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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 = |
| | |[[File:Siren.gif|30px|link=Metabolic acidosis resident survival guide]]||<br>||<br> |
| Caption = |
| | |[[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}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.D.]] [mailto:psingh@perfuse.org]
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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]], the other being [[respiratory acidosis]].
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| ==Pathophysiology==
| | '''For patient information page, click [[{{PAGENAME}} (patient information)|here]]''' |
| ===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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| ===Role of the urine anion gap in the patient with a normal anion gap metabolic acidosis===
| | {{CMG}}; {{AE}} [[Priyamvada Singh|Priyamvada Singh, M.D.]] [mailto:psingh13579@gmail.com] |
| * [[Urine anion gap]] helps to differentiate [[renal tubular acidosis]] (specifically a Type 1 or Type 4 RTA) from other causes of normal anion gap acidosis.
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| * The urine anion gap is calculated as the urine sodium plus urine potassium, minus the urine chloride
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| * Urine anion gap = (Urine Na + Urine K) - Urine Cl
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| * The pathophysiology behind this is:
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| ** When kidney is exposed to acidosis, the normal response of the kidney is to excrete acid.
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| ** Kidney excretes the excess acid in the form of ammonium, NH4+.
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| ** To maintain neutrality, Cl- is excreted along with ammonium, NH4+.
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| ** Thus, urine chloride act as a surrogate marker for urine ammonium (acidosis)
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| ** In Types 1 and 4 renal tubular acidosis, the kidney's function of acid excretion is compromised (decreased excretion of NH4+ and Cl).
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| ** Thus, in [[renal tubular acidosis]] (specifically a Type 1 or Type 4 RTA) urine anion gap will be high (> than zero).
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| ** A urine anion gap less than zero in the normal anion gap metabolic acidosis suggests the kidney is excreting acid, making [[renal tubular acidosis]] less likely.
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| ===Role of osmolar gap in differential diagnosis of elevated anion gap===
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| ===Buffer===
| | {{SK}} Acidosis, metabolic |
| * 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<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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| ==Causes== | | ==[[Metabolic acidosis overview|Overview]]== |
| The causes are best grouped by their influence on the ''[[anion gap]]'':
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| ===Low anion gap===
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| 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 albumin]] level. The mnemonic for low anion gap is '''BAM'''
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| * '''B''' - [[Bromism]]
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| * '''A''' - (Low) [[Albumin]] ([[hypoalbuminism]])
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| * '''M''' - [[Multiple myeloma]]
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| ===Normal anion gap ([[hyperchloremic acidosis]])=== | | ==[[Metabolic acidosis classification|Classification]]== |
| Usually the HCO<sub>3</sub><sup>-</sup> lost is replaced by a chloride anion, and thus there is 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. Urine anion gap is useful in evaluating a patient with a normal anion gap (see above).
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| The mnemonic for the most common causes of a normal-anion gap metabolic acidosis is "DURHAM."
| | ==[[Metabolic acidosis pathophysiology|Pathophysiology]]== |
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| * '''D'''- [[Diarrhea]]
| | ==[[Metabolic acidosis causes|Causes]]== |
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| * '''U'''- [[Ureteral diversion]]
| | ==[[Metabolic acidosis differential diagnosis|Differentiating Metabolic Acidosis from other Diseases]]== |
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| * '''R'''- [[Renal tubular acidosis]]
| | ==[[Metabolic acidosis epidemiology and demographics|Epidemiology and Demographics]]== |
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| * '''H'''- [[Hyperailmentation]]
| | ==[[Metabolic acidosis risk factors|Risk Factors]]== |
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| * '''A'''- [[Addison's disease]], [[acetazolamide]], [[ammonium chloride]]
| | ==[[Metabolic acidosis natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
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| * '''M'''- Miscellaneous ([[chloridorrhea]], [[amphotericin B]], [[toluene]] - toluene causes high anion gap metabolic acidosis followed by normal anion gap metabolic acidosis.
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| ===High anion gap=== | |
| 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 />
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| '''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:
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| '''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 [[salicylates]] 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.
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| '''Lactate''': including that caused by infection and shock
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| ===Coexistent elevated anion gap and normal anion gap metabolic acidosis===
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| * An elevated anion gap can coexist with a normal anion gap [[metabolic acidosis]].
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| * In a single [[acid-base disorder]] of elevated anion gap metabolic acidosis, serum bicarbonate (HCO3) will decrease by the same amount that the anion gap increases.
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| * However, a situation in which the [[anion gap]] increases less and serum bicarbonate decreases significantly indicates that there is another metabolic acidosis present, which is decreasing the the serum bicarbonate, but not affecting the anion gap i.e. normal anion gap metabolic acidosis is also present.
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| * Thus, it is advised to compare the changes in the anion gap with the changes in the serum bicarbonate.
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| * This is often referred as the delta-delta equation, or the corrected bicarbonate equation.
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| * '''Delta-Delta equation''': Change in anion gap = Change in bicarbonate
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| ==Diagnosis== | | ==Diagnosis== |
| ===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===
| | [[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]] |
| * Occasionally reveals signs of disease, but is otherwise normal
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| ====Eyes==== | | ==Treatment== |
| * [[retina]]l [[edema]] can be a sign of [[methanol]] ([[methyl alcohol]]) intoxication
| | [[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]] |
| ====Neurologic====
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| *[[Cranial nerve]] abnormalities can be observed in [[ethylene glycol]] poisoning
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| ====Extremities==== | | ==Case Studies== |
| * Longstanding chronic metabolic acidosis leads to [[osteoporosis]] and can cause [[fracture]]s.
| | [[Metabolic acidosis case study one|Case #1]] |
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| ===Laboratory Studies=== | | ==Related Chapters== |
| The following laboratory studies should be considered:
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| * [[Arterial blood gas]] sampling
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| * [[Anion gap]]
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| * Serum [[lactate]], [[ketone]]
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| * Toxicological screening, [[salicylate level]] ([[methanol]] or [[ethylene glycol]])
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| * [[ECG]] (to assess for [[arrhythmias]])
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| * [[Electrolyte]]s [[basic metabolic panel]]), [[complete blood count]].
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| * [[Urinalysis]] can reveal acidity, ([[salicylate]] poisoning) or alkalinity ([[renal tubular acidosis type I]]), and [[ketones]] in [[ketoacidosis]].
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| * Imaging of the kidneys
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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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|
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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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