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| '''For patient information page click [[{{PAGENAME}} (patient information)|here]]'''
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| | {| class="infobox" style="float:right;" |
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| | |[[File:Siren.gif|30px|link=Metabolic acidosis resident survival guide]]||<br>||<br> |
| | |[[Metabolic acidosis resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']] |
| | |} |
| | {{Metabolic acidosis}} |
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| {{Infobox_Disease |
| | '''For patient information page, click [[{{PAGENAME}} (patient information)|here]]''' |
| Name = Metabolic acidosis |
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| Image = Davenport Fig 12.jpg |
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| Caption = [[Davenport diagram]] |
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| DiseasesDB = 92 |
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| ICD10 = {{ICD10|E|87|2|e|70}} |
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| ICD9 = {{ICD9|276.2}} |
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| ICDO = |
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| OMIM = |
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| MedlinePlus = 000335 |
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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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| ==Signs and symptoms==
| | {{CMG}}; {{AE}} [[Priyamvada Singh|Priyamvada Singh, M.D.]] [mailto:psingh13579@gmail.com] |
| 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 respiration]]s 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 to form a respiratory alkalosis does not occur.
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| Extreme acidosis leads to neurological and cardiac complications:
| | {{SK}} Acidosis, metabolic |
| * Neurological: lethargy, stupor, [[coma]], [[seizure]]s.
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| * Cardiac: [[arrhythmia]]s ([[ventricular tachycardia]]), decreased response to [[epinephrine]]; both lead to [[hypotension]] (low blood pressure).
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| [[Physical examination]] occasionally reveals signs of disease, but is otherwise normal. [[Cranial nerve]] abnormalities are reported in [[ethylene glycol]] poisoning, and [[retina]]l [[edema]] can be a sign of [[methanol]] (methyl alcohol) intoxication. Longstanding chronic metabolic acidosis leads to [[osteoporosis]] and can cause [[fracture]]s. | | ==[[Metabolic acidosis overview|Overview]]== |
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| ==Diagnosis==
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| [[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.
| | ==[[Metabolic acidosis classification|Classification]]== |
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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 pathophysiology|Pathophysiology]]== |
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| Anion gap = ( [Na<sup>+</sup>]+[K<sup>+</sup>] ) - ( [Cl<sup>-</sup>]+[HCO<sub>3</sub><sup>-</sup>] )
| | ==[[Metabolic acidosis causes|Causes]]== |
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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 differential diagnosis|Differentiating Metabolic Acidosis from other Diseases]]== |
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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 epidemiology and demographics|Epidemiology and Demographics]]== |
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| ==Causes== | | ==[[Metabolic acidosis risk factors|Risk Factors]]== |
| The causes are best grouped by their influence on the ''[[anion gap]]'':
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| ===Increased anion gap=== | | ==[[Metabolic acidosis natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
| Causes include:
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| * [[lactic acidosis]]
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| * [[ketoacidosis]]
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| * [[chronic renal failure]] (accumulation of [[sulfate]]s, [[phosphate]]s, [[uric acid]])
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| * intoxication:
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| ** [[organic acid]]s ([[salicylate]]s, [[ethanol]], [[methanol]], [[formaldehyde]], [[ethylene glycol]], [[paraldehyde]], [[INH]], [[toluene]])
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| ** [[sulfates]], [[metformin]] (Glucophage®)
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| * massive [[rhabdomyolysis]]
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| ===Mnemonics for {{PAGENAME}}=== | | ==Diagnosis== |
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| The mnemonic MUDPILES is commonly used to remember the causes of Increased anion gap metabolic acidosis.<ref>{{MedicalMnemonics|1203|3255||}}</ref><ref>http://fitsweb.uchc.edu/student/selectives/TimurGraham/Anion_Gap.html</ref>
| | [[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]] |
| *M-[[Methanol]]
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| *U-[[Uremia]]
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| *D-[[Diabetic Ketoacidosis]]
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| *P-[[Paraldehyde]]
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| *I-[[Infection]], [[Iron]], [Isoniazid]]
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| *L-[[Lactic acidosis]]
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| *E-[[Ethylene glycol]], [[Ethanol]]
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| *S-[[Salicylate]]s
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| ===Normal anion gap=== | | ==Treatment== |
| Causes include:<ref>{{MedicalMnemonics|2001|||}}</ref>
| | [[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]] |
| * longstanding [[diarrhea]] (bicarbonate loss)
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| * [[pancreatic fistula]]
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| * uretero-sigmoidostomy
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| * [[Renal tubular acidosis]] (RTA)
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| * intoxication:
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| ** [[ammonium chloride]]
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| ** [[acetazolamide]] (Diamox®)
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| ** [[bile acid sequestrant]]s
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| ** [[isopropyl alcohol]]
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| * [[renal failure]] (occasionally)
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| 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).
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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. | |
| * [[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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| ===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:
| | ==Case Studies== |
| | [[Metabolic acidosis case study one|Case #1]] |
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| :pH=pKa + log [HCO<sub>3</sub><sup>-</sup>]/[CO<sub>2</sub>]
| | ==Related Chapters== |
| :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==
| | *[[Acid-base imbalance]] |
| 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]].
| | *[[Anion gap]] |
| | *[[Hypocalcemia]] |
| | *[[Metabolic alkalosis]] |
| | *[[Respiratory acidosis]] |
| | *[[Respiratory alkalosis]] |
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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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