MANIFESTASI KLINIK

MALARIA BERAT

P.N. Harijanto
SMF PENYAKIT DALAM, RSU BETHESDA
TOMOHON
Div. Penyakit Tropik & Infeksi, Bag. Penyakit Dalam
F.K. UNSRAT, Manado
Sulawesi Utara, Indonesia
 SEVERE MALARIA 2015

DEFINITION : Patients with plasmosium asexual parasitemia,with

one or more CLINICAL or LABORATORY FEATURES :
PROSTRATION
IMPAIRED CONSCIOUSNESS ( GCS SEVERE ANAEMIA ( Hb <5
<11, Blantyre < 3 ) PADA ANAK <12TH DAN
RESPIRATORY DISTRESS Hb<7 pd dewasa
HYPOGLYCAEMIA( < 40 )
MULTIPLE CONVULSIONS ( > 2/ 24 hrs)
ACIDOSIS (base def <8,
CIRCULATORY COLLAPSE / SHOCK ( HCO3 <15/ Pl. Lactate >5)
cap refil>3 or temp gradient on leg (mid to RENAL IMPAIRMENT ( >3,
prox limb), no hypotension; sys <80 blood urea > 20 mmol/L)
adults, 70 in children + impaired perfuss) HYPERPARASITEMIA, >10%
PULMONARY EDEMA (CX-Ray/ O2
sat<92% room air + resp >30/min)
ABNORMAL BLEEDING WHO: Guidelines for the
JAUNDICE ( > 3 mg/dL + par >100.000) Treatment of Malaria 2015
 PENYEBAB / ETIOLOGI
 Plasmodium falciparum
 Mixed plasmodium ( Falciparum+ vivax)
 Plasmodium vivax
 Plasmodium knowlesi
PLASMODIUM KNOWLESI
 Simian malaria ( Maccaca mullata)
 Unusual presentation P. Malariae
 Diagnosis by PCR
 Acute diare, abdominal pain, jaundice
Algid malaria, hypotension
Renal failure, respiratory failure
DIAGNOSIS SEVERE MALARIA
 CLINICAL :
 Information residence, travel history, blood
transfussion
 Mimics other diseases :
 CNS infection, sepsis, severe pneumonia, severe
typhoid, expended dengue syndrome, leptospirosis,
hepatitis, leptospirosis
 Children : febrile convulsions ( < 30 minutes)

 PARASITOLOGICAL :
 Microscopic
 RDT
Cerebral Malaria-2014
 cerebral capillaries and venules are packed tightly with
parasitised erythrocytes other not
 A distinct and specific malarial retinopathy with
haemorrhages and retinal and vessel whitening occurs
both in children and in adults
 systemic blood lactate–pyruvate ratios are increased
 Imaging shows no evidence of cerebral oedema in most
adults,
 adjunctive treatment with mannitol (to reduce brain
swelling) prolonged coma duration and increased mortality
 Glasgow Coma Scale
 Respon mata : spontan 4
dgn suara 3
dgn nyeri 2
tak ada reaksi 1

 Respon Bicara : normal respon 5

bingung 4
berkata kacau 3
suara merintih 2
tak ada suara 1

 Respon motorik : gerakan normal 6

dapat melokalisir nyeri 5
fleksi thdp nyeri 4
extensi 3
decerebrate rigidity 2
tak ada reaksi 1
TOTAL 3 -- 15
 Blantyre Coma Scale (modifikasi)
 Respon mata :
mengikuti wajah ibu 1
tak ada reaksi 0

 Respon Bicara :
menangis wajar 2
menangis merintih 1
tak ada suara 0

 Respon motorik :
melokalisir nyeri 2
menarik anggota o.k. nyeri 1
tak ada reaksi 0
TOTAL 0 --5
Extensi pada malaria cerebral
CLINICAL MANIFESTATION
NEUROLOGICAL SYNDROME : DIFFUSE, POTENTIALLY
RAPIDLY REVERSIBLE ENCEPHALOPATHY ASSOCIATED
WITH LOSS OF CONSCIOUSNESS AND FITTING
 mild meningism, no neck rigidity
 dysconjugate gaze
 vertical nystagmus +
 N.VI palsy +
 doll’s eye, oculovestibular reflex normal response
 symetri UMN, increased tone & jerk, clonus, extensor
 plantar response + , brisk Jaw jerk
 pout reflex + , abdominal reflex -, cremasteric reflex - .
 cerebellar sign present
FUNDUSCOPI PADA MALARIA SEREBRAL
Penunjuk Panah hitam besar : Perdarahan pada mata kiri
Penunjuk panah putih : bercak exudasi pada kedua mata berupa keputihan
Penunjuk panah hitam : perdarahan mata kedua mata
DIFFERENTIAL DIAGNOSIS CM

•INFECTION :
• MENINGITIS,
•ENCEPHALITIS,
•TYPHOID FEVER,
•SEPTIC SHOCK
•STROKE & HEAD INJURY
•METABOLIC COMA
•ECCLAMPSIA
•ALCOHOLISM , INTOXICATION
Malaria cerebral , jaundice, in Manado General Hospital
 GANGGUAN FAAL HATI
PADA MALARIA BERAT
 IKTERIK SERING DIJUMPAI ( RINGAN -
BERAT )
 IKTERIK TERGANTUNG JUMLAH PARASIT
 IKTERIK ( HEMOLISIS / DISFUNGSI HATI )
 “ BILIOUS REMITENT FEVER “
( IKTERIK, HIPERPARASITEMIA, SEREBRAL
& GAGAL GINJAL  “ Algid Malaria” )
 AKIBAT: - Hipoalbuminemia
- Gangguan koagulasi
- Penurunan klirens
 Malaria hepatitis ( Deller 1967 )
 Gagal hati jarang
 Hepatomegali sering, nyeri ringan,
splenomegali
 Hiperbilirubinemia ( direk & indirek )
 Transaminase meningkat ringan - sedang,
jarang > 200 i.u
 Waktu protrombin memanjang
 HIPOGLIKEMIA
 Bila gula darah < 40 mg%
 Sering dijumpai pada ibu hamil ( primi-
gravida)
 Pada anak-anak sering sebelum
pengobatan
 Pada orang dewasa sering terjadi
sesudah pengobatan kina ( 3 jam post
terapi kina )
 Patogenesa Hipoglikemia
 Parasit memerlukan karbo-hidrat untuk
metabolismenya
 Pada malaria dengan hiperbilirubin aemia,
terjadi kegagalan glukoneogenesis
 Kina menstimuli produksi insulin
( hiperinsulinemia )
 Peningkatan Tumor Necrosis factor
( TNF-alfa )
 ACUTE KIDNEY INJURY (AKI)
 Malaria related Acute Kidney Injury (MAKI)
 Penurunan fungsi ginjal dalam 48 jam :
 Peningkatan serum kreatinin 0.3 mg/dL, atau
 Peningkatan serum kreatinn 50% dan nilai dasar,
atau
 Penurunan urin output 0.5 ml/kg/jam untuk 6 jam

 WHO : serum kreatinin > 3 mg/dL

 Sering pada malaria dewasa dan jarang pada
anak
 AKI-2014
 Common in adult with SM, behave like ATN
 Pathogenesis is unclear, probably reduced
microvasculatory flow
 Acute kidney injury is frequently associated with
dysfunction of several other vital organs
 Acute kidney injury is oliguric in 60–70% of cases
 serum creatinine concentrations return to normal in
a mean of 17 days
 Early haemofiltration or dialysis substantially
improves out- comes, especially in acute
hypercatabolic renal failure.
 Renal Dysfunction
 2 catagoriesARF :
 Acute severe malaria + MOF
 Renal impairment with successful malaria
treatment ( anaemic, higher creatinine)
 Assoc : acidosis, hypoglycaemia, jaundice
and duration of coma prolonged
 Defined : creatinine > 3 mg/dl,/ urine
output < 400ml on rehydration
 ACUTE RENAL FAILURE IN SEVERE MALARIA
PRE-RENAL RENAL

Urine S.G >1.020 <1.010

Urine Osm. >500 <350
(mOsm/kg H2O)
Urine Na (meq/L) <10 >20
Plasma BUN/Creatinine >15:1 <10-15:1
U/P Urea >20:1 <10:1
U/P Creatinine >40:1 <10:1
U/P Osmolarity >2:1 <1:1
Renal failure Index <1 >1
Fractional excretion of
filtered Na <1 >1
 Faktor untuk mempermudah MAKI :
 Kehamilan
 Parasitemia tinggi
 Ikterik yang tinggi
 Dehydrasi
 NSAID

 Faktor yang penting prognosa MAKI

 Hipovolemia/ hipervolemia
 Hiperparasitemia
 Hemoconcentrasi
 Hiperbilirubinemia
 Hiperpireksia
 Fluid Balance
 Clinically hypovolemic ( low JVP, postural
hypotension, oliguria, high urine SG)
 Febrile & inadequate water intake:
dehydrated ( deceased skin turgor)
 Clinical assesment, CVP, invase monitoring
are inaccurate in predicting effective
circulatory blood volume, due to
microvascular obstruction due to
sequestration
 Management of fluid is DIFFICULT
ELECTROLYTE DISTURBANCES
 Mild hyponatremia is common ( 125-135 )
 ADH is appropriate
 Hypocalcaemia ~ hypoalbuminaemia
 36% asymptomatic hypocalcaemia,
associated with inappropriate low PTH
 Hypophosphatemia is common (43%) 
disturbances of cerebral, leucocyte &
platelet function and hemolysis
 Pulmonary Oedema-2014
 Occurred in SM ( pregnancy) in falcip, vivax, knowlesi
 Increased pulmonary capillary permeability develops in as
much as 30% of adult patients and often manifests after the
start of 1-2 days antimalarial treatment.
 Pathogenesis is not fully understood,maybe inflammation-
mediated endothelial damage
 Manifestations : fluid overload, raised CVP/ pulm wedge
pressure, grossly positive fluid balance,. Pulm. edema
 Careful fluid management is essential; rapid infusion of large
volumes of intravenous fluid can be lethal.
 In the absence of mechanical ventilation, the mortality of
acute respiratory distress syndrome exceeds 80%
 Prognosis is better in vivax malaria
 ARDS

A syndrome of severe respiratory

failure due to any causes
resulting in very low Pa O2 (<70
torr) during intermittent positive
pressure breathing (IPPB) with
FiO2 50%.
 A.R.D.S
 Occurs in P. Falciparum, P. Vivax, P. Ovale & ? P.
Knowlesi
 Common in adult than children, pregnancy and non-
immune
 Mechanism : Increased alveolar cappilary permeability
 intravascular fluid loss into the lungs
 Presentation : initial presentation or after initiation
treatment
 Predisposing factors : hyperparasitemia, renal failure,
pregnancy
 Clinical : acute onset dyspnea  respiratory failure
 CLINICAL FINDING
 Manifest abrupt onset dyspnoea, cough, tightness in the chest
that progresses rapidly over a few hours
 Disorientation and agitation is frequently present.
 Physical examination : raised respiration rate, signs of
respiratory distress ( air hunger, use of accessory muscles of
respiration, suprasternal and intercostal indrawing ), central and
peripheral cyanosis (arterial hypoxaemia), basal crepitations
and expiratory wheezing.
 In these patients, hypoglycemia, metabolic acidosis,
disseminated intravascular coagulation (DIC), and bacterial
sepsis usually co-exist.
 Chest radiography :
 Bilateral frontal opacities (alveolar pattern),
increased interstitial markings
 The cardiac size is usually normal
 Rarely, thickening of lung fissures, interlobular
septal lines
 Pleural effusion
 In assisted ventilator :
 complications pneumothorax, pneumomediastinum
, pneumonia may occur
 Malaria dengan edema paru:

 Komplikasi berat, sering fatal.

 Sering pada dewasa.
 Tinbul cepat ( 1-2 hari Tx)
 Ada 2 tipe :
1.Kelebihan cairan: tekanan vena sentral  ,
PAWP  ,balance cairan +.
2. ARDS : tekana vena sentral N/ ↓, balance
cairan N/+.
 ANEMIA BERAT
 Hb. < 5 gr% atau Ht < 15 %
 Parasit > 10.000 par/ uL
 Bukan thallasemia, iron deffeciency atau
keadaan lain yang dapat menyebabkan
anemia.
 MM4-1

A child, 5 months, malaria falciparum ++++, Hb. 1.6 gr%

In RSMM-Timika Hospital, Papua
 Malaria dengan perdarahan:
 Jarang, < 5%, aktivasivasi koagulasi sering,
10 % pasien SM mengalami DIC
 Gejala: perdarahan gusi,petikie/ hematom,
epistasis, hematemesis, perdarahan sub
conjungtiva.
 Tanda: anemia, trombositosis, koagulopati,
KID >10%.
 Berhubungan dengan komplikasi ginjal, paru,
ikterik, trombositopenia berat & koagulopati
Perdarahan pada malaria berat : Hematom di pipi
Purpura ( perdarahan dibawah kulit, pada malaria
dengan trombosit 2000/ mm3
Acidosis-2014
 Acidosis results from accumulation of organic acids,
including lactic acid, from anaerobic glycolysis in
tissues in which sequestered parasites obstruct
microcirculatory flow
 Lactate production by malaria parasites and failures
of hepatic and renal lactate clearance mechanisms
 Acidotic breathing (hyperventilation, Kussmaul
breathing) is a sign of poor prognosis  circulatory
failure refractory to volume expansion and inotropic
drugs  respiratory arrest.
 Plasma bicarbonate, base excess, or lactate
concentrations have the highest predictive value for
fatal outcomes.
 Asidosis metabolik 2:
 pH serum <7.2, bikarbonat rendah (<15 ml/l)
 Berkaitan dengan : edema paru, hiperparasitemia,
syok, gagal ginjal, hipoglikemia.
 Harus dibedakan dgn edema paru atau
neurogenic hyperventilation
 Kadar asam laktat  ,lactate/pyruvate ratio indicates
an ischaemic basis Lactic acidosis
 High plasma lactate poor prognosis; bila lactate
menurun prognosis baik
 Plasma lactate di periksa 4 jam
Cardiovascular abnormalites, shock (Algid malaria)
 10% cases of SM clinically shock, systole < 80
mmHg with circulatory failure
 Tanda-Tanda sirkulasi perifer↓:
(kulit dingin, lembab, nadi cepat, sianosis, vena
perifer konstriksi, waktu pengisian kapiler
memanjang.
 Dapat disebabkan P. knowlesi ( simian Malaria)
Berkaitan dengan :edema paru, asidosis, sepsis
bakteri gram -, perdarahan saluran cerna.
DD : -Dehidrasi berat – renjatan septik.
Setiap pasien malaria algid perlu kultur darah.
Hipotensi dapat juga disebabkan dehydrasi, terjadi
oliguria, bila perlu rehydrasi harus hati-hati terjadi
edema paru
 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)
 Infeksi sekunder bakteri:
 Pnemonia aspirasi ( sering)
 I.S.K ok kateter
 Ulkus dikubitus terinfeksi
 Infeksi pada tempat infus
 Gram –ve septicaemia >>
 Sering : pseudomonas, E.Coli, salmonela,
streptokokus dll.
 Curiga : fibris bekepanjangan parasit-, syok
menetap, leukositosis/neutropenia.
 Bacterial infection - 2014
 Reported in 5–8% of African children with severe
malaria ( enteric bacterial )
 Falciparum malaria is estimated to account for more
than half of invasive bacterial disease in children living
in malaria-endemic areas
 Neutrophil dysfunction might result from haemolysis-
induced haeme oxygenase-1 induction
 Plasma PfHRP2 concentrations can be used to
distinguish severe malaria from other disorders
 Nosocomial infection occurs in 12 of 37 deathof SM in
Vietnam with good ICU
 GASTRO-INTESTINAL SYMPTOMS

 Nausea, vomiting ( 20-30%), abdominal

pain, may be colicky.
 diarrhea ( 10-20%), watery but does not
contain blood and pus cells
 may lead misdiagnosis enteric fever.

 Diagnosis Banding:
 Malaria Cerebral: encepalitis/ meninggitis
(bakteri, virus, jamur), ggn metabolik, stroke,
intoksikasi alkohol/obat, trauma kepala.
 Malaria dengan ikterus :leptospirosis, hepatitis
tifosa, kolelitiasis dll.
 Malaria algid : Sepsis bakterial berat, IMA,
dehidrasi berat , perdarahan tersembunyi dll.
 Edema paru :pnemonia aspirasi, kelebihan
cairan, intoksikasi obat, dll.
 Prognosis :
 Jumlah & beratnya disfungsi organ
 Kecepatan diagnosis & mulai pengobatan yang adekuat.
 Indikator klinis:
- Derajat kesadaran ↓ prog jelek
- GGA +edema prog jelek
- asidosis berat  prog jelek
- gagal nafas prog jelek
- perdarahan mortalitas >>
- Imun ↓(splenektomi, steroid, dll)prog jelek
 Indikasi laboratorium:
 Hiperparasitemia +Shizont perifer
 Lekositosis
 Kadar asam laktat CSS>, serum >6 mmoll/l
 Kadar gula CSS<<
 Kadar anti trombin III <<
 Kreatinin>3 mg/dl, BUN >60 mg/dl
 Hb < 7,1 g/dl.
 GDS < 40 gr%
 Bikarbonat serum 
 Transaminase  > 3X N.
Lanjut penanganan malaria berat
PAKATUAN WO PAKALAWIREN
Till we meet again !
Dr. Paul Harijanto, Sp.PD
Div. Penyakit Tropik & Infeksi
SMF/ Bag. Penyakit Dalam
FK UNSRAT/ RSUP Manado
RSU Bethesda -Tomohon

Telp.: 0431-841581 (RSUP Manado)

0431-351024/65 ( RSU Bethesda)
HP : 0812-430-2869 ( Emerg)
0431-351187 (Res)
E-mail : paul@manado.wasantara.net.id