Electrolyte and endocrine emergencies

Life threatening emergencies, diagnose and treatment Anesthesiology, Intensive Care and Pain Management Department Faculty of Medicine Hasanuddin University

Electrolyte Emergencies

Hyponatremia
Decreased serum sodium Na+ <135 mEq/L

Hyponatremia
Causes Loss of salt and water
Diuretics Addisons disease Osmotic diuresis (DKA) Vomiting Diarrhea Diaphoresis

Hyponatremia

Causes Increase in body water (dilutional hyponatremia)

Excess water intake (water intoxication) CHF Renal failure Cirrhosis

Hyponatremia
Signs/Symptoms Lethargy, apathy secondary to cerebral edema Headache Muscle twitching, cramps Seizures
Na+ < 110 mEq/L

Hyponatremia
Treatment NS infused at a rate to restore normal sodium over 48 hours

Hypernatremia
Elevated serum sodium Na+ >150 mEq/L

Hypernatremia
Causes Pure water loss
Diabetes insipidus

Pure solute gain

NaHCO3 administration

Hypernatremia
Causes Water loss > Solute loss
Diarrhea Vomiting Sweating Osmotic diuresis

Hypernatremia

Signs/Symptoms Irritability, restlessness Coma Intracranial hemorrhage Blood sludging - thrombosis Seizures Thirst, dry mucus membranes, poor skin turgor

Hypernatremia
Treatment Infusion of D5W (free water) to correct water deficit over 48 hours

Hypokalemia
Decreased serum potassium K+ < 3.5 mEq/L

Hypokalemia
Causes Gastrointestinal losses
Diarrhea Vomiting NG suction

Urinary losses Diuretics

Osmotic diuresis

Hypokalemia
Causes Intracellular shifts
Alkalosis agents Theophylline

Inadequate intake

Hypokalemia
Signs/Symptoms Weakness, hyporeflexia, paresthesias Decreased GI motility Nausea, vomiting Increased sensitivity to digitalis

Hypokalemia
Signs/Symptoms EKG changes
Flat to inverted T waves U waves ST segment depression

Cardiac arrhythmias Ventricular ectopy

V-Fib

Hypokalemia
Treatment Correct underlying cause 10 mEq KCL IV over 1 hour, repeated until serum K+ > 3.5 mEq/L

Hyperkalemia
Elevated serum potassium K+ > 5.5 mEq/L K+ > 6 mEq/L - Emergency K+ > 7 mEq/L - Life Threat

Hyperkalemia
Causes Decreased excretion
Renal failure Addisons disease - blockers Hyperglycemia Acidosis

Hyperkalemia
Causes Increased intake
Crush injury, burns, sepsis Massive hemolysis Blood transfusion High-dose penicillin Increased oral intake

Hyperkalemia
Signs/Symptoms
Muscle weakness Numbness, tingling EKG changes

Tall, peaked T waves Broadening of QRS; decreased P wave size Sine wave leading to V-Fib then asystole

Hyperkalemia
Treatment
Calcium - 0.5 - 1.0g Antagonizes cardiac toxicity NaHCO3 - 50 mEq
Drives K+ into cells

D50W (25g)/insulin (10 units regular)

Drives K+ into cells

Hypocalcemia
Decreased serum calcium Ca2+ < 8.5 mg/100ml

Hypocalcemia
Causes Hypoparathyroidism Vitamin D deficiency Decreased dietary intake Alkalosis Massive blood transfusion
Citrate toxicity

Hypocalcemia
Signs/Symptoms Paresthesias Hyperreflexia, carpopedal spasm, tetany Seizures Trousseaus sign:
Carpopedal spasm following BP cuff compression of arm

Hypocalcemia
Signs/Symptoms Chvosteks sign
Contraction of facial muscles when face is tapped at angle of

jaw
Laryngospasms Prolonged QT interval Increased ventricular irritability

Hypocalcemia
Management Calcium chloride
1g over 10 - 20 minutes

Overly rapid administration of calcium can cause

bradycardia, hypotension, and cardiac arrest

Hypercalcemia
Increased serum calcium Ca2+ > 10.5 mg/100ml

Hypercalcemia
Causes Malignancies
Skeletal, breast, lungs

Hyperparathyroidism Vitamin D toxicity Addisons disease Milk/alkali syndrome

Hypercalcemia
Signs/Symptoms Apathy, fatigue, depression, coma Muscle weakness Hypertension Anorexia, nausea, abdominal pain

Hypercalcemia
Signs/Symptoms Kidney stones Short QT interval, heart block, cardiac arrest Bones, Stones, Hypertones, Abdominal moans

Hypercalcemia
Treatment 1 - 2 liters NS over 1 hour
Decrease Ca2+ reabsorption

Furosemide 40 mg IV Inhibits Ca2+ reabsorption Calcitonin Directly lowers Ca2+

Endocrine Emergencies

Endocrine Emergencies
Diabetic Ketoacidosis Thyroid Storm Adrenal Insufficiency

Diabetic Ketoacidosis (DKA)

Diabetic Ketoacidosis Physiology

Hyperglycemia
Increased hepatic production of glucose. Diminished glucose uptake by peripheral tissues Insulinopenia/hyperglucagonemia

Ketoacidemia Fluid and Electrolyte Depletion

Diabetic Ketoacidosis Physiology

Hyperglycemia Ketoacidemia The ketoacid is acetoacetic acid. Byproduct is acetone. The non-keto acid is beta-hydroxybutyric acid Increased lipolysis and hepatic ketogenesis Reduced ketolysis by insulin-deficient peripheral tissues Fluid and Electrolyte Depletion

Diabetic Ketoacidosis Physiology

Hyperglycemia Ketoacidemia Fluid and Electrolyte Depletion Osmotic diuresis and dehydration due to hyperglycemia On average, water deficit is about 5L, sodium 500mmol,

potassium 400mmol, chloride 400mmol.

Diabetic Ketoacidosis General Considerations

Initial presentation of Type 1 Diabetes (Can also occur in type 2

diabetics)

Increased insulin requirements in Type 1 diabetics (Infection, trauma,

myocaridial infarction, surgery)

Mortality 5% in patients under 40. Up to 20% in elderly. Estimates of 5-8 episodes per 1000 at risk diabetics annually. One of the more common serious complications of insulin pump

users occurring 1 per 80 months of treatment. Typically due to unrecognized pump failure.

Charfen MA, Fernandez-FrackeltonM. Diabetic Ketoacidosis. Emerg Med Clin North Am 2005;23:609-628

Diabetic Ketoacidosis
Essentials of Diagnosis Acidosis with blood pH <7.3 Serum bicarbonate < 15mEq/L Serum positive for ketones Elevated anion gap
Variable, may occur without gap.

Hyperglycemia > 250 No correlation between severity of hyperglycemia and severity of ketoacidosis
Gamblin GT, Ashburn RW, Kemp DG et al. Diabetic ketoacidosis presenting with a normal anion gap. Am J Med 1986;80:756-760 Brandt KR, Miles JM. Relationship between severity of hyperglycemia a nd metabolic acidosis in diabetic ketoacidosis. Mayo Clin Proc 1988;63:1071-1074

Diabetic Ketoacidosis Clinical Findings

Symptoms: Early: polyuria, polydipsia, fatigue, N/V Late: stupor Coma Signs: Rapid, Deep Breathing Fruity breath odor of acetone Tachycardia, Hypotension, mild hypothermia Abdominal Pain and Tenderness

Charfen MA, Fernandez-FrackeltonM. Diabetic Ketoacidosis. Emerg Med Clin North Am 2005;23:609-628

Diabetic Ketoacidosis Laboratory Findings

Glycosuria 4+, Ketonuria Hyperglycemia, ketonemia, low arterial blood pH, low plasma bicarb. Elevated serum potassium (despite total body potassium depletion) Elevated serum amylase (not specific for pancreatitis in this setting,

use lipase)

Leukocytosis If hyperthermic, likely due to infection since pts with DKA are

hypothermic if uninfected.

Diabetic Ketoacidosis Treatment

Insulin Replacement
Regular Insulin IV bolus 0.15 units/kg to prime insulin receptors Regular Insulin gtt at 0.1 units/kg/hr

Fluid Replacement
Typical deficit is 4-5L. Initially, NS 1L/hr x 2hrs. Then 300-400mL/hr. Switch to 1/2NS if serum NA >150.

Add D5 p glucose falls below 250 to maintain serum glucose 250-300mg/dL to prevent hypoglycemia and cerebral edema. Intensive insulin therapy is continued until ketoacidosis is corrected.
Sodium Bicarbonate
Clinical benefit has not been demonstrated. Use to correct pH to greater than 7.1.

Potassium
10-30mEq/hr replacement to be started during second or third hour of treatment

Phosphate
Replete hypophosphatemia of <1.0mg/dL. Replete slowly (3-4mmol/hr) to aviod hypocalcemic tetany.

Treatment of Associated Infection

Antibiotics as indicated Cholecystitis and pyelonephritis may be particularly severe in these patients

Diabetic Ketoacidosis Treatment

Insulin Replacement
Regular Insulin IV bolus 0.15 units/kg to prime insulin receptors Regular Insulin gtt at 0.1 units/kg/hr

Fluid Replacement
Typical deficit is 4-5L. Initially, NS 1L/hr x 2hrs. Then 300-400mL/hr. Switch to 1/2NS if serum NA >150.

Add D5 p glucose falls below 250 to maintain serum glucose 250-300mg/dL to prevent hypoglycemia and cerebral edema. Intensive insulin therapy is continued until ketoacidosis is corrected.
Sodium Bicarbonate
Clinical benefit has not been demonstrated. Use to correct pH to greater than 7.1.

Potassium
10-30mEq/hr replacement to be started during second or third hour of treatment

Phosphate
Replete hypophosphatemia of <1.0mg/dL. Replete slowly (3-4mmol/hr) to aviod hypocalcemic tetany.

Treatment of Associated Infection

Antibiotics as indicated Cholecystitis and pyelonephritis may be particularly severe in these patients

Diabetic Ketoacidosis Treatment

Insulin Replacement
Regular Insulin IV bolus 0.15 units/kg to prime insulin receptors Regular Insulin gtt at 0.1 units/kg/hr

Fluid Replacement
Typical deficit is 4-5L. Initially, NS 1L/hr x 2hrs. Then 300-400mL/hr. Switch to 1/2NS if serum NA >150.

Add D5 p glucose falls below 250 to maintain serum glucose 250-300mg/dL to prevent hypoglycemia and cerebral edema. Intensive insulin therapy is continued until ketoacidosis is corrected.
Sodium Bicarbonate
Clinical benefit has not been demonstrated. Use to correct pH to greater than 7.1.

Potassium
10-30mEq/hr replacement to be started during second or third hour of treatment

Phosphate
Replete hypophosphatemia of <1.0mg/dL. Replete slowly (3-4mmol/hr) to aviod hypocalcemic tetany.

Treatment of Associated Infection

Antibiotics as indicated Cholecystitis and pyelonephritis may be particularly severe in these patients

Diabetic Ketoacidosis Treatment

Insulin Replacement
Regular Insulin IV bolus 0.15 units/kg to prime insulin receptors Regular Insulin gtt at 0.1 units/kg/hr

Fluid Replacement
Typical deficit is 4-5L. Initially, NS 1L/hr x 2hrs. Then 300-400mL/hr. Switch to 1/2NS if serum NA >150.

Add D5 p glucose falls below 250 to maintain serum glucose 250-300mg/dL to prevent hypoglycemia and cerebral edema. Intensive insulin therapy is continued until ketoacidosis is corrected.
Sodium Bicarbonate
Clinical benefit has not been demonstrated. Use to correct pH to greater than 7.1.

Potassium
10-30mEq/hr replacement to be started during second or third hour of treatment

Phosphate
Replete hypophosphatemia of <1.0mg/dL. Replete slowly (3-4mmol/hr) to aviod hypocalcemic tetany.

Treatment of Associated Infection

Antibiotics as indicated Cholecystitis and pyelonephritis may be particularly severe in these patients

Diabetic Ketoacidosis Treatment

Insulin Replacement
Regular Insulin IV bolus 0.15 units/kg to prime insulin receptors Regular Insulin gtt at 0.1 units/kg/hr

Fluid Replacement
Typical deficit is 4-5L. Initially, NS 1L/hr x 2hrs. Then 300-400mL/hr. Switch to 1/2NS if serum NA >150.

Add D5 p glucose falls below 250 to maintain serum glucose 250-300mg/dL to prevent hypoglycemia and cerebral edema. Intensive insulin therapy is continued until ketoacidosis is corrected.
Sodium Bicarbonate
Clinical benefit has not been demonstrated. Use to correct pH to greater than 7.1.

Potassium
10-30mEq/hr replacement to be started during second or third hour of treatment

Phosphate
Replete hypophosphatemia of <1.0mg/dL. Replete slowly (3-4mmol/hr) to aviod hypocalcemic tetany.

Treatment of Associated Infection

Antibiotics as indicated Cholecystitis and pyelonephritis may be particularly severe in these patients

Diabetic Ketoacidosis Treatment

Insulin Replacement
Regular Insulin IV bolus 0.15 units/kg to prime insulin receptors Regular Insulin gtt at 0.1 units/kg/hr

Fluid Replacement
Typical deficit is 4-5L. Initially, NS 1L/hr x 2hrs. Then 300-400mL/hr. Switch to 1/2NS if serum NA >150.

Add D5 p glucose falls below 250 to maintain serum glucose 250-300mg/dL to prevent hypoglycemia and cerebral edema. Intensive insulin therapy is continued until ketoacidosis is corrected.
Sodium Bicarbonate
Clinical benefit has not been demonstrated. Use to correct pH to greater than 7.1.

Potassium
10-30mEq/hr replacement to be started during second or third hour of treatment

Phosphate
Replete hypophosphatemia of <1.0mg/dL. Replete slowly (3-4mmol/hr) to aviod hypocalcemic tetany.

Treatment of Associated Infection

Antibiotics as indicated Cholecystitis and pyelonephritis may be particularly severe in these patients

DKA vs HHS
Diabetic Ketoacidosis Hyperglycemic Hyperosmolar

State
Hyperglycemia >250 mg/dL Acidosis; pH<7.3 Serum bicarb <15 Serum Ketones Hyperglycemia >600mg/dL Serum Osmolality >310 No Acidosis; pH>7.3 Serum Bicarb >15 Normal anion gap <14

Thyroid Storm

Thyroid Storm
Extreme form of thyrotoxicosis. Occurs with stressful illness, thyroid surgery. Manifested by marked delirium, severe tachycardia, vomiting,

diarrhea, dehydration, and very high fever.

Mortality rate is high.

Franklyn JA. The management of hyperthyroidism. N Engl J Med 1994:330:1731-1738

Thyroid Storm Treatment

Beta-Receptor Antagonists Propanolol IV (1mg q 5min until desired effect) Propanolol PO (20-120mg q 6hrs until antithyroid drug therapy

effective

Antithyroid Drugs Methimazole 10-30mg daily Propylthiouracil 75-100mg tid Iodine Iodide (as Lugols solution 4gtts q 12hrs)
Migneco A, Ojeti V, Testa A, et al. Management of thyrotoxic crisis. Eur Rev Med Pharmacol Sci 2005;9:69-74

Acute Adrenal Insufficiency

Acute Adrenal Insufficiency General Presentations

Following Stress (trauma, surgery, infection, or prolonged fasting)

in patient with latent insufficiency. patient with chronic insufficiency

Following sudden withdrawal of adrenocortical hormone in a Following bilateral adrenalectomy or a functioning adrenal tumor

that had suppressed the other adrenal

Following sudden destruction of the pituitary gland (pituitary

necrosis) or when thyroid hormone is given to a pt with hypoadrenalism

Following injury to both adrenals by trauma, hemorrhage,

anticoagulant therapy, thrombosis, infection, or metastatic carcinoma.

Cooper MS, Stewart PM. Corticosteroid insufficiency in acutely ill patients. N Engl J Med 2003;348:727-734

Adrenal Insufficiency Diagnosis

Weakness, abdominal pain, fever, confusion, nausea, vomiting,

diarrhea Hypotension, dehydration, hyperpigmentation Hyperkalemia, Hyponatremia, Azotemia Cosyntropin (ACTH) test

Note: More than 90% of serum cortisol is protein bound. Pts

with serum albumin <2.5g/dL have low serum total cortisol levels but normal serum free cortisol levels and normal adrenal function. Serum FREE cortisol levels should be used in critically ill patients.

Hamrahian AH, Oseni TS, Arafah BM. Measurements of serum free cortisol in critically ill patients. N Engl J Med 2004;350:1629

Adrenal Insufficiency Diagnosis

Rapid ACTH Stimulation Test Not influenced by diurnal variations in cortisol secretion. Baseline cortisol sample. ACTH 250mcg. Post-ACTH plasma cortisol at 30min and 60min p injection. Baseline above 34 is normal and less than 15 is evidence of insufficiency. When between the two, the incriment increase with ACTH should be greater than 9mcg/dL.

Adrenal Insufficiency Treatment

In patients with high suspicion of insufficiency, dexamethasone (2mg) can be

started immediately. Does not interfere with ACTH assay.

After ACTH test is completed, Hydrocortisone can be started at 50mg IV

q6hrs until test results return

If test normal, hydrocortisone can be abruptly discontinued without a taper. If test reveals adrenal insufficiency, continue hydrocortisone 50mg IV q6hrs

until no longer in a stressed condition.

Taper to 20mg IV q6hrs or oral equivalent.

Cooper MS, Stewart PM. Corticosteroid insufficiency in acutely ill patients. N Engl J Med 2003;348:727-734