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In medicine, metabolic acidosis is a state in which the blood pH is low (under 7.35) due to increased production of H+ by the body or the inability of the body to form HCO3- 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 types of acidosis.
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 apetite (either anorexia or excessive eating) and weight loss (longer term), muscle weakness and bone pains. A slightly specific finding is when the patient reports rapid breathing, not due to shortness of breath but an unmotivated drive to hyperventilate. Kussmaul respiration is rare, but may indicate ketoacidosis.
Exteme acidosis leads to neurological and cardiac complications:
Physical examination occasionally reveals signs of disease, but is otherwise normal. Cranial nerve abnormalitites are reported in ethylene glycol poisoning, and retinal oedema 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 chlorine), 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 chlorine and bicarbonate levels from the sodium level. As sodium is the main extracellular kation, and chlorine and bicarbonate are the main anions, the result should reflect the remaining anions. Normally, this concentration is about 8-16 mmol/l. An elevated anion gap (i.e. >=17 mmol/l) can indicate particular types of metabolic acidosis, particularily 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:
- Normal anion gap:
- longstanding diarrhea (bicarbonate loss)
- pancreatic fistula
- urethro-sigmoidostomy
- RTA type II and IV (see below)
- intoxication:
- 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 other kations than sodium (e.g. potassium, 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.
- Blood buffering with bicarbonate. The enzyme carboxic anhydrase maintains the equilibrium between bicarbonate and H2CO3. This is, in turn, converted into carbon dioxide and water.
- Intracellular buffering by absorption of hydrogen atoms by various molecules, including proteins, phosphates and carbonate in bone.
- Respiratory compensation: chemoreceptors sense a deranged acid-base system, and there is increased breathing.
- Renal compensation: finally the kidney produces and excretes ammonia (NH4) and monophosphate, generating bicarbonate in the process while clearing acid.
Buffer
The elevated bicarbonate that distinguishes metabolic acidosis is therefore due to two seperate processes: the buffer (from water and carbon dioxide) and additional renal generation. The buffer reactions is: H+ + HCO3-- = H2CO3 = CO2 + H20
The Henderson-Hasselbalch equation mathematically describes the relationship between blood pH and the components of the H2CO3 buffering system:
- pH = 6.1 + log (HCO3-/H2CO3)
In clinical practice, H2CO3 can be calculated by using H2CO3 = P<CO2 x 0.03
RTA
Apart from the causes of increased acidity, there are four types of metabolic acidosis caused by the inability of the kidney to excrete acid. These conditions, termed renal tubular acidosis themselves have a number of potential (including hereditary) causes:
- Type 1 (distal) RTA: decreased acid secretion in the collecting ducts. The urine is relatively alkaline (pH>5.5)
- Type 2 (proximal) RTA: bicarbonate in pro-urine is poorly reabsorbed in the proximal tubules. It is mild, with bicarbonate levels between 14-20.
- Type 3 RTA: occurs in children
- Type 4 RTA: this form occurs in deficiency of aldosterone, the principal mineralocorticoid. Aldosterone is required for the secretion of potassium and hydrogen in the distal tubules, as well as retention of sodium. In this type of RTA there is mild hyperkalemia and metabolic acidosis due to acid retention.
Treatment
A pH under 7.1 is an emergency, due to the risk of cardiac arrhythmias, and may warrant treatment with intravenous bicarbonate (although this is probably unnecessary in ketoacidosis, in which rehydration and insulin are first-line treatments). Bicarbonate is given at 50-100 mmol at a time under scrupulous monitoring of the arterial blood gas readings.
If the acidosis is particularily 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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