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SEVERE AND COMPLICATED MALARIA DIAGNOSIS-MANAGEMENT (WHO GUILDELINES)

SEVERE AND COMPLICATED MALARIA DIAGNOSIS-MANAGEMENT (WHO GUILDELINES). PRESENTED BY- Dr.APOORVA.P MODERATOR- Dr.NAZIR ATTAR. INTRODUCTION. Malaria is a protozoan infection of red cells transmitted by bite of blood feeding female anopheline mosquito

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SEVERE AND COMPLICATED MALARIA DIAGNOSIS-MANAGEMENT (WHO GUILDELINES)

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  1. SEVERE AND COMPLICATED MALARIA DIAGNOSIS-MANAGEMENT(WHO GUILDELINES) PRESENTED BY-Dr.APOORVA.P MODERATOR-Dr.NAZIR ATTAR

  2. INTRODUCTION • Malaria is a protozoan infection of red cells transmitted by bite of blood feeding female anopheline mosquito • Six species of the genus Plasmodium cause nearly all malarial infections in humans. -P. falciparum - P. vivax -P. ovale - P. malariae， -P.knowlesi -in Southeast Asia-the monkey malaria parasite

  3. Fatality rate of 10-30% have been reported among children referred to hospital with severe malaria. • Malaria deaths have declined by 69% from 932 to 287 annually from 2000-2015.

  4. Malaria is one of the major public health problems of the country. • India reports around 1 million malaria cases annually • In India P.falciparum and P.vivax are the most common species causing malaria.

  5. SEVERE FALCIPARUM MALARIA Definition: Severe falciparum malaria is defined as one or more of the following occurring in the absence of an identified alternative cause and in the presence of P.falciparum asexual parasitemia

  6. MANIFESTATIONS OF SEVERE FALCIPARUM MALARIA

  7. SEVERE VIVAX MALARIA-It is defined as for Falciparum malaria but with no parasite density thresholds • SEVERE KNOWLESI MALARIA- It is defined as for falciparum malaria but with 2 differences Parasite density >1,00,000/microlt Jaundice and parasite density >20,000/microlt

  8. CEREBRAL MALARIA • Coma is a characteristic and ominous feature of falciparum malaria . • It is defined as unarousablecoma.This is usually Glasgow coma score of <11 • It is associated with death rates of 20% among adults and 15% among children,despite treatment. • The onset is gradual or sudden following a convulsion

  9. It manifests as diffuse symmetric encephalopathy, focal neurologic signs are unusual. SIGNS -Eyes-Gaze may be normal or divergent -Pout reflex is common(other primitive reflex absent)

  10. -Corneal reflex preserved -Muscle tone-increased or decreased -DTR-variable -Plantar-flexor or extensor -Abdominal and cremastric reflexes-Absent -Flexor or extensor posturing may be seen -Convulsions-generalised and repeated, occur in 10% adults and upto 50 % children -Opisthotonous posturing

  11. FUNDUS- -Retinal opacification -Papilledema -Cotton wool spots -Decolorization of retinal vessels • Adults rarely suffer neurological sequelae • 10% of children have residual neurological deficit when they regain consciousness.

  12. POST MALARIA NEUROLOGICAL SYNDROME AND DEFICITS • In approximately 1-3% of adults and 10-23% of children there is a clinically obvious persistent neurological deficit following cerebral malaria. • In 60% of cases with residual neurological deficit,there is hemiparesis with variable hemisensory deficit and sometimes hemianopia.

  13. Cortical blindness,diffuse cortical damage,tremors and occasionally isolated cranial nerve palsies may occur. • Late neurological complications like psychosis ,encephelopathy, parkinsonian rigidity and tremors and cerebellar dysfunction may develop.

  14. HYPOGLYCEMIA • It important and common complication of severe malaria. • It is associated with a poor prognosis and is particularly problematic in children and pregnant women • The usual physical signs like sweating,tachycardia are absent.

  15. It results from a failure of hepatic gluconeogenesis and an increase in the consumption of glucose by both the host and malaria parasites. • Quinine also causes hypoglycemia by stimulating pancreatic insulin secretion.

  16. METABOLIC ACIDOSIS • It results from accumulation of organic acids and is an important cause of death. • Renal failure and ketoacidosis compound the acidosis.

  17. Respiratory distress is a sign of poor prognosis. • It is followed often by circulatory failure refractory to volume expansion or inotropic drug

  18. Lactic acidosis is caused by

  19. RENAL IMPAIRMENT • Acute kidney injury is common in severe falciparum malaria. • It may be due to erythrocyte sequestration and agglutination interfering with renal microcirculatory flow and metabolism. • It manifests as acute tubular necrosis. • Early dialysis or hemofiltration considerably enhances the likelihood of a patient's survival.

  20. NON CARDIOGENIC PULMONARY EDEMA • The mortality rate is >80%. • The pathogenesis of this variant of the adult respiratory distress syndrome is unclear. • This condition can be aggravated by overly vigorous administration of IV fluid. • It is common in pregnant women and rare in children.

  21. HEMATOLOGIC ABNORMALITIES ACCELERATED RBC REMOVAL BY SPLEEN ANEMIA RBC DESTRUCTION AT PARASITE SCHIZOGONY INEFFECTIVE ERYTHROPOIESIS

  22. In nonimmune individuals and in areas with unstable transmission, anemia can develop rapidly and transfusion is often required. • Slight coagulation abnormalities are common in falciparum malaria and mild thrombocytopenia

  23. In severe malaria, <5% have significant bleeding with evidence of disseminatedintravascular coagulation.

  24. LIVER DYSFUNCTION • Severe jaundice is associated with P. falciparum infections. • It is more common among adults than children.

  25. It results from hemolysis, hepatocyte injury， and cholestasis • It leads to hypoglycemia,lactic acidosis and impaired drug metabolism.

  26. TREATMENT OF SEVERE MALARIA • Full dose of parentralartesunatetreatment be given promptly in initial treatment of severe malaria. • This should be followed by a full dose of effective ACT orally for 3 days.

  27. Two classes of medicine are available for parentral treatment of severe malaria: artemisininderevatives (artesunate or atemether) and Cinchona alkaloids (quinine and quinidine) • Parentralartesunate is the treatment of choice for all severe malaria. • Largest randomised clinical trial showed a substantial reduction in mortality with iv or imartesunate as compared with parentral quinine.

  28. ARTESUNATE • Treat adults and children with severe malaria (including infants,pregnant women in all trimesters and lactating women) with intravenous or intramuscular artesunate for atleast 24 hrs. • Once a patient has received atleast 24 hrs of parentral therapy and can tolerate oral therapy,complete treatment with 3 days of an ACT Strong recommendation, high–quality evidence

  29. Young children have a larger apparent volume of distribution for both artesunate and dihydroartemesinin. • Therefore they should receive slightly higher doses of parentralartesunate to achieve exposure comparable to that of older children. • Children <20 kg- 3 mg/kg/dose • Larger children and adults- 2.4 mg/kg/dose.

  30. Delayed haemolysis starting >1 week after artesunate treatment of severe malaria has been reported. • Post treatment hemolysis is a predictable event related to life saving effect of artesunate.

  31. If parenteralartesunate is not available,use intramuscular artemether in preference to quinine for treating children and adult with severe malaria. Strong recommendation,high-quality evidence.

  32. ARTEMETHER • It is less active than its metabolite Dihydroartemesinin. • It is given as oil based IM injection or orally. • Therapeutic dose: Initial dose- 3.2 mg/kg body wt IM(to anterior thigh) Maintainance dose- 1.6 mg/kg body wt IM daily

  33. QUININE • Several salts of quinine have been formulated for parentraluse,butdihydrochloride is most commonly used. • Loading dose of quinine 20 mg salt/kg bw provides therapeutic plasma concentration within 4 hrs.

  34. Maintainance dose 10 mg salt/kg bw is administered at 8 h interval, starting 8 h after loading dose. • Rapid IV administration of quinine is dangerous as it causes hypotension • It must be administered as a slow rate controlled infusion in saline or dextrose solution

  35. If there is no improvement in patient’s condition within 48 hrs, the dose should be reduced by one third i.e. to 10 mg salt/kg bw every 12 h.

  36. TREATMENT OF SEVERE VIVAX MALARIA • Treatment is same as for P.falciparummalaraia • Following parentralartesunate, treatment can be completed with a full course of oral ACT or chloroquine • A full course of radical treatment with primaquine should be given after recovery.

  37. Artesunate:2.4 mg/kg body weight i.v. or i.m. given on admission (time=0), then at 12 and 24 hours, then once a day • Quinine:20 mg quinine salt/kg body weight on admission (i.v. infusion in 5% dextrose/dextrose saline over a period of 4 hours) followed by maintenance dose of 10 mg/kg body weight 8 hourly; infusion rate should not exceed 5 mg/kg body weight per hour. Loading dose of 20 mg/kg body weight should not be given, if the patient has already received quinine. If parenteral quinine therapy needs to be continued beyond 48 hours, dose should be reduced to 7 mg/ kg body weight 8 hourly. www.nvbdcp.gov.in

  38. Artemether: 3.2 mg/kg body weight i.m. given on admission then 1.6 mg/kg body weight per day. • Alpha-beta Arteether: 150 mg daily i.m. for 3 days in adults only (not recommended for children). • Patients receiving artemisinin derivatives should get full course of oral ACT www.nvbdcp.gov.in

  39. ARTEMESININ BASED COMBINATION THERAPY ARTEMETHER+LUMEFANTRINE Formulations available:20+120 40+240

  40. ARTESUNATE+AMODIAQUINE Formulations available:25+67.5 mg 50+135 mg 100+270 mg

  41. ARTESUNATE+MEFLOQUINE Formulations available:100 mg artesunate+220 mg mefloquine hydrochloride(equivalent to 200 mg mefloquine base)

  42. ARTESUNATE+SULFADOXINE-PYRIMETHAMINE Formulations-50 mg/200 mg artesunate+ 500 mg Sulfadoxine+25 mg Pyrimethamine

  43. DIHYDROARTEMISININ +PIPERAQUINE Formulations:40+320 mg

  44. Due to treatment failures to artesunate + sulfadoxine-pyrimethamine in P. falciparum malaria, the national drug policy for malaria was changed in NorthEastern states in India. This led to the change in P. falciparum malaria therapy in these states to artemetherlumefantrine. www.nvbdcp.gov.in

  45. www.nvbdcp.gov.in

  46. Renal or hepatic dysfunction?? • The dosage of artemesinin derivatives does not have to be adjusted for patients with vital organ dysfunction. • Quinine accumulates in vital organ dysfunction hence dose should be reduced if no improvement in 48 h. • Dosage administration are not necessary if patient are receiving haemodialysis.

  47. MANAGEMENT OF COMPLICATIONS

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