Pediatric

1. CEREBRAL MALARIA
Dr. Muhammad Sajjad Sabir
MCPS, FCPS (Paediatrics)

2. GLOBAL BURDEN OF MALARIA
GLOBALLY 300 MILLION MALARIA CASES A YEAR

3. MALARIA EPIDEMIOLOGY

4. LIFE CYCLE

5. WHAT IS CEREBRAL MALARIA?
Sever form of malaria
caused by P. falciparum
Patient with malaria manifesting cerebral
dysfunction →cerebral malaria
manifested by
 Coma
 Convulsion and / or
 Hemoglobinuria

6. INCUBATION PERIOD
P. vivax and P.
ovale 13~15 days
P. malariae
24~30 days
P. falciparum
7~12 days

7. EPIDEMIOLOGY
More Sever in children as No of parasites
same in adult & child (proportionately smaller size)
Blood Gp A&B more protective than Gp O
Hb E & C more protective
HbF , sickle cell trait & G6PD deficiency
lesser tendency for falciparum malaria
 Malnutrition protective – immunity is low

10. Section of brain showing blood vessels
blocked with developing
P. falciparum parasites

11. CLINICAL FEATURES
PRODROMAL PHASE
FEBRILE PHASE
COMPLICATIONS –
CEREBRAL MALARIA

12. CAUSES OF CNS DYSFUNCTION IN
MALARIA
• HYPOGLYCEMIA
• HIGH GRADE FEVER ALONE
• RENAL FAILURE
• HEPATIC FAILURE
• SEPTICEMIA
• SHOCK

13. CEREBRAL MALARIA FEATURES
 High grade fever, Seizures & SOMI -VE
 IMPAIRMENT OF CONSIOUSNESS –delerium
stupor,obtundation ,coma
 SIEZURES – focal /generalised (common in children)
 MENINGISMUS
 NEURO-OPHTHALMOLOGIC SIGNS (gaze deviation,
oculomotor palsy, nystagmus)
 RETINAL HEMORRHAGE (in 15% patients)
 FOCAL NEUROLOGIC SIGNS (less common)
(aphasia, hemiplegia, ataxia, chorea, and tremor)

14. SEQUALE
 Transient neurologic sequelae -ataxia,
hemiparesis, memory disturbance, visual
field defects, cognitive impairment, and
behavioral abnormalities
 A postmalaria neurological syndrome
characterized by acute onset of confusion,
seizure, ataxia, myoclonus, tremor, and
aphasia

15. COMPLICATIONS
 Severe anaemia
 Renal failure
 Pulmonary oedema
 Shock
 Spontaneous bleeding
 Repeated generalized convulsions
 Acidemia or acidosis
Hypoglycemia

16. PROGNOSTIC FACTORS
the level of consciousness
presence of other organ dysfunction
Recurrent seizures,
decerebration
 retinal hemorrhage,
 age < 3 years,
 heavy parasitemia, (>20%),
lactic acidosis,
elevated CSF lactate
serum transaminase

17. DIFFERENTIAL DIAGNOSIS
Pyogenic meningitis
Viral encephalitis
Febrile fits
SOL
Hepatic coma
Hypoglycemic coma
Uremia

18. DIAGNOSIS
Demonstration of asexual
form of P. falciparum in
peripheral blood smear, in
thick and thin blood smear
films stained by Giemsa
stain.

19. LIGHT MICROSCOPY
 Thick blood film-
enhanced sensitivity , low levels of parasitemia
 Thin blood film.-
identification of the parasite to the species level
Recommendations
At least 3 smears 6 h apart should be examined
before excluding cerebral malaria
 Negative if anti-malarial given
 Upto 20% RBC’s may be infected
Thick & Thin film most specific

20. P. FALCIPARUM RINGS P. FACIPARUM GAMETOCYTES

21. Schizont stage –p vivax
TROPHOZOITE P. FACIPARUM

22. CSF EXAMINATION
Necessary to exclude other causes of febrile
encephalopathy
CSF is generally normal in cerebral
malaria
 Mild pleocytosis (10–50 cells/mm3)
 Protein rise up to 200 mg/dL
 Glucose - Normal

23. OTHER TESTS
 Immuno Chromatographic Assay (ICT-
Malaria)
Malaria antigen detection tests are a group of
commercially available rapid diagnostic tests that allow
quick diagnosis of malaria by people who are not
otherwise skilled in traditional laboratory techniques
 CBC
 Leucopenia
 Monocytosis
 Low Hb
 ↑sed Retics
 BSR – hypoglycemia
 Serum electrolytes

24. CT Scan and MRI
 usually normal or
 show edema
 cortical or subcortical infarcts
EEG
nonspecific abnormalities
 diffuse slowing,
 spike wave discharges
 burst suppression pattern

25. MANAGEMENT
Neurologic emergency requiring urgent
intervention.
 In endemic area, treatment should be started
without waiting for confirmation of the
diagnosis

26. SPECIFIC THERAPY
TREATMENT OF MULTI
ORGAN DYSFUNCTION
TREATMENT OF
COMPLICATIONS
MANAGEMENT

27. TREATMENT OF CEREBRAL MALARIA
Severe malaria should always be treated
with parenteral antimalarials
Drug of choice for cerebral malaria –
 Quinine
 Parenteral artemisinin derivatives or
 (widespread resistance to chloroquine)

28. QUININE
 a continuous and uniform flow of IV quinine in
dextrose solution should be maintained over a
period of four hours
 MONITORING
 Pulse
 Blood pressure
 Blood glucose
 QTc interval .
 Quinine should be discontinued if QTc interval exceeds
25% of the basal value
 IM injection carries the risk of necrosis at the injection
site and the injection is very painful
 never give as INTRAVENOUS push

29. IV quinine over 4Hrs in dextrose solution
1mg diluted in 1ml of 5% dextrose solution
20mg/kg I.V stat
10mg/kg I.V 8Hrly
For 07 days
Shift to oral when patient can take orally
 10mg/kg/dose TDS for 7 days
QUININE

30. ARTEMETHER
 Injectable
 3.2 mg /kg I.M stat
then
 1.6 mg /kg I.M BD for 2 days
CHLOROQUINE
 25 mg/kg body weight divided over three
days i.e.
 10mg/kg on day 1
 10mg/kg on day 2 and
 5mg/kg on day 3

31. SUPPORTIVE MANAGEMENT
Hydration by administration of fluids
Oral fluids should be given if the
patient is conscious and can swallow
High fever
 Paracetamol
 Brufen
 Tepid water sponging

32. MANAGEMENT OF
COMPLICATIONS
 INTENSIVE CARE UNIT
 VENTILATORY SUPPORT
 Pulmonary oedema
 RENAL FAILURE
 Care of hydration
 Dialysis(HEMODIALYSIS)
 1/3 ↓ dose of antimalarials

33. MANGEMENT OF COMPLICATIONS
Severe anaemia
 RCC transusion if Hb <6g/dl
Hypoglycemia
 Glucose bolus I.V(50%, 25%, 10%)
Repeated generalized convulsions
 Diazepam
 Phenobarbitone
Acidemia or acidosis
 Soda bicarb

34. PROGNOSIS
Mortality 10-30 %
Death mostly within 24 Hrs of
admission
Residual neurological deficit in 10% of
survivors