LAPORAN JAGA

RESIDEN KESEHATAN MATA

Sabtu, 15 Juli 2023 pukul 07.00 WIB s/d
Sabtu, 15 Juli 2023 pukul 19.00 WIB
Konsulen Jaga:
dr. Petty Purwanita, Sp.M, Subsp. IIM
Residen Jaga:
Jaga 2 : dr. Putri Dwi Kartini
Jaga 1B : dr. Avizena Muhammad Zamzam
Jaga 1A : dr. Gita Normala Dewi
: dr. Yesi Eka Molita
Data Dasar Permasalahan Asessment Planning
Ny. RA / PR / 43 VOD: 6/15 ph 6/7,5 - Saat ini tidak ditemukan tanda-tanda CMV retinitis - Informed consent
tahun / Dalam VOS: 6/21 ph 6/7,5 - Anomali refraksi ODS - Tidak terdapat tatalaksana khusus di bidang
Kota mata
Assesment TS Neurologi - Terapi lain sesuai TS Neurologi dan TS PDL
KU: DK:
- Obs. penurunan kesadaran (perbaikan) Tatalaksana TS Neurologi
Pasien - Parese N. VII sinistra tipe sentral Non farmakologis:
mengeluh
- Quadriparese tipe spastik - Obs GCS dan TTV
penglihatan
DE: - O2 5 lpm
berkurang
- Susp Toxoplasmosis Cerebri dd/ neoplasma dd/ - PRC 200 cc
secara perlahan tuberkuloma dd/ PCNSL - RB dengan TS PDL
sejak 1 minggu D(+): Farmakologis:
yang lalu - B20 -IVFD NaCl 0,9% gtt xx/m
- Susp pneumonia dd TB - Ranitidin 2 x 50 mg
RPP: - Aki stage I - Paracetamol 3x1gr
Slide berikutnya - Hiperkoagulasi - Dexametason 1x2 mg po (tappering off cepat)
- Hipokalemia - Neurodex 1x1 tab po
- Hiponatremia - Kapsul garam 3x500mg
- Anemia - KSR 1x600mg
- Clindamisin 4x600 mg po (H6)
Assesment TS PDL - Cotrimoxazole 3x960 mg po (H6)
HIV Stadium IV dengan Susp Meningitis Bakterial dd/
Meningoensefalitis TB dd/ Toxoplasmosis Cerebri Tatalaksana TS PDL
Anemia Penyakit Kronik dd/ Anemia Def Fe,Acute Non Farmakologis:
Kidney Disease dd/ Acute on CKD ec HIVICK, - Cek CD4, IgG/IgM TORCH, TCM Sputum
Hipokalsemia (8.0), Hiponatremia (129), Hipokalemia Farmakologis:
(3.2) - Ceftriakson 2gr/12 jam (Mulai 10/7/23)
ICD X - Ca Gluconas 1gr dalam NS 10 cc/8 jam 2 kali
H52 (Disorder of refraction and accomodation) - Nefrosteril 1x1 fl 3 hari
 Riwayat Perjalanan
Penyakit
Pasien mengeluh penglihatan kabur sejak 6 hari yang lalu,
Pandangan mulai dirasakan kabur setelah pasien sadar setelah
sebelumnya sempat penurunan kesadaran. Pandangan kabur dirasakan
saat melihat jauh dan dekat. Keluhan disertai dengan mata berair dan
mengganjal hilang timbul. Keluhan mata merah, kotoran mata, nyeri pada
mata, pandangan melihat benda hitam terbang disangkal oleh pasien.
Pasien mengaku terdapat keluhan penurunan kesadaran 1 minggu yang
lalu secara mendadak yang diawali dengan nyeri kepala dan juga lemas
beberapa jam sebelumnya. Pasien kemudian dibawa ke RSMH dan
mulai sadar 1 hari setelahnya.
 Riwayat Perjalanan Penyakit
R/ HT disangkal
R/ DM disangkal
R/ Penggunaan kacamata disangkal
R/ Trauma disangkal
R/ Bergonta-ganti pasangan disangkal
R/ Penggunaan jarum suntik secara bebas disangkal
R/ Suami menderita HIV (+) sejak 6 bulan yang lalu
R/ HIV (+) diketahui 1 minggu yang lalu
R/ Penurunan kesadaran 1 minggu yang lalu dan mulai sadar 1 hari
kemudian
 Status Generalis

Keadaan umum : Sakit sedang

 Sensorium : E4M6V5
 Nadi : 86 x/ menit
 Laju napas : 20 x/ menit
 Suhu : 36.9° C
 Status Oftalmologikus
OD OS
VA 6/15 ph 6/7,5 6/21 ph 6/7,5
TIO 13,1 mmhg 15,6 mmhg
KBM Ortoforia
GBM Baik ke segala arah Baik ke segala arah
 Segmen Anterior
OD OS
Palpaebra Tenang Tenang
Konjungtiva Tenang Tenang
Kornea Jernih Jernih,
BMD Sedang Sedang
Iris Gambaran baik Gambaran baik
Pupil B, C, RC (+), ᴓ 3 mm, B, C, RC (+) ᴓ 3 mm (-),
RAPD (-) RAPD (-)
Lensa Jernih Jernih
 Segmen Posterior
RFODS (+)

FODS
Papil:
Bulat, batas tegas, warna merah normal, C/D 0.3, A:V = 2:3 dengan
obscuration (-)
Makula:
RF (+) normal
Retina:
Kontur pembuluh darah baik, hard eksudat (-), cotton wool spot (-),
frosted branch angiitis (-), dot-blot haemorrhage (-), flame shaped
haemorrhage (-), cottage-cheese and ketchup appearance (-)
 PEMERIKSAAN
LABORATORIUM
Hasil Laboratorium (9/07/2023) di RSMH - Ca : 7.6*
- Hb : 7.8* - Ca Koreksi : 8.0
- Ht : 23 %* - Na :129*
- Eritrosit : 3.010.000* - K : 3.2*
- WBC : 8.120 - Cl : 109*
- PLT : 151.000* - Anti HIV reaktif
- PT : 16.2(16.2) - CRP reaktif
- INR :1.15
- APTT : 31.7(32.7)
- Fibrinogen : 558* (314)
- D-dimer : 2.82*
- SGOT : 50*

- SGPT :20
- Albumin :3.5
- Ureum :66*
- Creatinine :1.73*
 PEMERIKSAAN
LABORATORIUM
Hasil laboratorium tanggal 14/7/23 : - CMV igG : 159.80
- Ca : 9.0
- Ca koreksi : 9.8
- Albumin : 3
- K : 3.6
- Ur : 86
- Cr : 1.331
- CD 4 % : 1.6
- CD 4 absolut : 4Toxoplasma
- igG : 347.20
- Toxoplasma igM : 0.05

- Rubella Ig M : 0.13
- Rubella IgG : 69.40
- CMV Ig M : 0.16
Foto Pasien
 Foto Pasien

OD OS
 Retinal Drawing

OD OS
Terima Kasih
Segmen Posterior

OD OS
- Cytomegalovirus is a double- stranded DNA virus belong to the
betaherpesvirus subfamily in the Herpesviridae family
- The most common cause of congenital viral infection and causes clinically
relevant disease in neonates. It also causes illness in immunocompromised
children and adults (leukemia, lymphoma, or HIV/AIDS), transplant recipients,
and patients with conditions requiring systemic IMT.
- CMVR is most common opportunistic ocular infection and leading cause of
visual loss in AIDS patients
- Possible transmission paths include prenatal intrauterine infection, perinatal
infection through breast milkorgenital secretions, and post natal exchange of
bodily fluids such as blood, saliva, and sperm.
- Adult transmission
In the general adult population,the transmission of CMV through bodily fluids is
uncommon given the fact that the number of virus-shedding seropositive
individualsis very low. Like many other herpesviruses, once infected, CMV
remains latent peripheral blood leukocytes and bone marrow cells for the
remainder of the individual’s life. Bearing on the immune status of the individual,
reactivation and the non-symptomatic shedding of the virus is almost negligible in
individuals above the age of 30. In older populations of immune-suppressed and
HIV infected patients, CMV reactivates and sheds from bodily fluids mentioned
above
- Congenital transmission
Transmission may occur during CMV viremia in a pregnant woman allowing
exposure of the placenta and subsequent transmission of the fetus
Interestingly, perinatally infected children do not suffer from acute symptoms
mentioned above, although rare cases of infantile pneumonitis have been
reported

Active CMV in the eye primarily infects vascular endothelial cells followed by
retinal pigment epithelial cells in the retina causing viral cytopathyic effect and
subsequent retinal necrosis, as characterized in CMVR
The clinical appearance is similar regardless of clinical context, with 3 distinct variants :
• a classic or fulminant retinitis with large areas of retinal hemorrhage against a background of
whitened, edematous, or necrotic retina. The retinitis typically appears in the posterior pole,
near the vascular arcades, in the distribution of the nerve fiber layer, and associated with
blood vessels
• a granular or indolent form found more often in the ret i nal periphery, characterized by little
or no hemorrhage, edema, or vascular sheathing. Active retinitis may pro gress from the
borders of the lesion
• a perivascular form often described as a variant of “frosted- branch” angiitis, an
undifferentiated ret i nal perivasculitis initially described in immunocompetent children
The diagnosis of congenital CMV disease is suggested by the clinical
presentation; positive serum antibodies or PCR testing of urine, saliva,
or intraocular fluids; and systemic
- The diagnosis of CMV retinitis in patients with HIV/AIDS or undergoing
IMT is essentially clinical, but PCR testing can be helpful to confirm
etiology.
- Early CMV retinitis may present as a small, white retinal infiltrate and
look like a cotton-wool spot.
- Patients may have coincidental HIV-associated retinopathy (dot-blot
hemorrhages, cotton-wool spots), and early CMV retinitis is
distinguished by its inevitable progression without treatment.
- A, Retinal hemorrhages and areas of opaque retina are present. Note the
vascular sheathing in the superotemporal arcade and hard exudates in the
macular region.
- B, Histologically, full-thickness retinal necrosis is present. Note loss of the
normal lamellar architecture of the retina, including disruption of the RPE.
- C, Large syncytial cells (arrowheads) are present in areas of necrosis,
characteristic of CMV retinitis.
- D, Intranuclear “owl’s eye” inclusions (arrows) and intracytoplasmic
inclusions (arrowhead) are present in CMV-infected cells.
 Therapy
- In patients with a CD4+ T- cell count below 100 cells/µL (an effect not observed with counts
≥100 cells/µL).
- Options for systemic coverage include high- dose induction with either intravenous
ganciclovir (5 mg/kg twice daily) or foscarnet (90 mg/kg twice daily) for 2 weeks followed by
low- dose daily maintenance therapy or oral valganciclovir (900 mg twice daily) for 3 weeks
followed by maintenance therapy (900 mg/day).
- Intravitreal injection of ganciclovir or foscarnet effectively treats intraocular disease and is a
useful alternative in patients who cannot tolerate intravenous therapy because of
myelotoxicity.
- However, intravitreal therapy alone leaves extraocular systemic CMV and the fellow eye
untreated. Combination treatment with oral valganciclovir may ameliorate this limitation. This
combination is also useful for vision- threatening, posteriorly located retinitis. In patients with
CMV retinitis who are on antiretroviral regimens and experience sustained immune recovery
(CD4+ T lymphocytes ≥100 cells/µL for 3–6 months), systemic
- Guideline therapy intravitreal (harus kombinasi dengan oral)
• Step 1: Induksi
2 ns / 0,1 ml 2 x / week x selama 2-3 weeks
• Step 2: Membrance
2 ns / 0,1 ml 1 x / week x 4 weeks
• Step 3: Intermediate - dose maintenance
1 ns / 0,1 nl 1 x / week there after
- Kombinasi penyuntikkan intravitreal th/ CMV retinitas
• Visus O
• < 3 clock hours of disease in zone III
• No fundal view
• Pasien harus setuju penyuntikkan berkala
• External eyes disease