Accordingly, more studies are needed to determine whether the beneficial effects of daily moderate alcohol consumption outweigh the deleterious effects. Diabetics clearly should avoid heavy drinking (i.e., more than 10 to 12 drinks per day), because it can cause ketoacidosis and hypertriglyceridemia. Moreover, heavy drinking in a fasting state can cause hypoglycemia and ultimately increase diabetics’ risk of death from noncardiovascular causes. Hypomagnesemia and hypophosphatemia are common problems seen in the laboratory evaluation due to decreased dietary intake and increased losses.
- Alcoholic ketoacidosis (AKA) is a condition seen commonly in patients with alcohol use disorder or after a bout of heavy drinking.
- The accompanying lack of alcohol in the patient’s body and the fact that for some time, the only source of calories that a patient has is ethanol both contribute to the clinical syndrome that we see.
- Moreover, volume depletion increases the concentration of counter-regulatory hormones, further stimulating lipolysis and ketogenesis.
- In peripheral tissues, where NADH levels are lower, this lactate may be converted to pyruvate for metabolic needs.
- Although well described in international emergency medicine literature, UK emergency physicians rarely make the diagnosis of AKA.
- The condition is an acute form of metabolic acidosis, a condition in which there is too much acid in body fluids.
- The liver normally re-incorporates free fatty acids into triglycerides, which are then packaged and secreted as part of a group of particles called very low-density lipoproteins (VLDL).
Injury and surgery can lead to stress, which has been shown to trigger hyperglycemia. This is an undesirable consequence in people with diabetes, where hyperglycemia can be brought on quickly and should be treated as soon as possible. Viral or bacterial infections such as pneumonia, urinary tract infection, and sepsis can trigger DKA. This is because your body needs more insulin than usual during an infection. The majority of papers detected by this search focus primarily on diabetes mellitus and its complications, and were excluded.
Emergency Department Care
For example, obesity, inactivity, and cigarette smoking may worsen genetically determined insulin resistance. The FDA Adverse Event Reporting System database identified 20 cases of DKA in patients treated with SGLT2 inhibitors from March 2013 to June 2014. Several mechanisms are responsible for dehydration, including protracted vomiting, decreased fluid intake, and inhibition of antidiuretic hormone secretion by ethanol. Volume depletion is a strong stimulus to the sympathetic nervous system and is responsible for elevated cortisol and growth hormone levels. 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.
Heavy drinking, particularly in diabetics, also can cause the accumulation of certain acids in the blood that may result in severe health consequences. Finally, alcohol consumption can worsen diabetes-related medical complications, such as disturbances in fat metabolism, nerve damage, and eye disease. The mechanisms underlying the development of alcoholic ketoacidosis are complex. However, some typical contributing factors result in insulin lack and excess glucagon levels, thereby promoting the development of ketoacidosis. As mentioned earlier in this article, poor food intake can lead to depleted glycogen levels. Furthermore, continued alcohol metabolism results in diminished gluconeogenesis.
What is alcoholic ketoacidosis?
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 (NADH) and aids in normalizing the ratio of NADH to nicotinamide adenine dinucleotide (NAD+). 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.
The physical therapist should be involved in educating the patient on exercise and the importance of maintaining healthy body weight. For starvation ketosis, mild ketosis generally develops after a 12- to 14-hour 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.
Differential Diagnosis
This will cause the person with diabetes to jump between low and high blood sugar levels, which can be difficult to control. 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. If your body is unable to meet the demand, it may set off the liver’s ketone production to compensate for this need.
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. Arterial blood gas and biochemistry studies reveal a raised anion gap metabolic acidosis without evidence of lactic or diabetic ketoacidosis. Ketoacidosis, which occurs primarily in diabetics, is a condition characterized by excessive levels of certain acids called ketone bodies (e.g., acetone, acetoacetate, and β-hydroxybutyrate) in the blood. Elevated levels of those compounds can cause nausea, vomiting, impaired mental functioning, coma, and even death. Ketoacidosis is caused by complete or near-complete lack of insulin and by excessive glucagon levels.
Complications
Most importantly, insulin leads to the uptake of the sugar glucose into muscle and fat tissue and prevents glucose release from the liver, thereby lowering blood sugar levels (e.g., after a meal) (see figure). As a result of the immune system’s attack, the beta cells can no longer produce insulin. Because insulin is a key metabolic hormone, insulin deficiency leads to major impairment of the body’s regulation of carbohydrate, lipid, and protein metabolism.
In AKA, transaminitis, and hyperbilirubinemia due to concurrent alcoholic hepatitis may also be present. 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. 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.
In rare cases, however, the condition also may affect people with type 2 diabetes. In a milder form, ketoacidosis may even occur in people who are fasting. In those people, insulin levels are diminished, because the fasting has considerably lowered their blood sugar levels, thereby depriving the pancreas of its stimulus to produce and secrete insulin. In general, exogenous insulin is contraindicated in the treatment of AKA, because it may cause life-threatening hypoglycemia in patients with depleted glycogen stores. In most cases, the patient’s endogenous insulin levels rise appropriately with adequate carbohydrate and volume replacement. If the patient’s blood glucose level is significantly elevated, AKA may be indistinguishable from diabetic ketoacidosis (DKA).
- Clinicians underestimate the degree of ketonemia if they rely solely on the results of laboratory testing.
- People with type 2 continue to produce insulin in early disease stages; however, their bodies do not respond adequately to the hormone (i.e., the patients are resistant to insulin’s effects).
- Alcoholic ketoacidosis is the buildup of ketones in the blood due to alcohol use.
- That increase in prevalence was most apparent in patients with a disease duration of less than 4 years.
- Heavy drinking (i.e., more than 140 grams of pure alcohol, or approximately 12 standard drinks, per day) can cause alcohol-induced hypertriglyceridemia in both diabetics and nondiabetics (Chait et al. 1972).
- The acetic acid can be shunted towards ketogenesis in favorable insulin/glucagon concentrations, which is seen in hypoglycemia.
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 alcoholic ketoacidosis 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. The pancreas, which is located behind the stomach, serves two functions. The first function, which involves most of the pancreatic cells, is the production of digestive enzymes.