Examination should reveal a clear level of consciousness, generalised abdominal tenderness (without peritoneal signs), and tachypnoea. There may be concomitant features of dehydration or early acute alcohol withdrawal. Bedside testing reveals a low or absent breath alcohol, normal blood sugar, metabolic acidosis, and the presence of urinary ketones, although these may sometimes be low or absent. An altered level of consciousness should prompt consideration of alternative diagnoses such as hypoglycaemia, seizures, sepsis, thiamine deficiency, or head injury.
- Elevated cortisol levels can increase fatty acid mobilization and ketogenesis.
- Free fatty acids are either oxidized to CO2 or ketone bodies (acetoacetate, hydroxybutyrate, and acetone), or they are esterified to triacylglycerol and phospholipid.
- Take our free, 5-minute alcohol abuse self-assessment below if you think you or someone you love might be struggling with alcohol abuse.
- They provide some energy to your cells, but too much may cause your blood to become too acidic.
- All alcoholic patients presenting with acute illness should be offered contact with addiction services prior to or following discharge wherever possible.
- Despite the frequency of abdominal symptoms, objective findings other than tenderness were infrequent.
- In addition, AKA is often precipitated by another medical illness such as infection or pancreatitis.
What to Know About Alcoholic Ketoacidosis
- Given the frequency with which the condition is seen in other countries, the possibility exists that many cases may be unrecognised and misdiagnosed in UK EDs.
- Acetic acid (an acyl group carrier) is linked with coenzyme A (a thiol) to produce Acetyl-CoA.
- Energy (caloric) restriction secondary to abdominal pain, nausea, or vomiting usually occurs prior to the onset of AKA.
- Although well described in international emergency medicine literature, UK emergency physicians rarely make the diagnosis of AKA.
This literature review discusses the history, characterisation, pathophysiology, diagnosis, and management of AKA. In contrast to diabetic ketoacidosis, the predominant ketone body in AKA is β-OH. Routine clinical assays for ketonemia test for AcAc and acetone but not for β-OH.
BOX 3 MANAGEMENT OF AKA
The prognosis for alcoholic ketoacidosis is good as long as it’s treated early. However, the long-term prognosis depends on the severity of the underlying alcohol abuse disorder. The major causes of death in people with alcoholic ketoacidosis are diseases that occur along with the alcoholic ketoacidosis and may have caused it, such as pancreatitis, gastrointestinal bleeding, and alcohol withdrawal.
Clinical findings
There may be a history of previous episodes requiring brief admissions with labels of “query pancreatitis” or “alcoholic gastritis”. Nausea, vomiting, and abdominal pain were by far the most commonly observed complaints. Despite the frequency of abdominal symptoms, objective findings other than tenderness were infrequent. Abdominal distension, decreased bowel sounds, ascites, or rebound tenderness occurred rarely and only in the presence of other demonstrable intra‐abdominal pathology such as pancreatitis, severe hepatitis, and sepsis or pneumonia. Both Wrenn et al6 and Fulop and Hoberman5 found evidence of alcoholic hepatitis to be common, with frequent elevations in serum transaminase activities and bilirubin.
Alcoholic Ketoacidosis Treatment and Diagnosis
All alcoholic patients presenting with acute illness should be offered contact with addiction services prior to or following discharge wherever possible. Jenkins et al2 suggested that alcohol induced mitochondrial damage might account for AKA. Alcohol produces structural changes in human liver mitochondria within alcoholism days.
- Both Wrenn et al6 and Fulop and Hoberman5 found evidence of alcoholic hepatitis to be common, with frequent elevations in serum transaminase activities and bilirubin.
- Several mechanisms are responsible for dehydration, including protracted vomiting, decreased fluid intake, and inhibition of antidiuretic hormone secretion by ethanol.
- Nausea, vomiting, and abdominal pain were by far the most commonly observed complaints.
- Fever was seen in only two patients, both with other likely underlying causes.
- Usually, patients respond well and quickly to treatment, if it is started early in the course.
Who Is at Risk for Alcoholic Ketoacidosis?
This is why diagnosis and subsequent treatment can sometimes be challenging, but it’s crucial to receive alcoholic ketoacidosis a proper and timely diagnosis to obtain the correct treatment. Energy (caloric) restriction secondary to abdominal pain, nausea, or vomiting usually occurs prior to the onset of AKA. 7 Under conditions of starvation, the liver increases the production of ketones from fatty acids to supply the brain, kidney, and other peripheral tissues with a metabolic fuel that can replace glucose.
Management of alcoholic ketoacidosis
This drop in blood sugar causes your body to decrease the amount of insulin it produces. 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. Wrenn et al found altered mental status in 15% of patients, attributable in all but one case to hypoglycaemia, severe alcohol intoxication, or infection. Fever was seen in only two patients, both with other likely underlying causes.
More on Substance Abuse and Addiction
Both cause abdominal pain, with marked central nervous system depression, but methanol toxicity results in visual impairment, while ethylene glycol toxicity results in crystalluria, oliguria, and renal failure. 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. The patient might be tachycardic, tachypneic, profoundly orthostatic, or frankly hypotensive as a result of dehydration from decreased oral intake, diaphoresis, and vomiting.