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Diagnosis Malaria Menurut Depkes

A. Anamnesis
Keluhan utama pada malaria adalah demam, menggigil, berkeringat dan dapat
disertai sakit kepala, mual, muntah, diare dan nyeri otot atau pegal- pegal. Pada
anamnesis juga perlu ditanyakan:
1. riwayat berkunjung ke daerah endemik malaria;
2. riwayat tinggal di daerah endemik malaria;
3. riwayat sakit malaria/riwayat demam;
4. riwayat minum obat malaria satu bulan terakhir;
5. riwayat mendapat transfusi darah
B. Pemeriksaan Fisik
1. Demam (>37,5 oC aksila)
2. Konjungtiva atau telapak tangan pucat
3. Pembesaran limpa (splenomegali) 4. Pembesaran hati (hepatomegali)
5. Manifestasi malaria berat dapat berupa penurunan kesadaran, demam tinggi,
konjungtiva pucat, telapak tangan pucat, dan ikterik, oliguria, urin berwarna
coklat kehitaman (Black Water Fever ), kejang dan sangat lemah (prostration).
Keterangan :
penderita malaria berat harus segera dirujuk ke fasilitas
pelayanan kesehatan yang memiliki sarana dan prasarana
yang lebih lengkap untuk mendapatkan perawatan yang lebih lanjut.
C. Pemeriksaan Laboratorium
Untuk mendapatkan kepastian diagnosis malaria harus dilakukan pemeriksaan
sediaan darah:
1. Mikroskop: gold standard.
Membuat sediaan darah tebal dan tipis. Menentukan:
a) Ada tidaknya parasit malaria (positif atau negatif);
b) Spesies dan stadium Plasmodium;
c) Kepadatan parasit;
1) Semi Kuantitatif
(-)
=negatif (tidak ditemukan parasit dalam 100 LPB/lapangan pandang besar)
(+) = positif 1 (ditemukan 1 10 parasit dalam 100 LPB)
(++) = positif 2 (ditemukan 11 100 parasit dalam 100 LPB)
(+++)
= positif 3 (ditemukan 1 10 parasit dalam 1 LPB)
(++++)= positif 4 (ditemukan >10 parasit dalam 1 LPB)
Adanya korelasi antara kepadatan parasit dengan mortalitas yaitu:
- Kepadatan parasit < 100.000 /ul, maka mortalitas < 1 %
- Kepadatan parasit > 100.000/ul, maka mortalitas > 1 %
- Kepadatan parasit > 500.000/ul, maka mortalitas > 50 %
2) Kuantitatif
Jumlah parasit dihitung per mikro liter darah pada sediaan darah tebal (leukosit)
atau sediaan darah tipis (eritrosit).
Contoh :
Jika dijumpai 1500 parasit per 200 lekosit, sedangkan jumlah lekosit 8.000/uL
maka hitung parasit = 8.000/200 X 1500 parasit = 60.000 parasit/uL.
Jika dijumpai 50 parasit per 1000 eritrosit = 5%. Jika jumlah eritrosit 4.500.000/uL
maka hitung parasit = 4.500.000/1000 X 50 = 225.000 parasit/uL.
Sediaan darah tebal
Sediaan darah tipis
+/Konfirmasi stadium & spesies parasit
(morfologi lebih jelas)
Jumlah spesies
2. Pemeriksaan dengan tes diagnostik cepat (Rapid Diagnostic Test/RDT)
Mekanisme: deteksi antigen parasit malaria, metoda imunokromatografi.
DIgunakan pada:
1. unit gawat darurat,
2. terjadi KLB,
3. dan di daerah terpencil yang tidak tersedia fasilitas laboratorium mikroskopis.

Saat ini yang digunakan oleh Program Pengendalian Malaria adalah yang dapat
mengidentifikasi P. falcifarum dan non P. Falcifarum.
ParaSight- F Test
-use a specific antigen of P. falciparum (pfHRP-2) and present in the parasite
throughout the erythrocytic cycle.
OptiMAL
-detects parasite lactate dehydrogenase (pLDH)-> distinguish P. vivax from P.
falciparum
Kelemanahan RDT:
-tidak dapat mengukur densitas parasit (secara kuantitatif)
-dapat terjadi hasil positif palsu karena adanya antigen residual dan gametosit
muda
-biaya mahal
3. Polymerase Chain Reaction (PCR) dan Sequensing DNA
-Membedakan antara re-infeksi dan rekrudensi pada P. falcifarum.
-Identifikasi spesies Plasmodium yang jumlah parasitnya rendah atau di bawah
batas ambang mikroskopis.
-Membedakan antara parasit impor atau indigenous.
Cara Konvensional
Deteksi antigen/ RNA
Morfologi & jumlah parasit dapat dilihat Morfologi & jumlah parasit tidak dapt
dan dihitung-> evaluasi pengobatan
dilihat/ dinilai -> tidak dapat evaluasi
pengobatan
Jumlah parasit dibawah microscopic
Jumlh parasit sedikit-> positif (1-2
threshold-> tidak terlihat
parasit/ul)
4. Selain pemeriksaan di atas, pada malaria berat pemeriksaan penunjang yang
perlu dilakukan adalah: a. pengukuran hemoglobin dan hematokrit; b.
penghitungan jumlah leukosit dan trombosit;
c. kimia darah lain (gula darah, serum bilirubin, SGOT dan SGPT, alkali fosfatase,
albumin/globulin, ureum, kreatinin, natrium dan kalium, analisis gas darah); dan
d. urinalisis

box 7.3

dHa+ppQ is an act option for first-line treatment of uncomplicated P.


falciparum malaria worldwide. Strong recommendation, high quality evidence
GraDE evaluation (see Annex 7, tables A7.3.1A7.3.3) In clinical trials directly
comparing DHA+PPQ and the currently recommended ACTs, DHA+PPQ was at
least as effective at treating uncomplicated P. falciparum malaria (as measured by
PCR adjusted treatment failure) as:
artesunate plus mefloquine in Asia (day 63, 3 trials, 1182 participants; RR 0.39,
95% CI 0.190.79; high quality evidence);
artemether plus lumefantrine worldwide (day 42, 4 trials, 1492 participants; RR
0.42, 95% CI 0.260.67; high quality evidence);
artesunate plus amodiaquine worldwide (day 28, 2 trials, 679 participants; RR
0.47, 95% CI 0.230.94; moderate quality evidence).
Other considerations
At the time of publication, no DHA+PPQ product has been prequalified by WHO or
registered by any stringent medicine regulatory authority.
In summary, the ACT options now recommended for treatment of
uncomplicated falciparum malaria in alphabetical order are:
artemether plus lumefantrine,
artesunate plus amodiaquine,
artesunate plus mefloquine,
artesunate plus sulfadoxine-pyrimethamine,7
dihydroartemisinin plus piperaquine.

second-line treatments are recommended, in order of preference:


an alternative ACT known to be effective in the region,
artesunate plus tetracycline or doxycycline or clindamycin (given for a total of 7
days),
quinine plus tetracycline or doxycycline or clindamycin (given for a total of 7
days).

box 7.5 recommendations: treatment of uncomplicated falciparum malaria in


pregnancy
first trimester:
Quinine plus clindamycina to be given for 7 days (artesunate plus clindamycin
for 7 days is indicated if this
treatment fails).
An ACT is indicated only if this is the only treatment immediately available, or if
treatment with 7-day
quinine plus clindamycin fails, or if there is uncertainty about patient compliance
with a 7-day treatment.
second and third trimesters:
ACTb known to be effective in the country/region or artesunate plus clindamycin
to be given for 7 days orquinine plus clindamycin to be given for 7 days.
Pharmacovigilance programmes need to be established to continually monitor
safety of antimalarial medicines in all trimesters, including inadvertent exposures
in the early first trimester.
a.If

clindamycin is unavailable or unaffordable, then the monotherapy should be given.


the exception of DHA+PPQ for which there is insufficient information in second and third
trimesters of pregnancy to use as firstline therapy.
b.With

Lactating women
The amounts of antimalarials that enter breast milk and are consumed by the
breastfeeding infant are relatively small. Tetracycline is contraindicated in
breastfeeding mothers because of its potential effect on the infants bones and
teeth. Primaquine should not be used in nursing women, unless the breastfed
infant has been determined not to be G6PD-deficient.
box 7.6 recommendation: treatment for lactating women with uncomplicated
falciparum malaria
lactating women should receive the recommended antimalarial
treatment (including acts), except for dapsone, primaquine and
tetracycline.
box 7.8recommendations: treatment for travellers returning to non-endemic
countries with uncomplicated falciparum
for travellers returning to non-endemic countries with uncomplicated
malaria:a
atovaquone plus proguanil (15/6 mg/kg [adult dose 4 tablets] once a day for 3
days)
artemether plus lumefantrine
dihydroartemisinin plus piperaquine
quinine plus doxycyclineb or clindamycin
for severe malaria:
the antimalarial treatment in travellers is the same as shown in Section 8
travellers with severe malaria should be managed in an intensive care unit
a.Halofantrine

is not recommended as first-line treatment for uncomplicated malaria


because of cardiotoxicity.
b. Doxycycline should not be used in children under 8 years of age.

table 8.1 immediate clinical management of severe manifestations and

complications of P. falciparum malaria


manifestation/complication-immediate managementa
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 adrenaline; intubate if necessary.
Hyperpyrexia Administer tepid sponging, fanning, a cooling blanket and
antipyretic drugs. Paracetamol is preferred over more nephrotoxic drugs (e.g.
NSAIDsb).
Convulsions Maintain airways; treat promptly with intravenous or rectal
diazepam or intramuscular paraldehyde. Check blood glucose.
Hypoglycaemia Check blood glucose, correct hypoglycaemia and maintain with
glucose- containing infusion.
severe anaemia Transfuse with screened fresh whole blood.
acute pulmonary oedemac Prop patient up at an angle of 45, give oxygen,
give a diuretic, stop intravenous fluids, intubate and add positive end-expiratory
pressure/ continuous positive airway pressure in life-threatening hypoxaemia.
acute renal failure Exclude pre-renal causes, check fluid balance and urinary
sodium; if in established renal failure add haemofiltration or haemodialysis, or if
unavailable, peritoneal dialysis.
spontaneous bleeding and coagulopathy Transfuse with screened fresh whole

blood (cryoprecipitate, fresh frozen plasma and platelets, if available); give


vitamin K injection.
Metabolic acidosis Exclude or treat hypoglycaemia, hypovolaemia and
septicaemia. If severe, add haemofiltration or haemodialysis.
Shock Suspect septicaemia, take blood for cultures; give parenteral broadspectrum antimicrobials, correct haemodynamic disturbances.

box 9.1

in areas with chloroquine resistant P. vivax, artemisinin-based


combination therapies (particularly with those whose partner medicines
have long-half lives) are recommended for the treatment of P. vivax
malaria. Weak recommendation, moderate quality evidence
GraDE evaluation (see Annex 9, tables A9.6.1 and A9.6.2) Two trials compared
DHA+PPQ to alternative ACTs (AL6 and AS+AQ) in Indonesia where all groups
were also given primaquine to clear the liver stage parasites. DHA+PPQ reduced
the number of relapses by day 42 compared to AL (1 trial, 126 participants; RR
0.16, 95% CI 0.070.38; moderate quality evidence) and AS+AQ (1 trial, 84
participants; RR 0.16, 95% CI 0.050.49; moderate quality evidence). There are no
trials comparing DHA+PPQ and AS+MQ in P. vivax mono-infection. At day 42, the
patients in the DHA+PPQ groups were also less likely to be anaemic, although this
data includes participants with P. falciparum mono-infection at baseline, and
recurrence of P. falciparum was also lower with DHA+PPQ. This effect is likely to
be a prophylactic effect related to the longer half-life of DHA+PPQ.
Other considerations
The panel noted the programmatic advantage of these ACTs also being highly
effective against P. falciparum. This effect is likely to be a prophylactic effect
related to the longer half-life of DHA+PPQ.

box 9.2

at least a 14-day course of primaquine is required for the radical


treatment of P. vivax Strong recommendation, very low quality evidence
GraDE evaluation (see Annex 9, table A9.7.1) A 14-day course of primaquine
significantly reduces the relapse rate of P. vivax compared to a 5-day course (2
trials, 186 participants; RR 0.1, 95% CI 0.030.35; low quality evidence).
Other considerations
In addition, in clinical trials, CQ plus 14 days of primaquine has been shown to be
superior to CQ alone in reducing relapses (6 trials, 1071 participants; OR 0.24,
95% CI 0.12 0.45). No difference has been shown between CQ plus 5 days of
primaquine and CQ alone (3 trials, 2104 participants).

box 9.3 uncomplicated p. vivax malaria

chloroquine 25 mg base/kg body weight divided over 3 days, combined


with primaquine 0.25 mg base/kg body weight, taken with food once
daily for 14 days is the treatment of choice for chloroquine-sensitive
infections. in oceania and south-east asia, the dose of primaquine should
be 0.5 mg/kg body weight.
acts combined with primaquine for chloroquine-resistant vivax malaria.
in mild-to-moderate G6pd deficiency, primaquine 0.75 mg base/kg body
weight should be given once a week for 8 weeks. in severe G6pd
deficiency, primaquine is contraindicated and should not be used.
Where act (exception as+sp) has been adopted as the first-line
treatment for P. falciparum malaria, it may also be used for P. vivax
malaria in combination with primaquine for radical cure. artesunate plus
sulfadoxine-pyrimethamine is not effective against P. vivax in many
places.
Patofisiologi Metabolic Acidosis
This has been considered to be mainly a lactic acidosis, although ketoacidosis
(and sometimes salicylate intoxication) may predominate in children and the
acidosis of renal failure is common in adults.
Pathogenesis: lactatepyruvate ratios often exceed 30 reflecting tissue hypoxia
and anaerobic glycolysis.

-Lactic acidosis results from several discrete processes:


1.the tissue anaerobic glycolysis consequent upon microvascular obstruction
impeded by adherence of infected erythrocytes to the endothelium of postcapillary venules and/or increased rigidity of uninfected cells-> reduce O2 delivery
to tissues
a..Cytoadherence-> Rosetting-> Marked reductions in the deformability of
uninfected RBCs-> compromises blood flow
b. Dehydrated and hypovolemia can exacerbates microvascular obstruction by
reducing perfusion pressure
c. Destruction of RBCs and anemia further compromises oxygen delivery: digested
host Hb: haemozoin (malaria pigment) containing leucocytes -> high level of
proinflammatory cytokines (TNF-, IFN-, Interleukins, Th1) -> sequestration
(contributing to microcirculatory obstruction) ->cellular dysfunction in endothelial
cells, dendritic cells, monocytes/ macrophages -> provoke a metabolic shift within
host cells to anaerobic glucose metabolism and increased lactic acid production;
2. a failure of hepatic and renal lactate clearance;
3. and the production of lactate by the parasite (through direct stimulation of
cytokines).
Parasit matur konsumsi glukosa -> 90% konversi-> L+lactic acid (plasmodia tidak
memiliki enzim untuk masuk citric acid cycle) -> Hyperlactataemia (associated
with hypoglycaemia and is accompanied by hyperalaninaemia and elevated
glycerol concentrations reflecting the impairment of gluconeogenesis through the
Cori cycle).
Triglyceride and free fatty acid levels are also elevated in acute malaria and
plasma concentrations of ketone bodies are raised in patients who have been
unable to eat. Ketoacidosis may be prominent in children. In severe malaria, there
is dysfunction of all organ systems, particularly those with obligatory high
metabolic rates. The endocrine glands are no exception. Pituitarythyroid axis
abnormalities result in the sick euthyroid syndrome and also parathyroid
dysfunction. Mild hypocalcaemia is common and hypophosphataemia may be
profound in the very seriously ill. By contrast, the pituitaryadrenal axis appears
normal in acute malaria. Management:
1. Maintain airway patency & O2 delivery; unconsciuous, severe shock,
unstable-> intubate
2. IV line; tachycardia, hypotension, or other poor tissue perfusion-> replace
adequate intravascular fluid volume
3. Monitor cardiac dysrhytmias
4. Sodium bicarbonate is controversial and generally should be avoided
Hemoglobinuria
- results form severe intravascular hemolysis; usually seen in non-immune or
semi-immune individuals
- -due to non-immune destruction of parasitized red cells in case of high
parasitemia or immune mediated destruction of parasitized as well as nonparasitized red cells.
- G6DP Deficiency develop hemolysis when treated with oxidant drugs like
primaquine
- Oocur rapidly, Hb drop significantly in few hours
- Urine is dark red to almost black, output slowly drops
- May be associated with severe anemia, ARF, peripheral circulatory failure
- Black water fever: increase Hb into the circulation
- Repeated exposure to quinine -> black water fever
- Occurs when the capacity of haptoglobin
Treatment: Treatment is directed towards anemia and renal failure.
Transfusion of whole blood or packed cells should be started if the hemoglobin
level is less than 5g%.
Renal failure can be treated conservatively by careful fluid-electrolyte
management and use of diuretics like furoscemide. Dialysis must be considered in

patients who do not respond to conservative treatment.


Antimalarial therapy
- In cases with hemolysis following primaquine therapy, Glucose 6 phosphate
dehydrogenase assay should be done and the drug should be stopped.

Pengendalian Vektor Malaria


Vektor: nyamuk Anopheles, dengan ciri khas menungging saat hinggap atau
menghisap darah, mempunyai siklus hidup sempurna terdiri dari telur (1-2 hari),
jentik (6-8 hari), kepompong (1-2 hari) dan nyamuk (2-3 bulan).
tempat perkembangbiakan vektor malaria dibagi menjadi 2 tipe yaitu :
Tipe permanen seperti: Rawa-rawa, laguna, sawah non teknis dengan aliran air
gunung, Mata air, Kolam.
1. Tipe temporer seperti: Muara sungai tertutup pasir di pantai, genangan air
payau di pantai, kobakan air di dasar sungai waktu musim kemarau,
genangan air hujan, sawah tadah
Medications
Malaria Prophylaxis
-3-6 month temporary stay in malaria endemic areas
1. Doxycicline 100 mg/ daily for P. falciparum, starting 1-2 days before departure
to endemic areas, until 1-2 weeks after coming back
2. or Mefloquine weeky for all parasites starting 2 weeks before departure to
malaria endemic areas until 4 weeks after arrived.
Health Education
Promoting awareness
Fisik
Menghasilkan keadaan tidak menguntungkan bagi nyamuk.
-penimbunan kolam
-pengangkatan tumbuhan air
- pengeringan sawah secara berkala (2 minggu sekali)
-pemasangan kawat kasa pada jendela
Secara kimiawi
-penyemprotan rumah serta bangunanbangunan lainnya dengan menggunakan
fenitrothion, Dichloro Diphenyl Trichloroethane (DDT) dan lain-lain.
-Kelambu (Long Lasting Insecticide Treated Nets)
-Indoor residual spray: DDT, pyerethroids cyfluthrin, deltamethrin
-repellents: DEET (diethyl-meta-toluamide), icaridin
-larvasida
Biologi
Menggunakan beberapa agent biologis: predator pemakan jentik (clarviyorous
fish) yaitu gambusia, guppy, ikan nila dan ikan kepala timah, patogen misalnya
dengan virus yang bersifat cytoplasmic polyhedrosis, dengan bakteri seperti
Bacillus thuringiensis subsp. dengan protozoa seperti Nosema vavraia dan dengan
fungi seperti Coelomomyces (WHO, 1995; Sigit dan Hadi, 2006).
Fauna yang bersifat sebagai predator jentik nyamuk menurut Bates (1970) adalah
filum Rotifera, filum Annelida, filum Colenterata: Hydra, filum Mollusca: Limnea.
Predator dari kelompok hewan vertebrata adalah Pisces, Amphibia, Reptilia dan
Aves. Sedangkan predator dari filum Arthopoda meliputi 3 kelas yaitu kelas
Crustasea contohnya Entomostraca dan udang, kelas Arachnida yaitu laba - laba,
kelas insekta terdiri atas Ephemeroptera (lalat sehari), Odonata (capung),
Hemiptera (kepik-kepik), Coleoptera (kumbang-kumbang) dan Diptera (sebangsa
lalat). Tetapi predator yang paling penting adalah ikan pemakan jentik.