A discussion of the causes of a high anion gap metabolic acidosis are frequently required by the CICM SAQs, and lactate often comes up as a differential. Beyond that, there are a series of questions which ask specifically about the causes of lactic acidosis.
These questions are numerous. There is practically one in every paper.
A few specific examples include:
- Question 3.1 from the second paper of 2019
- Question 12 from the second paper of 2018
- Question 4.1 from the first paper of 2016
- Question 3.3 from the second paper of 2015
- Question 27 from the second paper of 2014
- Question 23 from the second paper of 2013
- Question 26.4 from the second paper of 2013
- Question 28 from the second paper of 2012
- Question 9.1 from the first paper of 2011
- Question 15.3 from the second paper of 2009
- Question 3.3 from the second paper of 2009
Many of these questions for some reason focus repetitively on the plight of a certain middle-aged diabetic with a history of alcohol abuse. A specific feature of these questions is the use of red cell transketolase as a test of thiamine deficiency, reminding the candidates that this is an important differential.
Lactic acidosis is discussed at greater length in a series of chapters dedicated to acid-base disturbances in their various forms and permutations. In order to simplify revision, a tabulated list of aetiologies is offered below, organised according to an increasingly irrelevant classification system from the 1980s.
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Type A lactic acidosis: impaired tissue oxygenation
Type B1 lactic acidosis, due to a disease state
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Type B2 drug-induced lactic acidosis
Type B3 : inborn errors of metabolism
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In order to simplify revision, I have paired these causes with helpful investigations. The college frequently asks for investigations.
Type A lactic acidosis: impaired tissue oxygenation |
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Shock: circulatory collapse |
Clinical features of shock; supportive history |
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Regional ischaemia |
CK levels, relevant leaking enzymes (eg. troponin) |
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Severe hypoxia |
Supportive history; neuron-specific enolase (assuming it was global hypoxia) |
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Severe anaemia |
Hb level, iron studies, haemolytic screen |
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Carbon monoxide poisoning |
Serum carboxyhaemoglobin levels |
Type B1 lactic acidosis, due to a disease state |
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Malignancy |
Tumour markers, LDH (particularly in haematological malignancy and tumour lysis) |
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Thiamine deficiency |
Red cell transketolase |
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Ketoacidosis /HONK |
Blood and urine ketone levels; BSL and serum osmolality |
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Septic shock |
Supportive history, fever, inflammatory markers |
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Impaired hepatic or renal clearance |
Clinical features of ascites, encephalopathy, icterus; deranged LFTs |
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D-lactic acidosis |
D-lactate level, the presence of encephalopathy, history of short gut syndrome |
Type B2 drug-induced lactic acidosis |
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Beta-2 adrenoceptor agonists |
Isoprenaline, adrenaline, salbutamol |
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Metformin |
History of diabetes |
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Isoniazid |
History of tuberculosis; seizures responsive to vitamin B6 |
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Cyanide (and by extension nitroprusside) |
Aside from cold war spies and malignant hypertension ...History of smoke inhalation |
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Xylitol, sorbitol, fructose |
Consumption of unusual dietary supplements, or use of unusual TURP irrigation fluid |
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Propofol |
Prolonged stay in ICU; infusion rate in excess of 4mg/kg/hr for over 24 hrs |
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The toxic alcohols eg. methanol |
Methanol, formate, oxalate levels. |
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Paracetamol |
Paracetamol levels, history of overdose attempt, and of course LFT derangement |
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Salicylates |
Salicylate levels; characteristic respiratory alkalosis followed by metabolic acidosis |
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NRTIs (anti-retroviral drugs) |
History of Hep C or HIV |
Type B3 : inborn errors of metabolism |
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Pyruvate dehydrogenase deficiency |
Specific genetic testing is called for |
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Electron transport chain enzyme defects |
Specific genetic testing |
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G6PD |
Rapid fluorescent spot test detecting the generation of NADPH from NADP |