Alcoholic Ketoacidosis Endocrine and Metabolic Disorders

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. Glycogen is a large molecule that consists of numerous glucose molecules and serves as a storage form of glucose in the tissues, particularly the liver. In the fasting state, as a first line of defense against hypoglycemia, glycogen is broken down into its constituent glucose molecules, which are secreted by the liver into the blood to maintain normal or near-normal blood sugar levels. Generally, the glycogen supply is depleted after 1 or 2 days of fasting. Thus, a person who has been drinking alcohol and not eating for 1 or more days has exhausted his or her glycogen supply. Two additional medications—metformin and troglitazone—are now being used to treat people with type 2 diabetes.

What’s the Outlook for Lactic Acidosis?

Hypoglycemia can have serious, even life-threatening, consequences, because adequate blood sugar levels are needed to ensure brain functioning. The two most common forms of diabetes are type 1 and type 2 diabetes, with type 2 diabetes accounting for at least 90 percent of all cases. Type 1 diabetes is an autoimmune disease—that is, a disease in which the body’s immune system attacks and destroys not only foreign molecules or organisms but also some of the body’s own cells.

Missed Insulin Treatment

Medications that increase certain hormones or glucose levels have the potential to lead to DKA. Therefore, discussing these risks with your healthcare professional and keeping them up to date on your medication and symptoms can help you avoid DKA. Cardiovascular disease, particularly myocardial infarction (heart attack), can rarely put people with diabetes at risk for DKA. However, DKA can worsen heart conditions and cause cardiopulmonary complications, including pulmonary edema and respiratory failure.

What are the complications of alcoholic ketoacidosis?

Ketone bodies are fat-derived fuels used by tissues at the time of limited glucose availability. Hepatic generation of ketone bodies is usually stimulated by the combination of low insulin levels and high counter-regulatory hormone levels, including glucagon. When the signal from insulin in the body is so low that glucose can’t go into cells to be used as a fuel source, the liver makes a huge amount of emergency fuel in ketones, and fat is broken down too rapidly for the body to process. When they are produced too quickly and build up in the blood, the blood becomes acidic, which causes vomiting and abdominal pain. Toxicity from methanol or ethylene glycol is an important differential diagnosis. Toxic metabolites of both substances result in severe metabolic acidosis with wide anion gap and wide osmolal gap.18 Neither, however, causes ketosis.

The dextrose will also increase glycogen stores and diminish counterregulatory hormone levels. It is essential to administer thiamine before any glucose administration to avoid Wernicke’s encephalopathy preci[itation. If severe hypokalemia is present dextrose containing fluids can be held until potassium levels are normalized.

Emergency Department Care

• Similar symptoms in a person with alcohol use disorder may result from acute pancreatitis, methanol (wood alcohol) or ethylene glycol (antifreeze) poisoning or diabetic ketoacidosis.
• It is not uncommon for the ingested ethanol to have already been metabolized, leading to low or normal serum levels when checked.
• During starvation, there is a decrease in insulin secretion and an increase in the production of counter-regulatory hormones such as glucagon, catecholamines, cortisol, and growth hormone.
• Lactate is a natural fuel source for cells and is a product of anaerobic metabolism, a process whereby cells break down glucose (sugar) for energy in the presence of low oxygen levels.
• Also, an infection can cause your body to produce higher levels of certain hormones, such as adrenaline or cortisol, that counter the effect of insulin.
• 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.
• These conditions have to be ruled out before a medical professional can diagnose you with alcoholic ketoacidosis.

The alcohol level itself need not be elevated as the more severe ketoacidosis is seen once the level falls, and the counter-regulatory response begins and shunts the metabolism towards lipolysis. Hypokalemia and increased anion-gap are usually seen with similar mechanisms to those seen in DKA. For starvation ketosis, mild ketosis generally develops after a 12- to 14-hour alcoholic ketoacidosis fast. If there is no food source, as in the case of extreme socio-economic deprivation or eating disorders, this will cause the body’s biochemistry to transform from ketosis to ketoacidosis progressively, as described below. It can be seen in cachexia due to underlying malignancy, patients with postoperative or post-radiation dysphagia, and prolonged poor oral intake.

Alcoholic ketoacidosis is a recognised acute complication in alcohol dependent patients. 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. AKA should be included in the differential diagnosis of alcohol dependent patients presenting with acute illness.

• Fever was seen in only two patients, both with other likely underlying causes.
• 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.
• Glycogen is a large molecule that consists of numerous glucose molecules and serves as a storage form of glucose in the tissues, particularly the liver.
• Hyperglycemia is the typical finding at presentation with DKA, but patients can present with a range of plasma glucose values.
• Note information about the patient’s social situation and the presence of intoxicating agents besides alcohol.
• Patients are usually tachycardic, dehydrated, tachypneic, present with abdominal pain, and are often agitated.

You should also follow all of your doctor’s recommendations to ensure proper nutrition and recovery. If you are diagnosed with alcoholic ketoacidosis, your recovery will depend on a number of factors. Seeking help as soon as symptoms arise reduces your chances of serious complications. Treatment for alcohol addiction is also necessary to prevent a relapse of alcoholic ketoacidosis. These conditions have to be ruled out before a medical professional can diagnose you with alcoholic ketoacidosis.

Alcohol Abuse

They may have a rapid and deep respiratory effort as a compensatory mechanism, known as Kussmaul breathing. They may have a distinct fruity odor to their breath, mainly because of acetone production. AKA patients may have signs of withdrawal like hypertension and tachycardia. There are signs of muscle wasting in patients with starvation ketoacidosis like poor muscle mass, minimal body fat, obvious bony prominences, temporal wasting, tooth decay, sparse, thin, dry hair and low blood pressure, pulse, and temperature. Patients with DKA may have a myriad of symptoms on presentation, usually within several hours of the inciting event. Symptoms of hyperglycemia are common, including polyuria, polydipsia, and sometimes more severe presentations include unintentional weight loss, vomiting, weakness, and mentation changes.

Watch out for early signs of DKA, including thirst or a very dry mouth, frequent urination, high blood glucose levels, and high levels of ketones in the urine. Seek emergency medical attention or call 911 immediately if you have these symptoms and suspect DKA. Diabetic eye disease (i.e., retinopathy) is another troublesome tissue complication of diabetes and one of the leading causes of blindness in the United States today.