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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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| }}
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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>. An [[ECG]] can be useful to anticipate cardiac complications. | |
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| Other tests that are relevant in this context are [[electrolyte]]s (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.
| | {{SK}} Acidosis, metabolic |
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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.
| | ==[[Metabolic acidosis overview|Overview]]== |
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| Anion gap = ( [Na<sup>+</sup>]+[K<sup>+</sup>] ) - ( [Cl<sup>-</sup>]+[HCO<sub>3</sub><sup>-</sup>] )
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| 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.
| | ==[[Metabolic acidosis classification|Classification]]== |
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| As the [[differential diagnosis]] is narrowed down, certain other tests may be necessary, including toxicological screening and imaging of the kidneys.
| | ==[[Metabolic acidosis pathophysiology|Pathophysiology]]== |
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| ==Causes== | | ==[[Metabolic acidosis causes|Causes]]== |
| The causes are best grouped by their influence on the ''[[anion gap]]'':
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| ===Low anion gap=== | | ==[[Metabolic acidosis differential diagnosis|Differentiating Metabolic Acidosis from other Diseases]]== |
| 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]])=== | | ==[[Metabolic acidosis epidemiology and demographics|Epidemiology and Demographics]]== |
| 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.
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| * Enteral causes
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| ** [[Diarrhea]] (note: vomiting causes hypochloraemic alkalosis)
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| ** [[Pancreatitis]], Pancreatic fistula
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| ** [[Arginine]] and [[lysine]] during [[total parenteral nutrition]]
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| ** Ureteroenterostomy
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| ** Ileal stoma
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| * [[Ammonium chloride]] and Acetazolamide ([[Carbonic anhydrase inhibitors]])
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| *[[Renal]] loss of HCO<sub>3</sub><sup>-</sup> i.e. proximal [[renal tubular acidosis]], [[renal failure]], [[hypoaldosteronism]], distal [[renal tubular acidosis]]
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| * Alcohol (such as ethanol) can effect anion gap by inducing [[alcohol dehydrogenase]] enzyme.
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| * Recovery from [[diabetic ketoacidosis]]
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| ===High anion gap=== | | ==[[Metabolic acidosis risk factors|Risk Factors]]== |
| The bicarbonate lost is replaced by an unmeasured anion and thus you will see a high anion gap.
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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 natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
| '''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:
| | ==Diagnosis== |
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| '''K''' - [[Ketones]] <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]] |
| '''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.
| | ==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]] |
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| '''Ketones''': more straightforward than remembering diabetic ketosis and starvation ketosis, etc.
| | ==Case Studies== |
| | [[Metabolic acidosis case study one|Case #1]] |
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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.
| | ==Related Chapters== |
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| '''Lactate''': including that caused by infection and shock
| | *[[Acid-base imbalance]] |
| | *[[Anion gap]] |
| | *[[Hypocalcemia]] |
| | *[[Metabolic alkalosis]] |
| | *[[Respiratory acidosis]] |
| | *[[Respiratory alkalosis]] |
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| ==Pathophysiology==
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| ===Compensatory mechanisms===
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| 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.
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| * [[bicarbonate buffering system]]
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| * [[Intracellular]] buffering by absorption of hydrogen atoms by various molecules, including proteins, phosphates and carbonate in bone.
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| * [[Respiratory compensation]]
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| * [[Renal compensation]]
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| ===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.
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| * 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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