Alcoholic ketoacidosis

Alcoholic ketoacidosis is the buildup of ketones in your blood caused by very heavy alcohol use. Alcoholic ketoacidosis can occur in adults of any age; alcoholic ketoacidosis more often occurs persons aged 20-60 years who are chronic alcohol abusers. Rarely, alcoholic ketoacidosis occurs after a binge in persons who are not chronic drinkers ¹. Ketones are a type of acid that form when the body breaks down fat for energy. Alcoholic ketoacidosis most often occurs in a malnourished person who drinks large amounts of alcohol every day. Alcoholic ketoacidosis is an acute form of metabolic acidosis, a condition in which there is too much acid in body fluids.

Alcoholic ketoacidosis can be a life-threatening condition. Complications may include:

• Coma and seizures
• Gastrointestinal bleeding
• Inflamed pancreas
• Pneumonia

If you or someone else has symptoms of alcoholic ketoacidosis, seek emergency medical help.

Alcoholic ketoacidosis treatment may involve fluids (salt and sugar solution) given through a vein. You may need to have frequent blood tests. You may get vitamin supplements to treat nutritional deficiencies caused by excess alcohol use.

People with alcoholic ketoacidosis are usually admitted to the hospital, often to the intensive care unit (ICU). Additional medicines may be given to prevent alcohol withdrawal. The patients need to be treated with fluid and volume resuscitation. The patient will need intravenous therapy (IV) normal saline volume replacement. If the initial blood glucose level is normal or low, five%dextrose should be added to the IV fluids. The patient will need volume replacement to replenish circulating volume and to increase the elimination of ketoacids. Dextrose will increase glycogen stores, diminish counterregulatory hormones and increase insulin secretion. Dextrose will help to suppress and eliminate ketoacid formation. Hypokalemia needs to be treated, and dextrose containing fluids can be held until potassium levels are normalized. Intravenous saline will also diminish serum potassium levels. Thiamine administration should proceed with the IV fluids. Magnesium and Phosphate can be repleted if the serum levels are found to be low. Intravenous Benzodiazepines should be given for seizure prophylaxis and to prevent full-blown alcoholic withdrawal. An antiemetic such as Ondansetron or Metoclopramide may also be given to control nausea and vomiting.

Alcoholic ketoacidosis causes

The cause of alcoholic ketoacidosis stems from the patient’s inability to ingest, absorb and utilize glucose from their diet ². The vomiting and nausea prevent the patient from keeping foodstuffs in the gastrointestinal tract that can cross over and provide nourishment. The alcohol further depressed gluconeogenesis in the body and keeps blood sugar levels low. An anxiety state and alcohol withdrawal further exacerbate the patient’s ability to eat. The lack of nutrients other than alcohol causes the creation of ketones and an elevated gap ketoacidosis in the absence of diabetes ³.

Patients present in a dehydrated state after a bout of heavy drinking and then an ongoing lack of oral intake. This period of poor oral intake lasts from 1 to 3 days. The pathophysiology of alcoholic ketoacidosis starts with low glycogen stores and a lack of oral food intake, which shifts the metabolism from carbohydrates to fats and lipids. The decreased oral intake causes decreased insulin levels and an increase in counter-regulatory hormones, Cortisol, Glucagon, and Epinephrine. The lack of insulin also allows an increase in the activity of hormone sensitive lipase. These changes are further enhanced, for as Ethanol is metabolized to Acetaldehyde and AcetylCOA, the nicotinamide adenine dinucleotide (NADH)/nicotinamide adenine dinucleotide (NAD+) ratio increase. The resultant increased NADH/NAD+ ratio increases lipid metabolism. All of these changes increase the breakdown of lipids to Ketoacids. The elevated NADH/NAD+ ratio further encourage the conversion of Acetoacetate to Beta-Hydroxybutyrate. Beta-hydroxybutyrate is the predominate ketoacid in alcoholic ketoacidosis. Ketoacids further accumulate as dehydration and decreased renal perfusion limit the removal of ketoacids. The differential diagnosis includes other causes of an increased anion gap metabolic acidosis. In a patient with diabetes, there must also be a consideration of diabetic ketoacidosis. A hemoglobin A1C may help in that consideration ⁴.

Alcoholic ketoacidosis prevention

Limiting the amount of alcohol you drink may help prevent alcohol induced ketoacidosis.

Alcoholic ketoacidosis symptoms

Alcoholic ketoacidosis symptoms include:

• Nausea and vomiting
• Abdominal pain
• Agitation, confusion
• Changed level of alertness, which may lead to coma
• Fatigue, slow sluggish movements
• Deep, labored, rapid breathing
• Loss of appetite
• Symptoms of dehydration, such as dizziness, lightheadedness, and thirst

Alcoholic ketoacidosis diagnosis

Diagnosis of alcoholic ketoacidosis is made on a clinical basis. Patients are usually tachycardic (fast heart rate), dehydrated, tachypneic (rapid breathing), present with abdominal pain and are often agitated. Most patients will often have a ketone odor on their breath.

1. Tachycardia is common and due to several factors including:
   • Several days of ethanol ingestion, which blocks antidiuretic hormone (ADH) and causes diuresis and increased urinary frequency,
   • Nausea and vomiting which result in decreased oral intake 1 to 3 days prior to presentation,
   • Abdominal pain which exacerbates decreased oral intake. Patients develop acidosis, which causes an increase in respirations and fluid loss.
2. Dehydration causes an elevated heart rate and dry mucous membranes. A degree of alcohol withdrawal and agitation are likely to present, resulting in an increased heart rate as well.
3. Patients are often become tachypneic due to acidosis, dehydration, alcohol withdrawal and abdominal pain.
4. Abdominal pain is commonly present although may be secondary to alcoholic gastritis or pancreatitis. Rebound tenderness is not common, and the pain is commonly epigastric in nature. If rebound tenderness or peritoneal signs are present, another cause should be sought for the pain.

Neurologically, patients are often agitated, but may occasionally present lethargic on examination. Alcohol withdrawal, in combination with nausea and vomiting, makes most patients agitated. However, if an alcoholic ketoacidosis patient is lethargic or comatose, an alternative cause should be sought.

Laboratory tests may include:

• Arterial blood gases (measures the acid/base balance and oxygen level in blood). The blood gas analysis will most likely reveal a pH that is low or normal. There will be a metabolic acidosis present with a decreased HCO3 level. If the patient is capable, a respiratory alkalosis will be mounted by the patient. The presence of a mixed disorder may also be present as significant vomiting can cause a metabolic alkalosis.
• Blood alcohol level
• Blood chemistries and liver function tests. The basic metabolic panel will likely be abnormal. Potassium levels can be normal or low, as dehydration and decreased oral intake frequently decrease the serum K level. Bicarbonate or HCO3 will likely be decreased with the presence of a metabolic acidosis. The BUN (blood urea nitrogen) to Cr ratio may be elevated if the patient is dehydrated. Glucose levels are usually mildly elevated but are not generally above 250mg/dl. The initial glucose levels are more likely to be in the normal range.
• Beta-hydroxybutyrate level will be significantly elevated. The degree of elevation of beta-hydroxybutyrate will be much greater than the elevation of lactate. If the lactate is greater than four mmol/L, another cause of the acidosis should be investigated. Serum alcohol levels are often low or absent.
• CBC (complete blood count), measures red and white blood cells, and platelets, which help blood to clot). The complete blood count may be elevated. The white blood cell, hemoglobin and the hematocrit may be elevated in a dehydrated patient. An elevated mean corpuscular volume (MCV) is often seen in chronic alcoholics.
• Prothrombin time (PT), a different measure of blood clotting, often abnormal from liver disease)
• Toxicology (poison) screening
• Urinalysis may show an elevated specific gravity as the patient is usually dehydrated. The specific gravity of the urine can be in the normal range if the patient has been drinking recently enough for the effect of antidiuretic hormone (ADH) inhibition to be still present. The patient may have been able to tolerate oral fluids over the last 24 hours, but no significant solid food.
• Nitroprusside test – Ketonuria should be present as the nitroprusside test will be positive with the present of Acetoacetate. It may be weakly positive despite the presence of significant ketosis as the urine Nitroprusside test may vastly underestimate the presence of beta-hydroxybutyrate which is the major ketoacid present in alcoholic ketoacidosis. Glucosuria will likely be absent.

Electrocardiography (EKG):

• The EKG will likely show sinus tachycardia, but atrial fibrillation or atrial flutter can be seen in a dehydrated alcohol abuser in alcoholic ketoacidosis. The initial Chest x-ray is usually negative.

Alcoholic ketoacidosis treatment

Diagnosis of the condition of alcoholic ketoacidosis is the first step in treatment. Treatment of alcoholic ketoacidosis is directed toward reversing the 3 major pathophysiologic causes of the syndrome, which are:

1. Extracellular fluid volume depletion
2. Glycogen depletion
3. An elevated ratio of the reduced form of nicotinamide adenine dinucleotide (NADH) to nicotinamide adenine dinucleotide (NAD+)

This goal can usually be achieved through the administration of dextrose and saline solutions ⁵.

Carbohydrate and fluid replacement reverse the pathophysiologic derangements that lead to alcoholic ketoacidosis by increasing serum insulin levels and suppressing the release of glucagon and other counterregulatory hormones. Dextrose stimulates the oxidation of nicotinamide adenine dinucleotide (NADH) and aids in normalizing the NADH/NAD+ ratio. Fluids alone do not correct alcoholic ketoacidosis as quickly as do fluids and carbohydrates together. Indeed, evidence-based guidelines by Flannery et al, on the management of intensive care unit patients with a chronic alcohol disorder, including symptoms that mimic or mask Wernicke encephalopathy, recommend that in cases of suspected alcoholic ketoacidosis, dextrose-containing fluids be used in place of normal saline during the first day of admission ⁶.

In alcoholics, thiamine (100 mg IV or IM) should be administered prior to any glucose-containing solutions. This will decrease the risk of precipitating Wernicke encephalopathy or Korsakoff syndrome ⁷.

Phosphate depletion is also common in alcoholics. The plasma phosphate concentration may be normal on admission; however, it typically falls to low levels with therapy as insulin drives phosphate into the cells. When present, severe hypophosphatemia may be associated with marked and possibly life-threatening complications, such as myocardial dysfunction, in these patients.

Bicarbonate therapy should be considered only in the face of severe, life-threatening acidosis (ie, pH < 7.1) that is unresponsive to fluid therapy.

Institute appropriate treatment for serious, coexisting, acute illnesses. These may include pancreatitis, hepatitis, heart failure, or infection.

Prevention of alcoholic ketoacidosis involves the treatment of chronic alcohol abuse.

Management of alcohol withdrawal syndrome

Evaluate the patient for signs of alcohol withdrawal syndrome, which may include the following:

• Tremors
• Agitation
• Diaphoresis
• Tachycardia
• Hypertension
• Tremors
• Agitation
• Seizures
• Delirium

Exclude other causes of autonomic hyperactivity and altered mental status. If the diagnosis of alcohol withdrawal syndrome is established, consider the judicious use of benzodiazepines, which should be titrated to clinical response.

Alcoholic ketoacidosis prognosis

Prompt medical attention improves the overall outlook. How severe the alcohol use is, and the presence of liver disease or other problems, may also affect the outlook.

References

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