Following brain injury, a range of secondary complications may occur which should be addressed.  Complications may include:

  • Intracranial complications of brain injury e.g. further bleed or intracranial pressure change. Arrange imaging if indicated.
  • Sepsis: assess inflammatory markers if indicated by Early Warning Scores. If abnormal consider the possibility of infection:
    • Intracranial causes including meningitis, encephalitis or ventriculitis (inflammation of the ventricles in the brain).
    • Extra-cranial causes (respiratory and urinary tract infections are the most common).
  • Renal or hepatic failure.
  • Metabolic (Sodium Balance or Pituitary Problems) or nutritional causes of confusion, in particular in patients with potential for nutritional deficiency should be considered. Screen the patient for supplementation with minerals (Magnesium, Iron, Zinc, Selenium, Calcium) and/or vitamins A/B1/B2/B6/E. During the post-acute phase oral nutritional supplements are probably appropriate. It is important to understand the rationale for vitamin replacement:
    • Deficiency of Thiamine/Vitamin B1 is a significant factor underlying alcohol induced brain damage. Thiamine is a cofactor required by enzymes involved in carbohydrate metabolism, and a reduction can lead to interference in generation of essential molecules in nerve cells.
    • Chronic alcohol consumption may result in thiamine deficiency by causing inadequate nutritional thiamine intake, decreased absorption of thiamine from the gastrointestinal tract, and impaired thiamine utilization in the cells.
    • Over-rapid administration of glucose in acute illness depletes any remaining body stores of thiamine and aggravates risk of damage, especially in vulnerable areas of the brain, creating potential for Wernicke’s encephalopathy; Korsakoff psychosis or alcoholic cerebellar degeneration.  This is why glucose replacement is not given in alcohol withdrawal prior to parenteral administration of B vitamins.  Oral vitamin B would be inadequate due to the decreased absorption of thiamine from the gastrointestinal tract in this patient group.