AFTERNOON REPORT

Duty on 6TH May of 2017

 Identity

Name : SAMW (17024308)

Age : 40 yo
Gender : Female
Ethnicity : Balinese
Religion : Hindu
Address : Dusun Pancoran Desa Gelgel Klungkung
Marital Status : Married
ToA : Tuesday, 06th of May 2017, 18:00
 Anamnesis

Chief Complaint: Fever

Patient came to ER Sanglah Hospital 6th May 2017, reffered from Klungkung
Hospial with pansitopenia with the chief complaint of fever.
Patient said that the fever started 2 weeks before admitted to the hospital.
Patient stated that the fever’s temperature was around 38oC-39oC. Patient
consumed medication Paracetamol to lower the fever, but it increased again.
Patient said that the fever never reached normal condition. Patient also
mentioned that the fever got worsened during the night
Patient said that the fever somehow disturb her activities.
Accompanied by the fever, patient also said that she got cold sweat mostly
during the night. It was started together with the fever which was 2 weeks ago.
 Anamnesis

Patient also complained of decreasing of body weight. She stated that since
1 month ago, her body weight decrease for almost 10 kg.

Patient also complained weakness and decreasing activities during day.

Patient stated that she got gum bleeding since 1 week ago. Bleeding in
another location was denied.

Patient’s menstrual period usually normal, with the cycle 28 days and
duration mostly 3-4 days with 3 times changing pads.
Patient complained that this month menstrual cycle was different than
usual. She said that her menstrual duration is longer. She started this’
month menstrual time since 27th of May 2017 and haven’t stopped until
today.
The blood wasn’t heavily flow, but only like blackish spots.

Other complains like diarrhea, chronic cough, bloody cough was denied by
 Anamnesis

Past Illness History

Patient never get the same condition like this before.
Patient already went to hospital and do the laboratory check. The doctor
told to go to Sanglah Hospital to do further medical check up
Other systemic disease was denied

Family History
None of the family member has the same complaint as the patient.
Systemic disease in family was denied

Social History

Patient owns little market at her home selling basic needs

Physical Examination

General Appearance : Moderately ill

Level of Consciousness : Compos Mentis (E4V5M6)

Vital Sign
Blood pressure : 95/70 mmHg
Heart rate : 96 x/min
Respiration rate : 16 x/min
Tax : 39 oC
VAS : 0/10
Physical Examination

Eyes : anemis(+/+); icterus (-/-),oedema palp. (-/-)

ENT : Tonsils T1/T1; pharyngeal hyperemia (-);

tongue normal; lip cyanosis (-)

Neck : JVP PR + 0 cmH2O;

lymph node enlargement (-)
Physical Examination

Thorax : Symmetrical, retraction (-)

Cor
Inspection : Ictus cordis unseen
Palpation : Ictus cordis unpalpable
Percussion :
UB : ICS II
LB : at MCL S ICS V
RB : at PSL D
Auscultation : S1 S2 single regular, murmur (-)

Po
Inspection : Symmetric (static and dinamic)
Palpation : VF N/ N
Percussion : sonor/sonor
Auscultation : vesikular + / + , Rh -/-, wh -/-
Physical Examination

Abdomen :
Inspection : Distention (-); ascites (-)
Auscultation : Bowel sounds (+) normal
Percussion : Tympani
Palpation : Liver& spleen not palpable

Extremities:
Warm +/+; edema -/-
 Complete Blood Count (6/6/2017)

Parameter Result Unit Remarks Reference range

WBC 2.30 103/μL L 4,5 – 11,00
-Ne 64,28% 1,48 L 103/μL L 47,00 – 80,00
-Ly 22,05% 0,51 L 103/μL L 13,0 – 40,0
-Mo 12,52% H 0,29 103/μL 2,00 – 10,00
-Eo 0,19% 0,00 103/μL 0,00 – 5,00
-Ba 0,96% 0,02 103/μL 0,0 0 – 2,00
RBC 2,92 106/μL L 4,50 – 5,90
HGB 7,27 g/dL L 13,50 – 17,50
HCT 23,74 % L 41,00 – 55,00
MCV 84.67 fL 80,00 – 100,00
MCH 24,91 pg L 26,00 – 34,00
MCHC 30,64 g/dL L 31,00 – 36,00
RDW 14,78 % H 11,60 – 14,90
PLT 75,60 103/μL L 150,0 – 440,0
Retikulosit 1,9 % 0,62-2,24
 Blood Chemistry Panel (6/62017)

Parameter Result Unit Remarks Reference range

SGOT 68.9 U/L H 11,00 – 33,00
SGPT 108.70 U/L H 11,00 – 50,00
BUN 7.4 mg/dL 10,00 – 23,00
Creatinine 0.58 mg/dL 0,50 – 1,20
Na 138 mg/dL 136-145
K 3.9 mg/dL 3,5-5,1
LDH 500 U/L H 240-480
Alkali Phosphatase (ALP) 72 U/L 42-98
Bilirubin Indirek 0,36 mg/dL
Bilirubin Total 0,55 mg/dL 0,30-1,10
Bilirubin Direk 0,19 Mg/dL 0,00-0,30
 Assessment

•Pansitopenia ec Anemia Aplastic dd/ Acute Leukaemia

- Gum bleeding
- Vaginal bleeding
- Moderate Anemia N-N (7,27)
•Transaminitis ec reactive dd/ viral
 Treatment

Therapy
•IVFD Nacl 0,9% 20 tpm
•Paracetamol 500 mg @ 8 hours per oral
•PRC Transfusion until Hb ≥ 10 gr/dL

Planning Diagnostic
•Blood smear
•BMP
•Tes HbsAg & Anti HCV

Monitoring
•Vital sign
•Complaint
Thank you
Gejala Klinik Akut Leukemia
Serological Patterns of Acute & Chronic Hepatitis B
 Viral Hepatitis
HAV HBV HCV HDV HEV
Incubation 4 weeks 4 – 12 weeks 7 weeks 4 – 12 weeks 6 weeks

Onset Acute Acute / insidious Insidious Acute / insidious Acute

Transmission Fecal – oral Parenteral +++ +++ +++ Fecal - oral

Perinatal +++ variable +
Sexual ++ + ++

Clinical
Fulminant 0.1 % 0.1 – 1 % 0.1 % 5 – 20 % 1 – 2%
Progression to None Neonates 90% Infect 80-90% Common None
chronicity Adults 1-10% Hepatitis –70%

HCCancer + + +
Prophylaxis Immune globulin Immune globulin NONE HBV vaccine NONE
Inactivated vacc Recombinan vacc

Therapy NONE IFN Interferon Interferon + None

Lamivudine Ribavirin
 LIVER FUNCTION TESTS
• ALT
• AST (SGOT)
• ALKALINE PHOSPHATASE
• BILIRUBIN
 ALT and AST
– Enzymes, found in Hepatocytes
– Released when liver cells damaged
– ALT is specific for liver injury
– AST (SGOT) is also found in skeletal and cardiac
muscle
 Transaminitis:
• ALT predominant • AST predominant
– Chronic Hep B / C – Alcohol-related liver dz
– Acute A-E, EBV, CMV – Steatosis/ Steatohep
– Steatosis / Steatohep – Cirrhosis

– Hemochromatosis
– Medications / Toxins • Non-hepatic source
– Hemolysis
– Autoimmune Hepatitis
– Myopathy
– Alpha-1-antitrypsin
– Thyroid disease
– Wilson’s Disease – Strenuous exercise
– Celiac Disease
 Severe AST & ALT Elev: >15x
• Acute Viral Hepatitis • Autoimmune Hepatitis
– does not predict • Wilson’s Disease
outcome • Acute bile duct obstr
– Bili > 20 poor prognosis • Hepatic Artery ligation
• Ischemic Hepatitis • Budd-Chiari Syndrome
– hypotension • Medications / Toxins
– sepsis – acetaminophen
– hemorrhage – CCl4
– MI
Anemia aplastik
 Definisi : suatu keadaan dimana terdapat
kegagalan sumsum tulang dalam memproduksi sel
darah  ditandai dengan pansitopeni
 Etiologi :
 Primer : anemia fanconi
 Sekunder : (paling sering)
Anemia Fanconi
• suatu keadaan anemia aplastik kongenital
yang sangat jarang,
• ditemukan pertama kali oleh Fanconi pada
pangamatan terhadap 3 saudara laki-laki yang
semuanya terkena anemia saat dilahirkan.
• Diturunkan secara autosomal resesif. Biasanya
disertai dengan mikroencephaly, retardasi
mental, perwakan pendek dan kelainan
genetic lainnya.
 Anemia sekunder
– Obat-obatan; misal: chlorampenicol, sulfonamide,
phenytoin, prophyltiouracil, chloroquin, thiazides
– Zat kimia; misal: bensin, pelarut organic, TNT,
insektisida, cat rambut
– Sinar radiasi; isotop radioaktif
– Infeksi; infeksi virus hepatitis A, hepatitis non A-
non B, TBC milier. Parasit
 Patogenesis
1. Absent or defective stem cells (stem cell failure).
2. Abnormal marrow micro-environment.
3. Inhibition by an abnormal clone of hemopoietic
cells.
4. Abnormal regulatory cells or factors.
5. Immune mediated suppression of
hematopoiesis.

It is believed that genetic factors play a role. There is a higher

incidence with HLA (11) histo comp.
Antigen. Immune mechanism is involved.
 Pathogenesis
Potential mechanisms:

– Absent or defective stem cells (stem cell failure).

– Abnormal marrow micro-environment.
– Inhibition by an abnormal clone of hemopoietic cells.
– Abnormal regulatory cells or factors.
– Immune mediated suppression of hematopoiesis.

Faktor genetik juga sangat berpengaruh

 Gejala klinis
• Gejala klinis terjadinya anemia aplastik ini
dapat perlahan-lahan atau akut (terjadi secara
tiba-tiba), gejala yang timbul sama seperti
anemia pada umumnya, dan sering kali
disertai dengan infeksi. Tidak terdapat
pembesaran kelenjar limfonodi, hati maupun
limpa.
 Clinical Features
• Pemeriksaan Hematologi:
– Anemia normositik-normokromik; dapat juga
hipokrom
– Pemeriksaan hitung retikulosit cenderung rendah.
– Leukopenia; ada penurunan selektif pada seri
granulositik, namun kadang-kadang dapat juga
terjadi penurunan seri limfosit.
– Trombositopenia
– Pada sediaan hapus darah tepi tidak ditemukan
sel-sel abnormal.
• Pemeriksaan Kimia Darah:
– Serum iron normal,
– Bilirubin baik direk maupun indirek juga normal.
• Pemeriksaan Sumsum Tulang:
– Pada aspirasi sumsum tulang didapatkan gambaran
hiposeluler, dengan pengurangan jumlah sel
hematopoetik
– Pada biopsy sumsum tulang didapatkan suatu
gambaran hipoplasia atau aplasia, dimana selularitas
akan menurun dan digantikan oleh jaringan lemak
lebih dari 75%.
• DIAGNOSIS
~ Anamnesis:
- Riwayat paparan terhadap zat toksik (obat,
lingkungan kerja, hobi),menderita infeksi virus 6
bulan terakhir (hepatitis, parvovirus), pernah
mendapat transfusi darah.
- Gejala anemia: rasa lemas/lemah, pucat, pusing,
sesak napas/gagal jantung, berkunang-kunang.
- Tanda-tanda infeksi: sering demam
- Akibat trombositopenia: perdarahan (menstruasi
lama, epistaksis, perdarahan gusi, perdarahan di
bawah kulit, hematuria, buang air besar campur
darah, muntah darah).
 ~ Pemeriksaan fisik:
konjungtiva pucat, takikardi, tanda perdarahan
~ Pemeriksaan penunjang:
darah tepi lengkap ditemukan pansitopenia,serologi
virus (hepatitis, parvovirus)
~ Diagnosis pasti:
sitologi dan histopatologi sumsum tulang

• DIAGNOSIS BANDING
Mielofibrosis, anemia hemolitik, anemia defisiensi,
anemia karena penyakit kronik, anemia karena penyakit
keganasan sumsum tulang, hipersplenisme, leukimia akut
• PEMERIKSAAN PENUNJANG
~ Laboratorium: darah tepi lengkap, serologi virus
~ Aspirasi dan biopsi sumsum tulang

• TERAPI
Terapi penunjang:
~ Transfusi komponen darah (PRC dan/atau TC)
sesuai indikasi (pada transfusi darah)
~ Menghindari dan mengatasi infeksi
~ Kortikosteroid: prednison 1-2 mg/kgBB/hari
~ Androgen : Metenolol asetat 2-3 mg/kgBB/hari,
maksimal diberikan selama 3 bulan
~ Transplantasi sumsum tulang  definitif
Respons terapi:
~ Komplit: granulosit >1000/ul, trombosit >100.000/ul,
Hb normal
~ Parsial; granulosit >500/ul, tidak membutuhkan
transfusi darah merah dan trombosit
~ Minimal: granulosit >500/ul, membutuhkan transfusi
darah merah dan trombosit
~ Tidak berespons: anemia aplastik berat menetap
• KOMPLIKASI
Infeksi bisa fatal, perdarahan, gagal jantung pada anemia
berat

• PROGNOSIS
~ Dubia, tergantung tingkat hipoplasinya
~ Pada umumnya pasien meninggal karena infeksi,
perdarahan atau komplikasi transfusi darah