Metabolic acidosis resident survival guide
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ogheneochuko Ajari, MB.BS, MS [2]
Definition
Metabolic acidosis is a state in which the blood pH is low (less than 7.35) due to increased production of H+ by the body or the inability of the body to form bicarbonate (HCO3-) in the kidney.
Causes
Life Threatening Causes
Common Causes
Low Anion Gap Metabolic Acidosis
Normal Anion Gap Metabolic Acidosis
The mnemonic for the most common causes of a normal-anion gap metabolic acidosis is "DURHAM."
- D- Diarrhea
- U- Ureteral diversion
- R- Renal tubular acidosis
- H- Hyperalimentation
- A- Addison's disease, acetazolamide, ammonium chloride
- M- Miscellaneous: congenital chloride diarrhea, amphotericin B, toluene
High Anion Gap Metabolic Acidosis
The mnemonic "MUDPILES" is used to remember the common causes of a high anion gap.
- M - Methanol/ Metformin
- U - Uremia
- D - Diabetic ketoacidosis
- P - Paraldehyde/ Propylene glycol
- I - Infection/ Ischemia/ Isoniazid
- L - Lactic acidosis
- E - Ethylene glycol/ Ethanol
- S - Salicylates/ Starvation
Management
Step 1
[pH]<7.35 And [HCO32-]<24 meq/L | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
[Metabolic acidosis] | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Calculate the [anion gap] (AG) Na+ - Cl- - HCO32- | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Low AG AG<8 | Normal AG 8<AG<16 | High AG AG>16 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
Check [albumin] Correct the AG if albumin is low For every decrease of 1 g/dl of albumin, AG is decreased by 2.5 meg/L | Check Ca2+, Mg2+, K+, [immunoglobulins] High levels of these unmeasured cations decrease the AG | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Check urine AG Na+ + K+ - Cl- | Check ΔAG/ΔHCO32- | R/O low Ca2+, Mg2+, K+ | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
Negative urine AG [GI] causes [RTA type II] | Positive urine AG [Renal failure] [RTA type I] [RTA type IV] | ΔAG/ΔHCO32-<1 High AG metabolic acidosis combined with normal AG metabolic acidosis | 1<ΔAG/ΔHCO32-<2 Pure high AG metabolic acidosis | ΔAG/ΔHCO32->2 High AG metabolic acidosis combined with [metabolic alkalosis] | |||||||||||||||||||||||||||||||||||||||||||||||||||||
Step 2
Shown below is the algorithm summarizing the management of metabolic acidosis
History, symptoms and physical examination Blood pH < 7.35 | |||||||||||||||||||||||||||||||||||||||||
Physical examination Eyes Extremities Neurologic (cranial nerves) | Labs/EKG Anion gap, Arterial blood gas analysis Electrolytes (Na, K, Cl, HCO3) CBC Serum lactate, ketone Urinalysis Toxicological screening (salicylate, methanol, ethylene glycol) EKG for arrhythmias | History Arrhythmias Kussmaul breathing Headache, altered mental status | |||||||||||||||||||||||||||||||||||||||
Place patient on EKG monitor for arrhythmias, hyperkalemia | Replace electrolytes if there are losses | If DKA, IV Insulin, normal saline Potassium and phosphate may be necessary | Send consult to nephrologist for dialysis for renal failure, poisoning | Toxicological consult | |||||||||||||||||||||||||||||||||||||
IV bicarbonate if there is cardiac arrhythmias 50-100mmol while monitoring arterial blood gas readings | Detoxification agents/toxin antidotes Fomepizole Activated charcoal Emesis Folic acid for methanol overdose Thiamine and pyridoxine for ethylene glycol overdose | ||||||||||||||||||||||||||||||||||||||||
Do's
- Treatment of the underlying cause should be the primary therapeutic goal.
- Bicarbonate should be given only when there is a severe case of acidosis with an arterial pH of less than or equal to 7.2
- Patient should be placed on SaO2 and blood pressure/heart rate monitor
- Consider intubation and ventilation for airway if the SaO2 level is deteriorating or there is a loss of consciousness
- Consider doing catherization to monitor the urine output and obtaining urine for urinalysis
Dont's
- Do not administer vasoconstrictors in the presence of lactic acidosis