Flashcards in Metabolic Acidosis Deck (12):
Metabolic acidosis with High Anion Gap
- Methanol poisoning
- Ethylene glycol toxicity
- Salicylates (= mixed metabolic acidosis and respiratory alkalosis)
- TCA OD (Severe poisoning)
- Severe Rhabdomyolysis (also assoc w Hyperkalaemia)
Metabolic Acidosis with Normal Anion Gap
- Cocaine toxicity
- Renal Tubular Acidosis T1, T2 (T1 and T2 assoc with Hypokalaemia), T4 (T4 assoc with Hyperkalaemia)
Unwell Patient ABG Interpretation: Example Question
A 49-year-old man was brought in by ambulance after he had a prolonged tonic-clonic seizure for 45 minutes. He had no previous history of seizures, and this episode was witnessed by people passing by, who claimed he was jerking throughout his body and wet himself during the course of the fit. On admission, he was postictal after. His seizures stopped after administration of rectal diazepam, phenytoin infusion and intubation, and he was admitted to the intensive care unit. He remained drowsy and lethargic for the next 2 days, and attempts to wean him off the ventilator was slow.
His blood results on day 2 showed:
Na+ 140 mmol/l
K+ 5.8 mmol/l
Urea 11.1 mmol/l
Creatinine 180 µmol/l
Serum corrected calcium 2.15 mmol/l
Serum bilirubin 21 µmol/l
Serum alkaline phosphatase 97 IU/l
Serum aspartate aminotransferase 62 IU/l
Creatine kinase (CK) 9000 IU/l
Serum lactate 4.5 mmol/l
C-Reactive protein (CRP) 5 mg/l
Haemoglobin 13.6 g/dl
White cell count 7.2 x 10^9/L
Which of the following values would likely be seen on his arterial blood gas result?
> pH 7.25 pO2 16 kPa pCO2 4.6 kPa HCO3 11mmol/l BE -10mmol/l, Cl- 101mmol/l
pH 7.46 pO2 16 kPa pCO2 2.4 kPa HCO3 31mmol/l BE 5mmol/l, Cl- 101mmol/l
pH 7.29 pO2 15 kPa pCO2 6.6 kPa HCO3 36mmol/l BE 6mmol/l Cl- 111mmol/l
pH 7.48 pO2 17 kPa pCO2 6.4 kPa HCO3 11mmol/l BE -10mmol/l, Cl- 101mmol/l
pH 7.36 pO2 17 kPa pCO2 4.6 kPa HCO3 27mmol/l BE -2mmol/l , Cl- 101mmol/l
This man has rhabdomyolysis, as evidenced by his acute kidney injury, and markedly raised CK values, secondary to status epilepticus. Rhabdomyolysis is the clinical syndrome resulting from the breakdown of muscle cells, resulting in the release of the intracellular contents into the circulation eg. myoglobin and potassium, resulting in electrolyte imbalances and acute kidney injury. It can also be caused by crush injuries, overexertion, compartment syndrome, drugs eg. statins, neuroleptic malignant syndrome.
In severe cases, it results in metabolic acidosis secondary to raised serum lactic acid levels from the ischaemic muscle fibres. The serum lactate is raised which would suggest an acidotic picture over a normal blood gas picture, ruling out options (b), (d), (e). Option D is a spurious result - it is alkalotic despite a high pCO2 and low HCO3. Option (c) is a picture of respiratory acidosis, leaving option (a) as the only correct answer.
Metabolic Acidosis with a Raised Anion Gap
Causes of a raised anion gap metabolic acidosis
lactate: shock, hypoxia, metformin, rhabdomyolysis
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol, cyanide, ethylene glycol
Metabolic Acidosis with a Normal Anion Gap
Causes of a normal anion gap or hyperchloraemic metabolic acidosis:
gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis (inc Fanconi Syndrome)
drugs: e.g. acetazolamide
ammonium chloride injection
NB: Why does vomiting/diuresis cause metabolic alkalosis whereas diarrhoea causes acidosis?
- Secretions into the large and small bowel are mostly alkaline with a bicarbonate level higher than that in plasma. Excessive loss of these fluids can result in a normal anion gap metabolic acidosis.
- Vomiting and Diarrhoea > Loss of Na+ and Cl- > activation of RAAS > Aldosterone retains Na+ in exchange for H+
NB - Diarrhoeas which are caused by predominantly colonic pathology may cause a metabolic alkalosis: this includes chronic diarrhoeas due to ulcerative colitis, colonic Crohns disease and chronic laxative abuse.
Hyperchloraemic Metabolic Acidosis - Example Question
A 29-year-old female is admitted to the Emergency Department following an episode of collapse. She denies prodromal symptoms and woke up after an undetermined period to find herself lying face down on the ground. She has recently consulted her GP regarding feelings of generalised weakness, intermittent palpitations and dizziness.
Her past medical history is remarkable for hypothyroidism and rheumatoid arthritis, previously managed with infliximab, and complicated 3 months ago by a diagnosis of TB. Her regular medications include methotrexate, folic acid, levothyroxine, artificial tears, rifampicin, and isoniazid.
During the examination, the patient complains of recurrent palpitations. The cardiac monitor shows broad-complex tachycardia. Her blood pressure is stable at 117/68mmHg and she is given a bolus of amiodarone.
Her venous blood gas is as follows:
pCO2 4.3 kPa
pO2 6.3 kPa
Na+ 137 mmol/l
K+ 2.1 mmol/l
Cl- 114 mmol/l
iCa2+ 1.05 mmol/l
Glucose 5.4 mmol/l
HCO3 15.6 mmol/l
BE -9.5 mmol/l
Some additional investigations are requested:
Urine dipstick pH 5.0 glucose ++ protein +
XR chest unremarkable
XR abdomen normal bowel gas pattern, no evidence of abnormal renal calcification
What is the most likely cause of the metabolic abnormalities described?
> Fanconi syndrome
The patient has a normal anion gap hyperchloraemic metabolic acidosis associated with hypokalaemia. This, in combination with the absence of GI symptoms, should alert you to the possibility of underlying renal tubular acidosis.
Fanconi syndrome is a disorder of proximal renal tubular function that leads to abnormal loss of bicarbonate, glucose, potassium, phosphate, uric acid and amino acids in the urine. Patients have features of type 2 renal tubular acidosis, accompanied by hypophosphataemia, glycosuria, and aminoaciduria. Presenting features include polyuria, polydipsia, osteomalacia (rickets and growth failure in children) and symptoms secondary to the electrolyte abnormalities associated with the disorder. Rifampicin has recently been implicated in the development of Fanconi syndrome and is the most likely cause in this case.
Rheumatoid arthritis and Sjögren's syndrome are causes of type 1 (distal) renal tubular acidosis; a failure of hydrogen ion secretion in the distal tubule that causes hypokalaemia and nephrocalcinosis. The absence of abnormal renal calcification on the patient's x-ray points away from this as the diagnosis.
Addison's disease typically causes hyperkalaemia, often associated with other electrolyte abnormalities including hyponatraemia and hypoglycaemia. It would, therefore, be inconsistent with the biochemistry provided.
Liver cirrhosis does not typically cause renal tubular acidosis unless it is itself a manifestation of Wilson's disease. There is nothing in the question to suggest Wilson's disease as the underlying diagnosis, however, and the occurrence of this pattern of metabolic abnormality would still be predicated on the development of a complicating Fanconi syndrome.
Classified according to the Anion Gap:
It is always useful to first calculate the anion gap:
Anion gap = (sodium + potassium) - (bicarbonate + chloride)
= (143 + 2.3) - (7 + 124) = 12.3 mmol/l
A normal anion gap is 8-14 mmol/l
Metabolic Acidosis 2dry to HIGH LACTATE Levels
Subdivided into 2 types
1) Lactic Acidosis Type A = shock, hypoxia, burns
2) Lactic Acidosis Type B = Metformin
Metabolic acidosis is classified according to the Anion gap
= (Sodium + Potassium) - (Chloride + Bicarbonate)
Normal range = 10-18mmol/L
Metabolic Acidosis with Hyperkalaemia
Renal tubular acidosis T4
Causes a mixed metabolic and respiratory acidosis
Carbon Monoxide Poisoning
Causes a metabolic acidosis secondary to lactic acidosis from systemic ischaemia.