Alcoholic ketoacidosis (AKA) is a metabolic disorder that arises due to alcohol abuse and starvation in a chronic alcoholic. Specifically, this condition is associated with ketonemia and high anion gap metabolic acidosis.
Alcoholic Ketoacidosis is the consequence of this process: Poison.
A patient with AKA has the profile of a chronic alcoholic who binge drinks and starves or eats poorly. The clinical presentation may vary from one individual to another depending on the quantity of alcohol consumed and their level of plasma ketones.
The symptoms include abdominal pain, nausea, vomiting, loss of appetite, sluggish movement, and fatigue. Mental status changes such as confusion, agitation, and/or a decline in alertness are common. Furthermore, patients may suffer from dehydration which manifests as thirst, dizziness, and light-headedness. Additionally, patients may exhibit the Kussmaul's sign which is described as irregular, deep and fast breathing. Finally, serious cases of AKA may result in coma.
When a chronic alcoholic presents with signs of AKA, the clinician should carefully evaluate the patient, obtain a history, perform a physical exam, and order the appropriate laboratory tests.
Laboratory tests and results
A comprehensive metabolic profile will allow the medical team to determine the overall clinical picture of the patient. This includes measurement of serum electrolytes, glucose, blood urea nitrogen (BUN), creatinine, lipase, amylase, and plasma osmolality. Also, urinalysis is helpful to detect ketones. Another useful tool is the blood alcohol level . Finally, critically ill patients with positive ketones must have an analysis of their arterial blood gas (ABG) and serum lactate levels.
With regards to expected findings, all patients demonstrate ketonuria and a majority display ketonemia. Also common are electrolyte imbalances such as hypokalemia, hyponatremia, hypophosphatemia, and hypomagnesemia. Additionally, the serum glucose may range from low to modest elevation while another abnormality is an increased osmolar gap (secondary to increased acetone and possibly ethanol).
Most importantly, AKA is typically characterized by a high anion gap metabolic acidosis, which may be complicated by metabolic alkalosis secondary to concurrent vomiting. In cases where the pH is normal, the increased anion gap is an indicator of ketoacidosis. If there is a normal gap, this is the result of the excretion of ketoacid ions. Additionally, lactic acidosis is observed in more than 50% of cases due to hypoperfusion .
If alcohol intoxication is not conclusive, serum methanol and ethylene glycol levels should be obtained. A urinalysis is also beneficial because it can reveal calcium oxalate crystals, which is suggestive of ethylene glycol poisoning.
The therapeutic approach for patients with AKA aims to correct the extracellular hypovolemia, glycogen depletion, and the increased NADH/NAD ratio. These three pathophysiologic mechanisms are reversed with IV fluid therapy consisting of 5% dextrose in 0.9% saline. Specifically, this dextrose-saline solution will provide the carbohydrate and fluid that the patient is lacking. Furthermore, it will elevate the insulin levels and inhibit glucagon and other hormones. Also, the dextrose will promote oxidation of NADH and normalize the ratio.
Note that administration of thiamine should precede treatment with dextrose-saline fluids as thiamine can reduce the risk of developing Wernicke encephalopathy or Korsakoff syndrome .
Electrolyte abnormalities such as hypokalemia, hypophosphatemia, and hypomagnesemia should be addressed since these pose life-threatening risks. Note that while phosphate may be normal initially, the levels may decline due to the release of insulin.
With regards to recovery, the gastrointestinal manifestations and ketoacidosis will improve rapidly with the dextrose-saline infusion. However, if the acidosis is not responding to fluid resuscitation, bicarbonate may be given.
Cessation of the offending substance is also a component of the treatment. Note that when the individual stops alcohol intake, the NADH/NAD ratio normalizes and gluconeogenesis returns to normal. Hence, the impaired metabolic pathways are restored.
Of importance, the clinician must be vigilant of alcohol withdrawal symptoms in these individuals. The signs include diaphoresis, tremors, agitation, tachycardia, hypotension, delirium, and seizures. If the patient meets the diagnostic criteria of alcohol withdrawal syndrome, then the cautious use of benzodiazepine is warranted.
As part of the long-term management of alcoholism, patients should be advised of and educated on the significance of quitting alcohol. There are resources such as rehabilitation programs, support groups, and psychotherapy available for those who wish to attain sobriety.
The earlier the treatment of AKA commences, the better the prognosis. However, the overall long-term outcome in these patients reflects on their cessation of alcohol intake.
While morbidity and mortality of AKA are uncommon, death is usually secondary to coexisting medical or surgical conditions such as alcohol withdrawal syndrome and gastrointestinal bleeding .
It is to be noted that AKA has been attributed as causing death in a number of alcoholic individuals as profoundly raised beta-hydroxybutyric acid levels have been proven to be fatal .
AKA is most likely to occur in a malnourished chronic alcoholic who partakes in a drinking binge. The patient will experience nausea, vomiting, and abdominal pain, which will cause this individual to cease or reduce food intake. In many cases, an underlying cause such as pancreatitis or infection will lead to AKA.
This metabolic disorder arises from a complicated interaction of decreased food consumption, dehydration, and hormonal imbalances. The latter contributes to the increase in hydroxybutyric acid, acetoacetic acid, and acetone .
The prevalence of this condition is associated with the predominance of alcohol abuse in a particular setting or community.
The demographics of AKA shows a frequent occurrence in longstanding alcohol abusers within the age range of 20 to 60 years of age although there is a case report of an 11 year-old male who developed AKA after consumption of mouthwash containing alcohol .
AKA is seldom seen in occasional alcohol drinkers. Also, there is no preference for race or gender.
To understand the pathophysiology of AKA, it is imperative to explain how the body processes ethanol and how chronic drinkers develop ketoacidosis.
Metabolism of ethanol
Ethanol is metabolized mainly through the alcohol dehydrogenase pathway in a 3 step oxidation reaction that proceeds sequentially to form acetaldehyde, acetic acid, and then finally acetyl coenzyme A (acetyl-CoA). During this process, NAD is reduced to NADH, of which the latter builds up in the mitochondria.
There is a complex interplay of hormones that leads to ketogenesis in long-term alcoholics. Often this population tends to have a poor nutritional status attributed to starvation and vomiting. They exhibit a profound deficiency in protein and carbohydrates as well as a depletion of glycogen stores. Additionally, these patients cannot rely on gluconeogenesis to meet their energy demands as high levels of NADH (produced in the metabolism of alcohol) inhibits this key metabolic pathway. Hence, acute alcoholic poisoning in these individuals causes hypoglycemia. To complicate matters, alcohol-induced vomiting can cause hypovolemia and hypotension, which can trigger the sympathetic nervous system.
The resultant hormone cascade strives to correct the patient's hypoglycemia and hypotension. To solve the energy insufficiency, the body increases the production of glucagon, cortisol, growth hormone, and adrenaline while reducing that of insulin as a collective effort to facilitate lipolysis. Additionally, raised glucagon levels and increased free fatty acids generate production of acetyl-CoA which can be used for ketogenesis.
Cellular effect of ethanol
It is believed that the accumulation of NADH in hepatic mitochondria disrupts the metabolic activity. Furthermore, some hypothesize that mitochondrial damage secondary to alcohol toxicity is responsible for the development of AKA  as this toxic substance induces alterations in the mitochondrial structure. However, others surmise that functional impairment of the mitochondria is the likely etiology of AKA .
All individuals are advised to adhere to a healthy lifestyle, which includes being careful about alcohol use. Moderate amounts are acceptable, however, excessive drinking over long periods of time is detrimental to one's health. Furthermore, everyone should remain vigilant about the signs of alcoholism and when in doubt, there is plenty of education and information available. Also, it should be emphasized to people of all ages and backgrounds that alcohol can lead to many diseases and illnesses. Hence, abstaining/quitting will vastly improve the health of the individual.
If an alcoholic chooses to cease drinking, there are numerous resources available including alcohol rehabilitation programs, support groups, psychotherapy, etc.
Alcoholic ketoacidosis (AKA) is a metabolic condition that occurs in malnourished chronic alcoholics. In this population, poor carbohydrate intake/starvation leads to a decline in the production of insulin and an increase in production of glucagon and other hormones. Additionally, the metabolic pathways in these individuals are altered as gluconeogenesis is impaired while lipolysis is stimulated. Both of these mechanisms lead to ketoacid formation .
Patients with AKA typically manifest with gastrointestinal symptoms, mental status changes, dehydration, fatigue, respiratory difficulty, and possibly even coma. Since this disorder can be life-threatening, prompt diagnosis and treatment are paramount.
The clinician will assess the patient, ascertain the history, perform a physical exam, and order diagnostic tests. The latter includes a metabolic panel to determine the presence of ketones and to measure the electrolytes, glucose, renal functions, pancreatic enzymes, and blood alcohol level. The typical findings include ketonemia, ketonuria, and high anion gap metabolic acidosis.
The treatment of AKA consists of intravenous (IV) fluids of saline containing dextrose,which is preceded by thiamine administration to prevent Korsakoff syndrome. Fluid therapy will relieve the symptoms and correct the metabolic acidosis. Another important consideration that the clinician must be cognizant of is the development of alcohol withdrawal syndrome in these patients. This serious disease requires treatment with benzodiazepines.
Since alcohol abuse contributes to a wide variety of multisystem illnesses, patients should be educated and informed of the harmful effects of alcohol addiction. Moreover, there are numerous resources available to help the patient cease the consumption of alcohol and such other substances.
What is alcoholic ketoacidosis?
This is a condition in which ketones, a type of acid, build up in the blood. Ketones form when the body does not have enough carbohydrate stores and therefore breaks down the fat for energy.
What causes this condition?
This develops when malnourished individuals drink large quantities of alcohol for a long time. Since these people do not consume food regularly and tend to vomit, they suffer from periods of starvation. The body responds to this by breaking down fat storage for energy, which causes the ketoacidosis.
What are symptoms of this condition?
The symptoms depend on how much alcohol is consumed and the amount of ketones present in the blood. Common signs are as follows:
This can be a life-threatening illness resulting in coma or death.
How is alcoholic ketoacidosis diagnosed?
When a patient presents with symptoms that are suspicious for this condition, the clinician will obtain a full history, perform a physical exam, and order the appropriate laboratory studies. The latter includes serum chemistries that will measure the electrolytes including sodium, potassium, magnesium, phosphate, etc. Also, very important labs such as ketones, glucose, BUN, creatinine. amylase, lipase, and plasma osmolality should be performed. A urinalysis should also be done to test for the presence of ketones.
The laboratory findings typically reveal ketones in the blood, metabolic acidosis, and reduced levels of potassium, magnesium, and phosphate.
How is it treated?
The treatment includes intravenous fluid therapy with dextrose in a saline solution. Prior to this, the patient should be treated with intravenous thiamine to prevent alcohol-induced diseases such as Wernicke encephalopathy or Korsakoff psychosis. The ketoacidosis and gastrointestinal signs improve rather quickly with fluid treatment.
Also, low levels of potassium, magnesium, and phosphate should be replaced since a deficiency of these electrolytes can lead to complications.
Note that patients are likely to suffer from alcohol withdrawal syndrome, which is characterized by excessive sweating, tremors, agitation. rapid heart rate, low blood pressure, delirium, and even seizures. The clinician must watch out for these symptoms. These patients are cautiously treated with benzodiazepines.
How can it be prevented?
If one has an addiction to alcohol, education should be provided to help understand why it is important to quit. While it is challenging to do so, there are numerous resources available to help an individual succeed at quitting drinking. For example, there are alcohol and drug rehabilitation programs, support groups, psychotherapy, etc.