Alcoholic ketoacidosis

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Alcoholic ketoacidosis
Other namesAlcoholic ketosis, alcoholic acidosis [1]
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It generally occurs in chronic alcoholics or those who binge drink [2]
Specialty Internal medicine
Symptoms Abdominal pain, vomiting, agitation, fast respiratory rate, specific "fruity" smell [2]
Risk factors Alcoholism, binge drinking [2]
Diagnostic method Based on symptoms [2]
Differential diagnosis Other causes of high anion gap metabolic acidosis (diabetic ketoacidosis, toxic alcohol ingestion, starvation ketosis), pancreatitis [2] [3]
Treatment Intravenous fluids, thiamine [2]
Prognosis Good with treatment [1]

Alcoholic ketoacidosis (AKA) is a specific group of symptoms and metabolic state related to alcohol use. [3] Symptoms often include abdominal pain, vomiting, agitation, a fast respiratory rate, and a specific "fruity" smell. [2] Consciousness is generally normal. [1] Complications may include sudden death. [1]

Contents

AKA most commonly occurs in long term alcoholics and less commonly in those who binge drink. [2] Onset is generally after a decreased ability to eat for a few days. [2] Diagnosis is generally based on symptoms. [2] Blood sugar levels are often normal or only mildly increased. [2] Other conditions that may present similarly include other causes of high anion gap metabolic acidosis including diabetic ketoacidosis. [2]

Treatment is generally with intravenous normal saline and intravenous sugar solution. [2] Thiamine and measures to prevent alcohol withdrawal are also recommended. [2] Treatment of low blood potassium may also be required. [2] Those who are affected are most frequently between the ages of 20 and 60. [2] The condition was initially recognized in 1940 and named in 1971. [3]

Signs and symptoms

Nausea, vomiting, and abdominal pain are commonly present and people may also have tachypnea, tachycardia, and hypotension. [4] In contrast to diabetic ketoacidosis, people with alcoholic ketoacidosis are usually alert and lucid despite the severity of the acidosis. [1]

Causes

Alcoholic ketoacidosis is caused by complex physiology that is the result of prolonged and heavy alcohol intake, usually in the setting of poor nutrition. Chronic alcohol use can cause depleted hepatic glycogen stores and ethanol metabolism further impairs gluconeogenesis. This can reduce glucose availability and lead to hypoglycemia and increased reliance on fatty acid and ketone metabolism. [1] [5] An additional stressor such as vomiting or dehydration can cause an increase in counterregulatory hormones such as glucagon, cortisol and growth hormone which may further increase free fatty acid release and ketone production. Ethanol metabolism can also increase blood lactic acid levels (lactic acidosis), due to pseudohypoxia, which may also contribute to a metabolic acidosis. [6]

Diagnosis

Diagnosis is generally based on symptoms. [2] An elevated anion gap metabolic acidosis and ketosis is the classic present. [3] However, a mixed acid-base disorder may be present especially if vomiting is contributing to a hypochloremic alkalosis. [2] The ketone which is present is mostly beta-hydroxybutyrate rather than acetoacetate resulting in only a weakly positive nitroprusside test. [2] People usually do not present with high blood sugar or sugar in the urine. [2] This can cause false negative results when testing urine ketones as they only measure acetoacetate. Ethanol level are often low or negative despite a chronic alcohol use history. [6] Electrolyte disturbances may include hypokalemia or hypomagnesemia may also be present. [2]

Differential diagnosis

Other conditions that may present similarly include other causes of high anion gap metabolic acidosis such as diabetic ketoacidosis, toxic alcohol ingestion, and starvation ketosis. [2] Toxic alcohol ingestion includes methanol and ethylene glycol poisoning. [6] Pancreatitis, alcoholic hepatitis, and gastritis may also result in similar symptoms. [3] The ratio of beta-hydroxybutryate to acetoacetate is usually higher in AKA (8:1) in contrast to diabetic ketoacidosis (3:1). [2]

Management

Treatment includes administration of intravenous saline to rehydrate and 5% dextrose to turn off gluconeogenesis. Electrolyte imbalances, specifically hypokalaemia, should be corrected. Thiamine supplementation is often included to prevent Wernicke encephalopathy. Insulin is generally not used due to risk of hypoglycemia. [5] Other potential causes of the symptoms should be ruled out. [6]

Prognosis

Outcomes are generally favorable with treatment but up to 10% may develop cardiac arrest. [5] It is proposed that alcoholic ketoacidosis is a significant cause of death among people with chronic alcoholism although the true prevalence is unknown. Estimation of prevalence and outcomes of this population is limited by difficulty in diagnosing the condition and the presence of multiple disorders at presentation. [6]

History

In 1940, Edward S. Dillon, W. Wallace, and Leon S. Smelo, first described alcoholic ketoacidosis as a distinct syndrome. They stated that "because of the many and complex factors, both physiologic and pathologic, which influence the acid-base balance of the body, a multitude of processes may bring about the state of acidosis as an end result". [7]

In 1971, David W. Jenkins and colleagues described cases of three non-diabetic people with a history of chronic heavy alcohol misuse and recurrent episodes of ketoacidosis. This group also proposed a possible underlying mechanism for this metabolic disturbance, naming it alcoholic ketoacidosis. [8]

Related Research Articles

<span class="mw-page-title-main">Diabetic ketoacidosis</span> Medical condition

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion and occasionally loss of consciousness. A person's breath may develop a specific "fruity" smell. The onset of symptoms is usually rapid. People without a previous diagnosis of diabetes may develop DKA as the first obvious symptom.

<span class="mw-page-title-main">Ketone bodies</span> Chemicals produced during fat metabolism

Ketone bodies are water-soluble molecules or compounds that contain the ketone groups produced from fatty acids by the liver (ketogenesis). Ketone bodies are readily transported into tissues outside the liver, where they are converted into acetyl-CoA – which then enters the citric acid cycle and is oxidized for energy. These liver-derived ketone groups include acetoacetic acid (acetoacetate), beta-hydroxybutyrate, and acetone, a spontaneous breakdown product of acetoacetate.

<span class="mw-page-title-main">Acetoacetic acid</span> Chemical compound

Acetoacetic acid is the organic compound with the formula CH3COCH2COOH. It is the simplest beta-keto acid, and like other members of this class, it is unstable. The methyl and ethyl esters, which are quite stable, are produced on a large scale industrially as precursors to dyes. Acetoacetic acid is a weak acid.

<span class="mw-page-title-main">Ketosis</span> Using body fats as fuel instead of carbohydrates

Ketosis is a metabolic state characterized by elevated levels of ketone bodies in the blood or urine. Physiological ketosis is a normal response to low glucose availability. In physiological ketosis, ketones in the blood are elevated above baseline levels, but the body's acid–base homeostasis is maintained. This contrasts with ketoacidosis, an uncontrolled production of ketones that occurs in pathologic states and causes a metabolic acidosis, which is a medical emergency. Ketoacidosis is most commonly the result of complete insulin deficiency in type 1 diabetes or late-stage type 2 diabetes. Ketone levels can be measured in blood, urine or breath and are generally between 0.5 and 3.0 millimolar (mM) in physiological ketosis, while ketoacidosis may cause blood concentrations greater than 10 mM.

<span class="mw-page-title-main">Diabetic coma</span> Medical condition

Diabetic coma is a life-threatening but reversible form of coma found in people with diabetes mellitus.

<span class="mw-page-title-main">Ketogenesis</span> Chemical synthesis of ketone bodies

Ketogenesis is the biochemical process through which organisms produce ketone bodies by breaking down fatty acids and ketogenic amino acids. The process supplies energy to certain organs, particularly the brain, heart and skeletal muscle, under specific scenarios including fasting, caloric restriction, sleep, or others.

Acidosis is a biological process producing hydrogen ions and increasing their concentration in blood or body fluids. pH is the negative log of hydrogen ion concentration and so it is decreased by a process of acidosis.

<span class="mw-page-title-main">Ketoacidosis</span> Medical condition

Ketoacidosis is a metabolic state caused by uncontrolled production of ketone bodies that cause a metabolic acidosis. While ketosis refers to any elevation of blood ketones, ketoacidosis is a specific pathologic condition that results in changes in blood pH and requires medical attention. The most common cause of ketoacidosis is diabetic ketoacidosis but it can also be caused by alcohol, medications, toxins, and rarely, starvation.

<span class="mw-page-title-main">Metabolic acidosis</span> Imbalance in the bodys acid-base equilibrium

Metabolic acidosis is a serious electrolyte disorder characterized by an imbalance in the body's acid-base balance. Metabolic acidosis has three main root causes: increased acid production, loss of bicarbonate, and a reduced ability of the kidneys to excrete excess acids. Metabolic acidosis can lead to acidemia, which is defined as arterial blood pH that is lower than 7.35. Acidemia and acidosis are not mutually exclusive – pH and hydrogen ion concentrations also depend on the coexistence of other acid-base disorders; therefore, pH levels in people with metabolic acidosis can range from low to high.

Ketotic hypoglycemia refers to any circumstance in which low blood glucose is accompanied by ketosis, the presence of ketone bodies in the blood or urine. This state can be either physiologic or pathologic; physiologic ketotic hypoglycemia is a common cause of hypoglycemia in children, often in response to stressors such as infection or fasting. Pathologic ketotic hypoglycemia is typically caused by metabolic defects, such as glycogen storage disorders.

<span class="mw-page-title-main">Glycogen storage disease type I</span> Medical condition

Glycogen storage disease type I is an inherited disease that prevents the liver from properly breaking down stored glycogen, which is necessary to maintain adequate blood sugar levels. GSD I is divided into two main types, GSD Ia and GSD Ib, which differ in cause, presentation, and treatment. There are also possibly rarer subtypes, the translocases for inorganic phosphate or glucose ; however, a recent study suggests that the biochemical assays used to differentiate GSD Ic and GSD Id from GSD Ib are not reliable, and are therefore GSD Ib.

The anion gap is a value calculated from the results of multiple individual medical lab tests. It may be reported with the results of an electrolyte panel, which is often performed as part of a comprehensive metabolic panel.

In physiology, base excess and base deficit refer to an excess or deficit, respectively, in the amount of base present in the blood. The value is usually reported as a concentration in units of mEq/L (mmol/L), with positive numbers indicating an excess of base and negative a deficit. A typical reference range for base excess is −2 to +2 mEq/L.

<span class="mw-page-title-main">Ketonuria</span> Medical condition

Ketonuria is a medical condition in which ketone bodies are present in the urine.

Hyperosmolar hyperglycemic state (HHS), also known as hyperosmolar non-ketotic state (HONK), is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis. Symptoms include signs of dehydration, weakness, leg cramps, vision problems, and an altered level of consciousness. Onset is typically over days to weeks. Complications may include seizures, disseminated intravascular coagulopathy, mesenteric artery occlusion, or rhabdomyolysis.

β-Hydroxybutyric acid Chemical compound

β-Hydroxybutyric acid, also known as 3-hydroxybutyric acid or BHB, is an organic compound and a beta hydroxy acid with the chemical formula CH3CH(OH)CH2CO2H; its conjugate base is β-hydroxybutyrate, also known as 3-hydroxybutyrate. β-Hydroxybutyric acid is a chiral compound with two enantiomers: D-β-hydroxybutyric acid and L-β-hydroxybutyric acid. Its oxidized and polymeric derivatives occur widely in nature. In humans, D-β-hydroxybutyric acid is one of two primary endogenous agonists of hydroxycarboxylic acid receptor 2 (HCA2), a Gi/o-coupled G protein-coupled receptor (GPCR).

<span class="mw-page-title-main">High anion gap metabolic acidosis</span> Medical condition

High anion gap metabolic acidosis is a form of metabolic acidosis characterized by a high anion gap. Metabolic acidosis occurs when the body produces too much acid, or when the kidneys are not removing enough acid from the body. Several types of metabolic acidosis occur, grouped by their influence on the anion gap.

Complications of diabetes are secondary diseases that are a result of elevated blood glucose levels that occur in diabetic patients. These complications can be divided into two types: acute and chronic. Acute complications are complications that develop rapidly and can be exemplified as diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar state (HHS), lactic acidosis (LA), and hypoglycemia. Chronic complications develop over time and are generally classified in two categories: microvascular and macrovascular. Microvascular complications include neuropathy, nephropathy, and retinopathy; while cardiovascular disease, stroke, and peripheral vascular disease are included in the macrovascular complications.

<span class="mw-page-title-main">Intravenous sodium bicarbonate</span> Pharmaceutical drug

Intravenous sodium bicarbonate, also known as sodium hydrogen carbonate, is a medication primarily used to treat severe metabolic acidosis. For this purpose it is generally only used when the pH is less than 7.1 and when the underlying cause is either diarrhea, vomiting, or the kidneys. Other uses include high blood potassium, tricyclic antidepressant overdose, and cocaine toxicity as well as a number of other poisonings. It is given by injection into a vein.

Pseudohypoxia refers to a condition that mimics hypoxia, by having sufficient oxygen yet impaired mitochondrial respiration due to a deficiency of necessary co-enzymes, such as NAD+ and TPP. The increased cytosolic ratio of free NADH/NAD+ in cells (more NADH than NAD+) can be caused by diabetic hyperglycemia and by excessive alcohol consumption. Low levels of TPP results from thiamine deficiency.

References

  1. 1 2 3 4 5 6 McGuire, LC; Cruickshank, AM; Munro, PT (June 2006). "Alcoholic ketoacidosis". Emergency Medicine Journal. 23 (6): 417–20. doi:10.1136/emj.2004.017590. PMC   2564331 . PMID   16714496.
  2. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 Howard, RD; Bokhari, SRA (January 2019). Alcoholic Ketoacidosis (AKA). PMID   28613672.
  3. 1 2 3 4 5 Allison, MG; McCurdy, MT (May 2014). "Alcoholic metabolic emergencies". Emergency Medicine Clinics of North America. 32 (2): 293–301. doi:10.1016/j.emc.2013.12.002. PMID   24766933.
  4. ↑ Wrenn, KD; Slovis, CM; Minion, GE; Rutkowski, R (August 1991). "The syndrome of alcoholic ketoacidosis". The American Journal of Medicine. 91 (2): 119–28. doi: 10.1016/0002-9343(91)90003-g . PMID   1867237.
  5. 1 2 3 Cartwright, Martina M.; Hajja, Waddah; Al-Khatib, Sofian; Hazeghazam, Maryam; Sreedhar, Dharmashree; Li, Rebecca Na; Wong-McKinstry, Edna; Carlson, Richard W. (Oct 2012). "Toxigenic and Metabolic Causes of Ketosis and Ketoacidotic Syndromes". Critical Care Clinics. 28 (4): 601–631. doi:10.1016/j.ccc.2012.07.001. PMID   22998993.
  6. 1 2 3 4 5 Höjer, Jonas (Oct 2017). "[Alcoholic ketoacidosis – a review]". Läkartidningen. 114. ISSN   1652-7518. PMID   28994854.
  7. ↑ Dillon, E.; Dyer, W. Wallace; Smelo, L. S. (November 1940). "Ketone Acidosis in Nondiabetic Adults". Medical Clinics of North America . 24 (6): 1813–1822. doi:10.1016/S0025-7125(16)36653-6.
  8. ↑ Jenkins, David W.; Eckel, Robert E.; Craig, James W. (12 July 1971). "Alcoholic Ketoacidosis". JAMA: The Journal of the American Medical Association. 217 (2): 177–183. doi:10.1001/jama.1971.03190020037007. PMID   5108780.
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