Cerebral malaria

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By Dr Sankalp Mohan
Senior resident Neurology
Under guidance of Dr Vijay Sardana (HOD Neurology)

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Cerebral malaria

  1. 1. GUIDELINES FOR CEREBRAL MALARIA DR SANKALP MOHAN SENIOR RESIDENT NEUROLOGY
  2. 2. Global burden of malaria GLOBALLY 300 MILLION MALARIA CASES A YEAR
  3. 3. Malaria epidemiology
  4. 4. Indian scenario  Mortality most often due to P. falciparum P. vivax (50-55%)  P. falciparum (48-52%)  P. malariae (small #, foothills of Orissa)  P. ovale (not found)  95% of pop. live in malaria risk areas  90% of malaria unstable (low incidence and  epidemics every 7-10 yrs)
  5. 5. Life cycle
  6. 6. Section of brain showing blood vessels blocked with developing P. falciparum parasites
  7. 7. Incubation period P. vivax and P. ovale 13~15 days P. malariae 24~30 days P. falciparum 7~12 days
  8. 8. CLINICAL FEATURES PRODROMAL PHASE FEBRILE PHASE COMPLICATIONS – CEREBRAL MALARIA
  9. 9. WHAT IS CEREBRAL MALARIA?  Most clinicians consider any manifestation of cerebral dysfunction in a patient with malaria as cerebral malaria.
  10. 10. CAUSES OF CNS DYSFUNCTION IN MALARIA • HYPOGLYCEMIA • HIGH GRADE FEVER ALONE • RENAL FAILURE • HEPATIC FAILURE • SEPTICEMIA • SHOCK
  11. 11. CEREBRAL MALARIA FEATURES  IMPAIRMENT OF CONSIOUSNESS –DELERIUM STUPOR,OBTUNDATION ,COMA  SIEZURES – FOCAL/GENERALISED (COMMONER IN CHILDREN )  MENINGISMUS  FOCAL NEUROLOGIC SIGNS(LESS COMMON)(aphasia, hemiplegia, ataxia, chorea, and tremor) neuro-ophthalmologic signs (gaze deviation, oculomotor palsy, nystagmus, and ocular bobbing) -Retinal hemorrhage may occur in 15% of patients.
  12. 12. DEFINITION OF CEREBRAL MALARIA
  13. 13. Coma Scale for Children Best Motor response Verbal Response Eye Movements Localizes painful stimulus Withdraws limb from pain Non-specific or Absent response Appropriate Cry 2 Moan or Inappropriate cry None Directed (e.g. follows mother’s face) Not directed Total 2 1 0 1 0 1 0 0-5
  14. 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. 15. 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,
  16. 16. DIAGNOSIS  Demonstration of asexual form of P. falciparum in peripheral blood smear, in thick and thin blood smear films stained by Giemsa stain.
  17. 17. LIGHT MICROSCOPY  Thick blood film- enhanced sensitivity , low levels of parasitemia -Thin blood film.- identification of the parasite to the species level
  18. 18. PL FALCIPARUM RINGS PL FACIPARUM GAMETOCYTES
  19. 19. Schizont stage –p vivax TROPHOZOITE PF
  20. 20. Recommendations  At least 3 smears 6 h apart should be examined. before excluding cerebral malaria.  Parasitological confirmation of the diagnosis of malaria provided by high-quality microscopy or, where this is not available, by RDTs is recommended for all suspected cases of malaria
  21. 21. OTHER DIAGNOSTIC TESTS -DETECTION OF MALARIAL ANTIGENS 1.Pl Glutamate Dehyrogenase 2.Pl Falciparum HRP II- only in Falciparum 3. Pl LDH - DIAGNOSIS USING FLUORESCENCE MICROSCOPY -Fluorescent dyes have an affinity for the nucleic acid in the parasite nucleus (ACRIDINE ORANGE)
  22. 22. CSF EXAMINATION -Necessary to exclude other causes of febrile encephalopathy. -CSF is generally normal in cerebral malaria, however, mild pleocytosis (10–50 cells/mm3) and protein rise up to 200 mg/dL may be seen.
  23. 23.  CT and MRI are usually normal or show edema and cortical or subcortical infarcts in watershed zone in 15%–20% patients.  EEG shows nonspecific abnormalities, such as diffuse slowing, spike wave discharges, and burst suppression pattern
  24. 24. TREATMENT  Neurologic emergency requiring urgent intervention.  In endemic area, treatment should be started without waiting for confirmation of the diagnosis
  25. 25. SPECIFIC THERAPY TREATMENT OF MULTI ORGAN DYSFUNCTION TREATMENT OF COMPLICATIONS
  26. 26. UNCOMPLICATED FALCIPARUM MALARIA  ACT options now recommended for treatment of uncomplicated falciparum malaria  artemether plus lumefantrine,  artesunate plus amodiaquine,  artesunate plus mefloquine,  artesunate plus sulfadoxine-pyrimethamine,  dihydroartemisinin plus piperaquine.
  27. 27.  Artesunate plus sulfadoxine-pyrimethamine – containing 50 mg of artesunate and tablets containing 500 mg of sulfadoxine and 25 mg of pyrimethamine Therapeutic dose- artesunate given once a day for 3 days and a single administration of sulfadoxinepyrimethamine on day 1,
  28. 28.  Artemether plus lumefantrine: standard tablets containing 20 mg of artemether and 120 mg of lumefantrine given twice a day for 3 days Artesunate plus tetracycline or doxycycline or clindamycin These are reserved for very rare occasions of treatment failures to the recommended ACTs Any of these combinations should be given for 7 days.
  29. 29.  Non-artemisinin based combination therapy sulfadoxine-pyrimethamine plus chloroquine (SP+CQ) or amodiaquine (SP+AQ) - PROVEN TO BE INFERIOR Artemisinins should not be used as monotherapy, as this will promote resistance
  30. 30. P VIVAX AND MIXED INFECTION  P.vivax -Chloroquine for 3 days and Primaquine for 14 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.  Treatment of mixed infections (P.vivax + P.falciparum) cases: course of ACT and Primaquine 0.25 mg per kg body weight daily for 14 days.
  31. 31. TREATMENT OF SEVERE FALCIPARUM MALARIA
  32. 32.  Severe malaria should always be treated with parenteral antimalarials  Drug of choice for cerebral malaria parenteral artemisinin derivatives or quinine because of widespread resistance to chloroquine.
  33. 33. QUININE  it should never be given as a push INTRAVENOUS  a continuous and uniform flow of IV quinine in dextrose solution should be maintained over a period of four hours  require monitoring of pulse, blood pressure, and blood glucose.  IM injection carries the risk of necrosis at the injection site and the injection is very painful.
  34. 34.  Patients with cardiac disease and in older people, QTc interval should be monitored  Quinine should be discontinued if QTc interval exceeds 25% of the basal value.
  35. 35. ARTESUNATE  Artesunate has been reported to reduce mortality by 34.7% compared to quinine in a randomized controlled trial in Asian adults.  Artemether and artesunate are advantageous because of low toxicity, ease of administration  Artesunate, which is water soluble has the advantage of i.v. or im. administration  Does not produce hypotension or hypoglycemia
  36. 36.  Mefloquine is not preferred for cerebral malaria because of neuropsychiatric complication  Corticosteroids are not beneficial IN cerebral malaria  BENEFICIAL IN POST MALARIA SYNDROME  Phenobarbitone reduces the seizures, it increases mortality specifically in children
  37. 37. SUPPORTIVE MANAGEMENT  Hydration by administration of fluids  Oral fluids should be given if the patient is conscious and can swallow.  High fever should be reduced by the use of oral paracetamol and tepid water sponging
  38. 38. MANAGEMENT OF COMPLICATIONS  INTENSIVE CARE UNIT  VENTILATORY SUPPORT  HEMODIALYSIS
  39. 39. MANGEMENT OF COMPLICATIONS  severe anaemia  renal failure  pulmonary oedema,  shock  spontaneous bleeding,  repeated generalized convulsions  acidemia or acidosis
  40. 40. MALARIA IN PREGNANCY  Pregnant women in the first trimester with uncomplicated falciparum malaria should be treated with quinine plus clindamycin for seven days  artemisinin derivatives in the second and third trimesters  Primaquine and tetracyclines should not be used in pregnancy

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