Metabolic acidosis

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Metabolic acidosis
Davenport diagram
ICD-10	E87.2
ICD-9	276.2
DiseasesDB	92

Template:Search infobox Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

In medicine, 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. 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.

Symptoms

Symptoms are non-specific, 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)
• weight loss (longer term)
• Muscle weakness and bone pains
• Kussmaul respirations (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.
• Lethargy, stupor, coma, seizures.
• Arrhythmias (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
• retinal edema can be a sign of methanol (methyl alcohol) intoxication
• Longstanding chronic metabolic acidosis leads to osteoporosis and can cause fractures.

Diagnosis

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 lungs), the bicarbonate is elevated, due to increased conversion from H₂CO₃. An ECG can be useful to anticipate cardiac complications.

Other tests that are relevant in this context are electrolytes (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 plus potassium levels.

Anion gap = ( [Na⁺]+[K⁺] ) - ( [Cl^-]+[HCO₃^-] )

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:

Low anion gap

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 serum albumin level.

• Electrolyte abnormality - hypercalcemia, hypermagnesemia, hypernatremia, underestimation of serum sodium
• Hyperviscosity-multiple myeloma, paraproteinemia
• Hypoalbuminemia
• Lithium toxicity
• Pheochromocytoma
• Bromism
• Dilution

Normal anion gap (hyperchloremic acidosis)

Usually the HCO₃^- 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.

• Enteral causes
  • Diarrhea (note: vomiting causes hypochloraemic alkalosis)
  • Pancreatitis, Pancreatic fistula
  • Arginine and lysine during total parenteral nutrition
  • Ureteroenterostomy
  • Ileal stoma
• Ammonium chloride and Acetazolamide (Carbonic anhydrase inhibitors)
• Renal loss of HCO₃^- i.e. proximal renal tubular acidosis, renal failure, hypoaldosteronism, distal renal tubular acidosis
• Alcohol (such as ethanol) can effect anion gap by inducing alcohol dehydrogenase enzyme.
• Recovery from diabetic ketoacidosis

High anion gap

The bicarbonate lost is replaced by an unmeasured anion and thus you will see a high anion gap. The mnemonic "MUDPILES" is used to remember the causes of a high anion gap.

M - methanol/metformin
U - uremia
D - diabetic ketoacidosis
P - paraldehyde/propylene glycol
I - Infection/ischemia/isoniazid
L - lactate
E - ethylene glycol/ethanol
S - salicylates/starvation

Some people, especially those not in the emergency room, find the mnemonic KIL-U easier to remember and also more useful clinically:

K - Ketones
I - Ingestion
L - lactic acid
U - uremia

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.

Ketones: more straightforward than remembering diabetic ketosis and starvation ketosis, etc.

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.

Lactate: including that caused by infection and shock

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

Respiratory compensation of metabolic acidosis

• For 1 meq/L fall of serum HCO3 levels there is a 1.2 mmHg fall in arterial pCO2.
• The respiratory compensation of metabolic acidosis is fast and begins within half an hour of metabolic acidosis.
• In cases where the metabolic acidosis develops slowly, the respiratory compensation occurs simultaneously with the metabolic acidosis.
• The respiratory compensation usually completes within 12 to 24 hours
• A failure to develop adequate respiratory response indicates an acute underlying respiratory diseases, neurologic disease or a very acute development of metabolic acidosis.
• Formula for checking appropriate respiratory compensation to metabolic acidosis include:
  • Arterial pCO2 = 1.5 x serum HCO3 + 8 ± 2 (Winters’ equation)
  • Arterial pCO2 = Serum HCO3 + 15

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⁺ + HCO₃^- <--> H₂CO₃ <--> CO₂ + H₂O

The Henderson-Hasselbalch equation mathematically describes the relationship between blood pH and the components of the bicarbonate buffering system:

pH=pKa + log [HCO₃^-]/[CO₂]

Using Henry's Law, we can say that [CO₂]=0.03xPaCO₂

(PaCO₂ is the pressure of CO₂ 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 arrhythmias, 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.