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Alcoholic Ketoacidosis
Article Last Updated: May 26, 2006
AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Irina Robinson, MD, Fellow, Department of Internal Medicine, Division of Endocrinology and Metabolism, University of New Mexico Health Sciences Center
Irina Robinson is a member of the following medical societies: American Association of Clinical Endocrinologists and American College of Physicians
Coauthor(s):
Sofya ;
David S Schade, MD, Chief, Division of Endocrinology and Metabolism, Department of Internal Medicine, Professor, University of New Mexico School of Medicine and Health Sciences Center
Editors: Ghassem Pourmotabbed, MD †, Division of Endocrinology and Metabolism, Former Associate Professor, Department of Internal Medicine, University of Tennessee School of Medicine and Health Science Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS, Affiliate Research Professor, School of Computational Sciences; Principal, Bioinformatics and Computational Biology Program, C/A Informatics, LLC; Mark Cooper, MD, Head, Vascular Division, Baker Medical Research Institute; Professor of Medicine, Monash University; George T Griffing, MD, Professor of Medicine, Director of General Internal Medicine, St Louis University
Author and Editor Disclosure
Synonyms and related keywords:
alcoholic ketoacidosis, AKA, binge drinking, alcohol binge, ethanol binge, alcoholic acidotic coma, metabolic acidosis, elevated anion gap, chronic alcohol abuse, alcohol abuse, ethanol abuse, chronic ethanol abuse, alcoholism, alcoholic, gastritis, alcoholic gastritis, pancreatitis, alcohol withdrawal, gastrointestinal bleeding, GI bleeding, metabolic acidosis
Background
In 1940, Dillon et al first described alcoholic ketoacidosis (AKA) as a distinct syndrome. Metabolic acidosis with an elevated anion gap and a normal or low glucose concentration characterize AKA. The disorder often occurs in chronically malnourished ethanol abusers after a drinking binge that culminates in severe vomiting with resulting dehydration, acute starvation, and ketoacidosis. Some patients also have withdrawal symptoms, and others have acute illnesses such as gastritis, pancreatitis, or infections.
Pathophysiology
The pathogenesis of AKA is complex. Although the general physiological factors and mechanisms leading to AKA are understood, the precise factors have not been fully defined. The following are the 3 main predisposing events: - Delay and decrease in insulin and excess in glucagon secretion induced by starvation
- Elevated ratio of the reduced form of nicotinamide adenine dinucleotide to nicotinamide adenine dinucleotide secondary to alcohol metabolism
- Volume depletion resulting from vomiting and poor oral intake of fluids
These inciting events result in the rapid accumulation of the metabolic acids hydroxybutyric acid and acetoacetic acid. Metabolism of ethanol The metabolism of alcohol itself is a probable contributor to the ketotic state. Alcohol dehydrogenase metabolizes alcohol to acetaldehyde in the cytoplasm of hepatocyte mitochondria. Acetaldehyde is metabolized further to acetic acid by aldehyde dehydrogenase. Because both alcohol dehydrogenase and aldehyde dehydrogenase require nicotinamide adenine dinucleotide as a cofactor, nicotinamide adenine dinucleotide is consumed and the reduced form of nicotinamide adenine dinucleotide is generated. The resulting increase in the ratio of the reduced form of nicotinamide adenine dinucleotide to nicotinamide adenine dinucleotide inhibits hepatic gluconeogenesis and elevates the ratio of hydroxybutyric acid to acetoacetic acid. Acetic acid is converted by coenzyme A to acetyl-coenzyme A, which, in turn, is used for the conversion to adipose tissue, in the formation of ketone bodies, and in the citric acid cycle. Low insulin levels and increased glucagon, catecholamine, growth hormone, and cortisol levels inhibit the hepatic metabolism of acetyl-coenzyme A by the citric acid cycle and triglyceride synthesis, thereby further enhancing ketogenesis. Diminished pyruvate dehydrogenase activity as a result of decreased nicotinamide adenine dinucleotide availability and/or magnesium or thiamine deficiency inhibits utilization of pyruvate in the citric acid cycle. Dehydration All patients with severe AKA are dehydrated. Several mechanisms are responsible for dehydration, including protracted vomiting, decreased fluid intake, and inhibition of antidiuretic hormone secretion by ethanol. Volume depletion is a strong stimulus to the sympathetic nervous system and is responsible for elevated cortisol and growth hormone levels. Dehydration and volume constriction directly decrease the ability of the kidneys to excrete ketoacids. Profound dehydration can culminate in circulatory collapse, lactic acidosis, or both. Fasting Energy (caloric) restriction secondary to abdominal pain, nausea, or vomiting usually occurs prior to the onset of AKA. Under conditions of starvation, the liver increases production of ketones from fatty acids to supply the brain, kidney, and other peripheral tissues with a metabolic fuel that can replace glucose. Increased ketogenesis secondary to utilization of hepatic glycogen stores with subsequently increased lipolysis and a decreased insulin-to-glucagon ratio causes starvation ketosis. Triglycerides stored in adipose tissue undergo lipolysis and are released into the circulation as free fatty acids bound ionically to albumin. Free fatty acids are removed by the liver, where they primarily undergo oxidation to hydroxybutyric acid and acetoacetate and subsequently are re-esterified to triglyceride. Decreased insulin and elevated glucagon, cortisol, catecholamine, and growth hormone levels can all increase the rate of ketogenesis. Ketogenesis Increased availability of free fatty acids, which provide the major substrate for ketone body formation, stimulates ketogenesis. Low insulin levels and elevated glucagon, catecholamine, growth hormone, and cortisol levels provide a hormonal milieu that inhibits hepatic metabolism of acetyl-coenzyme A via the citric acid cycle into triglyceride synthesis and that stimulates ketogenesis. In AKA, the increased ratio of the reduced form of nicotinamide adenine dinucleotide to nicotinamide adenine dinucleotide increases the proportion of beta-hydroxybutyrate relative to acetoacetate. Ketone body clearance is decreased by 2 major mechanisms, as follows: - The low insulin level characteristic of AKA prevents ketone body utilization by insulin-sensitive tissues.
- Dehydration impairs excretion of ketones by the kidneys.
Elevated cortisol levels can increase fatty acid mobilization and ketogenesis. Growth hormone can enhance precursor fatty acid release and ketogenesis during insulin deficiency. Catecholamines, particularly epinephrine, increase fatty acid release and enhance the rate of hepatic ketogenesis. Insulin release from the pancreatic beta cells might be abnormally sensitive to catecholamine inhibition. The pivotal variable appears to be a relative deficiency of insulin. Individuals with higher insulin levels are more likely to present with the syndrome of alcohol-induced hypoglycemia without ketoacidosis. The major factors separating AKA from alcohol-induced hypoglycemia are dehydration and starvation.
Frequency
United States
Dillon et al first described alcohol ketoacidosis in 1940. More than 100 patients with AKA have now been described in English literature, although many cases have likely remained undetected and unreported.
Mortality/Morbidity
- Mortality and morbidity are rare in uncomplicated AKA
- Medical complications are secondary to concomitant medical conditions such as gastrointestinal bleeding and alcohol withdrawal.
- Complications occur in less than 20% of patients. Markedly elevated beta-hydroxybutyric acid could lead to death.
Race
AKA has no race predilection.
Sex
AKA has no sex predilection.
Age
AKA can occur in adults of any age.
History
- Patients almost always are alcoholics who engage in a period of very heavy drinking preceding ketoacidosis.
- Abrupt cessation of alcohol consumption is usually present one or more days prior to presentation because of a physical complaint, such as abdominal pain, often resulting from alcohol gastritis or pancreatitis.
- Alcohol gastritis or pancreatitis leads to the inability to tolerate food, nausea, and/or vomiting.
- Poor energy intake is almost always present.
- Most patients do not have concomitant diabetes mellitus.
- If the plasma glucose level is elevated above 300 mg/dL upon presentation, consider diabetic ketoacidosis.
- Recurrence of AKA is reported to be common.
Physical
- Physical examination might reveal a multitude of pathologic conditions.
- Typical characteristics of an alcohol abuser may be present: rhinophyma, tremulousness, hepatosplenomegaly, peripheral neuropathy, gynecomastia, testicular atrophy, and palmar erythema. The patient might be tachycardic, tachypneic, profoundly orthostatic, or frankly hypotensive as a result of dehydration from the decreased oral intake, diaphoresis, and vomiting.
- The patient's breath might carry the fruity odor of ketosis.
- A tachypnea in the form of the Kussmaul respiration varieties is usually present when the pH is less than 7.2.
- Hypothermia is common in AKA; a fever can be a sign of an underlying infectious process.
- Symptoms of abdominal tenderness consistent with a diagnosis of alcoholic liver disease, pancreatitis, gastritis, or peptic ulcer disease may be revealed during abdominal examination and may mimic an abdominal emergency.
- Hemoccult-positive stools might be present.
- Mental status might be normal or slightly impaired as a result of derangements in electrolytes or vital signs.
- Severe obtundation, fixed dilated pupils, and, finally, death might occur.
Causes
- The alcoholic patient who has been on a drinking binge suddenly decreases energy intake because of abdominal pain, nausea, or vomiting.
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- AKA is the result of the accumulation of the ketoacids, hydroxybutyric acid, and acetoacetic acid because of the complex interaction caused by alcohol cessation, decreased energy intake, volume depletion, and the metabolic effects of hormonal imbalance.
Diabetic Ketoacidosis
Lactic Acidosis
Metabolic Acidosis
Uremia
Other Problems to be Considered
Ethylene glycol intoxication
Methanol intoxication
Salicylate intoxication
The AKA differential diagnosis includes all metabolic conditions that can cause an increased anion gap metabolic acidosis in a person who abuses ethanol. All patients with AKA have ketonuria and, usually, ketonemia. A normal, or even high, blood pH does not exclude the diagnosis because patients with AKA might have a concomitant metabolic alkalosis resulting from vomiting or a compensatory respiratory alkalosis. However, a compensatory respiratory alkalosis alone cannot correct the pH to normal because the drive for compensation decreases as the pH approaches normality. This implies that a significant noncompensatory metabolic alkalosis also must be present if the pH is near the normal range.
Lab Studies
- Usual laboratory findings include the following:
- The arterial pH is less than 7.3, and the serum bicarbonate level is less than 15 mEq/L.
- The calculated anion gap is greater than 14 mmol/L.
- The partial pressure of carbon dioxide is decreased secondary to compensatory hyperventilation.
- In some patients, severe vomiting results in chloride depletion and metabolic alkalosis, with consequently higher pH values than in patients with diabetic ketoacidosis.
- In AKA, the average ratio of hydroxybutyric acid to acetoacetic acid (5:1) tends to be higher than in diabetic ketoacidosis (3:1).
- Because the nitroprusside reaction measures acetoacetate but not beta-hydroxybutyrate, serum ketones estimated by this method might only be weakly positive or even negative.
- Use reagent strips that only measure beta-hydroxybutyrate.
- The hallmark of AKA is ketoacidosis without marked hyperglycemia.
- Serum glucose levels above 300 mg/dL usually indicates diabetic ketoacidosis, unless AKA develops in diabetic patients.
- Free fatty acid levels are usually markedly elevated, which is secondary to increased lipolysis.
- Insulin levels are low, glucagon levels are high.
- Cortisol and catecholamine levels are markedly elevated, and modest elevations of growth hormone are common.
- Because many of these patients are alcoholics and might have intercurrent or chronic disease, a variety of other laboratory parameters can be present, including elevated liver function test results, an increased amylase level, a decreased hemoglobin/hematocrit value, a decreased WBC and thrombocyte count, macrocytosis (MCV 100-110 fL), and an abnormal BUN-to-creatinine ratio.
- Hyponatremia and hypokalemia are common laboratory findings. Vomiting and extracellular volume depletion might cause hyponatremia. Hypokalemia is often associated with hypomagnesemia.
- Phosphate levels might be low, normal, or elevated.
- An elevated lactate level (usually does not exceed 3 mmol/L) might be the result of dehydration, seizure, or the direct metabolic effect of alcohol.
- Hyperuricemia is commonly observed, due to decreased renal perfusion, tissue catabolism, competitive inhibition of renal uric acid excretion by ketone bodies, and direct ethanol enhancement of adenine nucleotide degradation.
- True hypocalcemia might be present, associated with hypomagnesemia. Concomitant pancreatitis also might contribute to true hypocalcemia. Factitious hypocalcemia might result from a markedly decreased serum albumin level following prolonged malnutrition with alcoholism.
Imaging Studies
- Chest radiography is routinely preformed.
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- Perform abdominal radiography to exclude concurrent medical or surgical conditions such as perforated viscus, small bowel obstruction, or pneumonia.
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- The presence of pancreatic calcification suggests chronic and acute pancreatitis.
Medical Care
- Treatment of AKA is directed toward reversing the 3 major pathophysiologic causes of the syndrome, which are (1) extracellular fluid volume depletion, (2) glycogen depletion, and (3) an elevated ratio of the reduced form of nicotinamide adenine dinucleotide to nicotinamide adenine dinucleotide.
- Extracellular volume repletion with normal saline inhibits the release of counterregulatory hormones and facilitates urinary ketone excretion. The degree of weight loss is a good indicator of the extent of dehydration and the quantity of fluid required. Normal saline at about 20 ml/kg over 30-60 minutes is required in patients with severe hypotension or hypovolemic shock. After restoration of blood pressure and renal perfusion (urine flow is 50-100 mL/h) the fluid choice and rate depends on the state of hydration, serum electrolytes, and urine output. The rate is decreased to 5-10 mL/kg/h until resolution of ketoacidosis (usually within 24 h). The acid-base parameters that define resolution of ketoacidosis are serum bicarbonate levels greater than 18 mmol/L, pH greater than 7.30, and anion gap les than 14 mmol/L. Normal saline alone does not correct the acidosis of AKA as rapidly as dextrose and saline. Glucose administration interrupts ketogenesis by stimulationof insulin secretion and repletion of glycogen stores.
- Patients presenting with moderate-to-severe hypoglycemia (glucose levels <50 mg/dL) may require intravenous administration of 25-50 g of 50% dextrose followed by continuous 10% dextrose infusion until glucose level is greater than 120 mg/dL. Glucagon injections alone might not correct hypoglycemia due to the depletion of hepatic glycogen stores. Hypoglycemia can be a potentially lethal complication of AKA.
- Generally, insulin is not indicated in the treatment of AKA but should be used judiciously in very low doses in patients with blood glucose concentrations greater than 250 mg/dL. Consider diabetic ketoacidosis in these patients.
- Potassium repletion is indicated in hypokalemic and normokalemic patients with acidemia. These patients should initially receive at 10-30 mEq of potassium chloride per hour intravenously. The subsequent rate and total dose of potassium are determined by subsequent potassium measurements.
- In the absence of renal insufficiency, magnesium repletion is indicated in all patients to help restore calcium and potassium homeostasis and to forestall alcohol withdrawal. Magnesium sulfate can be given safely at a rate of up to 1 g/h intravenously. Calcium repletion is rarely needed. Magnesium repletion usually allows spontaneous correction of hypocalcemia.
- Routine use of phosphorus is not encouraged, but when severe hypophosphatemia is present, intravenous phosphate repletion at rate of 0.08-0.16 mmol/kg over 6 hours is recommended.
- Bicarbonate therapy is rarely needed. In AKA, regeneration of bicarbonate from the metabolism of lactate, ketoacids, and acetate occurs with conservative treatment.
- Thiamine repletion (100 mg/d) is routinely indicated to increase pyruvate dehydrogenase activity and to provide prophylaxis against the development of Wernicke encephalopathy.
Consultations
- The underlying severity of the disease process and underlying diseases associated with AKA determine the role of the consultant.
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- Patients with uncomplicated AKA might need nothing more than appropriate treatment and observation until metabolic and systemic abnormalities are resolved.
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- Patients with an acute abdomen need consultation with a surgeon.
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- Patients with underlying medical problems might need consultation with the appropriate specialist.
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- If indicated, provide follow-up for AKA patients to assess the problem of alcohol abuse, with possible referral to a counselor at an alcohol treatment center.
Potassium repletion is indicated in hypokalemic patients and normokalemic patients with acidemia.
Magnesium repletion is indicated in all patients to help restore calcium and potassium homeostasis and to prevent alcohol withdrawal.
Phosphate repletion is recommended only if severe hypophosphatemia is present.
Thiamine repletion is indicated routinely to provide prophylaxis against the development of Wernicke encephalopathy.
Drug Category: Electrolyte supplements, parenteral
Used to replenish electrolyte levels that have been depleted.
| Drug Name | Potassium chloride |
|---|
| Description | Essential for transmission of nerve impulses, contraction of cardiac muscle, maintenance of intracellular tonicity and skeletal and smooth muscles, and maintenance of normal renal function. Gradual potassium depletion occurs via renal excretion through GI loss or because of low intake. |
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| Adult Dose | 5-10 mEq/h IV; not to exceed 40 mEq/h; subsequent rate and total dose of potassium determined by frequent measurement |
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| Pediatric Dose | 1 mEq/kg IV over 1-2 h initially and prn based on frequently obtained laboratory values |
|---|
| Contraindications | Hyperkalemia, renal failure, conditions in which potassium retention is present; patients with oliguria or azotemia, crush syndrome, severe hemolytic reactions, anuria, or adrenocortical insufficiency |
|---|
| Interactions | Concurrent use with ACE inhibitors might result in elevated serum potassium concentrations; potassium-sparing diuretics and potassium-containing salt substitutes can produce severe hyperkalemia; hypokalemia might cause digoxin toxicity; caution if discontinuing potassium administration in patients maintained on digoxin |
|---|
| Pregnancy | A - Safe in pregnancy
|
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| Precautions | Do not infuse rapidly; high plasma concentrations of potassium can cause death as a result of cardiac depression, arrhythmias, or arrest; plasma levels do not necessarily reflect tissue levels; monitor potassium replacement therapy whenever possible by continuous or serial ECG; when a concentration >40 mEq/L is infused, local pain and phlebitis can result |
|---|
| Drug Name | Magnesium sulfate |
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| Description | Cofactor in enzyme systems involved in neurochemical transmission and muscular excitability. |
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| Adult Dose | 2 g/h IV |
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| Pediatric Dose | 25-50 mg/kg/dose q4-6h for 3-4 doses; maximum single dose of 2 g can also be administered and repeated if hypomagnesemia persists |
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| Contraindications | Documented hypersensitivity, heart block, Addison disease, myocardial damage, severe hepatitis, renal impairment, hypermagnesemia, hypocalcemia, anuria |
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| Interactions | Concurrent use with nifedipine might cause hypotension and neuromuscular blockade; might increase neuromuscular blockade observed with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; might increase CNS effects and toxicity of CNS depressants or betamethasone and cardiotoxicity of ritodrine |
|---|
| Pregnancy | B - Usually safe but benefits must outweigh the risks.
|
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| Precautions | Magnesium can alter cardiac conduction, leading to heart block in digitalized patients; monitor respiratory rate, deep tendon reflex, and renal function when electrolyte is administered parenterally; caution when administering magnesium dose because it can produce significant hypertension or asystole; in overdose, calcium gluconate, 10-20 mL IV of 10% solution, can be administered as antidote for clinically significant hypermagnesemia |
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Drug Category: Electrolyte supplements
Replenish depleted levels of electrolytes.
| Drug Name | Phosphate salt |
|---|
| Description | Response to IV serum phosphorus supplementation is highly variable and is associated with hyperphosphatemia and hypocalcemia. Base rate of infusion and choice of initial dosage on severity of hypophosphatemia and presence of symptoms. IV preparations are available as sodium or potassium phosphate. |
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| Adult Dose | Severe hypophosphatemia: 0.08-0.16 mmol/kg IV over 6 h recommended |
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| Pediatric Dose | 0.25-0.5 mmol/kg over 4-6 h; repeat if symptomatic hypophosphatemia persists |
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| Contraindications | Hyperphosphatemia, hypocalcemia, hypomagnesemia, hyperkalemia, renal failure |
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| Interactions | Magnesium- and aluminum-containing antacids or sucralfate can act as phosphate binders and decrease serum phosphate levels; potassium-sparing diuretics, ACE inhibitors, and salt substitutes can increase serum phosphate levels |
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| Pregnancy | C - Safety for use during pregnancy has not been established.
|
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| Precautions | Caution in patients with renal insufficiency and metabolic alkalosis; admixture of phosphate and calcium in IV fluids can result in calcium phosphate precipitation; serum concentrations do not always reflect total body load |
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Drug Category: Vitamins
Essential for normal DNA synthesis and cell function.
| Drug Name | Thiamine (Vitamin B-1) |
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| Description | For thiamine deficiency, including Wernicke encephalopathy syndrome. |
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| Adult Dose | 50-100 mg/d IV/IM |
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| Pediatric Dose | 50 mg IV initially followed by 10-25 mg/d IV/IM |
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| Contraindications | Documented hypersensitivity |
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| Interactions | Can enhance effect of neuromuscular blocking agents |
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| Pregnancy | A - Safe in pregnancy
|
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| Precautions | Sensitivity reactions can occur (intradermal test dose recommended if sensitivity possible); deaths have resulted from IV use; sudden onset or worsening of Wernicke encephalopathy following glucose might occur in thiamine-deficient patients; administer before or together with dextrose-containing fluids if thiamine deficiency suggested |
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Further Inpatient Care
- Institute appropriate treatment for serious, coexisting acute illnesses.
Further Outpatient Care
- Arrange follow-up to evaluate patients after the resolution of symptoms to detect other complications of chronic alcohol abuse.
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- The patient might benefit from an alcohol rehabilitation program.
Transfer
- Patients generally do not need to be transferred to special facilities.
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- Always assess the patient's stability for transfer.
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- Appropriately evaluate the patient for any life-threatening complications before a transfer is considered.
Deterrence/Prevention
- Treatment of the chronic alcohol abuse
Complications
- Seizure
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- Sudden cardiac arrest
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- Life-threatening arrhythmias
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- Shock
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- Infection
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- Pulmonary edema
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- Delirium tremens
Prognosis
- The major cause of morbidity and mortality is not the acidosis but rather the failure to adequately treat concurrent medical or surgical conditions.
Patient Education
Medical/Legal Pitfalls
- Failure to recognize underlying diseases associated with AKA
- Failure to inform patients and families about the possibility of treatment at an alcohol rehabilitation center
- Failure to recognize and treat a major alcohol withdrawal or delirium tremens
- Failure to recognize and treat hypoglycemia in patients presenting with altered mental status, seizure, or both.
Special Concerns
- The AKA differential diagnosis includes all metabolic conditions that can cause an increased anion gap metabolic acidosis in a person who abuses ethanol.
-
- All patients with AKA have ketonuria and, usually, ketonemia. A normal, or even high, blood pH does not exclude the diagnosis because patients with AKA might have a concomitant metabolic alkalosis due to vomiting or a compensatory respiratory alkalosis.
-
- A compensatory respiratory alkalosis alone cannot correct the pH to normal because the drive for compensation decreases as the pH approaches normality.
- This implies that a significant noncompensatory metabolic alkalosis also must be present if the pH is near the normal range.
| Media file 1:
Diagram of pathogenesis of alcoholic ketoacidosis. |
 |  View Full Size Image | |
Media type: Graph
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Alcoholic Ketoacidosis excerpt Article Last Updated: May 26, 2006
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