Treatment alcoholism uk. Alcoholic Ketoacidosis,


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. Pathophysiology of alcoholism.

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].

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 [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.

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.

Treatment of alcoholic jaundice

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.

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


To understand the pathophysiology of AKA, it is imperative to explain how the body processes ethanol and how chronic drinkers develop ketoacidosis.

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.

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].


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.

Describe the pathophysiology of alcoholism and addictive disorders

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.

Patient Information

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.

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.

The symptoms depend on how much alcohol is consumed and the amount of ketones present in the blood. Common signs are as follows:

Slow or sluggish movement

Abnormal breathing with an irregular pattern that is deep and rapid

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.

What is pathophysiology of alcoholism

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.

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.

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.

Posted by at 08:11PM

Tags: treatment alcoholism uk, pathophysiology of alcoholic liver disease, pathophysiology of alcoholism abuse, pathophysiology of alcoholic cirrhosis, treatment of alcoholic hepatitis, treatment of non alcoholic fatty liver, pathogenesis of alcoholic liver disease, treatment of alcoholic jaundice, what is pathophysiology of alcoholism, describe the pathophysiology of alcoholism and addictive disorders

Overall rating page: 3.92/5 left 53875 people.


There are no comments for this post "Alcoholic Ketoacidosis,". Be the first to comment...

Add Comment