ICU Handbook

The Intensive Care Unit

at the

Mid Yorkshire Hospitals NHS Trust

20th July 2010

1

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Contents

1 Administration 9

1.1 Staffing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

1.1.1 Clinical Lead . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

1.1.2 Consultant Medical Staff . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

1.1.3 Nursing Staff . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

1.1.4 SHO’s . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

1.2 Weekly Program . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

1.2.1 ICU Problem List Formulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

1.3 Orientation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

1.4 Patient admission policy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

1.4.1 Patient Triage: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

1.4.2 Elective admissions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

1.4.3 Refusal of patient admission . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

1.4.4 Management of patients in ICU . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

1.5 Patient discharge policy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

1.5.1 Discharge procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

1.5.2 Deaths in the ICU . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

1.6 Clinical duties in the Intensive Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

1.6.1 General comments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

1.6.2 Patient Admission . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

1.6.3 Doctor’s Documentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

1.6.4 Daily management issues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16

1.7 Clinical Duties Outside the Intensive Care Unit . . . . . . . . . . . . . . . . . . . . . . 17

1.7.1 Cardiac Arrest Calls . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

1.7.2 Trauma Call . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

1.7.3 Intra-hospital patient transport . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

1.7.4 Out of hospital transfers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

1.8 Infection Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

1.8.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

1.8.2 Hand Hygiene and Standard Precautions . . . . . . . . . . . . . . . . . . . . . 19

1.8.3 Isolation and transmission-based precautions . . . . . . . . . . . . . . . . . . 20

1.8.4 General Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

1.9 Information Technology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

1.10Consent in the Intensive Care Setting . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

1.10.1Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

1.10.2Consent by relatives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

1.10.3Consent at the Mid Yorks ICU . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

1.11Hospital Emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

1.11.1Fire and building emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

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2 Clinical Procedures 23

2.0.2 ICU Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23

2.0.3 Restricted procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23

2.1 Peripheral IV Catheter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23

2.2 Arterial Cannulae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24

2.3 Central Venous Cannulae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25

2.3.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25

2.3.2 Types of catheter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25

2.3.3 Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26

2.3.4 Site . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26

2.3.5 Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26

2.3.6 Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27

2.3.7 Documentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29

2.3.8 Line Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29

2.4 Pulmonary artery catheterisation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29

2.4.1 Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30

2.4.2 Insertion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30

2.4.3 Monitoring PA trace . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30

2.4.4 Measurement of pressures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30

2.4.5 Measurement of haemodynamics . . . . . . . . . . . . . . . . . . . . . . . . . . 30

2.5 Pleural Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30

2.5.1 Pleurocentesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

2.5.2 IntercostalCatheter / Underwater Sealed Drain . . . . . . . . . . . . . . . . . . 31

2.6 Endotracheal Intubation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32

2.6.1 Intubation Guideline . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33

2.7 Fibre-optic Bronchoscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37

2.8 Cricothyroidotomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37

2.9 Tracheostomy-Percutaneous . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

2.9.1 Patient selection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

2.9.2 Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

2.9.3 Contraindications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39

2.9.4 Timing of the procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40

2.9.5 Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40

2.9.6 Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

2.9.7 Post Insertion Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44

2.9.8 Decannulation of the Trachea . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44

2.10Nasojejunal tube insertion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45

2.11Intra-abdominal pressure manometry . . . . . . . . . . . . . . . . . . . . . . . . . . . 46

3 Drugs and Infusions 47

3.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47

3.1.1 Prescription practice . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47

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3.2 Cardiovascular Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48

3.2.1 Inotropes and Vasoactive drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . 48

3.2.2 Assess and correct hypovolaemia . . . . . . . . . . . . . . . . . . . . . . . . . 48

3.2.3 Instituting inotropic therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48

3.2.4 Vasopressors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 50

3.2.5 Steroid use in patients requiring vasopressors . . . . . . . . . . . . . . . . . . 51

3.3 Anti-hypertensive Agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52

3.4 Antiarrhythmic Drugs in Critical Care . . . . . . . . . . . . . . . . . . . . . . . . . . . 53

3.4.1 General Principles of Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . 53

3.4.2 Drug Therapy of Bradyarrhythmias . . . . . . . . . . . . . . . . . . . . . . . . . 54

3.4.3 Supraventricular Arrhythmias . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55

3.4.4 Ventricular Arrhythmias . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57

3.5 Respiratory Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58

3.5.1 Nebulised bronchodilators . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58

3.5.2 Parenteral Therapy in treatment of reversible obstructive airways disease . 59

3.6 Sedation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59

3.6.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59

3.6.2 Principles of Sedation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 60

3.6.3 Monitoring Sedation : Sedation Scoring . . . . . . . . . . . . . . . . . . . . . . 60

3.6.4 Sedation Holds/ Sedation Assessment . . . . . . . . . . . . . . . . . . . . . . . 61

3.6.5 Accumulation of Sedatives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62

3.6.6 Sedative Dependence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62

3.6.7 Sleep on the ICU . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63

3.6.8 Non-Pharmacological Methods of aiding sleep . . . . . . . . . . . . . . . . . . 63

3.6.9 Pharmacological Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63

3.6.10Management of Delirium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69

3.6.11References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73

3.7 Anticoagulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73

3.7.1 General Principles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73

3.7.2 Indications for the use of warfarin . . . . . . . . . . . . . . . . . . . . . . . . . 73

3.7.3 Indications for the use of heparin . . . . . . . . . . . . . . . . . . . . . . . . . . 74

3.7.4 Prophylactic use of heparin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74

3.7.5 Systemic anticoagulation using unfractionated heparin . . . . . . . . . . . . 75

3.7.6 Heparin Induced Thrombocytopaenia . . . . . . . . . . . . . . . . . . . . . . . 75

3.8 Endocrine Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76

3.8.1 Insulin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76

3.8.2 DDAVP . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77

3.8.3 Steroids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78

3.9 Renal Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79

3.9.1 General Principles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79

3.9.2 Diuretics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79

3.10Gastro-intestinal drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80

3.10.1Prophylaxis of gastric ”stress ulceration” . . . . . . . . . . . . . . . . . . . . . 80

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3.10.2Active GI Bleeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83

3.10.3Use of gastro-intestinal pro-kinetic agents . . . . . . . . . . . . . . . . . . . . 84

3.11ICU Antibiotic Guidelines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84

3.11.1Prologue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84

3.11.2Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84

3.11.3Principles of prescription . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84

4 Fluids and Electrolytes 85

4.1 Principles of Fluid Management in Intensive Care . . . . . . . . . . . . . . . . . . . . 85

4.1.1 Fluid charting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85

4.1.2 Assessment of fluid balance and hydration . . . . . . . . . . . . . . . . . . . . 86

4.1.3 Body Fluid and Electrolyte Physiology . . . . . . . . . . . . . . . . . . . . . . . 87

4.2 Electrolyte Abnormalities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87

4.2.1 Approach . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87

4.2.2 Hyponatraemia: Na+ < 130 mmol.L-1 . . . . . . . . . . . . . . . . . . . . . . . 88

4.2.3 Hypernatraemia: Na+ > 145 mmol.L-1 . . . . . . . . . . . . . . . . . . . . . . . 89

4.2.4 Hypokalaemia: K+ < 3.5 mmol.L-1 . . . . . . . . . . . . . . . . . . . . . . . . . 90

4.2.5 Hyperkalaemia: K+ > 5.0 mmolL-1 . . . . . . . . . . . . . . . . . . . . . . . . . 91

4.2.6 Hypophosphataemia: Serum Phosphate < 0.7 mmol.L-1 . . . . . . . . . . . . 92

4.3 Acid-Base Disturbances in the ICU . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93

4.3.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93

4.3.2 General principles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94

4.3.3 Metabolic Acidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 95

4.3.4 Metabolic Alkalosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96

4.3.5 Respiratory Acidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97

4.3.6 Respiratory Alkalosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97

4.4 Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98

4.4.1 Enteral Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98

4.4.2 Parenteral Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101

4.5 Blood and Blood Products . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102

4.5.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102

4.5.2 Blood transfusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102

4.5.3 Platelet transfusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102

4.5.4 Fresh Frozen Plasma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103

4.5.5 Cryoprecipitate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104

4.5.6 DIC . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104

4.5.7 Blood transfusion reaction guidelines . . . . . . . . . . . . . . . . . . . . . . . 105

5 Clinical Management 106

5.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106

5.2 Cardio-Pulmonary Resuscitation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106

5.2.1 Key Points in the management plan for an adult collapse . . . . . . . . . . . 106

5.2.2 Induced hypothermia following cardiac arrest . . . . . . . . . . . . . . . . . . 107

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5.3 Respiratory Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108

5.3.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108

5.3.2 Respiratory Failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108

5.3.3 Aetiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109

5.3.4 When Should I Consider Ventilating (± intubating) Patients? . . . . . . . . . . 109

5.3.5 Humidification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110

5.3.6 Mechanical Ventilation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110

5.3.7 Ventilator settings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112

5.3.8 Positive Pressure Ventilation and Hypotension . . . . . . . . . . . . . . . . . . 115

5.3.9 Supportive Therapies for Severe Hypoxia . . . . . . . . . . . . . . . . . . . . . 115

5.3.10Weaning from Mechanical ventilation . . . . . . . . . . . . . . . . . . . . . . . 119

5.3.11Ventilation in the prone position . . . . . . . . . . . . . . . . . . . . . . . . . . 122

5.3.12Non-invasive ventilation (NIPPV) . . . . . . . . . . . . . . . . . . . . . . . . . . 123

5.3.13Corticosteroids in ARDS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 124

5.4 Bibliography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 124

5.5 Aspects of Renal Failure in Intensive Care . . . . . . . . . . . . . . . . . . . . . . . . . 125

5.5.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125

5.5.2 Aetiology of renal failure in the ICU . . . . . . . . . . . . . . . . . . . . . . . . . 125

5.5.3 Assessment of renal function in a given patient . . . . . . . . . . . . . . . . . 126

5.5.4 Renal protective strategies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 126

5.5.5 Renal Replacement Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127

5.6 Neurosurgical Guidelines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130

5.6.1 Neurotrauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130

5.6.2 Status Epilepticus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 132

5.6.3 Subarachnoid haemorrhage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133

5.7 Microbiology Guidelines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 134

5.7.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 134

5.7.2 Glossary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135

5.7.3 Screening for sepsis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135

5.7.4 Investigation of Pneumonia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 136

5.7.5 Vascular Catheter Sepsis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137

5.7.6 Fungal infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138

5.8 Drug / Toxin Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139

5.8.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139

5.8.2 Admission to ICU . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139

5.8.3 Specific Overdoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140

5.9 Withdrawal of Treatment in the Intensive Care . . . . . . . . . . . . . . . . . . . . . . 140

5.9.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140

5.9.2 Principles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140

5.9.3 Deciding not to treat (or treat any further) . . . . . . . . . . . . . . . . . . . . 141

5.10Brain death and organ donation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141

5.10.1Declaration of brain death . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141

5.10.2Clinical certification of brain death . . . . . . . . . . . . . . . . . . . . . . . . . 142

6

Contents Contents

6 Appendices 144

6.1 Haemodynamic Principles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144

6.1.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144

6.1.2 Diagnosing hypotension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144

6.1.3 Is there any evidence of shock ? . . . . . . . . . . . . . . . . . . . . . . . . . . 144

6.1.4 Does this patient require more fluid resuscitation? . . . . . . . . . . . . . . . 145

6.2 The Pulmonary Artery Catheter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146

6.2.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146

6.3 The PiCCO-catheter / monitor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147

6.3.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147

6.3.2 Estimation of cardiac output . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148

6.4 Principles of ventilation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149

6.4.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149

6.4.2 Ventilatory strategies to provide total ventilatory support . . . . . . . . . . . 150

6.4.3 Objectives of mechanical ventilation . . . . . . . . . . . . . . . . . . . . . . . . 151

6.4.4 Other Ventilatory strategies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151

6.4.5 Ventilation Mechanics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 152

6.5 The Sedation - Agitation Score . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153

6.6 Classification of anti-arrhythmic drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . 154

6.6.1 Classification of Antiarrhythmic Drugs by Their Action . . . . . . . . . . . . . 154

6.7 Guidelines for the use of patient controlled anaesthesia (PCA) . . . . . . . . . . . . 155

6.7.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155

6.7.2 Acute Pain Service Standard Orders . . . . . . . . . . . . . . . . . . . . . . . . 155

6.7.3 Programmable Variables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 156

6.7.4 Standard Prescriptions for PCA . . . . . . . . . . . . . . . . . . . . . . . . . . . 157

7

Contents Contents

Foreword

Caring for patients in the intensive care setting is a challenging but potentially rewarding

experience. As we enter the intensive care environment each one of us brings a unique mix

of skills and knowledge. Inevitably though we must find a common ground on which to base

our management, without which optimal patient care and safety cannot be achieved. The

purpose of this document is not to provide definitive answers for each problem, nor is it meant

to be prescriptive in nature, but rather it describes a number of standardised approaches and

helpful guidelines to facilitate good patient care.

I must acknowledge that this guide has been heavily based on the one produced by the Inten-

sive Care Staff of The Waikato Hospital in New Zealand. In particular, my thanks to Dr John

Torrance and Dr David Gamble for their permission to use their manual as a template.

All those who access, use or disseminate these guidelines do so at your own risk. While you

are working in this unit, no matter what your level of experience, you will encounter situations

where you feel uncomfortable, confused or even scared. While this manual is intended to as-

sist you in caring for your patients, you should not be embarrassed to seek help from those

around you, including the Consultant Intensivist/Anaesthetist and senior nursing staff. You will

find references to articles which are useful further reading.

Rajiv Srinivasa

25th June 2008

8

1 ADMINISTRATION

Mid Yorkshire Hospitals Intensive Care Units

The Mid Yorkshire Hospitals NHS Trust is a 900 bed district general hospital and trauma centre

of the West Yorkshire region and serves a population area of 800 000. It is composed of 3

Hospitals: Pinderfields, Pontefract and Dewsbury.

The Intensive Care Units are located in Pinderfields General Hospital and Dewsbury District

Hospital with a total of 14 Level 3 and 8 Level 2 beds and admits over 1200 patients a year.

There are also 2 Level 3 beds on the Burns unit. Approximately 30% of the admissions are

surgical. The remainder are a mixture of trauma, medical and surgical patients. 76% of ad-

missions are ventilated. Our average APACHE II score is 16 and we have a crude mortality rate

of about 24%. The intensive care consultant staff also assist in the management of patients

in the High Dependency Unit which has 8 beds and admits over 1800 cases per year. The

intensive care also provides medical and nursing transport teams for inter-hospital transfers.

The ICUs are affiliated to the West Yorkshire Critical Care Network.

The Intensive Care unit senior medical staff consists of 13 consultants. The junior cover is

provided by senior SHO’s. We have a nursing staff of about 65 full time equivalents for ICU and

25 for HDU.

1 Administration

1.1 Staffing

1.1.1 Clinical Lead

Dr Rajdeep Singh Sandhu

1.1.2 Consultant Medical Staff

Dr Hugh O’Beirne

Dr Anthony Main

Dr Jaqueline Brook

Dr Paul Clarke

Dr Sameer Bhandari (Burns)

Dr Tendai Mbengaranwa (Burns)

Dr Jamie Yarwood (Burns)

Dr Christine Hildyard

Dr Rajiv Srinivasa

Dr Anne Thickett

Dr James Dodman

Dr Helen Buglass

9

1.2 Weekly Program 1 ADMINISTRATION

1.1.3 Nursing Staff

General Manager (Pain, Anaesthesia, Critical Care, Theatres) - Julie Clark

Head of Nursing PACCT – Steve Fenn

Nursing and Service Manager Critical Care – Carol Wood

Senior Sister/Charge Nurses

Suzanne Brompton (Practice Development)

Jean Garner

Jan Newton (Practice Development)

Mick Reynolds

Lindsay Shields

Jane Womersley

1.1.4 SHO’s

The junior medical team consists of SHO’s (or ST1/2’s) who have completed their ICU blocks

and are deemed competent in intensive management. They form the resident medical struc-

ture. They operate a day/night shift pattern, with the change over occurring at 0800 and 2000

hours (vide infra).

Non-intensive Care Trainees

Rotation through the intensive care is made by the following specialty based training pro-

grams: the Acute Care Common Stem for Emergency Medicine and Intensive Care. There is

also provision for a Foundation Year 1 placement (a 4 month rotation).

1.2 Weekly Program

08h00 morning handover (30 minutes) in the Handover Room.

08h30 Consultant led bedside ward round, followed by HDU

16h00 Afternoon ward round and HDU review. (30min-1hr)

20h00 Evening hand over between trainees and HDU review

All times other than that allocated above should involve patient review, not only in response

to request by nursing staff, but also in the interests of optimising patient care and progress.

1.2.1 ICU Problem List Formulation

The ICU runs a problem list sheet to help you keep up to date with each patient. It is the

responsibility of the night registrar to review the list for each patient, and to enter new data or

patients where appropriate. Towards the end of the night shift a report should be generated

10

1 ADMINISTRATION 1.3 Orientation

for each patient, and this is handed to the team following on. The generated document is then

filed in a folder as evidence of the handover. The process is repeated for the night handover.

1.3 Orientation

Prior to commencing an ICU on call rota, trainees will have to demonstrate competence in

managing patients on Intensive Care. The training block consists of 2 months on ICU as a

supernumary.

1.4 Patient admission policy

No patient may be accepted into the Intensive Care Unit without the knowledge and consent

of the ICU Consultant or the Consultant Anaesthetist on call (out of hours).

Resuscitation or admission must not be delayed where the presenting condition is imminently

life threatening unless specific advance directives exist. In general patients should be admit-

ted to the Intensive Care where it is perceived they would benefit in some way as a result.

Usually this means patients with actual or potential organ system failure, which appears re-

versible with the provision of intensive support measures.

1.4.1 Patient Triage:

A critical care Outreach team operates at the PGH and DDH sites between the hours of 0800

and 1800. Their primary function is to assist the ward nurses in managing and troubleshooting

critically ill patients on the ward. They will activate the MEWS pathway if required. The patients

at this point are still under the care of the primary medical team.

ICU admission criteria should select patients who are likely to benefit from ICU care. Patients

not admitted should fall into two categories, ”too well to benefit” and ”too sick to benefit”.

Defining substantial benefit is difficult, and no pre-admission model exists to predict outcome

in a given patient. Rather than listing arbitrary objective parameters, patients should be as-

signed to a prioritization model to determine appropriateness of admission.

• Priority 1: Critically ill patients in need of intensive treatment and monitoring that is not

available outside of the ICU. Generally these patients would have no limits placed on their

care.

• Priority 2: Patients that require intensive monitoring, and may need immediate interven-

tion. No therapeutic limits are generally stipulated for these patients.

• Priority 3: Unstable patients who are critically ill but have a reduced likelihood of recovery

because of underlying disease or the nature of their acute illness. If these patients are to

be treated in ICU/HDU, limits on therapeutic efforts may be set (such as not for intuba-

tion). Examples include patients with metastatic malignancy complicated by infection.

• Priority 4: These patients are generally not appropriate for ICU admission as their disease

is terminal or irreversible with imminent death (e.g. CVA). Included in this group would be

11

1.5 Patient discharge policy 1 ADMINISTRATION

those patients not expected to benefit from ICU based on the low risk of the intervention

that could not be administered in a non-ICU setting (e.g.: haemodynamically stable DKA,

or an ”awake” patient following an overdose). This category of patients also present

a conundrum and often are the subjects of passionate debates between the referring

physician and Intensivist as to what may reasonably be achieved on the ICU.

1.4.2 Elective admissions

Where possible, elective surgical admissions should be booked at least 48hrs in advance. A

book exists into which the names of prospective patients must be entered, following discus-

sion with the surgical team and anaesthetist responsible for that patient. Confirmation of bed

availability is the responsibility of the anaesthetist and surgeon, and must be confirmed by

prior to commencing the anaesthetic on the morning of surgery. Beds will be ring-fenced only

in exceptional circumstances. No elective surgical patient will be admitted into the ”last

bed” scenario.

1.4.3 Refusal of patient admission

When an outside team contacts the ICU with regard a patient, it is imperative that you clar-

ify whether this is a referral or a courtesy call. If it is a referral, then the patient should be

assessed (at the bedside if possible), and the problem discussed with the Consultant Anaes-

thetist/Intensivist at the earliest opportunity.

Where a patient is reviewed but not admitted to the Intensive Care Unit, the pertinent findings

and reason for refusal must be clearly communicated to the referring team and documented

in the notes. Where appropriate a directive regarding future review must be noted, and the

managing team encouraged to define resuscitation status.

This directive holds for patients placed in the HDU following ICU referral.

1.4.4 Management of patients in ICU

• Patients in Intensive Care Unit are managed primarily by the ICU staff. Visiting Teams

should be discouraged from charting drugs, fluids or other treatment directly.

• However, the opinion of all Specialists involved in the case is valued.

• The Consultant Intensivist must be kept fully informed of their opinion.

1.5 Patient discharge policy

1.5.1 Discharge procedure

All discharges must be approved by the Consultant Anaesthetist/Intensivist.

The parent team must accept care of the patient, this acceptance must be recognised at the

medical level, either through the SHO/Registrar, or in some cases to the Consultant directly.

12

1 ADMINISTRATION 1.5 Patient discharge policy

All other teams involved should be advised, including the pain team, dietician, special phar-

macy requirements (e.g.. TPN).

A careful plan for the immediate discharge period must be discussed with the accepting team,

and be clearly documented in the notes including:

• Limitation of treatment where appropriate

• Non-return orders

• Clear medical management plan, including charting of the following for the next 24hrs:

– Fluids

– Feeding

– Analgesia

Documentation to be completed prior to discharge:

• Entry in the ICU database - this also allows printing of the discharge note. The database

is designed in MS Access, and resides on the Desktop of the 2 computer terminals in the

ICU nurses station.

Nurses will not send patients to the ward without first checking with the on call SHO.

1.5.2 Deaths in the ICU

Withdrawal of therapy is a Consultant-only decision.

The Consultant Intensivist must be notified as soon as the patient has been examined and

certified dead, unless other specific arrangements exist (eg. where death is the expected

outcome and the issue of a death certificate issue has been discussed).

The ICU SHO must ensure:

• A death certificate has been completed or arranged (please speak to the General Office

regarding this)

• The parent team is notified

• Referring colleagues (including GP’s) are notified

• Post-mortem consent has been acquired from the family (if indicated)

• If appropriate, an End of Life Care Pathway must be completed and the process docu-

mented in the patient’s notes.

• If relevant and appropriate, initiate discussions with the Transplant Coordinator (via switch-

board at St James’ University Hospitals - 70020)

The Coroner must be notified as below:

• Every death that appears to have been without known cause, as a result of suicide, or

unnatural or violent death.

• Every death in respect of which no doctor has given (or is prepared to give) a death

certificate.

• Every death that occurs while the person concerned was undergoing a medical , surgical

or dental procedure, or some similar operation or procedure.

13

1.6 Clinical duties in the Intensive Care 1 ADMINISTRATION

• Death that appears to have been a result of any such operation or procedure.

• Death that occurred while the person was affected by an anaesthetic or that appears to

have been a result of the administration to the person of an anaesthetic.

• Death of any patient detained in an institution pursuant to an order.

• Death of any patient committed in a hospital under the Mental Health Act.

• The death of any inmate within the meaning of the Penal Institutions Act of 1954

• The death of any person in police custody, or in the custody of a security officer.

Where a death is referred to the coroner, no death certificate may be issued by the ICU doctor.

1.6 Clinical duties in the Intensive Care

1.6.1 General comments

Staff will always shoulder a major part of the burden of continuity. Continuity is central to

quality patient care and this expectation is not diminished with a decrease in working hours.

The responsibility for maintaining continuity and for effective communication both with other

unit staff and with outside teams rests largely with the SHO’s. Effective communication is a

basic medico-legal requirement.

There are guidelines covering the medical procedures and the administration of most of the

drugs used in the ICU. These guidelines are under constant review. The resident staff are

required to be familiar with these guidelines and to consult them when required. In addition,

any inconsistencies or discrepancies within them should be brought to the attention of the

consultant staff.

When asked by a team to review a patient, SHO’s are required to obtain a full history from

the patient and the patient notes, to perform a comprehensive examination of the patient

and to formulate a differential diagnosis. They should then have an outline of a suggested

investigation and treatment plan, to be presented to the Consultant Anaesthetist/Intensivist.

The final plan should be clearly documented in the patient record.

It is important that there is a complete transfer of information at the handover between shifts.

This will be facilitated by

• Comprehensive admission notes.

• Completion of a standardised daily update note.

• Daily review of all clinical laboratory tests, microbiology and radiological tests.

• An update of the problem list by the night on call SHO. This will contain details of the pre-

sentation, the provisional diagnosis, investigations, consults and opinions and unresolved

issues that require follow up.

The on call doctor should briefly familiarise themselves with the patients before the formal

ward rounds.

When leaving the unit for whatever reason, all doctors must inform their colleagues, or if out

of hours, the Charge Nurse. The ICU must never be left unattended unless in extraordinary

14

1 ADMINISTRATION 1.6 Clinical duties in the Intensive Care

circumstances and with the permission of the Consultant, and the knowledge of the Nurse in

charge.

1.6.2 Patient Admission

1.6.2.1 Primary patient survey

• A: Ensure patient protecting airway / GCS / cognition (is the patient receiving supplemen-

tary oxygen?)

• B: Breathing pattern acceptable, Pulse Oximetry acceptable

• C: Patient cardiovascularly stable, venous access acceptable

• Obtain hand over information from the referring doctor

1.6.2.2 Secondary survey

Examine patient thoroughly

• Notify Consultant Intensivist if this has not already been done.

• Document essential orders:

– Ventilation

– Sedation, analgesia, drugs and infusions

– Fluid therapy

• Discuss management with nursing staff and team: Everyone must be aware of the plan!

• Basic monitoring and procedures:

– ECG

– Invasive / non-invasive monitoring

• Urinary catheter / NG tube

• Basic Investigations (usually a full blood count, coagulation profile, ICU specific electrolyte

profile)

• Advanced Investigations; CT, ultrasound

• Case note documentation (see below)

• Inform and counsel relatives in general terms

1.6.3 Doctor’s Documentation

Doctors are responsible for documenting an admission note for all patients and a daily entry

into the clinical notes as well as:

• Discharge summary (includes database entry)

• Death certificate

15

1.6 Clinical duties in the Intensive Care 1 ADMINISTRATION

• Admission Note: a pro forma sheet should be used, documentation must include:

– Date / time

– Name/bleep of admitting doctor

– Reason for admission: primary and secondary

– Standard medical history including current medications

– Thorough examination findings

– Results of important investigations

– Assessment / severity / differential diagnosis

– Management plan

– Document notification of parent team and duty senior.

• Parent teams should be encouraged to write a short note (at least!) when they visit the

Unit.

1.6.3.1 Daily entry in clinical notes

• Use the Daily Notes pro forma page.

• Ensure each page is dated and labelled with the patients name and hospital number.

• Date / time / name of Senior ICU Doctor conducting the round.

• A: Mental state, GCS, airway.

• B: Ventilation, saturation (or PaO2), chest findings.

• C: Pulse / BP / peripheral perfusion / Precordial exam.

• Abdominal examination and description of feeding mode.

• Peripheries

• Assessment or Impression

• Plan

Additional notation must be made in the notes when:

• Invasive procedures are undertaken: please use the stickers when inserting central/arterial

lines.

• Important management decisions are made.

• Significant interaction is made with patient family.

1.6.4 Daily management issues

The daily handover ward round at 0800 is attended by the night on-call doctor, the incom-

ing day staff, the Consultant or senior Anaesthetist, Consultant Microbiologist and the Charge

Nurse (if not too busy).

The night doctor responsible will present a concise report of every patient. It is the responsi-

bility of the night registrar to review the list for each patient, and to enter new data or patients

16

1 ADMINISTRATION 1.7 Clinical Duties Outside the Intensive Care Unit

where appropriate. Towards the end of the night shift a report should be generated for each

patient, and this is handed to the team following on. The generated document is then filed in

a folder as evidence of the handover. The process is repeated for the night handover.

Important decisions regarding patient discharge and specialist investigations may be made

at this meeting and it is important that junior staff have a good understanding of the patient

status, including:

• Patient details and demographics

• Day of admission

• Diagnosis and major problems

• Relevant pre-morbid problems

• Progress and significant events

• Important results

• Plan for the next 24 hours

1.7 Clinical Duties Outside the Intensive Care Unit

1.7.1 Cardiac Arrest Calls

1.7.1.1 Indications Cardiac arrest calls may be called for the following:

• In-hospital cardiac arrest

• Collapse of unknown origin in the hospital environs

• Out of hospital arrest arriving in the A&E

The anaesthetic input for cardiac arrests is nominally the Acutes on call team. However, if the

Acutes team is otherwise occupied, the ICU doctor may attend provided the patients on ICU

are stable, and only after informing the Charge Nurse.

1.7.1.2 CPR (Cardio Pulmonary Resuscitation) We encourage the use of the UK Resus-

citation Council Guidelines for CPR http://www.resus.org.uk/pages/als.pdf. The anaesthetist

is responsible for securing the airway and establishing effective ventilation, whilst the Medi-

cal team should concern themselves with cardiac and general aspects. It would be expected

however that directing advanced life support be the responsibility of the most senior doctor

present.

Where CPR has been ”successful” but further active treatment may not be in the interests of

the patient, the decision to withdraw care must only made following consultation with senior

doctors involved - this will usually be the Anaesthetic and Specialty Consultants.

All involvement in an arrest call must be documented in the patient case notes.

1.7.2 Trauma Call

Again, the first responder for trauma calls is usually a member of the Acutes on call team.

However, should that team be busy, or in the event of a poly trauma, the ICU doctor may be

17

http://www.resus.org.uk/pages/als.pdf

1.8 Infection Control 1 ADMINISTRATION

called upon to assist.

Ensure that the ICU Charge Nurse and Consultant Intensivist are aware of where you are go-

ing, and communicate with the ICU team once the patient has been assessed and the likely

admission destination known.

1.7.3 Intra-hospital patient transport

No patient may be transported from the unit without the direction of the Senior Anaesthetist/Intensivist

on ICU or on call.

Medical escort is the rule if the patient is Level 2 or 3. In a minority of circumstances a nurse

escort may be sufficient, providing it is acceptable to the Senior Anaesthetist and the Charge

Nurse. It may not be appropriate for all ICU doctors to undertake prolonged transport, or

transport to unfamiliar areas. Always ask the senior Anaesthetist if you are unsure.

Prior to embarking on an escort all equipment, oxygen supply and emergency drugs must be

checked.

All problems encountered on the escort must be recorded in the notes, and an incident form

completed if appropriate.

If a test is deemed urgent the medical escort should endeavour to get an informal report

written in the notes, failing which they should request formal review and notification to the

unit as soon as possible.

1.7.4 Out of hospital transfers

Should a patient require Level 3 care in the absence of bed availability, the transfer process

must be initiated by the parent team with assistance from the ICU team. The first point of

contact must be the West Yorkshire Critical Care Network Bed Bureau.

The doctor who accompanies the patient must be competent to transfer the ventilated patient,

and to manage a compromised airway during transfer. The doctor must also have attended a

Transfer Training course.

Transfer of a Level 2 patient is fraught with danger. It may be safer to intubate/ventilate

prior to transfer, especially if there is respiratory compromise. Discuss with the Consultant

Anaesthetist/Intensivists at both ends (i.e. Mid Yorks and the receiving ICU/HDU).

1.8 Infection Control

1.8.1 Introduction

Patients requiring intensive care are highly susceptible to infection due to immunosuppressive

effects of drugs and disease, the use of invasive monitoring techniques and the severity of the

underlying illness requiring admission. The use of broad-spectrum antibiotics may predispose

to infection with resistant organisms.

18

1 ADMINISTRATION 1.8 Infection Control

Nosocomial infection delays patient discharge from the intensive care unit (ICU) and con-

tributes significantly to morbidity. The prevalence of hospital-acquired (nosocomial) infection

in the ICU can be considerably higher than other clinical areas of the hospital.

Significant risk factors for infection include:

• mechanical ventilation

• prolonged length of stay

• trauma or burns

• intravascular catheterisation

• urinary catheterisation

• prior antibiotic use

The four most common nosocomial infections seen in ICU are:

• Pneumonia

• urinary tract

• intra-vascular catheter-related bacteraemia

• surgical wound infection

All ICU staff are responsible for ensuring good infection control policies are adhered to, in

particular good hand hygiene practice. In keeping with Trust Infection Control policies, you are

required to ensure you are ”bare below the elbows”, and to hand wash with alcohol gel before

and after every patient contact.

Skin preparation for invasive procedures (CVP catheters, VasCath, ICD tracheostomy) must be

with the prefilled 2% chlorhexidine/alcohol swabs. Please ensure you adopt suitable barrier

protection (gowns, masks, gloves).

1.8.2 Hand Hygiene and Standard Precautions

Hand washing and hand disinfection remain the most important measures in the prevention

of cross infection. Hands should be washed before and after contact with every patient and

after manipulation of the patient environment, especially after contact with a patients with C.

difficile infection or if the hands are soiled. Either use a 15-second handwash with soap and

water, or alternatively the waterless hand gel may be used if hands are not visibly soiled.

A longer handwash with antibacterial soap is required prior to any major invasive procedures

such as insertion of central venous catheter.

In addition to hand hygiene standard precautions are used for all patients:

• Wear gloves for all contact with blood and body fluids including dressings and wounds.

Gloves must be changed and discarded between patients. Hands must be decontami-

nated after the removal of gloves.

• Wear a disposable plastic apron or fluid-resistant gown to protect the skin and clothing

for procedures likely to generate splash or cause soiling.

• Wear a mask and eye protection to protect mucous membranes of the eyes, nose and

mouth during procedures likely to generate splash or cause soiling.

19

1.8 Infection Control 1 ADMINISTRATION

• Ensure patient-care equipment is cleaned and disinfected appropriately between patient

use.

• Staff who generate a sharp product (e.g.: needle or blade) are responsible for its safe

disposal into an approved puncture resistant sharps container.

1.8.3 Isolation and transmission-based precautions

In addition to standard precautions, isolation and appropriate transmission-based precautions

are to be used with the following:

Multi-resistant organisms (MRO) Patients infected or colonised with the following MRO’s

require isolation and contact precautions (gloves and gown/apron for direct patient care):

• Methicillin Resistant Staph. Aureus (MRSA)

• Vancomycin Resistant Enterococcus (VRE)

• Extended Spectrum Beta Lactamase (ESBL) producing enterobacters

• Multi-resistant gram negative organisms

Meningococcal disease - proven or suspected

• Patients require isolation and droplet precautions (surgical mask within 1 meter of the

patient) until 24hrs of completed antibiotic treatment.

Miscellaneous

• Burns patients require isolation and contact precautions

• Febrile neutropaenic patients require isolation and contact precautions

• High risk immunosuppressed patients require isolation and contact precautions

• Respiratory syncytial virus require contact precautions

1.8.4 General Measures

The ICU should be kept tidy and uncluttered. Equipment not in use should be stored in a clean

area.

Movement of people through the unit should be kept to a minimum. This applies equally to

colleagues and relatives.

All visitors are to be encouraged to wash their hands before and after visiting the patient.

Staff with communicable diseases should take sick leave. If suffering from D&V, ensure at

least 48 hours have elapsed since the last symptom before returning to work.use

20

1 ADMINISTRATION 1.9 Information Technology

1.9 Information Technology

There are numerous terminals in the intensive care unit. All computers are networked to the

Intranet, which also functions as a gateway to the Internet. The computers are logged in as a

generic ICU-user, with permissions to view Pathology results.

The intranet allows access to all inpatients in the hospital. The ward administrator section

allows you to view the pathology results of patients on the ICU and HDU.

All imaging is now film-less, and may only be viewed on the computer terminals. You should

have completed a tutorial, and received a smartcard following this in order to view the images.

You will be given a separate login by the IT department. This allows you access to your own

account. You will have an e-mail address with access to the Outlook mail program via a link on

the Intranet front page.

The local area network provides access to the Internet. This is controlled and closely monitored

by the IT department. Access to the Internet requires personal login, and all websites visited

may be monitored. Please ensure you close the browser window when you have finished. This

prevents fraudulent and unauthorised access to websites in your name.

1.10 Consent in the Intensive Care Setting

1.10.1 Introduction

A competent patient may give or withhold consent for any medical treatment.

Unfortunately, patients in ICU often cannot have their competency established with certainty.

When a patient cannot give consent in an emergency, in the absence of convincing evidence to

the contrary (e.g. presence of a person with enduring power of attorney who can categorically

state that the person does not wish to receive the treatment in question, or applicable advance

directive) consent to treatment is implied.

1.10.2 Consent by relatives

Relatives or friends cannot give or withhold consent for the performance of a medical treat-

ment.

However, it is strongly recommended the treating doctor takes the families views into account

in deciding whether to perform a particular treatment.

1.10.3 Consent at the Mid Yorks ICU

The consent form and the attendant process can record the attempt to take the families views

into account. In any case, completion of the appropriate form is necessary to comply with

hospital policy in certain procedures.

A written record of informed consent is unnecessary for the vast majority of bedside proce-

dures in ICU.

21

1.11 Hospital Emergencies 1 ADMINISTRATION

When it is necessary to obtain consent for a particular procedure to be performed on an ICU

patient, it is appropriate for ICU medical staff to play a role in this process. That role may not

necessarily mean obtaining consent directly, but may mean ensuring that the staff performing

a procedure make the requisite information available to the ICU doctor to enable them to get

consent, or in many cases obtain consent themselves.

1.11 Hospital Emergencies

• Mass casualty

• Communications or utility failure

• Cardiac Arrest

• Earthquake

• Fire (or smoke smell)

• Hazardous substance spill

• Personal safety threat

• Threat from telephone, letter or suspicious object

• Bomb or arson

• Radiation spill

Dialling 4444 and thereby contacting the switchboard will in most circumstances allow you to

initiate an emergency response that is appropriate to the threat.

1.11.1 Fire and building emergencies

• Attend formal fire training sessions

• Become familiar with location of fire exits

• Assess medical condition of persons in an emergency area, and the likely effects of evac-

uation on them.

• Follow instructions of trained accredited staff.

22

2 CLINICAL PROCEDURES

2 Clinical Procedures

Introduction It is inevitable that during your stay in the Intensive Care Unit you will be

exposed to a number of procedures with which you are not familiar. All staff are encouraged

to become proficient with routine procedures:

2.0.2 ICU Procedures

• Endotracheal intubation

• Peripheral venous catheterisation

• Central venous catheterisation

• Arterial cannulation / PiCCO insertion

• Pulmonary artery catheterisation

• Urinary catheterisation

• Lumbar puncture

• Intercostal drain insertion or pleurocentesis

• Naso-gastric / jejunal tube insertion

Patient consent should be obtained if appropriate as outlined elsewhere in these guidelines.

No member of staff is permitted to attempt a procedure without adequate training. Staff with

previous experience must affirm this with the Senior

Anaesthetist or Consultant Intensivist prior to attempting unsupervised procedures. All junior

staff should be supervised for their first 2 arterial cannulations and at least 5 central venous

access procedures prior to performing these procedures unsupervised.

No matter how experienced you are, repeated unsuccessful vascular punctures are unaccept-

able and a more experienced member of staff should be asked to help.

All procedures must be annotated in the case notes, including the indication / complications

for the procedures.

2.0.3 Restricted procedures

Specialised procedures should only be performed by the Senior Anaesthetist or Consultant

Intensivist. They may not be attempted prior to discussion with the

Consultant.

• Percutaneous tracheostomy

• Fibreoptic bronchoscopy

2.1 Peripheral IV Catheter

2.1.0.1 Indications

23

2.2 Arterial Cannulae 2 CLINICAL PROCEDURES

• Initial IVI access for resuscitation

• Stable or convalescent patients where more invasive access is not warranted.

2.1.0.2 Management All lines placed in situations where aseptic technique was not fol-

lowed must be removed (eg. Placement by emergency staff at the roadside). Peripheral lines

must be removed after 72 hours (or before, if not required), and replaced if there is a continu-

ing need for peripheral IV access.

Acceptable aseptic technique must be followed including:

• Thorough hand-washing

• Skin preparation with alcohol swab

• Occlusive but transparent dressing

• All lines should be removed if not being actively used, or if > 2 days old. An exception

may be made where venous access is challenging (eg. IV drug abusers).

2.1.0.3 Complications

• Infection

• Thrombosis

• Extravasation

2.2 Arterial Cannulae

2.2.0.4 Indications

• Invasive measurement of systemic blood pressure in ICU or during patient transport /

retrieval.

• Multiple blood gas sampling and laboratory analysis

2.2.0.5 Site and catheter choice

• 1st choice: Radial artery

• 2nd choice: Femoral.

Site of choice for PiCCO catheter monitoring (Pulsiocath 5F 16 cm catheter) is generally the

femoral artery.

The axillary artery may be considered after consultation with the Consultant (usually 4F catheter).

The Brachial artery is an end-artery, and catheterisation has been considered a risk for distal

arterial complication (although this has also been disputed). It may be used if there are no

alternatives.

24

2 CLINICAL PROCEDURES 2.3 Central Venous Cannulae

2.2.0.6 Technique

• All catheters should be inserted with full sterile technique (gown, sterile gloves, topical

antiseptic)

• The arterial line must be firmly anchored (suturing is not recommended)

• The insertion site and all connectors must be visible through the applied dressing.


• Infection

• Thrombosis

• Digital Ischaemia

• Vessel trauma and fistula formation.

NB: Interpretation of arterial waveforms requires familiarity with normal arterial waveforms

as well as trace damping, amplification and arterial harmonics. If you are unsure as to the

reliability of a trace / reading you must seek assistance before removing the arterial cannula.

2.3 Central Venous Cannulae

2.3.1 Introduction

The use of CVCs is associated with adverse effects both hazardous to patients and expensive

to treat. More than 15% of patients with CVCs have some complication from them:

Mechanical 5-19%

Infectious 5-26%use

Thrombotic 2-26%

The first 5 CVC insertions performed by the trainee should be performed under direct su-

pervision and then (if the competency is signed off) the trainee may insert the lines without

supervision, on the understanding that when a difficult catheterisation is anticipated, they will

ask for senior assistance.

Failure to insert the catheter after 3 attempts, should prompt the clinician to seek help rather

than continue to attempt the procedure, as the incidence of mechanical complications after

three or more insertion attempts is six times the rate after one attempt.

2.3.2 Types of catheter

2.3.2.1 Anti-microbial-Impregnated Catheters These catheters have been shown to

lower the rate of catheter-related bloodstream infections.

Consider the use of an Anti-microbial-Impregnated CVC for adult patients who require short-

term (1-3 weeks) CVC and who are at high risk for catheter-related blood stream infection

(CR-BSI)

It may be appropriate to use this type of CVP in selected patients, ie those with neutropaenic

sepsis.

25

2.3 Central Venous Cannulae 2 CLINICAL PROCEDURES

2.3.2.2 Single-lumen and Multi-lumen catheters The number of lumina does not di-

rectly affect the rate of catheter-related complications, so the choice of either single- or multi-

lumen catheter should be dictated by clinical need.

2.3.3 Indications

2.3.3.1 Monitoring haemodynamic variables

• Fluid administration (particularly if large volumes of fluids or blood products are required)

• Infusions of

– TPN

– Inotropes

– Hypertonic solutions

– Irritant solutions

– Chemotherapy

– Potassium solutions

• For haemofiltration or haemodiafiltration

2.3.4 Site

• Subclavian

• Internal Jugular

• Femoral

Internal jugular catheterisation can be difficult in morbidly obese patients, although with ultra-

sound may be made easier.

Subclavian venous catheterisation should be avoided in patients with severe hypoxaemia, as

the risks and complications of pneumothorax and haemothorax are greater than with internal

jugular approach.

Femoral catheterisation should be avoided in patients with grossly contaminated inguinal re-

gions, as the risk of development of catheter-related infections is increased.

If central venous access is needed rapidly in the shocked patient, the femoral approach may

be the fastest technique and used for the initial resuscitation.

2.3.5 Technique

• Asepsis

– Full scrub

– Sterile gown

– Sterile gloves

26

2 CLINICAL PROCEDURES 2.3 Central Venous Cannulae

– Large sterile drape

• Skin decontamination

– Alcoholic chlorhexidine gluconate for skin

– Allow to dry before cannulation

• Use Seldinger technique to access vein

NICE guidance on use of ultrasound for placing CVCs

1.1 Two-dimensional (2-D) imaging ultrasound guidance is recommended as the

preferred method for insertion of central venous catheters (CVCs) into the

internal jugular vein (IJV) in adults and children in elective situations.

1.2 The use of two-dimensional (2-D) imaging ultrasound guidance should be

considered in most clinical circumstances where CVC insertion is necessary

either electively or in an emergency situation.

1.3 It is recommended that all those involved in placing CVCs using two di-

mensional (2-D) imaging ultrasound guidance should undertake appropri-

ate training to achieve competence.

1.4 Audio-guided Doppler ultrasound guidance is not recommended for CVC in-

sertion.

• Flush all parts of catheter with heplock prior to insertion

• Trendelenburg tilt for internal jugular or subclavian routes

• Use blade to ensure insertion site on skin will allow passage of dilator and catheter

• Insert catheter to estimated appropriate depth, according to insertion site and patient

anatomy

• Aspirate from each port. Easy aspiration of blood should be possible from each line, and

then flush each line with heplock, and the the catheter ports must then be closed with

caps.

• Secure the catheter to the skin by suturing the holder on the catheter to the skin (not the

clip for adjusting the catheter position)

• Apply a sterile semi-permeable polyurethane dressing to the catheter insertion site eg

Tegaderm. If the insertion site is bleeding or oozing, a sterile gauze dressing may be

used.

• Chest X-Ray when the catheter is secure, to look for pneumothorax and assess catheter

tip position

2.3.6 Complications

• At Insertion

27

2.3 Central Venous Cannulae 2 CLINICAL PROCEDURES

– Arterial puncture

– Pneumothorax

– Neural injury

– Guidewire induced arrhythmia

– Air embolus

• During catheter presence

– Infection

– Thrombosis

– Embolism

– Pulmonary infarct or PA rupture (with PAF catheter)

– Arterio-venous fistula

2.3.6.1 Mechanical complications Arterial puncture, haematoma and pneumothorax are

the commonest

Frequency of mechanical complications, according to approach :

Internal Jugular Subclavian Femoral

Arterial Punture 6.3-9.4% 3.1-4.9% 9-15%

Haematoma <0.1-2.2% 1.2-2.1% 3.8-4.4%

Haemothorax NA 0.4-0.6% NA

Pneumothorax <0.1-0.2% 1.5-3.1% NA

Total 6.3-11.8% 6.2-10.7% 12.8-19.4%

2.3.6.2 Infectious complications The available evidence is that subclavian catheterisa-

tion is less likely to result in catheter-related infection than use of the internal jugular or femoral

approach.

Data from a systematic review of complications of CVS has shown the rate of bloodstream

infections may be as high as 8.6% with jugular access, and 4.0% with subclavian access.

2.3.6.3 Thrombotic complications The risk of catheter-related thrombosis varies accord-

ing to site of catheter.

Approximate figures are:

21% of patients with femoral catheters

2% of patients with subclavian venous catheters

8% of patients with internal jugular

The clinical importance of catheter-related thrombosis remains undefined, although all throm-

boses have the potential to embolize.

28

2 CLINICAL PROCEDURES 2.4 Pulmonary artery catheterisation

2.3.7 Documentation

Documentation of the procedure undertaken should appear in the patient case notes using

a procedure sticker. ALL complications or difficulties encountered, should be documented

beneath the sticker.

2.3.8 Line Management

• Routine line replacement is not necessary

• The practice of changing the central line over a guidewire should be avoided unless it is

the only option

• Lines should be removed

– as soon as a clinical indication no longer exists

– if patient shows signs of unexplained systemic infection

– if insertion site appears infected or blood cultures suggest infection with a skin or-

ganism (eg staph epidermidis). The catheter-tip should be sent to microbiology for

culture and sensitivities

• If suspecting catheter-related bloodstream infection, a wound swab should be taken from

the catheter insertion site, and blood should cultured from the suspect line and from a

sample taken from a peripheral stab.

References

1. NICE Technology Appraisal Guidance No.49, ultrasound locating devices for placing central venous

catheters - September 2002. Moved to static list of guidance November 2005 following period of

consultation.

2. Guidelines for the prevention of intravascular catheter-related infections. Centers for Disease Con-

trol and Prevention. MMWR 2002;51(NoRR-10):1-33

3. Preventing Complications of Central Venous Catheterization. McGee DC, Gould MK The New England

Journal of Medicine. 2003 Vol 348:1123-1133

4. National Evidence-based guidelines for preventing healthcare associated infections in NHS hospi-

tals in England. London. Richard Wells Research Centre, Thames Valley University, 2006 epic2.

5. Complications of central venous catheters: Internal jugular versus subclavian access – A systematic

review. Ruesch S, Walder B, Tramer M. Critical Care Medicine 30(2):454-460, February 2002

2.4 Pulmonary artery catheterisation

The PA Catheter is not a resuscitation tool and should only be inserted in a controlled environ-

ment after discussion with the senior Anaesthetist.

Dwindling use of the PA catheter has resulted in a loss of familiarity with its use. Junior medical

staff and nursing staff not familiar with this instrument should not manipulate / advance /

inflate the PA catheter balloon.

29

2.5 Pleural Procedures 2 CLINICAL PROCEDURES

2.4.1 Indications

• Haemodynamic measurement: (cardiac output, stroke volume, systemic vascular resis-

tance)

• Measurement of right heart pressures (pulmonary hypertension, pulmonary embolus)

• Estimation of preload to the left ventricle - controversial.

2.4.2 Insertion

PA Catheter insertion is technically difficult and requires a working knowledge of right heart

pressures and waveforms. They should only be inserted by accredited staff.

See appendix on pulmonary artery catheterisation

2.4.3 Monitoring PA trace

An adequate tracing should be visible on the monitor at all times. A damped tracing may

represent a wedged catheter, clot at the catheter tip or inappropriate equipment set-up (wrong

monitor calibration, faulty pressure transducer).

• Flush the distal lumen generously (using closed mechanism)

• Withdraw catheter until a trace is present. NB: Never withdraw the catheter with an

inflated ballon.

2.4.4 Measurement of pressures

• Pressure should be referenced to the mid-axillary line

• The true wedge pressure is measured at end-expiration

PEEP may influence wedge pressures, however this is not a factor at PEEP < 10 mmHg, and

patients should not be disconnected from the ventilator to measure PAC pressures.

2.4.5 Measurement of haemodynamics

Cardiac output measurement should only be attempted by staff familiar with the use of PA

Catheters.

10 ml 5% dextrose at room temperature is rapidly injected into the appropriate lumen.

This is usually repeated three times, with results varying > 10% from average discarded.

2.5 Pleural Procedures

As with all invasive procedures this should not be attempted by inexperienced staff.

30

2 CLINICAL PROCEDURES 2.5 Pleural Procedures

Indications for accessing pleural space

• Pneumothorax (± temporising procedure if under tension)

• Haemothorax

• Symptomatic or infected pleural effusion

Needle Thoracostomy for Tension Pneumothorax

• 16G cannula placed in mid clavicular line, 2nd intercostal space

• Proceed to formal intercostal drain insertion.

2.5.1 Pleurocentesis

2.5.1.1 Indications

• Diagnostic procedure: Exudate vs Transudate, or to exclude infected collection or malig-

nancy.

• Therapeutic procedure: Drainage of an infected collection requires an underwater sealed

drain. It is not appropriate to perform ”one-off” drainage. The practice of draining

non-infected pleural collections by pleurocentesis is controversial and should not be per-

formed without direction by the senior Anaesthetist.

2.5.1.2 Technique Local anaesthesia and sterile technique.

Unless the fluid collection is grossly detectable on clinical examination and on plain radiology,

pleurocentesis should be ultrasound directed.

Investigation of pleurocentesis fluid Aspirated fluid should , at the very least, be sub-

mitted for pH or analysed in ICU blood gas analyser (pH < 7.20 = empyema, 7.20-7.25 =

equivocal)

2.5.2 IntercostalCatheter / Underwater Sealed Drain

2.5.2.1 Insertion

• Local Anaesthesia is mandatory in awake patients, and should be used in sedated patients

• Strict aseptic technique

• 28F catheter inserted into 3-4th intercostal space, mid-axillary line, using blunt dissection

as described and recommended in the ATLS guidelines.

• The Catheter must be guided through the ribs without use of sharp instruments (prefer-

ably finger). Trochar aided insertion techniques are not acceptable.

31

2.6 Endotracheal Intubation 2 CLINICAL PROCEDURES

2.5.2.2 Maintenance Drains placed in un-sterile environs should be removed as soon as

possible.

Drains should remain in-situ until radiological resolution has occurred and there is no further

bubbling or drainage of significance ( < 150 ml.24-hr)

In patients at risk (due previous large air leak, or multiple rib fractures) who remain on positive

pressure ventilation, the drain may be clamped for 4hrs prior to removal as a safety measure,

although this is by no means universally practiced.

Drains placed electively in theatre are the responsibility of the surgeon


• Incorrect placement

• Pulmonary laceration

• Pneumothorax

• Bleeding as a result traumatic drain insertion (intercostal or, lateral thoracic artery, lung

etc)

• Microbial innocculation

2.6 Endotracheal Intubation

2.6.0.4 Introduction Endotracheal intubation in ICU patients is a high risk but vital emer-

gency procedure in patients who often have limited reserve, are difficult to position and may

have a difficult airway.

All staff should familiarise themselves with the intubation trolley and equipment.

Whenever possible make sure that you have capable and trained staff to assist you. If you

are alone or inexperienced always call for assistance. If the senior anaesthetist cannot be

reached for some reason, or is detained, then assistance should be sought from an anaesthetic

colleague.

Rapid sequence induction is the rule in ICU patients unless previously discussed with senior

medical staff.

2.6.0.5 Indications

• Institution of mechanical ventilation

– To maintain an airway

– Upper airway obstruction or threat

– Control of arterial carbon dioxide content (eg. in the setting of traumatic brain injury)

• Patient transportation

• To protect an airway

– Patients at risk of aspiration

32

2 CLINICAL PROCEDURES 2.6 Endotracheal Intubation

– Altered conscious state

– Tracheal toilet

2.6.0.6 Techniques Orotracheal intubation is the rule.

Blind nasal awake intubation, or fibreoptic awake intubation, may be indicated in selected

patients with cervical spine injury, limited mouth opening or oro-facial surgery / trauma. These

techniques should only be undertaken by staff with current experience of these techniques,

and only after discussion with and the presence of the Consultant Intensivist.

2.6.0.7 Standard endotracheal tube choice All patients in the Intensive Care Unit should

be intubated with a low pressure high volume PVC tube (eg Portex blue line oral/nasal tube)

2.6.0.8 Non-standard tubes Patients returning from theatre (or transported from another

centre) may have a different ET tube (eg. armoured ETT) in situ. Where there is no good

reason for this to remain it should be changed to the standard ETT if it is anticipated that the

patient will require intubation > 48 hrs, and would not be exposed to significant risk during the

ETT change.

2.6.1 Intubation Guideline

2.6.1.1 Personnel

• Skilled assistance is mandatory, where possible a team of 4 is required.

• ”Intubator” who controls and co-ordinates the procedure.

• ”Drug administration”

• A person to apply in-line traction where the stability of the cervical spine is unclear.

• ”Cricoid Pressure”: Cricoid pressure is recommended in all emergency situations and

should be applied at the commencement of induction. Cricoid pressure may distort the

larynx so that intubation is made more difficult. It should be modified at the discretion of

the intubator, and requires an understanding of the procedure.

2.6.1.2 Preparation

• Secure adequate IVI access

• Check all equipment prior to intubation:

– Adequate lighting

– Selection of oropharyngeal airways

– Working suction with Yankauer attachment

– AMBU bag assembly and appropriate mask

– 100% oxygen with flow capability > 15 l/min

33


– 2 working laryngoscopes with appropriate choice of blade

– Magill forceps

– Malleable introducer and gum-elastic bougie

– 2 × ETT: estimated patient size and one smaller size. (Female = 7-8 mm, Male = 8-9

mm)

– A selection of laryngeal masks

– Emergency cricothyrotomy kit: (#15 scalpel and 6.0mm cuffed ETT)

• Ensure adequate monitoring

– Pulse oximetry

– Reliable blood pressure monitoring (eg. invasive if necessary)

– ECG telemetery

Difficult intubationKit A ”difficult intubation” kit can be found on the side of the intubation

trolley. This contains:

• An intubating LMA

• McCoy laryngoscopes

• Light wands

• Emergency cricothyrotomy kit

• Jet ventilation system

2.6.1.3 Drugs

Induction agent

• eg. Thiopentone, Fentanyl, Ketamine, Midazolam

Muscle relaxant

• Suxamethonium 1-2 mg/kg

• Consider Rocuronium 1-2 mg/kg if Suxemethonium contra-indicated ie:

– Burns patients > 48 hrs post injury

– Spinal injury patients where spasticity is present

– Chronic neuromuscular disease (Myasthenia Gravis, GBS)

– Hyperkalaemic states

Miscellaneous

• Atropine 0.6-1.2 mg

• Adrenaline 10 ml of 1:10 000 solution.

• Metaraminol 0.5 mg/ml (usually in 10 ml)

34

2 CLINICAL PROCEDURES 2.6 Endotracheal Intubation

2.6.1.4 Procedure: Rapid sequence induction and orotracheal intubation

• Pre-oxygenate for 3-4 minutes with 100% oxygen. Patients receiving non-invasive venti-

lation should continue on this form of ventilation until the point of induction, and a PEEP

valve applied to the AMBU-bag mask assembly.

• Administer induction agent and suxamethonium

• Apply cricoid pressure

• Intubation under direct visualisation

• Inflate ETT cuff until there is no air leak during ventilation

• Confirm ETT placement with capnograph and chest auscultation with manual ventilation.

• Release cricoid pressure

• Secure ETT at correct length (Female = 19-21cm at incisors, Males = 21-23 cm at incisors)

• Do not cut ETT at less than 26 cm (if at all).

• Connect patient to ventilator

• Ensure adequate sedation and analgesia to cover period of muscle relaxant and continue

as indicated by clinical scenario.

• Insert naso-/-orogastric tube or naso-jejunal tube if not already present.

A follow-up CXR should be performed as soon as convenient.

2.6.1.5 Maintenance of endotracheal tubes

Tapes ETT are generally secured with white tape.

Tapes are changed daily or PRN by nursing staff.

In certain circumstances personalised ETT security may be required.

Cuff integrity Sufficient air should be placed into the cuff to prevent an air leak, as assessed

by auscultating over the trachea.

ETT manometry is not routinely required, and may be misleading as the correlation with mu-

cosal pressure is unreliable.

Persistent cuff leakage Any ETT that constantly requires additional air instilled into the

cuff should be reviewed for:

• Herniation above the cords

• Cuff damage (rare)

• Malfunctioning pilot tube valve (which can be excluded by placing distal pilot tube into

container of water and observing for bubbling)

35


Airway suctioning Airway suction may be performed every 2-3 hrs prn

Routine suctioning should be avoided where:

• it requires disconnection of PEEP (open suction system)

• may exacerbate the patients condition (asthma, reactive Intra-cranial pressure, florid

pulmonary oedema).

2.6.1.6 Endotracheal tube change

Equipment and assistance The procedure / setup is the same as for intubation de novo

Ensure patient is adequately oxygenated (Saturation 98-100%). An FiO2 of 1.0 may be exces-

sive and promote atelectasis.

Ensure adequate anaesthesia and muscle relaxation

Procedure Perform direct laryngoscopy:

If a good view of the larynx and vocal cords is obtained then proceed to manual exchange of

ETT with application of cricoid pressure, or proceed as below using gum-elastic bougie.

If direct laryngoscopy reveals abnormal or swollen anatomy, or only partial view of anatomy,

then proceed as follows:

• Place gum elastic or ventilating bougie through the ETT and insert to a length correspond-

ing to a few cm distal to the end of the ETT.

• With an assistant stabilising the bougie, and applying cricoid pressure, remove faulty ETT

under direct laryngoscopy, while maintaining bougie in the same position.

• Confirm the bougie is still in place through cords once ETT removed, and then replace

new ETT over the top of the bougie apparatus.

• If the ETT does not progress smoothly through the cords, rotate 90 deg anti-clockwise and

attempt again (ie. realign beveled edge of ETT along upper border of bougie)

• Check position of ETT and secure as for de novo intubation procedure.

2.6.1.7 Extubation guideline Ensure adequate assistance, monitoring and equipment as

for intubation

Extubation should generally not be performed overnight, or when the responsibility to re-

intubate might fall on a less experienced staff member.

Patients may be extubated if this action is part of an established care plan or algorithm (eg.

cardiothoracic), or at the direction of the duty specialist.

No patient should be extubated without medical staff being aware and available to assist.

36

2 CLINICAL PROCEDURES 2.7 Fibre-optic Bronchoscopy

Patient Selection For a more extensive description see section on mechanical ventilation

The patient must be awake enough to maintain their own airway.

Any threat to airway patency as a result of surgery or injury may require consultation with the

co-managing team (ENT/Plastic surgery/MaxFac) prior to extubation.

Patient should demonstrate adequate pulmonary reserve. There are a number of ways of

assessing pulmonary reserve although none is perfect:

• Resp rate < 30

• FVC > 15 ml.kg-1

• Pa02 / FiO2 ratio > 200

• Resp rate / tidal volume 1 min after disconnection from ventilator (use T-piece )

The last method has the best predictive value.

All patients should receive supplemental oxygen post extubation.

2.7 Fibre-optic Bronchoscopy

Policy Only to be performed by adequately trained staff, after authorisation by the Consul-

tant Intensivist.

2.7.0.8 Indications

• Persistent lobar collapse that is refractory to normal bronchial toilet

• Foreign body in airway

• Diagnostic broncho-alveolar lavage (BAL): This is not routinely performed to diagnose

nosocomial infection, but may be employed in selected circumstances.

• Fibre-optic intubation

2.8 Cricothyroidotomy

Policy The recommended procedure for urgent surgical airway access (not percutaneous

tracheostomy).

When urgent surgical airway is required, call for help then proceed without delay.

2.8.0.9 Indications Failed intubation drill

Inability to maintain an airway despite basic manoeuvres.

2.8.0.10 Equipment Purpose made kits exist in the unit using direct access and/or a seldinger

technique. In the event of these not being available, the simplest technique

is described below.

• # 15 scalpel and handle

37

2.9 Tracheostomy-Percutaneous 2 CLINICAL PROCEDURES

• Size 6.0 cuffed ETT

• Oxygen delivery circuit and ventilation device (eg. Laerdal bag)

2.8.0.11 Procedure

• Palpate cricothyroid membrane

• Perform 2cm horizontal incision through skin and cricothyroid membrane

• Insert blade handle into wound and turn vertically to enlarge wound (do not use blade or

sharp instrument such as a pair of scissors)

• Insert ETT into trachea

• Connect oxygen circuit

• Confirm correct placement with end-tidal CO2, auscultation, and if possible CXR.

• Perform tracheal toilet as soon as adequate oxygenation achieved

Arrange definitive surgical airway as soon as possible.

2.9 Tracheostomy-Percutaneous

Tracheostomy is a very common procedure in critical care. Its history is quite ancient and

although the percutaneous route is a relatively new procedure, it is by far the commoner

means of performing tracheostomy in the critical care setting.

2.9.1 Patient selection

Patients on whom tracheostomy is being considered should have a reasonable likelihood of

survival and have a reversible condition. The benefits of performing the procedure and sub-

sequent critical care management must outweigh the risks. It is not good practice to perform

this treatment in a patient whose demise is inevitable.

Policy Percutaneous tracheostomy is the preferred method for elective tracheostomy in suit-

able critically ill patients.

The decision to perform percutaneous tracheostomy rests with the Consultant Intensivist.

Consent should be obtained if appropriate as outlined in the unit guidelines.

Percutaneous tracheostomies may only be performed by experienced specialist staff.

2.9.2 Indications

• as for surgical tracheostomy

• Airway maintenance:

– Prolonged intubation ( > 10 days), or anticipation thereof

– Prolonged upper airway obstruction

38

2 CLINICAL PROCEDURES 2.9 Tracheostomy-Percutaneous

– Laryngeal pathology

– Subglottic stenosis

• Airway protection

– Delayed return of glottic reflexes

– Tracheal toilet / ineffective cough mechanism

2.9.2.1 Benefits over prolonged transtracheal intubation (> 7 days)

• less use of sedative drugs and inotropes

• better communication

• patients able to eat and drink

• reduced time on invasive ventilation

• reduced length of stay

• facilitates physiotherapy

2.9.3 Contraindications

General

• unacceptable cardiovascular instability

• unacceptable risk of inducing hypoxaemia during the procedure: i.e. PEEP > 10 cmH2O,

peak airway pressures > 25 cmH2O, FiO2> 0.5 with borderline blood gases

• coagulopathies: platelets < 50 × 109, INR > 1.5, APTT > 1.5x

• local infection

• Elevated or unstable measured intra-cranial pressure

• Renal failure with uncorrected uraemic state

• high likelihood of difficult intubation/ventilation (should the need arise during the proce-

dure)

• lack of personnel or equipment

Local

• altered anatomy in the region of the trachea

• fat neck

• bony cervical pathology causing inadequate access

• previous tracheostomy

• prominent vessels overlying the trachea on ultrasound imaging

• short cricosternal distance

• Previous neck surgery

• Unstable cervical spine injury

39


2.9.4 Timing of the procedure

Once the indications are met and all contraindications are excluded, the patient must be as-

sessed clinically. One must consider whether the procedure would jeopardise the patient’s

safety, and test the likelihood of weaning. If the patient characteristics exhibit features of be-

ing able to wean, it would be reasonable to allow the patient the benefit of the procedure and

attempt to wean, with an emphasis on safety and doing no harm.

Such factors may include

• Clinical examination: crackles/wheeze, sputum production

• Respiratory: FiO2, Paw, PEEP, respiratory rate, SpO2, ABG, CXR

• Cardiovascular: stability, inotropic requirement, myocardial injury

• Metabolic: acid-base status, fluid balance, uremia

• Neurological: sedation requirements, mental state when conscious, effectiveness of cough,

muscular strength

• Nutritional state

If these parameters are satisfactory, a further assessment is made following a short period

of minimally assisted ventilation (PSV 8 cmH2O, PEEP ≯5 cmH2O, FiO2 < 0.4) when minimally

sedation. This may give an indication of likelihood of weaning and extubation.

If the patient fails this assessment on three consecutive days after 5 days of ventilation (or 3

days after re-intubation), a tracheostomy may be considered. This approach allows for a more

consistent and effective decision making process regarding the need for tracheostomy.

The TracMan study considering the benefit of early vs late tracheostomy is in progress. A fur-

ther meta-analysis concluded demonstrated that early tracheostomy led to decreased period

of ventilation, length of stay on ICU, and overall hospital stay.

2.9.5 Procedure

The patient is not consented, unless consent was obtained before the patient was anaes-

thetised or intubated, or is awake and able to comprehend and understand the procedure

and its implications. However, it is good practice to inform the relatives of the patient of the

indications, benefits and risks of the procedure.

Percutaneous tracheostomy is commonly performed using two experienced operators

• Anaesthetist / endoscopist: Responsible for administering a suitable anaesthetic and

managing the airway.

• Surgeon-operator

• Monitoring and drugs are as for standard endotracheal intubation, with the recommended

addition of the fibreoptic bronchoscope.

• Adequate lighting essential

An ultrasound imaging of the neck is performed to identify any prominent vessels, thyroid

mass, or displaced trachea.

The patient is ventilated on 100% oxygen utilising a pressure controlled ventilation mode.

40


2.9.5.1 Equipment A Cook Ciaglia®kit using a ”blue rhino” dilatational technique or the

Ohmeda UltraPerc®kit are standard.

Tracheostomy tubes: The ”Portex blue line” tracheostomy tube is the standard tube used in

this unit. All tubes inserted must have an inner cannula available as part of the kit or as an

add-on. The usual size inserted is a acuffed 8.0mm ID Portex BlueLine®tube.

All equipment necessary for resuscitation should available and at hand - this includes ET tubes,

functioning laryngoscopes (McCoy), syringes, bougie, suction.

No patient should leave the ICU without the inner cannula being placed prior to

discharge

2.9.5.2 Education and training SpRs and selected advanced trainees will be invited to

learn how to perform percutaneous tracheostomies. This will involve hands-on training with a

skilled operator scrubbing alongside the trainee.

2.9.5.3 Airway management Endoscopic confirmation of surgical technique is not prac-

ticed universally, but it is a useful adjunct to correct placement.

Method 1

• Place the fibreoptic bronchoscope in the trachea beyond the distal tip of the ETT.

• Under direct laryngoscopy retract the ETT (with deflated cuff) so that the cuff is above

the vocal cords and inflate the cuff with 10-15 ml of air.

• Use an assistant to secure tube in place and apply slight downward force on the ETT to

maintain a seal to ventilate the patient.

• Retract bronchoscope to a point proximal to planned tracheal puncture.

Method 2

• Place the fibreoptic bronchoscope in the trachea beyond the distal tip of the ETT

• Withdraw the ETT 2-3 cm with the cuff deflated, then reinflate cuff.

• Request the surgeon-operator apply digital pressure over intended tracheal puncture site,

and confirm this is distal to ETT tip and bronchoscope.

• Beware ETT puncture or bronchoscope damage.

• Observe correct placement of needle-guidewire by Seldinger technique, and sequential

dilatation.

• Once tracheal tube in situ, connect to ventilator and insert bronchoscope into tracheostomy.

• Confirm tip of tracheostomy clear of carina, and absence of ongoing haemorrhage.

2.9.5.4 Tracheostomy insertion technique

• Position patient: 30 deg head up, with neck in extension but supported.

41


• Both the anaesthetist and the operator don adequate protection (mask, goggles) to guard

against splashes/spraying of biological fluids.

The anaesthetist suctions the oral cavity and the endotracheal tube. The anaesthetist

then ensures the patient is monitored for anaesthesia (BP, ECG, SpO2, ETCO2 as a mini-

mum), and all equipment necessary for resuscitation is available and at hand. Anaesthe-

sia is administered utilising a propofol/alfentanil infusion.

• Adopt strict aseptic technique

• Infiltrate with 10 ml of 1% lignocaine / 1:100 000 adrenaline over the pre-tracheal rings

• Check trachy cuff, lubricate and insert dilator into trachy tube making sure there is a good

fit.

• Perform a 1-2cm horizontal incision over the 2nd tracheal ring.

• Dissect bluntly to fascia.

• Insert sheathed needle catheter in to trachea at midline. Confirm placement by aspirating

air and confirming with endoscopist.

• Remove needle, and feed guidewire through sheath.

• Remove sheath and dilate with mini-dilator.

• Place white dilator -guide over sheath.

• Proceed to dilatation with ”rhino” (to appropriate size according to desired size tracheostomy)

• Remove dilator and use guidewire to insert dilator and tracheostomy into the trachea.

• Remove dilator and wire, inflate cuff.

• Correct placement of the tube is confirmed by

– bronchoscopy

– capnography

– chest wall inspection and auscultation

• Once it is confirmed the tube is in place, the oral endotracheal tube is withdrawn.

• Secure with tapes.

• Perform a control CXR.

2.9.6 Complications

The overall early and late complication rate is between 4% and 30%, which compares favourably

with surgical tracheostomy (6-50%).

Before decannulation, the main complications are infection and bleeding. Surgical tracheostomies

have 2-3 times the rates as percutaneous. Post decannulation, airway stenosis predominates,

and it is difficult to compare between the two procedures.

Death Death directly due to tracheostomy is low ('0.4%). Overall survival to decannulation

is in the order of 50%.

42


Bleeding Up to 6% bleed problematically leading to technical difficulty or airway soiling.

It usually arises from large superficial vessels encountered during dissection, or on needling

the trachea. Tamponade by the tracheostomy tube usually controls the bleeding in the vast

majority of cases.

Infection Stomal infection can occur in up to 4% in the percutaneous group and 29% in the

surgical group. It can result in sternal osteomyelitis or mediastinitis.

Granulation tissue deposits These occur anyway between the stoma and where the tube

abuts the tracheal tissues. Occult granulomas may manifest themselves in bleeding during

decannulation, or causing obstruction in a fenestrated tube when phonation is attempted.

Paratracheal misplacement This is avoided by using intraoperative tracheoscopy.

Pneumothorax Rates of up to 2% have been suggested. It may be due to needle injury to

the pleura, malposition followed by positive pressure ventilation, or guide wire damage to the

small airways if the J-tip is not used.

Subcutaneous emphysema This is usually due to tracheal injury caused by multiple at-

tempts to needle the trachea, or laceration of the posterior wall of the trachea. Rarely, it may

be associated with a pneumothorax.

Tracheal cannula displacement This is said to occur in less than 1% of cases and may be

suspected in the presence of

• high airway pressures

• subcutaneous emphysema

• an inability to suction the trachea

• an audible speech with an intact inflated cuff

A track between skin and tracheostomy hole takes about 7-10 days to become established.

Changing the tube during this period increases the likelihood of displacement. A bougie or

airway exchange catheter must be used in these circumstances.

Tracheo-oesophageal fistula This is a rare complication associated with pulmonary infec-

tion due to recurrent aspirations, a high level of tracheal secretions, high cuff inflation pres-

sures and an ongoing air leak from the breathing system.

43


Tracheo-innominate fistula This is another rare but immediately lethal complication asso-

ciated with low placement of the tracheostomy. One option is for the tracheostomy tube to be

replaced by a translaryngeal tube with the cuff below the fistula. The other is to extend the

tracheostomy wound down to the sternal notch and digitally compress the artery against the

mediastinum.

Tracheocutaneous fistula Prolonged dependence on the tracheostomy or recurrent stomal

infection and granulation allows epithelialisation of the track.

Airway injury Tracheal stenosis occurs in up to 26% of percutaneous tracheostomy (60%

following surgical tracheostomy). However, only 2% of these are severe enough (>75% occlu-

sion of the lumen) to cause symptoms.

Symptoms usually occur after 2-12 weeks post decannulation, and are non-specific such as

cough, dyspnoea, stridor, and failure to clear secretions.

Transtracheal tubes are more likely to be associated with subglottic lesions, and tracheostomy

tubes with tracheal lesions.

The lesions occur at the stoma, cuff site, or the cannula tip. Obliquely placed tubes, or those

just below the cricoid are associated with stenosis. Cuff related stenosis is not as prevalent

now that high volume low pressure cuffs are the norm.

2.9.7 Post Insertion Management

The tracheal cannula is secured by tapes to prevent dislodgement.

Cuff pressures must be monitored to help prevent tracheal mucosal damage or stenosis. The

stoma must not be subject to weight loading from the breathing system.

The lumen must be kept clean by regular debridement of the inner tubes and the use of

warmed humidified oxygen.

Changing the tube is variable, and is dependent on clinical, patient and tube factors - but is

best avoided before 10 days post procedure.

Nasogastric feeding is commenced early and is only stopped if there is evidence of gross

aspiration.

Oral intake is facilitated when the patient is more alert, has a good cough reflex, and the cuff

deflated to help with coordination of swallowing.

2.9.8 Decannulation of the Trachea

The patient should be well into the recovery phase of their illness. They must have an effective

cough capable of expectoration into the mouth past the deflated cuff, and have intact upper

airway reflexes.

Factors that indicate a sustainable work of breathing include

44

2 CLINICAL PROCEDURES 2.10 Nasojejunal tube insertion

• normal respiratory rate

• FiO2 5 0.4 yielding acceptable SpO2 or blood gases

• clinically acceptable breathing pattern

The patient should have minimal CPAP (5 5 cmH2O) requirements with the cuff inflated or

be on a high flow circuit with the cuff deflated and maintained at this level without resort to

positive pressure ventilation or increasing CPAP for at least 48-72 hours.

Following decannulation, the patient must be observed for an appropriate period of time on the

HDU before transfer to the wards. Supplemental oxygen may be required during this period.

Some patients may be discharged to the ward with the tracheostomy tube in-situ. This requires

a careful consideration of the ability of the receiving ward to adequately and appropriately care

for the patient with a tracheostomy tube. The parent Consultant and the Nurse in charge on

the ward must be made aware and agree to the transfer (as with all patients).

2.10 Nasojejunal tube insertion

2.10.0.1 Indications Instillation of feed into the jejunum is an effective way of feeding pa-

tients with:

• Prolonged gastric stasis ( > 3 days)

• Gastric stasis resistant to treatment with pro-kinetic agents (erythromycin, metoclopramide)

• Pancreatitis or other scenario?s where feeding distal to the duodenum is desired.

2.10.0.2 Procedure

• Position the patient Rt side down to at least 45o, Remove any gastric tube.

• Use a Bengmark 10 Fr tube 140 cm long with stylet.

• Close tube sideport and attach 3 way tap to flow through stylet hub.

• Measure out Xiphisternum to ear plus ear to nose distance from the tip of the tube.

• Insert tube to this distance, confirm intragastric placement by auscultation during air

injection.

• Administer 200 mg of erythromycin or 10-20 mg of metoclopramide as slow IVI bolus.

• Inflate the stomach with 500 ml of air while the prokinetic is being administered.

• Gently advance the tube. You should feel a steady resistance. If there is increasing then

sudden loss of resistance this means you have thrown the tube into a loop in the stomach.

Withdraw the tube until resistance is felt and start slowly advancing the tube again. Insert

the tube to the 120-125 cm mark if possible.

• Try to aspirate fluid from the tube. If fluid can be aspirated check the pH with a urine

dipstick. An alkaline pH suggests duodenal or further insertion (may be a false positive if

the patient is on PPI’s).

• Position the patient flat again and order an upper abdomen-lower chest x-ray.

• Just before x-ray exposure inject 10 mls of contrast (Gastroview) down the tube.

45

2.11 Intra-abdominal pressure manometry 2 CLINICAL PROCEDURES

Check tube position on x-ray.

If the tube is in a satisfactory position a gastric tube can now be inserted to decompress the

stomach if this is desired.

Remember to leave the stylet in any fine bore tube during manipulation of the nasogastric

tube. Keep the stylet in a plastic bag at the head of the bed so it can be reinserted into the

oesophageal and gastric segment of the fine bore tube during procedures such as NG tube or

ET tube removal to stiffen the fine tube and prevent its accidental partial removal.


• Endobronchial placement

• Other ectopic placement

• Migration., Kinking or Knotting

2.11 Intra-abdominal pressure manometry

Policy Renal perfusion pressure may be compromised by raised intra-abdominal pressure

following:

• Surgery

• Trauma

• Intra-abdominal pathology (eg: pancreatitis)

The occurrence of acute renal failure in an intensive care patient significantly increases the

risk of adverse outcome.

The measurement of intra-abdominal pressures in patients that are at risk of developing ab-

dominal compartment syndrome may allow renal salvage in patients where there is a remedial

cause.

A measured pressure of > 20 mmHg (referenced to the symphysis pubis) may precipitate

acute abdominal compartment syndrome and renal failure.

2.11.0.4 Procedure

• Connect a 100ml bag of saline to a ?metriset? which is then connected to a manometer.

A 20G needle is then attached to the manometer tubing.

• Place patient supine

• Empty bladder

• Clamp indwelling catheter distal to the culture aspiration point. Clean aspiration point

with an alcohol swab and insert 20G needle (prepared as above).

• Inject 100 ml warmed sterile saline into patient’s bladder.

• Open stopcock to transducer and allow 30 seconds to equilibrate.

• Once pressure measurement completed, remove 20G needle from aspiration point, un-

clamp urinary catheter and allow free drainage of the bladder.

46

3 DRUGS AND INFUSIONS


• Instillation of bacteria into the bladder

• Triggering autonomic dysfunction (NB vagal) on injecting into the bladder, particularly if

the bladder is incompletely drained.

• Patient discomfort (if awake)

• Artificially elevated readings due to bladder spasm or local pelvic haemorrhage may pre-

cipitate interventions that are associated with significant morbidity.

3 Drugs and Infusions

3.1 Introduction

Most patients admitted to the ICU will have had medications prescribed for concurrent or pre-

morbid conditions. A new ICU drug chart must be started on each patient’s arrival in ICU.

Re-charting of all drugs implies an active review of the appropriateness of drug administration

and dosage, in changing clinical conditions.

It is important that drug charts are accurate, legal and legible. Use of drug trade names is

not acceptable practice. Similarly only drugs which are approved by the ICU medical staff may

be given to ICU patients. For this reason only ICU medical staff may write (prescribe) in the

patient’s drug chart while the patient is in the ICU.

Charting of drugs by outside teams must be discouraged.

On discharge to the ward it is the responsibility of the discharging medical person to review

patient drug and fluid orders.

3.1.1 Prescription practice

In general the following principles should be considered when prescribing any drugs for ICU

patients.

• A drug should only be instituted where the potential benefit is well described, or the risk

for adverse effects low when benefit is unproven.

• Unit protocols and guidelines should be used where these exist for a given drug.

• ICU patients often have vastly altered drug pharmacokinetics (what the body does to the

drug) and pharmacodynamics (what the drug does to the body). Where therapeutic drug

monitoring is available this should be undertaken with the assistance of the Pharmacist.

• Good drug prescribing practice is mandatory, including: Legible hand writing, use of

generic (not trade) names for drugs, clear delineation of dose, frequency and duration

of treatment.

Extensive guidelines for drugs commonly used in critically ill patients are available within the

ICU and in the BNF.

47

3.2 Cardiovascular Drugs 3 DRUGS AND INFUSIONS

3.2 Cardiovascular Drugs

3.2.1 Inotropes and Vasoactive drugs

Inotropes & Vasopressors are commonly prescribed drugs on Critical Care areas.

These drugs include Norepinephrine, Dobutamine, Dopexamine & Vasopressin. Epinephrine is

a drug of resuscitation & should only be instituted by infusion in exceptional circumstances.

Epinephrine is known to cause lactic acidosis, and may increase oxygen demand to a greater

extent than dobutamine for a given increase in cardiac output.

All patients should be adequately fluid resuscitated before starting vasoactive drugs.

Hypotension should be established :

Absolute: Systolic Blood Pressure < 90 mmHg

Relative: Systolic 30% < normal for that patient.

Consideration should be taken into end organ hypo-perfusion:

Renal: urine output < 0.5ml/Kg/hr

Cerebral: cognitive state

Peripheries: unreliable in septic patients

Several methods of cardiac output monitoring are available (pulmonary artery flotation catheter

- PAFC, oesophageal Doppler, LidCo), and should be used if there is any doubt as to the patho-

physiology. However, PAFC’s have not been shown to improve patient outcome and are as-

sociated with significant morbidity. They should therefore only be inserted on the advice of a

senior Anaesthetist, preferably an Intensivist.

3.2.2 Assess and correct hypovolaemia

This simple concept is in practice very difficult to perform accurately. In the ICU there are a

number of ways to assess intravascular volume status although each has shortcomings.

• Clinical assessment of fluid status including JVP

• Variation of arterial waveform characteristics with ventilatory cycle.

• Measurement of CVP.

• Right heart catheterisation.

• Calculation of intrathoracic blood volume and extrapolation to extravascular lung water

using the PiCCO meter.

• Echocardiographic techniques.

Except in very clear-cut cases (ie gross fluid overload or cardiac failure), in a situation where

there is doubt as to the patients fluid status a trial of fluid administration should be considered.

3.2.3 Instituting inotropic therapy

Only once the above steps have been considered should inotrope therapy be considered.

48

3 DRUGS AND INFUSIONS 3.2 Cardiovascular Drugs

No single inotrope (or mixture of inotropes) has been shown to be superior to another.

Please consult appendix on haemodynamic principles.

3.2.3.1 Short notes on using common agents Dopamine / adrenaline / noradrenaline:

For ease of application many claim these three agents have a β-adrenergic action in low dose

and a progressive α-effect in increasing doses. Each however has a characteristic feature

worth noting:

Dopamine in low doses (2.5 µg.kg-1.min-1) has a direct diuretic effect which may result in

increased urine volume, there is no evidence of a renal sparing or protective effect. In

fact, there is evidence that it may be harmful to patients.

Adrenaline is a useful α/β-agonist, however it does have significant β2-effect which may re-

sult in unwanted metabolic effects (hyperglycaemia, excess lactate production unrelated

to organ perfusion).

Noradrenaline is generally held to have a predominant α-effect and is therefore useful as a

inotrope-vasopressor, particularly in septic shock.

Dobutamine a synthetic inotrope, does not have significant α-effects (may have some my-

ocardial α-effect) and is therefore useful in increasing heart rate and stroke volume, but

may cause a paradoxical fall in blood pressure due to peripheral β-adrenergic activity.

Dopexamine acts via DA1 receptors, and is used at a low dose to promote splanchnic perfu-

sion.

Adrenaline and noradrenaline infusions should be started at 0.1 µg.kg-1.min-1 and titrated to

response. Infusions of these agents require 3-5 minutes to achieve steady state. Changes in

rate more frequently than every 3-5 minutes (unless in an emergency) should be discouraged

as it may lead to a ”roller-coaster” effect.

3.2.3.2 Inotropes Inotropes increase myocardial contractility, and mediate their effect through

cardiac β1-receptors. This leads to both an enhanced force of contraction, together with a

variable increase in heart rate. As a consequence, they have variable effects on myocardial

oxygen demand. They alter peripheral vascular tone & regional blood flow to a varying degree

(β2-mediated). This should be taken into account when considering which drug to use.

There is marked inter-individual variation in response to a chosen inotrope, due to:

• Qualitative & quantitative changes in adrenergic receptor kinetics in both acute illness

(sepsis) & chronic conditions (heart failure)

• Underlying variability in disease state (cardiogenic shock, sepsis, hypovolaemia)

3.2.3.3 Dobutamine This is a synthetic derivative of Dopamine. It is a very potent β1- &

β2-agonist, providing direct inotropic action, together with systemic vasodilatation & afterload

reduction.

49

3.2 Cardiovascular Drugs 3 DRUGS AND INFUSIONS

3.2.3.4 Dopexamine This is also a synthetic derivative of Dopamine. It is a very potent

β2-agonist, and a rather weak β1-agonist. It improves splanchnic perfusion and also promotes

a diuresis. It is not thought to alter outcome in renal failure, but the diuresis may be beneficial.

3.2.3.5 Phosphodiesterase inhibitors (Milrinone and Amrinone) Phosphodiesterase

inhibitors increase cAMP by non-adrenergic mechanisms. They are not therefore affected by

down-regulation of adrenoreceptors as occurs in sepsis or heart failure. For this reason mil-

rinone is the drug of choice for refractory (ie following adequate volume resuscitation) low

cardiac output states.

They result in:

• Increased myocardial contractility

• Systemic and pulmonary vasodilatation (often requires co-administration of a vasopres-

sor / noradrenaline)

• Improved diastolic relaxation (useful in patients with diastolic heart failure)

Notes on pharmacology of milrinone These drugs usually require a loading dose on com-

mencement which may predispose to additional hypotension by virtue of vasodilatation.

The relatively long half-life of these agents requires forethought before administration, as their

action is not easily reversed, and titration of infusions to effect cannot be effected rapidly.

Phosphodiesterase inhibitors use is extremely infrequent in this Unit, which reflects the uncon-

vincing evidence for its use in sepsis.

3.2.4 Vasopressors

3.2.4.1 General Principles

• These agents are used primarily to induce vasoconstriction & thus elevate blood pressure

• They may increase cardiac afterload and thus cardiac wall stress

• These agents should not be used to treat hypotension due to hypovolaemia

Vasopressors should be used with extreme caution in patients with a suspected low cardiac

output state, as they may have a detrimental effect. In cases of doubt, senior advice should

be sought or adjuncts to monitoring should be used.

3.2.4.2 Norepinephrine is the vasopressor of choice in critical care. Indirectly acting

agents (phenylephrine, metaraminol) should generally be restricted to peri-operative practice

where temporary vasodilatation results from specific intervention (general or regional anaes-

thesia).

It exerts its vasopressor action by the α1-receptor, and also exhibits α1-agonist activity. Its

peripheral action is to induce intense vasoconstriction in the splanchnic & pulmonary visceral

beds. This may oppose its inotropic effect in a dose dependent fashion.

50

3 DRUGS AND INFUSIONS 3.2 Cardiovascular Drugs

Consideration should be taken as to the effects on the splanchnic, renal & peripheral circula-

tions at higher doses.

3.2.4.3 Vasopressin (Argipressin) may be indicated (after discussion with an Intensivist)

where hypotension is refractory to norepinephrine. In early septic shock, endogenous levels

of vasopressin are (appropriately) high. In established septic shock levels fall, the reasons for

which are unclear. Replacement therapy may therefore reduce, or even abolish the need for

inotrope & vasopressors. Vasopressin enhances the sensitivity of vessels to catecholamines.

High doses may induce angina, hypertension and water intoxication. It has variable effects on

renal vessels and urine output.

3.2.5 Steroid use in patients requiring vasopressors

In patients with severe sepsis, & hypotension refractory to high doses of vasopressors, the co-

administration of physiological doses of intravenous steroid is potentially beneficial. However,

the Sepsis Guidelines published in March 2008 now recommend that steroids be instituted

only if the patient is unresponsive to inotropes (taken to mean increasing requirement for

inotropes and/or noradrenaline rate ≥0.5µg.kg-1.min-1). Hydrocortisone is prescribed at 50mg

four times daily. It is not necessary to taper the dose prior to discontinuation.

Agent Standard Infusion Dose

Dobutamine 250 mg / 50 ml 5% Dextrose 5-20 µg.kg-1.min-1

Dopexamine 50 mg / 50 ml 5% Dextrose 2-3 µg.kg-1.min-1

Norepinephrine 8 mg / 100 ml 5% Dextrose 0.02-1.0 µg.kg-1.min-1

Vasopressin 20 Units /50 ml 5% Dextrose 1-6 ml.hr-1

Norepinephrine should be infused through a central line. Dobutamine, Dopexamine & Argi-

pressin may be infused peripherally in some circumstances, although a CVP should be in situ

to allow assessment of filling.

References

1. Sladen RN. Inotropic agents. Chapter 17.1.19 In: Oxford Textbook of Critical Care.

2. Delinger RP, Carlet JM, Masur h, Gerlach H et al. Surviving Sepsis Guidelines, Crit Care Med

2004; 32: 858-873

3. Holmes CL, Patel BM, Russell JA, et al. Chest 2001; 120 (3) 989-1001. Physiology of Vaso-

pressin relevant to septic shock

4. Tsuneyoni I, Yamada H et al. Critical Care Medicine 2001; 29 (3) 487-93. Haemodynamic

and Metabolic effects of low dose vasopressin infusions in vasodilatory septic shock

51

3.3 Anti-hypertensive Agents 3 DRUGS AND INFUSIONS

Table 1: Inotropic agents commonly used in ICU

Agent Standard Infusion Indications

Adrenaline 10 mg in 100mls 5% Dex

CPR

Cardiogenic Shock

Acute severe asthma

Anaphylaxis (correct hypovolemia!)

Medical pacing

Noradrenaline4mg in 100mls 5% Dex (single

strength)

Septic Shock (1stline inotrope)

Conditions where mixed α/β effect required with predominant

α effect

Dopexamine50mg in 50 mls 0.9% NaCl, run

at 2.4 mls.hr-1Promote splanchnic perfusion

Dobutamine 250mg in 100mls 5% Dex

Pure β adrenergic agent used in low CO/high SVR states

Effect diminished in sepsis and CCF (down regulation of β

receptors

Milrinone

Loading dose:

12.5-50µg.kg-1 over 20 min

Infusion: 10mg in 50 mls 5%

Dex, infuse @ 0.375-0.75

µg.kg-1.min-1 (8-15 mls.hr-1in

70kg patient)

Cardiogenic shock due to diastolic failure

Pulm hypertension

Rescue following catecholamine induced downregulation ofreceptors

The drugs may accumulate in renal failure

3.3 Anti-hypertensive Agents

3.3.0.1 General Principles Elevated blood pressure should be viewed in the context of

each patient, and should include an appraisal of pre-morbid blood pressure.

Acute hypertension in the intensive care should not elicit direct treatment, but rather a review

of the cause of blood pressure elevation.

Elevated blood pressure is commonly seen in patients who are agitated, delirious, or who have

some other cause for overt sympathetic drive. This should be addressed with analgesia and

sedation where appropriate. A dual purpose drug such as an α2-agonist (clonidine) may be

useful.

”Neurogenic Hypertension” in the setting of intra-cranial pathology may be self limiting. No at-

tempt should be made to actively lower elevated blood pressure with anti-hypertensive agents

unless the intra-cranial pressure is being monitored, and cerebral perfusion pressure is not

threatened.

Vasodilators particularly may increase intra-cranial pressures further while dropping cerebral

perfusion pressure to dangerous levels.

52

3 DRUGS AND INFUSIONS 3.4 Antiarrhythmic Drugs in Critical Care

3.3.0.2 Indications

• Acute

– Peri-operative control of hypertension post-cardiac, carotid or other vascular surgery,

or for patients with critical myocardial ischaemia. In this instance target blood pres-

sures should be discussed with the surgeon involved, and confirmed with the Consul-

tant Intensivist

– Accelerated hypertension: ”Malignant Hypertension”

– Hypertensive Proteinuric Pregnancy states (Eclampsia)

– Active Phaeochromocytoma (NB: always preceed β-blockade with alpha blocker.

• Non-hypertensive indications

– Reduction of afterload in cardiac ischaemia and failure

– Decrease ∆P / ∆t in patients with aortic dissection


• Hypotension

• Tachyphylaxis (GTN - consider ”rescue” therapy with N-acetylcysteine if necessary to

continue GTN, although efficacy unproven)

• Cyanide Toxicity-Sodium Nitroprusside

• Pulmonary vasodilatation causing increased pulmonary shunting and hypoxia

3.4 Antiarrhythmic Drugs in Critical Care

3.4.1 General Principles of Treatment

In therapy of arrhythmias, prior consideration should be given to causal or aggravating factors:

• Hypoxæmia

• High, occasionally low, pH

• Hypokalæmia, hypomagnesæmia

• Pre-existing drug effects or toxicity (including bronchodilators and inotropes)

• Presence of right heart lines (including pacemakers)

• Myocardial or coronary compromise, especially pulmonary oedema

The need for therapy should be carefully evaluated. For instance atrial tachyarrhythmias with a

ventricular response similar to that of the preceding sinus rhythm need not be slowed down or

abolished at the cost of additional hypotension. Reperfusion VT associated with myocardial in-

farction (fascicular or otherwise) or non-paroxysmal junctional tachycardia (NPJT) at 130 min-1

may be as acceptable as sinus or junctional bradycardia at 40 min-1 and equally self-limiting.

Non-pharmacological therapy should also be always considered - even if only to be dismissed,

as in the case of precordial thump for VT. In patients with permanent pacemakers, a magnet

may abolish both VT or SVT by fixed overdrive pacing. DC cardioversion is always available.

53

3.4 Antiarrhythmic Drugs in Critical Care 3 DRUGS AND INFUSIONS

The value of precise diagnosis is increasingly deconstructed by the likes of sotalol or amio-

darone. Still, as a general rule, if antiarrhythmics are to be used, a 12-lead ECG should be

obtained.

Arrhythmias can only be defined electrocardiographically. On the other hand, a full ECG ob-

tained on a pulseless patient is medico-legally indefensible.

In many ICU patients the need for continued therapy ceases as they improve and the drug -

often the ubiquitous amiodarone - can be stopped.

3.4.2 Drug Therapy of Bradyarrhythmias

The cognoscenti prefer pacing when this is mentioned, but there are clinical situations when

pacing is either impracticable or fails. A number of drugs have some utility in the setting of

bradycardia-bradyarrhythmia.

3.4.2.1 Adrenaline A mixed α- / β- agonist, adrenaline has declined in popularity mainly

due to its metabolic side effects mediated by β-receptor stimulus (increased lactic acid pro-

duction, hyperglycaemia). In emergency situations where bradycardia is asscciated with hy-

potension and patient compromise adrenaline remains the first line agent, at least in the short

term.

3.4.2.2 Atropine Alkaloid from Atropa belladonna, competitive acetylcholine antagonist at

post-ganglionic parasympathetic endings. It comes in 0.6 mg ampoules. Small doses (or early

stages of administration) may cause central vagal stimulation.

Its vagolytic action is useful in the very early stages of (usually inferior) myocardial infarction

complicated by significant bradycardia or block; later stages of AV block are more likely to

respond to aminophylline. Intraventricular, Möbitz II block is made worse. Escape-capture

bigeminy may be replaced by slower 2:1 block.

It may also be used in reflex bradycardia associated with upper airway manoeuvres, such as

suctioning.

In brady-asystolic cardiac arrest, it is next to useless; its administration here is confined to

junior hospital staff and protocol-driven ambulance officers.

The main hazard of atropine is tachycardia in the presence of critical coronary ischæmia. Ac-

tual poisoning is now rare; the victim is memorably ”hot as a hare, blind as a bat, dry as a

bone, red as a beet and mad as a hen”.

3.4.2.3 Isoprenaline Isoproterenol is a ”pure” β agonist producing marked vasodilatation

and cardiac stimulation; these actions have long ago necessitated its replacement by selective

β2 bronchodilators in asthma. It is sometimes used for:

• 3o or advanced 2o AV block as a bridge to pacing

54


• to promote tachycardia and shorten the QT interval, against potential or manifest torsade

de pointes. Here, too, pacing offers greater flexibility and stability.

It is less useful than even atropine in bradyarrhythmic arrest due to the vasodilation and very

high oxygen cost; it usually precludes successful resuscitation.

3.4.2.4 Aminophylline It may be indicated for symptomatic 2o or 3o AV block in later stages

of inferior myocardial infarction, as mentioned above.

3.4.3 Supraventricular Arrhythmias

Some agents control the ventricular response through AV blocking action, some interrupt the

reentry circuit and abolish the paroxysm; many do both.

3.4.3.1 Adenosine Endogenous adenosine production is enhanced by ischæmia and it may

well be the mediator of sustained AV block following inferior infarction. Its half-life is only 0.6-

1.5 sec, requiring larger dose with peripheral access, e.g. 6 mg where 3 mg given centrally

would do.

In SVT, both AV nodal and non-nodal re-entrant tachycardias (AVNRT and AVRT), the slow path-

way is blocked and cycle length alternans may occur. With incremental doses, over 90% ef-

fectiveness is seen. The response can also be used to differentiate broad complex tachycardia

due to aberrancy from its ventricular look-alike, even though adenosine-sensitive VT needs

consideration.

Chest pain induced by adenosine, like that of dipyridamole, can be severe; other side effects

include flushing, headache, dyspn?a and cough. Sinus bradycardia or arrest and ventricular

arrhythmias are frequent, but almost never actionable. AF or flutter may follow cardioversion

of SVT; they are less durable than with verapamil. SVT recurs early in 10-30% of cases.

Indications for adenosine

• Narrow complex tachycardia: Adenosine may be the drug of choice in investigating and

or treating such arrhythmia. It may terminate AV-nodal and AV re-entry tachycardia, or

reveal underlying atrial flutter or fibrillation.

• Broad complex tachycardia: Adenosine may terminate SVT with intra-ventricular conduc-

tion block. It will not cardiovert true VT. It may be useful therefore in treatment of regular

broad complex tachycardia not thought to be of ventricular origin.

Dose: Adults: Incremental 3 mg, 6 mg, 12 mg, 18 mg. Given via large peripheral or central

vein followed by saline flush. Some practitioners use 6mg as first dose.

Please be aware that administration of adenosine may cause the patient to feel very unwell

(hot, flushed, nauseous) and you should warn the person beforehand if possible

55

3.4 Antiarrhythmic Drugs in Critical Care 3 DRUGS AND INFUSIONS

3.4.3.2 Verapamil Verapamil inhibits the slow inward Calcium channel and blocks the slow

antegrade pathway in AVNRT; it stops AVRT by AV block. Its effect on SVT should be apparent

within three minutes. If a 1-5 mg bolus (tailored to age and co-morbidity) is ineffective, a

bigger (5-10 mg) dose 10 minutes later is recommended. Before adenosine, verapamil was

the drug of choice in treatment of SVT.

It can be used to slow the ventricular response in AF, but this is rarely done now. It remains

quite useful for the same purpose in multifocal atrial tachycardias (where atrial rate may also

be slowed), usually as an infusion.

Hypotension may be a problem. It is obviated by preceding the bolus by 5 mmol of Calcium;

there is no loss of anti-arrhythmic activity. Verapamil should be given slowly in patients with

known myocardial disease.

Other side effects are similar to those of adenosine-sinus pauses, bradycardia and occasion-

ally AF. Unlike adenosine, it should never be given to diagnose a broad-complex tachycardia:

cardiogenic shock or cardiac arrest may result.

3.4.3.3 Amiodarone This is currently the drug of choice for AF with rapid response in the

ICU, given as a 5-10 mg.kg-1 loading dose over 20-60 minutes (occasionally bolus) and followed

by 1200 mg.day-1 infusion. Its advantage over digoxin is the rapid (within one hour) control

of the ventricular rate; unlike digoxin, it also propitiates the return of sinus rhythm. It is also

quite successful for cardioversion of SVT although it is rarely used for this purpose

Acutely, amiodarone blocks the AV node (prolonging the PR interval in sinus rhythm); there is

no immediate effect on the sinus rate, QRS duration or QT interval. It prolongs action potential

and lengthens the effective refractory period throughout the heart; hence slowing of the sinus

rate and prolongation of the QT interval follow.

Amiodarone has to be given via a central vein as it causes severe thrombophlebitis. Other side

effects are flushing, nausea and transient hypotension.

In patients with LV dysfunction, overt failure and shock may occur. In these patients it is wise

to omit the bolus and start with an infusion.

Long-term side effects are serious and well known; they are rarely of great moment in the ICU.

3.4.3.4 Flecainide It slows the phase zero of the action potential, interfering with the fast

inward Sodium current; it depresses the diastolic repolarisation. The action potential is not

prolonged-hence its 1C classification. PR, QRS and QT are prolonged.

It is a potent ”PVC killer” but has suffered greatly in the CAST trial: its pro-arrhythmic propen-

sity precludes its long-term use in post-MI patients.

The bad reputation has spread. This has little to do with its benefits in the ICU, where it

remains the drug of choice for both SVT and AF & flutter in patients with WPW syndrome. It

slows conduction in the atrium. It is also a good drug for pharmacological cardioversion of AF

and flutter in patients with normal conduction. Its pro-arrhythmic effects are of less moment

in continuously monitored ICU patients.

56


Preferred dose in the ICU = 150 mg in 5% dextrose IVI over 30 minutes.

One important side effect is the elevation of the pacing threshold; the patient may become

un-paceable. This limits its use in the pacemaker-dependent post-CABG patients.

3.4.4 Ventricular Arrhythmias

The pharmacological therapy is mostly concerned with treatment of VT and prevention of VF.

Isolated VEBs, accelerated idiofocal rhythms, escape beats or parasystole are usually treated

by mistake.

3.4.4.1 Lignocaine Lignocaine has for a long time been the drug of choice for the emer-

gency treatment of ventricular arrhythmias. At one stage it was de rigueur in the early man-

agement of acute infarction, as a prophylactic; it was also used to suppress the ”warning

arrhythmias” in this setting.

Its great advantage is its relative lack of toxicity; its equally great disadvantage is the frequent

(80-90%) ineffectiveness in VT.

The toxicity is mostly on the CNS, with slurred speech, twitching and seizures; a rare change

in intraventricular conduction is usually trivial, but interesting.

The standard dose is 75 mg, followed by 2-4 mg / min infusion in 5% D.

3.4.4.2 Amiodarone The drug is effective for sustained monomorphic VT and has some

activity, like the now withdrawn bretylium, even in VF. It is the drug of choice for VT in ICU.

3.4.4.3 Sotalol Sotalol, in addition to its amiodarone or bretylium-like class activity, is also a

non-selective β-blocker (in its l-isomer). It prolongs QT and PR intervals and appears to produce

more episodes of torsade de pointes than amiodarone (but probably less than flecainide). It is

excreted unchanged in the urine.

A loading dose is 0.5-1.5 mg.kg-1 over 10 minutes, followed by infusion of 0.2-0.4 mg.kg-1.hour-1

in 5% Dextrose or by oral tablets. It is a significant negative inotrope; some VT patients in the

emergency department setting had to be shocked ”at the end of the needle”. A lower initial

dose is prudent. Other side effects, like asthma, are shared with β-blockers. On the other

hand, the β-blockade is a reason for its being the drug of choice for VT in patients with IHD.

Its use in the treatment of supraventricular tachycardias is not recommended.

3.4.4.4 Magnesium A major indication is true torsade de pointes VT, where 2-4 g bolus is

followed by 3-20 mg.min-1 infusion.

Polymorphous VT with normal preceding QT is usually seen in the setting of acute ischæmia

and responds to Magnesium with the same frequency as sustained monomorphic VT: very

rarely. Amiodarone, β-blockers and urgent revascularisation are the best strategy here.

57

3.5 Respiratory Drugs 3 DRUGS AND INFUSIONS

3.4.4.5 Procainamide Its effects are very similar to those of quinidine; it is a Class 1A

Sodium channel blocker, prolonging the QRS complex (25% ”effect”, 50% ”toxicity”) and the

QT interval. It is less vagolytic than quinidine and has little, if any, ganglion-blocking proper-

ties.

Dose:

• loading dose: 1 g in 50 cc 5% D (20 mg.ml-1) at 10-20 mg.min-1.

• Alternatively, 100 mg boluses over 1 minute can be repeated at 5 min intervals, watching

the BP.

It is quite effective drug for VT and probably most effective of all drugs to slow down the

conduction by an anomalous pathway in WPW, AF or flutter. It is rarely used; part of the

problem is the relatively long time (20 min) to load an effective dose.

3.4.4.6 Phenytoin Beside KCl, diphenylhydantoin is the drug of choice for VT caused by

digoxin toxicity; it is also effective for digitalis-induced paroxysmal atrial tachycardia with

block, but less so for non-paroxysmal junctional tachycardia. It is best given, like procainamide,

as 100 mg boluses every 5 min; the usual antiarrhythmic dose is approximately 700 mg (be-

yond 1000 mg it is unlikely to succeed).

3.5 Respiratory Drugs

3.5.1 Nebulised bronchodilators

3.5.1.1 General principles These agents are used in the treatment of bronchospasm in

Intensive Care (including acute severe asthma).

These agents do not necessarily need to be delivered by nebuliser, but can be administered

as a metered dose inhaler into the appropriate port on the inspiratory limb of the ventilator

circuit. This is particularly important in patients that cannot afford to lose applied PEEP while

inserting the nebuliser into the circuit , and resultant lung de-recruitment.

Once these agents have been commenced they should be reviewed daily, as is the case with

all prescribed drugs. This is usually assessed by improvements in audible wheeze, lung com-

pliance, respiratory rate and blood gases.

3.5.1.2 Indications

• Pre-existing obstructive airways disease where reversibility is suspected

• Acute severe asthma

• Acute exacerbation of obstructive airways disease

• Problematic sputum plugging or poor sputum clearance.

58

3 DRUGS AND INFUSIONS 3.6 Sedation

3.5.2 Parenteral Therapy in treatment of reversible obstructive airways disease

3.5.2.1 Indications Adjunctive therapy for acute severe asthma in patients not responding

to nebulised agents


• Hypokalaemia, metabolic alkalosis

• Arrhythmias (theophylline)

• Intercurrent infection

• Polyneuropathy

• Lactic acidosis (β2-stimulants)

3.6 Sedation

This section is authored by Dr Simon Enright and Dr Jacquiline Brook, and covers the delivery

and monitoring of sedative agents used on the Intensive Care Units at Pinderfields General

Hospital and Dewsbury District Hospital (Mid Yorkshire NHS Trust).

It has been agreed by Consultant Intensivists and senior nursing staff who work on both units.

It is intended as a guide and will outline the reasons for sedation, sedation monitoring and the

commonly used drugs on the units

3.6.1 Introduction

Sedation is an extremely important part of the management of the critically ill.

It allows the depression of awareness of the environment and reduction in the response to

external stimulation. The intensive care is a frightening place for patients for a number of

reasons, and adequate sedation can reduce this. With the development of post-ICU follow-up

clinics, the need for adequate sedation on ICU has been shown to be even more important and

can reduce the incidence of longer term psychological complications.

There is not a simple prescription for all, and sedation requirements will depend on many fac-

tors including age, general medical condition, presence or absence of painful stimuli (such as

recent surgery), previous alcohol/drug habits and so on. There is no perfect sedative regimen

but below commonly used agents are considered.

Generally, patients should be given the sedation necessary to tolerate the presence of an

endotracheal tube, other catheters (N/G tube, urinary catheter), practical procedures (such

as central line changes, physiotherapy), painful stimuli and artificial ventilation. Sedatives

should be regularly reviewed and changed if appropriate (for example much less sedation is

required to tolerate IPPV after tracheostomy is performed). Always consider the pharmaco-

logical actions of all drugs used. Particular attention must be given to patients who are given

neuromuscular blocking agents.

59

3.6 Sedation 3 DRUGS AND INFUSIONS

The guidelines given below will cover most patients. There will be occasions when patients will

have different requirements, these must be discussed with senior medical staff.

3.6.2 Principles of Sedation

• Patients should be made as comfortable as possible and general measures taken when

considering sedation (eg pain relief especially post-operatively, urinary catheterization,

quiet environment). Any avoidable source of physical discomfort should be excluded .

• The need for any uncomfortable or disturbing therapies should be reviewed (eg line in-

sertion)

• A perceived need to increase sedation may be due to clinical deterioration.

• Drug, alcohol and nicotine withdrawal need to be considered and treated appropriately

before increasing sedation.

• Presence of parents/relatives may have an effect on sedative requirements (positively or

negatively) especially with paediatric patients.

• Sedation should be tailored to a patient’s needs eg may require increased sedation for

procedures such as physiotherapy.

• Patients should be comfortable but rousable, co-operative and able to tolerate uncom-

fortable procedures

3.6.3 Monitoring Sedation : Sedation Scoring

Both oversedation and undersedation can have adverse effects on patients and may lead to

an increased stay in intensive care. Therefore, there is a clear need to assess levels of patient

sedation and titrate sedative drugs accordingly ( Saggs, P 1998).

3.6.3.1 Complications of Under-sedation

• Agitation

• Pain and discomfort

• Displacement of monitoring

• Inadequate ventilation/disco-ordination with ventilator – potential hypoxi

• Hypertension

• Tachycardia

• Patient awareness (especially when using neuro-muscular blockers)

• Complications of raised intra cranial pressure (if patient is at risk)

• Sudden changes in level of conciousness : displacement of invasive lines, haemodynamic

instability

60


3.6.3.2 Complications of Over Sedation

• Withdrawal syndromes

• Respiratory depression

• Hypotension

• Bradycardia

• Intra abdominal complications

• Immunosuppression, increased risk of infection

• Nosocomial infections

• Renal dysfunction

• Deep vein thrombosis

• Hepatotoxicity

• Reduced mobilisation and muscle wasting

• Psychological disturbances

• Metabolic abnormalities

• Cost

3.6.3.3 Sedation Scores There are a number of sedation scoring systems available eg

modified Ramsay, Riker.

On the ICU’s at Mid Yorkshire Trust, the scoring system used is the Richmond Agitation Se-

dation Score (RASS), which combines a commonly used scoring system (increasing negative

for deepening sedation, increasing positive for increasing agitation). This scoring system can

be used in conjunction with the inattention scoring to detect delirium.

Table 2: RASS Scoring systemScore Term Description

+4 Combative combative, violent, immediate danger to staff

+3 Very Agitated Pulls tubes, aggressive

+2 Agitated Frequent non-purposeful movements

+1 Restless Anxious, but movements not aggressive

0 Alert and Calm

-1 Drowsy Opens eyes to voice in <10secs, eye contact

-2 Light sedation Opens eyes to voice in >10secs, eye contact

-3 Moderate sedation Movement or eye open to voice, no eye contact

-4 Deep sedation Movement or eye opening to physical stimulation

-5 Unrousable No response to voice or physical stimulation

3.6.4 Sedation Holds/ Sedation Assessment

A sedation hold (also known as “sedation holiday”) involves stopping a patient’s sedation to

allow assessment, usually on a daily basis. After sedation is stopped, the patient is assessed

61


and sedation is then gradually recommenced, hopefully at a lower level. Sedation holds have

been shown to reduce the overall length of stay on the ICU.

After stopping the sedation, drugs may be recommenced when the patient is considered to be

‘awake’, i.e. to be able to respond to at least 3 out of 4 of the following commands:

• Opens eyes in response to voice

• Uses the eyes to follow the assessor on request

• Sticks out the tongue to command

• Squeezes the hand to command

Ideally sedation should be stopped on a daily basis at around 08.00hrs to evaluate neurological

status and prevent accumulation of sedative agents, unless:

• Patients achieving target score i.e. 0 on sedation scoring tool

• Patient is receiving neuromuscular blocking agents

• Patient is ventilated in prone position

• Patient difficult to ventilate in previous few hours

• Patient is suffering from status asthmaticus or severe bronchospasm

• Patient is cardiovascularly unstable

As prolonged use of sedative infusions may lead to numerous complications as previously men-

tioned, daily interruptions of these infusions can be an easy and effective way of addressing

this. (Gehlbach B.K. Kress J.P. 2002)

3.6.5 Accumulation of Sedatives

This occurs commonly especially if there is hepatic or renal dysfunction. This can lead to

over-sedation, haemodynamic instability and prolonged duration of intubation. The action of

IV anaesthetic agents (eg propofol) is generally terminated by redistribution not clearance ;

therefore drugs with a low clearance given as infusion may accumulate. Accumulation and

over-sedation may be reduced or avoided by the use of sedation scoring and sedation holds.

3.6.6 Sedative Dependence

Patients exposed to more than 1 week of high dose opioid or sedative may develop tolerance

and/or dependence.

The symptoms of opioid withdrawal are: pupillary dilatation, sweating, lacrimation, rhinorrhea,

yawning, tachycardia, irritability, anxiety.

Symptoms of BDZ withdrawal : dysphoria, tremor, headache, nausea, sweating, agitation,

anxiety, sleep disturbance, myoclonus, delirium, seizures. Propofol withdrawal is not well

described but is reported to resemble BDZ withdrawal.

62


3.6.7 Sleep on the ICU

Sleep is a natural periodic state of rest for the mind and body, in which the eyes are usually

closed and conciousness is completely or partially lost, so that there is a decrease in bodily

movement and responsiveness to external stimuli. It is an important component in recovery

from critical illness and sleep deprivation may impair tissue repair and overall cellular immune

function. Sleep is difficult to assess and achieve on the ICU.

3.6.8 Non-Pharmacological Methods of aiding sleep

Modification of environment and reduction in excess noise. Sleep occurs best below 35dB

(80dB will cause arousal from sleep). Lighting to give diurnal rhythm (day-night) is helpful.

Music therapy can decrease HR, myocardial oxygen demand, anxiety and aid sleep.

3.6.9 Pharmacological Methods

Benzodiazepines such as zopiclone can be used, although they may also precipitate delirium.

They decrease sleep latency while increasing total sleep time, without affecting sleep archi-

tecture in stages 3 and 4 and decrease REM sleep. Concerns included addiction, morning

hangover, rebound insomnia. A newer melatonin receptor agonist, ramelteon, is being used

experimentally for sleep deprivation on the ICU, with promising early results.

3.6.9.1 Commonly Used IV Anaesthetic/Sedative Agents Below is a list of the agents

which are generally used on the units :

• Propofol

• Alfentanil

• Remifentanil

• Benzodiazepines : Diazepam, Midazolam, Lorazepam

• Clonidine

• Morphine (less commonly)

(On the ICU’s in the Mid Yorkshire Trust, the usual combination of sedative agents for the vast

majority of patients is Propofol + Alfentanil).

PROPOFOL

General: Rapid onset IV anaesthetic agent with excellent sedative properties. Vasodilator

properties similar to GTN (this property may be useful eg reduction of preload/afterload,

warming patient post-operatively). “Milk of amnesia” : similar degree of amnesia as

BDZs. No analgesic properties.

Onset: Rapid < 1min

Offset: Rapid < 10 mins (longer in elderly)

63


Table 3: Sedative Drugs in ICU

Dose: 0.5-4 mg.kg−1.hr−1 by infusion (occasionally may need to higher)

Problems: ↓ BP (potent vasodilator), lipid overload (triglycerides should be checked if used >

3 days), pancreatitis. Requires dedicated line.

Admin: 1% or 2% form is available. The 2% formulation has the advantage of less volume

and less lipid load, but it must be remembered that only half the volume should be given.

Nb :The dose must be prescribed in mg.hr−1 not ml.hr−1.

The standard formulation in Mid Yorks is 1% propofol

ALFENTANIL

General: Short acting opioid analgesic with sedative properties

Onset: Rapid 1-2 min

Offset: Rapid (depends on duration of infusion)

Dose: Adult 0.5 - 5mg.hr−1 (half dose in elderly)

Problems: Respiratory depression, chest rigidity, prolonged duration of action in renal/hepatic

disease

Admin: IV infusion 0.5mg.ml−1

REMIFENTANIL

64


General: Ultra-short acting opioid, potent µ agonist, usually given as a single agent. Not

generally “first-line” agent, should be discussed with consultant before use.

Onset: Very rapid, highly predictable

Offet: Very rapid, predictable, not dependent on normal hepatic/renal function, stable context-

sensitive half-time (3-10 mins)

Dose: only given by infusion, rate 0.1-0.15 µcg.kg−1.min−1 to start, adjusted at 5 min intervals

by increments of 0.025 µcg.kg−1.min−1 according to response. If adequate sedation is not

achieved at 0.2 µcg.kg−1.min−1, then additional agent may be required

Problems: haemodynamic (reduction in MAP, HR) esp if greater dose than 0.1 µcg.kg−1.min−1.

Acute-onset withdrawal symptoms and tolerance have occurred. The cost of remifentanil

is significantly higher than alfentanil.

Admin: IV infusion (variable concentration depending on weight)

BENZODIAZEPINES (BDZs) In general they offer greater cardiovascular stability than IV

anaesthetic agents and should be considered as the major sedative in patients with severe

haemodynamic instability (such as septic shock with inotropic support).

They produce sedation by modulating the effects of GABA, the main inhibitory neurotransmit-

ter in the CNS. They bind to the GABAA ligand gated Cl- ion channel. They may be given by

bolus or continous infusion.

However, we suggest that they are generally given by by intermittent bolus and generally

not by infusion on the ICU due to high lipid solubility, long elimination half-life and prolonged

duration of action. Diazepam (preferred) and midazolam are most commonly used. The bolus

should be titrated slowly to the response and it must be remembered that these drugs can

cause respiratory depression and hypotension. Concerns with their use include dependence,

withdrawal agitation and acute delirium.

MIDAZOLAM

General: Highest clearance of benzodiazepines (most suitable BDZ for infusion), metabolised

to active compounds in the liver

Dose: Bolus : 1-4 mg prn, or infusion : 0.04 – 0.2 mg.kg−1.hr−1

Onset: around 1 min

Duration: 1-2 hours, the most suitable BDZ to be given by infusion

DIAZEPAM (diazemuls)

General: Effective sedative/anxiolytic with amnesic action

Dose: Adult : up to 10mg (given 2mg at a time) by slow IV bolus. This may be prescribed

as frequently as hourly. If frequent boluses are required, the sedative regime should be

reassessed. Remember to reduce dose in elderly. May be given orally.

Onset: 1-2 mins

65


Duration: 1-8 hours (longer in elderly, renal failure, hepatic failure). Metabolized in the liver

to active compounds, should not be given as infusion

Problems: prolonged effect, active metabolites

Infrequently used IV Sedative/Anaesthetic agents :

SODIUM THIOPENTONE The only use of sodium thiopentone is by continuous infusion in the

management of refractory status epilepticus. It has a low clearance and tends to accumulate.

When given as an infusion its metabolism becomes linear (zero order) due to saturation of

hepatic enzymes. Accumulation can give toxicity including immunosuppression and cardiac

depression.

ETOMIDATE Etomidate has a good haemodynamic profile but is not administered by infusion

due to its suppressive effect on adrenocortical function . Etomidate is not recommended for

use on the ICU.

KETAMINE Ketamine is a phencyclidine derivative which acts as an antagonist to glutamate

(excitatory) at NMDA receptors. It is an excellent analgesic and produces a dissociative anaes-

thesia/sedation. Ketamine is a sympathomimetic agent, causing stimulation of heart rate and

increased cardiac work. Common side-effects include hallucinations, nausea, delirium and

nausea/vomiting. It is a potent bronchodilator : its only role on ICU is in the management of

refractory bronchospasm (status asthmaticus). It may also be used for control of pain in awake

patient.

3.6.9.2 NEUROMUSCULAR BLOCKADE Neuromuscular blockade (paralysis, muscle relax-

ation) on ICU has specific indications and should not be used routinely. Special attention to

detail is necessary to avoid paralysis without adequate sedation. If the decision is made on

clinical grounds to instigate neuromuscular blockade, then blockade should be complete (there

is no indication for partial N-M blockade). The adequacy of N-M blockade should be checked

with a peripheral nerve stimulator. These drugs should be stopped when there is no clinical

indication.

Indications for neuromuscular blockers include :

• poor oxygenation with high FiO2 (such as ARDS), reduction in oxygen consumption

• poor compliance with ventilator (“fighting the ventilator”) despite adequate sedation

• complex ventilation modes (inverse ratios, high pressures)

• management of raised intracranial pressure

• special circumstances eg prone ventilation

66


3.6.9.3 Problems

• inadequate sedation leading to awareness (while paralysed)

• prolonged paralysis or muscle weakness (major factor in critical illness polyneuropa-

thy/myopathy)

• hypostatic pneumonia

• venous thromboembolism (all reasonable measures should be taken to reduce this)

• peripheral oedema

ATRACURIUM

General: useful on ICU due to non-enzymic elimination and predictable duration of action

Dose: bolus 0.5mg/kg then infusion 0.5-1mg/kg/hr (remember tachyphylaxis develops and

increased dose needed if patient pyrexial)

Onset: 2-3mins (initial bolus)

Duration: 10-30 mins after stopping infusion

Problems: ↓ BP (histamine release), tachyphylaxis (less with cis-atracurium)

If complete neuromuscular blockade is difficult to achieve with high doses of atracurium but

necessary clinically, it is worth adding in another drug such as pancuronium (0.1mg.kg−1) or

vecuronium (0.1mg.kg−1) by bolus every 1-2 hourly. Both of these drugs have a synergistic

action with atracurium.

3.6.9.4 Centrally acting α-agonists Unlike other sedatives, α2-agonists do not cause ma-

jor problems with respiratory depression or haemodynamic instability. They may therefore

be given as a sedative to both mechanically ventilated and spontaneously breathing patients.

They are often given as an adjunct to other sedatives, especially when there are concerns over

withdrawal from other drugs, alcohol or nicotine.

CLONIDINE α2 > α1 -agonist

Clonidine is an α2-agonist. Initial pressor effect due to α1 stimulation of arterioles, then central

α2 stimulation in CNS inhibits sympathetic activity, reduces plasma epinephrine and nore-

pinephrine levels

It is useful in the management of agitation and withdrawal of benzodiazepines, opioids or

alcohol. It can be given as a bolus (50-150 mcg TDS) or infusion (0.5-1.5 mg/24hrs).

DEXMEDETOMIDINE More selective α2-agonist than clonidine and therefore more potent.

Stronger sedative and analgesic properties. It has a shorter elimination half-life than clonidine.

Not widely used in UK at present.

67


3.6.9.5 Difficult sedation patients This may be a problem in alcoholic or opioid abusers

and in long-term ICU patients who develop what has previously been named an “ICU psy-

chosis”. This term covers a host of psychological disturbances on the ICU. Butyrophenones

(haloperidol) and phenothiazines (chlorpromazine) are occasionally used in small doses. Haloperi-

dol 1-5mg (oral or IM), chlorpromazine (5-25mg IV). These drugs should be used with caution

as they may cause drop in blood pressure and over-sedation. Delirium is discussed in detail in

the last part of the guidelines.

Alcohol/Drug Withdrawal Alcohol or opioid withdrawal in adults is best treated with CLONI-

DINE (50-200mcg IV OD) and not traditional therapies such as Heminevrin (this accumulates

and leads to severe sedation, respiratory depression and possibly pulmonary aspiration).

Examples of Sedative Regimes :

1. 50yr old (70kg) man admitted to ICU for IPPV after laparotomy for perforated duodenal

ulcer.

• Sedation problems :

sedation required to tolerate presence of endotracheal tube and facilitate IPPV

analgesia required (post-laparotomy)

• Regimen :

a) Propofol infusion (up to 200mg/hr, 20ml 1% propofol)

b) Alfentanil infusion (up to 5 mg/hr)

c) Diazemuls (5-10mg) by intermittent bolus, given by nursing staff (can be given

in anticipation of stimulating procedures (eg line insertion, physiotherapy)

d) Remember adjuncts to analgesia such as thoracic epidural, morphine PCAS

2. 80yr old lady (50kg) with acute exacerbation of COAD.

• Sedation problems :

sedation reqd to tolerate endotracheal tube and IPPV

no painful stimuli

may be difficult to comply with ventilator so may require neuromuscular blockers

possibly hypovolaemic due to dehydration

• Regimen

a) Propofol infusion 120mg per hour (12 ml/hour of 1% propofol)

b) Alfentanil infusion (up to 1.5mg/hr)

c) Diazemuls up to 5mg by intermittent bolus (given very slowly to titrate response)

d) Remember, sedation requirements will fall to around 30% if tracheostomy per-

formed

68


3.6.10 Management of Delirium

Definition: an acute, reversible, organic mental syndrome with:

(a) disorders of attention and cognitive function,

(b) increased/decreased psychomotor activity

(c) disordered sleep-wake cycle

Typical onset: after 2 days, typical duration 4 days

Cognitive impairment :

• Memory: especially registration and recall of recent events

• Orientation: in time>place>person

• Attention: increased distractibility

• Perception: increased misinterpretations, illusions, hallucinations

• Logical thought: muddled thinking and speech

3.6.10.1 Types of delirium

Hyperactive: Agitated/paranoid (1%)

Hypoactive: withdrawn, quiet, paranoid (35%)

Mixed: combination of 2 types (64%)

Hypoactive

• lethargic, drowsy, quiet, disorientated,

• easily missed as patient is quiet, often treated as depression (nb disorientation is rare in

depression)

Hyperactive

• Continual movement, disorientated, may use violence, may not follow commands, inap-

propriate, pain exaggerated, abnormal vital signs

Mixed

• most common, combination of above

Delirium is under-recognised in the critically ill (70% missed and symptoms wrongly attributed

to dementia or confusion)

Delirium is a medical emergency

Delirium should not be ignored : it results in : increased 6 month mortality, longer stay in venti-

lated patients, longer hospital stay, neuropsychological disturbances after ICU stay, increased

cost,

Common : 15-80% in critically ill

69


Prevention

Non-pharmacological: provide support and orientation, provide an unambiguous environ-

ment, maintain competence, remove potential organic drivers

Pharmacological: stop medication no longer required

3.6.10.2 Risk Factors

• Age over 70

• Transfer from nursing home

• History of depression, dementia, epilepsy, alcohol abuse

• Psychoactive drugs

• Hypo/hyper-natraemia/glycaemia/thyroidism/thermia

• Renal dysfunction

• Liver disease

• CCF

• HIV

• CVP/bladder catheters

• Malnutrition

• Visual/hearing impairment

3.6.10.3 Associated Drugs :

• Analgesics

• Antidepressants

• Anticonvulsants

• Antihistamines

• Antiemetics

• Antipsychotics

• Antimuscarinics

• Cardiovascular agents

• Corticosteroids

• Hypnotic agents

• Miscellaneous agents (ranitidine, furosemide)

3.6.10.4 Assessment /Screening for Delirium

• Assess patient with RASS scale and use CAM-ICU tool

• Exclude or minimise organic drivers of delirium (hypoxia, hypercarbia, acidosis, pain,

unnecessary medications)

70


• Consider whether alcohol withdrawal or alcohol withdrawal syndrome is likely

• Continue to assess patient with RASS scale and use CAM-ICU tool, at least daily, even

when on treatment

3.6.10.5 TREATMENT SUGGESTIONS

Alcohol withdrawal

• LORAZEPAM 1-4mg (IV or IM)

• Consider PROPOFOL

• Consider CLONIDINE

Alcohol withdrawal delirium

• LORAZEPAM 1-4mg (IV or IM)

• Consider HALOPERIDOL if still agitated / altered perception / disturbed thinking

• Consider PROPOFOL

• CLONIDINE is unlikely to help

Delirium detected by screening

• HALOPERIDOL – low dose regular enterally / IV route, or

• OLANZAPINE 5mg enterally

Overtly delirious

• with IV access HALOPERIDOL IV – use titration method or

• OLANZAPINE 2.5 – 10 mg IM, repeat if necessary

• MIDAZOLAM 5 – 10 mg IV (for dangerous motor activity), repeat as needed

Night sedation

• 50mg TRAZADONE enterally at night for seven days or 2-5mg

• HALOPERIDOL intravenously at night

How to manage patient with hypoactive delirium

• Ensure the diagnosis is not depression or dementia

• Management is as for hyperactive / mixed delirium, although methylphenidate may be

useful if this treatment fails or cannot be used

• METHYLPHENIDATE - Consider 10-30mg methylphenidate daily in divided doses in addi-

tion to normal therapy if not responding.

71


– Titrate to maximum 50mg daily in divided doses if required. This is a stimulant, and

a controlled drug)

• OLANZAPINE 5-10mg enterally or IV (This is an antipsychotic)

Notes on Haloperidol use

• Do not use in patients with Parkinsons disease

• Start with low dose if any concern over cardiovascular status or if elderly (ie 1-2mg)

• If extra-pyramidal side effects occur, treat with Procyclidine 5-10mg iv

• If using IV titration, (doubling dose every 20-30 minutes until effect achieved) do not

exceed 80mg per 24 hours without consultant approval

• For any patient on regular haloperidol, perform daily 12-lead ECG to ascertain QTc value,

reduce dose if QTc exceeds 480 ms

• Perform daily measurement of serum magnesium and potassium

• If treatment is effective in controlling delirium, plan to reduce haloperidol (or other drug

for delirium) dosing regime gradually over a few days

Notes on Lorazepam use for alcohol withdrawal and alcohol withdrawal delirium

LORAZEPAM (Parenteral)

• Lorazepam 1-4mg intravenously every 5 to 15 minutes until calm (or 1-4mg intramuscu-

larly every 30to 60 minutes until calm), then every hour to maintain light somnolence.

LORAZEPAM (Enteral)

• Lorazepam 2mg every six hours for 4 doses, then 1mg every 6 hours for 8 doses. Addi-

tional doses can be given when required if needed for poorly controlled symptoms

Problems with commonly used drugs traditionally used for sedation / agitated be-

haviour

Benzodiazepines diazepam is deliriogenic and REM

Chlordiazepoxide deliriogenic and REM

Clonidine NOT deliriogenic, but REM

Opioids Codeine, Fentanyl, Morphine, Pethidine are all deliriogenic and all REM

Propofol NOT believed to be deliriogenic or to result in REM-rebound when stopped

Antipsychotics Chlorpromazine is deliriogenic

SSRI eg citalopram, paroxetine REM

Zolpidem or Zopiclone are not recommended substitutes for short acting benzodiazepines for

night sedation

72

3 DRUGS AND INFUSIONS 3.7 Anticoagulation

Other Drugs commonly used in critical care that have been shown to be deliriogenic

• Amitriptyline

• Phenytoin, Phenobarbital, Thiopental,

• Chlorphenamine, Promethazine

• Prochlorperazine

• Atropine, Hyoscine

• Atenolol, Digoxin, Dopamine

• Lidocaine

• Dexamethasone, Hydrocortisone, Prednisolone

• Furosemide, Ranitidine

3.6.11 References

www.icudelirium.org

UKCPA: Detection, prevention and treatment of delirium in critically ill patients. June 2006

3.7 Anticoagulation

3.7.1 General Principles

Anticoagulation in critically ill patients is a challenging issue, with patients at risk of bleeding

diatheses as well as hypercoagulable states. Often a single patient will move through a state

with a high risk of bleeding (including surgical sites) to one of high risk of developing venous

stasis and thrombosis. The decision to administer anticoagulation is often based on a relative

risk-benefit assessment.

Where anticoagulants are contra-indicated, alternative methods should be employed to pre-

vent venous stasis in the lower limbs (graded compression stockings and sequential calf com-

pressors), although it is unclear as to whether these confer adequate protection against throm-

bosis and embolisation.

As a general rule heparin infusions should be used to effect anticoagulation, titrated intra-

venously to a therapeutic APTT where this is required, or administered subcutaneously for

DVT prophylaxis. Low molecular weight heparins require measurement of anti-factor Xa to

quantify effect, and are more difficult to reverse than unfractionated heparin.

Where any doubt exists with regard the use of an anticoagulant in a given surgical or trauma

patient, this should be confirmed with the Surgeon involved.

3.7.2 Indications for the use of warfarin

• Post operative prosthetic valve (According to cardiothoracic guidelines)

• Previous thrombo-embolism: Selected cases only

• Maintenance of thromboprophylaxis in selected high risk patients only

73

3.7 Anticoagulation 3 DRUGS AND INFUSIONS

3.7.3 Indications for the use of heparin

• DVT prophylaxis (LMWH)

• Proven venous or arterial thrombo-embolism

• Myocardial ischaemia syndromes

• Prosthetic heart valves

• Prior to commencing oral anticoagulants

• During an acute illness where oral anticoagulation is unsuitable

• Atrial Fibrillation-sustained

• Continuous Renal Replacement Therapy (CRRT - See below)

3.7.4 Prophylactic use of heparin

DVT prophylaxis should be commenced within 24- 36 hrs of admission to the ICU. Low molecu-

lar weight heparin is generally considered as safe, and in some instances marginally superior

(eg. orthopaedic patient populations) to unfractionated heparin. Enoxaparin (Clexane) is the

chosen LMWH in the ICU (20mg s/c daily).

Non-pharmacological methods of DVT prophylaxis :elasticated compression stockings (ECS) or

sequential compression devices (SCD) may confer some protection against DVT formation.

3.7.4.1 Exclusions to heparin DVT prohylaxis

• Clinical coagulopathy or thrombocytopaenia

• Therapeutic anticoagulation (eg Warfarin, heparin)

• Significant intra-cerebral haemorrhage

• Heparin Induced Thrombocytopaenia.

3.7.4.2 DVT prophylaxis by category

• Medical ICU patients: Enoxaparin when bleeding risk felt to be minimal. When bleeding

risk high, use ECS and SCD.

• Surgical patients: ECS plus Enoxaparin when possible. Add SCD if enoxaparin contraindi-

cated.

• Head injury with CT evidence of frank haemorrhage or haemorrhagic stroke: ECS and SCD

for 72 hrs. Substitute enoxaparin for SCD at 72 hours if appropriate.

• Spinal Cord injury with intra-spinal haemorrhage on MRI: As for intra-cerebral haemor-

rhage above.

• Pelvic fractures and patients with significant trauma: Thrombotic and initial bleeding risk

high. If enoxaparin felt inappropriate at 24-36hrs then consider placement of temporary

caval filter.

74

3 DRUGS AND INFUSIONS 3.7 Anticoagulation

3.7.5 Systemic anticoagulation using unfractionated heparin

Weight based nomograms are more effective in achieving therapeutic anti-coagulation in a

shorter period of time.

• Proceed with loading dose if safe: 70 units / kg.

• Continue with 20 units.hr-1.kg-1 as continuous infusion (10 000 units heparin in 100 ml

Normal Saline = 100 iu.ml-1

• Check APTT 4-6 hrly and adjust infusion rate according to chart.

N.B. For APTT’s within 12 hours of starting thrombolytic therapy do not discontinue or decrease

the infusion unless:

• significant bleeding occurs

• APPT is > 150 secs

Adjust the infusion as per nomogram if APPT < 50 secs.

Heparin toxicity (prolonged APTT) in a patient that is actively bleeding should be reversed

with Protamine Sulphate 50 mg aliquots IVI (usually diluted). Administration of Protamine may

aggravate peripheral vasodilatation and hypotension in susceptible patients.

3.7.6 Heparin Induced Thrombocytopaenia

3.7.6.1 Introduction HIT occurs in two forms.

• Dose related: Platelet clumping as an effect of the larger glycosaminoglycans containing

the active pentasaccharide of heparin. Immediately obvious, dose related and usually

mild.

• Auto-immune: IgG antibody mediated. Therefore usually occurs 7-10 days after exposure

in non-sensitised patients. Idiosyncratic, often severe.

HIT may appear more common in the setting of continuous renal replacement therapy. This

might reflect patient condition and platelet adsorption to dialysis filter.

3.7.6.2 Diagnosis

• Decrease in platelet count: Usually < 50 000×109 .L-1. Rarely <20 000×109 .L-1

• Skin lesions at heparin injection sites

• Dominant finding of thrombosis (not bleeding)

• Formation of Heparin antibodies (heparin ? PF4 ELISA = Sensitive but not specific).

3.7.6.3 Treatment Measures Stop all Heparin immediately and reconsider indication for

anti-coagulation. Warfarin, if commenced, should not be used alone as it exacerbates throm-

botic risk.

Use of Low Molecular Weight Heparin in these patients is not considered safe (cross-reactivity

rates in excess of 90% reported).

75

3.8 Endocrine Drugs 3 DRUGS AND INFUSIONS

3.8 Endocrine Drugs

3.8.1 Insulin

3.8.1.1 Introduction Glycaemic control in the critically ill has become one of the most

debated aspects of care. There is some evidence that tight control of blood sugar (4.4-6.0

mmol.L-1) is associated with improved outcome. This effect may be preserved at levels less

than 8 mmol.L-1. This area of ICU practice is evolving and requires regular review.

Target blood sugar levels between 4.4-6.0 mmol.L-1, levels above 8.0 mmol.L-1must be aggres-

sively treated.

3.8.1.2 Indications for insulin in the ICU

• Diabetic emergencies: NB Rapid glycaemic control is not a priority in patients with either

hyperosmolar or ketotic diabetic states. In fact rapid correction of severe hyperglycaemic

states may aggravate cerebral oedema. Patients admitted to the ICU with these condi-

tions should be actively co-managed with the endocrine service.

• Perioperative diabetic patients

• Glucose intolerant or overtly diabetic patients with acute coronary syndromes

• Hyperglycaemia (single blood glucose >15 mmol.L-1 or 2 readings 4 hours apart > 10

mmol.L-1) or glycosuria associated with acute illness orsteroid administration.

• Hyperglycaemia associated with catecholamine infusions.

• Treatment of hyperkalaemia: ie 50 ml 50% dextrose administered with 10 units actrapid

insulin.

3.8.1.3 Administration of insulin Mix regular short acting insulin (actrapid) with normal

saline to a concentration 1 IU.ml-1.

Administer in a 50 ml syringe via syringe driver.

Maximum infusion rate never to exceed 25 IU.hr-1.

Discard at 24 hrs of use.

3.8.1.4 Monitoring of blood glucose Blood sugar levels should be monitored hourly until

stable within desirable range. Once stable, monitor at least 2 hrly in the first 48 hrs of ICU

admission, and 4 hrly thereafter.

Ongoing requirement for insulin beyond acute phase: Patients requiring insulin for

established or known diabetes should be converted to subcutaneous insulin as a medium or

long acting form with/without a short acting insulin constructed according to subcutaneous

sliding scale. As these patients may need long term follow-up, they should be referred to the

endocrine service for assistance.

76

3 DRUGS AND INFUSIONS 3.8 Endocrine Drugs

3.8.2 DDAVP

3.8.2.1 For Diabetes Insipidus

General DI may occur in the following settings:

• Evolving brain death or severe brain injury

• Post ablative pituitary surgery, or injury to pituitary stalk (anterior cranial fractures)

• Nephrogenic causes are typically mild and do not require treatment.

• Fluid mobilisation during convalescent phase of injury should not be mistaken for DI.

Indications for DDAVP in diabetes insipidus

• Persistent polyuria >300 ml.hr-1 for more than 3-4 hours with incremental hypernatraemia.

• Low urine osmolality in the presence of high plasma osmolality (or hypernatraemia)

• Pre-existing hyperosmolar state or intravascularly deplete patient.

Dose of DDAVP in diabetes insipidus 1-2 µg IVI bd as required.

Fluid orders: Isotonic fluid replacement in under-resuscitated patients.

5% Dextrose or 0.45% Saline in patients where hypernatraemia exists (maximum decrease in

serum Sodium should not exceed 2 mmol.L-1.hour-1)

3.8.2.2 For Platelet dysfunction

Indications Adjunctive treatment in bleeding patients with platelet dysfunction as a result

of

• Uraemia

• Cirrhosis

• Von-Willebrand’s Disease

• Drug (NSAIDs or aspirin) or cardiac surgery related platelet dysfunction

Contraindications Use in patients with severe oronary or cerebrovascular atherosclerosis

may cause arterial thrombosis.

Dose 0.3 µg.kg-1 IVI over 30 minutes or 300 µg intra-nasally.

In some instances a second dose may be administered, although a rapid ”fall-off” in effect per

dose (tachyphylaxis) is the norm.

77

3.8 Endocrine Drugs 3 DRUGS AND INFUSIONS

3.8.3 Steroids

3.8.3.1 General The use of steroids in the critically ill has been the subject of much debate

and some research. At present their use in ICU is dependant upon the personal experience

and practice of the consultant staff involved with the case.

Steroids should not be prescribed by junior staff, except for those indications listed below as

proven, unless this has first been discussed with the Consultant.

Proven Indications

• Hypoadrenalism (Addison’s disease or crisis)

• Acute severe asthma

• Panhypopituitarism

• Haemophilus meningitis in children (discuss with paediatric team first)

• Pneumocystis Carinii pneumonia (PaO2 < 6.0 kPa)

• Collagen Vascular diseases

• Active Immunosuppression (GVHD, solid organ transplant)

• Myasthenia Gravis

Unproven ICU indications

• Non-infected (fibroproliferative) ARDS: Meduri protocol = Methylprednisolone 2 mg.kg-1

for 14 days, tapered 1.0-0.5 mg.kg-1 for next 14 days.

• Shock associated with vasodilated states which are refractory to high dose, or prolonged

administration of, inotropes.

• Myocarditis

• Exacerbation of chronic airway obstruction

• Bronchiolitis obliterans

• Reduction of cerebral oedema around non-traumatic CNS lesions.

• Anaphylaxis

3.8.3.2 Conditions where steroids are not indicated or actively contra-indicated

• Active infection (except in the inotrope dependent septic shock scenario)

• Acute Head or spinal cord injury

• Guillain-Barre Syndrome

• Fat embolism syndromes

78

3 DRUGS AND INFUSIONS 3.9 Renal Drugs

3.9 Renal Drugs

3.9.1 General Principles

Acutely ill patients are at risk for developing, or exacerbating, renal dysfunction. Good inten-

sive care practice, and renal care, encompasses:

• Avoiding renal hypoperfusion: ICU patients generally do not have the ability to autoreg-

ulate renal blood flow and GFR, as these become increasingly dependant on systemic

perfusion pressures. For this reason urinary output is a good marker of total body perfu-

sion, and resuscitation status.

• Ensure adequate volume resuscitation

• Avoid renal toxins if possible: aminoglycoside antibiotics, contrast mediums etc

• Consider local complicating conditions: eg. abdominal compartment syndromes.

Administration of agents such as dopamine in low dose, or frusemide, are not however reno-

protective, and their use strongly deprecated.

3.9.2 Diuretics

3.9.2.1 Indications

• Symptomatic fluid overload without intravascular depletion

• Pulmonary oedema

• Congestive Cardiac Failure / Cor Pulmonale

• Ascitic states where abdominal volume is thought to be a compromising factor

• Hypertension

• Conjunctive therapy in Cardiac failure (not primarily diuretic): ACEI and thiazide, Low

dose (25 mg.day-1) spironolactone.

• Metabolic alkalosis: e..g recovering ventilated patients allowed permissive hypercap-

noea, prolonged renal replacement therapy with bicarbonate overshoot. (ie. acetazo-

lamide).

3.9.2.2 Contraindications

• Hypovolaemia

• Anuria: Frusemide in particular acts on the luminal side of the renal tubule. States where

there is no, or low, GFR will not respond to drug administration, and may complicate

hypotension by direct afterload reduction.

• Failure to respond to trial dose

• Drug hypersensitivity: NB Sulphonamides

79

3.10 Gastro-intestinal drugs 3 DRUGS AND INFUSIONS


• Hypovolaemia (often hyperosmolar)

• Hyponatraemia or hypernatraemia

• Electrolyte disturbance of K+, Mg2+ and PO43-.

3.10 Gastro-intestinal drugs

3.10.1 Prophylaxis of gastric ”stress ulceration”

Evidence base

Critically ill patients commonly develop gastrointestinal tract problems as a result of severe

physiological stress. These include stress related mucosal disease, gastrointestinal motility

problems and mucosal oedema. Gastric acidity has been identified as a significant risk factor

for stress ulcer bleeding and stress ulcer prophylaxis has become standard practice in critically

ill patients.

Initial studies looked at efficacy of available agents for stress ulcer prophylaxis [1]. These

included antacids, sucralfate and H2 receptors antagonists. Studies reported an increased

risk of ventilator associated/ nosocomial pneumonia with the use of H2 receptor antagonists

compared to sucralfate [2, 3, 4, 5, 6]. Other studies however were unable to support this

[7, 8]. These conclusions were then resolved in a meta analysis which suggested that there

was strong evidence of reduced clinically important gastrointestinal bleeding with H2 receptor

antagonists and sucralfate may be as effective in reducing bleeding as gastric pH altering

drugs and is associated with lower rates of pneumonia and mortality. There is insufficient data

to determine the net effect of sucralfate compared with no prophylaxis [9]. A further study

observed a lower incidence of clinically important stress ulcers with ranitidine and a lower

incidence of nosocomial pneumonia with sucralfate. Mortality and length of ICU stay were

similar in both groups [10].

Administration of sucralfate through a nasogastric tube probably limits its use and has pos-

sibly contributed to the success of intravenous H2 antagonists such as ranitidine as the first

choice agent for stress ulcer prophylaxis. The use of intravenous proton pump inhibitors is

now becoming widespread. They decrease the rate of peptic ulcer re-bleeding after endo-

scopic haemostasis [11, 12], and are effective in gastro-oesophageal reflux disease. This data

is likely to be extrapolated to suggest that proton pump inhibitors are superior in stress ulcer

prophylaxis. There is preliminary work to suggest that PPI’s are safe and effective for stress

ulcer prophylaxis [13, 14] but further studies are required to fully define the role of PPI’s in this

role [15, 16].

The comparison between drugs used for first line prophylaxis and second line or high-risk

patient groups is consistent with the understanding that PPI’s are more efficacious than H2

receptor antagonists. Ranitidine is effective for stress ulcer prophylaxis in first line therapy

but the evidence is less clear for high-risk groups.

80

References References

Nosocomial or ventilator associated pneumonia has been associated with the use of drugs

which alter gastric pH and leads to increased bacterial growth coupled with aspiration into

the trachea leading to pneumonia. This lead to the support for sucralfate as it does not alter

gastric pH. Several studies have been completed and the results are inconclusive [6, 20].

Comparisons between H2 receptor antagonists and proton pump inhibitors are inconclusive

[21].

Stress ulcer prophylaxis is once again a topical issue in the United Kingdom with the develop-

ment of Ventilator Care Bundles that have a stress ulcer prophylaxis component.

References

[1] Priebe HJ, Skillman JJ, Bushnell LS et al. Antacid versus cimetidine in preventing acute gas-

trointestinal bleeding. A randomised trial in 75 critically ill patients. New England Journal

of Medicine 1980; 302: 426-30. 80

[2] Driks MR, Craven DE, Celli BR et al. Nosocomial pneumonia in intubated patients given

sucralfate as compared with antacids or histamine type 2 blockers. The role of gastric

colonisation. New England Journal of Medicine 1987; 317:1376-82. 80

[3] Tryba M. Risk of acute stress bleeding and nosocomial pneumonia in ventilated inten-

sive care unit patients: Sucralfate versus antacids. American Journal of Medicine 1987;

83(3B): 117-24. 80

[4] Apte NM, Karnad DR Medhekar TP, et al. Gastric colonisation and pneumonia in intubated

critically ill patients receiving stress ulcer prophylaxis: A randomised controlled trial. Crit-

ical Care Medicine 1992; 20: 590-93. 80

[5] Eddleston JM, Vohra A, Scott P, et al. A comparison of the frequency of stress ulceration

and secondary pneumonia in sucralfate or ranitidine treated intensive care unit patients.

Critical Care Medicine 1991; 19: 1491-96. 80

[6] Prodhom G, Leuenberger P, Koerfer J, et al. Nosocomial pneumonia in mechanically ven-

tilated patients receiving antacid, ranitidine, or sucralfate as prophylaxis for stress ulcer.

A randomised controlled trial. Annals of Internal Medicine 1994; 120: 653-62. 80, 81

[7] Simms HH, DeMaria E, McDonald L, et al. Role of gastric colonisation in the development

of pneumonia in critically ill trauma patients: Results of a prospective randomised trial.

Journal of Trauma 1991; 31: 531-36. 80

[8] Pickworth KK, Falcone RE, Hoogeboom JE, et al. Occurrence of nosocomial pneumonia

in mechanically ventilated trauma patients: A comparison of sucralfate and ranitidine.

Critical Care Medicine 1993; 21: 1856-62. 80

[9] Cook DJ, Reeve BK, Guyatt GH, et al. Stress Ulcer Prophylaxis in Critically Ill Patients:

Resolving discordant Meta-analyses. Journal of the American Medical Association; 1996:

275: 308-14. 80

[10] Cook DJ, Guyatt GH, Marshall J, et al. A comparison of sucralfate and ranitidine for the

81


prevention of upper gastrointestinal bleeding in patients requiring mechanical ventila-

tion. New England Journal of Medicine 1998; 338: 791-97. 80

[11] Lin HJ, Lo WC, Lee FY, et al. A prospective randomised comparative trial showing that

omeprazole prevents rebleeding in patients with bleeding peptic ulcer after successful

endoscopic therapy. Archives of Internal Medicine 1998; 158: 54-8. 80

[12] Lau JYW, Sung JJY, Lee KKC, et al. Effect of intravenous omeprazole on recurrent bleeding

after endoscopic treatment of bleeding peptic ulcers. New England Journal of Medicine

200; 343: 310-16. 80

[13] Phillips JO, Metzler MH, Huckfeldt RE, et al. A multicenter, prospective, randomised clinical

trial of continuous infusion IV ranitidine vs. omeprazole suspension in the prophylaxis of

stress ulcers. Abstract. Critical Care Medicine 1998; 26(Supplement): A101. 80

[14] Jung R, Maclaren R. Proton pump inhibitors for stress ulcer prophylaxis in critically ill

patients. Annals of Pharmacotherapy 2002; 36: 1929-37. 80

[15] Steinberg KP. Stress related mucosal disease in the critically ill patient: Risk factors

and strategies to prevent stress-related bleeding in the intensive care unit. Critical Care

Medicine 2002; 30 (Supplement): S362-64. 80

[16] Cash BD. Evidence based medicine as it applies to acid suppression in the hospitalised

patient. Critical Care Medicine 2002; 30(Supplement): S373-78. 80

[17] Maclaren R, Jarvis CL, Fish DN. Use of enteral nutrition for stress ulcer prophylaxis. Annals

of Pharmacotherapy 2001; 35: 1614-23.

[18] Fennerty MB, Pathophysiology of the upper gastrointestinal tract in the critically ill pa-

tient: Rationale for the therapeutic benefits of acid suppression. Critical Care Medicine

2002; 30 (Supplement) S531-55.

[19] Raff T, Germann G, Hartmann B. The value of early enteral nutrition in the prophylaxis of

stress ulceration in the severely burned patient. Burns; 1997: 23:313-18.

[20] Tryba M. Sucralfate versus antacids or H2 antagonists for stress ulcer prophylaxis: A

meta-analysis on efficacy and pneumonia rate. Critical Care Medicine 1991; 19: 942-48.

81

[21] Mallow S, Rebuck JA, Osler T, et al. Do proton pump inhibitors increase the incidence

of nosocomial pneumonia and related infectious complications in critically ill trauma pa-

tients? Current surgery 2004; 61: 452-58. 81

GIT Stress Ulcer Prophylaxis Guideline for Critical Care

Start Enteral feeding ASAP

Ranitidine 50mg tds i.v.

• First line antacid prophylaxis

• Prescribe if enternal feeding not established

Omeprazole 40mg once daily i.v.

• For high risk groups:

82


– Burns victims

– Major trauma

– Acute brain injury

– Patients with history of PUD / GORD

– Patients already on PPI pre Critical care admission.

• Patients admitted post endoscopy with proven ulcer will need Omeprazole infusion as per

Trust protocol

On a daily basis check:

• Is possible to start enteral feeding?

– If not why not?

– Need for prokinetic?

– Need for N/J tube?

• Review prescription chart

• Take advice from Critical Care Dietician

• Involve the Nutritional Support team

Not indicated in enterally fed patients, even at low volumes, unless the patient is known to

have pre-existing or subsequently (in-hospital) proven peptic ulceration.

Consider use of a prophylactic agent (ranitidine 50 mg IVI 8 hrly) if patient is not enterally fed

and:

• Pre-existing or intercurrent coagulopathy

• Mechanical ventilation > 48hrs

3.10.2 Active GI Bleeding

3.10.2.1 Diagnosis

• Revealed blood: Nasogastric blood, haematemesis, malaena

• A fall in systolic blood pressure > 20 mmHg

• Drop in Hb > 20 g.L-1 in 24 hours, or requiring transfusion of blood

3.10.2.2 Management

• ABC / resuscitate

• Correct coagulopathy/cease heparin

• Omeprazole40-80 mg IVI 12-8 hrly, consider oral/nasogastric once stable.

• Endoscopy ± sclerotherapy/colonoscopy/angiography and attempted vessel embolism if

clinically appropriate.

83

3.11 ICU Antibiotic Guidelines References

3.10.3 Use of gastro-intestinal pro-kinetic agents

3.10.3.1 General Gastric stasis, colonic and small intestinal ileus are common manage-

ment problems in the intensive care unit. It may be necessary to explore jejunal feeding tube

placement and or the use of prokinetic agents to facilitate enteral feeding (see algorithm on

enteral feeding).

3.10.3.2 Contra-indications Erythromycin interacts significantly with other drugs metabolised

by the Cytochrome P450 enzyme system, with potentially lethal side effects (eg. arrhythmia).

Potential drug interactions must be reviewed prior to commencing these medications.

3.11 ICU Antibiotic Guidelines

3.11.1 Prologue

Emerging bacterial resistance is one of the major challenges facing modern intensive care. It is

the duty of all members of staff to actively participate in the appropriate use of anti-microbials,

while adopting proven infection control behaviour.

3.11.2 Introduction

This section cannot be a comprehensive guide, but should aid staff as to the unit preferences

in antibiotic prescribing practice.

Junior staff may not prescribe or change antibiotics without prior discussion with the Intensivist

or the Consultant Microbiologist.

All antibiotic charting must be reviewed daily.

The unit microbiological results must be reviewed daily and recorded in the patient notes.

All suggested drug dosages (magnitude and frequency) given in this section are intended for

the general population, with normal renal function. When prescribing drugs in the elderly, and

any patients with significant renal or hepatic insufficiency, you must allow for modified drug

handling.

3.11.3 Principles of prescription

3.11.3.1 Prophylaxis

General Prophylactic antimicrobial therapy should be restricted to situations in which it has

been shown to be effective, or where the consequences of

infection are disastrous.

Antimicrobials should be directed against likely causative organisms, however it is not rational

to attempt to cover all possible microbes.

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4 FLUIDS AND ELECTROLYTES

Timing Antibiotics for the purpose of prophylaxis should be administered at the time of

anaesthetic induction, and to cover the period of surgery and / or microbe implantation.

A second dose of antibiotic may be warranted if the operation continues beyond one half of

the normal dosing interval for the agent being used.

There may be some evidence in specific types of surgery (eg. vascular surgery) for extending

prophylactic cover beyond the immediate operative period, however in general there is little

evidence to support such a practice.

Preferred antibiotics Please confirm antibiotic choice and duration with each individual

surgeon at the time of admission of the patient to the Intensive Care Unit. The antibiotic

choices given below would constitute a rational approach, however it is generally not the role

of the ICU staff to direct surgical choice of agent or duration of prophylaxis.

3.11.3.2 Complications of antibiotic use

• Drug hypersensitivity: Dermal eruptions, anaphylactoid/anaphylactic reactions

• Drug toxicity: Idiosyncratic (non-dose related) or dose related.

– Flucloxacillin-hepatotoxicity

– Aminoglycoside-renal toxicity

• Emergence of bacterial resistance

• Selection of nosocomial colonising organisms (and potential pathogens)

– Pseudomembranous colitis

4 Fluids and Electrolytes

4.1 Principles of Fluid Management in Intensive Care

4.1.1 Fluid charting

4.1.1.1 Prologue

• All fluid prescriptions must be reviewed daily.

• Non-standard / bolus fluid orders must be charted individually

• Fluid orders should be considered in two components

4.1.1.2 Maintenance or replacement fluids

• Daily total fluid administration including enteral feeding = 30-40 ml.kg-1day-1 or 80-100

ml.hr-1, selected according to patient serum Sodium and/or glucose tolerance + addi-

tional fluid tailored to excessive losses where appropriate.

• 4% dextrose and one 5th normal saline

85

4.1 Principles of Fluid Management in Intensive Care 4 FLUIDS AND ELECTROLYTES

• 5% dextrose

Patients who are anuric or fluid overloaded should not necessarily receive maintenance fluids.

4.1.1.3 Resuscitation fluids The intensive care community is divided on the relative suit-

ability of each fluid in the resuscitation of a critically ill patient. In general if crystalloid (0.9%

saline or Hartmanns solution) is chosen in the first instance, no more than 2000 ml should be

administered, followed by colloid.

Fluid boluses should optimally be titrated against a measurable end-point, although most in

current use are at best imperfect.

4.1.2 Assessment of fluid balance and hydration

4.1.2.1 Clinical markers

• Skin turgor, mucous membrane hydration (poor indicator)

• Heart rate and blood pressure

• Peripheral perfusion, capillary refill

• Biochemical markers

– Serum Na+, Cl-, osmolality

– Urea/creatinine

– Bicarbonate

• Haematocrit

• Charted fluid balance - at best a rough guide

– Charted intake (Charted losses of all types + Insensible losses)

4.1.2.2 Predictors of increased cardiac output in response to administration of fluid

• JVP / CVP: Useful in patients with normal lungs and right heart function. In other patients

a trend in pressures may be useful.

• Pulmonary artery pressures (particularly diastolic), and pulmonary capillary pressure. At

best these are poorly related to a response to further fluid (pre-load), and are not widely

employed in Mid Yorks ICUs.

• PiCCO derived estimates of intra-thoracic blood volume and extra vascular lung water.

• Variation in arterial wave form peak with positive pressure ventilatory cycle.

This is a notoriously difficult aspect of critical care practice. Often the decision to administer

fluid is governed by a conglomeration of each of the following. If you are in any doubt consult

the senio Anaesthetist, but do not delay the administration of fluid in the acute resuscitation

phase.

86

4 FLUIDS AND ELECTROLYTES 4.2 Electrolyte Abnormalities

4.1.3 Body Fluid and Electrolyte Physiology

A working knowledge of the distribution of fluid and electrolytes throughout the body is re-

quired before any rational prescribing process can begin.

What follows are salient notes on fluid and electrolyte distribution, and some of the more

common disorders encountered in the intensive care setting.

4.1.3.1 Determinants of solute movement and concentration

Passive transport mechanisms

• Diffusion: movement of a solute from an area of higher concentration to one of lower

• Non-ionic diffusion

• Gibbs-Donnan effect: The unequal distribution of diffusible ions on either side of a mem-

brane can be explained if one side contains a poorly diffusible ion (eg. albumin-anion),

since at equilibrium:

– The product of the diffusible ions in one compartment will equal the product of the

same ions in the other compartment.

– Within each compartment the total cationic charges equal the total anionic charges-

electrical neutrality must be maintained in passive systems.

Active transport mechanisms

• Energy requiring mechanisms which distribute a substance across a membrane, in a man-

ner not achievable by physical forces alone. These are essential for establishing electrical

and ionic differences across membranes, the basis for tissue excitability and other funda-

mental functions of the body.

4.2 Electrolyte Abnormalities

4.2.1 Approach

Electrolyte derangement should be viewed as resulting from one of the following.

• Erroneous results:

– Lab error

– Haemolysed specimen

• Factitious results: eg hyperglycaemia and hyponatraemia; lipaemic serum.

• Blood taken in proximity to an intravenous infusion

• Decreased or increased intake

• Decreased or increased loss (renal versus extra-renal)

• Shifts between compartments: eg potassium driven intra-cellularly by insulin.

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4.2 Electrolyte Abnormalities 4 FLUIDS AND ELECTROLYTES

Treatment of electrolyte disturbance should be aimed at not only the apparent problem but

also the underlying cause.

Consideration should be given to the consequences of rapid correction of measured plasma

electrolyte imbalances, particularly the longstanding and chronic forms, where there may have

been some intracellular accommodation.

4.2.2 Hyponatraemia: Na+ < 130 mmol.L-1

4.2.2.1 Aetiology

Factitious

• Measured plasma osmolarity > 290 mmol.L-1:

– Hyponatraemia in hyperglycaemia: For every 10 mmol.L-1 increase in glucose, serum

sodium falls 3 mmol.L-1. It is in a sense a real hyponatraemia, however treatment

aimed at correcting the blood glucose will resolve the hyponatraemia.

– Mannitol: not usually a clinical issue, however later diuresis and hypernatraemia may

be.

– Alcohol (including methanol)

• Measured plasma osmolarity 270-290 mmol.L-1

– Hyperlipidaemia

– Hyperproteinaemia

Neither of the above should be a problem with current ion-specific electrodes.

Measured plasma osmolarity < 270 mmol.L-1 Hypovolaemia with Sodium depletion

• Renal

– diuretics

– Addisons

– Polyuric renal failure or diuretic recovery phase of renal dysfunction

• Extra-renal

– GIT loss

– Burns

Hypervolaemia (water excess)

• Renal failure: acute or chronic

• Extra-renal

• Excessive intake (IVI 5% dextrose)

• Oedematous states: CCF, cirrhosis, nephrotic syndrome, hypoalbuminaemia.

Normovolaemia

88


• Psychogenic polydipsia

• SIADH

• Hypothyroidism

• Acute adrenal insufficiency

4.2.2.2 Management of Severe Hyponatraemia with fitting or decreased LOC Re-

suscitative measures and ABC principles should not be delayed.

Hypertonic saline (3, 20, 29% ) may be indicated but should not be used without prior discus-

sion with the Consultant Intensivist, unless the patient is actively fitting.

Hypertonic saline is very irritant and is best administered via central venous access where

time allows.

An infusion of 50-70 mmol.hr-1 of sodium should increase the serum sodium by approximately

2 mmol.L-1hour-1.

The serum sodium should not be allowed to increase more than 20 mmol.L-1 in the first

24 hours, and certainly should not be overcorrected (serum sodium > 130 mmol.L-1).

In very rare circumstances where fitting or encephalopathy are life threatening, 500 ml of 20%

mannitol has been used.

Hypovolaemic states Restore volume with normal saline or colloid according to clinical

estimate (fluid balance, weight, JVP, CVP).

Urine Sodium may be misleading in the context of diuretic administration or use of cate-

cholamines.

Hypervolaemic states-most common scenario clinically

• Fluid restriction if safe to do so ( < 15 ml.kg-1day-1)

• Excess should correct as ADH levels re-set (often ADH ↑ post surgery)

• Address underlying cause (cardiac failure etc)

SIADH-often misdiagnosed Diagnosis:

• Low serum osmolarity

• Urine osmolarity > plasma osmolarity

• Urine Sodium > 40 mmol.L-1 with normal renal, hepatic and cardiac function, and no

diuretic use.

Management:

• Fluid restriction ( < 1000 ml / day)

4.2.3 Hypernatraemia: Na+ > 145 mmol.L-1

Aetiology

89


Water depletion Virtually all body fluids have a Sodium concentration less than that of

plasma

• Renal loss

– Diuretics or osmotic diuresis

– ARF / CRF

– Diabetes insipidus:

* Neurogenic (including Guillain-Barre)

* Nephrogenic: Hypercalcaemia, hypokalaemia, drug related (lithium), congenital

– GIT losses: diarrhoea, vomiting fistulae, small bowel obstruction

– Skin losses: fever, vasodilated states, burns, thyrotoxicosis

– Inappropriate fluid restriction or under administration (elderly, post operative nil by

mouth)

Salt gain

• Iatrogenic administration of Sodium containing feed or IVI fluids.

• Mineralocorticoid excess

Management

Water depletion / hypovolaemia Resuscitate if necessary

Restore volume over 24-28 hrs using a relatively hyponatraemic fluid (half normal saline or 5%

dextrose), if necessary a rough estimate of fluid

deficit can be calculated:

Water deficit =(measured serum Na+)−140

140 ×body weight×0.6

e.g. a 70kg male with a serum sodium of 160 mmol.L-1 might be expected to have a fluid

deficit of 6 litres.

Do not correct Sodium by more than 2 mmol.hr-1.

Consider DDAVP if central diabetes insipidus has been confirmed.

Excess salt intake Address cause

4.2.4 Hypokalaemia: K+ < 3.5 mmol.L-1

4.2.4.1 Aetiology/classification

• Increased loss

– Renal

90


– Diuretics

– ↓serum Magnesium, ↓ serum Calcium

– Steroids and mineralocorticoid excess

– Renal tubular acidoses

– GIT: diarrhoea, hypersecretory states (villous adenoma, small bowel fistulae)

– Inadequate dietary intake or daily administration

• Transcellular shifts:

– β-stimulants (catecholamines, salbutamol)

– Insulin (endogenous or exogenous)

– Familial periodic paralysis and related syndromes (consider thyrotoxic states).

– ↑ pH

4.2.4.2 Management Potassium replacement intravenously or orally.

Intravenous replacement should not exceed 40 mmol.hr-1, concentrated solutions should

be administered centrally and the patient carefully monitored.

Concentrated solutions should not be administered peripherally.

Address cause of K+ loss.

A low threshold should be adopted for co-administration of magnesium as an essential co-

factor in Na+-K+ pumps. Patients who are magnesium deficient will remain hypokalaemic

despite generous administration of potassium.

4.2.5 Hyperkalaemia: K+ > 5.0 mmolL-1

4.2.5.1 Aetiology/classification

• Factitious

– Sampling in proximity to venous infusion

– Haemolysis: i.e. collection using vacuum tube systems (venous sampling via vacu-

tainer with narrow gauge needle)

– Extremes of thrombocytosis and leukocytosis.

• Release from intra-cellular compartments:

– Acidosis: ↓pH by 0.1 ∼= serum K+ ↑ by 0.5 mmol.L-1.

– Tissue disruption: tumour lysis syndromes, rhabdomyolysis, intravascular haemoly-

sis, burns

– Suxamethonium (note: see section on drugs for intubation 2.6.1.3)

– ”Insulin deficiency”: the hyperkalaemia associated with diabetic ketoacidotic states

is related to lack of insulin and a change in serum pH but is usually associated with a

total body potassium deficit.

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• Increased intake: Not usually a problem unless patient has impaired renal function.

• Reduced potassium clearance:

– Acute renal failure

– Renal tubular acidosis: type 4

– Potassium sparing diuretics: spironolactone, amiloride

4.2.5.2 Management Patients with a slow rise in serum potassium usually tolerate ele-

vated levels better than following an acute rise.

Where elevated serum potassium (generally > 6.0 mmol.L-1) is associated with acute ECG

changes or haemodynamic compromise this should be considered a medical emergency and

treated as follows:

• Calcium Chloride 10 ml IVI stat, repeated in 20 minutes if appropriate. Membrane sta-

bilisation. First line action. Has no effect on serum potassium concentration.

• Insulin Bolus: 10 units actrapid equivalent insulin with 50 ml 50% dextrose infusion OR

20 units of actrapid insulin in 500 ml 10% dextrose over 30-60 min. Intracellular transfer

of potassium. Temporising measure. Probable decrease in serum potassium concentra-

tion of 1 mmol/L for 30-60 minutes with some effect up to 3 hours (either method)

Calcium and a dextrose-insulin preparation are appropriate measures to institute in the short

term, pending use of definitive treatment (eg. resuscitation, exchange resin, or haemodialy-

sis).

• Bicarbonate bolus equivalent to 50-100 mmol. Promotes cellular uptake of potassium by

reducing hydrogen-potassium exchange. Temporising measure only. Do not administer

with Calcium salts. Not appropriate in hypovolaemic acidotic patients.

• Exchange resins: resonium sodium (or Calcium) resonium 30-60g orally or rectally 8

hourly. Sometimes given with lactulose 20ml. Exchanges K+ for alternative cation in gut,

therefore action delayed for > 120 minutes. Definitive but delayed treatment. May be

difficult to administer in ICU patients with abnormal gut motility.

• β2 stimulants: Nebuliser: 10-20 mg by nebuliser over 10 minutes. IVI: 0.5 mg IVI over

10-15 minutes. Intra-cellular transfer of potassium. Temporising agent although concern

exists over the use of an arrhythmogenic agent in the critically ill.

4.2.6 Hypophosphataemia: Serum Phosphate < 0.7 mmol.L-1

Low serum phosphate is associated with serious clinical consequences, and is probably under-

appreciated in critically ill patients.

Some studies suggest an incidence of up to a third of all ICU patients may be phosphate

deficient.

4.2.6.1 Aetiology

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4 FLUIDS AND ELECTROLYTES 4.3 Acid-Base Disturbances in the ICU

• Inadequate input

– GIT phosphate binders (eg. laxatives, antacids)

– Starvation

– Vomiting or nasogastric suctioning

– Relative or absolute Vit D deficiency

• Transcellular shifts

– Carbohydrate loading, re-feeding phenomenon.

– Drugs: Insulin, catecholamines, steroids, ?2-agonists

• Excessive losses

– Massive diuresis

– Dialysis, including continuous replacement modalities.

4.2.6.2 Clinical effects All energy requiring processes may be involved.

• Cardiac: Decreased contractility.

• Respiratory: Failure to wean.

• Muscle / bone: Myopathy, Rhabdomyolysis, Osteomalacia.

• Haematological: Dysfunction of all formed elements of blood.

• Renal: Acute tubular necrosis.

4.2.6.3 Phosphate replacement

>0.7mmol.L-1 0.16 mmol.kg-1 over 4-6 hrs

0.5-0.7mmol.L-1 0.32 mmol-1kg over 4-6hrs

<0.5mmol.L-1 0.64 mmol.kg-1 over 8-12hrs.

4.3 Acid-Base Disturbances in the ICU

4.3.1 Introduction

Critically ill patients commonly have a deranged acid base status. Despite this, explanations

of the physiology behind the process are not universally accepted. It is necessary to have an

approach to the clinical importance of each of the common major abnormalities, even given

the complex and often mixed scenarios you might encounter. You are encouraged to read

widely on the subject of acid-base disorders and the opposing ideologies put forward to explain

them.

Correction of acid-base disturbance should be aimed at the underlying cause, and not at cor-

rection of the superficial abnormality.

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4.3 Acid-Base Disturbances in the ICU 4 FLUIDS AND ELECTROLYTES

4.3.2 General principles

The concept of pH:

pH = negative log of the hydrogen ion concentration. Normal range = 7.36 -7.40

4.3.2.1 Regulation of pH Without regulation of acid-base, the daily production of non-

volatile H+ in a normal person (about 70 mmol) would reduce the pH in a volume of water

similar to that of a 70kg man (42 L) from 7.4 to a pH of 2.78.

The human body is an open system in which other organ systems and tissues contribute to the

maintenance of the free [H+] within a narrow, biologically tolerable range.

Henderson Equation: [H+] =K × CO2

[HCO−3 ]

Henderson/Hasselbach Equation: pH =6.1 + log[HCO−

3 ]PaCO2 × 0.03

From both the above it is clear that any mechanism responsible for regulating or affecting pH

does so by changing the relative concentrations of HCO-3, PaCO2 or H+ directly.

The response of the body to an enforced change in one of these parameters takes place in

three broad groups:

• Adjusting minute ventilation (increasing respiratory rate or tidal volume) to manipulate

PaCO2

• Buffering systems:

– Bicarbonate ion

– Haemoglobin

– Protein substrates

– Phosphate

• Renal compensation: delayed > 6-12hrs

Primary and secondary acid-base derangements End point: ”constant” PCO2 : HCO-3

ratio

• Respiratory acidosis

– Primary change: ↑ PCO2

– Compensatory change: ↑ HCO-3

• Respiratory alkalosis

– Primary change: ↓ PCO2

– Compensatory change: ↓ HCO-3

• Metabolic acidosis

– Primary change: ↓ HCO-3

94


– Compensatory change: ↓ PCO2

• Metabolic alkalosis

– Primary change: ↑ HCO-3

– Compensatory change: ↑ PCO2

Compensatory changes are never complete, and certainly overcompensation does not occur.

Adequacy of compensation

The expected magnitude of compensation for a primary abnormality is given below. In critically

ill or ventilated patients this compensation may not be possible, presenting as a mixed or

complex problem.

4.3.3 Metabolic Acidosis

4.3.3.1 The anion gap Classically metabolic acidoses are classified according to the con-

cept of anion gap. Whilst the body must maintain overall electrical neutrality there are a

number of unmeasured ions which result in a difference when the major cations are compared

to the major anions.

ie. Anion Gap = [Na++ K+]-[Cl- + HCO-3] = 12-17 mmol.L-1 = unmeasured anions

Unmeasured anions

• Proteins (albumin) 15 mmol.L-1

• Organic acids (lactate, ketones) 5 mmol.L-1

• Phosphates 2 mmol.L-1

• Sulphates 1 mmol.L-1

Unmeasured cations

• Calcium 2.5 mmol.L-1

• Magnesium 1.2 mmol.L-1

• IgG

• Other

An increase in anion gap usually means an increase in an organic acid. In some patients with

low serum albumin this may be masked unless you adjust accordingly.

4.3.3.2 Aetiology

Raised anion gap metabolic acidosis

• Lactic acidosis

• Ketoacidosis

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4.3 Acid-Base Disturbances in the ICU 4 FLUIDS AND ELECTROLYTES

• Rhabdomyolysis

• Drugs or toxins:

– Aspirin (may result in elevated salicylate, lactate, ketones

– Ethanol

– Methanol

– Ethylene glycol

– Paraldehyde

• Renal failure: usually only mildly elevated anion gap ( < 23)

Low or normal anion gap acidosis

• Hyperchloraemic metabolic acidosis:

– Infusion IVI of NaCl

– Resolving renal failure

– Renal tubular acidosis / carbonic anhydrase inhibitors

– GIT losses including fistulae

• Hypoalbuminaemia

• Myeloma

4.3.3.3 Management

High anion gap Address cause. Bicarbonate administration is not indicated

Normal anion gap Address underlying cause.

In some situations (eg. renal tubular acidosis) it may be appropriate to replace / administer

bicarbonate directly.

Approx deficit = (24-[HCO-3]) × (body weight × 0.6) in mmol.

Generally one third to one half of the estimated deficit should be replaced and then acid-base

status reviewed.

4.3.4 Metabolic Alkalosis

4.3.4.1 Aetiology

Common causes

• Diuretics

• Vomiting

96


• Post hypercapnoea > 48 hrs

• Any fluid loss replaced with insufficient Na+, associated with H+ loss (contraction alkalo-

sis).

• Association with hypovolaemia and / or hypokalaemia

H+/Proton loss

• Renal

– Na+ reabsorption

– Cushings syndrome including exogenous steroid administration

– Proximal tubulopathies: Bartters syndrome, Liddles syndrome

– Hypercalcaemia / hypomagnesaemia associated with diabetes insipidus

– Diuretics

• GIT

– NG suctioning or protracted vomiting

– Diarrhoea (acidosis more likely)

Increased administration of bases CVVHDF-lactate buffered solution

4.3.4.2 Management Correct hypovolaemia and electrolyte abnormalities. Review drugs,

and administration of exogenous bases (lactate buffered dialysate, citrate).

Acetazolamide has been used to increase renal losses of bicarbonate, however this should not

be considered routine practice.

4.3.5 Respiratory Acidosis

4.3.5.1 Aetiology Any cause of hypoventilation, whether respiratory failure or planned (per-

missive hypercapnoea ventilation).

4.3.5.2 Treatment Address underlying respiratory pathology

4.3.6 Respiratory Alkalosis

4.3.6.1 Aetiology

• Any cause of hyperventilation in ICU eg. early sepsis

– Early hypoxic situations

– Anxiety

– Hysteria (NB this is a diagnosis by exclusion, and presumes normal oxygenation)

– Neurogenic hyperventilation: usually a marker of severity of head injury.

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4.4 Nutrition 4 FLUIDS AND ELECTROLYTES

4.3.6.2 Treatment Treat underlying problem.

4.4 Nutrition

4.4.1 Enteral Nutrition

The prevalence of malnutrition is increasing in hospitalised patients due to the aging process

of the general population and the development of aggressive medical and surgical treatments

for chronic debilitating diseases.

The positive consequences of enteral feeding however may go beyond nutrition and extend to

immune modulation, and possibly bacterial translocation through the gut.

Enteric feeding is the preferred mode of nutritional support and should be considered in all

patients admitted to the ICU.

4.4.1.1 Advantages

• In some patient subgroups (trauma) early enteral feeding improves patient outcome.

• Enteral feeding helps retain gut integrity and reduce atrophic changes.

• May reduce the incidence of gastric erosions and stress ulceration

• Cost effective: Cheaper than TPN (2p.day-1 vs £80.day-1)!

• Complications of central access for TPN are reduced (invasive procedures, infective risk)

4.4.1.2 Disadvantages

• Regurgitation / aspiration (no difference gastric versus distal feeding)

• Diarrhoea: diarrhoea may be a result of osmotic load to the gut, however it is not the most

likely reason for diarrhoea in critically ill patients, and other causes should be sought and

excluded.

4.4.1.3 Indications All ICU patients with a secure airway and functioning gut may receive

enteral feeding.

Patients admitted post surgical intervention should have the intention to feed cleared with the

surgeon in charge.

Patients with operatively placed jejunostomy may commence feeding within 6 hours of place-

ment (again, confer with the surgeon).

Where gastric feeding has not been established by day 5 of ICU admission (or earlier if un-

dernourished), a post-pyloric (duodenal / jejunal) tube should be considered for distal feeding.

Use of hypercaloric feeds may be considered to ensure reasonable intake.

Consider placing a fine bore feeding tube, to reduce irritation and ulceration, once feeding has

been established for a reasonable length of time (5-7 days).

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4 FLUIDS AND ELECTROLYTES 4.4 Nutrition

4.4.1.4 Contra-indications

Absolute

• Non-functional gut: anatomical disruption, obstruction, gut ischaemia

• Generalised peritonitis

• Severe shock states

Relative

• Expected short period of fasting (except trauma patients)

• Abdominal distension while feeding enterically

• Localised peritonitis, intra-abdominal abscess, severe pancreatitis

• Comatose patients at risk of aspiration

• Extremely short bowel ( < 30 cm)

4.4.1.5 Feeding Guideline

• Place a 12F or larger nasogastric tube to allow reliable aspiration (orogastric tube should

be considered in patients with anterior and middle cranial fossa trauma).

• Check position of feeding tube with abdo X-ray prior to feeding. It may not be obvious

from standard CXR or AXR that the tube is adequately placed, requiring a modified film

or both views.

• Nurse the patient at 30-45 degrees head up.

• Commence feeds at 30 ml/hr and feed continuously according to the attached protocol.

• Aspirate the tube 4 hrly (do not attempt routine aspiration of jejunostomies, naso-duodenal

or naso-jejunal tubes.

• Flush jejunostomy or gastrostomy tubes with 10-20 ml of saline 6 hourly if not being used.

4.4.1.6 Prokinetics: If feeding is persistently not tolerated > 48hrs then consider

• Reduction in narcotic dosage

• Use of a prokinetic agent: metoclopramide 10 mg IVI 6 hrly, then if necessary ery-

thromycin 70 mg mg IVI od.

• Post-pyloric feeding

4.4.1.7 Choice of enteral feed (see appendix for enteral feed content)

Most patients should be commenced on a standard isocaloric feed such as Osmolyte (standard)

Nutritional supplementation should be adjusted to provide approximately 20-35 kCal.kg-1.day-1

of non protein energy, and 1.5 g.kg-1 body weight of protein per day.

Immuno-fortified feed (with glutamine, arginine, nucleotides, omega-3-fatty acids) have shown

some benefit in small studies to date. Their use is accepted to be of benefit in polytrauma pa-

tients. Despite this there is as yet no defined place for these feed types in the ICU setting

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4.4 Nutrition 4 FLUIDS AND ELECTROLYTES

Figure 1: Enteral Feeding Agorithm

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4 FLUIDS AND ELECTROLYTES 4.4 Nutrition

4.4.2 Parenteral Nutrition

4.4.2.1 General Historical attempts at hyper-alimentation may have resulted in the role

of TPN in the ICU diminishing over the last 10 20 years. Concerns still exist over potential

immuno-suppression, hyperglycaemia and the infection risk coupled with central venous ac-

cess.

TPN should not be ordered unless requested by the Consultant Intensivist.

4.4.2.2 Indications Total parenteral nutrition should only be considered in patients who are

not suitable for enteric feeding.

Short term:

• No oral intake likely > 2 weeks

• Weight loss > 10 % starting body weight

Long term:

• Structural or functional short bowel syndrome

4.4.2.3 Vascular access TPN is generally administered by central venous access.

Where duration of TPN is envisaged to be less than 2 weeks it may be acceptable to consider

peripheral IV nutrition.


• Depression of immune function

• Gut villous atrophy

• Metabolic imbalance:

– Electrolyte disturbance

– Glucose intolerance

– Hyperosmolar dehydration syndrome

– Rebound hypoglycaemia on ceasing TPN

– Hyperbilirubinaemia

• Fluid imbalance

• Trace element and vitamin deficiency

• Complications of central venous access.

4.4.2.5 Charting TPN

Choice of formula

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4.5 Blood and Blood Products 4 FLUIDS AND ELECTROLYTES

4.5 Blood and Blood Products

4.5.1 Introduction

The decision to transfuse a patient, or administer other blood products, is the prerogative of

the Consultant Intensivist.

Whenever reasonable, the patients informed consent to proceed with transfusion should be

obtained.

4.5.2 Blood transfusion

4.5.2.1 Acute resuscitation Excessive ongoing haemorrhage is usually surgical in origin.

In these circumstances transfusing blood products should be viewed as a bridging procedure

until definitive treatment is undertaken.

Platelet count and coagulations studies should be performed, and if abnormal addressed as

required.

Blood replacement in an otherwise fit patient should be considered once blood loss is antici-

pated to exceed 25% of total blood volume (or 1000-1500ml).

A full cross match may take up to 20 minutes, if blood is required faster than this consider one

of the following:

Group specific (ABO, Rh+) blood without full compatibility testing may be available faster (5-10

minutes).

O negative blood can be issued immediately in a true emergency, while similarly O positive

blood can be used for men, or women past child bearing age.

4.5.2.2 Elective transfusion Traditionally a haematocrit of 30% or absolute haemoglobin

of 10 g.dL-1 have been used as a trigger to transfuse a patient.

In stable patients with adequate oxygenation there is no need to transfuse until Hb < 7.0

g.dL-1.

Critically ill patients with poor oxygenation, myocardial ischaemia, acute head injury or ongo-

ing risk of blood loss may require earlier transfusion.

4.5.3 Platelet transfusion

4.5.3.1 Indications Permission may have to be sought from a Haematologist prior to platelets

being issued.

Spontaneous haemorrhage is rare at platelet counts of > 10 × 109.µL-1 (or > 20 ×109 .µL-1 in

febrile patients)

Prophylactic transfusion before surgery or invasive procedure:

• Platelet count < 50 × 109.µL-1

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4 FLUIDS AND ELECTROLYTES 4.5 Blood and Blood Products

• Platelet count > 50 × 109.µL-1 where there is evidence of abnormal platelet function (eg.

uraemia, aspirin therapy)

Uncontrolled haemorrhage:

• Transfuse platelets at platelet count < 100 × 109.µL-1

• Consider transfusing platelets at any threshold if there is reason to suspect platelet dys-

function.

Bone Marrow failure, TTP ,ITP, or H.I.T.S.

• Seek advice from haematology team.

• Seek input from haematology team.

4.5.3.2 Dosing of platelets One dose of platelets usually means pooled donor platelets

from 4 or more donors.

One dose approximates 3-3.5 × 1011 platelets, or enough to increase the platelet count by

20-25 × 109.µL-1 at 24 hours, in the absence of further problems.

4.5.3.3 Risk of transfusion In general the risk is similar to that for blood transfusion with

the following addition:

There is a higher risk of bacterial contamination than whole blood (0.6 / 1000 cases per dose)

HLA allo-immunisation may occur in 45-62% of long term recipients, resulting in transfusion

resistant thrombocytopaenia.

Platelet specific antibodies may develop (4% of patients)

4.5.3.4 Adjunctive treatment Administration of DDAVP 0.3-0.4 µg.kg-1 over 30 minutes

may increase levels of factor VIII:C and VIII:vWF with increased platelet adhesion.

Indication

• Haemophilia A, type I von Willebrands Disease.

• Bleeding post cardio-pulmonary bypass

• Uraemia

• Platelet dysfunction secondary to aspirin

Other scenarios where platelet dysfunction is suspected and platelet transfusion might be

delayed, or stock exhausted.

4.5.4 Fresh Frozen Plasma

4.5.4.1 Indications

• Prophylactic transfusion prior to surgery or other invasive procedure

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4.5 Blood and Blood Products 4 FLUIDS AND ELECTROLYTES

– Patients on warfarin ro vit K deficiency: consider partial reversal with 1 mg Vit K or

full reversal with 10 mg Vit K if time allows (24-36hrs).

– Prolonged INR or APTT in patients with liver disease

– Inherited coagulation factor deficiency when factor concentrates not available.

• Uncontrolled haemorrhage

– Warfarin or Vit K deficiency

– Prolonged INR or APTT in patients with liver disease

– Inherited coagulation factor deficiency when factor concentrates not available

– DIC

• Massive transfusion:

– Consider administering Calcium as citrated stored blood is Calcium deficient, retard-

ing the clotting cascade.

– Whole stored blood does not contain clotting factors in any appreciable number

– Consider transfusion when INR > 1.5 or APTT > 40 seconds.

• Plasma exchange in TTP and related syndromes.

4.5.4.2 Dosing of FFP 10-15 ml.kg-1 (average 2-4 units) according to clotting profile.

4.5.4.3 FFP in the setting of heparin overdose Protamine is the drug of choice for re-

versing excessive unfractionated heparin effect. Protamine is not effective in the setting of

Low Molecular Weight Heparin, and it may be tempting to administer FFP. Theoretically this

carries the risk of potentiating bleeding by further increasing ATIII availability.

4.5.5 Cryoprecipitate

4.5.5.1 Indications

• Diffuse microvascular bleeding and fibrinogen < 1.0 g.L-1

• DIC

• Massive transfusion

• Hereditary hypofibrinogenaemia

4.5.5.2 Dose Ten units of cryoprecipitate would be expected to increase plasma fibrinogen

by 1.0 g.L-1

4.5.6 DIC

Definition: A process representing disordered balance of the haemostatic and fibrinolytic

systems, usually in response to severe pathophysiological stimuli as part of mul-

tisystem organ dysfunction.

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4 FLUIDS AND ELECTROLYTES 4.5 Blood and Blood Products

Characterised by:

• Microthrombi formation causing microvascular obstruction

• Consumption of platelets and clotting factors

• Thrombocytopaenia

4.5.6.1 Diagnosis-DIC screen

• Blood smear examination for evidence of red cell fragmentation, haemolysis, thrombocy-

topaenia.

• Extended coagulation screen:

– Prolongation of thrombin clotting time, APTT, Prothrombin time.

– Hypofibrinoginaemia

– Low factor VIII

– Elevated fibrin breakdown products (FDPs).

• Liver function tests and renal function review.

4.5.6.2 Treatment Treat the underlying cause!

Replace blood components as assessed by above DIC screen if patient bleeding or at risk of

bleeding.

4.5.6.3 Controversial therapies Heparin, fibrinolytics, antifibrinolytics (aminocaproic acid)

and other agents have been described in the literature. They do not form part of standard ther-

apy and should not be attempted without ICU consultant approval, and not before exhausting

other therapies at the advice of the haematology specialty service.

4.5.7 Blood transfusion reaction guidelines

4.5.7.1 Introduction A wide range of reactions can be manifest upon infusion of blood

products.

The response to a suspected reaction depends on the urgency of the transfusion and the

magnitude of the adverse reaction.

4.5.7.2 Suspected transfusion reaction Stop the infusion and check the patient details

against that of the blood product. If there is any discrepancy then discontinue the transfusion.

If patient and product details are correct then proceed as follows.

Mild reactions

Temperature rise < 1.5o C without hives, rash, bronchospasm or cardiovascular compromise:

restart transfusion at slower rate.

Moderate reactions

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5 CLINICAL MANAGEMENT

If temperature rise > 1.5o C with other manifestations, administer antipyretic (paracetamol

1g) and restart transfusion of the same unit after 20 minutes.

Severe reactions

If any signs or symptoms in addition to temperature rise, discontinue the transfusion and

return the blood product to blood bank for re-crossmatch and culture.

Treat as for anaphylaxis:

• Volume resuscitation

• Adrenaline or vasopressor as necessary.

• Bronchodilators if significant airway outflow obstruction.

• Adjuncts: anti-histamine, theophylline, corticosteroids may not be appropriate in ICU pop-

ulation and should be discussed with the Consultant.

5 Clinical Management

5.1 Introduction

The purpose of this chapter is not to dictate rigid policies on the most appropriate way to

manage every patient. Rather it is to provide guidelines on reasonable clinical practice based

on the available evidence and where that is lacking, based on consensus practice.

As you will come to realise during your stay in the ICU very few patients read the appropriate

textbooks prior to becoming ill. Patients therefore may not behave in a classical or expected

manner. It is in these patients that these guidelines may help you to adopt a reasonable and

standardised approach.

5.2 Cardio-Pulmonary Resuscitation

5.2.0.3 Introduction It is clearly beyond the scope of this document to outline the skills,

knowledge and algorithms required to implement advanced cardiac life support.

Whilst we have little control at present over community cardiac arrests, and to a lesser ex-

tent hospital cardiac arrest, it must be stressed that vigilance and pro-active management of

critically ill patients may abort a process precipitating a cardiac arrest within the ICU.

For ease of referral the combined basic life support and Advanced Cardiac Life Support Algo-

rithm appear below. Please refer to the appendix ACLS Algorithms for a more comprehensive

list.

5.2.1 Key Points in the management plan for an adult collapse

In adult cardiac arrest, VF / VT is the most likely rhythm, and a defibrillator the only effective

treatment.

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5 CLINICAL MANAGEMENT 5.2 Cardio-Pulmonary Resuscitation

Start effective CPR as soon after the circulatory arrest as possible. Effective artificial circula-

tion requires controlled, uninterrupted chest compression. The ratio of compressions to venti-

lation is 15:2 in all instances except when an ETT is in place, when it is 5:1 with no compression

pause. The rate of compression is 100 / min.

As soon as possible (especially in unmonitored patient) switch the defibrillator on and check

or confirm the rhythm via the paddles.

• Defibrillate as soon as possible. Defibrillation should take precedence over all other inter-

ventions. Assess for, and shock, VF / pulseless VT, up to 3 times (200J, 200J to 300J, 360J

or equivalent biphasic) if necessary.

Endotracheal intubation, IV insertion and ECG electrode placement / replacement should occur

between defibrillation attempts. The order of priority for these adjuncts is

• secure airway

• ventilate with 100% oxygen

• IV administration.

Augmentation of aortic diastolic pressure should be an adjunctive goal of therapy since coro-

nary perfusion is low during conventional CPR.

Adrenaline and other alpha agonists will significantly increase aortic diastolic pressure. Ad-

minister adrenaline to maintain coronary blood flow if the first three defibrillations fail. 1 mg

of adrenaline every 3 minutes is an acceptable minimum. Vasopressin 40.i.u IV is a suitable

alternative in VF/VT arrests.

Consider and correct if possible any reversible causes of circulatory arrest. (see 5Hs and 5Ts

on algorithm below)

During CPR, adequate ventilation is the mainstay of therapy for acid-base abnormalities. The

indications for Sodium Bicarbonate are:

• Hyperkalaemia

• Tricyclic antidepressant overdose where metabolic acidosis existed prior to arrest.

• Late in cardiac arrest situation (at least > 10 minutes) in intubated hyperventilated pa-

tients.

If VT / VF persists after 9 defibrillating shocks, give amiodarone 150 mg IVI. Give earlier if a

defibrillating shock seems

transiently successful.

5.2.2 Induced hypothermia following cardiac arrest

5.2.2.1 Introduction Patients subjected to therapeutic hypothermia as soon as possible fol-

lowing resuscitation from cardiac arrest may have a better outcome (15-25% absolute survival

advantage). Following consultation with the Consultant Intensivist, short term hypothermia

should be induced as below.

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5.3 Respiratory Therapy 5 CLINICAL MANAGEMENT

5.2.2.2 Patient selection Apply to patients with

• Suspected hypoxic encephalopathy.

• Motor score of GCS 4 or less (ie flexion to pain or worse)

5.2.2.3 Cooling guideline

• Cool as soon as possible following return of circulation.

• Sedate with propofol and alfentanil, with intermittent muscle relaxant to ablate shivering

if prominent

• Actively cool, using water cooled blanket to temperature target of 33 (32.5-33.5) oC for

12 hours, as measured with rectal temp probe.

• After 12 hours actively re-warm to 37 degrees.

• Conduct sedative free neurological assessment. Progress to somato-sensory evoked po-

tentials if awakening slow or absent.

5.2.2.4 Rapid Cooling Rapid onset cooling can be achieved by administering 30ml.kg-1 of

Ringers lactate or other crystalloid, cooled to 4 oC, over a 30 minute period. Do not attempt

this method unless discussed with the Consultant.

5.3 Respiratory Therapy

5.3.1 Introduction

Traditionally the major reason for referral to intensive care, respiratory failure and our under-

standing of how best to manage it is constantly evolving.

Recent advances in ventilatory strategy, and their impact on not only lung injury but also on

other organ dysfunction, necessitates that all staff within the ICU acquire some understanding

of the pathophysiology involved.

While Registrars and residents are encouraged to understand the principles of ventilation, and

indeed participate in the management of ventilated patients; decisions regarding ventilation,

weaning, extubation and other extra-ordinary actions (such as patient proning) remain the

domain of the Consultant Intensivist.

5.3.2 Respiratory Failure

Definition Failure of efficient gas exchange. Either failure to oxygenate adequately, or failure

to ventilate.

5.3.2.1 Failure to oyxygenate adequately PaO2 < 8 kPa under the following conditions:

• FiO2 21% (ie. room air)

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5 CLINICAL MANAGEMENT 5.3 Respiratory Therapy

• Barometric Pressure 101 kPa (sea level)

• No intracardiac shunt

NB: This does not mean taking a patient off oxygen to perform an arterial blood gas, but rather

inferring the need for assistance as stated below.

5.3.2.2 Failure to ventilate adequately PaCO2 > 7 kPa, unless in the presence of a pri-

mary metabolic alkalosis (pH normal or elevated)

5.3.3 Aetiology

• Lung insult

– Pulmonary oedema (hydrostatic-cardiogenic, or leaky capillary-ARDS)

– Pneumonia

– Contusion

– Haemorrhage

• Airway pathology

– Proximal

– Distal: COAD, asthma, bronchiectasis, sputum retention

• Neuromuscular

– Depressant drugs

– Intra-cranial pathology

– Guillan Barré

– Myasthenia Gravis

• Skeletal

– Loss of chest wall integrity: flail chest

– Loss of chest wall elasticity: severe kyphosis or scoliosis

• Intra-thoracic space occupying lesion: Pneumo-/ Haemothorax, pleural effusions.

5.3.4 When Should I Consider Ventilating (± intubating) Patients?

5.3.4.1 Indicators Clinical assessment outweighs any result such as an ABG / CXR or other

objective measurement (see below)

Consider institution of ventilation in the presence of:

• Threatened airway

• Fatigue or imminent exhaustion

• Inability to effectively cough or clear secretions

• Respiratory failure

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5.3.4.2 Objective measurements In the appropriate clinical setting, and where time al-

lows a combination of the following may assist your decision.

• Resp rate > 35 breaths per minute

• Tidal volume < 5 ml.kg-1

• Vital capacity < 15 ml.kg-1

• Abnormal oxygenation as indicated by:

– PaO2 < 10 kPa on an FiO2 > 0.4 (40% O2)

– PaO2 to FiO2 ratio < 150

• Abnormal ventilation as indicated by:

– PaCO2 > 8 kPa

5.3.5 Humidification

5.3.5.1 General Poor conditioning of the temperature and humidity of inspired gases leads

to airway damage, sputum plugging and may even increase morbidity and mortality of during

an ICU stay.

All patients that are intubated/tracheostomised must have adequate humidification of inspired

gases using one of two mechanisms

5.3.5.2 Heat and Moisture Exchangers (HMEs) Effective first line humidifier: Con-

serves patients exhaled water vapour and temperature (gas re-inspired at about 20 oC). Still

requires patient to be able to warm and humidify inspired gas to some degree.

• Not effective at minute volume in excess of 10 l.min-1.

• Must be changed daily

• Cannot be used with an in-line nebuliser.

• Incorporates a bacterial filter.

5.3.5.3 Heated water humidifiers (Fisher and Paykel evaporative humidifier) Where

any doubt exists about adequate humidification, a heated water humidifier should be the de-

fault humidifier, particularly those patients in whom there is bronchorrhoea, sputum inspissa-

tion or haemoptysis.

Generally these devices supply gas to the upper proximal airways at 29-32oC and 95-100%

relative humidity, requiring minimal modification within the lungs.

5.3.6 Mechanical Ventilation

5.3.6.1 Introduction Mechanical ventilation is one of the mainstays Intensive Care Medicine

and you should attempt during your stay to develop an understanding of the basic principles

and practice of ventilation.

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ST1/2s are not expected to manage patient ventilation alone. While most patients can be

ventilated using a default setting (see below), ventilation of complex patients remains the

domain of the Consultant Intensivist.

Senior Critical Care Nursing Staff may be useful resource people to aid in troubleshooting, and

assisting with instituting ventilation using a default setting.

No change may be made to a ventilator without clear written order on the appropriate chart

and communication with bedside staff.

5.3.6.2 Indications for mechanical ventilation

• Respiratory failure

• Maintenance of cardiopulmonary homeostasis in an unstable or high risk environment:

– Following cardiac arrest

– Post-operative support in high risk surgical patients

– Control of intracranial pressure

– Patient Transport / assessment

• Relaxant anaesthesia

• To facilitate treatment in confused state

5.3.6.3 When to consider Intubating and ventilating Patients

• Clinical assessment

– Threatened airway

– Fatigue or imminent exhaustion

– Inability to effectively cough or clear secretions

– Respiratory failure

• Objective measurements

– Respiratory rate > 35 breaths per minute

– Tachycardia

– Hypertension

5.3.6.4 Objectives of mechanical ventilation

• Improve patient oxygenation and improve ventilation perfusion mismatch.

• To improve alveolar ventilation and reduce PaCO2

• To increase end expiratory lung volume, preventing or treating lobar or pulmonary col-

lapse and atelectasis.

• To increase functional residual capacity: PEEP may help improve oxygenation through

lung recruitment, and reduce lung injury with the prevention of repeated opening and

closing of alveoli.

111


• To unload the respiratory muscles when there is respiratory muscle insufficiency or ven-

tilatory failure.

• To allow adequate sedation and paralysis of the patient to aid control to enable the un-

derlying disease state to be adequately treated.

• In some conditions such as trauma where there is loss of chest wall integrity such as in

a flail chest, ventilation may be needed to stabilise the chest wall and to initiate other

treatment such as analgesia with safety.

5.3.6.5 Complications of mechanical ventilation

Haemodynamic Increased intrathoracic pressure-unmasking of hypovolaemia (although there

is significant benefit to LV performance with application of PEEP).

Respiratory

• Nosocomial pneumonia

• Volutrauma

• Barotrauma

• Ventilator dependancy

Metabolic

• Post-hypercapnoeic metabolic alklosis

• SIADH

Local

• Pressure effects from ETT, tracheostomy or face masks.

5.3.7 Ventilator settings

5.3.7.1 Default ventilator settings, and principles in optimizing ventilation in ICU

patients Where there is no reason to expect mechanical ventilation will be complex the

following settings should be chosen:

Mode BI-LEVEL Resembles Pressure controlled Ventilation (PCV) but differs in its ability to

allow spontaneous breathing at both upper and lower pressure levels.

Pressure and inspiratory time are set by operator. Volume and flow are variable according to

patient need. Patients can breathe spontaneously during inspiratory and expiratory phase.

Active value allows free breathing during any phase of breath delivery.

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Initial set up PEEPL: 3cmH20 above lower inflection point (“Best PEEP value”)

PEEPH : adjust to achieve 6ml.kg−1 tidal volume(TV) (maximum 30cmH20 unless set by Con-

sultant Intensivist)

TH : 1.5 sec

Rate: 10 bpm

PS: adjust to achieve 6mls.kg−1 TV(maintain at less than PEEPH value)

FiO2: adjust for SpO2 >92% or PaO2 > 10kPa (unless otherwise directed by intensivist)

FAP (Flow acceleration Percent)/ Rise time: 50%

Ventilator Maintenance Oxygen

Increase FiO2 and TimeH to improve oxygenation.

PEEPL

Adjust PEEPL to just above the lower inflection points on PV curves. This combined with low

volume tidal volume has shown to improve outcome in severe ARDS.

Tidal Volume

The ARDS-net trial suggested 6-8 ml per kilogram ideal body weight per breath (450-550 ml

per delivered breath in a 60 kg woman, 500-650 ml in a 70 kg male). Generally 6-8mls per

kilogram ideal body weight per breath. Inspiratory pressure should be adjusted after initial set

up of ventilation and thereafter to achieve this.

Peak and Plateau pressure should not exceed 30 cmH2O to achieve this unless set by Consul-

tant Intensivist.

Respiratory Rate

10-25 breathes per minute adjusted to an arterial blood gas PaCO2 in the normal range or

approximating pre-morbid level.

It is essential that in patients with ARDS and critical oxygenation that normal PaCO2 is not

chased at the detriment of the patient exposing the patient to the risk of barotrauma and or

volu-trauma. In these patients it is acceptable to allow PaCO2 to rise to 12kPa if the patient is

able to tolerate affect of associated respiratory acidosis on cardiovascular system.

Reverse I:E Ratio

Conventional inspiratory to expiratory ratio(I:E) is 1:2 to 1:4

Reverse ratios can used in critical oxygenation. The alveolus is held at its inspiratory volume

longer. This allows more mixing time and an improvement in ventilation perfusion mismatch-

ing.

There is incomplete lung emptying and auto PEEP develops.

Ensure patient is adequately sedated and paralysis is sometimes required for patient to fully

synchronize with the ventilator.

There may be negative effects on cardiac output (increased intrathoracic pressure impeding

venous return)

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Table 4: PEEP-O2 nomogramFiO2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0

PEEP 5 7.5 10 10 12 12 14 15

Rise time (FAP)

Following Analysis of pressure time curve, and observing patient for signs of increased patient

comfort and synchrony this can be increased or decreased.

Expiratory Sensitivity (ESENS)

Defines the percentage of the projected peak inspiratory flow (Vmax) at which the ventilator

terminates flow, and thus cycles from inspiration to expiration during spontaneous breathing.

If inspiratory flow terminates too early, it can lead to a decreased tidal volume, or increased

inspiratory muscle work load if the patient effort persists after the ventilator has cycled off.

Conversely, if the inspiratory flow persists beyond patient effort, which may happen when

leaks are present, it can result in unnecessary expiratory work and patient/ ventilator dysfunc-

tion.

PEEP As a guideline, PEEP may be applied using the nomogram below, titrated to arterial

oxygen content:

5.3.7.2 Spontaneous mode of ventilation

Indications Consider if

• FiO2 <0.4 and PEEP <12cmH2O and

• PEEP and FiO2 values are trending downwards

• The patient has spontaneous breathing efforts

• Haemodynamically stable

Proportional Assist Ventilation (PAV) PAV harmoniously augments the patients’ respi-

ratory effort – it amplifies the effort – no effort, no support. PAV harmoniously unloads the

patients’ inspiratory muscles. PAV samples the patients’ inspiratory effort every several mil-

liseconds and unloads the patient effort. Amplication is set as function % support, which

ranges between zero and just under 100% support. Zero support is the equivalent of classic

CPAP. Maximal support is 95% when PA is active throughout the entire respiration.

Set up:

• Turn on PAV on spont mode

• The ventilator analyses the work of breathing of the patient(WOBPT )over a series of

breaths

• This is then displayed

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• The aim is to keep the WOBPT within the green zone

– If towards the left decrease the support, and increase if towards the right

• Once support about 30% patients can be switched to wall CPAP.

Pressure Support (PS)

PS is an all or none event, triggered by patient effort. Once triggered, the ventilator drives the

pressure to a clinical preset value regardless of patient effort. Lung –thorax compliance(CL)

and insufflation pressure lung pressure(PL) combine to determine the lung volume (VL=CL×PL).

The goal of PS is to balance an appropriate insufflation pressure that, combined with patient

effort, will yield the desire VL and that will not tax the patient’s inspiratory reserve. Both

insufficient and excessive PS can increase patient inspiratory work load and cause the patient

to tire and become tachypnoeic and tachycardic.

Support level: titrate level of PS from 10- 20 cmH2O to achieve satisfactory tidal volumes

and respiratory rate below 30 breaths.min−1 (preferably less than 25 breaths.min−1.

This should be slowly reduced.

PEEP set at 5-12 cmH2O according to oxygenation.

Rise time should be adjusted for optimal ease of ventilation by optimizing the flow delivery.

FAP should be set at 50% initially then adjusted as required.

Tube Compensation (TC)

Spontaneous ventilation mode that overcomes the WOB(work of breathing) for the artificial

airway (ET or tracheostomy tube). TC accomplishes this support by assisting the patient’s

spontaneous breaths with positive pressure proportional to the inspired flow and the diameter

of the artificial airway. It then allows a constant PEEP to apply. The patient does not experience

the resistive work due to inspiring through an artificial airway.

• Percentage of support set at 100-70%

• Decreasing the level of the support can be used to train respiratory muscles

5.3.8 Positive Pressure Ventilation and Hypotension

Positive pressure ventilation may exacerbate or induce hypotension by increasing relative in-

trathoracic pressure and therefore decreasing venous return to the heart. ie

• Mild moderate: Loss of negative phase of inspiration and initiation of PEEP

• Extreme: Excessive increase in intrathoracic pressure (auto-PEEP or tension pneumotho-

rax)

5.3.9 Supportive Therapies for Severe Hypoxia

5.3.9.1 Rotational Beds Is the patient on the correct bed? Consider rotational beds for

patients with High Oxygen requirements.

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5.3.9.2 Fluid Management In patients with ALI/ARDS, there is an increase in lung water

due to changes in vascular permeability. After early haemodynamic stabilization, studies have

shown that fluid restriction and diuresis have shown to improve lung function and shorten

the duration of mechanical ventilation and intensive care stay, improved neurological function

and decrease the sedation use, without increasing non pulmonary – organ failure though no

difference in 60 day mortalityi.

Aim for neutral fluid balance, consider use of diuretics or increase fluid removal in patients on

renal support with ALI/ARDS.

5.3.9.3 High frequency oscillatory ventilation(HFOV) Consider in patients with pneu-

monia, ARDS/ALI with severe hypoxia and patients with bronchopleural fistula. It is better to

consider early.

Paw > 30, FiO2 > 0.6 with PaO2 <8, PEEP >12-15

• Prior to use,

– Complete all circuit connections including the Aerogen Solo nebuliser if available.

– Prime the humidifier with 350 mls of sterile water prior to switching it on

• Once familiar with the controls

– Power up and calibrate the O2 analyser if present then with a test lung check func-

tions

– Review settings and alarms, make appropriate changes before use.

• 3 Key Controls for HFOV

Frequency = CO2 clearance - adjust ↓ 1Hz according to PaCO2

Mean = Recruitment and Oxygenation - adjust ↑ by 5cmH2O according to PaO2

Cycle Volume = CO2 clearance - adjust ↑ by 10ml according to PaCO2

• Initial settings for HFOV

Base Flow 15 Lpm (the continuous gas flow through the circuit)

SI Setting 5cmH2O > mean airway pressure

FiO2 100 %

Frequency 8 Hz (rate of oscillations per second)

MAP 5cmH2O > than conventional ventilation MAP (20cmH2O if unknown)

Cycle volume 175ml (the size of each circulating volume)

Actions

1. Optimise PaO2 (Lung Recruitment)

a) start oscillation using initial settings→ wait 20 mins→ confirm baseline blood gasses

b) ↑ MAP by 5cmH2O → wait 20 minutes → check bloods for improved PaO2 → repeat

cycle until PaO2 no longer improves (fully recruited) or deteriorates (over distended)

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c) Consider correcting over distension by ↓ MAP again by 5cmH2O to optimise PaO2

2. Optimise PaCO2

a) ↑ cycle volume by 10 ml → wait 20 minutes → check bloods for reduced PaCO2 →repeat until PaCO2 reduces to within acceptable limits (or no further adjustment is

possible)

b) If CO2 clearance remains insufficient → ↓ frequency in 1 Hz steps → wait 20 minutes

→ check bloods for reduced PaCO2 → repeat until PaCO2 value is acceptable

c) If CO2 clearance is still insufficient→ check for ETT patency, pneumothorax, consider

introducing an ET cuff leak or the prone position. *If PaCO2 remains unacceptable

consider extra-corporeal CO2 extraction (i.e. using a Novalung ILA)

3. Optimise FiO2

a) When PaO2 and PaCO2 are optimised and stable, ↓FiO2 in 10% steps whilst PaO2 re-

mains acceptable

Weaning from HFOV

• ↓ FiO2 in 10% steps aiming for maintenance < 40%

• ↓ MAP in 2cmH2O steps aiming for maintenance < 25cmH2O

• If stable at above for 24 hours consider changing mode

• Insufficient spontaneous effort? → set to VENT mode (PCV+SIMV or CMV+SIMV)

• Effective spontaneous effort? → consider setting to SPONT mode (CPAP+PS),

Charting Mode, Base Flow, FiO2, Frequency, Mean Airway Pressure, Cycle Volume and Am-

plitude

Amplitude is the difference between the high and low airway pressures during oscillation and

is expressed in cmH2O. It may be visualised between the peaks and troughs of the displayed

waveform.

Closed Suction and Bronchoscopy ↑ MAP by 5cmH2O 5 minutes before, during and for 5

minutes after the procedure.

↑ base flow to 40 L.min-1 only during the procedure

Green Paw Tube This airway pressure (Paw) tube allows volume and pressure to be monitored

inside the machine.

VIP – run the green Paw tube over the circuit support arm to prevent moisture ingress at the

Y-piece.

Volume and Pressure sensing automatically calibrates hourly.

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S.I. “Suspend Intervention” stops oscillation but maintains the airway pressure at the set

value whilst the operator presses the button showing lungs. This may be used for lung recruit-

ment, ECG, x-ray or listening to heart sounds. Check the set value before use!

Accidental Disconnection System alarms → HFOV stops → on reconnection it gently re-

recruits and alarm cancels automatically.

Spontaneous Breathing Effort Is indicated by wandering MAP LED’s at the top of the dis-

play panel and measured values in the display. Consider resetting MAP high / MAP low alarms

Base flow may be ↑ incrementally to support spontaneous breathing efforts.

Cardiovascular Effect Observe for cardiovascular insufficiency as ↑ MAP in HFOV may ↓cardiac output.

Conventional Mode ETS = Expiratory Trigger Sensitivity terminates inspiratory support dur-

ing assisted breaths. Set as a % of the inspiratory trigger setting.

RSB = Rate of Spontaneous Breaths.

Inspiratory pressure setting in PCV is in addition to PEEP.

Only use closed suction in PCV with a high flow rate, if using VCV switch to PCV during closed

suction.

The humidifier Prime with 350mls H20 before switching on, is fully automatic, schematic

display shows alarm locations.

After 30 days an alarm for replacement sounds but allows a further 72 hours allows for re-

placement.

P23 alarm = overfilling of the reservoir - close the water inlet line, power off the humidifier for

3 minutes, turn power back on, leave the giving set closed for 1 hour to allow excess water to

clear the reservoir before reopening the giving set.

Further Points The vent circuit is PVC and latex free.

Circuit breakers are provided on the rear of the machine for easy user access.

* Vision α has no integral battery, connect to a UPS protected mains supply if concerned.

After use Switch off at front of machine then press and hold the alarm mute button for three

seconds to cancel the alarm.

The impedance valve (at the front of the diaphragm), oxygen analyser and humidifier heater

cables are not disposable and should be retained. The circuit, diaphragm and humidifier cham-

ber can be discarded.

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5.3.9.4 Prone positioning Prone position has been demonstrated to improve oxygenation,

and decrease the incidence of VAP in patients with ARDS, but does not improve mortality.

Majority of patient’s oxygenation respond quickly to prone position and should then be left in

prone position for at least 12 hours.

Rationale for prone ventilation Improvement in ventilation perfusion matching, recruit-

ment of atelectatic areas following a gravitational gradient and an increase in end-expiratory

volume.

Indications

• Severe ARDS PaO2:FiO2 ratio <20

• Non responsive to standard supportive / ventilatory care

Relative Contraindications

• Inadequate staff to perform procedure safely

• CRRT

• Anterior chest drain

Complications

• Difficult airway management and access

• Accidental removal of invasive catheters

• Pressure necrosis, pressure neuropraxia and blindness

5.3.10 Weaning from Mechanical ventilation

5.3.10.1 Introduction In many patients, especially those requiring short-term support, me-

chanical ventialtion can be removed quickly and easily. In more complex cases however con-

siderable difficulty may be encountered

The actuarial risk of nosocomial pneumonia increases by about 1% per each day of MV, being

6.5% at 10 days and 19% at 20 days. It is crucial to discontinue ventilatory support and ex-

tubate at the earliest time that a patient can sustain spontaneous ventilation safely. Planning

for weaningshould start as soon as the patient is intubated, using the following parameters:

How long can we expect this patient to require mechanical ventilation (MV)? Is a tracheostomy

likely to be needed?

What is the underlying disease process and how may this impact on weaning?

Premature attempts at weaning can result in respiratory muscle fatigue and atelectasis.

Premature extubation with resultant reintubation carries an appreciable risk to the patient.

119


5.3.10.2 Minimum requirements for extubation

• Improving clinical condition.

• Patient stable on FiO2 < 0.4 with a PaO2 > 8 kPa

• PEEP < 5-8 cmH2O

• Acceptable neurological state: ie the expectation exists that the patient will be awake

enough to protect their airway, and have the local ability (intact cranial nerve function or

tracheostomy) to do so.


• No prospect of major intervention planned in the ensuing 24 hours

5.3.10.3 Predicting successful weaning from mechanical ventilation In a small per-

centage of patients, there may be some doubt as to whether the patient will cope with removal

of respiratory support despite meeting the above criteria. A number of parameters have been

studied, however at present a spontaneous breathing trial is considered the most useful, with

a positive predictive value of about 80%.

Spontaneous breathing trial

• The patient should receive no more than a PEEP of 5 cmH2O through a T-piece system.

Generally if an SBT is conducted while on the ventilator, no more pressure support than

is sufficient to overcome system resistance to flow should be allowed (see ETT compen-

sation mode on newer generation Puritan-Bennett).

• Allow 120 minute trial (some suggestion 30 minutes may predict adequately)

• If trial successful extubate

Markers of successful Spontaneous Breathing Trial Objective

• Gas exchange acceptable ( Oxygen sat > 90% , PaO2 > 8 kPa , Increase in PaCO2 < 10

1.5 kPa)

• Stable ventilatory pattern (RR < 30 35 min-1 , RR not changed > 50%)


Subjective

• No onset or worsening of discomfort

• Diaphoresis

• Clinical evidence increased work of breathing

5.3.10.4 Chosen mode of weaning to extubate There is no evidence that a trial of un-

supported breathing using a T-piece apparatus is any better or worse than decremental levels

of pressure support ventilation.

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The duration of the trials is not defined but those that fail usually do so early on. Probably 30

minutes to two hours is all that is needed.

Clinical signs of failure include tachypnoea, tachycardia, hypertension, obtundation, and de-

saturation.

5.3.10.5 Factors that influence success of weaning

Increase in work of breathing

• Increase metabolism (increasing CO2 production)

– Fever, sepsis, carbohydrate excess

• Reduction in pulmonary or chest wall compliance

– Pulmonary oedema, acute respiratory distress syndrome, atelectasis, pneumonia

– Bronchospasm, retention of secretions

– Obesity, abdominal distension

• Unfavourable respiratory circuit characteristics

– Delayed response and high negative pressure to trigger high resistance circuitry

– Inspiratory flow rate unable to match peak inspiratory flow

– Reduction in respiratory muscle power

• Electrolyte abnormalities

– Hypokalaemia, hypomagnesaemia, hypophosphataemia, metabolic alkalosis

• Cardiovascular failure

– Left ventricular failure, shock, anaemia

• Polyneuropathy of the critically ill

• Myopathy (eg endocrine or carcinomatous)

Depression in respiratory centre

• Excess respiratory depressant drugs

• Hypothyroidism

Pain

Brain Injury

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5.3.11 Ventilation in the prone position

5.3.11.1 Introduction Ventilating a patient in the prone position has not been shown to im-

prove mortality, however in up to 60% of selected patients there is a significant improvement

in oxygenation, often persisting beyond the period spent prone.

It is unclear how long a patient should be ventilated in the prone position. The majority of

patients that do respond do so quickly, however up to 30%may exhibit delayed improvement.

Available evidence suggests > 12hrs is recommended.

The decision to prone a patient should not be made lightly, and is the domain of the ICU

Consultant.

Once the decision has been made to prone a patient, this should be done under the direction

of an experienced nursing team.

5.3.11.2 Rationale for prone ventilation

• Increased uniformity of regional pleural pressure gradient.

• Improvement in dorsal ventilation with a reduction in shunt fraction

• Improved ventilation-perfusion heterogeneity.

• Uniform distribution of lung water and exudate

• Improvement in FRC with further alveolar recruitment

• Reduction in diaphragmatic splinting and improved movement of the posterior diaphragm

• Non-restriction of abdominal contents

5.3.11.3 Indications

• Severe ARDS as given by: PaO2: FiO2 ratio < 100

• Non response to standard supportive / ventilatory care

• Local or anatomical factors (eg. posterior burns)

5.3.11.4 Relative Contraindications

• Inadequate staff to perform procedure safely

• Anterior intercostal catheter

• Continuous renal replacement therapy

• Morbid obesity

5.3.11.5 Hazards

• Difficult airway management and access (including ETT kinking and dislodgement)

• Accidental removal of invasive catheters (and possible occult haemorrhage)

• Obstruction or disconnection of abdominal / thoracic drains.

• Pressure necrosis, pressure neuropraxia and blindness

• Labour intensive procedure-distraction from other patients

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5.3.12 Non-invasive ventilation (NIPPV)

5.3.12.1 Introduction Mechanical ventilation not requiring endotracheal intubation may

avoid many of the complications of invasive ventilation (ie. generally associated with less ICU

acquired infection, results in shorter ICU and hospital length of stay, and may be more accept-

able to patients. Appropriate patient selection is important (restrict to indications below), as

is appropriate monitoring and a controlled environment with the capacity to initiate invasive

ventilation without delay where necessary.

Modes

• Continuous positive airway pressure (CPAP)

– Single continuous positive airway pressure

– No augmentation of tidal volume

– Generally seen to be useful in hypoxic states

• Biphasic positive airway pressure (BiPAP)

– Usually PEEP plus augmentation of tidal volume

– Useful in the treatment of hypercarbic states

5.3.12.2 Indications This section does not attempt to address the role of NIPPV outside

of acute conditions. The groups outlined below are those that have been studied, often in a

limited way.

Accepted indications

• Acute exacerbations COAD: Good evidence, albeit with some conflicting data, that NIPPV

useful in hypercapnoeic patients.

• Pulmonary oedema.

• Patients with underlying neuromuscular, parenchymal or restrictive lung disease: NIPPV

useful only if decompensation is a result of reversible infection and not disease progres-

sion.

Less accepted indications NIPPV should only be applied in the following situations on a

trial basis, with well defined end points, and in a well controlled environment (ICU generally).

• Weaning or early discontinuation of invasive ventilation.

• Stable airway obstruction (eg: post operative patient with obstructive sleep apnoea).

• Pneumonia or ARDS

• Asthma

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5.4 Bibliography 5 CLINICAL MANAGEMENT

5.3.12.3 Contra-indications to NIPPV

• Patient with impaired level of consciousness, including those that are in-extremis

• Haemodynamic instability

• Bowel obstruction or upper GI haemorrhage (increased risk of aspiration)

• Agitation such that mask not tolerated well

• Impaired cough, including low GCS and bulbar dysfunction

• Non-reversible disease process

• Untreated pneumothorax

5.3.12.4 Pre-requisites

• The patient must be able to protect their own airway sufficiently.

• The patient must be accepting of the face mask

• There must be a reversible problem requiring bridging respiratory support.

• There must be adequate monitoring:

– Continuous pulse oximetry, telemetry and at least intermittent blood pressure and

ABG recording.

– Nursing ratio no worse than 1:2.


• Aerophagia or gastric distension - Aspiration lung injury

• Mask intolerance and heightened anxiety

• Pressure necrosis of the face

5.3.13 Corticosteroids in ARDS

High dose intravenous Corticosteroids have intermittently been used through the years to try

and prevent the fibro-proliferation stage of ARDS progressing to end stage fibrosis. However

concerns about sample size in Meduri et al study lead to the ARDS network looking at this. The

late Steroid rescue study(LaSRS) showed no difference in hospital mortality. Among the corti-

costeroid related complications, infection rate was no different while neuromuscular weakness

was higher in the treatment group.ii These results do not support the routine use of methyl-

prednisolone in patients with persistent ARDS.

5.4 Bibliography

VillarJ Kacmareck RM. A high in positve end-expiratory pressure, low tidal volume ventilatory strategy improves outcome in persistentacute respiratory distress syndrome: a randomised, controlled trial. Crit Care Med. 2006;34:1311-1318

The National heart, lung and blood Institute Acute Respiratory distress syndrome (ARDS) Clincial Trial Network. Ventilation with lowertidal volumes as compared with traditional tidal volumes for acute lung injury and acute respiratory distress syndrome. NEJM 2000,May 4.342(18):1301-8

124

5 CLINICAL MANAGEMENT 5.5 Aspects of Renal Failure in Intensive Care

ARDS Clinical Trial network. Comparision of two fluid management strategies in acute lung injury. N Engl J Med 2006a;354(24):2564-75

Gattinoni L, Tognoni G et al. Prone-supine Study Group. Effect of prone Positioning on the survival of patients with acute respiratoryfailure. N Engl J Med 2001;345: 568-73

McAuley DF et al. What is the optimal duration of ventilation in the prone position in the ARDS. ICM 2002;28:414-418

Meduri GU, headley AS et al.Effect of prolonged methylprednisolone therapy in unresolving ARDS. JAMA1998;273:159-65

The National heart, lung and blood Institute Acute Respiratory distress syndrome (ARDS) Clincial Trial Network. Efficacy and safety ofcorticosteriods for persistent ARDS. NEJM 2006b; 354(16):1671-84

5.5 Aspects of Renal Failure in Intensive Care

5.5.1 Introduction

Renal failure in ICU is invariably involves at least one other organ dysfunction or failure, and

carries a mortality of up to 70% in this setting.

The advent of continuous renal replacement therapies has revolutionised this aspect of care.

Conversely renal protective strategies, established therapy in many units have not been proven

beneficial in large multi-centre trails.

Acute renal failure that develops in isolation, due intrinsic renal disease and not part of critical

illness should be referred to the Specialist Renal physicians in Leeds for further management

and investigation.

5.5.2 Aetiology of renal failure in the ICU

The classical compartmentalisation of pre-renal, intra-renal and post-renal factors hold true in

ICU with the following considerations:

• A missed, but reversible, cause of renal failure has dire consequences-time is kidney.

• The commonest cause of an acute kidney injury is hypovolaemia or hypoperfusion and

should be excluded and treated as a matter of urgency. Renal perfusion (blood flow and

GFR) in critically ill patients may become directly related to systemic blood pressure as

local autoregulation fails. Hypotension, even a marginal decrease, will not be well toler-

ated.

• Nephrotoxic agents and sepsis may act alone or in combination with hypovolaemia to

complicate the picture.

• The renal interstitium is relatively hypoxic even under optimal conditions. When sub-

jected to a multilevel endothelial insult as a result of sepsis or SIRS there is a ready

predisposition to a vasomotor nephropathy and progession to overt ATN.

• The pharmacokinetics of many drugs in ICU are severely deranged, exposing the patient

to a much greater risk of nephrotoxic effects. Drugs and toxins (including radio-contrast)

should not be administered without consideration of their toxicity.

• Occult or overt increases in intra-abdominal pressure should always be considered in pa-

tients with abdominal distension with or without previous surgery. When considered it

should be measured and if necessary addressed (see Intra-abdominal pressure measure-

ment, section 2.11).

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5.5 Aspects of Renal Failure in Intensive Care 5 CLINICAL MANAGEMENT

5.5.3 Assessment of renal function in a given patient

5.5.3.1 Biochemical markers Serum creatinine is a poor marker of renal reserve. A rise in

serum creatinine > 120 µmol.L-1 may not occur until more than 75% of renal function is lost.

All patients should have their renal function calculated, and drugs tailored according to the

Cockroft and Gault equation:

Creatinine Clearance (ml.sec-1) =(140−Patient age)− weight in kg × 0.8(for females)

50000× Serum creat conc in mmol.L−1

From this equation it can be appreciated that a 20 year old 100kg male will have 6 times the

creatinine clearance of an 80 year old 50kg woman, even though they have the same serum

creatinine concentration.

5.5.3.2 Urine The minimum urine output required to excrete obligatory daily solute load is

0.5 ml.kg-1.hr-1

Urine electrolyte analysis is of little use in ICU to diagnose aetiology of renal failure but maybe

useful in specific electrolyte abnormalities.

Urine sediment: Unhelpful unless a specific reason exists (true vasculitis, nephritis)

5.5.3.3 Renal imaging Ultrasound or nuclear imaging techniques may be useful where pre-

existing pathology is suspected, or the renal vasculature has been compromised by surgery or

trauma.

Supra-renal aortic aneurysm or dissection may extend distally and compromise renal blood

flow, particularly where a significant false lumen exists. As soon as is practical following acute

repair, investigation of aorto-renal vascular anatomy should be performed to facilitate a fen-

estration procedure if necessary.

Post-renal pathology, whilst uncommon in ICU, is embarrassing to miss and should be excluded

where there is any doubt about the cause of renal failure.

5.5.4 Renal protective strategies

5.5.4.1 Good practice The cornerstones of good renal protection are not the administration

of various drugs, but critical care practice ie.

• Adequate fluid resuscitation (sometimes a difficult concept).

• Haemodynamic support to maintain both a good renal perfusion pressure and adequate

blood flow. Where necessary this may involve inotrope and/or vasopressor support. De-

spite historical anxiety about the use of vasopressors (noradrenaline), it is not harmful

to the kidneys and may in fact increase renal blood flow in animal studies. Ensure ad-

equate preload aiming for CVP 10-12 mmHg (higher if thought to have right ventricular

dysfunction e.g. COPD), aiming for an appropriate mean arterial pressure of at least 70

mmHg.

• Avoid nephrotoxic drugs where possible

126


• Treat intercurrent infection

• Active surveillance for abdominal compartment syndrome, where this is appropriate.

5.5.4.2 Drug therapy The following drugs have been used to promote urine output, but

have not been found to impact in a positive way on progression to dialysis or mortality.

• Low dose dopamine (increase in urine output secondary to direct tubular effect and minor

increase in β-effect) - however, dopamine has no place in the management of ARF and

there is evidence that it may be harmful.

• Frusemide (must be delivered to lumen of tubule to be effective)

• Dopexamine at 0.25-1 µg.kg-1.min-1 if GI perfusion thought to be at risk

• Mannitol

• Aminophylline

The routine use of these drugs (except dopexamine) is not advocated.

5.5.5 Renal Replacement Therapy

Indications for dialysis

• The threshold for dialysis in a critically ill patient is different from that of an ambulatory

ward patient. Mortality in critically ill patients is related to time averaged urea during

their stay, so that dialysis should be started earlier with the aim of maintaining a optimal

state, rather than cyclical clearance of urea and metabolites.

• The presence of two of the following would suggest dialysis should be considered

– Oliguria < 200 ml over 24hrs

– Oliguria < 50 ml over 12hrs

– Severe acidaemia

– Hyperkalaemia (K+ > 6.0) refractory to medical management

– Plasma Urea > 20 mmol.L-1 or uraemic syndrome (pericarditis, pneumonitis, bone

marrow suppression)

– Plasma Creatinine > 400 µmol.L-1

– Pulmonary oedema

– Diuretic resistant cardiac failure

– Anasarca (generalised oedema)

– Selected overdose (salicylates, methanol, theophylline)

– Severe dysnatraemia (Na+ <115 or Na+ >160)

– Severe metabolic acidosis - pH <7.1

– Critical oxygenation

– Refractory fluid overload

The attempted removal of cytokines and inflammatory mediators is not yet proven to reduce

mortality in humans.

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5.5 Aspects of Renal Failure in Intensive Care 5 CLINICAL MANAGEMENT

5.5.5.1 Modes of dialytic therapy in the ICU Standard intermittent dialytic therapy: Al-

though still used in some ICUs, it is limited by resource availability and is probably not suitable

for use in unstable patients

Continuous veno-venous renal replacement therapy: A growing field of therapy in the ICU,

this modality has become the mainstay of renal replacement in the critically ill. Continuous

Renal Replacement Therapy (CRRT) is for the support of patients with renal dysfunction that

develops as part of their critical illness. It is not for providing dialysis in patients with acute

renal failure as part single organ failure i.e. intrinsic renal disease such as glomerulonephritis.

Initiation of haemofiltration is a Consultant Intensivist decision only! It will only be initi-

ated/resumed during ”office” hours.

5.5.5.2 Continuous renal replacement:-Default Prisma settings

Mode CVVHD

Blood flow rate 100 ml.min-1

Dialysate flow rate 1500 ml.hr-1 (usual need: 15-25 ml.kg-1.hr-1)

Replacement 1500 ml.hr-1

Pre-dilution 30%

Fluid removal According to need

Anticoagulation If considered safe, a bolus of 2000-5000 units of heparin is administered

to the patient IVI at the commencement of dialysis.

There is no evidence that anticoagulation prolong filter life and prevents clotting in the filter.

Anticoagulation is however widely practiced, the aim being to anti-coagulate the filter but not

the patient. Therefore:

• Heparin 20 000 IU is made up to 20ml with Normal Saline, and starting at 10-15 units.kg-1.hr-1

is infused via stand alone syringe pump pre-filter.

• APPT should then be monitored after one hour, then two hourly x2, then 4 hourly until a

stable target APTT is reached. Once achieved, APTT can be monitored 12 hourly.

• Target APTT should be in the range of 1.5-2 times normal. The maximum APTT of 65s

should not be exceeded.

128


Patients with deranged coagulation due to sepsis or low / abnormal platelet function may not

require heparin administration at all.

Prostacyclin

Prostacyclin should be used when heparin is contraindicated, or heparin resistance has oc-

curred. It can be used concurrently with heparin (50% reduction in heparin dose), but this

does increase the risk of bleeding complications.

It should not be used during infusion of activated protein C.

Prostacyclin is made up as 500 µg in 50ml NaCl 0.9% (10 µg/ml) run via the Prismaflex or

systemically at a rate of 2-6 ml.hr-1.

It can cause an increase in intrapulmonary shunting.

Potassium replacement The haemodialysis counter current should mean that with an ef-

fective filter in situ, the plasma exiting the filter has the same potassium.

concentration as the dialysate entering the filter. Potassium supplementation should therefore

only occur in the dialysate fluid.

Standard haemofiltration fluid is lactate buffered and contains [K+] = 4 mmol.L-1.

Buffering solution Most dialysate solutions contain lactate as a buffer, as this results in a

stable solution. Lactate is then metabolised to bicarbonate in the liver.

Commonly therefore, patients on CVVHDF will have moderately elevated lactate levels. In the

context of a stable patient (unchanged or improvingwhole blood pH) this should not cause

alarm.

Solutions using bicarbonate as a buffer need to be prepared just prior to use. They are more

expensive, and more prone to contamination.

Bicarbonate buffer fluid is not indicated unless there is significant hepatic impairment.

Fluid removal The Prisma machine will allow you to set a net fluid removal volume per hour.

This is calculated by the machine based on the weight of the ultrafiltrate bag, and the set flow

rates of replacement and dialysate fluids. The volume to removed from the patient must be

discussed with the Consultant Intensivist, and form part of the daily management plan.

5.5.5.3 Complications of continuous renal replacement therapy

• Haemorrhage (and other consequences of exposure to heparin (HIT or HITT)

• Hypothermia, or masking of hyperthermia (prevention of hyperthermia may be clinically

useful)

• Complications of (prolonged) venous access.

• Exposure to extracorporeal circuits and filter (activation of complement, sequestering of

platelets)

• Air embolism

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5.6 Neurosurgical Guidelines 5 CLINICAL MANAGEMENT

• Increased requirement for experienced staff, and increased nursing workload.

5.6 Neurosurgical Guidelines

5.6.1 Neurotrauma

The effective management of neurotrauma relies upon early notification of the neurosurgical

team, and close liaison at all times.

For obvious reasons we have no control over the magnitude and mechanism of the primary

injury, however we can influence patient outcome by preventing a secondary insult through

hypoxia, hypotension, or electrolyte/metabolic derangement.

5.6.1.1 Acute trauma resuscitation Safe retrieval and transport around the hospital, and

during emergency surgery

Cardio-pulmonary / renal / metabolic homeostasis

Maintenance of cerebral perfusion.

5.6.1.2 Monitoring the head injured patient

• Real time (invasive) arterial blood pressure monitoring

• CVC accessed and pressure transduced.

• End-tidal CO2 monitoring (calibrate and establish arterial-end tidal difference).

5.6.1.3 Ventilation of the head injured patient Maintain PaO2 > 10 kPa

Maintain normocapnia: PaCO2 between 4.5-5.3 kPa. Hyperventilation to PaCO2 as low as 3.0

kPa may decrease ICP temporarily, however there is a short term trade off in cerebral blood

flow, and after 6 hours tachyphylaxis occurs with a potential hyperaemia on correction to a

normal PaCO2.

Hyperventialtion should not be used therefore unless it forms a short term bridge to definitive

treatment (ie. impending surgery).

Low level PEEP has not been proven to affect outcome of head injury adversely, and may

prevent secondary pulmonary pathology.

Nurse 30 degrees head up with head in neutral position.

5.6.1.4 Haemodynamic priorities Maintain perfusion pressure:

• Mean arterial pressure (MAP) > 90 mmHg in the absence of an ICP monitor,

• Cerebral perfusion pressure (see algorhythm below) > 70 mmHg where ICP is being mon-

itored (CPP = MAP-ICP)

• Avoid inotrope or vasopressor use until patient adequately fluid resuscitated.

Fluid maintenance

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5 CLINICAL MANAGEMENT 5.6 Neurosurgical Guidelines

• Aim for euvolaemia

• Use crystalloid (usually normal saline) unless a specific contra-indication exists

5.6.1.5 Osmotherapy

• Indications:

– Signs of trans-tentorial herniation

– Progressive neurological deterioration not attributable to systemic pathology.

• The patient should be euvolaemic prior to initiating osmotherapy.

• Bolus therapy may be better than infusions: consider-

– Mannitol 0.25 g.kg-1 or (100 ml of 20% )

– Hypertonic saline: 10-20 ml of 20% saline to a serum Sodium concentration of 150-

155 mmol.L-1

• Measured osmolality should not exceed 320 mmol/L.

• Prolonged serum hyperosmolality will promote intracellular generation of idiogenic os-

moles leading to a rebound in cellular fluid uptake (and ICP) if osmolality is allowed to

correct rapidly beyond day 3 of therapy.

5.6.1.6 Sedation

• First 24-48hrs: It may be appropriate to use a short acting agent such as propofol to facil-

itate repeated neurological assessment, particularly where no ICP measurement exists.

• Labile neurogenic hypertension, sympathetic storming or emergence agitation: Consider

β-blockade or clonidine.

• Barbiturate use (thiopentone: consider loading dose, 1-1.5 g IVI) see raised ICP algorithm.

5.6.1.7 Other management issues relating to neurotrauma

Steroids

• not proven useful in the trauma setting.

Antibiotics

• A single dose of antibiotic should be sufficient to cover insertion of monitoring catheters.

• A fracture base of skull is not an indication for antibiotic prophylaxis in the absence of a

CSF leak.

• CSF should be sent for MC&S daily. All sampling of CSF, or other disruption of the drainage

system should be performed using aseptic technique, including sterile gloves and gown.

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5.6 Neurosurgical Guidelines 5 CLINICAL MANAGEMENT

Seizure prophylaxis

• Consider use in patients with a closed head injury and structural damage, or penetrating

injury.

• Phenytoin 15 mg.kg-1 over 30 minutes followed by 300 mg daily for 10 days when used

for prophylaxis only.

Thromboprophylaxis

• All patients should be fitted with T.E.D. stockings.

• Consult the neurosurgical team on prophylactic heparin use.

• Those patients not suitable for using T.E.D. stockings should be considered for sequential

calf compressors.

Stress ulcer prophlaxis

• consider if patient likely to be ventilated for > 48hrs, and not tolerating enteral feeding

Avoid hyperthermia

• Hyperthermia should be avoided using simple measures such as regular paracetamol

• The role of active cooling is controversial, and should not be instituted without consent of

the Consultant.

5.6.2 Status Epilepticus

5.6.2.1 Definition

• Prolonged or repetitive seizures that occur without a period of recovery between attacks.

• Refractory status epilepticus refers to ongoing seizures for more than 20-30 minutes.

• Serial seizures may occur within a brief period, but as long as the patient regains con-

sciousness in between this is not an indication for ICU admission.

5.6.2.2 Principles of ICU management

• Basic resuscitation protocol: Secure Airway, Breathing, Circulation

• Acquire IVI access.

• Control Seizures using drugs described in table below.

• Consider precipitating causes and treat as appropriate:

– Glucose: administer an empiric dose if in doubt, or estimation delayed.

– Electrolytes: Ca2+, Mg2+, K+, PO3-4

– Metabolic derangement: hypoglycaemia, thiamine deficiency, intoxication or with-

drawal

– Known epileptic: review medication compliance and recent changes.

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5 CLINICAL MANAGEMENT 5.6 Neurosurgical Guidelines

– Intracranial pathology: CVA, tumour, infection

• Prevent secondary insult: Hypoxia, hyperpyrexia, prolonged seizures-rhabdomyolysis.

• Further investigations:

– CT scan head: where cause of seizure unknown, and of new onset.

– EEG. May be useful where pseudoseizures are suspected, the patient has complex

partial seizures with intermittent generalisation, or where muscle relaxants have

been administered to the patient.

– Lumbar Puncture: LPs are generally not indicated.

5.6.2.3 Useful Drugs in the treatment of refractofy status epilepticus

• Ketamine : NMDA receptor antagonist, may be helpful when GABA receptor response to

other drugs less effective

– Loading dose: 1-5 mg.kg-1

– Infusion: 1-5 mg.kg-1.hr-1

• Propofol : Anaesthetic agent used to control refractory status in the intubated patient

– 1-2 mg.kg-1 followed by 2-10 mg.kg-1.hr-1.

• Thiopentone : Reserved for failed standard treatment, where endotracheal intubation is

required

– Loading dose: 5 mg.kg

– Infusion: 1-3 mg.kg-1.hr-1 (approx 150 mg.hr-1) titrated to EEG activity at the bedside.

Once emergency treatment has been implemented it is expected that the assistance of the

neurology team will be sought in adjusting treatment in known epileptics, or those with focal

or complex partial seizures.

5.6.3 Subarachnoid haemorrhage

5.6.3.1 Introduction Patients will be admitted as a result of acute aneurysmal rupture,

generally with impaired level of consciousness.

5.6.3.2 Planning of surgical intervention in patients with acute rupture

• Early ( < 3 days):

– Advantages: Prevents re-bleeding, may assist with reduction in associated vasospasm

(blood products removed) and subsequent cerebral ischaemia.

– Disadvantages: More technically difficult, higher risk of intra-operative rupture.

• Late ( > 11 days):

– Advantages: Easier procedure. Allows a period of observation, avoiding surgery in

potentially non-salvageable patients.

– Disadvantages: re-bleed or rupture. Increased risk of vaso-spastic complications.

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5.7 Microbiology Guidelines 5 CLINICAL MANAGEMENT

5.6.3.3 Principles of ICU management

Monitoring

• Pulse oximetry

• Invasive arterial monitoring

• Central venous access (particularly during administration of nimodipine).

• Neurological observations hourly: A deterioration in GCS that cannot be easily explained

or corrected (eg. sedation) may be due to a re-bleed, vasospasm or hydrocephalus in

which case the neurosurgical team should be notified.

Therapeutic interventions Maintain adequate cerebral perfusion (generally a MAP > 20

mmHg above pre-morbid state, or > 90 mmHg if unknown).

Aim to minimise secondary damage due to cerebral vasospasm, using Nimodipine (Calcium

channel antagonist) 10 mg.hr-1 IVI (preferably via CVC)

• Nimodipine administration may precipitate hypotension, in general noradrenaline is used

to maintain the desired mean arterial pressure (MAP), although this should be discussed

with the Consultant Intensivist.

• Change to oral administration as soon as possible

• Usually continued for a total of 21 days

Fluid administration:

• Maintain at least normovolaemia using 0.9% saline IVI

• Hypervolaemia has been advocated as a means of maintaining cerebral flow, although

achieving hypervolaemia may be difficult.

• Measures of adequate volume status should include:

– Warm and well perfused patient

– Urine output at least 0.5 ml.kg-1.hr-1, preferably > 1.0 ml.kg-1.hr-1

– CVP > 12 mmHg

– Maintain normal serum electrolytes and total osmolality

Adjuncts to treatment Direct and chemical (papaverine) angioplasty may play a role in

refractory cerebral vasospasm, however they do not form part of routine practice at this stage.

5.7 Microbiology Guidelines

5.7.1 Introduction

Sepsis is the most common cause of death in critically ill patients. The detection of active

infection, as opposed to colonisation with ICU flora, is difficult but important.

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5 CLINICAL MANAGEMENT 5.7 Microbiology Guidelines

Regular routine microbiological examination is not cost effective in the ICU, and infective

screens should only be ordered for specific indications, using the guidelines listed below.

Simple preventative measures are extremely important in the containment of infection and

the prevention of bacterial resistance. ie Compulsory hand washing by all staff who come

into contact with patients. Hands should be washed both before and after patient contact.

Alternatively, alcohol gel may be used.

Strict aseptic technique for all procedures

Rational prescription of antibiotics.

5.7.2 Glossary

5.7.2.1 Systemic inflammatory response syndrome: SIRS Describes clinical picture

following any insult (trauma/major surgery, burns, pancreatitis, hypersensitivity reactions )

activating a significant inflammatory reaction.

Defined by the presence of at least 2 of the following:

• Temp > 38 oC or < 36 oC

• Heart rate > 90 bpm

• Respiratory rate > 20 bpm (or PaCO2 < 4.0 kPa spontaneously breathing)

• Plasma WCC > 12000 .mm-3 or < 4000 .mm-3 or > 10% immature neutrophils (band cells)

5.7.2.2 Sepsis The presence of SIRS as defined above in the presence of a proven microbi-

ological pathogen

5.7.2.3 Septic Shock Sepsis with hypotension, despite adequate fluid resuscitation, along

with the presence of perfusion abnormalities that may include but are not limited to

• Lactic acidosis

• Oliguria

• Acute alteration in mental status

5.7.2.4 Nosocomial infection Clinically evident infection that was neither present nor in-

cubating at the time of admission to hospital (generally held to appear > 48hrs after admis-

sion)

5.7.2.5 Colonisation The detectable presence of micro-organisms on / in a patient that are

not pathogenic or elicit an inflammatory response.

5.7.3 Screening for sepsis

5.7.3.1 Septic screen-empiric

135


• Urine microscopy and culture

• Tracheal aspirate and BAL fluid

• Blood cultures

5.7.3.2 Components of sepsis screen-directed

• Fungal cultures

• CSF

• Pleural Tap

• X-ray sinuses

• Directed or bronchoscopic examination of chest flora.

5.7.4 Investigation of Pneumonia

5.7.4.1 Community acquired pneumonia

Microbiology

• Common organisms:

– Strep pneumoniae, Haemophilus influenzae, Influenza A

• Other organisms:

– Bacteria: Legionella sp, Gram-bacilli, S. Aureus

– Viral: Influenza B, Parainfluenza, Adenovirus, RSV

– Other: Mycoplasma, Chlamydia Psittaci (birds), TB, Chlamydia pneumoniae

Investigations

• Full blood count and differential

• Biochem: ICU profile

• ABG

• CXR

Microbiology

• Blood cultures ×2

• Endotracheal aspirate or sputum for microscopy and culture (urgent gram stain)

• Respiratory viral antigen and culture (if not intubated then use nasopharyngeal swab)

• Serology: for atypical bacteria

• Direct antigen detection: Urine (pneumococcal Ag), serum (Legionella Ag) by PCR .

• Pleural fluid: where significant effusion present

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5 CLINICAL MANAGEMENT 5.7 Microbiology Guidelines

In immuno-compromised host

• Extend spectrum of detection on sputum: fungal stain and culture, Pneumocystis Carinii

stain and acid fast bacilli.

• Viral studies for CMV, HSV, EBV

• HIV serology if appropriate

• Consider broncho-alveolar lavage or lung biopsy if initial cultures negative.

5.7.4.2 Nosocomial pneumonia in the ICU

Introduction Incidence: Up 20% of all ICU patients, 70% of patients meeting criteria for

ARDS.

Clinical diagnosis, including use of tracheal aspirates, has poor sensitivity and specificity.

Diagnosis A diagnosis of nosocomial infection (including ventilator associated pneumonia)

should be considered if:

• New and persistent CXR changes

• Tachycardia and tachypnoea

• Fever or hypothermia

• Leucocytosis or leucopaenia

• Purulent sputum

• Deteriorating lung function or increasing ventilatory requirement.

Confirmation of diagnosis:

• Broncho-alveolar lavage: Only specimens with Epithelial cell count < 1 % considered

– > 5 % intracellular organisms considered diagnostic

– < 5 % intracellular organisms, treat with antibiotics only if patient unstable and sub-

sequent culture reveals > 104 CFU.ml-1.

Treatment Empiric treatment should be guided by the initial gram stain. See antibiotic

guideline.

5.7.5 Vascular Catheter Sepsis

5.7.5.1 Introduction It is no longer common practice to remove or replace central access

routinely, but only when infected or no longer required.

Suspect line sepsis in the presence of:

• New or unexplained fever

• Or ↑ in WCC

• Deterioration in organ function

137


• Positive blood culture with likely organism in a patient with sepsis.

• Evidence of local infection (inflammation or pus at the insertion site)

5.7.5.2 Guidelines Attempt to confirm bacteraemia by taking blood cultures from a periph-

eral vein (cultures from the line may only indicate colonisation).

Remove line on suspicion of infection. Intra-vascular catheters are not routinely submitted for

culture.

5.7.5.3 Treatment Removal of the infected line will usually result in resolution of clinical

sepsis.

Antibiotics are indicated only if sepsis is severe, progressive following removal of the line, or if

the patient is high risk (eg. prosthetic implants)

Refer to antibiotic guidelines for selection of antibiotics.

Subsequent venous access In ICU central access may be necessary for ongoing antibiotics

or inotropes, so that a new line may have to be inserted immediately.

Where possible wait 24 hours before re-inserting a new line at a new site.

Guidewire exchanges may only be performed where mechanical problems complicate a new

catheter site.

5.7.6 Fungal infections

5.7.6.1 Introduction The incidence of systemic fungal infections in Intensive Care has in-

creased in recent years as a result of

• Increased use of broad spectrum antibiotics

• Increasing numbers of immunosuppressed patients being referred to ICU.

• Prolonged use of intravascular catheters

• Co-existent use of immunosuppressive therapy.

The Consultant Microbiologist should be consulted where any doubt exists with regard initia-

tion of antifungal therapy.

5.7.6.2 Indications for antifungal therapy

• Prophylaxis in patients following bone marrow transplant or neutropaenic patients.

• Single positive blood culture in a high risk patient

• Isolation of candida from any sterile body site except urine, or isolation of fungi in two

anatomically discrete sites in selected patients.

• Histological evidence of yeast or mycelial forms in tissue from high risk patients.

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5 CLINICAL MANAGEMENT 5.8 Drug / Toxin Overdose

5.7.6.3 Treatment See antimicrobial guidelines.

5.8 Drug / Toxin Overdose

5.8.1 Introduction

The majority of overdoses are polypharmacological and respond to general supportive mea-

sures. Overall mortality is low and usually relates to cardio-respiratory arrest and / or uncon-

trolled siezures prior to admission.

Despite an unreliable correlation between depth of coma and preservation of glottic reflexes,

over the last decade emergency departments have become more aggressive at intubating

patients.

While specific reversal agents such as Naloxone (opioids) or flumazenil (benzodiazepines) have

some short term use, their relatively short half lives restrict their efficacy in definitive treat-

ment.

5.8.2 Admission to ICU

• Intubated patients

• Uncontrolled siezures

• Coma

• Persistent hypotension

• ECG abnormalities consistent with significant ingestion (may be suitable for HDU moni-

toring in the absence of other features listed above):

– Ventricular or supraventricular tachyarrhythmias

– Sinus tachycardia > 140 / min

– 2nd or 3rd degree heart block

– QT-prolongation (preferably index QTc)

– QRS duration > 0.12ms

5.8.2.1 Gastric lavage The place of gastric lavage in acute poisoning is debatable, and is

only of benefit in the hyperacute phase of poisoning ( < 1 hour).

Patients must be awake with a preserved gag reflex, or already be intubated, failing which

the risks and benefits of intubating specifically to perform gastric lavage patient need to be

evaluated.

Procedure

• Insert 16G nasogastric tube (not a large bore sump)

• Instil 1 ml.kg-1 warm water only, then attempt recovery of the lavage.

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5.9 Withdrawal of Treatment in the Intensive Care 5 CLINICAL MANAGEMENT

• Do not continue to instil water until the previous volume has been removed.

• Continue until lavage is clear.

5.8.2.2 Charcoal Charcoal aspiration has a high morbidity and mortality. As for gastric

lavage above, this should not be attempted in patients without a safe or protected airway.

Instil 50g as soon as possible and 50g 4 hrly thereafter while indication persists. Co-administration

with sorbitol has not been shown to increase efficacy.

In general charcoal should be given in a ratio of 10:1, charcoal dose to drug ingested dose.

Indications for administering activated charcoal Virtually all patients presenting with a

drug overdose.

Contra-indications

• Elemental metals (lithium, iron)

• Pesticides

• Strong acids or alkalis

• Cyanide

• Late presentations > 4-6 hrs post ingestion.

5.8.3 Specific Overdoses

The Hospital intra-net site contains a link to Medline and other Biomedical Databases, in which

directory you will find Micromedex which contains both Poisindex and Drugdex two accessible

and readable databases relating to drug and toxin ingestion.

Consult the ICU Consultant prior to commencing therapy not considered part of basic resusci-

tation measures.

5.9 Withdrawal of Treatment in the Intensive Care

5.9.1 Introduction

Withdrawal of treatment, or the decision not to initiate treatment, is a Consultant responsibility.

Junior staff are not expected, nor encouraged, to enter into an end-of-life discussion

with a patient or their family, unless requested by a Consultant to do so.

5.9.2 Principles

Patients have a right to receive quality end of life care including appropriate palliative care

and help making decisions regarding life-sustaining treatment.

Health providers are not however obliged to provide treatments that would be perceived to be

futile, or otherwise not in the best interests of a given patient.

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5 CLINICAL MANAGEMENT 5.10 Brain death and organ donation

5.9.3 Deciding not to treat (or treat any further)

The goal of intensive care is to prevent unnecessary suffering and premature death by treating

reversible illnesses for an appropriate period of time.

Patients in whom treatment is to be withdrawn or not initiated generally fall into one of the

following categories:

• Imminent death: A patient with an acute illness whose reversal or cure would be unprece-

dented, and will certainly lead to death.

• Lethal condition: Progressive, unrelenting terminal disease incompatible with survival

longer than 3-6 months. Life sustaining treatment should not be provided for the un-

derlying disease. Where treatment is provided for superimposed, reversible illness, this

should have cleargoals and limitations.

• Severe irreversible condition: A patient has a severe and irreversible condition impairing

cognition or consciousness, but where death may not occur for many months. Life sus-

taining treatment should not be instituted for the underlying condition, but again may be

used to achieve a specific goal (eg. waiting for arrival of a family member).

5.9.3.1 The decision making process Generally, there should be inter-professional team

consensus to withdraw therapy.

The ICU Consultant or primary specialist should:

• As early as possible discuss with patients while capable, their prognosis and wishes for

treatment.

• Explore why the patient or substitute decision maker wishes treatment to be continued.

• Discuss with the patient or decision maker the rationale for withholding or withdrawing of

life support systems.

• Describe palliative measures and emphasize patient comfort and dignity.

• Offer hospital resources such as social work, chaplaincy or bioethics to assist the patient

/ family with their psychosocial, cultural, spiritual and informational needs.

• Document pertinent details of this communication in the patient notes.

Where there is not consensus between the patient/family and staff, then:

• Negotiate a plan of care acceptable to all parties.

• Obtain a second opinion should this be appropriate

• Initiate a clearly defined trial of therapy

If none of these are successful then external mediation may become necessary although this

would be extremely rare.

5.10 Brain death and organ donation

5.10.1 Declaration of brain death

This procedure is an absolute requirement prior to beating-heart organ donation.

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5.10 Brain death and organ donation 5 CLINICAL MANAGEMENT

Where clinical examination is to be used alone, this must be performed by 2 doctors of the

status prescribed by local jurisdiction.

The two doctors may choose to present at each examination, however, each must perform ALL

of the brain death studies independently, and be responsible for one of the examinations.

In some circumstances, a clinical examination may be replaced by investigations as given

below.

5.10.2 Clinical certification of brain death

5.10.2.1 Pre-conditions A cause of coma must be identified and documented

Reversible causes of coma must be excluded

• coma caused by drugs / poisons-Morphine, Midazolam, barbiturates etc

• unresponsive state caused by neuromuscular blocking agents-vecuronium, pancuronium

etc

• coma caused by hypothermia-core temperature must be ? 35o C

• coma caused by metabolic or endocrine disturbance-the patients should have:

– normal renal function

– normal hepatic function

– normoglycaemia

– normal electrolyte profile

5.10.2.2 Clinical assessment of brain stem function It is recommended that this pro-

cedure is performed separately by 2 doctors at least 2 hours apart, to ensure that death is not

confirmed until a minimum of 6 hours after onset of coma.

A minimum of four hours observation and mechanical ventilation must occur, during which the

patient has been comatose (Glasgow Coma Score 3), had non-reactive pupils, absent cough

and gag reflexes, and no spontaneous breathing efforts. In some cases this period may be

longer (eg. in primary hypoxaemic injuries).

Testing brain stem function A response at any stage deems the patient is not brain dead

and further testing does not proceed

• absent pupillary responses to light (directional and consensual)

– tests cranial nerve III

• absent corneal reflexes (avoid unnecessary repetition so as not to injure the cornea)

– tests cranial nerve V + VII

• absent vestibulo-ocular reflex: (the tympanic membrane must be inspected and noted to

be intact before proceeding).-no nystagmus (no eye deviation to the stimulated side) on

the injection of 50 ml of iced water into the ear

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5 CLINICAL MANAGEMENT 5.10 Brain death and organ donation

– tests cranial nerve VII + VIII

• absent gag reflex

– tests cranial nerve IX + X

• absent cough reflex

– tests cranial nerve IX + X

• absent response to painful stimuli within the cranial nerve distribution

• absent respiratory function: should always be done last, and the following must be ad-

hered to following the disconnection of the ventilator:

– pre-oxygenate the patient by placing oxygen tubing into the ET tube and insufflate

with 100% oxygen at 2 l.min-1

– look for apnoea clinically

– sample ABG 10-15 minutes following disconnection from the ventilator.

– the PaCO2 should be > 8 kPa

Time of death The legal time of death is at the time of the completion of the second test

of brain death studies / or whatever time the doctor performing the second set of brain death

studies documents on the appropriate form and / or in the patient notes.

5.10.2.3 Non-clinical certification of brain death Objective demonstration of the ab-

sence of cerebral blood flow is required if brain death is suspected and the preconditions (2b)

for clinical certification cannot be met. For example:

• facial trauma or obstruction of the external auditory canals may not allow assessment of

all the brain stem reflexes.

• a high cervical injury will not allow assessment of all the brain stem reflexes

• Where the effects of sedation agents cannot be excluded

A 6 hour period of observation of absent brain function is preferred prior to radiological exam-

ination when the absence of cerebral blood flow may be established by either:

• radionuclide cerebral perfusion scan

• 4 vessel angiography

Certification of brain death is then undertaken after the respective scan has been verified by

a practitioner certified to do so.

The legal time of death is at the time of radiological testing.

5.10.2.4 Frequently asked questions: Exclusions to the diagnosis of brain death

The following observations do not exclude a diagnosis of brain death:

• spontaneous ”spinal” movements of the limbs

• respiratory-like movements (shoulder elevation and adduction, back arching or inter-

costal expansion without significant tidal volume)

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6 APPENDICES

• sweating

• blushing

• tachycardia

• absence of diabetes insipidus (normal osmolar control mechanism)

• deep tendon reflexes

• Up-going plantar reflex.

6 Appendices

6.1 Haemodynamic Principles

6.1.1 Introduction

When faced with a patient who may have some haemodynamic impairment you should have

a systematic approach to assessing and managing this important issue. The following is one

way:

Ask four questions:

• Is the blood pressure actually low?

• Is there any evidence of shock (or poor tissue perfusion)?

• Does this patient require more fluid?

• Do I need to introduce an inotrope, a chronotrope or a vasopressor substance?

6.1.2 Diagnosing hypotension

6.1.2.1 Absolutely low blood pressure

Definition Systolic BP < 90 mmHg or Mean arterial pressure < 60 mmHg.

These are implied limits at which vital organs continue to autoregulate blood flow.

6.1.2.2 Relatively low blood pressure Individual patients may normally have elevated or

indeed low blood pressure. Hypotension would then be considered as:

Systolic BP 30% lower than known values for that patient (or an absolute drop of 20 mmHg).

6.1.3 Is there any evidence of shock ?

6.1.3.1 Bedside indicators:

• Cerebral perfusion: restlessness or confusion

• Renal blood flow: oliguria ( < 0.5 ml..kg-1.hr-1)

• Cool peripheries (unreliable)

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6 APPENDICES 6.1 Haemodynamic Principles

6.1.3.2 Simple investigations

• ECG: evidence of regional ischaemic changes

• ↓ pH on arterial blood gas

• ↑ Serum lactate

• Central venous oxygen saturation.

6.1.3.3 Surrogate end-points Generally unwieldy eg. gastric tonometry and measure-

ment of gastric mucosal pH.

6.1.4 Does this patient require more fluid resuscitation?

6.1.4.1 Introduction-Assessment of Cardiac Preload This is the hardest question to

answer.

All texts and wise men will urge you to adequately volume resuscitate the patient, while simple

to say, it is difficult to fulfil.

6.1.4.2 Defining preload Pre-load refers to the degree of ventricular filling which infers the

degree of stretch of myocytes during diastole.

6.1.4.3 Starling Curve The more fluid returned to the heart (venous return), the greater

the contractile force of the heart and the greater the volume of blood expelled.

At some point the distension of the heart exceeds its ability to contract and the ventricle will

fail.

Should I give more fluid ? Patients on the volume responsive part of the Starling curve

should increase their cardiac output in response to further intravenous fluid.

How do I know where the patient is on the curve ? In a number of patients this is not

problematic as they have haemorrhagic shock, vomiting, diarrhoea or some other reason for

absolute or relative (eg. epidural, anaphylaxis) intra-vascular volume contraction.

There are a number of techniques for assessing or inferring left ventricular end-diastolic vol-

ume as the determinant of pre-load in patients where this is not clear-cut. Two of these, the

pulmonary artery catheter and the PiCCO are described separately in this appendix.

Clinical estimates of hydration (moist mucous membranes, skin turgor.) are almost useless in

ICU.

Estimation of JVP, or indeed invasive measures of right heart (CVP) or left heart(pulmonary

capillary wedge pressure) filling pressures have some relevance in patients with hearts that

have normal structure and function. Often this is not the case in ICU.

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6.2 The Pulmonary Artery Catheter 6 APPENDICES

So what should I do ? Often clinical practice relies on your impression and an assessment

of the risk of giving more fluid than not doing so. ie. It would be easier to give fluid to a

hypotensive person with a clear chest who is ventilated, than one with chest crackles who is

developing respiratory failure, even if this is due to some other pathology.

The decision to implement a fluid challenge is inextricably linked with a duty to closely observe

the results and act accordingly.

Do I need to introduce an inotrope, a chronotrope or a vasopressor ? Once the three

questions above have been addressed adequately it may become necessary to use an agent

to bring about an increase in blood pressure and therefore organ perfusion. ie.

Organ perfusion: Q = (Pi-Po) × C , where

• Q = organ perfusion

• C = regional conductance (a function of vascular radius, and blood rheology)

• Pi-Po = pressure gradient across the tissue bed or organ (generally blood pressure, BP)

BP = Systemic vascular resistance (SVR) × cardiac output , (ie = HR × Stroke volume × SVR).

Manipulation of blood pressure and therefore organ perfusion relies on changing one of the

following three parameters therefore: heart rate, stroke volume and vascular resistance.

6.2 The Pulmonary Artery Catheter

6.2.1 Introduction

The PAC was designed in an effort to quantify and therefore manipulate haemodynamic pa-

rameters ie.

1. Estimation of cardiac pre-load by measuring pulmonary artery occlusion pressure

2. Estimation of cardiac output by thermodilution

6.2.1.1 Pulmonary artery occlusion pressure (or PCWP Pulmonary Capillary Wedge

Pressure) Under conditions described in the clinical procedures section of this guideline the

PA catheter is inserted into a central vein.

The PA catheter is introduced into a segmental pulmonary artery using a flow directed tech-

nique.

The premise behind the use of this catheter is that PAOP is determined by left atrial pressure

which bears a relationship to left ventricular end diastolic pressure and this in turn relates to

left ventricular end-diastolic volume as the final arbiter of pre-load.

This relationship does not hold true if:

• There is not a continuous column of fluid between sensor and left atrium.

• There is mitral regurgitation.

• The compliance characteristics of the left ventricle are abnormal.

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6 APPENDICES 6.3 The PiCCO-catheter / monitor

Given the above it is not surprising that the PAOP has proven to be an unreliable predictor of

preload in clinical practice.

6.2.1.2 Complications of Pulmonary Artery Catheterisation

• Time spent inserting the catheter may distract from resuscitating the patient.

• Insertion and mechanical problems, thrombosis and infection are similar to those ob-

served with central access cannulation.

• Balloon induced problems:

– Balloon rupture

– Catheter knotting

– Pulmonary infarction

– Pulmonary artery rupture

– Pulmonary and tricuspid valve damage

– Endocarditis

– Arrhythmias

6.2.1.3 Place in therapy The impact of a PA catheter, and the haemodynamic variables

obtained with it on management, and outcome, are not well defined. Particularly disappointing

has been the inability of pulmonary wedge (or occlusion) pressure to reflect in any useful way

the pre-load status of a given patient.

Understanding of the catheters limitations and usefulness varies widely among doctors and

nursing staff and requires ongoing education to reduce morbidity associated with its use, and

correct interpretation of the data it provides.

Proponents of its use argue that failure of clinical judgement in diagnosing type of shock,

or instituting successful treatment is an indication for catheterisation of the right heart, to as-

sess haemodynamic and metabolic variables reflecting type, severity and course of circulatory

compromise.

Those who do not favour use of the PA catheter argue that clinical judgement (or less invasive

monitoring) is not inferior to catheterisation of the right heart.

The lack of direct evidence to support the use of this type of catheter, and the increasing

body of evidence documenting its inability to predict response to fluid loading have resulted

in declining use of the PA catheter in clinical practice.

6.3 The PiCCO-catheter / monitor

6.3.1 Introduction

This method evolved as an alternative to cathterisation of the right heart in an attempt to

elucidate further the concept of cardiac pre-load, and patient fluid status.

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6.3 The PiCCO-catheter / monitor 6 APPENDICES

6.3.1.1 Aims

• Measurement of cardiac output by less invasive means than catheterisation of the right

heart.

• Estimation of pre-load, intra-thoracic blood volume and by inference extra-vascular lung

water.

6.3.1.2 Technique: Trans-pulmonary thermodilution measurement and analysis of pulse

contour.

6.3.2 Estimation of cardiac output

A bolus of injectate, usually cold fluid, given into a large central vessel (eg. superior vena cava)

can be detected in a large artery (eg. femoral or axillary) as a temperature change, giving rise

to a pulse contour.

This is similar in theory to the thermodilution principle used in the PA catheter where cold fluid

of a known volume and temperature is injected proximally into the catheter and a temperature

change detected more distally by a temperature sensor as the colder fluid mixes with blood.

The magnitude of the temperature change detected at the thermistor can be used to estimate

the volume of blood into which the cold fluid was diluted, and hence the cardiac output.

When this is done across the entire pulmonary circulation however, and is detected in an artery

the pulse contour generated by the temperature change is flatter and longer, but nevertheless

still gives reliable results when extrapolated to predict cardiac output.

6.3.2.1 Estimation of pre-load, intra-thoracic blood volume and extra-vascular lung

water The derivation of these parameters using this technique is not simple, nor intuitive,

and requires extensive extrapolation of data.

6.3.2.2 Inferences inherent in estimation of cardiac pre-load using the PiCCO tech-

nique By examining the contour of the temperature pulse wave generated in the systemic

arterial tree by injecting cold fluid centrally, it is possible to make some inferences relating to

given blood volumes.

Inference 1 An injected indicator (cold fluid) always mixes with largest volume accessible.

Cold water injected into a central vein will mix into fluid in the following spaces, which together

comprise the intra thoracic thermal volume or ITTV.

Inference 2 By analysing the shape and time characteristics of the temperature wave form

(or pulse) it is possible to make certain assumptions with regard to the volumes of mixing as

given above.

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6 APPENDICES 6.4 Principles of ventilation

The leap of faith is that wave form analysis produced by a transpulmonary thermodilution

technique, can be used to calculate cardiac output.

Derived fluid volumes may allow estimation of both preload (using global end diastolic volumes

or intra thoracic blood volumes), and the amount of extravasated fluid into the lungs (given by

extra vascular lung water).

Once you accept this principle you can the use these numbers to guide both further fluid

therapy and administration of inotropes or vasopressors.

6.4 Principles of ventilation

6.4.1 Introduction

Mechanical ventilation serves two basic functions: ventilatory support and oxygenation sup-

port.

Ventilatory support is designed to provide either total or partial gas transport between the

environment and the alveoli. Usually this is done by providing positive airway pressure in a

manner that mimics the normal tidal volume and breathing frequency pattern.

In contrast oxygenation support is designed to supplement the FiO2 and to optimise ventilation

perfusion matching to effect alveolar gas transport.

The most common technique to accomplish this is the application of positive end expiratory

pressure (or PEEP), but manipulations of the ventilatory pattern and other strategies can also

be used.

6.4.1.1 Classification of ventilators Mechanical ventilators have been classified accord-

ing to the characteristics of the inspiratory phase.

• If they provide a constant inspiratory pressure they are known as pressure generators.

• If they provide a constant inspiratory flow they are known as flow generators.

Flow Generators These usually deliver a preset volume of gas to the lung independent of

the change in pulmonary or chest wall compliance or airway resistance.

The pulmonary and chest wall compliance and airway resistance determine the proximal air-

way pressure produced by these machines.

Pressure Generators These deliver gas at a preset pressure.

They are often simple, small, robust and cheap.

The volume of gas that they deliver can be altered by a change in the patients lung or chest

wall compliance or airway resistance.

Modern ventilators encompass both types of generator. They can ventilate the patient either

by preset volume, independent of compliance, or preset pressure which is interactive with

pulmonary compliance and resistance, thus altering tidal volume.

149

6.4 Principles of ventilation 6 APPENDICES

It is important to become familiar with the mechanics of both modes.

6.4.2 Ventilatory strategies to provide total ventilatory support

Current approaches to total ventilatory support generally attempt to duplicate the normal bulk

flow ventilatory pattern and use tidal volumes (VT) of 5-10 ml.kg-1.

Machine breath rates of 10-30 breaths per minute and inspiratory to expiratory ratios (I:E) of

1:4 to 1:2.

These positive pressure breaths are generally delivered as either flow limited volume cycle

breaths or pressure limited time cycle breaths.

Positive pressure ventilatory support is usually used in conjunction with elevations in baseline

(end expiratory) pressure (PEEP) and supplementary oxygen.

These settings generally provide safe and effective total ventilatory support in most patients

in respiratory failure.

In more complex patients, conventional approaches do not provide ideal blood gas values, or

airway pressures may be excessively high. Under these circumstances other strategies may

be considered.

6.4.2.1 Controlled mechanical ventilation This is the most basic form of mechanical

ventilation supplying all ventilation in the apnoeic patient.

Spontaneous breaths are not available.

During pressure control ventilation (PCV) each breath is delivered as time pressure controlled

breaths and tidal volume varies, dependent on the resistance of the airway, elastance and the

total PEEP.

6.4.2.2 Assist control ventilation (ACV) In addition to a preset background rate of CMV

breaths the patients inspiratory effort initiates a standard CMV breath.

The ability to control respiratory rate means that less sedation is required, however the respi-

ratory muscles continue to contract during these assisted breaths with only a small reduction

in work compared to unassisted spontaneous breaths.

6.4.2.3 Intermittent mandatory ventilation (IMV) This was introduced to allow unim-

paired spontaneous breaths while still ventilated with intermittent CMV breaths to minimise

sedative use and to reduce respiratory muscle discoordination, allowing more rapid weaning.

6.4.2.4 Synchronised intermittent mandatory ventilation (SIMV) Is designed to avoid

breath stacking by partitioning the inspiratory time into patient initiated or spontaneous breaths.

Neither IMV nor SIMV has been clearly shown to allow easier weaning than T-piece trials.

150

6 APPENDICES 6.4 Principles of ventilation

6.4.2.5 Pressure support ventilation (PSV) During this type of ventilation the patient

breaths are supported to a preset pressure using additional gas flow.

Inspiration is usually terminated when the inspiratory gas flow falls to about 25% of the initial

flow rate.

The main disadvantage of pressure support ventilation is that the tidal volume may alter so

that minute volume will alter depending on respiratory drive, pressure support level and res-

piratory system compliance.

Excessively large tidal volumes resulting in overstretch of the lung may occur, possibly con-

tributing towards ventilator associated lung damage.

On some ventilators there is a similar type of ventilation called volume support (VS) which is a

mode of adaptive pressure support ventilation where breath to breath logic is used to assure

preset tidal volume.

There are many other forms of ventilation which at the moment are still being investigated.

These include airway pressure release ventilation, bilevel ventilation and proportional assist

ventilation.

Note: PSV and VSV are spontaneous modes. They cannot be used in paralysed patients.

6.4.3 Objectives of mechanical ventilation

• To improve alveolar ventilation and reduce PaCO2.

• To improve oxygenation and ventilation perfusion mismatch.

• To increase end expiratory lung volume to prevent or treat lobar or pulmonary collapse

and atelectasis.

• To increase functional residual capacity through the use of PEEP, which may help improve

oxygenation or reduce lung injury through adequate recruitment with the prevention of

repeated opening and closing of alveoli.

• To unload the respiratory muscles when there is an unbalance between load and the

ability to cope. This results in respiratory muscle insufficiency or ventilatory failure.

• To allow adequate sedation and paralysis of the patient to aid control to enable the un-

derlying disease state to be adequately treated.

• In some conditions such as trauma where there is loss of chest wall integrity such as in

a flail chest, ventilation may be needed to stabilise the chest wall and to initiate other

treatment such as analgesia with safety.

6.4.4 Other Ventilatory strategies

6.4.4.1 Reverse I:E Ratio The conventional inspiratory to expiratory (I:E) ratio is generally

1:2 to 1:4.

This range of I:E ratio tends to synchronise with the patients spontaneous ventilatory drive and

permits adequate expiratory time for the lung to return to functional residual capacity (FRC)

using the recoil pressure of the lung.

151

6.4 Principles of ventilation 6 APPENDICES

Lengthening the inspiratory time to I:E ratios approaching 1:1 or even exceeding it (inverse

ratio ventilation) can be accomplished in either volume or pressure cycled modes.

Prolonging inspiration has several physiological effects.

• The alveolus is held at its inspiratory volume for a longer period. This should allow more

mixing time between the alveolus and the conducting airway and more exposure of the

capillary blood to fresh gas. Some studies have shown an improvement in ventilation

perfusion (V̇ /Q̇) mismatching with this technique and increases in the PaO2.

• Incomplete lung emptying. Under these conditions the lung cannot return to its normal

FRC and intrinsic PEEP or auto-PEEP develops.

Many of the studies on long inspiratory time and inverse ratio ventilation showing an improve-

ment in gas exchange have probably had this occur as a consequence of auto or intrinsic PEEP.

Long inspiratory times with air trapping may also improve V̇ /Q̇ mismatching because it func-

tions like applied PEEP, however there is often a trade-off to allow permissive hypercapnoea.

This is largely a consequence of lower set respiratory rates to allow adequate expiration per

breath.

Baseline alveolar pressure rises and thereby this raises maximum alveolar pressure for a con-

stant tidal volume.

The main role of inverse ratio ventilation is in alveolar recruitment in acute lung injury and

ARDS. In these conditions it is used as a ventilatory strategy in an attempt to improve oxy-

genation.

It is important to realise that once the I:E ratio has been inverted the need for increased

sedation and neuromuscular paralysis starts to increase.

The mode is inherently uncomfortable and is poorly tolerated in lightly sedated patients.

There may be negative effects on cardiac output (increased intrathoracic pressure impeding

venous return)

6.4.5 Ventilation Mechanics

6.4.5.1 Tidal volumes Traditionally an average tidal volumes of around 10-15 ml.kg-1 were

used, and 10 ml/kg can be considered a reasonably safe tidal volume in most patients including

children. In patients with poorly compliant lungs or acute respiratory distress syndrome lower

tidal volumes should be used ( < 8 ml.kg-1).

6.4.5.2 Respiratory frequency The respiratory frequency required in an adult varies be-

tween 8 and 25 inflations per minute and depends on the patients expiratory time and lung

compliance.

6.4.5.3 Peak inspiratory airway pressure Generally this alarm should be set on the ven-

tilator to at or below 35 - 40 cmH2O to reduce side-effects of barotrauma. Plateau pressure is

probably a more reliable guide to risk of barotrauma than peak pressure. Please note: The

actual peak airway pressure generated in the patient should be ≤ 30 cmH2O.

152

6 APPENDICES 6.5 The Sedation - Agitation Score

Table 5: Sedation-Agitation Score

6.4.5.4 Positive end expiratory pressure

Introduction PEEP is defined as the pressure above atmospheric maintained at the airway

at the end of expiration.

It is a supportive technique used to increase arterial oxygen content without increasing the

FiO2 and maintain alveolar / small airways recruitment.

Using PEEP PEEP may be indicated in patients with pulmonary oedema of cardiogenic or

non cardiogenic origin.

The usual range of applied PEEP varies anywhere from 5 to 15 cmH2O and rarely up to 20.

Problems with using PEEP PEEP is generally contraindicated in patients who have a bron-

chopleural fistula or severe barotrauma as it may further predispose to barotrauma including

mediastinal air leak and pneumothorax.

PEEP may also

• Increase physiological dead-space

• Reduce the capacity to excrete carbon dioxide

• Reduce cardiac output, which is due in part to a decrease in venous return and an increase

in alveolar and therefore pulmonary blood pressure, i.e. an increase in RV afterload, and

alteration of left ventricular geometry (intraventricular septum shifted towards the left).

• Other complications may include a decrease in renal blood flow and possibly a reduction

in portal blood flow.

Weaning from PEEP In general to wean from PEEP we usually reduce the fractional inspired

oxygen concentration first until it is down to approximately an Fi02 of 0.5.

The PEEP is then slowly removed in aliquots of 3-5 cmH2O providing the PaO2 is maintained at

8 kPa or greater.

6.5 The Sedation - Agitation Score

One of many sedation scores developed to assess and target depth of sedation.

This score is not interchangeable with Glasgow Coma Score, the purpose of which is to assess

depth of coma following an insult to the brain.

153

6.6 Classification of anti-arrhythmic drugs 6 APPENDICES

6.6 Classification of anti-arrhythmic drugs

6.6.1 Classification of Antiarrhythmic Drugs by Their Action

The standard classification of antiarrhythmic drugs was developed by Singh and Vaughan

Williams based upon the drug’s electrophysiological mechanisms of action:

• Class I drugs act by blocking the Sodium channel, and are divided into 3 groups, IA, IB,

and IC based on their effects on repolarization and potency towards blocking the Sodium

channel

– Subclass IA drugs are potent Sodium channel blockers (prolong QRS interval), and

also usually prolong repolarization (prolong QT interval) through blockade of potas-

sium channels (quinidine, procainamide, disopyramide)

– Subclass IB drugs have the lowest potency as Sodium channel blockers, produce

little if any change in action potential duration (no effect on QRS interval) in nor-

mal tissue, and shorten repolarization (decrease QT interval) (lignocaine, mexiletine,

tocainide, phenytoin)

– Subclass IC drugs are the most potent Sodium channel blocking agents (prolong

QRS interval), and have little effect on repolarization (no effect on QT interval) (en-

cainide, flecainide, propafenone)

• Class II drugs act indirectly on electrophysiological parameters by blocking beta-adrenergic

receptors (slow sinus rhythm, prolong PR interval, no effect on QRS or QT intervals) (pro-

pranolol, esmolol, acebutalol, l-sotalol)

• Class III drugs prolong repolarization (increase refractoriness) by blocking outward potas-

sium conductance (prolong QT interval), with typically little effect on the rate of depolar-

ization (no effect on QRS interval) (dofetilide, amiodarone„ ibutilide, bretylium, d/l-sotalol

• Class IV drugs are relatively selective AV nodal L-type Calcium-channel blockers (slow si-

nus rhythm, prolong PR interval, no effect on QRS interval) (Verapamil, diltiazem, bepridil)

• Miscellaneous: In addition to the standard classes, IA-C, II, III, and IV, there is also

a miscellaneous group of drugs that includes digoxin, adenosine and Magnesium with

actions that don’t fit the standard four classes.

• The Vaughan Williams classification is relatively simple and is useful as a conversational

shorthand based on mechanism of action, for its ability to predict adverse effects, and

for preliminary decisions regarding drug therapy, but it has a number of important draw-

backs:

– Drugs within a class are not necessarily clinically similar; a patient may respond well

to one drug in a given class, but not another

– Almost all of the currently available drugs have multiple actions; it is rarely apparent

which of these actions is responsible for suppression of an arrhythmia in a given

patient

– The metabolites of many of the drugs contribute to or are primarily responsible for

their antiarrhythmic actions (e.g.-procainamide and its metabolite, N-acetylprocainamide;

154

6 APPENDICES 6.7 Guidelines for the use of patient controlled anaesthesia (PCA)

encainide and its metabolite, 3-methoxy-O-desmethylencainide)

– The stereoisomers of several drugs can have different actions:

* The stereo isomers of disopyramide (Class IA) have opposite effects on repo-

larization; the predominant effect in a given patient depends on the degree of

stereospecificity exhibited in elimination of the drug by that patient

* Only the l-isomer of sotalol has beta-adrenergic blocking activity

– Some of the most widely used drugs (procainamide, disopyramide, amiodarone, so-

talol) have multiple actions which might explain their utility in treating a broad range

of arrhythmias.

6.7 Guidelines for the use of patient controlled anaesthesia (PCA)

6.7.1 Introduction

Generally, PCA has been associated with better pain relief and greater patient satisfaction

compared with intermittent opioid injections. The reasons for this include:

• Small and frequent intravenous bolus doses of opioid can be given whenever the patient

becomes uncomfortable, or when a painful stimulus is anticipated, enabling individual

titration of pain relief. This flexibility helps to overcome the wide interpatient variation in

opioid requirements.

• The intensity of acute pain is rarely constant, and PCA means that the amount of opioid

delivered can be rapidly titrated.

• Patients can also titrate the amount of opioid delivered against dose-related side effects.

The inherent safety of the technique lies in the fact that, as long as the machine is in PCA

mode only (ie. there is no continuous infusion), further doses of opioid will not be delivered

should the patient become excessively sedated.

6.7.1.1 Contraindications

• Patient confusion

• Inability to understand the technique.

• Untrained staff (medical and nursing)

6.7.2 Acute Pain Service Standard Orders

Oxygen is routinely ordered for at least the first 8 hours.

No additional opioids or sedatives, unless ordered by the APS.

Only the patient may press the demand button.

The IV line must contain a non-return valve.

Change syringe every 24 hours and line every 48 hours.

155

6.7 Guidelines for the use of patient controlled anaesthesia (PCA) 6 APPENDICES

6.7.2.1 Observations Pain score, sedation score, vomiting score, and respiratory rate hourly

for 8 hours, then 2 hourly for duration of PCA.

Total demands, good demands, amount in syringe, and cumulative dose hourly for 8 hours,

then 2 hourly.

SpO2 to be recorded each nursing shift.

6.7.2.2 Opioids and equipment The PCA machines currently in use require a code to

change bolus or infusion rate. This information will be provided in the course of your train-

ing.

6.7.3 Programmable Variables

6.7.3.1 Loading Dose Patient controlled analgesia may not be effective for some time if

moderate to severe pain is present from onset.

Generally, the same opioid to be used in the PCA should be given by the anaesthetist as

intraoperative analgesia.

During the recovery period, to make the patient comfortable before PCA is commenced, a

loading dose of opioid may be required.

There is enormous inter-patient variation in the amount of opioid needed, and it is better to

individualise for each patient

6.7.3.2 Bolus Dose The optimum bolus dose is that which results in appreciable analgesia

without significant side effects.

The best predictor of dose required is patient age, as patient weight is of relatively little im-

portance.

An estimation of the first 24 hour Morphine requirements can be given by the formula (for

patients aged 20 years and older).

• Morphine requirements (mg) = 100-(age in years)

From this formula it can be seen that, on average, Morphine requirements for a 70 year old

patient are less than half the dose of a 20 year old.

The size of the bolus dose should generally be halved in patients over 70 years of age, and

consideration should be given to further reducing the size of the bolus dose in patients aged

over 80 years.

6.7.3.3 Dose Duration Dose duration is usually set at stat. However, the rate of delivery

can be slowed to as much as 10 minutes.

6.7.3.4 Lock-out interval This is the time from the end of delivery of one dose until the

machine will respond to another demand. This allows the patient to feel the effect of one dose

156


before receiving a subsequent dose. Most patients have an inherent maximum frequency of

demand-the average rate is 3-5 doses per hour.

6.7.3.5 Continuous (background) infusion A continuous infusion decreases the inherent

safety of PCA, as opioid will be delivered regardless of how sedated the patient may be. This

mode should only be used on the advise of the APT or the ICU Consultant.

6.7.3.6 Drug concentration Standard prescriptions are employed (see below). However,

delivery of the drug may not be accurate if the volume delivered is less than 0.5mls.

Hence, dilutions are used for children and the very elderly.

6.7.4 Standard Prescriptions for PCA

6.7.4.1 Morphine Usually the opioid of first choice.

Standard orders For patients aged 15 to 70 years: Bolus 1 mg, lockout 5 minutes

70 to 80 / 85 years: Bolus 0.5 mg , lockout 5 minutes

If analgesia is inadequate (in all age groups), consider doubling the size of the bolus dose, or

alternative agent (eg: Tramadol).

6.7.4.2 Special Situations

PCA and the opioid tolerant patient

• These patients are likely to require much larger doses of opioids and a background in-

fusion benefits many. To calculate an appropriate background infusion, base it upon 50-

100% of the patients usual opioid requirements.

• The bolus dose which is ordered (in mg.) is normally the same as the background infusion

in mg/hr.

Incomplete Cross Tolerance The degree of cross tolerance that occurs between opioids is

unpredictable, and appears to be incomplete. If a change is made from one opioid to another,

especially when doses have been high, it may be best to commence the new opioid at a dose

that is about 50% of the calculated equianalgesic dose of the new opioid. The equianalgesic

doses given above are based on single dose studies in opioid naïve patients and should be

used cautiously in patients on long term opioids.

In particular, if changing opioid therapy to oral methadone, doses that are about 10-15% of

the expected equianalgesic dose may be more appropriate. This lower than expected dose

may be due to the long and variable half life of methadone and also because methadone is

thought to have NMDA receptor antagonist properties.

157

6.7 Guidelines for the use of patient controlled anaesthesia (PCA) 6 APPENDICES

Illicit Opioids Where a patient has been using illicit opioids the amount and purity of the

drug they have been using is difficult to ascertain. As a rough guide, one should assume purity

to be no more than 50% . It is safer to be conservative.

6.7.4.3 Problem Solving and PCAs

Patient Confusion Patient confusion and inability to understand the use of a PCA is an

absolute contraindication and other means of analgesia should be used.

Inadequate Analgesia Assess the patient.

Exclude technical issues, including pump programming and function, and reliability of vascular

access.

If there is increasing pain, increasing analgesic requirements, or pain out of proportion to that

expected for the procedure or for the number of days elapsed since the procedure, then there

may be another cause for the pain. A complication may have developed (eg. a leaking anas-

tomosis following bowel surgery), or the patient may have colicky wind pain which responds

poorly to opioids.

If these are excluded and the patient is receiving 3 bolus doses per hour on average, encourage

the patient to use the demand button more frequently.

If side effects are limiting use of the PCA, treat these.

If the patient is receiving 3 bolus doses per hour, and still has inadequate analgesia, increase

the size of the bolus dose (usually double).

If the patient complains of waking in severe pain frequently at night, and PCA use is high, then

consider adding a background infusion. The size of the background infusion should not be

greater than the bolus dose.

Nausea and Vomiting An appropriate antiemetic should be given.

If the patient has low analgesic requirements, then a decrease in the size of the bolus dose

should be tried.

Non-opioid analgesia such as regular paracetamol and NSAID suppositories (if no contraindi-

cations such as lower GI surgery) should be added.

If the patient feels a wave of nausea soon after pressing the demand button, then slowing the

rate of administration of the bolus dose (increasing the dose duration) may be of benefit.

Individual patients may be more sensitive to a particular opioid. If other measures have failed,

then it is worth considering a change to a different opioid. However, remember that opioids

are not the sole cause of post-operative vomiting.

Pruritus Pruritus may be caused through both histamine release and u-receptor activation.

It is more commonly seen with Morphine that Fentanyl. In the hospital setting, pruritus is most

often caused by lying on a plastic covered mattress! (pruritus is present on the back only).

158


If the distribution of the pruritus is on the face and trunk, then it is likely to be due to the opioid.

Treatment options are:

• Change the opioid. eg. Morphine to Fentanyl.

• Titrate small (50-100 mcg) doses of Naloxone.

• Antihistamines-but these may lead to sedation and respiratory depression.

Sedation and Respiratory Depression These are unusual with a pure PCA - i.e. with no

background infusion, with an appropriate size of bolus dose and no additional sedative agents.

If a patient does have a sedation score of -1 (constantly or frequently drowsy-falls asleep

during conversation but easy to rouse), then a reduction in bolus dose (usually by half) and

ceasing any background infusion is indicated.

If the patient has a respiratory rate of 8 or less, in addition to a sedation score of -1, then

titration of Naloxone in 100mcg doses should be considered, in addition to the above.

If the patient has a sedation score of -2 or less (somnolent, difficult to rouse) then Naloxone

should be administered regardless of the respiratory rate.

Problems not infrequently arise in the opioid dependent patient, who becomes sedated, yet

complains of high pain scores. It should be explained to these patients that they cannot be

safely given more opioid, and that complete pain relief may be an unrealistic aim for them.

Addition of non-opioid pain relief may be of value.

Urinary Retention Urinary retention can occur, and should be treated with catheterisation.

Be wary of the possibility of sedation / respiratory depression in the patient who has been

treating the pain of a distended bladder with their PCA, who then has the pain relieved by a

catheter.

Inhibition of Bowel Motility To some extent, inhibition of bowel function is inevitable. Pa-

tients should be discouraged from using their PCA to treat wind pains.

Hypotension Opioids will not in themselves cause hypotension, but may unmask hypo-

volaemia (through a reduction in sympathetic tone).

159

Index

Acid Base Disturbances, 93

Metabolic acidosis, 94

Metabolic alkalosis, 95

Respiratory acidosis, 94

Respiratory alkalosis, 94

acidosis

metabolic, 94, 95

respiratory, 94, 97

adenosine, 55

Admission

patient, 15

primary survey, 15

secondary survey, 15

admission

elective, 12

policy, 11

refusal, 12

Adrenaline, 49

alkalosis

metabolic, 95, 96

respiratory, 94, 97

Aminophylline, 55

amiodarone, 56, 57

Amrinone, 50

anion gap, 95

anti-arrhythmic drugs, 154

Anti-hypertensive, 52

Antiarrhythmic drugs, 53

antibiotic

prescription, 84

antibiotics

guideline, 84

anticoagulation, 73

Arterial Cannulae, 24

Atropine, 54

bicarbonate, 96

Bradyarrhythmias, 54

brain death, 141

brain stem testing, 142

bronchodilators, 58

Bronchoscopy, 37

cardiac arrest

CPR, 17

Central venous cannulae, 25

Charcoal, 140

Clinical duties

on ICU, 14

outside ICU, 17

cardiac arrest, 17

Trauma, 17

Clinical Lead, 9

clonidine, 52

Consent, 21

Consultants, 9

Coroner referral, 13

CPR, 106

induced hypothermia, 107

Cricothyroidotomy, 37

Cryoprecipitate, 104

DDAVP, 77

ddrenaline, 54

diabetes

Insipidus, 77

DIC, 104

Difficult intubation, 34

dipyridamole, 55

discharge

policy, 12

procedure, 12

diuretics, 79

Dobutamine, 49

Documentation, 15

Dopamine, 49

Dopexamine, 49

DVT, 73

DVT prophylaxis, 74

Electrolyte abnormalities, 87

160

Index Index

Hyperkalaemia, 91

Hypernatraemia, 89

Hypokalaemia, 90

Hyponatraemia, 88

Hypophosphataemia, 92

SIADH, 89

Enteral Netrition, 98

erythromycin, 84

Feeding guideline, 99

FFP, 104

fluids

management, 85

replacement, 85

resuscitation, 86

Fresh Frozen Plasma, 103

Fungal infections, 138

gastric lavage, 139

gastric stress ulcer, 80

glucose

blood, 76

Guideline

feeding, 99

Microbiology, 134

Guidelines

PCA, 155

head injury, 130

Henderson equation, 94

Henderson/Hasselbach equation, 94

heparin, 74

heparin induced thrombocytopaenia, 75

unfractionated, 75

HFOV: see Mechanical ventilation, 116

HMEs, 110

Hospital Emergencies, 22

Humidification, 110

Hyperkalaemia, 91

Hypernatraemia, 89

Hypokalaemia, 90

Hyponatraemia, 88

Hypophosphataemia, 92

hypotension, 144

ICU Procedures, 23

Arterial Cannulae, 24

Bronchoscopy, 37

Cricothyroidotomy, 37

CVC, 25

ICD, 31

intraabdominal pressure manometry, 46

intubation, 32

extubation guideline, 36

intubation guideline, 33

rapid sequence, 35

Nasojejunal, 45

Peripheral IV catheters, 23

Pleural Procedures, 30

Pulmonary artery catheter, 29

Tracheostomy, 38

IMV, 150

induction

rapid sequence, 35

Infection Control, 18

Information Technology, 21

Inotropes, 48

insulin, 76

Intercostal catheter, 31

Intra-abdominal pressure manometry, 46

intubation

difficult, 34

Intubation, endotracheal, 32

Isoprenaline, 54

lignocaine, 57

magnesium, 57

Mannitol, 131

Mechanical Ventilation, 110

HFOV, 116

Pressure Support, 115

prone position, 122

Prone positioning, 119

proportional assist ventilation, 114

Tube Compensation, 115

weaning, 119

Milrinone, 50

161

Index Index

Nasojejunal tube insertion, 45

Neurotrauma, 130

Nimodipine, 134

NIPPV, 123

Noradrenaline, 49

Nutrition

Enteral, 98

parenteral, 101

Omeprazole, 83

organ donation, 141

Orientation, 11

Osmotherapy, 131

Overdose, 139

Parenteral Nutrition, 101

paroxysmal atrial tachycardia, 58

patient

admission, 15

PCWP, 146

PEEP, 114, 153

pH, 94

phenytoin, 58

Phosphodiesterase inhibitors, 50

PiCCO, 147

platelets

dose, 103

transfusion, 102

Pleurocentesis, 31

pneumonia

invesitgation, 136

Nosocomial, 137

policy

admission, 11

discharge, 12

Preload, 145

procainamide, 58

Prokinetics, 99

Proportional Assist Ventilation, 114

Prostacyclin, 129

PSV, 151

Pulmonary Artery catheterisation, 29

quinidine, 58

Renal

preotective strategies, 126

replacement therapy, 127

Renal Failure, 125

Respiratory Failure, 108

Sedation, 59, 131

Sedation Agitation Score, 153

Sepsis, 135

sepsis

screening, 135

Vascular catheter, 137

Septic Shock, 135

shock, 144

SIADH, 89

SIMV, 150

SIRS, 135

sotalol, 57

spontaneous breathing trial, 120

status epilepticus, 132

refractory, 133

steroids, 78

subarachnoid haemorrhage, 133

Supraventricular arrythmia, 55

Suxamethonium, 34

torsade de pointes, 57

Tracheostomy

Percutaneous, 38

complications, 42

decannulation, 44

policy, 38

procedure, 40

timing, 40

transfusion

blood, 102

FFP, 103

Massive, 104

platelet, 102

reaction, 105

risk, 103

Triage

patient, 11

162

Index Index

ventilation

assist control, 150

CMV, 150

IMV, 150

inverse ratio, 151

PSV, 151

SIMV, 150

Ventilator settings, 112

ventilators, 149

Ventricular arrythmias, 57

Verapamil, 56

warfarin, 73

Weekly Program, 10

Withdrawal of therapy, 13

Withdrawal of treatment, 140

163

Index Index

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Documents

ICU Handbook