4. malaria

MALARIA

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Dr. H. Harun Hudari, SpPD, FINASIM

Divisi Penyakit Tropik Infeksi

Bagian Ilmu Penyakit Dalam

RS Dr. Moh. Hoesin/FK UNSRI

Batasan

Malaria : penyakit infeksi menular akut /kronis yg disebabkan oleh sporozoa dari spesies plasmodium sp dan ditularkan oleh nyamuk anopheles yg ditandai oleh demam paroksismal, menggigil, berkeringat, disertai dengan anemia, dan hepatosplenomegali

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Latar Belakang

Morbiditas dan mortalitas malaria tinggi

Kasus klinis 300-500 juta tiap tahun

1,5 – 2,7 juta kematian

Resiko terkena malaria : 2,3 miliar, atau 41% dari jumlah pddk dunia

Menyebar lebih dari 100 negara tropis

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Di Indonesia ; 15 juta kasus malaria/thn

30.000 diantaranya meninggal

35% pddk resiko terkena malaria

Daerah dgn kasus klinik tinggi ;

Papua, NTT, Maluku, Sulawesi Tenggara,

Kalimantan Barat, Bangka Belitung, Bengkulu dan Riau

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Adanya resistensi thd klorokuin

Dilaporkan pd thn 1973 di Kalimantan Timur

Hampir semua propinsi resisten klorokuin dg RI – RIII

Resisten sulfadoksin pirimetamin (RI-RIII) :10 propinsi (Irja, Lampung, Jateng, Sumut, Aceh, Palu, Sulsel,DKI Jakarta, Kaltim dan Sulut)

Resistensi thd kina : 5 propinsi (Jabar, Jateng, NTT, Irja dan Kaltim)

Depkes (1997) : 1986 – 1990 kasus malaria falsiparum di Bangka,resisten klorokuin 50% dg RII

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Distribusi Malaria :

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Sejarah Malaria :

- Pada tahun 3000 – 4000 Sebelum Masehi terjadi di Lembah Nil dan Asia Kecil.

- Dijelaskan pada zaman Yunani Kuno tahun 400 Sebelum Masehi.

- Tahun 1880 : Charles Laveran menemukan parasit malaria dalam darah manusia.

- Tahun1897 : Ronald Ross mendemonstrasikan penularan malaria oleh nyamuk.

- Shortt dan P.C., C. Garnham menemukan hypnozoites pada tahun 1948.

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Epidemiologi Malaria :

- 300 – 500 juta manusia di seluruh dunia terinfeksi malaria.- 120 juta kasus klinis setiap tahun.- 40% populasi dunia tinggal di wilayah dimana terjadi

transmisi endemis, terutama di Sub-sahara Afrika ( 92 negara ).

- 1,4 – 2,7 juta kematian setiap tahun, terutama anak < 5 tahun dan wanita hamil (primigravida).

- Kematian disebabkan malaria berat, gagal organ multipel, malaria serebral, anemia kronik, Acute Respiratory Distress Syndrome (ARDS) dan malaria plasental yang disebabkan Plasmodium falciparum.

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Epidemiologi

Kejadian luar biasa telah menyerang 11 propinsi, meliputi 13 kabupaten pada 93 desa dg jumlah kasus mencapai 20000 dg kematian 74 penderita.

Case fatality rate (CFR) malaria berat yg dilaporkan dari bbrp RS berkisar 10-50%.

Daerah yg resisten thd obat malaria pd th 2000 ditemukan di 77 kabupaten, 158 kecamatan.

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MALARIA- Penyakit yang disebabkan parasit protozoa genus Plasmodium yang ditularkan melalui gigitan nyamuk anopheles betina yang terinfeksi Plasmodium.- Penyakit klasik ditandai oleh demam tinggi periodik dari demam tipe intermiten.

- Empat spesies Plasmodium yang dapat menginfeksi manusia : * P. falciparum * P. vivax * P. ovale * P. malariae

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Penularan :

Vektor – Nyamuk Anopheles

Transfusi darah

Transplantasi organ

Kongenital

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Gambar Plasmodium Falciparum :

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Plasmodium falciparum :

- Malaria yang paling berbahaya : resiko malaria serebral, gagal ginjal, Acute Respiratory Distress Syndrome , anemia berat.

- Terapi segera sangat penting.- Infeksi yang tidak diobati pada orang yang non-imun

biasanya fatal.- Bila pasien diobati dan sembuh, tidak ada resiko relaps

karena P. falciparum tidak mempunyai stadium hepar dormant ( hypnozoite ).

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Gambar Plasmodium vivax :

Stad.cincin

Tropozoit

Schizont

Merozoit

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Gambar Plasmodium Ovale :

Ring

Trophozoite

Schizont

Gametocyte

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P. vivax dan P. ovale :

- Tidak mengancam jiwa seperti Pl.falciparum.- Gejala ( terutama demam) masih menonjol.- Digunakan obat yang berbeda untuk menghilangkan

parasit stadium darah dan hepar.

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Gambar Plasmodium Malariae :

Ring stage

Gametocyte

Trophozoite

Schizont

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Tiga stadium siklus hidup parasit malaria :

Hepar

Sel darah merah (eritrosit)

Nyamuk

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Siklus Hidup Parasit Malaria :

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Masa Inkubasi Malaria :

Berhubungan dengan stadium hepar dari parasit malaria :– P. falciparum 12 hari– P. vivax 14 hari*– P. ovale 14 hari*– P. malariae 30 hari

*dapat 8 – 10 bulan atau lebih pada beberapa strain

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Gejala Klinis Malaria :

- Parasit stadium darah bertanggung jawab terhadap manifestasi klinis.

- Demam merupakan gejala yang paling umum.- Gejala Paroksismal siklik yang klasik :

* Stadium dingin : menggigil dan bergoyang

* Stadium panas : badan hangat, sakit kepala, muntah

* Stadium berkeringat : lemah.

- Gejala lain dapat berupa : mual, diare, nyeri otot, dan perubahan status mental.

- Merasa sehat dalam suatu periode waktu, lalu siklus berulang dengan sendirinya.

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MALARIA– clinical syndromesChronic Disease

Chronic or Recurrent Asymptomatic

Infection

Placental Malaria

& AnemiaAnemia

InfectionDuring

Pregnancy

Developmental Disorders

Transfusions

Death

LowBirth weight

IncreasedInfant

Mortality

Acute Disease

Non-severeAcute Febrile

disease

CerebralMalaria

Death

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Struktur knobs eritrosit parasit.

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Fig. 2. Integration of mini-var transgenes into the IT4var3 locus.A. Schematic of a native PfEMP1 and miniPfEMP1 proteins depicting their predicted organization and topology. The top row shows a generic PfEMP1 with its protein head structure (composed of NTS, DBL1 and CIDR1 head domains, a variable number of internal domains, a TM and an ATS). The Type 3 var encodes the smallest PfEMP1 protein and lacks a CIDR1 domain (Gardner et al., 2002; Kraemer et al., 2007). The red cell membrane is indicated by two black bars, with predicted extracellular sequence to the left. The miniPfEMP1 recombinant molecule NTS-V5-GFP is depicted as residing within the intracellular space (note that the parasite vacuolar and plasma membranes have been omitted for clarity). V5, V5 epitope.B. Schematic diagram depicting Bxb1 integrase-mediated recombination of a mini-var transgene into the attB-tagged IT4var3 locus. Coding regions are indicated by their grey shading. This schematic also indicates the probe hybridization site (black bars), the human dhfr cassette, the blasticidin resistance marker (bsd cassette), ef-1a 5′ UTR, hrp3 5′ UTR, hsp86 3′ UTR, the attP site, the attB element, the neomycin resistance cassette (neo cassette), the Bxb1 integrase cassette (Integrase cassette) and the HA tag. This schematic also shows the positions of primers used to verify integration.

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Fig. 3. Confirmation of mini-var transgene integration into the IT4var3 locus and miniPfEMP1 expression.A. PCR analysis of transfected lines was performed using the following primers: 1091 and 1094 to detect unrecombined attB sites; 1091 and 1090 to amplify the 5′ attL junction; 594 and 1094 to amplify the 3′ attR junction; and 594 and 1090 to detect unrecombined plasmid or plasmid that integrated as a concatemer. PCR product sizes are indicated. ‘P’ indicates the attP plasmid used in the generation of each line.B. Western blot of protein extracts from transgenic parasite lines expressing miniPfEMP1s. These extracts were probed with antibodies to GFP (top panel), or BiP (used as a loading control and shown on the bottom panel). The expected miniPfEMP1 product sizes are listed to the left of panel.

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Fig. 4. Localization of miniPfEMP1 proteins in the infected RBCs by live cell fluorescence imaging.A. Characteristic fluorescence patterns observed in the miniPfEMP1-expressing parasite lines: the first row: localization to the intracellular parasite; the second row: association with the parasite membrane/PVM; the third row: export into the RBC; the fourth row: export to or near the RBC membrane. White arrowheads indicate GFP signal in lipid-enclosed vesicles in the RBC cytoplasm.B. Percentage of each fluorescence pattern observed in each miniPfEMP1-expressing parasite line, as determined by cell counts of fluorescence patterns of at least 50 infected RBC per line.

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Fig. 5. Export of miniPfEMP1 proteins to the RBC cytoplasm. Representative fluorescence images showing the localization of miniPfEMP1-GFP fusion proteins. Parasite lines are indicated on the left. The first column of images represents GFP fluorescence, the second column BODIPY lipid staining, the third column DAPI staining of parasite DNA and the fourth column an overlay of the three images. The NTS-V5-GFP construct was confined to the parasite and other miniPfEMP1 constructs were typically exported to the RBC cytoplasm. Exported proteins had a punctate staining pattern and GFP signal generally colocalized with BODIPY-labelled structures in the RBC cytoplasm(white arrowheads).

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Fig. 7. Ultrastructural analysis of miniPfEMP1 transport. The NTS-V5-TM-ATS-GFP or R29var-V5-GFP-TM-ATS parasite lines were analysed by immunogold EM with anti-GFP antibodies.A. NTS-V5-TM-ATS-GFP, immunogold particles were observed in association withan electron dense structure in the RBC cytoplasm.B. NTS-V5-TM-ATS-GFP localized close to the parasite plasma membrane.C. R29var-V5-GFP-TM-ATS immunogold particles were observed close to the PVM.D–H. R29varV5-GFP-TM-ATS parasites were labelled with anti-GFP, revealing miniPfEMP1 fusion proteins at the RBC surface at or near knob structures, as well as near a Maurer’s cleft in the RBC cytoplasm (H). Anti-GFP immunogold label is found at the RBC surface or in close proximity to Maurer’s clefts (H). Labelling with 10 nm immunogold was performed after cryosectioning (A to F and H) or prior to fixation with 2% glutaraldehyde (G). White arrowheads, Maurer’s clefts; black arrowheads, surface knobs of infected RBCs. Scale bars 200 nm, p parasite, rbc red blood cell cytoplasm.

MALARIA BERATMALARIA SEREBRALMALARIA DGN BILIRUBIN > 3 MG% & gagal organ lainnyaGAGAL GINJAL AKUT < 400 ml/24 jam & Kreat > 3 mg% HIPOGLIKEMI < 40 mg%SYOK SISTOLIK < 70 mmHg / Anak < 50 mmHgANEMIA BERAT HB < 5 gr% / Ht < 15%EDEMA PARU / ARDSPERDARAHAN SPONTAN / DICKEJANG BERULANGASIDOSIS Ph <7.15 , Plasma Bicarb < 15 mmol/LHAEMOGLOBINURIAHIPERPARASITEMIA > 5 %HIPERTERMIA > 40 C ( rectal)

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Malaria serebral :

- Sindrom yang didefinisikan sebagai Koma yang tidak disebabkan oleh penyebab lain, dengan berbagai

kadar parasitemia P. falciparum.

- 1% infeksi P. falciparum berlanjut menjadi malaria serebral dan 10-20% kasus ini meninggal.

- Biasanya terjadi pada anak usia < 2 tahun.

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Malaria serebral

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Malaria Berat :

Anemia : - disebabkan oleh P. falciparum dan P. vivax- destruksi eritrosit yang mengandung parasit karena berkurangnya kemampuan transport oksigen.- meningkatnya kecepatan pemindahan eritrosit yang tak terinfeksi dari sirkulasi.- supresi eritropoiesis- destruksi imun eritrosit - biasanya terjadi pada usia < 2 tahun.

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3. Respiratory Distress Syndrome (RDS) :

- suatu gambaran malaria pada anak di Afrika dan orang dewasa di Asia.

- dapat disebabkan oleh injury terhadap endotel mikrovaskuler paru dan epitel alveolar melalui mekanisme proinflamasi

- dapat disebabkan oleh gagal jantung, pemecahan parasit, atau kebutuhan respirasi yang meningkat.

- sering berhubungan dengan asidosis metabolik.

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Acute Respiratory distress Histopatologi

Infiltrasi sel mononuklear paru, edema

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Faktor yg menyebabkan meningkatnya insiden malaria :

1. Resistensi obat

- penggunaan salah obat anti malaria

- sedikitnya pengembangan obat anti malaria oleh perusahaan obat dan pemerintah.

2. Resistensi insektisida

- penggunaan salah insektisida dalam bidang pertanian

- pengaruh pada lingkungan

3. Faktor ekonomi

4. Kekacauan politik

5. Kurangnya infrastruktur kesehatan masyarakat

6. Kurangnya minat secara global

7. Perilaku manusia.

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Prinsip proteksi terhadap Malaria :

1. Waspada thd resiko, masa inkubasi, dan gejala utama.

2. Hindari digigit nyamuk terutama antara senja hingga fajar.

3. Minum obat anti malaria sbg kemoprofilaksis untuk menekan infeksi bila diperlukan.

4. Mencari diagnosis dan terapi dini bila timbul demam satu minggu atau lebih setelah memasuki wilayah dimana ada resiko malaria, sampai satu tahun setelah meninggalkan wilayah tsb.

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Proteksi Personal thd Malaria :

- Hindari wilayah / daerah malaria- Tinggal di dalam rumah dari senja sampai fajar di dalam

kamar kelambu atau kamar AC- Memakai semprot serangga di dalam kamar dan kelambu- Memakai baju lengan panjang dan celana panjang- Oleskan losion DEET pada kulit yang tidak tertutup

pakaian.- Menggunakan kelambu.

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DEET lotion

NSN 6840-01-284-3982

• Apply a thin coat to EXPOSED skin

• One application lasts up to 12 hours

Insect Repellents For Skin And Clothing

• Individual Dynamic Absorption Kit (IDA)

• Treatment lasts for for over 50 launderings

NSN 6840-01-345-0237

NSN 6840-01-278-1336

• Aerosol spray can

• Treatment lasts through 5-6 washes

Permethrin

US Army Center for Health Promotion and Preventive Medicine

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Faktor-faktor yang mempengaruhi pemilihan obat kemoprofilaksis malaria :

1. Tipe malaria2. Resistensi obat pada lokasi/daerah tertentu.

Indonesia termasuk wilayah dimana P. falciparum, P. vivax, dan P. malariae sudah resisten thd chloroquine.

3. Riwayat alergi atau reaksi lain terhadap obat anti malaria yang terpilih

4. Keterbatasan yang berhubungan dg pekerjaan ( misalnya mefloquine tidak dibolehkan untuk penerbang dan penyelam )

OBAT untuk kemoprofilaksis malaria primer :3. Klorokuin 4. Mefloquine (Lariam)5. Doxycycline6. Atovaquone-proguanil (Malarone)

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ACTs (Artemisinin Combination Therapy )

for uncomplicated falciparum malaria

The following ACTs are recommended:–artemether-lumefantrine–artesunate - amodiaquine–artesunate + mefloquine–artesunate + sulfadoxine-pyrimethamine–dihydroartemisinin – piperaquine*

efficacy of ACTs depend on the efficacy of the partner medicine

The artemisinin derivatives (oral formulations) and partner medicines of ACTs should not be used as monotherapy in the treatment of uncomplicated malaria

*Update in 2009 WHO Revised Guidelines*Update in 2009 WHO Revised Guidelines

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First line therapy of P.FALCIPARUM in adult man :

day 1 : 4 Artesunate tabs 4 Amodiaquine tabs 2 – 3 Primaquine tabs

day 2 : 4 Artesunate tabs 4 Amodiaquine tabs

day 3 : 4 Artesunate tabs 4 Amodiaquine tabs

Second line therapy of P.FALCIPARUM in adult man :

day 1 : Quinine 3 x 2 tabs Tetrasiklin / doksisiklin 4 x 1 capsule Primaquine 2-3 tabs

day 2 – 7 : Quinine 3 x 2 tabs Tetrasiklin / doksisiklin 4 x 1 capsule

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Dosage and administration Coartem (Artemether 20 mg/Lumefantrine 120 mg) for uncomplicated

malaria falciparum

Age group Weight group Blistercolor (Day 1) (Day 2) (Day 3)

4 months to 5yrs 5 to 14 kg Yellow

1 tb R, 1 tb R, 1 tb R,

1 tb Z 1 tb Z 1 tb Z

6 to 11y 15 to 24 kg Blue2 tb R, 2 tb R, 2 tb R,

2 tb Z 2 tb Z 2 tb Z

12 to 14y 25 to 34 kg Orange3 tb R, 3 tb R, 3 tb R,

3 tb Z 3 tb Z 3 tb Z

> 14y > 34 Green4 tb R, 4 tb R, 4 tb R,

4 tb Z 4 tb Z 4 tb Z

Source: Guideline for the treatment of malaria, WHO; 200649

PENGOBATAN MALARIA BERAT

TERHADAP PARASITEMIANYA– JENIS OBAT ( ARTESUNATE, ARTEMETER, KINA )– DOSIS ( ARTEMISININ, KINA ?? ) DAN CARA PEMBERIAN– RESISTENSI PARASIT / M.I.C PARASIT– TRANSFUSI GANTI

TERHADAP KERUSAKAN ORGAN – GAGAL GINJAL ( DIALISIS )– GAGAL PERNAFASAN ( RESPIRATOR )

TERHADAP KEADAAN UMUM ( Nutrisi/ Cairan )HASIL SEKUESTRASI PARASIT/ METABOLISMENYA– OBSTRUKSI --> EDEMA SEREBRAL (GINJAL ?/HATI?)– HEMOLISIS– SLUDGING/ ROSETTE– SITOKIN

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SPECIFIC TREATMENT SEVERE MALARIA ( Anti Malaria)

PARENTERAL

START IMMEDIATELY

DOSAGE, WEIGHT THE PATIENT

MONITORING RESPONSE

SWITCHED TO ORAL WHEN POSSIBLE

MONITORING SIDE EFFECTS

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Dextrose 5%

Kina

Microdrips 100-200 cc

PiggyBackCairan

Maintenance

CARA PEMBERIAN

KINA PADA

MALARIA BERAT52

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SUPPORTIVE MANAGEMENT C.M.

AIRWAYFLUID REQUIREMENT : HYDRATION / OVERHYDRATIONCONVULSION : DIAZEPAMMONITORING GCS & VITAL SIGNLAB : FBC, GLUCOSE, PAR.COUNT, CREATININE, UREUM, BLOOD GAS, URINE S.G, SODIUM, POTASSIUM.PREVENT : SHOCK, SEPTICAEMIA, ACIDOSIS, ARDS, HYPOGLYCAEMIA, ASPIRATION, BEDSORES.TREAT HYPERPYREXIAVOLUME URINE & CATHETERIZATION

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Initial management of Severe Malaria

Clear & maintain airwayPosition semiprone or on sideWeight patient, calculate dosageStart antimalarial chemotherapyMake rapid clinical assesmentExclude or treat hypoglycaemiaAsses state of dehydrationMeasure & monitor urine output, if nes. Catheter, S.GDiagnostic smear, rapid test, other lab testPlan first 8 hrs i.v. fluid, including anti malarial, glucose, blood trasfussionConsider CVP lineIf temp. rectal > 39 C, r. clothes, tepid sp., fan, coolingLumbal puncture, to exclude meningitisAnti convulsant, anti-microbials, vit.K

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ANTI MALARIAL THERAPY FOR S.M

ARTEMISININ :– ARTESUNATE : I.V/ I.M / – ARTEMETHER : I.M– ARTEMISININ SUPP

QUININE

QUINIDINE

CHLOROQUINE

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RECOMMENDED DOSES OF ANTI MALARIAL DRUGS FOR TREATMENT OF

SEVERE/CEREBRAL MALARIA

i.v. 2,4 mg/kg BB pada jam 0, dan jam 12, kemudian dilanjutkan jam 24, 48 dst sampai 7 hari. Dosis total 17 – 18 mg/ 7 hari ( 1 Amp= 60 mg)

Alternatif 1,2 mg/ Kb BB dengan waktu pemberian seperti diatas

3.2 mg/kg im pada hari I dibagi 2 dosis, dilanjutkan 1.6 mg/kg/ hari. TIDAK iv (1 amp = 80 mg)

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

Artemeter

DRUGS SIDE EFFECTS

Artemisinin

ARTESUNATE

Neurotoxicity in animal not human

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RECOMMENDED DOSES OF ANTI MALARIAL DRUGS FOR TREATMENT OF

SEVERE/CEREBRAL MALARIA

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

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

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

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

Quinine

DRUGS SIDE EFFECTS

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TREATMENT OF ORGAN FAILURE

ENCEPHALOPATHY/ CONVULSION

RENAL FAILURE

ACIDOSIS

HYPOGLYCAEMIA

HYPERBILIRUBINAEMIA

RESPIRATORY FAILURE

HYPOTENSION

SEPSIS

SEVERE ANAEMIA

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Oksigenasi

Pencegahan kejang : diazepam,

luminal, largactil

Mencegah trauma/ jatuh

Mengatasi anxiety, delirium state

Penanganan insufisiensi serebral

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PENANGANAN IKTERIK

Tidak ada yang khusus

Hati-hati hipoglikemia

Hati-hati terhadap perdarahan

Pemberian vit. K pada ikterus yang dalam/ tanda perdarahan : 10 mg/ hari selama 3 hari.

Ulangi bilirubin, SGOT/ SGPT hari ke -3

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HYPOGLYCAEMIA ( Bl. Sugar < 40 mg% )

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

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

Hypoglycaemia may developed Day 1 --- 7

Pushed 50% dextrose if necessary

Glucagon injection

Via nasogastric , beware gastric distension

In peritoneal dialysis, add glucose in dialysis fluid

Somatostatin analoque octreotide (Sandostatin)

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Exclude pre-renal/ hypovolemic

Dopamine /& dobutamine or diuretic

Dialysis early

MANAGEMENT ACUTE RENAL FAILURE

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MANAGEMENT OF RESPIRATORY FAILURE

PRINCIPLES :

*Consider severity & cause.

*Correct pH, if < 7.1

*Maintain PaO2 : 50 - 60 torr

* Rapid Rx anti-malarial

* Consider aggravating factors :

- secreting obstructing airways

- pneumothorax

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METABOLIC ACIDOSIS

Occur in : - acute renal failure- hypovolaemia- shock- pulmonary oedema- hyperparasitemia

Management :* Dialysis* Sod.bicarbonate if pH< 7.15, beware

of sodium overload Pulm edema* Preverable THAM tris (hydroxymethyl)- amino

methan, no sodium* Pyruvate dehydrogenase activator dichloro –

acetate

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HYPOTENSION (algid malaria)

Causes: gram - ve bacteriaemia, MOF

Management :

1. CVP : 0 -- 5 cm H2O with crystalloid/

colloid infusion

2. I.V. Dopamine +/ dobutamine

3. Blood culture

4.Antibiotic ( Cephalosporin III)

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GENERAL SUPPORTIVE MEASURES

Urinary catheterization should be used to monitor output

Patients should be observed for vomiting. To ensure patient’s safety, cot-sides may be required

Regular re-positioning of patient is necessary to prevent development of pressure sores

Nasogastric tube should be avoided because of the risk of aspiration

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KemoprofilaksisTujuan : mengurangi resiko terinfeksi malaria, shg kalau terinfeksi maka gejalanya tidak terlalu berat.

Utk orang yg akan bepergian ke daerah endemis.

Dulu : kloroquin resisten

diganti : doxisiklin, 1hr sblm brkt.

selama 12 mg, dosis 2mg/kgbb.

KI: ibu hamil, anak < 8th.

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PROTOKOL MALARIA SEREBRAL

Definisi: Infeksi parasit Plasmodium falsifarum stadium aseksual disertai penurunan kesadaran dan bukan disebabkan oleh penyakit lain. Anamnesis: Demam intermiten, menggigil, berkeringat, riwayat pergi ke daerah endemis malaria.Pemeriksaan Fisik:Hiperpireksia (suhu rektal>400C) Konjungtiva palpebra pucat, sklera ikterik, splenomegali, gangguan kesadaran, kelemahan otot tanpa kelainan neurologis.Laboratorium: Hb turun, bilirubin>3mg/dl, hiperparasitemia >5%.

Bantuan hidup dasar

Anti malaria Penyulit

Bebaskan jalan nafas.Berikan O2

atau atau

Psg IV-line CVP jk memungkinkan (CVP 8-12cmH2O)

Psg Dauer kateter (vol.urin 1ml/kg/jam)

Artesunat 2 amp (@60mg) iv pelan (2mnt), diulang 12 jam kemudian

Dilanjutkan 2amp iv/ hari sampai 5hari

Artemeter 2 amp(@80mg) im dilanjutkan 1 amp/hari sampai 5 hari.

Kina 2 ampul (@500mg) dlm 500ml D5% /NaCl0,9% selama 4jam ke-1 gtt 40/’

D5% atau NaCl selama 4jam 40 gtt/’

Kina 1 ampul dlm 500ml D5% /NaCl selama 4 jam gtt 40/’

Selanjutnya 500ml D5%/NaCl diselang-seling dg drip Kina 1 amp tiap 4 jam sampai pasien sadar (maksimal 7 hr)

T ≥38,50C Parasetamol 15mg /kgbb/kali bs diulang /4jam

Kejang Diazepam 5-10mg iv bs diulang tiap 15’ (maks 100mg/24 jam) atau phenobarbital 2x100mg im

Hb< 10 g% Transfusi PRC

GDS <70mg/dl D40% 2fls + IVFDD10

TDS< 100mmHg kristaloid 20-30cc/kgBB/jam selama 6 jam

TDS<100mmHg, MAP≤60 NaCl 500ccPasien sadar

-Kina (@500mg) 3x1 tab sampai 7 hari (dihitung mulai drip kina) -Primakuin 3 tab

Monitor :-Vital sign tiap 30 mnt-Hb dan Ht per hari-Bil. dan Cr hr I dan III-BSS tiap 6 jam

Pasien sadar-Artesunat-amodiakuin 2x4 tab-Primakuin3 tab (@15mg)

TDS<100, MAP ≤65Dobutamin 5-20mcg/kg/mnt Dopamin 5-20mcg/kgbb/mnt Epinefrin0,05-2mcg/kgbb/mnt Norepenefrin 0,05-5 mcg/kgbb/mnt

Tidak respon

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