Electrolic Management

8/12/2019 Electrolic Management

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Management of Life-Threatening

Electrolyte and MetabolicDisturbances

S.Gaus,M.D,Ph.DAnesthesiologist

Dept. of Anesthesiologi, ICU and Pain ManagementFaculty of Medicine Hasanuddin University


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Introduction

Common in critically ill & injured patients

Alter physiologic function and contribute tomorbidity & mortality

The most common electrolyte disturban-cein critically ill patients are: disturbance inK, Na, Ca, Mg, P levels

Metabolic disturbance accompany manysystemic disease processes or result ofaltered endocrine function


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Objectives

Review causes and clinical manifestationsof severe electrolyte disturbances

Outline emergent management ofelectrolyte disturbances

Recognize acute adrenal insufficiency andappropriate treatment

Describe management of severehyperglycemic syndromes


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Principles of Electrolyte Disturbances

Implies an underlying disease process

Treat the electrolyte change, but seek the

cause

Clinical manifestations usually not specific

to a particular electrolyte change, e.g.,

seizures, arrhythmias


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Principles of Electrolyte Disturbances

Clinical manifestations determine urgency

of treatment, not laboratory values

Speed and magnitude of correctiondependent on clinical circumstances

Frequent reassessment of electrolytes

required


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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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Metabolic Disturbances

Severe hyperglycemic syndromes

Acute adrenal insufficiency


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Potassium (K)

Essential for maintenance of the electricalmembrane potential

Alteration of K primarily effect the CV,

neuromuscular, and GI systems.


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Overview of Potassium Balance


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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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Hypokalemia

Neuromuscular manifestations:

weakness, fatigue, paralysis, respiratory

dysfunction

GI:constipation, ileus

Nephrogenic DI

ECG changes:U waves, flattened Twaves

Arrhythmias


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Mosby items and derived items 2005, 2002 by Mosby, Inc.

Box 26-1.Symptoms of hypokalemia.


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Effect of hypokalemia

Cardiovaskular:- ECG changes/dysrhythmias

- Myocardial dysfunction

Neuromuscular:

- Skeletal muscle weakness

- Tetany

- Rhabdomyolisis

- Ileus

Renal:

- Polyuria (nephrogenic DI)

- Increased ammonia production

- Increased bicarbonate reabsorption

Hormonal:

- Decreased insulin secretion- Decreased 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 and Company, 1986.


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Due to Delayed ventricular repolarization: T wave flattening and inversion

Prominent U wave

ST segment depression

Increased P wave amplitude

Prolongation of the PR interval


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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 20-30mEq via centralvenous catheter (sequential infusion: 10mEq in 100

mL fluid over 20 mins, infusion rate can be slowedafter symptoms resolve)

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

K


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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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Lund GJ. Fluid and electrolyte. The Harriet Lane Handbook. 8thEd, 2009

K+deficit (mEq/L) =

fluid deficit (L) x proportion from ICF x K+

concentration (mEq/L) in ICF


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Monitoring

Continuous ECG monitoring is necessa-

ry (during parenteral administration of

high concentration of KCl)

Serum K levels must be monitored atfrequent interval during repletion (every

1-2 hrs during initial replacement)


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Blood-Gas Analysis


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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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ECG change:

Peaked T-wave Widening of QRS complex PR prolongation Loss of P wave Loss of R wave amplitude ST depression (occationally elevation) Sine wave Ventricular fibrillation and asystole


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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 bodyinvolved in the regulation of extracellular

volume

Abnormalities in circulating Na primarily

effect neuronal & neuromuscularfunction.


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Overview of Sodium Balance


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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 and

hypervolemic conditions The presence of a nonsodium solute: glucose and

mannitol (characterized by an elevated serumosmolality

Pseudohyponatremia: occurs in the presence of

severe 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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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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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 muchNaCl 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/kg/hour, thisamount 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 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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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 fromwater loss only, then total body osmoles areunchanged. 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 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 prefer

administration 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

T (3)


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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)

M it l l l


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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, Course Text, 3rdedition, Society of Critical Care Medicine

Lange Clinical Anesthesiology, 3rd edition, LangeMedical Books/McGraw-Hill Medical Publishing

Division Physiologic and Pharmacologic Bases of Anesthesia,

2ndedition, Williams and Wilkins

Textbook of Critical Care, 3rdedition, W.B. SaundersCompany

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