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Dengue encephalopathy

Varatharaj A. Encephalitis in the clinical spectrum of dengue infection. Neurol India 2010;58:585-91

Three types of neurological manifestations have been

associated with confirmed dengue infection:

•Classic signs with acute infection (headache, dizziness, delirium,

sleeplessness, restlessness, mental irritability and depression)
•Encephalitis with acute infection (depressed sensorium, lethargy,
confusion, somnolence, coma, seizure, stiff neck and paresis)
•Post-infection disorder (epilepsy, tremors, amnesia, dementia, manic
psychosis, Bell’s palsy, Reye’s syndrome, meningoencephalitis and GBS)
http://www.mrcindia.org/journal/issues/483180.pdf
Dengue encephalopathy

http://www.spc.int/phs/pphsn/outbreak/Dengue/WHO_dengue_classification_and_case_management-flyer.pdf
 Dengue encephalopathy

• Management: careful monitoring and

replacement of intravascular fluid and
electrolyte losses

http://bioline.org.br/showimage?ni/photo/ni10153t7.jpg\

http://www.spc.int/phs/pphsn/outbreak/Dengue/WHO_dengue_classificatio
n_and_case_management-flyer.pdf
Cerebral malaria
• WHO definition– A clinical syndrome with:
1. Coma at least 1 hr after termination of seizure or correction of
hypoglycemia
2. Asexual forms of Plasmodium falciparum paracites on peripreal blood
smears
3. No other causes to explain the coma
• Clinical hallmark: impaired consciousness,
coma = most severe manifestation
• Outcome = fatal without treatment

Cerebral Malaria; Mechanisms Of Brain Injury And Strategies For Improved Neuro-Cognitive Outcome. Pediatr Res. 2010 October ; 68(4): 267–274.
Cerebral malaria

Cerebral Malaria; Mechanisms Of Brain Injury And Strategies For Improved Neuro-Cognitive Outcome. Pediatr Res. 2010 October ; 68(4): 267–274.
Cerebral malaria
• Neuroprotective & adjuvant therapy:
• Murine model: low molecular weight thiol (B5 complex pro-vitamin pantethine) prevented
development of cerebral malaria by down-regulating platelet reactivity and release of microparticles
from activated endothelium
• Glatiramer acetate (immuno-mdulatory agent)  lower risk of cerebral malaria in treated animals
• Erythropoietin: neuroprotection in animal models and protection against endothelial injury in heart &
reduce apoptosis

• Rehabilitation of children with sequele

• Physical and occupational therapy
• Behaviour and speech therapy
• Cognitive rehabilitation and hearing aids

Cerebral Malaria; Mechanisms Of Brain Injury And Strategies For Improved Neuro-Cognitive Outcome. Pediatr Res. 2010 October ; 68(4): 267–274.
 Electrolyte disorders encephalopathy
Normal serum & body fluid Calculating osmolality: Osmolal gap should be:
osmolality: 275-295 mOsm/kg <10 mOsm/L

HYPEROSMOLALITY

Hypertonicity = effective hyperosmolality; increased extracellular osmoles to draw

water (↓serum Na) e.g. diabetic hyperglycemia e.c. diabetes mellitus

Non-hypertonic hyperosmolality (serum Na not altered)

e.g. azotemia e.c. renal failure/inadequate perfusion

Generalized encephalopathy

Treatment
Calculation of apparent water loss  replace water losses with water or D5W 
serum sodium falls no faster than 2 mEq/L/h
Renal failure  dialysis may be required
Hyperglycemia rapid acting insulin 0.1 U/kg IV (cont 0.05U) + blood sugar testing

Samuels MA, Seifter JL. Encephalopathies Caused by Electrolyte Disorders. SEMINARS IN NEUROLOGY. 31 (2). 2011
 Electrolyte disorders encephalopathy

HYPEROSMOLALITY:
HYPERNATREMIA

Serum Na >145 mEq/L  loss of intracellular water  cell shrinkage

Compensation: nervous system generate idiogenic osmoles  minimize shrinkage
ADH released, thirst increases

Severe hypernatremia (>160 mEq/L)  compensation mech fails  encephalopathy

Treatment
Calculation of apparent water loss  replace water losses  serum sodium falls no
faster than 2 mEq/L/h
Central diabetes insipidus  D-arginine vasopressin, ADH analog
Nephrogenic diabetes insipidus  salt restriction & thiazide diuretics

Samuels MA, Seifter JL. Encephalopathies Caused by Electrolyte Disorders. SEMINARS IN NEUROLOGY. 31 (2). 2011
 Electrolyte disorders encephalopathy

HYPONATREMIA

Serum Na <135 mEq/L (may be asymptomatic if chronic)

Maybe isotonic, hypertonic, or hypotonic (hypervolemic, euvolemic, hypovolemic)

Acute (≤hours)  seizures, cerebral edema  life threatening in seum Na 125 mEq/L
Chronic (≥days)  serum Na 110 mEq/L can still be tolerated (be careful of rapid
correction  osmotic demyelination)

Treatment
Hypertonic: treat underlying disorders (e.g. hyperglycemia) + replace only salt loss
Hypovolemic hypotonic: replace volume with isotonic saline
Hypervolemic hypotonic: free water restriction, treat edema
Chronic isovolemic hypotonic: water restriction, ADH antagonist
Acute (<48hrs) isovolemic hypotonic: 3% saline(513 mEq/L Na/mL) by 4-6 mEq/L 
rate then slowed to 10 mEq/L/24hrs  free water restriction; if resistant: vasopressin
receptor antagonists used

Samuels MA, Seifter JL. Encephalopathies Caused by Electrolyte Disorders. SEMINARS IN NEUROLOGY. 31 (2). 2011
 Electrolyte disorders encephalopathy

HYPOKALEMIA

Serum K <3.5 mEq/L

e.c. excessive losses (renal –hyperreninemia, hyperaldosteronism, renal tubular
acidosis, diuretic, hypomagnesemia/ extrarenal –,vomiting, diarrhea, sweating,
starvation), excessive uptake (insulin, cathecolamine, alkalosis, hypothermia)

Severe <3 mEq/L  cardiac arrhythmia, paralysis

Treatment
Correct K balance problems: reduce beta2 adrenergic agonists
Dietary Na restriction (<80 Meq/L)
Oral KCl supplement in resistant cases (30-50 mEq/d)
Severe  IV KCl with continuous cardiac monitoring not more than 20 mEq/h

Samuels MA, Seifter JL. Encephalopathies Caused by Electrolyte Disorders. SEMINARS IN NEUROLOGY. 31 (2). 2011
 Electrolyte disorders encephalopathy
HYPERKALEMIA

Serum K >5.5 mEq/L (rarely problematic unless exceeds 6 mEq/L)

e.c. excess potassium (Addison disease, aldosterone deficiency/resistance), muscle
injury, etc.
First sign = peaking T wave of ECG (~0.6 mEq/L)  QRS widen  amplitude reduction
 T wave disappear, heart block and loss of P waves + weakness, paresthesia
Diagnosis  measure serum K+

Sever muscle weakness  sudden cardiac arrest

Treatment
Cardiac protection: calcium gluconate 10% solution 20 mL rapid IV infusion
Redistribution of K+ into cells: glucose 50 g/hr IV + insulin 5 U rapid IV infusion every
15 min + albuterol 10-20 mg by inhaler
Removal of K+ : sodium polysterene sulfonate 15-60 g + sorbitol oral 50-100 g
Volume expanded patients: loop diuretic (furosemid) 40-240 mg IV over 30 min
Severe resistant cases: hemodialysis

Samuels MA, Seifter JL. Encephalopathies Caused by Electrolyte Disorders. SEMINARS IN NEUROLOGY. 31 (2). 2011