Ketoacidosis can Be alcohol in origin: A case report

Patient 1 saw resolution of their acidosis following 3 L of 10% dextrose over 10 hours, with potassium replacement. Following medical optimisation, this patient was admitted to the local inpatient psychiatry unit for further work-up and went onto receive a diagnosis of schizophrenia with catatonia requiring electroconvulsive therapy. The driver for ketone production in patients with SKA is a state of carbohydrate depletion, initial management therefore centres around replacing this with intravenous dextrose.1 Patient 1 received 10% dextrose IV as initial management. Patient 2 was incorrectly identified as having DKA initially and received variable rate insulin plus 10% dextrose overnight, before recognition of the correct diagnosis during the consultant post-take ward round the following morning. Furthermore, the patient cohort described here have higher rates of alcohol dependence and are therefore at risk of alcoholic ketoacidosis. It is important to recognise that these conditions may coexist and should be managed as such, with thiamine prior to carbohydrate replacement in all at-risk patients.

Fomepizole does not cause the slowing of mentation noted with alcohol. The rate of its elimination from the body is more predictable, making monitoring of blood levels less necessary; therefore, patients do not have to be treated in the intensive care unit (13,40,50,53,55,58–60). Alcohol predisposes to lactic acid production and can also damage the liver; however, ethanol is easily obtained and is inexpensive, whereas fomepizole can cost as much as $5000 for 48 h of therapy per patient and may not be available in all hospitals . Twenty-four chronic alcohol abusers hospitalized during a twenty-seven-month period were suspected of having “alcoholic ketoacidosis” because they had ketonuria or ketonemia with little or no glucosuria. Twenty-one had moderate or severe ketosis, with plasma 3-hydroxybutyrate of 5.2 to 22.5 mmol/L. Fifteen of this group were not diabetic, while six were later found to have mild postprandial hyperglycemia without glycosuria. Three patients who had continued to drink until shortly before admission, though at first suspected of having alcoholic ketosis, were found to have predominant lactic acidosis, with minor elevations of plasma 3-hydroxybutyrate.

Case ReportKetoacidosis can Be alcohol in origin: A case report

Given the potential severity and the need for frequent monitoring for intravenous insulin therapy and possible arrhythmias, patients may be admitted to the intensive care unit. Blood glucose levels and electrolytes should be monitored on an hourly basis during the initial phase of management.

  • Although randomized, controlled studies to compare ethanol and fomepizole have not been done, fomepizole is preferred by most experts .
  • However, this intoxication has primarily been reported in outbreaks in which the diethylene glycol was used as a solvent for medications (46,93–96).
  • In normal alcohol metabolism, the ingested ethanol is oxidized to acetaldehyde and then to acetic acid with the enzyme alcohol dehydrogenase, during which process the coenzyme nicotinamide adenine dinucleotide (NAD+) is reduced to NADH.
  • Although the metabolites for each alcohol differ, the initial metabolic step facilitated by the enzyme ADH is an important determinant of generation of these products and serves as an important therapeutic target.

In this case report, we discuss two patients presenting with a starvation ketoacidosis and psychiatric illness. This link between SKA and psychiatric disease is especially pertinent as this is a cohort of patients who may not be able to give an accurate history, which can potentially lead to a delay in diagnosis and treatment. Labs show a high anion gap, low bicarbonate, ketonemia, and normal glucose level. The diabetic nurse should follow all outpatients to ensure medication compliance, followup with clinicians, and adopting a positive lifestyle. Further, the nurse should teach the patient how to monitor home blood glucose and the importance of careful monitoring of blood sugars during infection, stress, or trauma. The physical therapist should be involved in educating the patient on exercise and the importance of maintaining healthy body weight.

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The patient will need volume replacement to replenish circulating volume and to increase the elimination of ketoacids. Dextrose will increase glycogen stores, diminish counterregulatory hormones and increase insulin secretion. Hypokalemia needs to be treated, and dextrose containing fluids can be held until potassium levels are normalized. Magnesium and Phosphate can be repleted if the serum levels are found to be low. Intravenous Benzodiazepines should be given for seizure prophylaxis and to prevent full-blown alcoholic withdrawal. An antiemetic such as Ondansetron or Metoclopramide may also be given to control nausea and vomiting.

Blood Ketone Meters: How to Test at Home – Verywell Health

Blood Ketone Meters: How to Test at Home.

Posted: Wed, 09 Nov 2022 08:00:00 GMT [source]

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Review Date 4/24/2021

Glucose comes from the food you eat, and insulin is produced by the pancreas. When you drink alcohol, your pancreas may stop producing insulin for a short time.

Failure to make the diagnosis can result in severe metabolic abnormalities, acidosis, and shock. Nitrogen and creatinine, glucose, ketones, amylase, lipase, and plasma osmolality should be measured. Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurement. Plasma glucose levels are usually low or normal, but mild hyperglycemia sometimes occurs.

Once the diagnosis of alcoholic ketoacidosis is established, the mainstay of treatment is hydration with 5% dextrose in normal saline to address the principal physiologic derangement, a lack of metabolic substrate . Carbohydrate and fluid replacement reverse this process by increasing serum insulin levels and suppressing the release of glucagon and other counterregulatory hormones and by providing metabolic substrate. Dextrose stimulates the oxidation of the reduced form of nicotinamide adenine dinucleotide and aids in normalizing the ratio of NADH to nicotinamide adenine dinucleotide (NAD+). Potassium levels can be normal or low, as dehydration and decreased oral intake frequently decrease the serum potassium level. Bicarbonate or HCO3 will likely be decreased with the presence of metabolic acidosis. The blood urea nitrogen to creatinine ratio may be elevated if the patient is dehydrated.

alcoholic ketoacidosis treatment guidelines

Isopropanol intoxication results from its accidental ingestion or its use in suicide attempts or when used in lieu of ethanol . In 1997, 1999, alcoholic ketoacidosis and 2004, a total of almost 27,000 exposures were reported to poison control centers; one third were in children who were younger than 6 y .

If the dehydration is profound enough to cause a decrease in the circulating blood volume, a rapid heart rate and low blood pressure may be observed. Often, a “ketotic” odor is present, which is often described as “fruity” or “like pear drops”.