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| '''For patient information page click [[{{PAGENAME}} (patient information)|here]]'''
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| {{Infobox_Disease | | | {| class="infobox" style="float:right;" |
| Name = Metabolic acidosis |
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| Image = Davenport Fig 12.jpg |
| | |[[File:Siren.gif|30px|link=Metabolic acidosis resident survival guide]]||<br>||<br> |
| Caption = [[Davenport diagram]] |
| | |[[Metabolic acidosis resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']] |
| DiseasesDB = 92 |
| | |} |
| ICD10 = {{ICD10|E|87|2|e|70}} |
| | {{Metabolic acidosis}} |
| ICD9 = {{ICD9|276.2}} |
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| ICDO = |
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| OMIM = |
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| MedlinePlus = |
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| MeshID = |
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| {{Search infobox}}
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| {{CMG}}
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| ==Overview==
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| In [[medicine]], '''metabolic acidosis''' is a state in which the blood [[pH]] is low (less than 7.35) due to increased production of [[hydrogen|H<sup>+</sup>]] by the body or the inability of the body to form [[bicarbonate]] (HCO<sub>3</sub><sup>-</sup>) in the [[kidney]]. Its causes are diverse, and its consequences can be serious, including [[diarrhea]], [[coma]] and [[death]]. Together with [[respiratory acidosis]], it is one of the two general types of [[acidosis]].
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| ==Symptoms==
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| Symptoms are non-specific, and diagnosis can be difficult unless the patient presents with clear indications for [[arterial blood gas]] sampling. Symptoms may include
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| * [[chest pain]]
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| * [[palpitations]]
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| * [[headache]]
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| * Altered mental status
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| * Decreased visual acuity
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| * [[Nausea]], [[vomiting]]
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| * [[Abdominal pain]]
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| * Altered appetite (either loss of or increased)
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| * [[weight loss]] (longer term)
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| * Muscle weakness and bone pains
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| * [[Kussmaul respiration]]s (deep rapid breathing, 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 to form a respiratory alkalosis does not occur.
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| * Lethargy, stupor, [[coma]], [[seizure]]s.
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| * [[Arrhythmia]]s ([[ventricular tachycardia]]), decreased response to [[epinephrine]]; both lead to [[hypotension]] (low blood pressure).
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| ==Physical examination==
| | '''For patient information page, click [[{{PAGENAME}} (patient information)|here]]''' |
| * Occasionally reveals signs of disease, but is otherwise normal
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| * [[Cranial nerve]] abnormalities are reported in [[ethylene glycol]] poisoning
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| * [[retina]]l [[edema]] can be a sign of [[methanol]] (methyl alcohol) intoxication
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| * Longstanding chronic metabolic acidosis leads to [[osteoporosis]] and can cause [[fracture]]s.
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| ==Diagnosis==
| | {{CMG}}; {{AE}} [[Priyamvada Singh|Priyamvada Singh, M.D.]] [mailto:psingh13579@gmail.com] |
| * [[Arterial blood gas]] sampling is essential for the diagnosis. The pH is low (under 7.35) and the bicarbonate levels are decreased (<12 mmol/l). In [[respiratory acidosis]] (low blood pH due to decreased clearance of [[carbon dioxide]] by the [[lung]]s), the bicarbonate is elevated, due to increased conversion from H<sub>2</sub>CO<sub>3</sub>.
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| * 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 plus potassium levels. Normally, this concentration is about 10-14 mmol/l (12±2). An elevated ''anion gap'' (i.e. > 16 mmol/l) can indicate particular types of metabolic acidosis, particularly certain poisons, lactate acidosis and ketoacidosis.
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| * Serum lactate, ketone
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| * An [[ECG]] can be useful to anticipate cardiac complications.
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| * [[Electrolyte]]s (including [[chloride]]), [[glucose]], [[renal function]] and a [[full blood count]].
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| * Urinalysis can reveal acidity, ([[salicylate]] poisoning) or alkalinity (renal tubular acidosis type I). In addition, it can show ketones in ketoacidosis.
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| * Toxicological screening, salicylate level (methanol or ethylene glycol)
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| * Imaging of the kidneys
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| ==Causes==
| | {{SK}} Acidosis, metabolic |
| The causes are best grouped by their influence on the ''[[anion gap]]'':
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| ===Low anion gap=== | | ==[[Metabolic acidosis overview|Overview]]== |
| A low anion gap is relatively rare but may occur from the presence of abnormal positively charged proteins, as in [[multiple myeloma]], or in the setting of a low [[human serum albumin|serum albumin]] level.
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| * Electrolyte abnormality - [[hypercalcemia|hypercalcemia]], [[hypermagnesemia]], [[hypernatremia|hypernatremia]], underestimation of serum [[sodium]]
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| * Hyperviscosity-[[multiple myeloma]], [[paraproteinemia]]
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| * [[Albumin|Hypoalbuminemia]]
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| * [[Lithium]] toxicity
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| * [[Pheochromocytoma]]
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| * Bromism <ref>Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:34 ISBN 1591032016</ref>
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| * Dilution
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| ===Normal anion gap ([[hyperchloremic acidosis]])===
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| Usually the HCO<sub>3</sub><sup>-</sup> lost is replaced by a chloride anion, and thus there is a normal anion gap. Urine anion gap is useful in evaluating a patient with a normal anion gap. In normal anion gap acidosis, the increased anion is chloride, which is measured, so the anion gap does not increase. Thus, normal anion gap acidosis is also known as hyperchloremic acidosis.
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| The mnemonic for the most common causes of a normal-anion gap metabolic acidosis is "DURHAM."
| | ==[[Metabolic acidosis classification|Classification]]== |
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| * '''D'''- Diarrhea
| | ==[[Metabolic acidosis pathophysiology|Pathophysiology]]== |
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| * '''U'''- Ureteral diversion
| | ==[[Metabolic acidosis causes|Causes]]== |
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| * '''R'''- Renal tubular acidosis
| | ==[[Metabolic acidosis differential diagnosis|Differentiating Metabolic Acidosis from other Diseases]]== |
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| * '''H'''- Hyperailmentation
| | ==[[Metabolic acidosis epidemiology and demographics|Epidemiology and Demographics]]== |
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| * '''A'''- Addison's disease, acetazolamide, ammonium chloride
| | ==[[Metabolic acidosis risk factors|Risk Factors]]== |
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| * '''M'''- Miscellaneous (chloridorrhea, amphotericin B, toluene - toluene causes high anion gap metabolic acidosis followed by normal anion gap metabolic acidosis.
| | ==[[Metabolic acidosis natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
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| ===High anion gap=== | | ==Diagnosis== |
| The bicarbonate lost is replaced by an unmeasured anion and thus you will see a high anion gap. Low serum albumin will decrease the apparent anion gap. To correct the anion gap for low serum albumin, we have to add 2.5 to the anion gap for every 1g/dl that serum albumin is decreased from the normal value of 4g/dl.
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| {{anchor|MUDPILES}}
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| The mnemonic "MUDPILES" is used to remember the causes of a high anion gap.
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| '''M''' - [[methanol]]/[[metformin]]<br />
| | [[Metabolic acidosis history and symptoms|History and Symptoms]] | [[ Metabolic acidosis physical examination|Physical Examination]] | [[Metabolic acidosis laboratory findings|Laboratory Findings]] | [[Metabolic acidosis electrocardiogram|Electrocardiogram]] | [[Metabolic acidosis other imaging findings|Other Imaging Findings]] | [[Metabolic acidosis other diagnostic studies|Other Diagnostic Studies]] |
| '''U''' - [[uremia]]<br />
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| '''D''' - [[diabetic ketoacidosis]]<br />
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| '''P''' - [[paraldehyde]]/[[propylene glycol]]<br />
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| '''I''' - [[Infection]]/[[ischemia]]/[[isoniazid]]<br />
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| '''L''' - [[lactate]]<br />
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| '''E''' - [[ethylene glycol]]/[[ethanol]]<br />
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| '''S''' - [[salicylates]]/[[starvation]]
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| Some people, especially those not in the emergency room, find the mnemonic KIL-U easier to remember and also more useful clinically:
| | ==Treatment== |
| | | [[Metabolic acidosis medical therapy|Medical Therapy]] | [[Metabolic acidosis secondary prevention|Secondary Prevention]] | [[Metabolic acidosis cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Metabolic acidosis future or investigational therapies|Future or Investigational Therapies]] |
| '''K''' - [[Ketones]] <br />
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| '''I''' - [[Ingestion]] <br />
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| '''L''' - [[lactic acid]] <br />
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| '''U''' - [[uremia]] <br />
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| All of the components of "mudpiles" are also covered with the "KIL-U" device, with the bonus that these are things that can kill you.
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| '''Ketones''': more straightforward than remembering diabetic ketosis and starvation ketosis, etc.
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| '''Ingestion''': methanol, metformin, paraldehyde, propylene glycol, isoniazid, ethylene glycol, ethanol, and salicilates are covered by ingestion. These can be thought of as a single group: "ingestions" during the initial consideration, especially when not triaging a patient in the emergency room.
| | ==Case Studies== |
| | [[Metabolic acidosis case study one|Case #1]] |
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| '''Lactate''': including that caused by infection and shock
| | ==Related Chapters== |
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| ==Pathophysiology==
| | *[[Acid-base imbalance]] |
| ===Compensatory mechanisms===
| | *[[Anion gap]] |
| 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.
| | *[[Hypocalcemia]] |
| * [[bicarbonate buffering system]] | | *[[Metabolic alkalosis]] |
| * [[Intracellular]] buffering by absorption of hydrogen atoms by various molecules, including proteins, phosphates and carbonate in bone. | | *[[Respiratory acidosis]] |
| * [[Respiratory compensation]] | | *[[Respiratory alkalosis]] |
| * [[Renal compensation]] | |
| ===Respiratory compensation of metabolic acidosis===
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| * For 1 meq/L fall of serum HCO3 levels there is a 1.2 mmHg fall in arterial pCO2. | |
| * The respiratory compensation of metabolic acidosis is fast and begins within half an hour of metabolic acidosis.
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| * In cases where the metabolic acidosis develops slowly, the respiratory compensation occurs simultaneously with the metabolic acidosis.
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| * The respiratory compensation usually completes within 12 to 24 hours
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| * A failure to develop adequate respiratory response indicates an acute underlying respiratory diseases, neurologic disease or a very acute development of metabolic acidosis.
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| * Formula for checking appropriate respiratory compensation to metabolic acidosis include:
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| ** Arterial pCO2 = 1.5 x serum HCO3 + 8 ± 2 (Winters’ equation)
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| ** Arterial pCO2 = Serum HCO3 + 15
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| ===Buffer===
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| 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:
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| :H<sup>+</sup> + HCO<sub>3</sub><sup>-</sup> <--> H<sub>2</sub>CO<sub>3</sub> <--> CO<sub>2</sub> + H<sub>2</sub>O
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| The [[Henderson-Hasselbalch equation]] mathematically describes the relationship between blood pH and the components of the bicarbonate buffering system:
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| :pH=pKa + log [HCO<sub>3</sub><sup>-</sup>]/[CO<sub>2</sub>]
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| :Using Henry's Law, we can say that [CO<sub>2</sub>]=0.03xPaCO<sub>2</sub>
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| : (PaCO<sub>2</sub> is the pressure of CO<sub>2</sub> in arterial blood)
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| :Adding the other normal values, we get
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| :pH = 6.1 + log (24/0.03x40)
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| : = 6.1 + 1.3
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| : = 7.4
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| ==Treatment==
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| A pH under 7.1 is an emergency, due to the risk of [[cardiac arrhythmia]]s, 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]].
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| 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.
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| ==References==
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| <references/>
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| [[Category:Nephrology]]
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| [[Category:Electrolyte disturbance]] | | [[Category:Electrolyte disturbance]] |
| | [[Category:Emergency medicine]] |
| [[Category:Intensive care medicine]] | | [[Category:Intensive care medicine]] |
| [[Category:Emergency medicine]] | | [[Category:Laboratory Test]] |
| | | [[Category:Medical tests]] |
| [[et:Metaboolne atsidoos]] | | [[Category:Medicine]] |
| [[fr:Acidose métabolique]] | | [[Category:Nephrology]] |
| [[it:Acidosi metabolica]] | |
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| [[Category:Inborn errors of metabolism]]
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