11

MalariaMalaria

22

MalariaMalaria

Malaria is a protozoan disease transmitted by the Malaria is a protozoan disease transmitted by the bite of female bite of female AnophelesAnopheles mosquitoes. mosquitoes.

Most important of the parasitic diseases of humans, Most important of the parasitic diseases of humans, with transmission in 103 countries affecting more with transmission in 103 countries affecting more than 1 billion people and causing between 1 and 3 than 1 billion people and causing between 1 and 3 million deaths each yearmillion deaths each year

Four species of the genus Four species of the genus PlasmodiumPlasmodium cause nearly cause nearly all malarial infections in humans : all malarial infections in humans : P. falciparumP. falciparum, , P. P. vivaxvivax, , P. ovaleP. ovale, and , and P. malariaeP. malariae

Almost all deaths are caused by Almost all deaths are caused by falciparum falciparum malaria. malaria.

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Causative Agent Causative Agent

Malaria is caused by one of four species of Malaria is caused by one of four species of the prototype the prototype plasmodium.plasmodium.

Female Female Anopheles Anopheles mosquitoes feed on mosquitoes feed on human blood to obtain the protein they human blood to obtain the protein they need to develop their eggs. need to develop their eggs.

44

Epidemiologi Epidemiologi Epidemiologi Epidemiologi

Malaria occurs throughout most of the tropical regions Malaria occurs throughout most of the tropical regions of the world of the world

Endemicity traditionally has been defined in terms of Endemicity traditionally has been defined in terms of parasitemia rates or palpable-spleen parasitemia rates or palpable-spleen

55

66

The Life Cycle of The Life Cycle of PlasmodiumPlasmodium

i.i. Mosquitoes transmit Mosquitoes transmit Plasmodium Plasmodium when they feed when they feed on an infected human host and absorb the on an infected human host and absorb the parasites gametes.parasites gametes.

ii.ii. These fuse and develop in the mosquito’s gut to These fuse and develop in the mosquito’s gut to form infective stages, which move to the form infective stages, which move to the mosquito’s salivary glands. mosquito’s salivary glands.

iii.iii. When the mosquito feeds again the infective When the mosquito feeds again the infective stages pass out into the blood together with an stages pass out into the blood together with an anticoagulant in saliva.anticoagulant in saliva.

iv.iv. The parasites enter the red blood cells, where The parasites enter the red blood cells, where they multiply.they multiply.

77

Patogenesis,patologiPatogenesis,patologi

Manusia mrpkan hospes perantara,sedang Manusia mrpkan hospes perantara,sedang nyamuk mrpkan hospes definitif untk nyamuk mrpkan hospes definitif untk infeksi plasmodium.infeksi plasmodium.

Sikluskehidupan Sikluskehidupan aseksual(skizogoni)ditemukan pd aseksual(skizogoni)ditemukan pd manusia,sedang siklus kehidupan parasit yg manusia,sedang siklus kehidupan parasit yg seksual(sporogoni)ditemukan pd nyamuk.seksual(sporogoni)ditemukan pd nyamuk.

Dalam siklus aseksual,satu eritrsit yg Dalam siklus aseksual,satu eritrsit yg terinfeksi akan menghasilkan 6-32 merozoit terinfeksi akan menghasilkan 6-32 merozoit pd setiap kejadian sporulasi.pd setiap kejadian sporulasi.

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Patogenesis,patologiPatogenesis,patologi

Infeksi oleh plasmodium malariae mrpkan Infeksi oleh plasmodium malariae mrpkan infeksi paling ringan,hanya eritrsit matang infeksi paling ringan,hanya eritrsit matang yg diserang;siklus aseksuqal berlangsung yg diserang;siklus aseksuqal berlangsung 72 jam;jadi baru setelah 72 jam timbul 72 jam;jadi baru setelah 72 jam timbul generasi baru(merozoit)yg akan generasi baru(merozoit)yg akan menyerang eritrosit yg lain.menyerang eritrosit yg lain.

Jumlah merozoitpun hanya 6-12 saja dari Jumlah merozoitpun hanya 6-12 saja dari hasil sporulasi dlm satu eritrosit.hasil sporulasi dlm satu eritrosit.

Infeksi oleh Plasmodium falciparum Infeksi oleh Plasmodium falciparum mrpakan yg terberat ok parasit ini mrpakan yg terberat ok parasit ini menyerang baik retikulosit eritrosit menyerang baik retikulosit eritrosit matang,skizogoni berlangsung cepat dlm matang,skizogoni berlangsung cepat dlm 36-48 jam.36-48 jam.

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Patogenesis,patologiPatogenesis,patologi Dari satu eritrosit dihasilkan banyak merozoit(20-32 Dari satu eritrosit dihasilkan banyak merozoit(20-32

merozoit).Juga terjadi perubahan fisik pd eritrosit yg tdk merozoit).Juga terjadi perubahan fisik pd eritrosit yg tdk dijumpai pd infeksi oleh pasmodium lainnya yi eritrosit yg dijumpai pd infeksi oleh pasmodium lainnya yi eritrosit yg terinfeksi lebih mudah saling mlekat pd endotel terinfeksi lebih mudah saling mlekat pd endotel kapiler,membentuk trombus(aglutinasi)eritrosit yg kapiler,membentuk trombus(aglutinasi)eritrosit yg terinfeksi jadi lebih tipis,lebih besar diameternya dan terinfeksi jadi lebih tipis,lebih besar diameternya dan mudah pecah di dalam sistem retikulo endotelial.mudah pecah di dalam sistem retikulo endotelial.

Pada setiap adanya destruksi eritrsit timbul demam yg Pada setiap adanya destruksi eritrsit timbul demam yg paroksismal peridik,ok reaksi alergi thdp zat pirogen yg paroksismal peridik,ok reaksi alergi thdp zat pirogen yg terbebas pd wkt sporulasi perjalanan khas demam malaria.terbebas pd wkt sporulasi perjalanan khas demam malaria.

Demam malaria yg khas : stadium Demam malaria yg khas : stadium 1:dingin(frigoris)berlangsung 20-60 mnt.Stadium 1:dingin(frigoris)berlangsung 20-60 mnt.Stadium 2:panas(febris) 1-4 jam,Stadium 2:panas(febris) 1-4 jam,Stadium 3:berkeringat(sudoris)berlangsun 1-3 jam.3:berkeringat(sudoris)berlangsun 1-3 jam.

Ketiga stadium berlangsung 3-4 jam kadang 6-12 jam lalu Ketiga stadium berlangsung 3-4 jam kadang 6-12 jam lalu disusul periode tidak demam(apireksia).disusul periode tidak demam(apireksia).

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Patogenesis,patologiPatogenesis,patologi Juga terjadi vasokonstriksi disusul vasodilatasi,yg seirama Juga terjadi vasokonstriksi disusul vasodilatasi,yg seirama

dg rasa menggigil dan demam.dg rasa menggigil dan demam. Pada infeksi dg P.Falsiparum,vasodilatasi ini dpat disertai Pada infeksi dg P.Falsiparum,vasodilatasi ini dpat disertai

HipotaensiHipotaensi Banyaknya eritrosit yg pecah,menimbulakan anemia. Banyaknya eritrosit yg pecah,menimbulakan anemia. Pigmen malaria,(heozoria),akan diambil lekosit segmen dan Pigmen malaria,(heozoria),akan diambil lekosit segmen dan

monosit lalu di deposit kedalam trabekula dan pulpa merah monosit lalu di deposit kedalam trabekula dan pulpa merah limpa,dan sistem retikuloendotelial lainnya(hati,otak).limpa,dan sistem retikuloendotelial lainnya(hati,otak).

Limpa akan membesar ok kongesti dan hiperplasi Limpa akan membesar ok kongesti dan hiperplasi sistemretikuloendotelial.sistemretikuloendotelial.

Pada infeksi dg P.Falsiparum,terdapat gangguan sirkulasi g Pada infeksi dg P.Falsiparum,terdapat gangguan sirkulasi g berat,anemi berat.berat,anemi berat.

Komplikasi pernisiosa,yi hiperpireksi,malaria Komplikasi pernisiosa,yi hiperpireksi,malaria serebral,ikterus/hepatitis,nekrosis tubuler akut.serebral,ikterus/hepatitis,nekrosis tubuler akut.

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Life cycle of malariaLife cycle of malaria Human infection begins when a female anopheline Human infection begins when a female anopheline

mosquito inoculates plasmodial sporozoites from its mosquito inoculates plasmodial sporozoites from its salivary gland during a blood meal salivary gland during a blood meal carried rapidly via carried rapidly via the bloodstream to the liver, where they invade hepatic the bloodstream to the liver, where they invade hepatic parenchymal cells and begin a period of asexual parenchymal cells and begin a period of asexual reproductionreproduction

By this amplification process (intrahepatic or By this amplification process (intrahepatic or preerythrocytic schizogony or merogony), a single preerythrocytic schizogony or merogony), a single sporozoite eventually may produce 10,000 to more than sporozoite eventually may produce 10,000 to more than 30,000 daughter merozoites 30,000 daughter merozoites discharging motile discharging motile merozoites into the bloodstream and symptomatic stage merozoites into the bloodstream and symptomatic stage of the infection begins. of the infection begins.

1212

Life cycle of malariaLife cycle of malaria

In In P. vivaxP. vivax and and P. ovaleP. ovale infections, a infections, a proportion of the intrahepatic forms do not proportion of the intrahepatic forms do not divide immediately but remain dormant for divide immediately but remain dormant for months to years before reproduction months to years before reproduction begins. These dormant forms, or begins. These dormant forms, or hypnozoites, are the cause of the relapses hypnozoites, are the cause of the relapses that characterize infection with these two that characterize infection with these two species.species.

1313

Life cycle of malariaLife cycle of malaria

After entry into the bloodstream, merozoites After entry into the bloodstream, merozoites rapidly invade erythrocytes and become rapidly invade erythrocytes and become trophozoites. Attachment is mediated via a trophozoites. Attachment is mediated via a specific erythrocyte surface receptor. During the specific erythrocyte surface receptor. During the early stage of intraerythrocytic development, the early stage of intraerythrocytic development, the small "ring forms" of the four parasitic species small "ring forms" of the four parasitic species appear similar under light microscopy. As the appear similar under light microscopy. As the trophozoites enlarge, species-specific trophozoites enlarge, species-specific characteristics become evident, pigment characteristics become evident, pigment becomes visible, and the parasite assumes an becomes visible, and the parasite assumes an irregular or ameboid shape. irregular or ameboid shape.

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Life cycle of malariaLife cycle of malaria

By the end of the 48-h intraerythrocytic life By the end of the 48-h intraerythrocytic life cycle (72 h for cycle (72 h for P. malariaeP. malariae), the parasite ), the parasite has consumed nearly all the hemoglobin has consumed nearly all the hemoglobin and grown to occupy most of the red cell and grown to occupy most of the red cell (merogony) (merogony) red cell ruptures to release red cell ruptures to release 6 to 30 daughter merozoites, each capable 6 to 30 daughter merozoites, each capable of invading a new red cell and repeating of invading a new red cell and repeating the cycle.the cycle.

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The disease in The disease in human human beings is caused by the direct beings is caused by the direct effects of red cell invasion and destruction by the effects of red cell invasion and destruction by the asexual asexual parasite and the host's reaction. After a series parasite and the host's reaction. After a series of asexual cycles (of asexual cycles (P. falciparumP. falciparum) or immediately () or immediately (P. P. vivaxvivax, , P. ovaleP. ovale, , P. malariaeP. malariae), some of the parasites ), some of the parasites develop into morphologically distinct long-lived sexual develop into morphologically distinct long-lived sexual forms (gametocytes) that can transmit malaria.forms (gametocytes) that can transmit malaria.

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After being ingested in the blood meal of a After being ingested in the blood meal of a biting female anopheline mosquito, the male biting female anopheline mosquito, the male and female gametocytes form a zygote in the and female gametocytes form a zygote in the insect's midgut. This zygote matures into an insect's midgut. This zygote matures into an ookinete, which penetrates and encysts in the ookinete, which penetrates and encysts in the mosquito's gut wall. The resulting oocyst mosquito's gut wall. The resulting oocyst expands by asexual division until it bursts to expands by asexual division until it bursts to liberate myriad motile sporozoites, which then liberate myriad motile sporozoites, which then migrate in the hemolymph to the salivary gland migrate in the hemolymph to the salivary gland of the mosquito to await inoculation into of the mosquito to await inoculation into another human at the next feeding.another human at the next feeding.

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Diagram of Malaria InfectionDiagram of Malaria Infection

Infection is by mosquito bite

Infects liver, then blood cells

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1919

½ - 1 jam½ - 1 jam

Ovale : tachisporozoit & bradisporozoit

Ovale : tachisporozoit & bradisporozoit

10-30 ribu parasit anak10-30 ribu parasit anak

Pre-patenPre-paten

2-10 hr2-10 hr

Lamina basalisLamina basalis

Masuk sirkulasiMasuk sirkulasi

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Pathogenesis Pathogenesis The vector, the The vector, the AnophelesAnopheles species mosquito, species mosquito,

passes plasmodia, which is contained in its saliva, passes plasmodia, which is contained in its saliva, into its host while obtaining a blood meal. into its host while obtaining a blood meal. Plasmodia enter circulating erythrocytes (RBCs) Plasmodia enter circulating erythrocytes (RBCs) and feed on the hemoglobin and other proteins and feed on the hemoglobin and other proteins within the cells. within the cells.

This protozoan brood replicates inside the cell. This protozoan brood replicates inside the cell. This replication induces RBC cytolysis and causes This replication induces RBC cytolysis and causes the release of toxic metabolic byproducts into the the release of toxic metabolic byproducts into the bloodstream bloodstream symptoms : chills, headache, symptoms : chills, headache, myalgias, and malaise in a cyclic pattern. The myalgias, and malaise in a cyclic pattern. The parasite also may cause jaundice and anemia. parasite also may cause jaundice and anemia.

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PathogenesisPathogenesis P falciparum,P falciparum, may induce kidney failure, coma, and death. may induce kidney failure, coma, and death. P vivaxP vivax and and P ovaleP ovale may produce a dormant form that may produce a dormant form that

persists in the liver persists in the liver Malaria-causing Malaria-causing PlasmodiumPlasmodium species metabolize hemoglobin and species metabolize hemoglobin and

other RBC proteins to create a toxic pigment termed hemozoin. other RBC proteins to create a toxic pigment termed hemozoin. The parasites derive their energy solely from glucose, and they The parasites derive their energy solely from glucose, and they

metabolize it 70 times faster than the RBCs they inhabit, thereby metabolize it 70 times faster than the RBCs they inhabit, thereby causing hypoglycemia and lactic acidosis. causing hypoglycemia and lactic acidosis.

The plasmodia also cause lysis of infected and uninfected RBCs, The plasmodia also cause lysis of infected and uninfected RBCs, suppression of hematopoiesis, and increased clearance of RBCs suppression of hematopoiesis, and increased clearance of RBCs by the spleen, which leads to anemia. Over time, malaria infection by the spleen, which leads to anemia. Over time, malaria infection also causes thrombocytopenia and hepatosplenomegaly. also causes thrombocytopenia and hepatosplenomegaly.

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The morbidity and mortality caused by The morbidity and mortality caused by P P falciparumfalciparum are increased greatly over that are increased greatly over that caused by other caused by other PlasmodiumPlasmodium species because species because of the increased parasitemia of of the increased parasitemia of P falciparumP falciparum and and its ability to cytoadhere. its ability to cytoadhere.

Infected RBC produces proteinaceous knobs Infected RBC produces proteinaceous knobs that bind to endothelial cells. The adherence of that bind to endothelial cells. The adherence of these infected RBCs causes them to clump these infected RBCs causes them to clump together in the blood vessels in many areas of together in the blood vessels in many areas of the body, leading to much of the damage the body, leading to much of the damage injurred by the parasite.injurred by the parasite.

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CLINICAL FEATURESCLINICAL FEATURES Clinical symptoms include the following: Cough, Fatigue, Clinical symptoms include the following: Cough, Fatigue,

Malaise, Shaking chills, Arthralgia, Myalgia, Paroxysm Malaise, Shaking chills, Arthralgia, Myalgia, Paroxysm of fever, and sweatsof fever, and sweats

The classic paroxysm begins with a period of shivering The classic paroxysm begins with a period of shivering and chills, which lasts for approximately 1-2 hours, and and chills, which lasts for approximately 1-2 hours, and is followed by a high fever. Finally, the patient is followed by a high fever. Finally, the patient experiences excessive diaphoresis, and the body experiences excessive diaphoresis, and the body temperature of the patient drops to normal or below temperature of the patient drops to normal or below normalnormal

Less common symptoms include the following:Less common symptoms include the following:Anorexia and lethargyAnorexia and lethargyNausea and vomitingNausea and vomitingDiarrheaDiarrheaHeadacheHeadache

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Laboratory examinationLaboratory examination

Giemsa-stained thick and thin peripheral blood smearsGiemsa-stained thick and thin peripheral blood smearsThese smears are the criterion standard for malaria These smears are the criterion standard for malaria

detection and should be sent to the laboratory detection and should be sent to the laboratory immediately, since malaria is a potentially life-immediately, since malaria is a potentially life-threatening infection.threatening infection.

When reading the smear, 200-300 oil-immersion When reading the smear, 200-300 oil-immersion fields should be examined (more if the patient fields should be examined (more if the patient recently has taken prophylactic medication, because recently has taken prophylactic medication, because this temporarily may decrease parasitemia).this temporarily may decrease parasitemia).

Rapid diagnosis testRapid diagnosis testPF test, ICT test, paracheck, OptiMALPF test, ICT test, paracheck, OptiMAL

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Manifestations of Severe Falciparum Malaria Signs Manifestations  

Unarousable coma/cerebral malaria Failure to localize or respond appropriately to noxious stimuli; coma persisting for >30 min after generalized convulsion

 

Acidemia/acidosis Arterial pH <7.25 or plasma bicarbonate level of <15 mmol/L; venous lactate level of >15 mmol/L manifests as labored deep breathing, often termed "respiratory distress"

 

Severe normochromic, normocytic anemia

Hematocrit of <15% or hemoglobin level of <50 g/L (<5 g/dL) with parasitemia level of >100,000/mL 

Renal failure Urine output (24 h) of <400 mL in adults or <12 mL/kg in children; no improvement with rehydration; serum creatinine level of >265 mmol/L (>3.0 mg/dL)

 

ARDS Noncardiogenic pulmonary edema, often aggravated by overhydration  

Hypoglycemia Plasma glucose level of <2.2 mmol/L (<40 mg/dL)  

Hypotension/shock Systolic blood pressure of <50 mmHg in children 1-5 years or <80 mmHg in adults; core/skin temperature difference of >10∞C

 

Bleeding/disseminated intravascular coagulation

Significant bleeding and hemorrhage from the gums, nose, and gastrointestinal tract and/or evidence of disseminated intravascular coagulation

 

Convulsions More than two generalized seizures in 24 h  

Hemoglobinuriaa Macroscopic black, brown, or red urine; not associated with effects of oxidant drugs and red blood cell enzyme defects (such as G6PD deficiency)

 

Other  

Impaired consciousness Obtunded but arousable  

Extreme weakness Prostration  

Hyperparasitemia Parasitemia level of >5% in nonimmune patients  

Jaundice Serum bilirubin level of >50 mmol/L (>3.0 mg/dL)  

a Hemoglobinuria may occur in uncomplicated malaria.

NOTE: G6PD, glucose-6-phosphate dehydrogenase.

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2727

Differential Diagnosis Differential Diagnosis

Typhoid feverTyphoid feverDengue FeverDengue FeverURTIURTILeptospirosis Leptospirosis

28

Recommended Therapeutic Doses of Antimalarial Drugs

Drug Uncomplicated Malaria (Oral) Severe Malariaa (Parenteral)

Chloroquine 10 mg of base/kg followed by 10 mg/kg at 24 h and 5 mg/kg at 48 h or by 5 mg/kg at 12, 24, and 36 h (total dose, 25 mg/kg); for P. vivax or P. ovale, primaquine (0.25 mg of base/kg per day for 14 daysc) added for radical cure

10 mg of base/kg by constant-rate infusion over 8 h followed by 15 mg/kg over 24 h or by 3.5 mg of base/kg by IM or SC injection every 6 h (total dose, 25 mg/kg)b

Sulfadoxine/pyrimethamine

25/1.25 mg/kg, single oral dose (3 tablets for adults)

æ

Mefloquine 15 mg/kg followed 8-12 h later by second dose of 10 mg/kg

æ

Quinine 10 mg of salt/kg q8h for 7 days combined with tetracyclined (4 mg/kg qid) or doxycycline (3 mg/kg once daily) or clindamycin (10 mg/kg bid) for 7 days

20 mg of salt/kg by IV infusion over 4 he followed by 10 mg/kg infused over 2-8 h every 8 h

Quinidine gluconate æ 10 mg of base/kg by constant-rate infusion over 1-2 h followed by 0.02 mg/kg per min, with ECG monitoringf

29

Recommended Therapeutic Doses of Antimalarial Drugs

Drug Uncomplicated Malaria (Oral) Severe Malariaa (Parenteral)

Artesunate In combination with 25 mg of mefloquine/kg, 12 mg/kg given in divided doses over 3-5 days (e.g., 4 mg/kg for 3 days or 4 mg/kg followed by 2 mg/kg per day for 4 days); if used alone, give for 7 days (usually 4 mg/kg initially followed by 2 mg/kg daily)

2.4 mg/kg IV or IM stat followed by 1.2 mg/kg at 12 and 24 h and then daily

Artemether Same regimen as for artesunate 3.2 mg/kg IM stat followed by 1.6 mg/kg per day

Atovaquone-proguanil

For adults >40 kg, each dose comprises 4 tablets (each containing atovaquone 250 mg and proguanil 100 mg) taken once daily for 3 days with food

æ

Artemether-lumefantrine

For adults ≥35 kg, each dose comprises 4 tablets (each containing artemether 20 mg and lumefantrine 120 mg) at 0, 8, 24, and 48 h (semi-immunes) or at 0, 8, 24, 36, 48, and 60 h (nonimmunes) taken after food

æ

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Management of Severe MalariaManagement of Severe Malaria

3131

SUPPORTIVE MANAGEMENT C.M.SUPPORTIVE MANAGEMENT C.M.

AIRWAYAIRWAY FLUID REQUIREMENT : HYDRATION / FLUID REQUIREMENT : HYDRATION /

OVERHYDRATIONOVERHYDRATION CONVULSION : DIAZEPAMCONVULSION : DIAZEPAM MONITORING GCS & VITAL SIGNMONITORING GCS & VITAL SIGN LAB : FBC, GLUCOSE, PAR.COUNT, CREATININE, LAB : FBC, GLUCOSE, PAR.COUNT, CREATININE,

UREUM, BLOOD GAS, URINE S.G, SODIUM, UREUM, BLOOD GAS, URINE S.G, SODIUM, POTASSIUM.POTASSIUM.

PREVENT : SHOCK, SEPTICAEMIA, ACIDOSIS, ARDS, PREVENT : SHOCK, SEPTICAEMIA, ACIDOSIS, ARDS, HYPOGLYCAEMIA, ASPIRATION, BEDSORES.HYPOGLYCAEMIA, ASPIRATION, BEDSORES.

TREAT HYPERPYREXIATREAT HYPERPYREXIA VOLUME URINE & CATHETERIZATIONVOLUME URINE & CATHETERIZATION

CM:cerebral Mal

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SPECIFIC TREATMENT SEVERE SPECIFIC TREATMENT SEVERE MALARIA ( Anti Malaria)MALARIA ( Anti Malaria)

PARENTERALPARENTERALSTART IMMEDIATELYSTART IMMEDIATELYDOSAGE, WEIGHT THE PATIENTDOSAGE, WEIGHT THE PATIENTMONITORING RESPONSEMONITORING RESPONSESWITCHED TO ORAL WHEN POSSIBLESWITCHED TO ORAL WHEN POSSIBLEMONITORING SIDE EFFECTSMONITORING SIDE EFFECTS

3333

ANTI MALARIAL THERAPY FOR S.MANTI MALARIAL THERAPY FOR S.M

QUININEQUININEQUINIDINEQUINIDINECHLOROQUINECHLOROQUINEARTEMISININ :ARTEMISININ :

ARTESUNATE : I.V/ I.M / ARTESUNATE : I.V/ I.M / SUPPOSITORIESSUPPOSITORIES

ARTEMETHER : I.MARTEMETHER : I.MARTEMISININ SUPPARTEMISININ SUPP

SM:Severe Malaria

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RECOMMENDED DOSES OF ANTI MALARIAL RECOMMENDED DOSES OF ANTI MALARIAL DRUGS FOR TREATMENT OF DRUGS FOR TREATMENT OF

SEVERE/CEREBRAL MALARIASEVERE/CEREBRAL MALARIA

Hypoglycemia, Hypoglycemia, chinchonism, tinnitus, chinchonism, tinnitus, hearing impairment, hearing impairment, nausea, dysphoria, nausea, dysphoria, vomiting, prolonged vomiting, prolonged QT interval, QT interval, dysrhythmias, dysrhythmias, hypotensionhypotension

20 mg of dihydrochloride salt/kg by 20 mg of dihydrochloride salt/kg by iv infusion over 4 hr, then after iv infusion over 4 hr, then after loading, followed by 10 mg/kg loading, followed by 10 mg/kg over 4 hr every 8 hr. Patients over 4 hr every 8 hr. Patients should not received quinine or should not received quinine or mefloquine within last 24 hrmefloquine within last 24 hr

Alternatively, 7 mg of salt/kg can Alternatively, 7 mg of salt/kg can be infused over a period of 30 be infused over a period of 30 min, followed by 10 mg salt/kg min, followed by 10 mg salt/kg over a period of 4 hr, orover a period of 4 hr, or

10 mg of salt/kg (500 mg for adult) 10 mg of salt/kg (500 mg for adult) by i.v infusion over 8 hr by i.v infusion over 8 hr continously 3 x a daycontinously 3 x a day

QuinineQuinine

DRUGSDRUGS SIDE EFFECTSSIDE EFFECTS

3535

RECOMMENDED DOSES OF ANTI MALARIAL RECOMMENDED DOSES OF ANTI MALARIAL DRUGS FOR TREATMENT OF DRUGS FOR TREATMENT OF

SEVERE/CEREBRAL MALARIASEVERE/CEREBRAL MALARIA

HypotensiHypotensionon

3.2 mg/kg im initially, followed 3.2 mg/kg im initially, followed by 1.6 mg/kg daily. Not to be by 1.6 mg/kg daily. Not to be given iv (1 amp = 80 mg)given iv (1 amp = 80 mg)

Suppositories, 10 mg/kg at 0 & Suppositories, 10 mg/kg at 0 & 4 hr followed by 7 mg/kg at 4 hr followed by 7 mg/kg at 24,36,48 & 60 hrs.24,36,48 & 60 hrs.

10 mg base/kg infusion at 10 mg base/kg infusion at constant rate over 8 hrs constant rate over 8 hrs followed by 15 mg/kg over 24 followed by 15 mg/kg over 24 hrs, orhrs, or

3.5 mg base/kg 6 hourly or 2.5 3.5 mg base/kg 6 hourly or 2.5 mg base/kg 4 hourly by im or mg base/kg 4 hourly by im or sc injection. Total dose 25 mg sc injection. Total dose 25 mg base /kgbase /kg

ArtemeterArtemeter

DRUGSDRUGS SIDE SIDE EFFECTSEFFECTS

ArtemisininArtemisinin

ChloroquineChloroquine

3636

ConvulsionsConvulsions

I.v. diazepam 10 mg –adult or rectal 0.5-I.v. diazepam 10 mg –adult or rectal 0.5-1.0 mg/kg1.0 mg/kg

i.m paraldehyde o.1 mg/kg – adulti.m paraldehyde o.1 mg/kg – adultRepeated conv- chlormethiazol infussion Repeated conv- chlormethiazol infussion

0.8 %,0.8 %,Phenytoin 5 mg/kg i.v. 20 minutesPhenytoin 5 mg/kg i.v. 20 minutesFosphenytoin 7.5 mg/kg i.v …20 mnutesFosphenytoin 7.5 mg/kg i.v …20 mnutes

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HYPOGLYCAEMIA ( Bl. Sugar < 40 mg% )HYPOGLYCAEMIA ( Bl. Sugar < 40 mg% )

Coma, 20 -50 ml 50% dextrose i.v. 5 – 10 Coma, 20 -50 ml 50% dextrose i.v. 5 – 10 minutes ( routine is not recommended )minutes ( routine is not recommended )

Infussion 10 % dextrose ( children – 5% Infussion 10 % dextrose ( children – 5% dextrose) – beware hyponatremiadextrose) – beware hyponatremia

Hypoglycaemia may developed Day 1 --- 7Hypoglycaemia may developed Day 1 --- 7 Pushed 50% dextrose if necessaryPushed 50% dextrose if necessary Glucagon injection Glucagon injection Via nasogastric , beware gastric distensionVia nasogastric , beware gastric distension In peritoneal dialysis, add glucose in dialysis fluidIn peritoneal dialysis, add glucose in dialysis fluid Somatostatin analoque octreotide (Sandostatin)Somatostatin analoque octreotide (Sandostatin)

The end