Table of Contents
- Introduction
- Epidemiology
- Etiology
- Causes of encephalopathy include
- Figure 1: Mechanism of Hypoglycemia induced encephalopathy
- Figure 2: Mechanism of Sepsis induced Acute encephalopathy
- Figure 3: Mechanism of Acute Metabolic Encephalopathy
- Clinical Features
- Differential Diagnosis
- Diagnosis
- Treatment
- Complications
- Prognosis
- Bibliography
Primary Category
Neurocritical Care
P-Category
Secondary Category
S-Category
Authors:
Introduction
- Change in level of consciousness associated with altered cognition and/or perception appearing over hours/days that is not secondary to prior/developing chronic dementia
- Encephalopathy results in acute structural brain changes to non-structural, metabolic, toxic, infection related brain dysfunction
- Change in mental status that affects a patient's perception
- Abrupt deterioration in mental status not secondary to seizure or syncopal episode
- Common neurological emergencies related to chronic neurological decline
- Important cause of morbidity and mortality in ICU and post-operative patients
Epidemiology
- Commonly seen in elderly and critically ill patients
- Over 250,000 patients affected in the US in the last decade
- Death rate increases with increased severity of encephalopathy
- Delirium/coma in septic encephalopathy doubles the risk of mortality
Etiology
Causes of encephalopathy include
- Metabolic Causes:
- Hepatic encephalopathy
- Hypoglycemia
- Hypoxia
- Hypercapnia
- Uremia
- Electrolyte abnormalities (hyponatraemia, hypo/hypercalcaemia, hypo/hypermagnesemia)
- Hyperammonemia
- Organic acid and amino acid disorders
- Fatty acid oxidation disorders
- Vitamin Deficiency: Thiamine, Folic acid, cobalamin, nicotinic acid
- Toxins/poisons: (carbon monoxide, organic solvents, lead, manganese, mercury, carbon disulphide, heavy metals)
- Infective causes:
- Meningitis/Encephalitis
- Parainfectious encephalomyelitis
- Cerebral abscess
- Neurosyphilis
- HIV syndromes
- Lyme disease
- Systemic infections with septicemia
- Progressive multifocal leukoencephalopathy
- Neurological causes:
- Stroke
- Seizure
- Subdural hematoma
- Intracerebral hemorrhage
- Subarachnoid hemorrhage with vasospasm
- Hydrocephalus
- Brain tumors
- Migraine
- Trauma:
- Traumatic brain injury
- Concussion
- Acid-base disorders:
- Acidosis
- Alkalosis
- Organ related causes:
- Liver failure: Hyperammonemia
- Renal failure: Uremia, electrolyte imbalance
- Lung disease: CO2 narcosis
- Thyroid dysfunction: Myxedema coma, hypothyroidism
- Parathyroid dysfunction: Hypo/hyperparathyroidism
- Pancreas dysfunction: Diabetes, hypoglycemia
- Adrenal dysfunction: cushing syndrome, pheochromocytoma, Addison disease
Figure 1: Mechanism of Hypoglycemia induced encephalopathy
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Figure 2: Mechanism of Sepsis induced Acute encephalopathy
Figure 3: Mechanism of Acute Metabolic Encephalopathy
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Clinical Features
- Altered mental status
- Altered sleep/wake pattern
- Coma
- Delirium
- Disorientation
- Hallucination
- Impaired thinking
- Impaired concentration
- Agitation
- Inappropriate behaviour
- Inattention
- Paratonic rigidity
- Loss of deep tendon reflexes
Differential Diagnosis
- Trauma
- Meningitis/encephalitis
- Intracranial Space-occupying lesion
- Drug overdose or withdrawal
- Hypoxia/ischemia
- Hypertension
- Cerebral vasculitis
- Metabolic causes
Diagnosis
- Complete Blood count
- Comprehensive metabolic profile
- Effective for metabolic acute encephalopathy
- CT scan of Head
- Can detect hematoma, neoplasms, structural brain changes
- MRI of brain
- Can identify recent stroke, cerebral blood vessels and white matter changes
- Lumbar puncture and CSF analysis
- Useful for septic encephalopathy
- Consider in Autoimmune encephalopathy
- Electroencephalogram:
- Most sensitive for sepsis induced acute encephalopathy
- Findings: mild, diffuse, reversible slowing of background frequencies in sepsis
- With deterioration of encephalopathy, changes in EEG are observed. Initial mild changes start with theta waves followed by delta waves then diffuse triphasic waves and eventually by Suppression
- Urine and blood culture:
- Detect septic changes
- Drug chart screening
Treatment
- Correction of the underlying cause is the mainstay of treatment as this improves the systemic inflammation and allows speedy recovery of multiple organs including the brain
- General management:
- Supportive treatment: maintain oxygenation, circulation, normal body temperature, prevent agitation
- Correction of electrolyte abnormalities, acidosis, seizures
- Correction of underlying abnormalities
- Avoidance of neurotoxic drugs
- Reduce raised intracranial pressure:
- Intubation and mechanical ventilation
- Restrict fluids
- Monitor Intracranial pressure
- Use Mannitol 0.25-0.5 g/kg then furosemide l mg/kg for raised ICP
- Pentobarbitone or thiopentone if necessary
- Specific Management:
- Hypoglycemia: IV bolus of glucose followed by infusion
- Hyperammonemia:
- Sodium Benzoate and Phenylacetic or phenylbutyric acid
- Hemodialysis in case of very high ammonia (500-700µmol/l) or poor response to therapy
- Organic acidemia: glycine, carnitine and hemodialysis
- Liver disease: For acute Wilson disease, use albumin infusion, plasmapheresis, dialysis, and liver transplantation
- Sepsis induced encephalopathy:
- Correction of underlying source of infection
- Intensive insulin therapy if hyperglycemia is observed
- Activated protein C
- Steroids
- Appropriate use of antibiotics
- Branched chain amino acids
Complications
- Coma
- Multiorgan failure
- Permanent neurological damage
- Death
Prognosis
- Poor prognosis in patients with severe cerebral dysfunction
- In sepsis induced encephalopathy, death rate depends upon the EEG changes
- Mortality rate 0% in normal waves
- Mortality rate 19% in theta waves
- Mortality rate 36% in delta waves
- Mortality rate 50% in triphasic waves
- Mortality rate 67% in suppression waves
- Death rate correlates with plasma level of biomarkers
- Symptoms are reversible in the early stage of encephalopathy
- Prognosis is poor as time passes
Bibliography
- American Psychiatric Association. Diagnostic and statistical manual of mental disorders: DSM-IV. Task Force on DSM-IV, editor. American Psychiatric Publication, 2000.
- Venkatesan A, Geocadin RG. Diagnosis and management of acute encephalitis: A practical approach. Neurol Clin Pract. 2014;4(3):206–215. doi:10.1212/CPJ.0000000000000036
- Lacobone E, Bailly-Salin J, Polito A, et al.: Sepsis-associated encephalopathy and its differential diagnosis Crit Care Med 2009 Vol. 37, No. 10 (Suppl.) DOI: 10.1097/CCM.0b013e3181b6ed58
- Sprung CL, Peduzzi PN, Shatney CH, et al. Impact of encephalopathy on mortality in the sepsis syndrome. Crit Care Med 1990;18:801–806
- Young GB, Bolton CF, Archibald YM, Austin TW, Wells GA. The electroencephalogram in SAE. J Clin Neurophysiol 1992; 9: 145-152.
- Young GB, Bolton CF, Austin TW, et al. The encephalopathy associated with septic illness. Clin Invest Med 1990; 13: 297-304.
- Brusilow, S. W. Inborn errors of urea synthesis. In Lloyd, J. K. and Scriver, C. R. (Eds.), Genetic and Metabolic Disease in Paediatrics, Butterworths, London, 1985, pp. 140-165.
- Sokol, R. J., Francis, P. D., Gold, S. H., Ford, D. M., Lure, G. M. and Ambruso, D. R. Orthotopic liver transplantation for acute fulminant Wilson disease. J. Pediatr. 107 (1985) 549-552.
- de Bont, B., Moulin, D., Stein, F., van Hoof, F, and Lauwerys, R. Peritoneal dialysis with D-penicillamine in Wilson disease. J. Pediatr. 107 (1985) 545-547.
- Wollff, J. A., Caroll, J. E,, Thuy, L. P., Haas, R. and Nyhan, W. L. Carnitine reduces fasting ketogenesis in patients with disorders of propionate metabolism. Lancet 1 (1986) 289-291.
- Walter, J. H. and Leonard, J. V. Inborn errors of the urea cycle. Br. J. Hosp. Med. 38 (1987) 176-183.
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