MANAGEMENT OF SEVERE & COMPLICATED MALARIA

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BY: Ephrem Bekele (MSC,CIDPH fellow at MU) Dec. 2011

Outline:

Outline Definition Etiology Pathogenesis Epidemiology Pathophysiology Clinical features Diagnosis Sever malaria/complicated malaria Malaria & HIV co-infection Management of sever malaria

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Malaria :is a protozoan disease transmitted by the bite of infected Anopheles mosquitoes Etiology More than 50 species of genus plasmodium Only Four species cause nearly all malarial infections in humans P. falciparum , P. vivax , P. ovale , and P. malariae

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Transmission Bite of female Anophilus mosquito Congental transmision (<5%) Blood transfusion Sharing of contaminated needles Organ transplantation

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Incubation period Varies based on species PF ≈12-14days Pv & PO ≈2wks Pm ≈18 days

Life cycle :

Life cycle

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Pathogenesis Human infection begins when a female anopheline mosquito inoculates plasmodial sporozoites Sporozoites carried via the bloodstream to the liver Invade hepatic parenchymal cells and begin a period of asexual reproduction single sporozoite may produce from 10,000 to >30,000 daughter merozoites

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Infected liver cell bursts, discharging motile merozoites into the bloodstream Merozoites invade the red blood cells (RBCs) and multiply every 48–72 h P. vivax and P. ovale infections, forms hyponozoites Hypnozoites , are the cause of the relapses

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merozoites invade erythrocytes and become trophozoites As the trophozoites enlarge, species-specific characteristics become evident, pigment becomes visible, and the parasite assumes an irregular or ameboid shape. After erythrocytic cycle of 48hrs(72hrs for p. malaraie ) changed to schizont

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RBC ruptures to release 6–30 daughter merozoites Invades a new RBC and repeating the cycle Disease caused by the direct effects of RBC invasion and destruction by the asexual parasite and the host's reaction Gamatocyte formation basic for transmision

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Host Response in malaria Splenic immunologic and filtrative clearance Removal of both parasitized and uninfected erythrocytes parasitized cells escaping splenic removal are destroyed when the schizont ruptures material released induces the activation of macrophages Release of proinflammatory mononuclear cell–derived cytokines Cause fever and exert other pathologic effects

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Both humoral immunity and cellular immunity are necessary for protection, but the mechanisms of each are incompletely understood Factors retard the development of cellular immunity to malaria absence of major histocompatibility antigens on the surface of infected RBCs malaria antigen–specific immune unresponsiveness enormous strain diversity of malarial parasites

Epidemiology :

Epidemiology Malaria is endemic throughout most of the tropics Three billion people living in 108 countries who are exposed, approximately 243 million will develop symptomatic malaria annually Around 863,000 deaths each year Most of these are attributable to P. falciparum ( 90 %)

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Over 80 % of the deaths occur among children in sub-Saharan Africa In endemic areas, young children and pregnant women are at high risk for severe malaria. Older children and adults develop partial immunity after repeated infection Travelers to areas where malaria is endemic are at high risk for severe disease

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In Ethiopia Estimated Number people living in malaria areas: 50 million(68%) Estimated number malaria cases per year: 9 million Number of extra cases in an epidemic year: 6 million Number of people dying in a 9-month malaria epidemic (e.g. 2003): 114,000

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Estimated number of lives saved annually if all malaria control interventions fully implemented (Child survival strategy, 2005): 70,400 According to FMOH, in 2008/2009, malaria was leading cause of outpatient visits(12%), health facility admissions(10%) and inpatient deaths

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PATHOPHYSIOLOGY Cytoadherence Important component of P. falciparum pathogenesis induce the formation of sticky knobs on the surface of erythrocytes((PfEMP-1) Knobs binds to reseptors on varities of cells i.e cappillaries , venules including endotilial cells human receptors include ICAM-1 (vascular endothelium & brain), CD36 (on endothelium and platelets), and chondrotin / CSA (in the placenta) binds to knobs Result in sequstration , inflammation & partial blood flow obstruction CEREBRAL MALARIA & RENAL FAILURE

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Rosetting / Aglutination parasitized red cells stick to uninfected red cells mediated by an interaction between PfEMP-1 within knobs and receptors on the surface of uninfected red cells, such as complement-receptor 1 (CR1) rosettes clog the microcirculation Parasitized RBCS bind togather ( form aglutination )

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parasite Biomass Vascular beds harboring sequstered parasites allow accumulation of high level of parasite biomass HRP-2 (a P. falciparum antigen expressed on the erythrocyte membrane) used as an indirect measure of parasite density Increased level correlate with severity

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Cytokines interaction between host endothelium and immune cells with malaria parasites is complex and not fully understood SIRS-like state with high circulating levels of TNF and nitric oxide C reactive protein (CRP), correlate directly with parasitemia . TNF, lymphotoxin , interleukin(IL)-6, IL-10, IL-12, and MIP-1 are consistently elevated in the setting of malaria

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Coagulation Activation of tissue factor is starting point Thrombocytopenia is a common feature of severe malaria Activation of the coagulation cascade in the absence overt bleeding is common Nitric oxide Low nitric oxide low arginine (the pre-cursor of nitric oxide) Parasite produce arginase enzyme( convert arginin to ornithine )

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Host factors Genetic factors Hemoglobin ( HbA /s) Red cell antigens TNF polymorphysm Immunity Humoral response- Cellular response- Ability to mount rebust INF- γ associated with protection againest high parasitemia

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Clinical features symptoms are nonspecific Head ach Fatigue Abdominal discomfort Muscle ach followed by fever Arthralgia N/V Chills & rigers Signs Fever Maliase Anemia Palpable spleen Mild joundice

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Diagnosis of malaria Clinical -non spesific Light microscopy blood smear( gold standard) RDT Other Tagged monoclonal antibodies for malaria antigen detection Fluorescence microscopy with acridine orange or other staining Quantitative buffy coat analysis Serology (detects past infection primarily) PCR

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Malaria in pregnancy It is estimated that 10,000 women and 200,000 infants die during pregnancy In endemic areas Prevalence is high in primigravidas prevalence of maternal maleria in holoendemic areas is 28% Prevalence of Placental malaria in stable transmision area is 26% pregnant women experience more severe disease, hypoglycemia(58%), and respiratory complications (pulmonary edema, acute respiratory distress syndrome) Anemia is a common complication(60%)

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OUTCOME Miscarriage Fetal growth restriction/small for gestational age (SGA) Preterm birth (<37 weeks of gestation) Low birth weight (LBW) (<2500 g at birth) Perinatal death Congenital infection Maternal anemia Maternal death

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Malaria in children 1–3 million persons who die of falciparum malaria each year are young African children Can develop sever form of disease Seizures and severe anemia are more common in children Children tolerate antimalarial drugs well and respond rapidly to treatment

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Severe malaria Is generally defined as acute malaria with high levels of parasitemia (>5 %) and/or major signs of organ dysfunction OR In a patient with P. falciparum asexual parasitaemia and no other obvious cause of symptoms, the presence of one or more of the following clinical or laboratory features

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Clinical features: – impaired consciousness or unrousable coma – prostration, i.e. generalized weakness so that the patient is unable walk or sit up without assistance – failure to feed – multiple convulsions – more than two episodes in 24 h – circulatory collapse or shock, systolic blood pressure < 70 mm Hg in adults and < 50 mm Hg in children – clinical jaundice plus evidence of other vital organ dysfunction - haemoglobinuria – abnormal spontaneous bleeding – pulmonary oedema (radiological) deep breathing, respiratory distress ( acidotic breathing)

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Laboratory findings : – hypoglycaemia (blood glucose < 2.2 mmol /l or < 40 mg/dl) – metabolic acidosis (plasma bicarbonate < 15 mmol /l) – severe normocytic anaemia ( Hb < 5 g/dl, packed cell volume < 15%) – haemoglobinuria – hyperparasitaemia (> 2%/100 000/ μl in low intensity transmission areas or > 5% or 250 000/ μl in areas of high stable malaria transmission intensity) – hyperlactataemia (lactate > 5 mmol /l) – renal impairment (serum creatinine > 265 μ mol/l).

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In malaria endemic area, young children (ages 2 to 5 years) are at high risk for severe malaria, as pregnant women Older children and adults develop partial immunity after repeated infection & at low risk for severe disease Travelers to malaria endemic area are at high risk for progression to severe disease if infected with P. falciparum consider malaria in the differential diagnosis

Poor Prognostic features :

Poor Prognostic features

Malaria & HIV co-infection :

Malaria & HIV co-infection

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Introduction HIV and malaria infections often coexist due to geographic overlap of these two diseases This is true in sub-Saharan Africa, where an estimated 40 million people are living with HIV and more than 350 million episodes of malaria occur yearly A study in MUMBAI, western India, showed HIV and malaria co-infection of 7.6%

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Study of Ugandan adults with malaria demonstrated that the HIV seroprevalence rate was 31% HIV increases the risk of malaria infection and the development of clinical malaria Conversely, malaria increases HIV replication

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Interactions between the two diseases might be limited by: differences in geographic distribution (HIV is more prevalent in urban areas and malaria is more prevalent in rural areas) and age patterns (HIV mainly affects adults, whereas the prevalence of malaria is higher in children in areas of high malaria transmission)

Impact of malaria on HIV:

Impact of malaria on HIV T cell activation In vitro, malarial antigens lead to T cell activation and productive HIV infection Viral load Malaria infection is associated with a temporary rise of HIV RNA A cohort study performed in Malawi prospectively enrolled 348 aparasitemic patients A near doubling of HIV RNA was demonstrated between baseline and follow-up in those patients who acquired malaria infection

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Rise was temporary, returning to baseline at two months after treatment of malaria If viral loads are being used to monitor response to HAART, testing should be delayed if the patient has had a recent malaria infection Transient increase predicted to have minimal impact on long term HIV progression unless infections were frequent or remained occult and untreated From public health standpoint, even a transient rise in HIV RNA at a population level could impact sexual transmission

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Malaria related mortality The prevalence of severe malaria and mortality in areas of stable transmission was not affected by HIV infection in previous studies But data from three recent studies challenge this finding In Burkina Faso, a positive blood smear for malaria was an independent risk factor for death in HIV-infected patients In a retrospective study in Senegal, malaria-related mortality was higher in HIV-infected patients than in HIV-uninfected patients (58% vs 19%, p<0·001)

Impact of HIV infection on malaria :

Impact of HIV infection on malaria HIV immunosuppression , affects the acquisition and persistence of immune response to malaria HIV infection could increase morbidity and mortality attributable to malaria in two ways: Immunosuppression increase susceptibility to malaria, with an increased occurrence of clinical and severe malaria Immunosuppressed patients have more frequent malaria infections and higher parasite density or delayed clearance of parasitaemia , thus increasing the parasite biomass and transmission

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In a systematic review of HIV-1 infection in Africa, malaria was identified as the third cause of HIV-related morbidity In 41 sub-Saharan African countries, HIV infection is thought to have caused an average increase in the prevalence of malaria of 1·3% and malaria-related mortality of 4·9%. Overall, an extra 3 million cases of clinical malaria and 65 000 malaria-related deaths can be attributed to HIV infection in Africa every year

Effect of HIV infection on malaria in children :

Effect of HIV infection on malaria in children Data from prospective cohort studies indicate a higher prevalence of clinical malaria in HIV-infected children than in children without HIV parasite density was similar for HIV-infected and HIV-uninfected children prevalence and severity of anaemia, transfusion requirements, hospitalisation rates, coma, and hypoglycaemia are higher in HIV-infected children In Kenya, the mortality at 3 months after malaria was 33% in HIV-infected children versus 3% in HIV-uninfected children (p<0·001)

Effect of HIV on malaria in pregnant women :

Effect of HIV on malaria in pregnant women pregnant women have more frequent parasitaemia and clinical malaria, with higher parasite densities Anaemia and maternal death are also more common in women with both HIV and malaria Most studies (but not all) show an increased occurrence of placental malaria, and higher parasite densities in HIV-infected women

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The difference in malaria infection is more pronounced after the third pregnancy In a review of 11 studies in Africa, the proportion of cases of placental malaria attributable to HIV co-infection increased with number of pregnancies: 21·3% (first pregnancy), 41·2% (second pregnancy), and 58·2% (more than two pregnancies) HIV and placental malaria co-infection increased risk of low birthweight and preterm delivery

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In a prospective study in Uganda, in which HIV-infected mothers and their children received daily co- trimoxazole prophylaxis, breastfeeding was associated with a significantly decreased risk of malaria in HIV-exposed (relative risk 0·62)

Effect of daily co-trimoxazole on parasitaemia and malaria in HIV-infected patients :

Effect of daily co- trimoxazole on parasitaemia and malaria in HIV-infected patients Daily co- trimoxazole reduces the occurrence of parasitaemia and clinical malaria in HIV-infected adults and children. Co- trimoxazole prophylaxis combined with the use of insecticide-treated nets reduced the prevalence of clinical malaria in children by 97% ITN alone reduced this prevalence by 43%. Cotrimoxazole in patients with CD4 cell counts of < 200 cells per μL , in combination with ITN, can therefore be considered as a part of preventive strategies against malaria

Effect of HIV on treatment of malaria :

Effect of HIV on treatment of malaria Increase the burden of malaria by increasing susceptibility of patients to infection or by decreasing the response to treatment treatment of malaria in HIV-infected patients is similar to treatment of HIV-uninfected In early studies, HIV infection was not associated with treatment failure, HIV infection has been suggested to impair treatment responses or favour recrudescence and reinfection

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A prospective study in western Kenya, Adults was followed for 28 days after treatment with SP for malaria infection. Treatment failure was higher in HIV- seropositive patients with a CD4 count <200 cells/ microL compared with HIV- seronegative patients (21%versus 8%). There was a higher rate of both new infections and recrudescent infections in the HIV positive cohort

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In a randomised study that compared sulfadoxine—pyrimethamine with artemether—lumefantrine for uncomplicated malaria, patients with CD4 cell counts of less than 300 cells per μL had an increased risk of recurrent parasitaemia (relative risk 2·24), and of recrudescence (relative risk 1·67)

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Effect of antiretroviral treatment on malaria ART that contains NNRTI when combined with co- trimoxazole decreases the prevalence of clinical malaria compared with co- trimoxazole alone PI lopinavir , saquinavir , indinavir , ritonavir , and atazanavir have inhibitory effects on P falciparum proliferation in vitro PI also have a synergistic effect with chloroquine and mefloquine on P falciparum Thus, ART is associated with a reduced prevalence of clinical malaria, and protease inhibitors have a specific antimalarial effect

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Drug interaction Limited data exist on pharmacokinetic interactions between antiretroviral therapy and antimalarial drugs

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HIV treatment Potential interaction Clinical implication Quinine EFV, NVP ↓ quinine conc. Monitor quinine conc. Quinine PI inhibitors ↑quinine conc. " Mefliquine retonavir ↓ retonavir conc. Atovaquine Lopinavir / retonavir ↓ Atovaquine conc. Lumefantrine PI inhibitors,EFV,NVP ↑ lumfantrin conc. & prolong QT interval Avoid coadminstration Chloroquine , SP retonavir Alteration of antimalaria drug metabolism - SP neverapine ↑ risk of cutaneuos & hepatic advers effects Do not initiate togather Artimesinin PI inhibitors Alteration of Artimesinin metabolism -

Management :

Management Management of severe malaria comprises four main areas: Clinical assessment of the patient Specific antimalarial treatment Adjunctive therapy and supportive care

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C linical assessment of the patient General principles Severe malaria is a medical emergency mortality of untreated severe malaria (particularly cerebral malaria) is thought to approach 100% With promt , effective antimalaria treatment and supportive care martality may falls to 15- 20% Death can occur within hours of presentation A full neurologic assessment should be performed(Glasgow coma scale) Temperature , heart rate and rhythm, respiratory rate and rhythm , blood pressure oxygen saturation

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Supportive measures ( eg , oxygen, ventilatory support, cardiac monitoring, and pulse oximetry ) Additional tests when indicated : electrolytes, full blood count, type and cross, blood culture, and clotting studies LP for unconscious patients to rule out concomitant bacterial meningitis

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Antimalarial treatment Two major classes of drugs available for parenteral treatment of severe malaria Artemisinin derivatives ( artesunate , artemether and artemotil ) Cinchona alkaloids (quinine and quinidine )

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1, Artemisinin derivatives IV artesunate should be used in preference to quinine for the treatment of severe P. falciparum malaria in adults and children.(Strong recommendation, high quality evidence) IV artesunate has been shown to significantly reduce the risk of death from severe malaria compared to iv quinine (6 trials, 1938 participants; RR 0.62, 95% CI 0.51–0.75; high quality evidence).

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Clear parasitemia more rapidly than quinine Active against a broader life-cycle range of blood stage parasites than quinine and they are active against gametocytes Not requiring rate controlled infusion or cardiac monitoring Artesunate was well tolerated, while quinine was associated with a threefold increased risk of hypoglycemia

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Dosing 2.4 mg/kg as first dose, followed by 2.4 mg/kg at 12 and 24 hours, followed by 2.4 mg/kg once daily Following four doses of intravenous artesunate , oral antimalarial treatment may be administered Intravenous therapy for more than three days may be indicated in very ill patients. Artesunate can also be administered im , orally, or via rectal suppository Artesunate dosing need not be adjusted for hepatic or renal failure

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2, Quinine/ quinidine Treatment of choice for areas where iv artesunate of reliable quality is not readily avialable IV quinine dihydrochloride 20 mg salt/kg (in 5% dextrose ) loading dose over 4 hours, followed by 20 to 30 mg salt/kg divided into two to three equal administrations of 10 mg salt/kg (over 4 hours) at 8 or 12 hour intervals ( maximum 1800 mg salt/day) IV quinidine gluconate 10 mg salt/kg loading dose (max. 600 mg salt) in normal saline over 1 hour, followed by 0.02 mg/kg/minute continuous infusion.

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If iv infusions cannot be given, quinine can be administered via im injection( have equal peak concentration) Two injections of 10 mg/kg quinine (diluted to 60 to 100 mg/ mL ) should be administered 4 hours apart(IM) The anterior thigh is preferred over the gluteal region to minimize the risk of sciatic nerve damage.

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Both quinine and quinidine can act as pancreatic secretagogues , leading to hyperinsulinemic hypoglycemia Other toxic effects include tinnitus, reversible hearing loss, nausea, vomiting, dizziness, and visual disturbances Quinidine can cause QT prolongation and should be administered with electrocardiographic monitoring

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Adjunctive therapy Aimed at management of complications of sever malaria Coma/cerebral malaria/ Maintain airway, place patient on his or her side, exclude other treatable causes of coma (e.g. hypoglycaemia , bacterial meningitis) avoid harmful ancillary treatment, such as corticosteroids, heparin and adrenalineintubate if indiceted

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Hyperpyrexia Administer tepid sponging, fanning, a cooling blanket and antipyretic drugs Paracetamol is preferred over more nephrotoxic drugs (e.g. NSAIDsb ) Seizure management Seizures occur in up to 70 percent of children Exclude firist seizure is not due to hypoglycemia or fever Benzodiazepines are useful first line agents for seizure treatment

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Diazepam (0.4 mg/kg) iv or per rectum; lorazepam (0.1 mg/kg) iv or intraosseously . Repeate once if seizures do not cease within 5 minutes of the initial dose Benzodiazepines should not be combined due to risk of respiratory depression

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If seizures are not controllable with benzodiazepines, phenobarbitone ( phenobarbital 15 to 20 mg/kg, slow IV push) or phenytoin (18 mg/kg diluted in 100 mL normal saline, infused over 20 minutes) If seizures recur, maintenance doses of phenobarbital (5 to 15 mg/kg/day, administered orally, via NG tube, or via slow IV push in divided doses every 12 hours) or phenytoin (5 mg/kg/day IV) may be initiated

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Anemia and coagulopathy Blood Transfusion In areas where malaria and HIV are common infections, blood transfusion is associated with important risks For these reasons, transfusion should be reserved for patients with altered consciousness, high output heart failure, respiratory distress, cool peripheries, hyperlactatemia , and/or high density parasitemia low hemoglobin concentration (≤4 to 5 g/ dL ) or low hematocrit (≤10 to 15%)

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10 mL /kg of packed red blood cells or 20 mL /kg of whole blood transfused over 2 to 4 hours is appropriate Blood transfusion is well tolerated duo to hypovolumia and no need of diuretics Exchange transfusion has been proposed eventhough who does not recommend, but CDC recommends for patients with parasite density of >10 percent with end organ complications

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Coagulopathy DIC is rare in sever malaria(<5%), but thrombocytopenia is common Treat the underlying cause & hemodynamic support Platelet transfusion and fresh frozen plasma Heparin Activated protein C Antithrombin

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Hypoglycemia Blood glucose <40 mg/ dL or <2.2 mmol /L suspected in any patient who is comatose or who deteriorates suddenly Case fatality rates approches 61% Parasite glucose consumption and/or impaired host gluconeogenesis , use of quinine or quinidine

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Initial bolus of dextrose (0.25 g/kg of body weight) Achieved with 2.5 mL /kg of 10% dextrose solution Blood glucose measurement after 15 minutes, administration of repeat boluses until the patient is normoglycemic . If glucose measurement is not possible, comatose patients with parasitemia at the time of initial assessment should receive a bolus of 2.5 mL /kg of 10% dextrose solution

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Maintenance intravenous fluids should contain at least 5% dextrose; patients with recurrent hypoglycemia should receive 10 % dextrose (10 % dextrose can be prepared by withdrawing 100 mL from a one liter bag of a 5% dextrose solution and replacing it with 100 mL of a 50 % dextrose solution

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Fluid management Adults with severe malaria are very vulnerable to fluid overload Children, on the other hand, are more likely to be dehydrated Fluid requirements should be assessed on an individual basis Clinical symptoms of hypovolemia frequently resolve with blood transfusion (when warranted)

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When transfusion is not indicated, data suggest that repeated boluses of normal saline may be counterproductive In a large study involving 3141 African children with severe infection and impaired consciousness with impaired perfusion (over half of whom had malaria), patients who received saline bolus had higher mortality at 48 hours than patients who received no bolus (10.6 versus 7.3 percent, respectively Therefore, aggressive fluid resuscitation has uncertain benefit in these setting

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Maintenance fluid shuold include 5 % dextrose Patients weighing 1 to 10 kg should receive fluids at a rate of 4 mL /kg/hour For patients weighing 10 to 20 kg, patients should receive 40 mL per hour for the first 10 kg PLUS 2 mL /kg/hour for each kg above 10 kg For patients who weigh more than 20 kg, 60 mL per hour for the first 20 kg PLUS 1 mL /kg/hour for every kg above 20 kg Total maintenance needs are generally capped near 2.5 liters daily. Intravenous fluid support should be continued until oral intake is tolerated

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Nutritional support NGT feeding for patients with prolonged coma who are unable to eat and drink within 24 to 48 hours (eggs, milk, sugar and oil) or high calorie drinks may be used IV fluids has to be decreased accordingly Most patients are able to eat and drink with in 5 to 7 days

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Fever Paracetamol ( 15 mg/kg every 6 hours; maximum dose 1000 mg) is a reasonable antipyretic agent If fever persists, ibuprofen (10 mg/kg every 6 hours; maximum dose 1200 mg per day) alone or on an alternating schedule with paracetamol every 3 hours.

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Bacterial infection Bacteremia is an important contributor to morbidity and mortality severe anemia has been implicated as a primary risk factor for nontyphoidal Salmonella septicemia A comprehensive study of bacteremia in Kenya identified falciparum infection as a major risk factor for bacteremia with multiple organisms When the prevalence of malaria parasitemia was 29 percent, 62 percent of bacteremia cases were attributable to malaria Bacterial infection should be suspected in patients with severe anemia together with signs or symptoms of sepsis Blood cultures and broad spectrum antibiotic therapy with activity against gram-negative bacilli

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PREGNANCY More likely to develop severe P. falciparum malaria, particularly in the second and third trimesters Hypoglycemia and pulmonary edema are more common than in nonpregnant individuals. Maternal mortality can approach 50 %, and fetal death and premature labor are common Prompt antimalarial therapy and supportive care s are crucial Artesunate or artemether are preferred over quinine in the second and third trimesters In the first trimester, either artemisinins or quinine are acceptable choices

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1 st line antimalarial drugs - artemeter plus lumefantrine - artesunate plusamodiaquine - artesunate plus mefloquine - artasunate plus sulfadoxine-pyrimethamine - dihydroartemisinin plus piperaquine

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2 nd line antimalarial drugs - artesunate plus TTC or Doxi or clindamycin - quinine plus TTC or Doxi or clindamycin

COMMON ERRORS IN MANAGEMENT OF SEVERE MALARIA:

COMMON ERRORS IN MANAGEMENT OF SEVERE MALARIA 1 .Failure to diagnose associated complications such as bacterial infections, Gram negative septicemia etc. 2. Missed hypoglycaemia 3. Misjudgement of severity

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4.Errors of fluid and electrolytic replacement 5.Errors in anti-malarial chemotherapy 6. Delay in starting treatment Unjustified withholding of antimalarial drug for the fear of toxicity e.g. Quinine in pregnant women, in hypoglycaemia -Inadequate dosage administration -Failure to control the rate of IV infusion

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7. Delay in considering obstetrics intervention pregnant women suffering from malaria 8.Missed / late diagnosis of ARDS, acute pulmonary oedema 9 Use of inappropriate ancillary therapies e.g. steroids, . 10. Delay in starting dialysis

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Prevention Use of Insectiside Avoid bite E liminating breeding grounds using repellents Malaria prophylaxis Vaccination ( under clinical trial)

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Reference UpToDate 2011 Consequences of HIV infection on malaria and therapeutic implications: a systematic review/The Lancet.com / Shankarkumar U,Shankarkumar A, Ghosh K. HIV and malaria co-infection in Mumbai, western India.National Institute of Immunohaematology , KEM Hospital, Mumbai, India / pubmed / Harrison’s, Internal medicine. 17 th edition Giudeline for the treatment of malaria, second edition,WHO , 2010.

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