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20-September-2008 09:55:49 - acidosis Merge arrows It has been suggested that this article or section be merged with acidosis. Discuss Metabolic acidosis Classification and external resources Davenport diagram ICD-10 E87.2 ICD-9 276.2 DiseasesDB 92 MedlinePlus 000335 eMedicine emerg/312 med/1458 ped/15 In medicine, metabolic acidosis is a process which if unchecked leads to acidemia i.e. blood pH is low less than 7.35 due to increased production of H+ by the body or the inability of the body to form bicarbonate HCO3- in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Contents 1 Signs and symptoms 2 Diagnosis 3 Causes 3.1 Increased anion gap 3.2 Normal anion gap 4 Pathophysiology 4.1 Compensatory mechanisms 4.2 Buffer 5 Treatment 6 References Signs and symptoms Symptoms are aspecific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite either loss of or increased and weight loss longer term, muscle weakness and bone pains. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Over compensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardiac complications: Neurological: lethargy, stupor, coma, seizures. Cardiac: arrhythmias ventricular tachycardia, decreased response to epinephrine; both lead to hypotension low blood pressure. Physical examination occasionally reveals signs of disease, but is otherwise normal. Cranial nerve abnormalities are reported in ethylene glycol poisoning, and retinal edema can be a sign of methanol methyl alcohol intoxication. Longstanding chronic metabolic acidosis leads to osteoporosis and can cause fractures. Diagnosis Arterial blood gas sampling is essential for the diagnosis. The pH is low under 7.35 and the bicarbonate levels are decreased 24 mmol/l. Due to respiratory compensation hyperventilation, carbon dioxide is decreased and conversely oxygen is increased. An ECG can be useful to anticipate cardiac complications. Other tests that are relevant in this context are electrolytes including chloride, glucose, renal function and a full blood count. Urinalysis can reveal acidity salicylate poisoning or alkalinity renal tubular acidosis type I. In addition, it can show ketones in ketoacidosis. To distinguish between the main types of metabolic acidosis, a clinical tool called the anion gap is considered very useful. It is calculated by subtracting the chloride and bicarbonate levels from the sodium. Anion gap = Na+ - Cl-+HCO3- As sodium is the main extracellular cation, and chloride and bicarbonate are the main anions, the result should reflect the remaining anions. Normally, this concentration is about 8-16 mmol/l 12±4. An elevated anion gap i.e. 16 mmol/l can indicate particular types of metabolic acidosis, particularly certain poisons, lactate acidosis and ketoacidosis. As the differential diagnosis is narrowed down, certain other tests may be necessary, including toxicological screening and imaging of the kidneys. Causes The causes are best grouped by their influence on the anion gap: Increased anion gap Causes include: lactic acidosis ketoacidosis chronic renal failure accumulation of sulfates, phosphates, uric acid intoxication: organic acids salicylates, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde, INH, toluene sulfates, metformin Glucophage massive rhabdomyolysis The mnemonic MUDPILES is commonly used to remember the causes of Increased anion gap metabolic acidosis.12 M-Methanol U-Uremia D-Diabetic Ketoacidosis P-Paraldehyde I-Infection, Iron, Isoniazid L-Lactic acidosis E-Ethylene Glycol S-Salicylates Note: Ethanol is sometimes included in this mnemonic as well, although the acidosis caused by ethanol is actually primarily due to the increased production of lactic acid found in such intoxication. Normal anion gap Causes include:3 longstanding diarrhea bicarbonate loss pancreatic fistula uretero-sigmoidostomy Renal tubular acidosis RTA intoxication: ammonium chloride acetazolamide Diamox bile acid sequestrants isopropyl alcohol renal failure occasionally It bears noting that the anion gap can be spuriously normal in sampling errors of the sodium level, e.g. in extreme hypertriglyceridemia. The anion gap can be increased due to relatively low levels of cations other than sodium and potassium e.g. calcium or magnesium. Pathophysiology Compensatory mechanisms Metabolic acidosis is either due to increased generation of acid or an inability to generate sufficient bicarbonate. The body regulates the acidity of the blood by four buffering mechanisms. bicarbonate buffering system Intracellular buffering by absorption of hydrogen atoms by various molecules, including proteins, phosphates and carbonate in bone. Respiratory compensation Renal compensation Buffer The decreased bicarbonate that distinguishes metabolic acidosis is therefore due to two separate processes: the buffer from water and carbon dioxide and additional renal generation. The buffer reactions are: H+ + HCO3- -- H2CO3 -- CO2 + H2O The Henderson-Hasselbalch equation mathematically describes the relationship between blood pH and the components of the bicarbonate buffering system: pH=pKa + log HCO3-/CO2 Using Henry's Law, we can say that CO2=0.03xPaCO2 PaCO2 is the pressure of CO2 in arterial blood Adding the other normal values, we get pH = 6.1 + log 24/0.03x40 = 6.1 + 1.3 = 7.4 Treatment A pH under 7.1 is an emergency, due to the risk of cardiac arrhythmias, and may warrant treatment with intravenous bicarbonate. Bicarbonate is given at 50-100 mmol at a time under scrupulous monitoring of the arterial blood gas readings. This intervention however, is not effective in case of lactic acidosis. If the acidosis is particularly severe and/or there may be intoxication, consultation with the nephrology team is considered useful, as dialysis may clear both the intoxication and the acidosis. References January 2008 ^ Mnemonic at medicalmnemonics.com 1203 3255 ^ Anion Gap: Acid Base Tutorial, University of Connecticut Health Center ^ Mnemonic at medicalmnemonics.com 2001 v d e Water-electrolyte imbalance and acid-base imbalance E86-E87, 276 Volume status Dehydration/Hypervolemia - Hypovolemia Electrolyte Na+ Hypernatremia/Hyponatremia K+ Hyperkalemia/Hypokalemia Cl- Hyperchloremia/Hypochloremia Acid-base Acidosis: Metabolic - Respiratory - Lactic - Ketosis Alkalosis: Metabolic, Respiratory Mixed disorder of acid-base balance Retrieved from http://en..org/wiki/Metabolic_acidosis Categories: All articles to be merged | Metabolic disorders | Nephrology | Electrolyte disturbances | Intensive care medicine | Emergency medicineHidden categories: Articles to be merged since June 2008 | Articles needing additional references from January 2008 Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Deutsch Eesti Français Italiano Polski This page was last modified on 20 August 2008, at 18:23
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