Synopsis
Recognise deficiency-related neuropathy, myelopathy, ataxia and encephalopathy, identify malabsorption and functional deficiency, and replace nutrients urgently without masking a second diagnosis or causing refeeding harm.
- Vitamin B12 deficiency can cause peripheral neuropathy, optic neuropathy, cognitive or psychiatric change and subacute combined degeneration, sometimes with a normal haemoglobin and mean cell volume.
- Posterior-column sensory loss plus corticospinal signs suggests B12 or copper-related myelopathy; a clear sensory level, sphincter dysfunction or rapid progression still requires urgent spinal imaging.
- Thiamine deficiency causes Wernicke encephalopathy, painful or weak neuropathy and cardiovascular beriberi; treat suspected neurological deficiency parenterally before or alongside carbohydrate when feasible rather than awaiting a blood concentration, without delaying emergency glucose.
Key red flags
Confusion, eye-movement abnormality or acute ataxia in malnutrition or alcohol dependence requires immediate parenteral thiamine before or alongside planned glucose-containing nutrition, while urgent hypoglycaemia is corrected without delay.
Investigation priorities
Identify confirmed or indeterminate B12 status using the current NICE diagnostic thresholds and clinical context.
Management branches
Paraesthesia, sensory ataxia, myelopathy, optic or cognitive symptoms occur with confirmed or strongly suspected B12 deficiency.
- Take total or active B12, full blood count and cause-directed samples before treatment when this creates no harmful delay and document supplements and nitrous oxide.
- Start intramuscular hydroxocobalamin promptly for significant neurological disease using the BNF or local loading regimen and do not wait for macrocytosis.