Metabolic acidosis
1333992
223937982
2008-07-06T16:34:09Z
89.246.207.1
{{Merge|acidosis|TALK:Metabolic acidosis|June 2008|date=June 2008}}
{{Infobox_Disease |
Name = Metabolic acidosis |
Image = Davenport Fig 12.jpg |
Caption = [[Davenport diagram]] |
DiseasesDB = 92 |
ICD10 = {{ICD10|E|87|2|e|70}} |
ICD9 = {{ICD9|276.2}} |
ICDO = |
OMIM = |
MedlinePlus = 000335 |
eMedicineSubj = emerg |
eMedicineTopic = 312 |
eMedicine_mult = {{eMedicine2|med|1458}} {{eMedicine2|ped|15}} |
MeshID = |
}}
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 [[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 [[coma]] and [[death]]. Together with [[respiratory acidosis]], it is one of the two general causes of acidemia.
==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 pain]]s. 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 via respiratory alkalosis to form an alkalemia does not occur.
Extreme acidemia leads to neurological and cardiac complications:
* Neurological: lethargy, stupor, [[coma]], [[seizure]]s.
* Cardiac: [[arrhythmia]]s ([[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 [[retina]]l [[edema]] can be a sign of [[methanol]] (methyl alcohol) intoxication. Longstanding chronic metabolic acidosis leads to [[osteoporosis]] and can cause [[fracture]]s.
==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 [[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.
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<sup>+</sup>] ) - ( [Cl<sup>-</sup>]+[HCO<sub>3</sub><sup>-</sup>] )
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 [[sulfate]]s, [[phosphate]]s, [[uric acid]])
* intoxication:
** [[organic acid]]s ([[salicylate]]s, [[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.<ref>{{MedicalMnemonics|1203|3255||}}</ref><ref>[http://fitsweb.uchc.edu/student/selectives/TimurGraham/Anion_Gap.html Anion Gap: Acid Base Tutorial, University of Connecticut Health Center<!-- Bot generated title -->]</ref>
*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:<ref>{{MedicalMnemonics|2001|||}}</ref>
* longstanding [[diarrhea]] (bicarbonate loss)
* [[pancreatic fistula]]
* uretero-sigmoidostomy
* [[Renal tubular acidosis]] (RTA)
* intoxication:
** [[ammonium chloride]]
** [[acetazolamide]] (Diamox)
** [[bile acid sequestrant]]s
** [[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<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
The [[Henderson-Hasselbalch equation]] mathematically describes the relationship between blood pH and the components of the bicarbonate buffering system:
:pH=pKa + log [HCO<sub>3</sub><sup>-</sup>]/[CO<sub>2</sub>]
:Using Henry's Law, we can say that [CO<sub>2</sub>]=0.03xPaCO<sub>2</sub>
: (PaCO<sub>2</sub> is the pressure of CO<sub>2</sub> 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 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]].
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==
{{Refimprove|date=January 2008}}
<references/>
{{Fluid, electrolyte, acid base metabolic pathology}}
[[Category:Nephrology]]
[[Category:Electrolyte disturbance]]
[[Category:Intensive care medicine]]
[[Category:Emergency medicine]]
[[de:Metabolische Azidose]]
[[et:Metaboolne atsidoos]]
[[fr:Acidose métabolique]]
[[it:Acidosi metabolica]]
[[pl:Kwasica metaboliczna]]