s.gaus-management of life-threatening (kuliah sistem)
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Management of Life-Threatening
Electrolyte and Metabolic Disturbances
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Introduction
Common in critically ill & injured patientsAlter physiologic function & contribute to
morbidity & mortalityThe most common electrolyte disturban-
ce in critically ill patients are: disturbance in K, Na, Ca, Mg, P levels
Metabolic disturbance accompany many systemic disease processes or result of altered endocrine function
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Electrolyte Disturbances
Potassium: hypo- & hyperkalemiaSodium : hypo- & hypernatremiaOthers: Calcium : hypo- & hypercalcemia
Phosphate : hypo- & hyperphosphatemia
Magnesium : hypomagnesemia
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Potassium
Essential for maintenance of the electrical membrane potential
Alteration of K primarily effect the CV, neuromuscular, and GI systems.
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Hypokalemia
Plasma [K+] <3.5mEq/L (<3.5mmol/L)Can occur as a result from:
1.increased K loss (renal or extrarenal losses)
2.intercompartmental shift / transcellular shift of K 3.inadequate or decreased K intake
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Causes of hypokalemia
Transcellular Shifts Renal Losses Extrarenal Losses
Decreased Intake
Alkalosis
Hyperventilation
Insulin
β-adrenergic agonists
Hypomagnesemia
Vomiting
Diuresis
Metabolic alkalos
Renal tub defects
Diabetic ketoacid
Drugs (diuretics, aminoglycosides, amphotericin B)
Diarrhea
Profuse sweating
Malnutrition
Alcoholism
Anorexia nervosa
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Clinical manifestation:
Cardiac system: arrhythmias (ventricular, & supraventricular,
conduction delay, sinus bradycardia) ECG abnormalities (U waves, QT prolo- ngation, flat or inverted T waves) Neuromuscular system: muscle weakness
or paralysis, paresthesia, ileus, abdominal cramps, nausea, and vomiting
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Effect of hypokalemiaCardiovaskular ECG changes/dysrhythmias Myocardial dysfunctionNeuromuscular Skeletal muscle weakness Tetany Rhabdomyolisis IleusRenal Polyuria (nephrogenic DI) Increased ammonia production Increased bicarbonate reabsorptionHormonal Decreased insulin secretion Decreased aldosteron secretionMetabolic Negative nitrogen balance Encephalopaty in patients with liver disease
Adapted from Schrier RE,ed: Renal and Electrolyte Disorders, 3 rd ed. Little, Brown and Company, 1986.
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Treatment (1)
Stop offending drugs (if possible)Correct hypomagnesemia & other
electrolyte disturbancesCorrect alkalosis
Treatment is aimed:Correcting the underlying causeAdministering potassium
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Treatment (2)
Arrhythmias or paralysis: KCl 20-30 mEq via central venous catheter (sequential infusion: 10 mEq in 100 mL fluid over 20 mins, infusion rate can be slowed after symptoms resolve)
Absence of life-threatening manifestation: KCl 10 mEq/hr IV
K <3 mEq/L (<3 mmol/L) & asymptomatic: K enterally (orally or NGT) (KCl 20-40 mEq every 4-6 hrs)
K <2-2.5 mEq/L (<3 mEq/L if on digoxin) or if symptoms are present: K intravenously
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Treatment (3)
Acedemia is present, correct the potassium level before correcting pH (K shift intracellularly as the pH increases)
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Monitoring
Continuous ECG monitoring is necessary (during parenteral administration of high concentration of KCl)
Serum K levels must be monitored at frequent interval during repletion (every 1-2 hrs during initial replacement)
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Hyperkalemia
Potassium >5.5 mEq/L (>5.5 mmol/L)Most often results from renal dysfunctionPseudohyperkalemia may result from a
white blood cell count >100,000/mm3 or platelet count >600,000/mm3.
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Causes of hyperkalemia
Renal dysfunction
Acidemia
HypoaldosteronismDrugs (potassium-sparing diuretics, ACE inhibitors, etc.)
Excessive intake
Cell death Rhabdomyolisis Tumor lysis Burns Hemolysis
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Clinical manifestation
Heart: arrhythmias (heart block, bradycardia, dimi- nished conduction and contraction) ECG abnormalities (diffuse peaked T waves, PR prolongation, QRS widening, diminished P waves, sine waves) Muscle: muscle weakness, paralysis, pares-
thesias, and hypoactive reflexes
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Treatment (1)
Recognition & treatment of underlying diseases Removal of offending drugs Limitation of potassium intake Correction of acidemia or eletrolyte abnorma-
lities Any serum potassium level >6 mEq/L should be
addressed, but the urgency of treatment depends on clinical manifestation
The presence of ECG changes mandates immediate therapy
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Treatment (2) ECG abnormalities present: CaCl 5-10 mL of a 10%
solution IV over 5-10 mins (the effect lasts only 30-60 mins & should be followed by additional treatment)
Redistribution of K: ■ Na bicarbonate 1 mEq/kg (1 mmol/kg) IV over 5-10 mins (beware of potential Na overload with Na bicarbonate) ■ 50 g of 50% dextrose over 5-10 mins with 10 U of regular insulin IV ■ Inhaled β2-agonists in high dose (albuterol 10-20 mg) Removal of K from body: ■ Increase urine output with a loop diuretic ■ Increase GI K loss with Na polystyrene sulfonate 25-50 g in sarbitol, enterally or by enema ■ Dialysis
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Monitoring
Should be monitored during evaluation & treatment:
◙ Repeat serum K levels
◙ Continuous cardiac monitoring
and serial ECG tracings
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Sodium
Primary functions: ◈ determinant of osmolality in the body ◈ involved in the regulation of extracellular volumeAbnormalities in circulating Na primarily
effect neuronal & neuromuscular function.
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Hyponatremia
Sodium <135 mEq/L (>135 mmol/L) Most common cause: associated with a low serum
osmolality is excess secretion of ADH (euvolemic hyponatremia) or associated with hypovolemic and hypervolemic conditions
The presence of a nonsodium solute: glucose and mannitol (characterized by an elevated serum osmolality
Pseudohyponatremia: occurs in the presence of severe hyperlipidemia, hyperproteinemia, or hyperglycemia
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Causes of hyponatremia
Euvolemia Hypovolemia Hypervolemia
SIADH
Psychogenic polydipsia
Hypothyroidism
Inappropriate water admi- nistration to infanst/chil- dren
Diuretic use
Aldosterone deficiency
Renal tubular dysfunction
Vomiting
Diarrhea
Third-space fluid losses
CHF
Cirrhosis
Nephrosis
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Clinical manifestation
CNS: disorientation, decreased mentation, irritability, seizures, lethargy, coma, nausea and vomiting
Muscle: weakness & CNS-driven respiratory arrest
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Algorithm for treatment of hypernatremia
hypernatremia
water & Na+ loss water loss increased Na+ content
replace isotonic loss replace water deficit loop diuretic
replace water deficit replace any water deficit
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Treatment (1)
Treating the underlying diseaseRemoving offending drugsImproving the circulating Na level
Hypovolemic hyponatremia: usually responds to IV volume repletion (with normal saline). Volume is replaced, ADH is suppressed & free water is excreted by the kidneys.
Hypervolemic hyponatremia: usually not severe & improves with successful treatment of the underlying condition
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Treatment (2)
Hyponatremia is acute or symptomatic: serum Na level should be increasedrestricting free-water intakeincreasing free-water clearence with loop
diureticsreplacing IV volume with normal saline
(154 mEq/L) or hypertonic 3% saline (513 mEq/L)
The goal of therapy: to remove free water & not Na
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The amount of NaCl necessary to raise plasma [Na+] to the desired value, the Na+ deficit, can be estimated by the following formula:
Na+ deficit=TBW x (desired [Na+]-present [Na+] )
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Example:
An 80-kg woman is lethargic and found to have a plasma [Na+] of 118 mEq/L. How much NaCl must be given to raise her plasma [Na+] to 130 mEq/L?
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[Na+] deficit = TBW x (130-118)
TBW is approximately 50% of body weight in females:
[Na+] deficit=80x0.5x(130-118)
=480 mEq
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Normal (isotonic) saline contains 154 mEq/L, the patient should receive 480 mEq : 154 mEq/L = 3.12 L of normal saline.
For correction rate of 0.5 mEq/L/hour, this amount of saline should be given over 24 hours (130 mL/hour)
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Hypernatremia
Sodium <145 mEq/L (>145 mmol/L)Indicates intracellular volume depletion
with a loss of free water, which exceeds Na loss
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Causes of hypernatremia
Water Loss Reduced Water
Intake
Excessive Sodium Intake
Diarrhea
Vomiting
Excessive sweating
Diuresis
Diabetes insipidus
Altered thirst
Impaired access
Salt tablets
Hypertonic saline
Sodium bicarbonate
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Clinical manifestation
CNS: altered mentation, lethargy, seizures, coma
Muscle function: muscle weaknessPolyuria: the presence of diabetes
insipidus or excess salt and water intake
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Treatment (1)
Centers on correcting the underlying cause of hypernatremia
The vast majority of patients require free-water repletion
The water deficit can be calculated using equation:
water deficit (L)=0.6 x wt (kg) [(Na2/Na1)-1]
Na1 = the normal sodium level
Na2 = the measured sodium level
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Example:
A 70-kg man is found to have a plasma [Na+] of 160 mEq/L. What is his water deficit?
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If one assumes that the hypernatremia if from water loss only, then total body osmoles are unchanged. Thus, assuming he had a normal [Na+] 140 mEq/L and a TBW content that is 60% of body weight:
Normal TBW x 140 = present TBW x [Na+]plasma
(70 x 0.6) x 140 = present TBW x 160 present TBW = 36.7 ltr Water deficit = normal TBW – present TBW = (70 x 0.6)- 36.7 = 5.3 L
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To replace this deficit over 48 hours, one would give 5% Dextrose in water intrave-nously, 5.300 mL over 48 hours, or 110 mL/hour
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METABOLIC DISTURBANCES
Acute Adrenal Insufficiency Hyperglycemic Syndromes
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Acute Adrenal Insufficiency
Lack of specific signs & symptoms makes early recognition of acute renal insufficiency difficult
May result from: ■ Failure of the adrenal glands (autoimmune disease, granulomatous disease, HIV infection, adrenal hemorrhage, meningococ- cemia, ketoconazole) ■ Failure of the hypothalamic/pituitary axis (withdrawal from glucocorticoid therapy)
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Clinical manifestation Weakness Nausea/vomiting Abdominal pain Orthostatic hypotension Hypotension refractory to volume or
vasopressor agents Fever
Suggestive laboratory findings: Hyponatremia Hyperkalemia Acidosis Hypoglycemia Prerenal azotemia
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Emergent treatment Indicated in critically ill patients, even if the
diagnosis is not established High-risk patients include: AIDS, disseminated
tuberculosis, sepsis, acute anticoagulation, post CABG patients, patients from whom glucocorticoid therapy was withdrawn within the past 12 months
If dexamethasone is used for emergent steroid replacement, a short adrenocorticotropic hormone stimulation test can be performed for diagnosis after resuscitative therapy is instituted
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Short ACTH Stimulating Test
Blood for serum cortisol is drawn at baseline Synthetic 1-24 ACTH (cortrosyn, cosyntropin), 250 ug,
is administered intravenously A serum cortisol level is drawn 60 mins after
cosyntropin administration A cortisol level >20 ug/dL (>552 nmol/L) at 60 mins
indicates adequate adrenal function Failure to attain adequate cortisol levels indicates the
need for further testing and expert consultation Since cortisol level may not be reported quickly,
corticosteroid should be administered, pending results, if the clinical situation is suggestive of acute adrenal insufficiency
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Treatment Obtain baseline blood samples for cortisol, electrolyte,
etc Infuse D5 normal saline to support blood pressure Administer dexamethasone 4 mg IV, then 4 mg IV
every 6 hrs Perform short adrenocorticotropic hormone stimulation
test if needed for diagnosis If the diagnosis of adrenal failure is confirmed,
hydrocortisone 100 mg IV, then 100 mg every 8 hrs, can be administered. Some physicians prefer administration of hydrocortisone as a continuous infusion, 300 mg over 24 hrs
Treat precipitating conditions
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Hyperglycemic Syndromes
Results from a relative or absolute lack insulin
Characterized by: hyperglycemia, keto-acidosis, and osmotic diuresis-induced dehydration
Life-threatening hyperglycemic syndromes: diabetic ketoacidocis (DKA) and hyper-glycemic hyperosmolar nonketotic syndro-me (HHNK)
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Clinical manifestations
Result from hyperglycemia & excess ketone productionHyperglycemia:
HyperosmolalityOsmotic diuresis-induced dehydrationFluid & electrolyte lossDehydrationVolume depletion
Ketone (DKA):AcidosisOsmotic diuresis
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Clinical features
Weakness Dehydration Polyuria Polydipsia Altered mental status Coma Tachycardia Arrhythmias Hypotension
Anorexia Nausea/vomiting Ileus Abdominal pain Hyperpnea Fruity odor to the
breath (DKA)
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Laboratory investigation
Hyperglycemia Hyperosmolality (more common in HHNK) Glukosuria Ketonemia/Ketonuria (DKA) Anion gap metabolic acidosis (DKA) Hypokalemia Hypophosphatemia Hypomagnesemia Leukocytosis Azotemia Elevated amylase Creatine phosphokinase
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Treatment (1)
The goal: to restore the fluid & electrolyte balance, provide insulin, & identify precipitating factors (infection, stroke, MI, pancreatitis)
Volume deficits correlate with the severity of hyperglycemia & are usually greater in HHNK
Normal saline: replenish IV volume & restore hemodynamic stability (1 L in the first hour, 250-500 mL/hr as needed)
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Treatment (2)
After 1-2 L of NS, fluids with less Cl (0.5 saline) should be used to avoid hyperchloremic metabolic acidosis
Urine output should be maintained at 1-3 mL/kg/hr (ensure adequate tissue perfusion & clearance of glucose)
Invasive hemodynamic monitoring (arterial catheter, PA catheter): required in patients with underlying CV disease
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Treatment (3)
DKA: Loading dose: 5-10 U regular human insulin IV route is the most reliable & easiest to titrate Continuous infusion is necessary with serial monitoring of the blood glucose & electrolyte concentration
HHNK: Smaller doses of insulin are usually adequate
(1-2 U)
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Monitor glucose levels
Frequently Glucose decreases to >250 mg/dL (<13.8
mmol/L), switch to glucose-containing fluids to avoid hypoglycemia
10% dextrose may be necessary to maintain glucose levels >150 mg/dL (>8.3 mmol/L) while continuing insulin infusion
Subcutaneous insulin (BS is controlled, ketonemia has cleared, the patient is stable)
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Insulin & correction of acidosis shift potassium intracellularly & may lead to precipitous drops in K levels
K deficit range from 3-10 mEq/kg K should be added to fluid therapy as soon as
serum K is recognized or thought to be normal or low and urine output is documented
K levels should be monitored frequently until levels stabilize & acidosis is resolved (DKA)
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Priorities in initial resuscitation of DKA
Institute crystalloid resuscitation, initially with NS Institute insulin infusion at 0.1 U/kg/hr Consider bicarbonate if pH<7.0 Look for precipitating of DKA (infection, MI, GI bleed) Add KCl to fluid resuscitation when serum K is known or
expected to be low or normal, and urine output is documented Add glucose to crystalloid infusion when serum glucose is <250
mg/dL. Do not decrease insulin infusion rate unless symptomatic hypoglycemia or precipitous drops in serum glucose. Administer 10% dextrose if necessary to maintain serum glucose >150 mg/dL
Continue insulin infusion until ketosis is cleared (negative serum ketones with correction of increased anion gap).
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References:
Fundamental Critical Care Support, Course Text, 3rd edition, Society of Critical Care Medicine
Lange Clinical Anesthesiology, 3rd edition, Lange Medical Books/McGraw-Hill Medical Publishing Division
Physiologic and Pharmacologic Bases of Anesthesia, 2nd edition, Williams and Wilkins
Textbook of Critical Care, 3rd edition, W.B. Saunders Company