Content
The reversal of ketosis and vigorous rehydration are central in the management of AKA. In addition to isotonic fluid replacement, dextrose-containing intravenous fluids are needed. Intravenous dextrose-containing fluid infusions should be stopped once the bicarbonate levels have reached mEq/L and the patient is tolerating oral intake.
Not eating enough or vomiting can lead to periods of starvation. Patients are usually tachycardic, dehydrated, tachypneic, present with abdominal pain, and are often agitated. Most patients will often have a ketone odor on their breath.
There is increasing evidence that rather than being benign and self limiting, AKA may be a significant cause of mortality in patients with alcohol dependence. This literature review discusses the history, characterisation, pathophysiology, diagnosis, and management of AKA. Generally, the physical findings relate to volume depletion and chronic alcohol abuse. Typical characteristics of the latter may include rhinophyma, tremulousness, hepatosplenomegaly, peripheral neuropathy, gynecomastia, testicular atrophy, and palmar erythema.
In particular, cases of AKA can be misdiagnosed as diabetic ketoacidosis (DKA). Subsequent mismanagement can lead to increasing morbidity and mortality for patients. AKA typically presents with a severe metabolic acidosis with a raised anion gap and electrolyte abnormalities, which are treatable if recognized early and appropriate management instituted. Given the increasing epidemic of alcohol-related healthcare admissions, this is an important condition to recognize and we aim to offer guidance on how to approach similar cases for the practising clinician. Growth hormone, epinephrine, cortisol, and glucagon are all increased. Plasma glucose levels are usually low or normal, but mild hyperglycemia sometimes occurs.
You may get vitamin supplements to treat malnutrition caused by excessive alcohol use. Your prognosis will be impacted by the severity of your alcohol use and whether or not you have liver disease. Prolonged used of alcohol can result in cirrhosis, or permanent scarring of the liver. Cirrhosis of the liver can cause exhaustion, leg swelling, and nausea.
Increasing volume status and providing increased perfusion to tissues help reduce lactic acid, ketoacids and acetic acid, which would all have been contributing to the severe acidosis. Alcoholic ketoacidosis (AKA) is a condition that presents with a significant metabolic acidosis in patients with a history of alcohol excess. The diagnosis is often delayed or missed, and this can have potentially fatal consequences. There are a variety of non-specific clinical manifestations that contribute to these diagnostic difficulties.
Alcohol dehydrogenase (ADH), a cytosolic enzyme, metabolizes alcohol to acetaldehyde in hepatocytes. Acetaldehyde is metabolized further to acetic acid by aldehyde dehydrogenase. Both steps require the reduction of nicotinamide adenine dinucleotide (NAD+) to reduced nicotinamide adenine dinucleotide (NADH). This goal can usually be achieved through the administration of dextrose and saline solutions (see Treatment). How severe the alcohol use is, and the presence of liver disease or other problems, may also affect the outlook. Treatment may involve fluids (salt and sugar solution) given through a vein.
Restoration of volume status and correction of the acidosis may be difficult to accomplish in the emergency department (ED). Evaluate the patient for signs of alcohol withdrawal syndrome, which may include tremors, agitation, diaphoresis, tachycardia, hypertension, seizures, or delirium. Exclude other causes of autonomic hyperactivity and altered mental status.
Although many patients had a significant ketosis with high plasma BOHB levels (5.2–14.2 mmol/l), severe acidaemia was uncommon. In the series from Fulop and Hoberman, seven patients were alkalaemic. In 1940, Dillon et al1 described a series of nine patients who had episodes of severe ketoacidosis in the absence of diabetes mellitus, all of whom had evidence of prolonged excessive alcohol consumption. It was not until 1970 that Jenkins et al2 described a further three non‐diabetic patients with a history of chronic heavy alcohol misuse and recurrent episodes of ketoacidosis. This group also proposed a possible underlying mechanism for this metabolic disturbance, naming it alcoholic ketoacidosis.
In addition, AKA is often precipitated by another medical illness such as infection or pancreatitis. One complication of https://ecosoberhouse.com/article/alcoholic-ketoacidosis-symptoms-and-treatment/ is alcohol withdrawal. Your doctor and other medical professionals will watch you for symptoms of withdrawal. Alcoholic ketoacidosis may lead to gastrointestinal bleeding.
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 reesterified to triglyceride. Decreased insulin and elevated glucagon, cortisol, catecholamine, and growth hormone levels can increase the rate of ketogenesis.
They attributed this to the administration of therapy (intravenous dextrose) rather than the withdrawal of the toxin, ethanol. However, following senior medical review, given a recent history of drinking alcohol to excess, the diagnosis of AKA was felt more likely. Whilst a decreased conscious level may have been expected, our patient was lucid enough to report drinking one to two bottles of wine per day for the past 30 years, with a recent binge the day prior to admission.
This drop in blood sugar causes your body to decrease the amount of insulin it produces. Your cells need insulin to use the glucose in your blood for energy. If they can’t use glucose because there’s not enough insulin, your body switches to another method to get energy — breaking down fat cells. Alcoholic ketoacidosis can develop when you drink excessive amounts of alcohol for a long period of time.
