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.

• Pain

  Symptoms of alcoholic ketoacidosis include Excessive thirst Nausea Vomiting Abdominal pain Breathing tends to become deep and rapid as the body attempts to correct the blood’s acidity. [merckmanuals.com]

  The most common symptoms were nausea, vomiting, and abdominal pain. The most common physical findings were tachycardia, tachypnea, and abdominal tenderness. [ncbi.nlm.nih.gov]

• Falling

  […] alcoholic ketoacidosis the fall in blood pH (acidosis) sometimes seen in alcoholics and associated with a rise in the levels of serum ketone bodies. alcoholic ketoacidosis Acute metabolic ketoacidosis classically seen 1–2 days after an alcohol binge coupled [medical-dictionary.thefreedictionary.com]

  Rehydration itself will cause a fall in blood glucose level. [ld99.com]

  Hormone-sensitive lipase is normally inhibited by insulin, and, when insulin levels fall, lipolysis is up-regulated, causing release of free fatty acids from peripheral adipose tissue. [emedicine.com]

• Fatigue

  Patients with AKA typically manifest with gastrointestinal symptoms, mental status changes, dehydration, fatigue, respiratory difficulty, and possibly even coma. [symptoma.com]

  Symptoms Abdominal pain Agitation Changed level of alertness, which may lead to coma Confusion Fatigue Slow, sluggish, lethargic movement Irregular deep, rapid breathing (Kussmaul’s sign) Loss of appetite Nausea and vomiting Symptoms of dehydration, such [coordinatedhealth.com]

  Symptoms of alcoholic ketoacidosis 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 [medlineplus.gov]

  Abdominal pain, fatigue, vomiting, and dehydration are the common symptoms of alcoholic ketoacidosis. Binge alcohol drinking often leads to repetitive vomiting. [rehabnear.me]

  Symptoms Symptoms of alcoholic ketoacidosis 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 [ufhealth.org]

• Collapse

  All cases displayed evidence of prolonged excessive alcohol consumption and elevated beta-hydroxybutyric acid levels and exhibited pulseless electrical activity (PEA) upon collapse. Severe metabolic acidosis was also seen in all cases. [ncbi.nlm.nih.gov]

  This would be an excellent indication for the Toxicologic Ultrasound in Shock and Hypotension (TUSH) exam, using bedside sonography to visualize collapsibility of the inferior vena cava to help guide fluid resuscitation. [thepoisonreview.com]

  Profound dehydration can culminate in circulatory collapse and/or lactic acidosis. [emedicine.com]

• Swelling

  The pancreas is normally asked to secrete juices that are used during digestion, but alcohol abuse causes the pancreas to swell and shut down. The U.S. [thecanyonmalibu.com]

  Cirrhosis of the liver can cause exhaustion, leg swelling, and nausea. It will have a negative effect on your overall prognosis. You can prevent alcoholic ketoacidosis by limiting your alcohol intake. [healthline.com]

• Vomiting

  People who go on a major alcohol binge often vomit repeatedly and stop eating. If the vomiting and starvation go on for a day or more, the liver's normal stores of sugar (glucose) decrease. [merckmanuals.com]

  Prolonged vomiting leads to dehydration, which decreases renal perfusion, thereby limiting urinary excretion of ketoacids. [emedicine.com]

  Alcoholic ketoacidosis is a complication of alcohol use and starvation that causes excess acid in the bloodstream, resulting in vomiting and abdominal pain. People who go on a major alcohol binge often vomit repeatedly and stop eating. [msdmanuals.com]

• Nausea

  A 43-year-old alcoholic presented in coma with ketoacidosis, after three days of nausea and feeling generally unwell, which had been preceded by a prolonged three-week period of heavy alcohol consumption with poor dietary intake. [ncbi.nlm.nih.gov]

  Symptoms of alcoholic ketoacidosis include Excessive thirst Nausea Vomiting Abdominal pain Breathing tends to become deep and rapid as the body attempts to correct the blood’s acidity. [merckmanuals.com]

• Abdominal Pain

  Symptoms of alcoholic ketoacidosis include Excessive thirst Nausea Vomiting Abdominal pain Breathing tends to become deep and rapid as the body attempts to correct the blood’s acidity. [merckmanuals.com]

  It generally is seen in the chronic alcoholic patient who has recently gone on a "binge" that was terminated because of complaints such as nausea, vomiting or abdominal pain. Caloric intake is diminished. [ncbi.nlm.nih.gov]

• Heart Disease

  Aetiology and characteristics of beri-beri heart disease. S. African Med. J. 46, 1707–1713 (1972). 27. Gloria, L. et al. Nutritional deficiencies in chronic alcoholics: relation to dietary intake and alcohol consumption. Am. J. [nature.com]

  Patients may develop acute renal failure, probably secondary to rhabdomyolysis, acute liver failure, acute pancreatitis, and rarely acute heart failure, probably secondary to beri beri heart disease. [pulmonarychronicles.com]

  The Charlson index includes 19 groups of major chronic diseases, including ischemic heart disease, cancer, diabetes, chronic lung diseases, and chronic renal failure. [ccforum.biomedcentral.com]

  Alcohol use disorder is a chronic disease not unlike diabetes or congestive heart failure. If alcoholism is considered a chronic disease, a treatment success rate of 50% is similar to the success rates in other chronic illnesses. [emedicinehealth.com]

• Liver Dysfunction

  Complications such as liver dysfunction, lactic acidosis, acute pancreatitis, Wernicke's encephalopathy, rhabdomyolysis and heart failure were present. Attention should be paid to multiple complications in the treatment of AKA. [ncbi.nlm.nih.gov]

• Suggestibility

  Vitreous ketone levels showed good correlation with blood and pericardial fluid levels, suggesting that vitreous could be used as an alternative autopsy specimen for this analysis. [ncbi.nlm.nih.gov]

  The striking preponderance of women, including one pregnant patient, reported with this condition also suggests a possible role for ovarian and placental hormones in its pathogenesis; fetal drain on carbohydrate reserves may further contribute to the [diabetes.diabetesjournals.org]

  Calcium oxalate crystals in the urine also suggests ethylene glycol poisoning. Lactic acid levels are often elevated because of hypoperfusion and the altered balance of reduction and oxidation reactions in the liver. [msdmanuals.com]

• Confusion

  I don’t know if I’m confusing myself….or if I made any sense. [valuemd.com]

  Symptoms Abdominal pain Agitation Changed level of alertness, which may lead to coma Confusion Fatigue Slow, sluggish, lethargic movement Irregular deep, rapid breathing (Kussmaul’s sign) Loss of appetite Nausea and vomiting Symptoms of dehydration, such [coordinatedhealth.com]

  Symptoms of alcoholic ketoacidosis 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 [medlineplus.gov]

  Symptoms Symptoms of alcoholic ketoacidosis 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 [ufhealth.org]

• Stupor

  /coma Stupor/coma Serum bicarbonate 15 to 18 mEq per L (15 to 18 mmol per L) 10 to < 15 mEq per L (10 to < 15 mmol per L) < 10 mEq per L (10 mmol per L) > 18 mEq per L (18 mmol per L) Serum ketone† Positive Positive Positive Small Urine ketone† Positive [aafp.org]

  Examination Lethargy, stupor and progression to a state of coma may occur, particularly in cases of poisoning. An intoxicated-appearing patient who has no smell of alcoholic drink on their breath may have ingested ethylene glycol. [patient.info]

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 [8]. 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 [9].

Differential diagnoses

Differentials include diabetic ketoacidosis (DKA),however, the absence of hyperglycemia excludes this. Pancreatitis may also present similar to AKA and should be ruled out.

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.

• Glycosuria

  On admission, blood glucose level was normal or moderately elevated, glycosuria was absent or trivial, and alcohol had disappeared from blood, but ketoacidosis was sometimes severe. [doi.org]

  The dissociation of severe ketosis from glycosuria and hyperglycemia in these patients raises important questions concerning coupling of ketogenesis to gluconeogenesis. [diabetes.diabetesjournals.org]

  Signs ● Ketonuria and Glycosuria ● Vomiting ● Kussmaul breathing: hyperventilation ● Acetone smell on breath ● Confusion and disorientation => Coma ● Hypokalaemia: blood potassium concentration 7. [slideshare.net]

  Laboratory results included absent blood alcohol with normal or low blood glucose level, no glycosuria, and a variably severe metabolic acidosis with a raised anion gap. [ncbi.nlm.nih.gov]

• Hyperglycemia

  The absence of hyperglycemia makes diabetic ketoacidosis improbable. Those with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated hemoglobin (HbA1C). [msdmanuals.com]

  Whether it is because of hyperglycemia or of ketoacidosis is unclear. [ncbi.nlm.nih.gov]

• Hypoglycemia

  This case, however, presented comatose status caused by hypoglycemia. Poor oral intake of this patient was assumed to be the cause of hypoglycemia. [ncbi.nlm.nih.gov]

  A subset of alcoholic patients in whom hypoglycemia and ketoacidosis are coexistent has been described. [emjournal.net]

  […] genotype, whiskey or shochu (distilled alcoholic beverages with no carbohydrates) as the drink of choice, hypoglycemia, lower body mass index, and smoking. [11] [emedicine.com]

• Triglycerides Decreased

  Triglycerides stored in adipose tissue undergo lipolysis and are released into the circulation as free fatty acids bound ionically to albumin. [emedicine.com]

• Glucose Increased

  and other peripheral tissues with a metabolic fuel that can replace glucose. [emedicine.com]

• Insulin Increased

  Alcoholic Ketoacidosis (AKA) Associations : History of alcohol abuse + normal glucose + ketones in urine Pathophysiology : Multifactorial: Decreases in insulin, increases in glucagon, impaired NADH to NAD+ ratios from alcohol metabolism and volume depletion [ebmconsult.com]

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 [10].

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.

Alcohol cessation

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.

Other

Coexisting medical conditions such as hepatitis, pancreatitis, cardiac failure, and infections should be promptly treated as well.

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 [6].

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 [7].

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 [2].

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 [3].

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.

Ketoacidosis

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 [4] 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 [5].

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 [1].

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:

• Nausea and vomiting
• Abdominal pain
• Loss of appetite
• Fatigue
• Slow or sluggish movement
• Dehydration and thirst
• Lightheadedness and dizziness
• Agitation
• Confusion
• Abnormal breathing with an irregular pattern that is deep and rapid
• Lethargy

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.

The clinician should be wary that other conditions may present similarly. Examples include diabetic ketoacidosis, pancreatitis, and methanol or ethylene glycol poisoning.

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.

1. Halperin ML, Hammeke M, Josse RG, Jungas RL. Metabolic acidosis in the alcoholic: a pathophysiologic approach. Metabolism 1983; 32:308.
2. Iten PX, Meier M. Beta-hydroxybutyric acid -- an indicator for an alcoholic ketoacidosis as cause of death in deceased alcohol abusers. Journal of Forensic Science. 2000; 45(3):624-32.
3. Manini AF, Hoffman RS, Nelson LS. Alcoholic ketoacidosis in an 11-year-old boy. Pediatric Emergency Care. 2008; 24(3):170-1.
4. Jenkins D W, Eckle R E, Craig J W. Alcoholic ketoacidosis. Journal of American Medical Association. 1971; 217(2): 177–183.
5. Fulop M, Hoberman H D. Alcoholic ketosis. Diabetes. 1975; 24(9): 785–790.
6. Ngatchu T, Sangwaiya A, Dabiri A, et al. Alcoholic ketoacidosis with multiple complications: a case report. Emergency Medicine Journal. 2007; 24(11):776-7.
7. Palmer JP. Alcoholic ketoacidosis: clinical and laboratory presentation, pathophysiology and treatment. Clinics in Endocrinology and Metabolism. 1983; 12(2):381-9.
8. Höjer J. Severe metabolic acidosis in the alcoholic: differential diagnosis and management. Human and Experimental Toxicology. 1996; 15(6):482-8.
9. Wrenn KD, Slovis CM, Minion GE, Rutkowski R. The syndrome of alcoholic ketoacidosis. American Journal of Medicine. 1991; 91(2):119-28.
10. Diltoer MW, Troubleyn J, Lauwers R, et al. Ketosis and cardiac failure: common signs of a single condition. European Journal of Emergency Medicine. 2004; 11(3):172-5.