Metabolic acidosis Totally Explained

Everything about Metabolic Acidosis totally explained

In medicine, metabolic acidosis is a process which if unchecked leads to acidemia (for example 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 coma and death. Together with respiratory acidosis, it's 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 pains. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations 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 doesn't occur.
Extreme acidemia leads to neurological and cardiac complications:

Neurological: lethargy, stupor, coma, seizures.
Cardiac: 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, and 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 (<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 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.
   Anion gap = ([Na⁺] ) - ([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 (for example > 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 sulfates, phosphates, uric acid)

intoxication:

organic acids (salicylates, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde, INH, toluene)
sulfates, metformin (Glucophage)

massive rhabdomyolysis The mnemomic MUDPILES is commonly used to remember the causes of Increased anion gap metabolic acidosis.

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:

longstanding diarrhea (bicarbonate loss)

pancreatic fistula

uretero-sigmoidostomy

Renal tubular acidosis (RTA)

intoxication:

renal failure (occasionally) It bears noting that the anion gap can be spuriously normal in sampling errors of the sodium level, for example in extreme hypertriglyceridemia. The anion gap can be increased due to relatively low levels of cations other than sodium and potassium (for example 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⁺ + 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, isn't 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.

Further Information

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