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ANGGRAENI PARWATI09-036
Kepaniteraan Ilmu NeurologiPeriode 15 Desember 2014 24 Januari 2015
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Toxoplasma gondii is known as one of the most common infectiousprotozoan parasites that has a worldwide distribution.
Toxoplasma infection is largely asymptomatic, but in those individuals
who are immune-compromised with AIDS, malignant patients underchemotherapy or organ transplant recipients can become disseminatedand cause severe toxoplasmosis and/or encephalitis .
T. gondii may serve as one factor that can enhance the immunodeficiencyfound after HIV-1 infections.
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Toxoplasmosis is generally a late complication of HIV infection andusually occurs in patients with CD4 + T-cell counts below 200/l.
In adults, most T.gondii infections are subclinical, but severe infectionscan occur in patients who are immunocompromised (A.I.D.S,Malignancy).
AIDS associated toxoplasma encephalitis results from reactivation ofchronic latent infection in more than 95% of patients.
In patients with AIDS seropositive for T.gondii, the risk for cerebraltoxoplasmosis approaches 30%.
Toxoplasmosis is the most common cause of focal brain lesions inpatients with AIDS and frequently localizes to the basal ganglia, althoughother sites in the brain and spinal cord may be affected, multiple foci areseen more often.
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In patients with AIDS, tissue cysts rupture and the released bradyzoitesmay multiply locally and spread to other organs.
The pathology of Toxoplasma infection is due to the invasion processinitiating the lytic cycle that consequently leads to cell and tissuedestruction.
In the host cell cytoplasm, T. gondii induces the formation of aparasitophorous vacuole that contains secretions of both parasite andhost proteins that normally promote phagosome maturation, , andthereby prevent lysosome fusion (Dubey et al, 1998; Carruthers, 2002).
T. gondii excretory/secretory antigens (ESAs) represent the majority of
the circulating antigens in host sera of patients with acute toxoplasmosis(Pereira-Chioccola et al, 2009).
ESAs include the tachyzoite, sporozoite and encysted bradyzoite stages(Tilley et al, 1997).
Pathogenesis
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Anti-ESA antibodies develop in high titers when circulating bloodtachyzoites are present in AIDS-associated CT patients (Meira et al,2008).
Toxoplasma infection results in pathological changes such asinflammation and is usually followed by necrosis.
Among patients with AIDS, CT is a multifocal process that occursspontaneously.
The use of the highly sensitive technique of magnetic resonance imaging(MRI) reveals that >80% of patients will have multiple lesions (Ciricillo &Rosenblum, 1990).
The spontaneous and simultaneous development of multifocal brainlesions strongly indicates that although CT arises because of reactivationof a latent infection, the multiple areas of the brain that are involved arelikely a result of the hematogenous spread of the parasite, andinvolvement of the brain is due to the particular proclivity of T. gondii forcausing disease in the CNS (Luft & Remington, 1992).
Pathogenesis
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An US study demonstrated a significant association between CD4 countsof 200-499 cells/mm3 and Toxoplasma-seropositivity in patients (Falusi etal, 2002).
The authors were unable to provide an explanation for this associationexcept that patients with low CD4 counts were more likely to be foreign
born.
Primary chemoprophylaxis or antiretroviral drugs including HAART (ifavailable) should be instituted to these patients after clinical evaluation.
Pathogenesis
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Congenital toxoplasmosis The level of anti-Toxoplasma (IgG) antibodies does not appear to be affected by
antiretroviral drugs or therapeutic regimes/prophylaxis used to treat toxoplasmosisin these patients (Machala et al, 2009)
In recent years, an HIV-infected pregnant woman with CT who was at risk fortransmitting HIV (low CD4 and high viral load) and Toxoplasma infections to herfetus; she responded well to anti-Toxoplasma therapy and HAART (Nogueira et al,2002).
In this case, the combined Toxoplasma therapy (pyrimethamine and sulfadiazine)and HAART were benefitial not only to the mother but also prevented transmissionto the fetus.
Cerebral toxoplasmosis
The risk of developing CT among seropositive patients with AIDS was 27 times thatof seronegative ones (Oksenhendler et al, 1994).
AIDS patients who are Toxoplasma seropositive, have CD4 count of
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Cerebral toxoplasmosis The clinical presentations of CT depend on the number of lesions and location.
Headache, hemiparesis and seizure (Nissapatorn et al, 2004; Vidal et al, 2005a) are
among the most common neurological presentations found in CT patients. Other
clinical manifestations include disarthria, movement disorders, memory and
cognitive impairments and neuropsychiatric abnormalities.
It is very rare for patients with CT to present as a neuropsychiatric illness with an
acute psychosis followed by a rapid mental and somatic decline, however one case
has been reported in a patient with AIDS (Ilniczky et al, 2006).
In hyperkinetic movements, holmes (also known as rubral or midbrain tremor)
tremor is the earliest reported symptom of CT and might present with other focal
neurological signs that indicates a midbrain localization (Koppel & Daws, 1980).
Clinical implication
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Cerebral toxoplasmosis The appearance of hemichoreahemiballism is considered as a pathognomonic of CT
and is most commonly associated with a subthalamic abscess (Navia et al, 1986;
Maggi et al, 1996). The presence of hemichoreahemiballism in CT patients is low
(7.4% of cases) compared to the pathological studies which show 50% of
Toxoplasma abscesses occur in the basal ganglia (Navia et al, 1986; Maggi et al,
1996). Generalized chorea may occur as a result of bilateral abscesses of toxoplasmosis
(Gallo et al, 1996).
Myoclonus, is generalized and elicited by sudden auditory stimuli that resembles a
startled response, has also been described in AIDS-associated CT patients (Maher et
al, 1997).
A case of focal dystonia of the left arm and hand has been reported in an AIDSpatient due to the right lenticular nucleus and thalamic abscesses of toxoplasmosis
(Tolge & Factor, 1991).
Clinical implication
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Extracerebral toxoplasmosis Occular toxoplasmosis is the most common form of ECT associated with CT, being
detected in 50% of ECT in AIDS patients and has the best prognosis (Rabaud et al,
1994; Zajdenweber et al, 2005).
Clinical implication
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Multifocal necrotizing encephalitis is the predominant neuropathologicalfinding of CT in AIDS patients.
Localization of multiple with ring enhancing lesions on neuroimaging inbasal ganglia, frontoparietal cortex and thalamus suggestshaematogenous spread.
Three morphological patterns of brain lesions based on the stage ofinfection and degree of tissue reaction (Shankar et al, 2005):
Acute stage: appearance of a necrotizing abscess or encephalitis seen as poorly
circumscribed necrotic foci with variable degrees of haemorrhage, perifocal edema,
acute and chronic inflammation, macrophage infiltration, with numerous T. gondii
tachyzoites and encysted bradyzoites along the periphery. Also common are
vascular thrombosis/fibrinoid necrosis of vessel walls, with polymorph infiltration,hypertrophy and the presence of tachyzoites in the hypertrophie arterial wall.
Neuropathology of toxoplasmosis
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Three morphological patterns of brain lesions based on the stage ofinfection and degree of tissue reaction (Shankar et al, 2005):
Chronic lesion :organized abscesses are found in CT cases treated for 2 weeks and
seen as well circumscribed foci of central necrosis with a rim of congestion. In
contrast to the acute phase, the central foci of an acellular necrosis is surrounded by
a granulomatous reaction, with macrophages containing tightly packed lipid and
haemosiderin, prominent hypertrophic occlusive arteritis with dense lymphocyticcuffing, and only a few organisms.
Patients treated for 1 month show chronic abscesses in CT appear as small cystic
cavities or linear orange-yellow scars and macrophages containing lipid and
haemosiderin surrounded by a dense gliotic reaction. Calcification of vessels occurs
and organisms are rarely found. In addition, a CAT scan can present as a diffuse,
non-necrotizing, rapidly progressive encephalitis. The histological appearance seen as nodules of micrioglial cells with
encysted bradyzoites and dispersed tachyzoites within the nodules.
Neuropathology of toxoplasmosis
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Empiric Anti Toxoplasmic
No history of toxo prophylaxis
Empiric Anti TB drug
CD4 > 200
Thorax photo : Miliar TB
Empiric Antibiotic for Bacterial Brain Absces
Neuroimaging study : compatible with bacterial brain absces
Choosing between Toxo TB BacterialAbsces
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Trimethoprim/sulfamethoxazole (Co-trimoxazole, 5/25mg/kg PO or intravenous (IV) every 12 h for 4-6 weeks)(Canessa et al, 1992).
Clindamycin and pyrimethamine or sulfadiazine (Katlama etal, 1996a; Tsai et al, 2002),
Clarithromycin and pyrimethamine (Fernandez-Martin et al,1991),
Clindamycin and 5- Fluoro-uracil (Dhiver et al, 1993),
Azithromycin and pyrimethamine (Saba et al,1993;Jacobson et al, 2001),
Clindamycin and fansidar (Nissapatorn et al, 2004),
Sulfadoxine and pyrimethamine (Amogne et al, 2006), and
Atovaquone (Torres et al, 1997).
Empiric anti Toxoplasmic Treatment
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Pyrimethamine and sulfadoxine twice a week appears to givepromising results for prevention of CT.
A current guideline recommends the use of a daily dose of a double-strength tablet of co-trimoxazole in Toxoplasma-seropositivepatients who have a CD4 cell count below 100 cells/cumm (CDC,2009).
Secondary prophylaxis for CT patients; the combination of pyrimethamine (25-50 mg/day) plus sulfadiazine (500 mg
every 6 h) plus eucovorin (10-20 mg/day), thrice weekly (Podzamczer etal, 1995) or the same doses of sulfadiazine twice a day (Jordan et al,2004) is an alternative option among non-compliance patients.
The recommendation is for pyrimethamine plus clindamycin (600 mg
clinidamycin every 8 h) for patients who are intolerant to sulfa drugs(CDC, 2009).
Co-trimoxazole (960 mg twice daily) is another potential drug used insecondary prophylaxis for patients with CT (Duval et al, 2004). Thisagent (2.5/12.5 mg/kg PO every 12 h)
Empiric anti Toxoplasmic Treatment
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2004
Pyrimethamine-sulfadoxine bid po
Drug allergy 34.2 %
Clindamycin 600 mg qd po2005 - present
Pyrimethamine 200 mg load 75 mg/d
Clindamycin 600 mg qd po
Empiric anti Toxoplasmic Treatment
Department of Neurology RSCM Hospital -Indonesia University
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HAART should be started at least 2 weeks after an anti-Toxoplasmaregimen was initiated in these patients (Manzardo et al, 2005; Pereira-Chioccola et al, 2009).
In HIV-infected patients receiving HAART, primary prophylaxis for CT canbe safely discontinued in patients whose CD4 cell counts increase to >200
cells/mm3 (CDC, 2009). Secondary prophylaxis can be safely discontinued in CT patients receiving
HAART with CD4 cell count of > 200 cells/cumm after 6 months (Pereira-Chioccola et al, 2009). This same prophylaxis should be reintroduced inpatients with CD4 cell count of < 200 cells/cumm (CDC, 2009).
While, primary and secondary prophylaxis against CT can also be safelydiscontinued after the CD4 cell count has increased to 200 cells/cumm formore than 3 months in HIV-infected patients receiving HAART (Miro et al,2006).
Highly active anti-retroviral therapy(HAART)
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Nama : Tn. AO
Usia : 22 tahun
Alamat : OKSOP
Suku : Ngalum
Tanggal masuk RS : 09 Desember 2014
IDENTITAS
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Keluhan utama : Sakit kepala sejak 1 tahun lalu.
Riwayat penyakit sekarang:
Pasien datang dengan keluhan sakit kepala sejak 1 tahun yang laludan dirasakan semakin memberat setiap harinya. Sakit kepala yang pasienrasakan seperti ditusuk-tusuk. Pasien tidak bisa beraktivitas karena sakit
kepala tersebut. Selain itu, pasien juga mual (+) serta muntah (+) apabilapasien batuk dan bangun dari tidur. Apabila kepala ditegakkan, sakit kepalaterasa semakin hebat. Demam (-), batuk sesekali, BAB dan BAK tidak adakeluhan. Mata kanan pasien sudah tidak dapat melihat dan mata kiri pasienpandangannya kabur sejak 5 bulan yang lalu.
Riwayat penyakit dahulu:
Hipertensi (-), diabetes mellitus (-)
Anamnesis
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PEMERIKSAAN FISIK
Kesadaran : Composmentis
GCS : E4V5M6
Nadi : 124 x/menit
Tekanan Darah : 120/70 mmHg
Suhu : 39,1C
Respirasi : 24 x/menit
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Umur Klinis : 30 an
Bentuk Badan : Atletikus
Gizi : Cukup
Kulit : Coklat tua
Kuku : Sianosis (-)
Turgor : Cukup
Kel. Getah Bening : Tidak teraba membesar
Pembuluh Darah :
A. Carotis : Palpasi kanan dan kiri : Teraba kuat, cukupangkat, reguler
Auskultasi : Bising (-)
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PEMERIKSAAN REGIONALKepala : Normocephali
Kalvarium : Tidak ada kelainan
Mata : Konjungtiva tidak pucat,
Sklera tidak ikterik
Hidung : Bentuk biasa, lapang, sekret -/-
Mulut : Tidak ada kelainan
Telinga : Bentuk biasa, serumen -/-
Leher : Tidak ada kelainan
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PEMERIKSAAN REGIONAL Toraks : Normochest
Jantung : Inspeksi :iktus kordis tidak terlihat Palpasi :Iktus kordis tidak teraba
Perkusi :Batas kanan jantung ICS V linea parasternaldextra, Batas kiri jantung ICS V linea midklavikularissinistra
Auskultasi :BJ I dan II normal, murmur -, gallop -
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PEMERIKSAAN REGIONAL Paru-paru Inspeksi :pergerakan dinding dada simetris Palpasi :vocal fremitus simetris Perkusi :sonor simetris kanan kiri Auskultasi :BND vesikuler, Wheezing -/-, Rhonki -/-
Abdomen Inspeksi :perut tampak datar Auskultasi :BU (+) 3 x/menit
Palpasi :supel, NT (-) Auskultasi :timpani, tidak ada nyeri ketok
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Hepar : Tidak teraba membesar
Lien : Tidak teraba membesar
Vesika Urinaria : Bulging -, nyeri tekan -
Extremitas : Simetris, Akral hangat, Oedem (-)Sendi : Tidak ada kelainan
Gerakan Leher : Tidak ada keterbatasan Range ofMovement
Gerakan Tubuh : Tidak ada keterbatasan Range ofMovement
Nyeri Ketok : -
Nyeri Sumbu : -
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PEMERIKSAAN NEUROLOGIS
Rangsang Meningeal
Kaku kuduk : -
Brudzinski I : -
Brudzinski II : -/-
Kerniq : -/-
Laseque : >70/ >70
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Saraf Kranial
N.I (Olfaktorius)
Kanan Kiri
Cavum nasi lapang lapang
Test Penghidu normosmia normosmia
N. II (Optikus)
Visus kasar 0 1/6
Lihat warna Baik Baik
Lapangan pandang Baik Baik
Funduskopi Tidak dilakukan
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(Okolomotorius, Trochlearis,Abdusen)
Pupil:Bentuk : BulatIsokor : 3mm/3mm,Tepi rata, ditengah.
Reflek cahaya:Langsung : + / +Tidak langsung : + / +
Reflek akomodasi : + / +
Sikap bola mata : simetrisPtosis : tidak adaStrabismus : tidak adaEksoftalmus : tidak ada
Endoftalmus : tidak adaDiplopia : tidak adaDeviasi Konjugee : tidak adaPergerakan Bola mata
Lateral kanan : BaikLateral Kiri : BaikAtas : Baik
Bawah : BaikBerputar : Baik
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N. V (Trigeminus)
Motorik- Membuka Mulut : Baik- Gerakan Rahang : Baik
- Menggigit : Baik
Sensorik- Rasa Nyeri : Baik Baik- Rasa Raba : Baik Baik
- Rasa Suhu : tidak dilakukan
Refleks:Reflek Kornea : + +
Reflek Masseter : + +
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N.VII (Fasialis)
Sikap wajah (saat istirahat) : Simetris
Mimik : Biasa
Angkat Alis : Simetris, kanan = kiriKerut Dahi : Simetris, kanan = kiri
Lagoftalmus : Tidak ada
Kembung Pipi : Simetris, kanan = kiri
Menyeringai : Sulcus nasolabialis kanan tampakmendatar
Fenomena Chovstek : -
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N.VIII (Vestibulocochlearis)
VestibularisNistagmus : -
Vertigo : tidak ada
KokhlearisSuara bisik : kanan = kiri
Gesekan jari : kanan = kiri
Tes Rinne : +/+
Tes Weber : Tidak ada lateralisasiTes Schwabach : Sama dengan pemeriksa
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N. IX, X (Glosofaringeus, Vagus)
Arkus Faring : simetris, uvula ditengah
Palatum Mole : intak, simetris
Disfoni : Tidak ada
Rinolali : Tidak ada
Disfagi : Tidak adaBatuk : Tidak ada
Menelan : Baik
Mengejan : Baik
Refleks Faring : BaikRefleks Okulokardiak : Positif
Refleks Sinus Karotikus : Positif
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N.XI (Asesorius)
Menoleh (kanan,kiri,bawah) : Baik
Angkat Bahu : Baik
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N.XII (Hipoglosus)
Sikap lidah dalam mulut : simetris
Julur lidah : simetris
Gerakan lidah : baik
Tremor : tidak ada
Fasikulasi : tidak ada
Tenaga otot lidah : Berkurang
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MOTORIK
Kekuatan motorik:5 5 5 5 5 5 5 5
5 5 5 5 5 5 5 5
Tonus Otot:Lengan kanan kiri
Fleksor : Normotonus NormotonusEkstensor : Normotonus Normotonus
TungkaiFleksor : Normotonus Normotonus
Ekstensor : Normotonus Normotonus
Trofi OtotLengan : Eutrofi EutrofiTungkai : Eutrofi Eutrofi
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Gerakan Spontan Abnormal
Kejang : tidak ada
Tetani : tidak ada
Tremor : tidak ada
Khorea : tidak ada
Atetosis : tidak adaBalismus : tidak ada
Diskinesia : tidak ada
Mioklonik : tidak ada
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Koordinasi
Statis
Duduk : baik.
Berdiri : tidak dilakukan
Tes Romberg : tidak dilakukanDinamis
Telunjuk Hidung : baik
Jari-jari : baik
Tumit lutut : baik
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REFLEKS
Refleks TendoBiseps : ++ / ++
Triseps : ++ / ++
Knee Pes Reflex : ++ / ++Achilles Pes Reflex : ++ / ++
Refleks Kulit
Telapak kaki : ++ / ++Kulit perut : ++ / ++
Kremaster : tidak dilakukan
Anus Interna : tidak dilakukan
Anus Externa : tidak dilakukan
Refleks Abnormal
Babinski : -/-
Chaddock : -/-Oppenheim : -/-Gordon : -/-Schaeffer : -/-Mendel Bechterew : -/-Hoffman Trommer : -/-Klonus lutut : -/-Klonus Kaki : -/-
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Sensibilitas
Eksteroseptif
- Rasa raba : kanan = kiri
- Rasa nyeri : kanan = kiri
- Rasa suhu : tidak dilakukan
Propioseptif- Rasa sikap : baik, kanan = kiri
- Rasa getar : tidak dilakukan
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Vegetatif
Miksi : Baik
Defekasi : Baik
Salivasi : tidak ada
Sekresi keringat : umum
Fungsi Seks : -
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Fungsi Luhur
Memori : baik
Bahasa : baik
Afek dan emosi : irritable
Kognitif : baik
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Tanda Regresi
Refleks menghisap : -
Refleks menggigit : -
Refleks memegang : -
Snout Reflex : -
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Laboratorium (9 Desember 2014) Masa pembekuan : 9 10
menit
APTT : 29.5
PT : 10.9
IMR : 1.0
Fibrinogen : 152 (L)
D-dimer : 350
Protein total : 5.9 (L)
Albumin : 2.6 (L)
Globulin : 3.3
SGOT : 23
SGPT : 43
Ureum : 36
Creatinin : 1.1
Asam urat : 4.6
Na : 145
K : 3.3 (L)
Ca : 8.9
HBsAg : non reaktif
Anti HCV : non reaktif
Anti HIV (ELISA) : 0.10 (non-reaktif)
Pemeriksaan
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Urin & parasitologi (10 Desember 2014)
Leukosit 0/LBP
Eritrosit 0/LBP
Epitel 0/LBP
Silinder 0/LBP
Bakteri 0/LBP
Berat jenis 1.015
Warna kuning
Kejernihan jernih
Esterase leukosit -
Nitrir -
Darah -
pH 6.0
Protein -
Glukosa -
Bilirubin -
Urobilinogen 0.2
Keton -
Pemeriksaan
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Pemeriksaan 9 Des 2014 13 Des 2014 14 Des 2014 16 Des 2014
LED 33 (H) 15 (H) 10 26
Hb 12.4 (L) 10.8 (L) 10.5 (L) 10
Leukosit 6.9 3.4 (L) 2.8 (L) 2.4
Eritrosit 5.15 4.56 4.44 (L) 4.23
Basofil 0 0 0 30
Eosinofil 0 (L) 3 2 1
Neutrofilbatang
0 (L) 0 (L) 0 (L) 0
Neutrofilsegmen
84 (H) 82 (H) 81 (H) 2
Limfosit 3 (L) 6 (L) 8 (L) 0
Monosit 13 (H) 9 (H) 9 (H) 81 Trombosit 128000 (L) 78 (L) 73 (L)
MCV 73 (L) 72 (L) 70 (L)
MCH 24.1 (L) 23.7 (L) 23.6 (L)
MCHC 32.8 33.1 33.7
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15 Des 2014
Kultur darah : -
Kultur urin : -
Protein total : 5.5 (L)
Albumin : 2.5 (L)
globulin` : 3.0
Pemeriksaan
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15 Desember 2014 11 Desember 2014
CT angiografi cerebral
Gambaran CVD infark di lobus
temporoparietooksipitalis sinistra
CT brain + kontras
Gambaran abses multipel di temporal dan
parietooccipital sinistra
USG abdomenSplenomegali, nefrolithiasis multipel
kanan, susp.cystitis
Pemeriksaan
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Kesan subtipe limfosit
Linfosit T helper rendah dan T
supressor rendah dengan rasio CD4-
CD8 normal
Hematologi
CD4
CD4 Absolute 70 (L)
CD4% 23 (L)
CD8
CD8 Absolute 89 (L)
CD8% 29
Rasio CD4:CD8 0.78
PEMERIKSAAN
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Choosing between Toxo TB Bacterial
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Empiric Anti Toxoplasmic
No history of toxo prophylaxis
Empiric Anti TB drug CD4 > 200
Thorax photo : Miliar TB
Empiric Antibiotic for Bacterial Brain Absces
Neuroimaging study : compatible with bacterial brain absces
Choosing between Toxo TB BacterialAbsces
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Diagnosis kllinik Cephalgia
Penurunan visus
Diagnosis topis
Temporal sinistra
Parieto-occipital sinistra
Diagnosis etiologik
Infeksi dd/ Toxoplasma gondii
Mycobacterium tuberculosis
Diagnosis patologi anatomi Sel mikroglia dengan bradiziot encysteddan tachyzoite yang berada di dalam nodul
Diagnosis
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Pengobatan