Fluid & Electrolytes

Advanced Concepts in Fluid and Electrolyte Disturbances The Kidney: Balancing Internal Environment Major controller of fluid & electrolyte homeostasis

Acid-base balance

Metabolic & endocrine functions:

BP regulation

EPO production

insulin degradation

prostaglandin synthesis

Ca2+/Phosphorous regulation

Vitamin D metabolism

Kidneys Receive ~25% of cardiac output

Filtration of plasma (~160170L/ 24hr.) Liver=other filtration system Proximal tubules:

Reabsorb Na, K, Cl, HCO3, Ca, Mg, Glu, AAs, proteins, vitamins + water

Distal tubules secrete:

H+, K, UA & excrete urea and Cr

**Major controller of fluid & electrolyte homeostasis

Metabolic & endocrine functions:

BP regulation: Renin, Angiotensin, Aldosterone

EPO production: Regulation of RBC production

Insulin degradation:

~25% of insulin produced by pancreas is degraded by kidneys daily

Prostaglandin synthesis:

The kidney increases prostaglandin synthesis to modulate renal vascular resistance d/t ischemia, vasoconstriction, or angiotensin II

Ca2+/Phosphorous Regulation:

Via Vitamin D absorption from food and promoting resorption of calcium in kidneys

Vitamin D metabolism:

Facilitates conversion of Vitamin D to its active form

Acute Renal Failure Abrupt ( of kidney function

~10% of kidney functioning

Sudden ( BUN and Creatinine (norm ratio 1:10) BUN: protein intake, muscle, hydration & bleeding affect BUN Cr: less factors that affect so more indicative of kidney function Urine output < 40ml/hr

Occurs in 530% of hospitalized patients

One of leading causes for inpatient mortality Not excreting waste -> metabolic acidosis

In acute phase pt may still be creating urine

S3, S4, weight gain , edema d/t fluid overload Decline in GFR

Anuria: < 100 ml/24 hrs.

Oliguria: < 400 ml/24 hrs (50% cases with ~80% mortality rate)

Azotemia: ( BUN

Symptoms: S3, S4; crackles, DOE, weight gain, edema

Types of ARF Prerenal: stems from heart d/t (ed perfusion

Intrarenal (Kidney): anything damaging kidney within the kidney ex: ABX processed through kidney

Postrenal: after the kidneys there is an obstruction; BPH, spinal cord injuryGlomerulonephritis

Inflammation of glomeruli ESRD (possibly leading to transplant) Initial stage:

Nephrotic syndrome (decreased Albumin, proteinuria >3.5g/day ( decreased plasma volume ( increased aldosterone ( fluid & sodium retention, edema) Hypertension

Hematuria Damaged kidney attempts to filter through, sloughs off tissue and causes blood in the urine

Little blood can cause it to look like more blood loss than actually occurred Late stage: Azotemia, N/V, pruritus (inability to excrete toxins -> lack of blood flow), dyspnea, malaise, fatigue, anemia, severe HTN (cardiac hypertrophy, heart failure) Lab Tests:

Urine: Proteinuria, hematuria, RBCs Serum: Increased BUN & creatinine Acute Tubular Necrosis

Damage to renal tubular epithelium due to:

Ischemic Injury

Decreased perfusion: decreased CO, intravascular volume loss (hemorrhage, dehydration), severe prolonged hypotension Shock: Hypovolemic, cardiogenic, septic Sepsis & anaphylaxis

Nephrotoxic injury

Endogenous: Rhabdomyolysis (seen in athletes, immigrants, crushing injuries), TLS Rhabdo: breakdoen of muscle, release myoglobin and it cannot be filteres Antimicrobials: Aminoglycosides, cephalosporins, antifungals, antivirals Immunosupressants: Cyclosporin, tacrolimus Chemotherapy

NSAIDS

Street drugs: Heroin, amphetamines, PCP Collaborative Treatment of ARF

Prerenal: crystalloid, colloid, pRBCs

fluid volume increase in vasculature to increase perfusion to kidneys

Intrarenal: fluid restriction depends on pt and function of kidneys ABX: monitor peak and trough of vanco before and after tx Phases of ATN

1. Onset: (initial phase)

Pathophysiology: Integrity of renal tubular epithelium disrupted

Duration: Hours to days (longer with toxic factors)

Reversible by early intervention

2. Oliguric/Anuric: Occurs within 1 day of onset; lasts 5 days to 16 days.

Pathophysiology: Accumulation of necrotic cellular debris blocks urine flow & damages tubular wall & basement membranes

Inability to excrete fluid, electrolytes, and waste

Oliguiria: 9

K > 6.0

Drug toxicity

FVE (fluid volume excess) Metabolic acidosis

Contraindications: Hemodynamic instability; inability to coagulate, no access Tx: about 3 hours 3x/week Continuous Renal Replacement Therapy (CRRT)

Gradual over 8-24 hrs.

Patients hydrostatic pressure (MAP >70) drives blood through the filter

Arterial-venous

Veno-venous

Indications:

Hemodynamic instability with FVE unresponsive to diuretics, MODS

Inability to coagulate

BUN >60 Changes in BUN & Cr seen quicker in CRRT then hemo; doesnt mean kidneys working better, just indicates better filtering

Short term use for BP management Main reason why CRRT used rather than dialysis Dialysis (es fluid & BP

Dialysis: Nursing Management

Monitor VS (hypotension)

Monitor fluid balance

Monitor electrolytes

Hyperkalemia: Kayaxelate

Metabolic acidosis: Bicarbonate

Hypocalcemia: Calcium supplements

Hyperphosphatemia: Phosphate binders

Administer medications at appropriate times

Fatigue management (EPO, iron, Vitamin B complex)

GI disturbance symptom control: antiemetics, laxatives

Psychological care

Teaching

Pre Dialysis Question A patient with ESRD is admitted for cellulitus of the right leg. The nurse is preparing a patient for hemodialysis. The patients VS are: T=99 F, HR= 100, BP= 148/98, RR=20. Which of the following medications should not be given before hemodialysis.

Vancomycin (IV) Will get filtered out Morphine sulfate IV

Give morphine; it will act quick & cellulitis painful

Diltiazem (PO)

Will drop BP Atenolol (PO)

BP will drop anyway Heparin (SQ) Will be getting heparin during HD MVI (PO)

Aspirin (PO) Senna PO Calcium PO Post Dialysis Question A patient with ESRD is admitted for cellulitus of the right leg. The nurse is receiving the patient from the hemodialysis unit. The patients VS are: T=99 F, HR= 112, BP= 98/66, RR=20. Which of the following medications should not be given be given after hemodialysis.

Vancomycin (IV) [Give after each Rx]

Morphine sulfate (IV)? [Give low dose PRN]

HR goes up with temp & pain Diltiazem (PO) Atenolol (PO)? Affects HR (Beta-blocker); possibly give for HR Call doc & ask Heparin subQ Calcium PO Nephrocap PO Aspirin PO Senna PO Delicate Balance of Fluids & Electrolytes in Complex Client Care Mrs. Black Case Study 87yo admitted to the intermediate care unit with pneumonia, CHF, and renal insufficiency.

PMHx: MI x2, Afib, HTN, Diabetes-type 2 x10yrs, osteoarthritis, osteoporosis, s/p right hip replacement 2mths ago

VS: T= 38.6C, HR= 106 with S3 present, EKG= Atrial fibrillation irregular with peaked T waves & widened QRS, BP= 158/90, RR= 20 at rest , pOx=90% on 30% VentiMask.

Weight/Height:185lbs/ 5ft 2in.

I/O: 2400/ 1200 via Foley catheter

Labs: Na= 130, Cl= 95, K= 5.5, CO2= 20, BUN= 10, Cr= 2.1, Glu= 302, Mg =1.5, Ca= 8, PO4= 5.5, Alb= 1.9

Current patient complaints: palpitations and SOB and being fuzzy in the head, right hip pain, diarrhea

Questions? Concerns?

What is the patient experiencing? Priorities?

Medications

Azithromycin 500mg IV daily

Digoxin .25mg po daily

Vancomycin 500mg IV every 12 hrs

Lisinopril 10mg po daily

Methylprednisolone 20mg IV every 12 hrs

Losartan 50mg po daily

Insulin continuous infusion (conc: 100Units/ 100ml) sliding scale Regular

Diltiazem 60mg po daily

IV Fluids: D5 1/2NS + 20mEq @ 125ml/hr

Furosemide 40mg IVP twice a day

KCl 40mEq po daily - discontinued

Other Orders:

Activity: OOB to chair x3/ day

Diet: Low sodium, low carbohydrate + high protein snacks BID

Questions? Concerns? What is the patient experiencing? Priorities?

Diabetes Insipidus:

Water diabetes

Occurs when secretion or action of ADH is abnormal

Hypothalamus produces insufficient ADH

Posterior pituitary fails to release ADH

Nephron does not respond to ADH

Results:

Severe dehydration, thirst, hypernatremia

Uncommon; 1 case in 25,000 people

Diabetes Insipidus: Causes 1. Central (decreased ADH)

CNS tumors

Cerebrovascular disease

Traumatic brain injury

CNS infections

Pregnancy: vasopressinase destroys vasopressin

2. Nephrogenic (kidney resistance to ADH)

Chronic tubulo-interstitial disease (such as ATN, PKD, MM, Lupus)

Medications: lithium, ampho B, phenytoin, steroids, aminoglycosides

Electrolyte problems: hypercalcemia, hypokalemia

Diabetes Insipidus: Symptoms Labs (diagnostic criteria):

Serum Osmo > 300

Serum Na > 145

Urine osmo < 300

SG < 1.005

IVF > 5 liters/24 hours

Symptoms: Onset = 5-10 days after initial injury

Polyuria: u/o 3 - 4 liters/day (>200ml/hr)

Polydipsia: intensive thirst

Hypernatremia Causes: Renal losses, severe (GLU, (thirst, fluid loss from skin/ lungs, hypertonic feedings, (sodium intake, hyperaldosteronism, increased cortisol, diabetes insipidus Symptoms: Dry flushed skin/ mucous membranes, thirst, fever, neuromuscular irritability, (HR, (BP, (CO, oliguria

Treatment:

Decrease Na level

Fluid resuscitation with hypotonic solution

Diabetes Insipidus: Collaborative Management Monitor intake & output hourly

Monitor electrolytes (esp. sodium & chloride)

Replace fluids hourly with hypotonic fluids (0.45% NaCl)

ml/ ml hourly replacement

Hormonal replacement

DDVAP, Vasopressin

Hormonal Replacement Therapy Syndrome of Inappropriate ADH Increased production of ADH

Increased water reabsorption in renal tubules

Increased water retention & dilutional hyponatremia

Causes:

Small cell lung cancer

Pulmonary disease: COPD, TB, bacterial pneumonia

GI malignancies

Medications

Chlorpropamide

Carbamazepine

Thiazide diuretics

Tricyclic antidepressants; SSRI

Nicotine

SIADH:

Pathophysiology Increased water reabsorption

Increased extracellular < intracellular fluid

Decreased sodium concentration (dilutional)

Hypo-osmolality ( cellular swelling

Intracranial ( includes increased ICP

Water Intoxication

Symptoms

Lab values:

Serum Na+: < 130 mEq/L Serum Osmolarity: < 280 mOsm/kg Urine Osmolarity: > 500 mOsm/kg Urine Na+: >20 mEq/L Symptoms:

Weakness, fatigue

Altered LOC (Increased ICP); seizures

Normal CV status

N,V,D

Oliguria (< 400ml/ 24 hr)

Increased weight

Hypoactive reflexes

Hyponatremia Causes: Diuretics, vomiting, diarrhea, diaphoresis, renal failure, hypervolemia, SIADH

Symptoms: N/V/D, hyperactive BS, (DBP, tachycardia, neuro Sx, dry skin, pallor, dry mucous membranes

Treatment:

Increase sodium to water ratio in ECF

Hypertonic saline replacement

Hyponatremia Treatment: 1. Assess plasma osmolality

2. Assess volume status of patient

Hypervolemic, Euvolemic, Hypovolemic

3. Assess Urine Sodium Concentration

Needed for definitive diagnosis, not needed for treatment purposes

4. Calculate Na+ Deficit

0.6 x weight (kg) x (130 plasma [Na+])

5. Correct at no more than 0.5mEq/L per hour or 12 mEq/L per 24 hours

SIADH: Collaborative Interventions Water restriction (~1L/ day)

Seizure precautions

Diet: high sodium

NS IV or hypertonic saline (3%)

Demeclocycline (derivative of tetracycline)

Inhibits effect of ADH on renal tubules

Allows diuresis of water

Comparision of DI & SIADH DI (Inadequate ADH) Hypernatremia >150

Dehydration

Increased serum osmolality Decreased urine osmolality Decreased urine Na+ SIADH (Excess ADH) Hyponatremia uric acid)

Cellular Destruction: Rhabdomyolysis Signs & Symptoms:

Myoglobulinuria brown urine

Hyperkalemia

Hyperphosphatemia

Hyperuricemia

Hypocalcemia cardiac arrhythmias

Acute renal failure, MODS

Collaborative Management:

Alkalinization of urine (prevent metabolic acidosis) with NS & NaHCO3

Correct electrolyte imbalances

Hydration and diuresis

Dialysis

Cellular Destruction: Tumor Lysis Syndrome Definition: Rapid tumor cell kill resulting from cancer therapy which causes rapid release of intracellular contents

At highest risk:

Large tumor burden (leukemia, lymphoma, SCLC, breast, neuroblastoma) on therapy,

Comorbidities (renal or cardiac)

Etiology: Release of cellular contents (potassium, phosphorus, nucleic acids -> uric acid)

Signs & symptoms:

Hyperkalemia ( cardiac arrhythmias

Hyperphosphatemia,

Hyperuricemia ( metabolic acidosis

Hypocalcemia ( cardiac arrhythmias

Acute renal failure (increased BUN & Cr), MODS

Collaborative Management:

Alkalinization of urine (prevent metabolic acidosis) with NS & NaHCO3

Urate oxidase; xanthine oxidase inhibitors

Correct electrolyte imbalances

Hydration and diuresis

Dialysis

Hepatic-Related Ascites Definition: Abnormal collection of fluid in abdominal cavity d/t advanced stage hepatic dysfunction

Causes:

colloid osmotic pressure d/t albumin

Inability of liver to metabolize protein

Cirrhosis Patiens: Increased Na retention by kidney ( expansion of intravascular volume ( fluid shifting to tissues ( decreased NaCl and water excretion r/t decreased albumen (colloidal), increased aldosterone (Na conservation), and increased ADH (H2O conservation)

Hepatic Related: Hepatorenal Syndrome Definition: Complication of ESLD ARF without underlying kidney pathology At highest risk:

Hepatic dysfunction

Cirrhosis

Etiology:

Type I ( decreased BP (s/p aggressive diuresis, large volume paracentesis, GI bleed, major surgical procedure) OR acute viral hepatitis in cirrhosis pt. Type II ( severe ascites, refractory to diuresis Signs & Symptoms: Type I: Rapid, progressive (doubling serum Cr over 2wks; >2.5mg/ dL) Type II: Chronic, slowly progressive (slow increase of serum Cr; >1.5mg/ dL) General: Liver failure with increased LFTs Oliguria (250mg/ dL but 5x osmotic than that of plasma

Nonhemorrhagic shock, burns, ascites, hepatic failure

No compatibility testing (no ABO antigens, antibodies)

Give 5% 2-4 ml/min; 25% in I ml/min

Fluid & Electrolyte Distrubances with Transfusions

Hyperkalemia

Destruction of RBCs when blood is stored

Hemolyzed blood (mismatched) Cell lysis -> release of K+ Hypocalcemia

Citrate preservative combines with ionized Ca in patients blood

5-8 units PRBC in < 4 hours, give Calcium gluconate Clinical manifestations: twitches, tremors in face, tingling lips Acid-Base Changes

Banked blood 2-3 wks old, pH 6.9

Overview of Electrolytes Conduct electricity across cell membranes

Maintain osmolality of body fluid compartments

Regulate acid/ base balance

Aid in neurological/ neuromuscular functioning

Electrolyte Composition of Body Fluid Electrolyte Excretion Excessive elimination of body fluids

Renal excretion after diuretics

GI elimination: Vomiting and diarrhea

LGI: Bicarbonate lost

UGI: Hydrogen, sodium and potassium lost

Excessive diaphoresis: Sodium and chloride loss

Surgical drains

Renal Function by Numbers **BUN, Cr, important to memorize Electrolyte Regulation Main regulators: Kidneys and endocrine system Kidneys: Glomerular filtration, tubular reabsorption, and secretion Endocrine: Pituitary adrenocorticotropic hormone -->release of aldosterone -->sodium reabsorption-->K+ excretion Endocrine: Cortisol ( sodium & water retention Excess cortisol (Cushings) would negatively affect ability to control CHF Endocrine: parathormone & calcitonin -> calcium/ phosphorus balance GI: Fluid & electrolyte absorption Cardio/ Pulmonary Electrolyte Documentation

Sodium Imbalance: (shifting Na+ should be done slowly to give cells time to adjust & prevent cell lysis) Neuro changes occur when shifting occurs too quickly Hyponatremia [145mEq/L] Causes: Renal losses, severe (GLU, (thirst, fluid loss from skin/ lungs, hypertonic feedings, (sodium intake, osmotic diuresis Symptoms: Dry flushed skin/ mucous membranes, thirst, fever, Neuromuscular irritability: Hyperactive reflexes, lethargy, (HR, oliguria Treatment: Decrease Na level using hypotonic solutions (except for D5W)

Potassium Imbalance: Hypokalemia [10.0mg/dL] Levels:

Mild: 10.5 11.9 mg/ dL

Moderate: 12 13.9 mg/ dL

Hypercalcemic crisis: 14 16mg/ dL

Causes: Metastatic malignancy, hyperparathyroidism, hypophosphatemia, thiazide diuretics, immobility

Symptoms:

Anorexia, dehydration, constipation, kidney failure, digoxin toxicity, bone pain and fractures

(mental acuity, arrhythmias, muscle weakness

Treament: Normalize calcium levels

IV NS @ high hourly rate

Loop diuretics

Calcitonin (decreases osteoclastic activity)

IV bisphosphonates *High Ca Low Phos Albumin [3.5-5g/dL] Produced in liver

Fluid connection: Assists in maintaining oncotic pressure

Relationship to total protein: 60% TP is albumin

Calcium connection (50% albumin bound)

Calculation for corrected Ca2+ =

(4.0g/dL pts albumin) (0.8) + patients serum Ca level

Protein binding of Ca2+ influenced by pH

Increased ionized Ca in metabolic acidosis

Decreased ionized Ca in metabolic alkalosis

Phosphorus Imbalance Hypophosphatemia [ phosphate shifts into cell)

Symptoms: Similar to hypercalcemia

Muscle weakness, fatigue, confusion) tachycardia

Treatment:

Prevention by monitoring po intake and TPN

Phosphorus supplements

Hyperphosphatemia [>4.5mEq/L] Causes: Hypocalcemia, hypoparathyroidism, poor nutrition, adrenal insufficiency, vitamin D toxicity, bone breakdown, cell lysis (rhabdomyolysis, TLS), acidosis (decrease pH > phosphate driven out of cell to buffer) Many phos issues are corrected when Ca corrected or underlying cause of Phos imbalance is corrected Symptoms: Similar to hypocalcemia, pruritus, renal failure

Treatment:

Normalize phosphorus levels

Calcium supplements

Phosphate binders

Dialysis (renal failure patients)

Regulation of Calcium & Phosphorus Balance 80% phosphorus is bound to Calcium in bone

Kidneys:

Filter & reabsorb ~ unbound serum Ca2+ Activate vitamin D3 promotes intestinal Ca2+ absorption & regulates phosphate excretion

Endocrine:

Parathyroid: PTH (acts on bone to release Ca2+, works with Vitamin D in GIT to increase Ca2+ absorption, kidneys respond by decreasing Ca2+ excretion)

Increased Ca2+ and decreased PO4

Thyroid: calcitonin (decrease Ca2+release from bones)

Albumin:

Albumin 3.5 + Ca2+ level = Ca2+ corrected

Magnesium Imbalance

Hypomagnesemia [2.1mEq/L]

Causes: Dehydration, renal failure, hypothyroidism, Addisons disease Symptoms: Similar to hyperkalemia (mental acuity, (BP, (HR, (RR, EKG changes, N/V, thirst, hypoactive DTRs Treatment: Normalize magnesium levels

Diuretic therapy

Calcium gluconate (decrease cardiac effects of Increased Mg)

Relationships: Ca2+ ,PO4, Mg, K+

Hypocalcemia may respond to Mg

Mg increases intestinal absorption of Ca

Mg , Ca, & K fluctuate together

Ca and PO4 fluctuate inversely

Insulin drives potassium, magnesium, & phosphate into cell

Chloride Imbalance

Hypochloremia [110mEq/L]

Causes: Excessive diarrhea, dehydration, cortisone/ corticosteroids d/t Na+ retention Symptoms: Metabolic acidosis d/t bicarb depletion (weakness, lethargy, tachypnea)

Treatment: Prevention Bicarbonate

Ratio of HCO3 to H2CO3 (carbonic acid) is 20 to 1

Reabsorption: In proximal tubule; used in chemical buffering system Formation: Produced by kidneys in response to hydrogen ion level

Hydrogen ion excretion: Maintains acid/ base balance What is the difference between BICARBONATE & pCO2? Blood Urea Nitrogen: 10 20mg/dL Directly related to metabolic function of liver & excretory function of kidney

Protein ( amino acids catabolized ( ammonia ( urea formed by combined ammonia molecules Creatinine: 0.5-1.2mg/dL Description: Product of skeletal muscle metabolism

Exclusively excreted by kidneys

Directly proportional to GFR

CrCl decreases 6.5ml/min with each decade of age

BUN/ Cr ratio: 10:1

Increased: Decreased renal blood flow, ATN, glomerulonephritis; rhabdomyolysis, acromegaly (increased muscle mass)

Decreased: decreased muscle mass

Glucose Imbalance Hypoglycemia

Causes: Starvation, Insulin overdose, Addisons disease, malignant disease

Symptoms: Headache, irritability, dizziness, weakness, lightheaded

Treatment: Carbohydrates, 5% Dextrose/ 50% Dextrose

Hyperglycemia Causes: Endocrine= DM, Cushings disease, acute stress, pituitary dysfunction, pancreatitis, Organ= chronic liver or renal disease Symptoms: Classic polys (thirst, hunger, diuresis) Treatment: Oral hypoglycemics, insulin High Risk for Fluid & Electrolyte Imbalances Cardiac disease: CHF Diabetes: Dehydration with increased glucose Renal disease: Overhydration & electrolyte imbalance GI dysfunction: Upper vs lower Respiratory dysfunction: Insensible fluid loss with related sodium loss Burns: General fluid & electrolyte loss IV therapy: Fluid overload, altered electrolytes Enteral feedings/ PPN/ TPN: Altered electrolytes Endocrine Addisons Disease or abrupt discontinuing of systemic long-term glucocorticoids Weakness, fatigue, nausea/ vomiting, lethargy, Decreased concentration, Hypotension, dehydration, Hyperpigmentation, Decreased urine output Burn units in AZ St Marys Hospital Burn Unit closed 2008 UAMC beginning burn unit now 2 burn units in Phoenix Arizona Burn Center at Maricopa Hospital and Grossman Burn Center at St Lukes Hospital Burn Teams Burns are complex systemic injuries. The interdisciplinary burn team consists of many experts with specialized knowledge: Surgeons

Social Workers

Nurses

Anesthesiologists

PT/OTs

CNAs/PCTs

Psychologists

Housekeepers

Dieticians (burn patients require high cal high protein diet) Child Life Specialists

Rehabilitation specialists (Scar management) Major vs. Minor Burns Major burns may involve:

> 20% TBSA

Inhalation injury

Chemical injury Electrical injury

Lg Full Thickness

Large fluid loss

Minor burns may involve:

1-10% TBSA

Minimal fluid loss

Superficial burns

NO inhalation

Some small chemical injury

Skin Anatomy

Zone of coagulation is the area of necrosis; the deepest part of the burn; it will not heal. The zone of stasis is characterized by decreased tissue perfusion; it has the potential to recover with adequate fluid resuscitation and oxygenation. The zone of stasis may convert to necrosis 24-48 hours after the initial burn. The zone of hyperemia (erythema-sunburn like) is the outermost zone that is noted by hyper-perfusion; this area is not lost and will return to normal Faschia: does not stretch

Can create compartment syndrome Burn Depth

1st Degree = Superficial 2nd Degree = Superficial Partial Thickness and Deep Partial Thickness

3rd Degree = Full Thickness 4th Degree = Subdermal Superficial=1st degree (involves epidermis only)

Pink or Red Painful No blisters Sensitive to air Immediate capillary refill Usually not admitted: mainly only if dehydrated & need hydration Superficial {atrial Thickness=2nd degree (damage extends into dermis) Very Painful

Epidermis opened up & nerve endings in dermis are opened up Edema

Blisters

Sensitive to air

Rapid capillary refill

Nerves, sweat glands, hair follicles intact

Deep Partial Thickness = 2nd Degree (damage deep into dermis) Painful Pale or mottled Edema Delayed capillary refill Nerves, sweat glands, hair follicles damaged May convert to a 3rd degree burn over next 24 hours

Full Thickness = 3rd Degree (All of dermal layer destroyed) Painless to pinprick or light touch Cause pain is deeper inside of tissues

Consistency of tennis show leather Edema White, gray, charred Cells need absolute excision

Does not stretch Leathery No capillary refill Subdermal = 4th degree

Damage extends through subcutaneous layer to deep tissues - fascia, muscle or bone Measuring Total Body Surface Area (TBSA)

The Rule of Nines Adult:

Head 9%

Each arm 9%

Ant. Trunk 18%

Post. Trunk 18%

Each leg 18%

Perineum 1% Child 2 years and under:

Head 18%

Each Arm 9%

Ant. Trunk 18%

Post. Trunk 18%

Each leg 14%

Measuring TBSA

Lund and Browder Palm Rule Pts. Palm and fingers = 1% of THEIR total body surface area Does not work in very obese patient Palm = 0.5%

Calculate TBSA Burned and Determine Depth 1st pic: 28-29%; 2nd degree burn that will probably turn to 3rd degree in 24 hours

2nd pic: ~1%; 2nd (red) & 3rd (where it is white) gasoline burn 3rd pic: ~9%; 3rd degree burn palm rule to count cause you cant see chest

4th pic: ~5%; 3rd degree with little 2nd degree **ONLY count what you can see Physiologic Response Coagulation of cellular proteins causing cell death Release of complement, cytokines, histamine, and oxygen free radicals Increased capillary permeability Fluid shift from intravascular to interstitial space Edema (ed cap permeability causes more fluid to shift Hemoconcentration Increased hematocrit (simply d/t leaking of fluid) Increased blood viscosity Increased risk of emboli formation Decreased intravascular volume Decreased cardiac output Vasoconstriction Increased systemic vascular resistance Decreased blood flow to the skin, kidneys, and GI tract in order to spare the vital organs (brain and heart) Inflammatory mediators lead to bronchoconstriction which may lead to acute respiratory distress syndrome (ARDS) Hypermetabolism: increased oxygen consumption, negative nitrogen and potassium balance lead to muscle wasting and catabolism Immunological down regulation of cell mediated and humoral immune pathways creates vulnerability to infection If the responses go uncorrected, the results will be:

Hypovolemic shock (burn shock)

Metabolic Acidosis

Hyperkalemia/Hypokalemia Hyper when burn 1st happens

Hypokalemic after getting hydrated (D/t dilution) Pulmonary Hypertension

Compartment Syndrome

Multiple organ failure and death

Renal failure Primary Survey

Airway

S/S of Inhalation Injury: Facial burns

Singed facial hair

Absence of nasal hair

Carbon deposits

Edema/erythema of oro/nasopharynx

Hoarse voice/Brassy cough Anxiety/Agitation SOB/Tachypnia Stridor (late sign of airway closure) Hypoxia Breathing Assess Breathing Carbon deposits in mouth or on face?

Hoarse voice or Brassy Cough?

Auscultate each lung field POSTERIORLY: base then go up Listen for crackles (Sounds indicating overhydration) Look for circumferential chest/neck burns

Assess rate and depth of respiration

Obtain oxygen saturation (not reliable in carbon monoxide poisoning)

Airway & Breathing Deliver 100% Oxygen to ALL pts with 20% TBSA or more Maintain patent airway Be prepared to intubate Avoid succinylcholine it exaggerates hyperkalemia poss. Cardiac arrest (Usually a problem in thermal burns 6-8hrs old. Immediate danger in electrical injuries)

Intense edema to soft tissues of lower face 24 hrs after a 21% TBSA flame burn

Same pt. 72hrs post burn. Elevation of all affected areas is essential to prevent complications of edema

**intubate early & with largest tube you can find (7 preferably; 8)

need to bronchoscope pt (can only be done with #7) Breathing

Circumferential trunk/neck burns: Loss of chest wall compliance Difficult to oxygenate Difficult oxygenation

Escharotomy Cut from healthy to healthy tissue if possible to release rib cage for expansion Other considerations Carbon Monoxide poisoning: CO has affinity to hemoglobin that is 200-500 times that of oxygen Give 100% oxygen until carboxyhemoglobin levels are less than 15% Pulse oximetery is of no value in CO poisoning since it is not specific to oxygen Hyperbaric oxygen is of unproven value in burn patients Circulation Assess Circulation hourly: Skin Color

Sensation

Peripheral pulses Call doctor/burn squad EARLY when you feel the pulse weakening Capillary refill

Circumferential burns

Disability, Neurologic Deficits Burn patients are typically alert and oriented Consider hypoxia, assoc. injury, substance abuse, pre-existing medical conditions Assess level of consciousness: AVPU A = Alert

If not why? -> head injury? Drugs? Diabetic coma? Etc.

V = Verbal Stimuli

P = Painful stimuli

U = Unresponsive

Expose and Examine Remove all clothing adherent clothing may be left undisturbed Clothes act as tourniquet Remove all jewelry including piercings Examine for deformities, foreign or protruding objects, or other injuries Log roll to examine posterior surfaces Fluid Resuscitation IV access 2 Large bore IVs May place IV in burned areas if necessary Begin fluid resuscitation for 20% or greater TBSA burns Lactated Ringers Weigh patient as soon a possible (estimate if necessary) Fluid resuscitation is based on weight Why Lactated Ringers for resuscitation? Large amounts of NS can lead to hyperchloremic metabolic acidosis As chloride levels rise, bicarbonate levels decline in a 1:1 ratio to maintain electroneutrality As bicarbonate drops, metabolic acidosis results Lactate in LR is converted by the liver to bicarbonate, so it makes up for the bicarbonate that is lost with the addition of chloride that is in the LR Consensus Formula: Lactated Ringers 2-4ml x pt wt. in kg x TBSA Burn = Amount to be infused in 1st 24 hours post burn. Start @ 4ml Dont convert TBA to decimal Give of total amount in 1st 8 hours from the time the injury occurred Give the remaining over the next 16 hours

*Note: Children need 3-4ml/kg/TBSA LR burn replacement plus maintenance fluids of 100ml/kg for up to 10kg in wt., 50ml/kg for additional 11-20kg, 20ml/kg for additional 21-30kg.

Fluid Resuscitation ex: Adult A 68 y/o woman sustained 2nd and 3rd degree burns to her anterior chest, abdomen and the front of both legs in a fire in her office building

TBSA = 36%1kg = 2.2lbs

154lbs 2.2 = 70kg

4ml x 36 x 70 = 10,080 over 24 hours

Give 5040ml in first 8 hours at 630ml/hr (5040ml 8hrs = 630ml/hr)

Give 5040ml over next 16 hours at 315ml/hr (5040 16hrs = 315ml/hr)

Fluid Resuscitation Place Foley catheter with urimeter (temp probe) Monitor urine output hourly ( amount of fluids given if even a drop causing eyes to protrude out (eyes never go back to normal completely) Does not regress with therapy Decrease edema with diuretics and glucocorticoids (prednisone) Clinical Manifestations Extreme agitation/irritability Hand tremors at rest Thin Loose BM Heat intolerance Profuse diaphoresis Skin is warm Hair is thin Mood swings Extreme fatigue Depression Diagnostics Confirmed on physical exam/clinical manifestations Labs Serum TH levels elevated Serum cholesterol levels are depressed Management Reduce excessive secretion of TH Prevent and treat complications Removal of thyroid tumors (surgery) Administration of adrenergic blocking agents (control SNS activity) Propranolol Administration of antithyroid medications Propylthiouracil (PTU) Tapazole Radio iodine therapy (potassium iodide) To treat thyroid storm Because radioiodine destroys thyroid cells, hypothyroidism is a complication. Patient/Family Education Exophthalmos (Bulging eyes) Wear dark eyeglasses to reduce discomfort and reduce risk of getting dirt/dust in eyes Use sleeping mask or lightly tape eyes shut with paper/non-allergic tape Elevate HOB at night Diet Restrict salt intake High calorie/high protein Supplemental vitamins Weigh daily Thyroidectomy Total Secondary to cancer Clients must take thyroid hormones permanently Partial To correct hyperthyroidism and extreme cases of goiter 5/6th the gland is removed. Since 1/6th of the functioning gland is left, hormone replacement therapy may not be necessary many times med control still needed Preoperative TH suppression a must! May take 2-3 months. Antithyroid meds/iodine preparations Diminishing chance of hemorrhage Postoperative, at risk for Infection/hemorrhage Thyroid storm Secondary to infection, thyroid surgery, stopping antithyroid meds Hypoparathyroidism Inadvertent removal of parathyroid glands Respiratory obstruction Secondary to swelling Observe for hypoxia Laryngeal edema Vocal cord injury Secondary to nerve damage Thyroid storm (thyrotoxicosis) All hyperthyroid manifestations are heightened High fever Severe tachycardia Increased B/P Increased RR Atrial fibrillation Delirium Dehydration Extreme irritability Potentially fatal acute episode Clinical diagnosis KNOW YOUR PATIENTS No lab tests differentiate hyperthyroidism from thyroid storm Management

Hypothermia blankets IV fluids Suppressing hormone release Inhibiting hormone synthesis Blocking conversion of T4 to T3 Amiodarone (antiarrythmic drug) K+ channel blocker Inhibiting effects of TH on body tissues Beta blockers Treat cause (if known) Thyroiditis Appears in three basic forms: Acute/sub-acute (painful) Uncommon Bacterial/viral invasion Following respiratory tract infection Most have pre-existing thyroid disorder Lymphocytic (silent/painless) Genetic predisposition Chronic (Hashimotos disease) Most common form of thyroiditis Long-term inflammatory disorder Auto immune destruction of thyroid gland Genetic predisposition Clinical Manifestations: Abrupt unilateral anterior neck pain which radiates to ear (acute/sub-acute) Fever Diaphoresis Sore throat About 50% present with thyroid storm Painless goiter in lymphocytic/chronic form Diagnostics TH levels Thyroid antibodies Management Antibiotics Pain management Prednisone Outpatient incision and drainage of thyroid glad (acute) Fine needle biopsy to rule out malignancy (chronic) Parathyroid & Parathyroid hormones Embedded in the posterior surfaces of thyroid gland Monitor calcium levels When calcium concentration falls below normal, cells secrete parathyroid hormone (PTH) PTH stimulates osteoclasts (to break down bone) Inhibits bone-building Reduces urinary excretion of calcium Hyperparathyroidism Over activity of parathyroid glands

Excessive PTH leads to bone damage, hypercalcemia, and kidney damage

Classified as primary, secondary, & tertiary

Primary (hyperactivity of glands themselves)

Secondary

Secondary to another condition that lowers calcium levels

Therefore, your parathyroid glands overwork to compensate for the loss of calcium

Tertiary

Persistent secondary hyperparathyroidism after successful renal transplantation

Idiopathic hypersecretion of parathyroid hormone

Clinical Manifestations Skeletal disease joint pain, Fractures, Deformity Renal involvement Polyuria (excessive urine) Calculi in urine Hypertension GI disorders (secondary to hypercalcemia) Polydipsia (excessive thirst) Psychiatric abnormalities Diagnostics Lab Serum calcium levels are elevated Serum phosphate are depressed X-ray findings Management Short-term Lowering severely elevated calcium levels Hydration (Lasix to flush out kidneys) NOT thiazides (which promote calcium reabsorption through kidneys)

Promote calciuria (urinating out excess calcium) Lasix - AFTER rehydration NO Thiazides! They promote calcium retention in kidneys Diet - Low in calcium and Vitamin D Long-term Increase bone resorption (medications) Phosphates Calcitonin Patient/Family Education Encourage fluids Monitor urine for stones and blood Hypoparathyroidism Hyposecretion of parathyroid glands due to accidental removal of parathyroid glands or damage to these glands thyroidectomy genetics Low Serum calcium levels High Serum phosphate levels Tetany (painful muscular spasms/tremors) may develop Clinical Manifestations Painful muscle spasms Numbness, tingling on fingers/toes Dysrhythmias Chvosteks Sign Unilateral spasm of the oris muscle is initiated by a slight tap over the facial nerve Trousseaus Sign Carpal spasm occurs when the upper arm is compressed, as by a tourniquet Diagnostics Physical Exam Labs Low calcium levels Low PTH level High phosphorus level Emergency Management Restore serum calcium levels to normal quickly (ONLY time youd give Calcium chloride is when coding cause very hard on body) 10% calcium gluconate IV (takes longer for body to convert to calcium chloride but less harsh) Prevent and treat seizures Control laryngeal spasms and respiratory obstruction which may lead to distress Long-term Oral calcium salts Vitamin D PTH replacement Diet high in calcium, but low in phosphorous Patient/Family Education Life long medications Visit health care provider regularly Monitor serum calcium levels Dietary modifications Omit cheese and milk The adrenal glands Two parts: Outer cortex Produces steroid hormones: Corticosteroids/glucocorticoids Cortisol Mineralocorticoids Aldosterone Androgens - Male sex hormones Inner medulla Produce: epinephrine norepinephrine Adrenal insufficiency Hypofunction of adrenal glands Primary Type (cause probs within organ itself) Addisons Disease (rare) Idiopathic destruction of adrenal glands (AIDS & metastasis from lung, breast, or GI) All steroids hormones are reduced Risk factors: History of other endocrine disorders Not tapering off glucocorticoids Adrenalectomy TB (infection can destroy glands) Clinical Manifestations Usually insidious Anorexia Mild fatigue Irritability Weight loss Nausea and vomiting Postural hypotension Diagnostics Low cortisol production rate High plasma ACTH concentration Serum electrolyte levels Blood glucose level CT/MRI of adrenal glands and pituitary Patient/Family Education Medication importance/tapering Maintain a normal electrolyte balance Follow-up visits with health care provider Monitor steroid levels Medic-Alert Band IM self-injection Dexamethasone Addisonian Crisis Emergent condition Acute adrenal insufficiency Causes

Stress Pregnancy Surgery Infection Dehydration Anorexia Fever Emotional upheaval Lack/insufficient hormone replacement Clinical Manifestations Penetrating pain in back Depressed or changed mentation Volume depletion Hypotension Loss of consciousness Shock Hyponatremia & hyperkalemia Management Correct fluid and electrolyte imbalances Rapid rehydration with .9% NS Replace steroids Hydrocortisone 100 mg IV, followed by 100mg q 8 hours x 24-hours, then PO hydrocortisone Correct hypoglycemia 5% Dextrose IV Vasopressors Kayexalate Treatment of hyperkalemia Adrenal Insufficiency

Secondary type, causes

Hypofunction of adrenal glands hypofunction of the pituitary-hypothalamic unit (lack of ACTH - Adrenocorticotropic hormone ) chronic treatment with glucocorticoids for non-endocrine uses Circulating levels of corticosteroids remain high. Patients do not experience manifestations of adrenocortical insufficiency unless therapy is stopped

Pituitary tumor Radiation Adrenocortical Hyperfunction Hyperfunction of adrenal cortex Result in excessive production of glucocorticoids, mineralocorticoids, and androgens Major conditions Hypercortisolism (glucocorticoid excess) Primary Aldosteronism (aldosterone excess) Hypercortisolism Cushings Syndrome Over activity of adrenal gland, with consequent hypersecretion of glucocorticoids Causes Medical interventions account for most cases Adrenal tumor Excessive ACTH secretion Pituitary hypersecretion secondary to pituitary tumor Rare Clinical Manifestations Normal function of the glucocorticoids become exaggerated Poor wound healing Masculine characteristics in women Memory loss, poor concentration Persistent hyperglycemia (steroid diabetes) Potassium depletion Sodium and water retention HTN Abnormal fat distribution Moon shaped face Fat pad on back of neck (buffalo hump) Obesity with slender limbs Purple striae on breasts and abdomen Diagnostics Physical exam Clinical manifestations ACTH levels 24 hour urine collection for free cortisol High dose dexamethasone suppression test checks to see how taking a corticosteroid medicine (dexamethasone) changes the levels of cortisol in the blood CT (pituitary and adrenal glands) MRI Management Reducing corticosteroid use over time while still managing condition (example: asthma/arthritis) Medications that interfere with ACTH production or adrenal hormone synthesis Mitotane (Lysodren) Surgical (adrenalectomy) Adrenal tumor Lifelong glucocorticoid mineralocorticoid replacement Surgical (resection of pituitary tumors) Transsphenoidal adenomectomy (through nose) Surgical removal of a small, well-defined pituitary adenoma Patient/Family Education Patients on glucocorticoids are at risk for Cushings Recognizing manifestations Don't reduce dose of corticosteroid drugs or stop taking them on your own. Hyperalosteronism Aldosterone conserves sodium and promotes potassium excretion Primary Hypersecretion of aldosterone secondary to adrenal lesion (usually benign) Produces secondary HTN, hypernatremia, & hypokalemia Secondary, results from Renal disease Laxative or diuretic abuse Dehydration Cirrhosis with ascites Heart failure Clinical Manifestations Primary May be asymptomatic HTN Hypernatremia Hypokalemia Excessive urinary excretion Muscle weakness Cardiac dysrhythmias Diagnosis Serum potassium levels Alkalosis Elevated urine or plasma aldosterone levels Management Primary Spironolactone (Aldactone) drug of choice To increase sodium excretion Treat HTN Improves hypokalemia Surgery Unilateral or bilateral adrenalectomy Temporary/permanent replacement therapy Secondary Manage causative disease Comply with treatment of disease Patient/Family Education Comply with treatment and maintain control of the causative disease process (secondary) Pheochromocytoma A rare condition characterized by an adrenal medulla tumor that produces excessive catecholamines The tumor is benign in most cases. The secretion of excessive catecholamines results in severe hypertension. If undiagnosed and untreated may lead to diabetes mellitus cardiomyopathy death Manifestations Severe, episodic hypertension accompanied by classic triad of severe, pounding headache tachycardia with palpitations and profuse sweating, and unexplained abdominal or chest pain. Attacks may be provoked by many medications, including Antihypertensives Opioids Radiologic contrast media Tricyclic antidepressants. The treatment consists of surgical removal of tumor (tumors can be very hard to find & small) Acromegaly Results from excess secretion of growth hormone (GH) It is a rare condition of bone and soft tissue overgrowth Bones increase in thickness and width but not length Clinical manifestations enlargement of hands and feet thickening and enlargement of face and head bony and soft tissue sleep apnea (d/t excessive soft tissue) signs of diabetes mellitus cardiomegaly hypertension (extreme) Diagnostic Studies History Physical Assessment CT MRI Oral glucose challenge Definitive test GH concentration falls during oral glucose tolerance test. In acromegaly, GH levels do not fall below 1ng/ml3 Treatment Focuses on returning GH levels to normal through surgery, radiation, and drug therapy Octreotide Acetate (Sandostatin) Transsphenoidal Hypophysectomy (surgical removal of pituitary gland) Treatment of choice Nursing Care Postoperatively includes Avoidance of vigorous coughing, sneezing & straining at stool (could cause CSF leaks) to prevent cerebrospinal fluid leakage from where the sella turcica (sphenoid bone) was entered Hypopituitarism

Rare and involves a decrease in one or more of the pituitary hormones

The anterior pituitary gland secretes adrenocorticotrophic hormone (ACTH) thyroid-stimulating hormone (TSH) follicle-stimulating hormone (FSH) luteinizing hormone (LH) growth hormone (GH) prolactin (PRL) Melanocyte-stimulating hormone (MSL) Posterior pituitary gland secretes ADH Oxytocin Normal changes in endocrine function d/t aging Endocrine system functions well in most older people Some changes do occur because of normal damage to cells during the aging process hormone production and secretion hormone metabolism (how quickly excess hormones are broken down and leave the body, for example, through urination) hormone levels circulating in blood target cell or target tissue response to hormones rhythms in the body, such as the menstrual cycle Hematopoiesis: Bone marrow manufactures all blood cells Blast cells are immature blood cells Bone marrow produced in long bones of the body & the sternum

Iliac crest produces the most followed by the femur

Epo stimulates bone marrow to produce RBCs

Marrow starts to decline at age 7

Stem cells: basic cell that everythings made from

Plant in body -> migrates to bone marrow -> generates to platelets & RBCs Aging Hematologic System

At ~ age 70yo, amount of bone marrow in long bones begins to decline

Decreased # stem cells in marrow Decreased effectiveness of EPO Decreased platelet adhesiveness & therefore they bruise easily Average H & H decreases slightly to low normal No changes: RBC life span, Blood volume, total WBC count, platelet structure & function CBC w/ differential & platelets

WBCs (5,000-10,000/cu mm) Differential: segs + bands (50 70%)

Determines individuals ability to fight off infection

lymphs (20 40%) rise in lymphs with ( in neuts

monos (2 8%) eos (1 4%) ( w/ allergic reaction

basos blasts RBCs Hct (men: 42-52%; women: 37-47%) Hgb (men: 14-18g/dl;women: 12-16g/dl) * Hgb x3 ~ Hct

Plts (150,000-400,000/ cu mm) Spontaneous bleeding @ Colony Stimulating Factors (CSF): GM-CSF, G-CSF, IL-3 act on bone marrow Immune response

24-48H when 1st exposed & for antigen to start the reaction

2nd time: could start in just minutes antigen will get picked up by neutrophils (1st line of defense)

macrophages are next

B-lymph is 3rd line of defense

These specialized cells manufacture antibodies against antigen

B-cell can hold memory to start response faster

T-cells:

Cytotoxic: directly kill

Have memory

Helper T-cells: help B cells develop into plasma cells that secrete antibody

Suppressor T cells: Turn off the whole immune system

IL/IFN: chemotactic (call next cells in & also fever causing antigen) Immunoglobulins

IgG: what we give to patients Case study:

Mrs. Brown is a 78yo with a history of hypertension, Type II diabetes, and chronic reactive airway disease. She is POD #2 for a hip replacement.

Patient-related data VS: 100.8F, 100/65, HR=110, RR=20 with pOx = 90% on 2L O2 nasal canula pOx @ 90%: sit pt up a little more; have her take DEEP breaths Heart: S1, S2 normal; stable Afib

Lungs: Course crackles in mid lobes & bases

GI: hypoactive BS; minimal appetite

Lab Values: WBC = 15,000 (15% segs, 10% bands, 50% lymphs); Hct = 32% ; Plts = 450,000 WBC: normal inflammatory response for post op patient

Expected to rise a little bit

Lungs are #1 place for infection; if WBC (ed greatly, this would be the 1st place to look besides surgical site Monitor lung sounds, TCDB, ISqh Questions? Concerns?

What is the patient experiencing? Priorities? Risk for infection

Checking skin & mouth

Dry mucous membrane (es ability to fight off bacteria

Skin: opportunity for infection Discussion Question: What would you expect to see as a normal immune response in this patient?

Factors affecting immune system

Aging

Stress

Nutrition

Trauma (es overall immune response cause body is in crisis and cannot attend to everything at once Aging Immune system

Decreased cellular immunity (helper & cytotoxic T cells)

Decrease humoral immunity: decreased response to antigen stimulation

Decreased speed, strength & duration of immune response & Immune regulation

*Results: atypical presentation of infections ie UTI, pneumonia (low grade fever & MS changes) Mrs. Brown is a 78yo with a history of hypertension, Type II diabetes, and chronic reactive airway disease. She is POD #3 for a hip replacement.

*Pt. was diagnosed with pneumonia confirmed by CXR and started on azithromycin IV. Pt. received the 2nd dose about 2hrs ago.

Patient-related data VS: 101.8F, 90/58, HR=112, RR=24 with pOx = 88% on 2L O2 nasal canula

Heart: S1, S2 normal; stable Afib; c/o lightheadedness

Lungs: Wheezes in all lung fields; c/o chest tightness

GI: hypoactive BS; nausea, cramping

Patient was observed as being anxious and restless with facial flushing , hives on her neck & itching.

Questions? Concerns? What is the patient experiencing? Allergic reaction to antibiotic; Watch for anaphylaxis Allergic reaction: wheezing

Progression to get worse -> stridor Give Benadryl: 25 mg (d/t elderly) IV STAT Priorities of care? Priority interventions?

Hypersensitivity response

Type I : allergic response

Requires repeated exposures

Priming (IgE attaches to mast cells)

Secondary or triggered response (rapid degradation of mast cells & release of mediators

Patho:

Primed mast cells release: histamine, leukotrienes, platelet activating factors, prostaglandins, chemotactic factors

Local: common allergies

Systemic: severe allergic reaction = anaphylaxis

Anaphylaxis Causes: drugs, insect venom, food proteins

System response

Skin: hives, urticaria (histamine)

Cardiovascular: capillary dilation, increased vascular permeability ->redness, swelling & hypotension, (histamine, leukotrienes, prostaglandins)

Pulmonary: bronchoconstriction (histamine, leukotrienes) When you hear stridor GI: smooth muscle contraction & edema of mucosa ->cramps, nausea, diarrhea

Treatment of Anaphylaxis Epinephrine: stimulates and receptors in SNS (increases HR, BP, CO; bronchodilation, decreases release of histamine) Tell pt they will feel like their heart is beating out of chest

Causes smooth muscle relaxation -> bronchodilation Antihistamines: blocks histamine release Glucocorticoids: anti-inflammatory & immunosuppressive actions Push inflammation away to open tube Beta2-agonists: act on beta2-receptors of smooth muscles ->bronchdilation; inhibit histamine release from mast cells Albuterol

Goal: ( inflammation & open breathing tube

Monitor BP to ensure adequate perfusion Type II (cytotoxic): transfusion incompatibility; drug-induced hemolytic anemia (PCN, quinine, sulfonamides)

Type III (Immune Complex-mediated): Involve IgG & Ig M antibody and antigen complexes commonly seen in transplant rejection, SLE, glomerulonephritis

Type IV (delayed): primarily involves T lymphocytes & involves tissue destruction (GVHD, HVGD, rheumatoid arthritis, Type 1 diabetes mellitus)

Priorities of care: Hypersensitive reactions Fluid Volume Deficit

Decreased Cardiac Output r/t fluid volume deficit Impaired Gas Exchange: #1 Risk for Infection

Imbalanced Nutrition: < Body Requirements

Hemostasis

Thrombocytopenia (Bleeding-related: petechiae (seen more on abd & legs), ecchymosis, scleral bleeding, oozing from IV lines, arterial lines, injured tissues & internal bleeding in response to low platelets >Microthrombosis-related:

*Superficial: cyanosis/ ishchemia fingers, toes, nose, ears

*Organ dysfunction: CNS (altered LOC), Cardiac (tachycardia, hypotension), Resp (dyspnea, tachypnea, cyanosis, hypoxemia, ARDS), renal failure

Labs: Prolonged: bleeding time, PT, PTT, thrombin time Increased: fibrin degradation products, d-dimer Decreased: clotting factors, fibrinogen level, plts. Treatment Goal: Maintain fluid and hemodynamic balance (IVFs, RBC, Plt, & FFP transfusions) and treat the cause Transfusions: platelet s, FFP (has clotting factors in it), RBCs Heparin drip Coagulation inhibitor: antithrombin III Leukocyte Disorders: Leukemia Malignant disease of the blood Dysfunction of the bone marrow Types: Acute (A) vs. Chronic (C) Cell type: Myeloid (M) *myeloblastic, myelocytic Cell type: Lymphoid (L) *lymphoblastic, lymphocytic) Nomenclature: AML, CML, ALL, CLL Chronic leukemia pt: on low dose chemo daily; live in community

Acute: rapid onset, many manifestations Etiologies: genetic, radiation & chemical exposure, drugs, viruses Pathophysiology: lack of normal regulatory mechanisms of bone marrow cell proliferation and maturation Primary symptoms: d/t granulocytopenia, anemia, thrombocytopenia Secondary symptoms: d/t leukemic cell infiltration of tissue & BMD Diagnosis:

Symptom profile (evidence of leukemic infiltrates and pancytopenia) CBC WBC range: 200,000/mm3 Differential will define type Platelets & Hemoglobin low Bone marrow aspiration: increased # immature cells (blasts) LP: blast cells in CNS (~5% pts) MRI & CT: infiltrates and sites of infection Therapeutic treatments: Induction of a remission using chemotherapy Chemotherapy maintenance (lower dose over longer time period)

Bone Marrow Transplantation Syngeneic Allogeneic (matched) Case example: Ms. Jones is a 26yo newly diagnosed leukemia patient who is admitted to the inpatient unit with fever and neutropenia five days after her first cycle of chemotherapy.

VS: 101.8F, 90/56, 110 (NSR), RR=20

Lab Data: WBCs=650/mm3

(5% segs, 7% bands,10% lymphs, 20% monos); Hct=23%, Hgb=6g/dL; Plts=5,000/mm3 Interventions:

Blood transfusion; Platelets; O2; iron

Birth control: dont want her to have menses

Brush teeth carefully w soft toothbrush; No flossing

No rigorous nose blowing

(es ICP

fall precautions if lightheaded No drugs to ( plt aggregation

Ibuprofen, aspirin

Protective isolation

No fresh fruits, veggies, pets, flowers *Concept of neutropenia Abnormal decrease in neutrophils (must have nutrition for bone marrow to work Alcoholism Lose all protein/drinking empty cals Malignancy Diabetes Blood sugars; perfusion probs; (ed immune system; infection; vasculature issues Cirrhosis Introduction of compromised immune system Male sex Genetic predisposition? SIRS The systemic response to a wide range of stresses Temperature >38C (100.4) or 90 beats/min. Respiratory rate >20 breaths/min or PaCO2 12,000 cells/ml or < 4,000 cells/ml or >10% immature (band) forms. Note Two or more of the following must be present These changes should be represent acute alterations from baseline in the absence of other known cause for the abnormalities Etiology of SIRS Mechanical Trauma Burns Can get infected or activate inflammatory response Surgery Chemical Toxic drugs/fumes Pancreatitis Ischemic Shock states Myocardial infarction Reperfusion injury: anaerobic metabolism occurs d/t cell death and lysed cells expel K+ Normal inflammatory immune response

This is a NORMAL response Injury ->bleeding (attempt to cleanse area) ->clot off ->immune system activated -> redness (area around wound vasodilates & gets warm d/t blood)-> exudate is being released (protein enriched substance in white cells being pushed to area) = localized response (think of it body wide) Multiple systems are activated to protect the host from insult and limit the extent of injury & promote rapid healing. Insult can be microbial, but also mechanical, chemical, ischemic. Mediators involve multiple pathways- from molecular to systemic. Patho:

Although inflammation is essential to host response against infection, SIRS results from a dysregulation of the normal response, with massive, uncontrolled release of pro-inflammatory mediators.

Triggers caused from bacterial, viral, etc. Inflammatory cells Monocytes/Macrophages Neutrophils Mast cells Endothelial cells Plasma protein systems Complement Kinin Coagulation Biochemical mediators C-reactive protein Interleukins Tumor necrosis factor (TNF) Platelet-activating factor (PAF) Oxygen radicals Arachidonic acid metabolites Prostaglandins Leukotrienes Thromboxanes Vasodilation occurs, thereby (ing afterload (norm=800-1200)

CVP (es -> HR (es, BP (es, CO (es Microvascular permeability: fluid in 3rd space

It is lost fluid but does NOT harm you

Its lack of fluid in vasculature that causes harm

Hypovolemic Loss of volume d/t change in permeability (3rd spacing)

Vasodilation: changes size of compartment * stage of progression: initial, compensatory, progression, refractory refractory: even with treatment, pt is still hypotensive SIRS or sepsis?

SIRS Inflammation gone WILD!! Sepsis Triggered by invading microbes Clinically SIRS and Sepsis can look the same (early on) except with SIRS, cultures will be negative BOTH can lead to shock Severe sepsis: inability of organs to metabolize O2 Sepsis

Etiology

Microbial infection Blood Bacteria Gram negative Gram positive Fungi Virus Abscess Bacterial translocation in gut Bacterial translocation when depleted of nutrients Just 10 cc going in gut will prevent this from happening Instrumentation/catheterization * The definitions for SIRS and sepsis can also be used to describe a disease continuum with respect to the severity of the illness Determining factor of progression: how good/bad immune system works * Septic shock is a subset of severe sepsis. Note that current definitions have dropped the term septicemia that may still be found in older textbooks. Bacteremia is the term for when organisms are cultured from blood.

Sepsis

General Temperature > 38.3 or < 36 Heart rate > 90 beats per minute Tachypnea Altered mental status Significant edema or positive fluid balance (> 20 ml/kg over 24 hours) Hemodynamic Systolic BP 40 decrease in SBP or MAP < 70 Cardiac index > 3.5 L/min Tissue perfusion Decreased capillary refill or mottling Lactate levels > 2 mmol/L Inflammatory WBC > 12,000 cc/mL, < 4,000, > 10% bands C-reactive protein levels > 2 times normal Severe Sepsis Sepsis with organ hypoperfusion

1st organ affected: lungs

2nd affected: kidneys acute tubular necrosis (ATN) oliguria->anuria

one of the followings : SBP < 90 mmHg Acute mental status change PaO2 < 60 mmHg on RA (PaO2 /FiO2 < 250) Increased lactic acid/acidosis Oliguria DIC or Platelet < 80,000 /mm3 Liver enzymes > 2 x normal Ability to filter impaired d/t hypoperfusion Organ dysfunction Arterial hypoxia, P/F ratio (PaO2/FiO2 0.5 mg/dL Kidneys hypoperfused Ileus (absent bowel sounds) hypoperfused Total bilirubin > 4 mg/dL Coagulation abnormalities (INR > 1.5 or a PTT > 60 sec) Thrombocytopenia (platelet count < 100,000) Platelets are getting used up quicker than production occurs Metabolic acidosis (pH < 7.30) d/t lactic acidosis

kidneys cant compensate

lungs cant compensate cause failing too Complications

Adult respiratory distress syndrome (ARDS) Disseminated Intravascular Coagulation (DIC) Acute Renal failure (ARF) Intestinal bleeding Liver failure Central Nervous System dysfunction Heart failure Death Prognosis

Overall mortality from SIRS/sepsis in the U.S. is approximately 20%. Mortality is roughly linearly related to the number of organ failures, with each additional organ failure raising the mortality rate by 15%.

Hypothermia is one of the worst prognostic signs. Patients presenting with SIRS and hypothermia have an overall mortality of ~80%

Surviving sepsis campaign

The SSC aimed to reduce mortality from sepsis via a multi-point strategy, primarily: Building awareness of sepsis Improving diagnosis Increasing the use of appropriate treatment Educating healthcare professionals Improving post-ICU care Developing guidelines of care Facilitating data collection for the purposes of audit and feedback Guidelines for Management of Severe Sepsis and Septic Shock

Early Goal-Directed Therapy Sepsis resuscitation bundle Sepsis management bundle Diagnosis

Before the initiation of antimicrobial therapy, at least two blood cultures should be obtained

At least one drawn percutaneously At least one drawn through each vascular access device if inserted longer than 48 hours Other cultures such as urine, cerebrospinal fluid, wounds, respiratory secretions or other body fluids should be obtained as the clinical situation dictates Lactate has direct correlation to survivability

CBC, ABG, coag panel Other diagnostic studies such as imaging and sampling should be performed promptly to determine the source and causative organism of the infection may be limited by patient stability Sepsis resuscitation bundle (must be accomplished within the first 6 hours*) The Sepsis Resuscitation Bundle describes below, but must be accomplished within the first 6 hours of presentation for patients with severe sepsis or septic shock.

Serum lactate measured Blood cultures obtained before antibiotics administered Improve time to broad-spectrum antibiotics within 3 hours of ED admission and within 1 hour of non-ED In the event of hypotension or lactate > 4 mmol/L (36 mg/dL)

a. Deliver an initial minimum of 20 mL/kg of crystaloid (or colloid equivalent) For a 85kg patient you would give 1.7 liters of NS/LR b. apply vasopressors for ongoing hypotension (vasopressors, inotropes) blood culture before fluid (or at same time)

give vasopressin to constrict (acts on smooth muscles); levophed doesnt work in acidotic states In the event of persistent hypotension despite fluid resuscitation or lactate > 4 mmol/L (36 mg/dL)

a. achieve central venous pressure of > 8 mmHg fluid will leak out faster than can be put in (must continually give fluid boluses to maintain CVP)

b. achieve central venous oxygen saturation of > 70% 4 mmol/L (36 mg/dl). Evaluation for adrenal insufficiency Stress dose corticosteroid administration Test for this condition: give pt adrenocorticotropin, draw cortisol level before and after administration. Should see an ( in level

Give steroids if levels are decreased (cause cant make their own and cortisol is essentially a steroid) Recombinant human activated protein C (xigris) for severe sepsis (Studies now indicates that Zigris has no effect on outcome on patients with septicemia) Low tidal volume mechanical ventilation for ARDS Tight glucose control (ed glucose impairs tissue healing

bacteria thrive on glucose; prevents healing & impairs vasculature

* to lower lactate level, stop anaerobic metabolism

flush out lactate (( urine output) Priorities of care

Ineffective tissue perfusion related to progression of septic shock with decreased cardiac output, hypotension, and massive vasodilatation Deficient fluid volume related to vomiting, diarrhea, high fever, and shift of intravascular volume to interstitial spaces Ineffective breathing pattern related to rapid respirations and progression of septic shock Anxiety related to feelings that illness is worsening and is potentially life threatening, and the transfer to the critical care unit Expected outcomes

Regain and maintain stable hemodynamic levels by the end of shift Maintain adequate circulating blood volume Regain and maintain blood gas parameters within normal limits by the end of shift Verbalize increased ability to cope with stressors by the time of discharge. *Injury ->bleeding (attempt to cleanse area) ->clot off ->immune system activated -> redness (area around wound vasodilates & gets warm d/t blood)-> exudate is being released (protein enriched substance in white cells being pushed to area) ->infection worsens (bacteria in blood)->bacteremia->Sepsis (vasodilation, microvascular permeability, cellular activation {early and late mediators], coagulation)-> (decreased preload -> decrease in SV -> ( in CO) Give norepi (#1) & vasopressin (#2) ABX!!

For change in permeability, must treat underlying cause

Must start w/in 3 hr of arrival at ED & 1 hr on floor

Sepsis case study

43-year-old male Flu-like symptoms for 1 day In ER Temp 39.5 ((ed) Pulse 130 ((ed HR) Blood pressure 70/30 ((ed) Respirations 32 ((ed) Petechial rash (D/t DIC; microemboli formation -> microemboli clotting occurs in capillaries Chest, CV, Abdominal exam normal Case 2 Laboratory

pH 7.29, Sat 89%, PaO2 72, PaCO2 29 (resp compensation) Lactate 6.0 (anything above 2 is (ed) ->the higher the lactate the higher the mortality Start sodium bicarb drip (mix with D5, NEVER NS-> sodium load will be too high)

3 amps/L Investigations pending

Blood, urine cultures Anything draining out of body Orally intubated and placed on mechanical ventilation Low tidal volumes

Pressure ventilation if hes bad enough instead of volume Central venous catheter inserted

Cefotaxime 2 g IV Normal saline 2 litres initially, repeated

Admitted to ICU

Case 3

In ICU:

Norepinephrine started to support blood pressure

Additional fluid (NS/ LR)

Volume expansion with pentastarch {hetastarch}) Albumin based on low CVP Once permeability has returned to normal limits, thats when you give albumin

Pentastarch: acts similar to albumin Blood products, (PRBC, FFP, cryoprecipitate)

Pulmonary artery catheter inserted to aid further hemodynamic management

Despite therapy patient remained anuric

Continuous venovenous hemofiltration initiated

Case 4

Early gram stain on blood revealed gram negative rods Patient started on: Hydrocortisone 100 mg IV q8h d/t adrenal insufficiency Recombinant activated protein C 24(g/kg/hour for 96 hours (Studies now indicates that Zigris has no effect on outcome on patients with septicemia) Use of vasopressin vs norepinephrine for BP support At high doses, stimulates contraction of smooth muscle causing vasoconstriction when catecholamine's fail (works better than catecholamines) Enteral nutrition via nasojejunal feeding tube Even without BS Prophylaxis for stress ulcers, deep venous thrombosis DVT: SCDs

Possible heparin

Final culture: meningococcal septicemia Hematopoiesis: Bone marrow manufactures all blood cells Blast cells are immature blood cells Erythropoiesis: production of RBCs; dependent upon the release of EPO from the kidney in response to blood cell oxygen demand CBC w diff & platelets WBCs (5,000-10,000/cu mm) Differential: segs + bands (50 70%), lymphs (20 40%), monos (2 8%), eos (1 4%), basos, blasts RBCs Hct (men: 42-52%; women: 37-47%) Hgb (men: 14-18g/dl;women: 12-16g/dl) *most important * Hgb x3 ~ Hct Men have more RBCs than women d/t: bigger bones, lack of menses Plts (150,000-500,000/ cu mm) Reticulocyte count: indicator of RBC production rate & EPO response RBC indices: MCV (mean corpuscular [cell] volume): tells us the average size of an RBC Small RBCs: blood loss, (ed #s of immature RBCs, (ed iron Normal size RBCs: normocytic anemia (normal size w (ed #s), acute blood loss Extra large RBCs: macrocytic anemia, vitamin B12 deficiency/folate deficiency (B12 & folic are building blocks of nucleic acid; (ed #s prevent cells from dividing properly so they are extra large) Pernicious anemia: B12 deficiency May be d/t alcoholism, gastric bypass, anorexia, malnutrition, long term/untreated hypothyroidism MCH (mean corpuscular [cell] hemoglobin): tells us the average (in weight) amount of Hgb in one RBC MCHC (mean corpuscular [cell] hemoglobin concentration): tells us the average Hgb concentration in one RBC (%) 1 RBC ~ 33% Hgb other components: enzymes, cytoplasm, etc.

RDW (RBC distribution with): red cell distribution =avg variance in sizes of RBCs

(ed RDW = great diff in sizes

(es efficacy of gas exchange in the body

normal size: maximizes gas exchange in the body Retic count: young RBC production; tells us how effectively our EPO response from the kidneys is working High production of young RBCs d/t anemia, hypoxia, sickle cell anemia*, altitude*, bleeding, (ed RBC destruction (burns) (ed retic count: bone marrow suppression, medication, infection, (ed EPO Heme (iron + oxygen molecule)

Iron deficiency decreases oxygen carrying capacity

Globin (protein)

Aging hematologic system

At ~ age 70yo, amount of bone marrow in long bones begins to decline

Decreased # stem cells in marrow Decreased effectiveness of EPO Decreased platelet adhesiveness Average H & H decreases slightly to low normal No changes: RBC life span, Blood volume, total WBC count, platelet structure & function Factors effecting the aging immune system Stress SNS stimulation -> hormonal changes -> decrease immune response -> especially cellular immunity Cortisol (stress hormones): suppresses immune system & bone marrow response Comorbidity *Chronic infection/ inflammation decreased EPO, decreased RBC survival, impaired iron transport

*Chronic liver disease decreased RBC production & survival, decreased serum iron and TIBC

*Renal insufficiency/ renal failure decreased EPO, decreased RBC survival

Exercise Exercise: may prevent decrease in cellular immunity

Nutrition Vitamins enhance cellular immunity (Vitamins A, B6, C, E, folic acid, iron, copper, selenium, zinc) Anemia: decreased RBCs, Hgb, Hct Mild anemia: 10-12 Hgb Mod: 7-10 Hgb

Severe: under 7 Hgb Neutropenia: decreased neutrophils 50-70%: 1st to show up on site Thrombocytopenia: decreased plts Less than 150,000 Pancytopenia: decrease in all cellular components of the bone marrow; caused by bone marrow supression Types of anemia

Reasons for Anemia

Blood loss: surgery, acute bleeding (hemorrhage, trauma), chronic bleeding (cirrhosis -> (ed vitamin K, colitis [Irritable Bowel Disease], cancer, peptic ulcers/gastric ulcers) Confirm: H&H, RBC indices (including retic count), endoscopy (for upper GI bleed), occult blood sample (for lower GI bleed) (ed RBC production: Vit D deficiency, (ed iron, (ed B12, folate, bone marrow issues (BM failure [aplastic anemia], suppression [Rx, Chemo, malignancy], insensitive to EPO Chronic inflammation/disease: (ed WBCs (specifically cytokines [IL-2, IL-6, INF]) (ed cytokines suppress bone marrow ( encourages cells to uptake iron ((ed iron to uptake RBCs) ( lysing of cells

Kidney issues Types of anemia

(ed RBC destruction: infections, Rx, blood vessel issues, sickle cell anemia, burns

General symptoms of anemia

S&S of anemia: Face

(ed pallor (Fe give Hgb its color) ( skin (mucous membranes ( conjunctiva (lids of eye) (ed O2 to brain ( fatigue ( HA ( (ed concentration

sore tongue/bald tongue (smooth & shiny tongue cause papillae not produced

Specific to Fe deficiency anemia (typically chronic) Cracking at side of mouth (patients like to chew on mouth) (pica (ice [no nutritional value]) Vitamin deficiencies d/t anemia (common wit other vit deficiencies)

Lungs

Report feelings of breathlessness ( (ed RR (compensatory mechanism) Heart

(ed HR (baseline ~110) Lower extremities

Cramping, Numbing/tingling ((ed B12) Physiologic Compensatory Mechanisms of Anemia

Increased synthesis of 2,3-DPG: more oxygen released to the tissues

Blood redistribution: decreased urine output, pallor of skin/ mucous membranes

Increased cardiac output: tachycardia, systolic flow murmur, orthostatic hypotension

Increased respiratory rate: DOE, orthopnea

Increased production of erythropoietin: generalized aches and pains, sternal tenderness

Symptoms of compensatory failure: decreased oxygenation to tissues

Angina

Headache Light-headedness

Nocturnal leg cramps

Irritability

Nursing Diagnoses for Patients with Anemia

Ineffective Tissue Perfusion

Fatigue

Activity Intolerance

Impaired Gas Exchange

Altered Skin Integrity

Altered Nutrition: < body requirements

Altered Mucous Membrane Integrity

Blood transfusion types

Blood transfusion basics

Pretransfusion (history, vital signs, premedication PRN) Transfuse blood with normal saline only 18g for blood products Older adults at high risk for fluid overload & CHF One unit RBC -> Hct by 3% Hgb by 1g/dlCare of patient with anemia

Questions

Which of the following statements would indicate that an anemic patient needs further teaching about taking iron supplements.

I can take my iron pills with milk to prevent an upset stomach.(Calcium inhibits iron absorption) I should take a stool softener when I am taking iron pills. Fe supplements very constipation I can take vitamin C to enhance iron absorption It is normal for my stool to be black when I take iron Client teaching about self management of the fatigue associated with anemia should include instructions to:

Continue bedrest (increases fatigue) Participate in all usual ADLs (may increase fatigue) Follow a progressive ambulatory program (gradually restores energy) Participate in aerobic exercise training (may increase fatigue) Sickle cell anemia Group of inherited disorders characterized by abnormal hemoglobin: Hb S Primarily found in African American population frequency 8% chance if both parents have gene = Hgb S Autosomal recessive mutation in the hemoglobin chain Hgb S (75 95%) Sickle Cell trait (mixed Hgb A & Hgb S) Heterozygous inheritance pattern Hgb S (34 45%) Carrier which rarely develops clinical manifestations Pathophysiology Hgb S is well oxygenated, then Hgb has normal function PaO2 and SaO2 drop, Hgb S forms a fibrous polymer; realignment of polymers =>sickle shape Rod shaped cells ( half moon shape( inflexible & very rigid

As these RBCs filter through capillaries they get stuck and cause issues

(ed retic count 5-8x the norm

RBC lasts 12-20 days

Sickle cell crisis/vaso-occluions

Dehydration

Hypoxic -> (ed O2

Cold -> (ed perfusion & (ed O2 to local areas

Affects all systems

PE ( priapism ( kidney failure* ( liver ( spleen (ruptures and dies away) (sepsis (pain

If spleen dies it can make pt septic Sickle Cell Characteristics Rigid RBC membrane -> decreased oxygen carrying capacity Increased blood viscosity -> slowed blood flow in small capillaries Increased adherence of cells to endothelium of vessel walls Shortened RBC lifespan to10 20 days (normal RBC lifespan = 120 days) Elevated erythropoiesis (5-8x normal) Abnormal RBCs destroyed in the spleen -> tissue ischemia & autosplenectomy Diagnosis: Sickle cell screening test Hemoglobin electrophoresis Lab Values: Decreased Hgb Decreased platelets Increased reticulocytes Clinical manifestations

Begin to occur at age 6 mths to 1 yr

Chronic hemolytic anemia

Microvascular occlusion which effects all organs

Brain: stroke

Lungs: acute lung injury (~25% deaths)

Spleen: infarction leading to organ loss which predisposes pts. to infection d/t chronic neutropenia

Renal: ARF (common cause death in adults)

Treatment Hydration (D51/2NS @ 150-200ml/hr) Oxygenation (O2 2-4L/min via NC) Pain management Morphine sulfate IV continuous with PCA Ketorolac for bone pain Diagnosis and treatment of infections Prompt anti-infective therapy Reverse sickling crisis Transfusion to increase Hct to >30%