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Warfarin overdose was also considered, although the patient repeatedly denied this and reports he did not have access to his medications. Further, vitamin K administration in our patient resulted in normalization of his INR. Although potassium is profoundly depleted in persons with DKA, decreased insulin levels, acidosis, and volume depletion cause elevated extracellular concentrations. Potassium levels should be monitored every two to four hours in the early stages of DKA. Hydration alone will cause potassium to drop because of dilution. Insulin therapy and correction of acidosis will cause cellular uptake of potassium.

  • Treatment for AUD looks different for everyone but can include inpatient programs, outpatient rehab, participation in mutual-help groups like Alcoholics Anonymous or SMART Recovery, attending individual or group counseling sessions, or a combination of these methods.
  • If history does not rule out toxic alcohol ingestion as a cause of the elevated anion gap, serum methanol and ethylene glycol levels should be measured.
  • Lipase activity increases, causing a breakdown of adipose tissue that yields free fatty acids.
  • Alcoholic ketoacidosis (AKA) is a condition seen commonly in patients with alcohol use disorder or after a bout of heavy drinking.
  • Dextrose is required to break the cycle of ketogenesis and increase insulin secretion.

If the potassium level is in the normal range, replacement can start at 10 to 15 mEq potassium per hour. During treatment of DKA, the goal is to maintain serum potassium levels between 4 and 5 mEq per L (4 and 5 mmol per L). If the potassium level is between 3.3 and 5.2 mEq per L (3.3 and 5.2 mmol per L) and urine output is normal, replacement can start at 20 to 30 mEq potassium per hour.

Clinical Scenario

Alcoholic ketoacidosis is the buildup of ketones in the blood due to alcohol use. Ketones are a type of acid that form when the body breaks down fat for energy. You can prevent alcoholic ketoacidosis by limiting your alcohol intake.

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. The patient received 4 liters of normal saline and was started on D5-1/2 NS prior to admission. He was given IV valium for alcohol withdrawal, and thiamine, folate, and phosphate were repleted. He was hospitalized for three days for management of AKA and alcohol withdrawal, then discharged once tolerating oral intake and in good condition.

How Is Alcoholic Ketoacidosis Treated?

This results in metabolic acidosis with elevated beta-hydroxybutyrate levels. Patients with AKA most commonly present with a history of alcohol use (acute or chronic), poor oral intake, gastrointestinal symptoms, and ketoacidosis on laboratory assessment. Patients are generally dehydrated, and serum glucose can be low, normal, or mildly elevated. An anion gap metabolic acidosis with ketosis and electrolyte abnormalities are usually present on laboratory evaluation. Management includes fluid resuscitation, glucose and vitamin supplementation, electrolyte repletion, and evaluation for other conditions. Similar symptoms in a person with alcohol use disorder Alcohol Use Alcohol (ethanol) is a depressant (it slows down brain and nervous system functioning).

  • Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent).
  • He was admitted to the internal medicine service for continued management.
  • He was given IV valium for alcohol withdrawal, and thiamine, folate, and phosphate were repleted.
  • He was seen three weeks later in the emergency department for a similar presentation.
  • Appropriately evaluate the patient for any life-threatening complications before a transfer is considered.

Magnesium and phosphate levels should be measured and repleted if the serum levels are found low. 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. This typically occurs 8 to 16 hours after the initiation of treatment.2 Alcohol withdrawal in these patients should be aggressively managed with intravenous benzodiazepines.

Vitamin supplementation

Meetings are widely available at little-to-no cost in most communities. Support groups can be a valuable source of support and can be combined with medication and therapy. Although the underlying pathophysiology is complex, a proper comprehension greatly aids in the diagnosis and management of this condition. He is actively involved alcoholic ketoacidosis smell in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE. He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world.

alcoholic ketoacidosis treatment