View
0
Download
0
Category
Preview:
Citation preview
PULMONARY EMBOLISM
JO-ANN VOSLOO
DEPARTMENT CRITICAL CARE
SBAH
Embolism
1. Thrombo-embolism DVT: legs/iliac veins/IVC**
2. Septic emboli infective endocarditis
3. Tumor e.g. choriocarcinoma
4. Fat embolism
5. Air
6. Amniotic fluid
7. Placenta
**VTE = venous thromboembolism
(PE plus DVT)
5% of in-hospital deaths
PE rare from below knee DVT
Venous thrombo-embolism(VTE)
Clinical presentation
Depends on : number, size and distribution of emboli
: underlying cardiovascular reserve
• Acutely breathless
• Hypoxia(mismatch ventilation/perfusion)
• Sudden collapse
• Unilateral pleuritic chest pain
• Uni- or bilateral changes on CXR
• Hemoptysis
• Tachicardia / fever
Diagnosis is difficult in critically ill patient
40% of pt with DVT will develop PE
5% of pt with VTE develop chronic pulm hypertension
Recurrent VTE due to activated Prot C resistance mediated by factor V Leiden mutation
Pathophysiology (VTE)
• Pulmonary arterial obstruction and release of vasoactive agents from platelets/hypoxia
pulmonary vascular resistance and pulmonary hypertension
RV preload increases /Decreased Rt heart perfusion(Rt coronary
artery)
Paradoxial interventricular shift/RV dilatation and dysfunction
(opening of foramen ovale with Rt to Lt shunt and paradoxical arterial
embolisation)
OR
• Massive pulmonary embolism
Sudden collapse due to acute low cardiac output (shock)
Investigations:VTE
• CXR:
Most useful to exclude pneumonia, pneumothorax (diff. diagnosis)
• ECG
Exclude MI
Sinus tachicardia, ant. T-wave inversion, S1 Q3 T3 Rt heart strain, ST-segment
changes, Rt bundle branch block.
• ABG: Low PaO2
N – low PaCO2 /widening end tidal to PaCO2 gradient
Increased A-a gradient
Metabolic acidosis (massive pulm emb with CVS collapse)
• D-Dimer/Trop I/Pro-BNP
D-Dimer: Negative predictive value -- limited value in ICU setting
Investigations: VTE
• CT pulmonary angiogram: 1st line diagnostic test
Visualize distribution and extend of PE/Identify alternative diagnosis: pneumonia, pneumothorax,
aorta dissection.
• Echocardiography
RV dilatation, interventricular septal shift, RV dysfunction, Thrombus in RV or PA
• Ventilation – perfusion scan
For pt with normal CXR and cardiopulmonary disease
Diagnosis in ICU
• Despite presence of risk factors still relatively uncommon in critically ill pt
• However the diagnosis is frequently overlooked should it occur
• Clinical prediction systems:
Wells score
Geneva score
Management VTE
• General:
Recognize the problem
Oxygen
IV fluids for circulating shock
Opiates for pain
• Anticoagulation:
Start immediately if high probability of PE
UFH or LMWH
Overlap LMWH and Warfarin. Stop LMWH when INR =2
• Thrombolytic therapy:
Pt with massive PE and CVS collapse
Useful up to 14 days post Non-massive PE
Administration must be followed by heparin treatment
Complications: Major bleedings in 10% of pt. (treatment: FFP and antifibrinolytic agent
Aprotinin)
Exclude contra-indication e.g. intracranial hemorrhage
VTE
• Management cont. Surgical embolectomy
When thrombolytic therapy is contra-indicated or fails
Free floating thrombus
• Combine surgical embolectomy and thrombolytic therapy
• Percutaneous embolectomy
Can combine extraction with embolus fragmentation or catheter directed
thrombolysis
• Caval filters
When thrombolytic/anticoagulation therapy is contra-indicated
Recurrent PE on anticoagulation treatment
Following surgical embolectomy
RVCPP < 30mmHg RV failure and shock
RVCPP = MAP – [CVP + 1/3(PAPs - CVP)]
(right ventricular coronary perfusion pressure)
Therefore increase MAP and lower PAP vasopressor NA to increase MAP, (preferred to phenylephrine
due to added β-adrenoceptor effect). Alternative = adrenalin,
dopamine and vasopressin
judicious fluids
systemic vasodilators can be harmful (no dobutamine,
nitroglycerine and nitroprusside, milrinone)
IABalloon pump counterpulsation / ECMO can be beneficial
Inhaled NO selective pulmonary vasodilatation
AMNIOTIC FLUID EMBOLISM
(AFE) • Unpredictable, unpreventable, uncertain pathophysiology
• Incidence; 1 in 40 000 deliveries
• 5 – 10% of maternal deaths
• 20-50% of proven AFE die within 1st hour
• Neonatal mortality: 40%. High incidence of neurological deficits in survivors
• Maternal mortality: 40 - 86%. Survivors may have neurological sequelae.
• Amniotic fluid enters through uterine/cervical laceration/uterine veins at site of placental separation/placenta abruptio amnion fluid and fetal debris complement activation/physical blockage of pulmonary arteries/pulmonary vasoconstriction. Mediators in amniotic fluid can cause a picture equal to anaphylaxis.
• Clinical picture: severe dyspnoea, cyanosis, sudden CVS collapse, coma/convulsions. Can develop coagulopathy (DIC)
• Diagnosis: Clinical suspicion.
Confirmed by presence of fetal debri in pulmonary circulation(pulm aretery
catheter sample. (presence of squamous cells not diagnostic – also seen in non-pregnant patients and other
parturients)
AFE
• Treatment:
- Cardiopulmonary resuscitation, 100% O2
- Early pulmonary artery catheterisation (RV failure, Pulm Ht, later LV
failure)
- Urgent delivery of fetus (C-section)
- Supportive treatment
- Cryoprecipitate, r-Factor VIIa
• Survivors may have neurological sequelae.
PULMONARY TUMOR
EMBOLISM • Cancer patients have increased incidence of thrombo-embolism, as well as tumor
embolism. Therefore important to diagnose to avoid aggressive treatment in terminally ill patients. Often misdiagnosed as pulmonary thrombo-embolism.
• Incidence: 8,5% (all kinds of cancer)
26% for Ca of breast, stomach, liver, kidney and ChorioCa
• Can be: - Macro tumor embolus: blocking the bigger pulmonary arteries
- Micro-embolism: Clusters of tumor cells block septal or smaller arterioles.
- Lymphatic spread: Pulmonary lympangitic carcinomatosis. Tumor growth in interlobular
septal vessels and subpleural lymphatic vessels.
• Microemboli triggers fibrin deposition and neutrophil sequestration:
Increased permeability of endothelial cells
Intimal fibrosis, media hypertrophy endartiritis obliterance
PULMONARY TUMOR
EMBOLISM • Endartiritis obliterance, vasoconstriction pulmonary hypertension myocardial
hypertrophy/dilatation RV and RA.
• Diagnosis:
ABG: Resp alkalosis, increased A-a gradient, hypoxemia.
ECG: S1Q3pattern, sinus tachicardia, RV hypertrophy
CXR: Prominent pulm artery, RV enlargement, atelectesis, pleural effusion, features suggestive of pulm
TB(miliary TB picture)
Doppler echocardiography: Dilated Rt heart chambers
Lung biopsy: Gold standard for definitive diagnosis open lung biopsy or video-assisted thoracoscopic.
Pulmonary wedge aspiration cytology: if too hypoxic to undergo lung biopsy
Ventilation-perfusion radionuclide scanning: Segmental contour pattern numerous small defects that
outlines the pulmonary fissures and bronchopulmonary segments (non specific
finding also seen with vasculitis, fat embolism, septic emboli).
Pulmonary angiography/CT pulmonary angiogram
PACatheter: Pulmonary wedge aspiration cytology unfortunately not 100% sensitive
RV pressures increased (50-60mmHg)
PAPm increased (50-100mmHg)
PAWP = normal
Tumor associated monoclonal antibody imaging: Injection radiolabelled antibodies
PULMONARY TUMOR
EMBOLISM • Managemenrt:
- Distinguish from thrombo-embolism
- Complete resection of primary tumor
- Inferior vana cava filter for large emboli
- Chemotherapy (add hormonal therapy for breast, prostate and choriocarcinoma)
- Steroid therapy and anticoagulation therapy showed no benefit
- Palliative therapy: fluids, vasopressors, oxygen and control pleural effusion.
SEPTIC PULMONARY
EMBOLI(SPE) • Uncommon disorder
• Presents with: Incidious onset of fever
: Resp symptoms
: Lung infiltrates (non specific) poorly marginated lung nodules that
has tendency to cavitate
• Associated with: IV drug use
: Pelvic thrombophlebitis
: Suppurative process in head and neck region
: Indwelling catheters and devices(Lamierre Syndrome; anaerobic
thrombophlebitis internal jugular vein metastatic infection)
: Immunocompromised patients
• Infected embolic clot pulmonary artery branches infarction focal abscess
SPE
• CT scan:
*Lung abscesses, multiple nodules, cavitation, lung infiltrates
*Pleural effusion
*Empyema
*Pneumothorax
• Echocardiography/TEE
* In patients with suspected infective endocarditis
* Valvular vegetations, leaflet perforations, valvular insufficiency or dehiscence,
congestive heart failure, paravalvular abscesses.
• Blood cultures
TREATMENT:
• Early appropriate antibiotics
Control of infectious source
FAT EMBOLISM
• Incidence: 2-22%
• More commonly seen with:
- Femur, pelvis and tibia fractures
- Young males
- Closed long bone fractures
- Non – immobilized long bone fractures
- Placement of medullary nails (reaming)
• Occur 12-72h following injury
• Pathophysiology:
Fat droplets enter circulation occlusion of pulmonary vessels = EARLY PRESENTATION
hydrolysis of fat molecule forms FA stimulates
inflammatory response (lung) interstitial
hemorrhage, oedema, chemical pneumonitis) = LATE
PRESENTATION
FAT EMBOLISM
• Clinical picture:
- Tachicardia, hypotension, elevated CVP, low Hb
- Dyspnoea, hypoxemia
- Fever
- Thrombocytopenia Peticheal hemorrhages upper ant. chest/neck/face and
upper arms, oral mucosa and conjunctiva = PATHOGNOMONIC
- Confusion, agitation, lethargy, seizure, coma
• Diagnosis:
High index of suspicion
CXR: *snow storm appearance
* dilation of Rt side of heart
Laboratory tests: * Increase s-lipase (non specific)
* Fat lobules in blood, urine, sputum absence does not
exclude FES
FAT EMBOLISM
Treatment:
• Reduce and immobilize long bone fractures as soon as possible
• Prevent/treat hypovolemic shock
Suggest Albumin as resus fluid (binds fatty acids and may decrease extend
of disease.
• Mechanical ventilation (ARDS)
• High dose corticosteroids (controversial)
AIR EMBOLISM
• Venous air embolism (VEA)
• Associated with:
- Placement of central lines
- Penetrating or blunt trauma of chest/abdomen (4-14% incidence)
- High pressure mechanical ventilation (pneumothorax)
- Thoracocentesis
- Interventional radiology (0.3% incidence)
- Decompression sickness
- Cardiovascular, otolaryngiological and orthopaedic procedures
- Neurosurgical procedures
- Lumber puncture
- Ingestion of hydrogen peroxide
AIR EMBOLISM
Symptoms and signs:
• Symptoms are non-specific
• High index of suspicion
• Shock and cardiac arrest: need 5ml/kg air
• 2-3ml Air into cerebral circulation: can be fatal
• 0.5ml Air in LAD coronary artery VT
• Large AE in RV outflow obstruction systemic cardiovascular collapse
• Small multiple emboli into pulmonary arteries inflammatory changes V/Q mismatch resp. failure/pulmonary HT/enlarged Rt heart
• Via patent foramen ovale to cerebral circulation paradoxical arterial embolism stroke
• Hemoptysis
• Dysrythmia
• Agitation, confusion
• Substernal pain
AIR EMBOLISM
• Special investigations:
Transcranial doppler: cerebral micro-emboli
TEE/TTE: presence of air in RV outflow
CXR: Usually normal
Gas in PA
Pulm oedema
PA dilation
CT scan: AE can be identified
ECG: resembles that of PE
ETCO2: Non specific
Diff diagnosis: PE, massive blood loss, circulatory arrest, upper
airway obstruction, disconnection of CO2 monitor
ETN2 : non specific
AIR EMBOLISM
• Treatment:
- Place in left lateral decubitus position (Durant manuevre) and Trendellenburg
- Identify and prevent further entry of air
- Intubate + 100% O2
- Direct aspiration of air via central line success doubtfull
- CPR if indicated break large air bubbles into smaller ones Prevent air
lock.
- Supportive therapy for hypotension fluids +/- vasopressors
- HBOT (hyperbaric oxygen therapy): 1st choice
Treatment window: immediate to 6h after incident
Compression of existing bubbles creates a high diffusion gradient
resolution
Reference
• Cook RJ, Ashton RW, Augenbaugh GL, Ryu JH. Septic pulmonary embolism.
Presentinf features and clinical course of 14 patients. Chest 2005: 128; 162-
166.
• Qaseem A, Snow V, Barry P, et. al. Current diagnosis of venous
thromboembolism in primary care: A clinical practice guideline from the
American Academy of Family Physicians and the American College of
Physicians. Annuls of Internal Medicine 2007: 146; 454-458.
• Mehrishi S, Awan A, Mehrishi A, Fein A. Pulmonary tumor microembolism.
Hospital Physician 2004: 23-30.
• Davidsons Handbook: Principles and Practice of Medicine
• Oh’s Intensive Care Manual Sixth Edition
Recommended