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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

  • 8/10/2019 cerebellar toxoplasmosis

    57/57

    Pengobatan