electrolyte & metabolic disturbance

7/27/2019 Electrolyte & Metabolic Disturbance

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Management of Life-Threatening

Electrolyte and Metabolic

Disturbances


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Introduction

Common in critically ill & injured patients

Alter physiologic function & contribute tomorbidity & mortality

The most common electrolyte disturban-ce in critically ill patients are: disturbancein K, Na, Ca, Mg, P levels

Metabolic disturbance accompany manysystemic disease processes or result ofaltered endocrine function


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Electrolyte Disturbances

Potassium: hypo- & hyperkalemia

Sodium : hypo- & hypernatremia

Others:Calcium : hypo- & hypercalcemia

Phosphate : hypo- & hyperphosphatemia

Magnesium : hypomagnesemia


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Potassium

Essential for maintenance of the electricalmembrane potential

Alteration of K primarily effect the CV,

neuromuscular, and GI systems.


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Hypokalemia

Plasma [K+]


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Causes of hypokalemia

Transcellular Shifts Renal Losses Extrarenal

Losses

Decreased Intake

Alkalosis

Hyperventilation

Insulin

-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, abdominalcramps, nausea, and vomiting


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Effect of hypokalemia

CardiovaskularECG changes/dysrhythmias

Myocardial dysfunction

Neuromuscular

Skeletal muscle weakness

Tetany

Rhabdomyolisis

Ileus

Renal

Polyuria (nephrogenic DI)

Increased ammonia production

Increased bicarbonate reabsorption

Hormonal

Decreased insulin secretionDecreased aldosteron secretion

Metabolic

Negative nitrogen balance

Encephalopaty in patients with liver disease

Adapted from Schrier RE,ed: Renal and Electrolyte Disorders, 3rd ed. Little, Brown andCompany, 1986.


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Treatment (1)

Stop offending drugs (if possible)

Correct hypomagnesemia & other

electrolyte disturbances

Correct alkalosis

Treatment is aimed:

Correcting the underlying cause

Administering potassium


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Treatment (2)

Arrhythmias or paralysis: KCl 20-30 mEq viacentral venous catheter (sequential infusion: 10

mEq in 100 mL fluid over 20 mins, infusion rate canbe slowed after symptoms resolve)

Absence of life-threatening manifestation: KCl 10mEq/hr IV

K


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Treatment (3)

Acidemia 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 dysfunction

Pseudohyperkalemia may result from awhite blood cell count >100,000/mm3 or

platelet count >600,000/mm3.


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Causes of hyperkalemia

Renal dysfunction

Acidemia

Hypoaldosteronism

Drugs (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 beaddressed, 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 2-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

volume

Abnormalities in circulating Na primarily

effect neuronal & neuromuscular function.


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Hyponatremia

Sodium 135 mmol/L)

Most common cause: associated with a low serumosmolality is excess secretion of ADH (euvolemichyponatremia) or associated with hypovolemic andhypervolemic conditions

The presence of a nonsodium solute: glucose andmannitol (characterized by an elevated serumosmolality

Pseudohyponatremia: occurs in the presence ofsevere hyperlipidemia, hyperproteinemia, orhyperglycemia


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Causes of hyponatremia

Euvolemia Hypovolemia Hypervolemia

SIADH

Psychogenic polydipsiaHypothyroidism

Inappropriate water admi-

nistration to infanst/chil-

dren

Diuretic use

Aldosterone deficiencyRenal tubular dysfunction

Vomiting

Diarrhea

Third-space fluid losses

CHF

CirrhosisNephrosis


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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 hyponatremia

hyponatremia

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 disease

Removing offending drugs

Improving 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 intake

increasing free-water clearence with loop

diuretics

replacing 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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Hypernatremia

Sodium 145 mmol/L)

Indicates intracellular volume depletion

with a loss of free water, which exceedsNa 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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CNS: altered mentation, lethargy,

seizures, coma

Muscle function: muscle weakness

Polyuria: 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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METABOLIC DISTURBANCES

Acute Adrenal Insufficiency

Hyperglycemic Syndromes


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Acute Adrenal Insufficiency

Lack of specific signs & symptoms makesearly recognition of acute renal insufficiencydifficult

May result from:

Failure of the adrenal glands (autoimmunedisease, granulomatous disease, HIV

infection, adrenal hemorrhage, meningococ-

cemia, ketoconazole)

Failure of the hypothalamic/pituitary axis

(withdrawal from glucocorticoid therapy)


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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 thediagnosis is not established

High-risk patients include: AIDS, disseminatedtuberculosis, sepsis, acute anticoagulation,

post CABG patients, patients from whomglucocorticoid therapy was withdrawn withinthe past 12 months

If dexamethasone is used for emergent steroidreplacement, a short adrenocorticotropichormone stimulation test can be performed fordiagnosis after resuscitative therapy isinstituted


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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 aftercosyntropin administration

A cortisol level >20 ug/dL (>552 nmol/L) at 60 minsindicates adequate adrenal function

Failure to attain adequate cortisol levels indicates theneed 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 adrenalinsufficiency


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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 IVevery 6 hrs

Perform short adrenocorticotropic hormone stimulationtest 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 preferadministration of hydrocortisone as a continuousinfusion, 300 mg over 24 hrs

Treat precipitating conditions


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Hyperglycemic Syndromes

Results from a relative or absolute lackinsulin

Characterized by: hyperglycemia, keto-

acidosis, and osmotic diuresis-induceddehydration

Life-threatening hyperglycemic syndromes:

diabetic ketoacidocis (DKA) and hyper-glycemic hyperosmolar nonketotic syndro-me (HHNK)


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Clinical manifestations

Result from hyperglycemia & excessketone productionHyperglycemia:Hyperosmolality

Osmotic diuresis-induced dehydrationFluid & electrolyte loss

Dehydration

Volume depletion

Ketone (DKA):Acidosis

Osmotic 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 thebreath (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 (0.5saline) should be used to avoidhyperchloremic metabolic acidosis

Urine output should be maintained at 1-3mL/kg/hr (ensure adequate tissueperfusion & clearance of glucose)

Invasive hemodynamic monitoring(arterial catheter, PA catheter): requiredin 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 (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


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References:

Fundamental Critical Care Support, CourseText, 3rd edition, Society of Critical CareMedicine

Lange Clinical Anesthesiology, 3rd edition,Lange Medical Books/McGraw-Hill MedicalPublishing Division

Physiologic and Pharmacologic Bases ofAnesthesia, 2nd edition, Williams and Wilkins

Textbook of Critical Care, 3rd edition, W.B.Saunders Company

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