VIN_Metabolic_Electrolyte emergencies

Page 1

1 sur 2

Front Page : Library : WVC 2003 : Specialty : Critical Care : Metabolic Emergencies Back to Critical Care Back to Table of Contents

Metabolic and Electrolyte Emergencies WESTERN VETERINARY CONFERENCE 2003 Michael Schaer, DVM University of Florida, College of Veterinary Medicine Gainesville, FL, USA 18272513

OBJECTIVES Describe clinical features of selected metabolic emergencies. Provide treatment principles for select metabolic emergencies.

KEY POINTS Hypokalemia: The general causes include: dilutional, alkalosis, gastrointestinal loss, and renal loss. Neuromuscular signs are seldom present until serum K+ has decreased to 2.5 mEq/L or less. Hyperkalemia: becomes a life-threatening disorder when myocardial toxicity occurs at serum levels in excess of 7.5 mEq/L. Hypocalcemia: The main causes include hypoparathyroidism, hypoproteinemia, vitamin D deficiency, hyperphosphatemia, malabsorption, acute pancreatitis, and chronic renal disease. Hypercalcemia: The more common causes include pseudohyperparathyroidism, primary hyperparathyroidism, and the newer cholecalciferol-containing rodenticides. Metabolic Acidosis: Metabolic acidosis can occur from two basic pathophysiologic processes: (1) accumulation of fixed acid and (2) loss of alkali. The diagnosis is characterized by a known or suspected predisposing cause, low pH, low total CO2 , and a decreased PCO2. Hypoglycemia: The brain is the main organ that is adversely effected by this metabolic abnormality. The signs include: bizarre behavioral changes, palpitations, hunger, anxiety, dementia, weakness, seizures, coma, and hypothermia. Hypo- and Hypernatremia: Hyponatremia can be caused by those conditions causing water excess (more common) or salt loss. Hypernatremia is caused by water loss (most common) or salt gain. The clinical neurological effects of each are brought about by the osmotic transfer of water in and out of the brain parenchyma.

OVERVIEW

AND

ADDITIONAL DETAIL

The treatment of severe or acute hypokalemia with or without metabolic alkalosis requires the administration of intravenous potassium chloride solution. The use of intravenous 0.9% saline solution supplemented with potassium chloride is essential for treating marked metabolic alkalosisassociated hypokalemia (< 2.5 mEq/L). When potassium chloride is given intravenously, the rate is more critical than the total amount administered. The rate should not exceed 0.5 mEq/Kg/hr. The total 24-hour needs will range from 3-10 mEq/kg body weight. The recommended treatments of hyperkalemia include: 1) intravenous sodium bicarbonate given at 1-2 mEq/kg by IV push, 2) dextrose and insulin infusions where regular crystalline insulin is administered at a recommended dose of ½ unit per kilogram along with 2 grams of dextrose per every 1 unit of insulin, and 3) calcium gluconate 10% given intravenously at 1 ml/kg. Symptomatic acute hypocalcemia is a medical emergency that requires immediate administration of 10% calcium gluconate solution. A safe dose for the small animal is 1.0-1.5 ml/kg given slowly IV over a 20-30 minute period. Heart rate should be monitored periodically. Maintenance treatment for hypocalcemia is provided with 10% calcium gluconate solution at a dosage of 5-10 ml/kg given slowly IV over a 24-hour period or 2 ml/kg IV over a 6-8 hour period and to be repeated as necessary. The four basic initial treatment objectives for treating hypercalcemia include: 1) correct


2 sur 2

dehydration, 2) promote calciuresis, 3) inhibit accelerated bone resorption, and 4) treat the underlying disorder. The most important therapeutic measure is to rehydrate the patient with intravenous 0.9% sodium chloride solution. Glucocorticoids are particularly beneficial when treating hypercalcemia of malignancy and cholecalciferol rodenticide intoxication. Surgical excision of the parathyroid tumor is the preferred treatment for primary hyperparathyroidism. The treatment principles for metabolic acidosis entail: (1) treat the underlying cause, (2) administer sodium bicarbonate at pH levels < 7.1, and (3) repeat blood acid-base measurements for monitoring further needs. The amount of HCO3 needed = 0.6 x B.W.(kg) x (desired TCO2 measured TCO2 ). The 0.6 value refers to the HCO3 distribution in both the extra- and intracellular spaces. Only 1/2 of the calculated amount should be given during the first 3-4 hours of therapy; the remaining to be titrated according to need. Treating hypoglycemia requires the immediate administration of glucose intravenously using 50% Dextrose at a dosage of 1 ml/kg (0.5 gm/kg) IV push. Glucagon Injectable can also be administered to counteract insulin overdose at a dosage of 0.03 mg/kg IV, SQ, or IM. If the patient is conscious, syrups (Karo) containing 1 gm of carbohydrate per 1 ml can be given orally at a dose of 0.5 to 1 ml/kg. Depending on the cause, the treatment for hyponatremia calls for either water restriction or sodium administration. That for hypernatremia entails hypotonic fluid administration. In chronic conditions, corrections must be made slowly over 48-72 hours.

SUMMARY The treatment of severe or acute hypokalemia with or without metabolic alkalosis requires the administration of intravenous potassium chloride solution. The most dramatic effect of hyperkalemia occurs at the neuromuscular cell membrane causing muscular weakness and disturbed cardiac excitation and conduction. Symptomatic acute hypocalcemia is a medical emergency that requires immediate administration of 10% calcium gluconate solution. The most important therapeutic measure for correcting hypercalcemia is to rehydrate the patient with intravenous 0.9% sodium chloride solution. Treatment of hypoglycemia requires the immediate administration of glucose intravenously using 50% Dextrose at a dosage of 1 ml/kg (0.5 gm/kg) IV push. References 1. Rose DB (ed). Clinical Physiology of Acid-Base and Electrolyte Disorders. 5 th ed. New York: McGraw-Hill, 2001.

SPEAKER INFORMATION (click the speaker's name to view other papers and abstracts submitted by this speaker) Michael Schaer, DVM Professor of Medicine and Associate Chief of Staff University of Florida Gainesville, FL

Front Page : Library : WVC 2003 : Specialty : Critical Care : Metabolic Emergencies 800.700.4636 | VINGRAM@vin.com | 530.756.4881 | Fax: 530.756.6035 777 West Covell Blvd, Davis, CA 95616 Copyright 1991- 2010, Veterinary Information Network, Inc.


Turn static files into dynamic content formats.

Create a flipbook
Issuu converts static files into: digital portfolios, online yearbooks, online catalogs, digital photo albums and more. Sign up and create your flipbook.