FAKULTAS KEPERAWATAN UNIVERSITAS

JEMBER RESUME ASUHAN KEPERAWATAN

MEDIKAL BEDAH

Nama Mahasiswa : Yeti Novitasari,

S.Kep NIM 202311101016

FORMAT RESUME KASUS KELOLAAN

I. Identitas pasien
a. Nama : Tn. M.S
b. Umur : 44 tahun
c. Jenis Kelamin : Laki-laki
d. Status : menikah
e. Agama : (tidak terkaji)
f. Pekerjaan : Penjual buah
g. Alamat : Surabaya
h. RM :-
i. Diagnosa Medis : HIV dengan pericarditis akut
j. Tanggal MRS : 19-05-2020 Jam:-
k. Tanggal Pengkajian : 24-12-2018 Jam: 19.00

II. Riwayat Kesehatan

a. Keluhan utama
Pasien mengeluh nyeri dada, sesak nafas saat beraktivitas, penurunan berat
badan dan nafsu makan
b. Riwayat kesehatan sekarang
Pasien mengeluh nyeri dada menusuk sejak 3 hari sebelum masuk. Nyeri
 dirasakan terus menerus di bagian tengah dada, diperparah dengan menarik
napas dan pasien merasa lebih baik saat dalam posisi duduk dan
membungkuk. Pasien menyangkal sensasi panas atau terbakar, nyeri tajam
di hipokondrium, dan mual dan muntah. Pasien juga mengeluhkan sesak
napas, terutama saat beraktivitas. Batuk disangkal. Pasien mengeluh demam
sejak> 1 bulan sebelum masuk, dan memburuk 1 minggu sebelum masuk.
pasien juga mengeluhkan penurunan berat badan sejak sebulan terakhir
sekitar 6 kg (dari 57kg menjadi 51kg), serta penurunan nafsu makan.
Berkeringat di malam hari, sariawan, nyeri saat menelan dan diare. Keluhan
kulit kemerahan, rambut rontok, nyeri persendian berkurang.
c. Riwayat kesehatan dahulu
Pasien mengatakan memiliki riwayat STEMI inferior dan riwayat
tuberkulosis tahun 1999, mendapatkan pengobatan selama 6 bulan dan
sudah dinyatakan sembuh
d. Pengkajian fisik head to toe (data fokus)
Kondisi umum : Glasgow Coma Scale (GCS) E4V5M6 (komposmetis)
Tekanan darah (TD) 112 / 67mmhg
Denyut nadi 120 x/m, teratur
RR : 22 x/menit
Suhu aksila 37,60C
Saturasi oksigen 98% dengan saluran hidung O2 3 lpm.
- Pemeriksaan kepala dan leher tidak menunjukkan pucat konjungtiva,
ikterus, dispneu, atau sianosis. Tidak ada peningkatan tekanan vena
jugularis (JVP) atau pembesaran kelenjar getah bening.
- Pada pemeriksaan dada, ada gesekan fiksi perikardial di batas parasternal
kiri, bunyi jantung dalam batas normal tanpa murmur, gallop atau sistol
ekstra; tidak ditemukan kelainan pada pemeriksaan paru.
- Pemeriksaan perut tidak menunjukkan adanya kelainan.
- Perfusi ekstremitas hangat dan kering, tidak ada edema, waktu pengisian
kapiler <2 detik.
e. Pemeriksaan penunjang
 - Dari pemeriksaan laboratorium, leukosit 8690 / μL, Hemoglobine11.2g / dL,
neutrofil 78.3%, limfosit 19.4%, hematrocrit 37.3%, trombosit 489000 / μL,
gula darah 75mg / dL, 17mg / dL, serum kreatinin 1.14mg / dL, AST 38 U /
L, ALT 39U / L, albumin 3.28 gr / dl, natrium 129mmol / L, kalium
3.8mmol / L, klorida 105mmol / L, HBs Ag non reaktif, HIV rapid test
reaktif, APTT 24.1 detik, PPT 9,5 detik , Troponin I 6.18pg / ml (Normal
<14pg / ml), CKMB 11.2U / L (Normal 7-25U / L), CRP 197.16 mg / L.
Hasil pemeriksaan BGA pH 7,41, pCO2 25mmHg, pO2131mmHg, HCO3
15,8mmol / l, Beecf-8.8mmol / l, SO2 99% dengan O2 kanul hidung 3 lpm.
- EKG menunjukkan seperti pada kita takikardia 124 denyut per menit
dengan elevasi ST cekung yang tersebar luas dan depresi PR di sebagian
besar sadapan ekstremitas (I, II, III, VL, VF) dan sadapan prekordial (V2-6),
ST timbal balik depresi dan peningkatan PR dalam memimpin VR dan V1.
- Rontgen dada menunjukkan adanya fibrosis suprahilar di paru kanan.
- Hasil Ekokardiografi masih dalam batas normal
f. Terapi pengobatan
- diet tinggi kalori dan protein tinggi 2100kkal per hari
- O2 kanula hidung 3 lpm
- ceftriaxone 1g setiap 12 jam (iv)
- ranitidine 50mg setiap 12 jam (iv)
- colchicine 0,5mg per oral setiap 24 jam
- ibuprofen 600mg per oral setiap 8 jam
- Tes antibodi HIV, apusan dahak dengan pewarnaan Gram dan Ziehl-
Nielssen (ZN), kultur darah dan sputum, dan GeneXpert MTB / RIF pada
sputum

III. Catatan Perawatan dan Perkembangan Klien (Here and

Now) S (Subjektif)
- Pasien mengeluh nyeri dada menusuk sejak 3 hari sebelum masuk.
- Pasien juga mengeluhkan sesak napas, terutama saat beraktivitas.
- Pasien mengeluh demam sejak> 1 bulan sebelum masuk, dan memburuk 1
 minggu sebelum masuk.
- Pasien juga mengeluhkan penurunan berat badan sejak sebulan terakhir
sekitar 6 kg (dari 57kg menjadi 51kg), serta penurunan nafsu makan.
Berkeringat di malam hari, sariawan, nyeri saat menelan dan diare.
(Objektif)
- Tekanan darah (TD) 112 / 67mmhg
- Denyut nadi 120 x/m
- RR : 22 x/menit
- Suhu aksila 37,60C
- Saturasi oksigen 98% dengan saluran hidung O2 3 lpm.
- Hemoglobine11.2g / dL, neutrofil 78.3%, limfosit 19.4%, hematrocrit
37.3%, trombosit 489000 / μL, gula darah 75mg / dL, serum kreatinin
1.14mg / dL, AST 38 U / L, ALT 39U / L, albumin 3.28 gr / dl, natrium
129mmol / L, kalium 3.8mmol / L, klorida 105mmol / L, HBs Ag non
reaktif, HIV rapid test reaktif, APTT 24.1 detik, PPT 9,5 detik , Troponin I
6.18pg / ml (Normal <14pg / ml), CKMB 11.2U / L (Normal 7-25U / L),
CRP 197.16 mg / L. Hasil pemeriksaan BGA pH 7,41, pCO2 25mmHg,
pO2131mmHg, HCO3 15,8mmol /L, Beecf-8.8mmol / l, SO2 99% dengan
O2 kanul hidung 3 lpm
-
A (Analisa/ Diagnosa Keperawatan yang ditegakkan berdasar DS dan DO)
(PPNI, 2017):
a. Gangguan pertukaran gas b.d perubahan membran alveolus-kapiler d.d
Pasien juga mengeluhkan sesak napas, terutama saat beraktivitas, RR 22
x/menit, pCO2 25mmHg, HCO3 15,8mmol /L, nadi 120 x/m
b. Nyeri akut b.d agen pencedera fisiologis d.d Pasien mengeluh nyeri dada
menusuk sejak 3 hari sebelum masuk, nadi 120 x/m, RR 22 x/menit, pCO2
25mmHg, HCO3 15,8mmol /L, nafsu makan menurun
c. Defisit nutrisi b.d ketidakmampuan mengabsorbsi makanan d.d
mengeluhkan berat badan berat tanpa sebab yang jelas> 10%, demam terus
menerus tanpa sebab yang jelas> 1 bulan, nafsu makan menurun, HIV rapid
 test reaktif
P (Perencanaan)
SLKI (PPNI, 2019)
a. Pertukaran gas L.01003
- Dipsnea menurun (5)
- Pola napas membaik (5)
- Takikardia membaik (5)
- PCO2 membaik (5)
- PO2 membaik (5)
b. Tingkat nyeri L.08066
- Keluhan nyeri menurun (5)
- Frekuensi nadi membaik (5)
- Pola napas membaik (5)
- Nafsu makan membaik (5)
c. Status nutrisi L.03030
- IMT cukup membaik (4)
- Berat badan cukup membaik (4)

SIKI (PPNI, 2018)

a. Pemantauan respirasi 1014
Observasi
1. Monitor frekuensi irama, kedalaman dan upaya napas
2. Monitor pola nafas
3. Auskultasi bunyi nafas
4. Monitor saturasi oksigen
5. Monitor nilai AGD
6. Monitor hasil x-ray thorax
Terapeutik
1. Dokumentasikan hasil pemantauan
Edukasi
1. Jelaskan tujuan dan prosedur pemantauan
2. Informasikan hasil pemantauan
b. Manajemen nyeri I.08238
Observasi
1. Identifikasi lokasi, karakteristik, durasi, frekuensi, kualitas intensitas nyeri
2. Identifikasi skala nyeri
3. Identifikasi respon nyeri non verbal
4. Identifikasi faktor yang memperberat dan memperingan nyeri
5. Identifikasi pengetahuan dan keyakinan tentang nyeri
6. Identifikasi pengaruh nyeri pada kualitas hidup monitor efek samping
penggunaan analgetik
Terapeutik
1. Kontrol lingkungan yang memperberat rasa nyeri
2. Fasilitasi istirahat dan tidur
3. Pertimbangkan jenis dan sumber nyeri dalam pemilihan strategi
meredakan nyeri
Edukasi
1. Jelaskan penyebab, periode dan pemicu nyeri
2. Jelaskan strategi meredakan nyeri anjurkan menggunakan analgetik
secara tepat
Kolaborasi
1. Kolaborasi pemberian analgetik
c. Manajemen Nutrisi I. 03119
Observasi
1. Identifikasi status nutrisi
2. Identifikasi kebutuhan kalori dan jenis nutrisi
3. Monitor asupan makanan
4. Monitor hasil pemeriksaan
laboratorium Terapeutik
1. Berikan makanan tinggi kalori dan tinggi protein
2. Berikan suplemen makanan
Edukasi
1. Ajarkan diet yang diprogramkan
Kolaborasi
1. Kolaborasi dengan ahli gizi untuk menentukan jumlah kalori dan jenis nutrien
yang dibutuhkan

I (implementasi)
Diagnosa 1
1. Memonitor frekuensi irama, kedalaman dan upaya napas
2. Memonitor pola nafas
3. Mengauskultasi bunyi nafas
4. Memonitor saturasi oksigen
5. Memonitor nilai AGD
6. Memonitor hasil x-ray thorax
7. Menjelaskan tujuan dan prosedur pemantauan
8. Mendokumentasikan hasil pemantauan
9. Menginformasikan hasil pemantauan

Diagnosa 2
1. Mengidentifikasi lokasi, karakteristik, durasi, frekuensi, kualitas
intensitas nyeri
2. Mengidentifikasi skala nyeri
3. Mengidentifikasi respon nyeri non verbal
4. Mengidentifikasi faktor yang memperberat dan memperingan nyeri
5. Mengidentifikasi pengetahuan dan keyakinan tentang nyeri
6. Mengidentifikasi pengaruh nyeri pada kualitas hidup monitor efek samping
penggunaan analgetik
7. Mengkontrol lingkungan yang memperberat rasa nyeri
8. Memfasilitasi istirahat dan tidur
9. Mempertimbangkan jenis dan sumber nyeri dalam pemilihan
strategi meredakan nyeri
10. Menjelaskan penyebab, periode dan pemicu nyeri
11. Menjelaskan strategi meredakan nyeri anjurkan menggunakan
analgetik secara tepat
12. Berkolaborasi pemberian analgetik

Diagnosa 3
1. Mengidentifikasi status nutrisi
2. Mengidentifikasi kebutuhan kalori dan jenis nutrisi
3. Memonitor asupan makanan
4. Memonitor hasil pemeriksaan laboratorium
5. Memberikan makanan tinggi kalori dan tinggi protein
6. Memberikan suplemen makanan
7. Mengajarkan diet yang diprogramkan
8. Berkolaborasi dengan ahli gizi untuk menentukan jumlah kalori dan jenis
nutrien

E (Evaluasi)
Diagnosa 1
S (Subjektif):
Pasien mengatakan sudah dapat bernafas dengan mudah
O (Objektif):
- Pasien kooperatif saat dilakukan implementasi
- Hasil monitor RR 20x/menit, nadi 98x/menit, PCO2 meningkat (37mmHg),
PO2 85 mmHg
A: masalah teratasi sebagian
P: lanjutkan intervensi:
1. Memonitor hasil x-ray thorax
2. Menjelaskan tujuan dan prosedur pemantauan
3. Mendokumentasikan hasil pemantauan
4. Menginformasikan hasil pemantauan

Diagnosa 2
S: Pasien mengatakan nyeri pada bagian dada, skala nyeri 6
Pasien mengatakan sulit untuk tidur
O: pasien terlihat gelisah
A: masalah belum teratasi
P: lanjutkan intervensi
1. Mengidentifikasi faktor yang memperberat dan memperingan nyeri
2. Mengidentifikasi pengetahuan dan keyakinan tentang nyeri
3. Mengidentifikasi pengaruh nyeri pada kualitas hidup monitor efek samping
penggunaan analgetik
4. Mengkontrol lingkungan yang memperberat rasa nyeri
5. Memfasilitasi istirahat dan tidur
6. Mempertimbangkan jenis dan sumber nyeri dalam pemilihan
strategi meredakan nyeri
7. Menjelaskan penyebab, periode dan pemicu nyeri
8. Menjelaskan strategi meredakan nyeri anjurkan menggunakan
analgetik secara tepat
9. Berkolaborasi pemberian analgetik

Diagnosa 3:
S: pasien mengatakan akan makan asupan makanan yang disediakan
O: pasien terlihat lahap makan yang diberikan
Pasien kooperatif saat dilakukan intervensi
A: masalah belum teratasi
P: Lanjutkan intervensi
1. Memonitor hasil pemeriksaan laboratorium
2. Memberikan suplemen makanan
3. Mengajarkan diet yang diprogramkan
4. Berkolaborasi dengan ahli gizi untuk menentukan jumlah kalori dan jenis
nutrien
 DAFTAR PUSTAKA

PPNI. 2017. Standar Diagnosis Keperawatan Indonesia: Definisi Dan

Indikator Diagnostik. Jakarta: DPP PPNI.
PPNI. 2018. Standar Intervensi Keperawatan Indonesia: Definisi Dan
Tindakan Keperawatan. Jakarta Selatan: DPP PPNI.
PPNI. 2019. Standar Luaran Keperawatan Indonesia. Jakarta Selatan: DPP PPNI.
Triyono, E. A. dan T. Fonda. 2019. A case report an hiv patient with acute
perikarditis. Journal of Dermatology & Cosmetology. 3(5)
 Journal of Dermatology & Cosmetology
Case Report
A case report an HIV patient with acute perikarditis
Introduction
Infection of Human immunodeficiency virus (HIV) and Acquired
immune deficeincy syndrome (AIDS) is a global issue. There were
around 36.7 million people in the world who were infected with
HIV in 2016 and 1 million people die each year.1 HIV infection
is often associated with heart problems . However, cardiac
involvement in this patient population is often underdiagnosed or
associated with other disease processes.2
The prevalence of cardiovascular disorders in HIV/
AIDS patientsreached 30-60% and up to 24% in one autopsy
series .3,4 Pericardial lesions are a frequent cardiovascular diseases,
the prevalence of pericardial lesions in HIV/AIDS patients nearly
28% in the Democratic Republic of the Congo (DRC) and 35.3%
in Congo Brazzaville. HIV/AIDS patients with pericardial effusion
accounted for 20% and 4% of them with massive effusion.3
Heart disease in patients with HIV/AIDS has many challenges
both in terms of diagnostic and therapeutic. The high prevalence of
cardiovascular disorders, especially pericardial lesions in HIV /
AIDS patients, further confirms the magnitude of the problem.
Pericarditis itself is a serious disease and is almost always fatal
because of late management. The pathogenesis of this event is also
unclear.5
Considering the magnitude of the problems that occur in patients
with HIV / AIDS with cardiovascular disorders , the authors would
like to discuss this issue further,especially in relation to acute
pericarditis. The authors present a case regarding a HIV/AIDS
patient with acute pericarditis.
Keywords: tattoos, acute pericarditis, sweating, oral ulcers
Case presentation
Mr. M.S., age 44 y.o., a fruit seller living in Surabaya came to
the emergency department of Dr. Soetomo Hospital. He was referred
from Karang Tembok Hospital with inferior STEMI and a history
of pulmonary TB. The patient complained of stabbing chest pain
since 3 days before admission . Pain was felt continuously in the
middle of the chest, worsened by breathing in and he felt better when
in sitting and bending position . He denied hot or burning sensation,
sharp pain in hypocondrium, and nausea and vomiting. He also
complained shortness of breath, especially on activity. Cough was
denied. He complained fever since >1 month before admission,
and worsened
1 week before admission. He also complained decrease of body
weight since last month for around 6kg (from 57kg to 51kg), and
also decrease of appetite. Night sweating, oral ulcers, pain on
swallowing and diarrhea were denied. Complaints of reddish skin,
hair loss, joint pain weredenied. There were no complaints of
tumors/lumps.
The patient didin’t have history of diabetes, high blood pressure,
jaundice, heart disease or kidney disease. The patient had a history of
tuberculosis in 1999, received treatment for 6 months and was
declared cured. His father-in-law, who had been living in the same
house with the patient,had a history of pulmonary tuberculosis, but
had received treatment and was declared cured. There weren’t other
family members suffering from lung diseas. The patient had been
married since 20
Open Access
Volume 3 Issue 5 - 2019
Erwin Astha Triyono,1 Troy Fonda2
1
Tropical and Infectious Diseases Division, Internal
Medicine Department, Indonesia
2
Faculty of Medicine Universitas Airlangga, Dr. Soetomo General
Academic Hospital, Indonesia
Correspondence: Erwin Astha Triyono,Tropical and Infectious
Diseases Division, Internal Medicine Department, Indonesia,
Email
Received: September 25, 2019 | Published: October 18, 2019
years ago and had two boys, now aged 10 and 18 years. His wife and
his two children denied any complaints. History of drugs, tranfusion,
tattoos were denied. He had multiple sexual partners before mariage,
and he admitted using prostitutes’ services several times during his
marriage.
On physical examination, he was alert, with Glasgow Coma
Scale ( GCS ) E4V5M6. Blood pressure (BP) was 112/67mmHg,
pulse 120 beats per minute, regular, respiratory rate (RR) 22 times
per minute and axillary temperature 37.6 0C, oxygen saturation was
98% with O2 nasal canule 3 lpm . Head and neck examination
showed no conjungtival pallor, jaundice, dyspneu, nor cyanosis.
There were no increase in jugular venous pressure ( JVP ) nor
lymph nodes enlargement. On chest examination, there was a
pericardial fiction rub in the left parasternal border, heart sounds
within normal limit without murmurs, gallops or extra systole; no
abnormality was found on pulmonary examination. Abdominal
examination did not reveal any abnormalities . Extremities perfusion
were warm and dry, no edema, capillary refill time < 2 seconds.
From the laboratory examination, leukocytes 8690/μL,
Hemoglobine11.2g/dL, neutrophils 78.3%, lymphocytes 19.4%,
hematrocrit 37.3%, platelet 489000/μL, Blood sugar 75mg/dL,
17mg/ dL, creatinin serum 1.14mg/dL,AST 38 U/L , ALT 39U/L ,
albumin
3.28 gr/dl, sodium 129mmol/L, potassium 3.8mmol/L, chloride
105mmol/L , HBs Ag non reactive, HIV rapid test reactive, APTT
24.1 seconds, PPT 9.5seconds, Troponin I 6.18pg/ml (Normal<14pg/
ml), CKMB 11.2U/L (Normal 7-25U/L), CRP 197.16 mg/L. BGA
examination results pH 7.41, pCO2 25mmHg, pO2131mmHg, HCO3
15.8mmol/l, Beecf-8.8mmol/l, SO2 99% with O2 nasal cannula 3
lpm. An ECG showed as in us tachycardia 124 beats per minute with
wide spread concave ST elevation and PR depression throughout
most of the limb leads (I, II, III, a VL, a VF) and precordial leads
(V2-6), reciprocal ST depression and PR elevation in lead a VR and
V1. Chest X-Ray showed the presence of suprahilar fibrosis on the
right lung. Echocardiography result was within normal limit:
• Valves within normal limit
• Cardiac chambers: LA, LV, RV, RA within normal limit,
thrombus (-)
Submit Manuscript | http://medcraveonline.com J Dermat Cosmetol. 2019;3(5):132‒136. 132
©2019 Triyono et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which
permits unrestricted use, distribution, and build upon your work non-commercially.

A case report an HIV patient with acute Copyright:

perikarditis ©2019 Triyono et al. 133

• LV systolic function within normal limit (EF 65%). RV 2

systolic

RR 16 times per minute, and temperature 36.5oC , O saturation

function within normal limit (TAPSE 2cm)
• LV normokinetic all segments
• Pericardial effusion (-)
Patient was diagnosedwith HIV stage III with acute pericarditis
and suspected relapse of pulmonary TB. As treatment, patient
recieved high calories and high proteins diet 2100kcal per day, O2
nasal cannula 3 lpm, ceftriaxone 1g every 12 hours (iv), ranitidine
50mg every 12 hours (iv), colchicine 0,5mg orally every 24 hours
and ibuprofen 600mg orally every 8 hours.An HIV antibody testing,
sputum smear with Gram and Ziehl-Nielssen (ZN) staining, blood
and sputum culture, and GeneXpert MTB/RIF on sputum were
ordered.Serial ECG monitoring was ordered. CD4 count was not
ordered because of financial issue.
Disease progression
On the second day of care,the patient’s chest painimproved. He
was alert, with blood pressure 110/70mmHg, pulse 110 beats per
minute, RR 20 times per minute, temperature 36.6°C, O 2 saturation
99% with O2 nasal cannula 3 lpm. The results of HIV antibody tests
were positive.
On the sixth day of care, the patient had no complaints. He was
alert, with blood pressure 120/70 mmHg, pulse 100 beats per minute,
Table 1 WHO HIV/AIDS clinical stadium in young adults and adults.16
99% without O2 support.Laboratory examinations: leukocytes 9410/
μL, Hb 11.9g/dL, neutrophils 87,5%, hematocrit 35.6 %, platelets
304000/μL. GeneXpertresult was negative for MTB. Sputum
staining for Gram and ZN were negative. Blood culture and sputum
culture were negative. ECG examination showed sinus rhythm 98
times per minute. The patient was diagnosed with HIV stage III with
improved acute pericarditis and a history of pulmonary TB. The
patientwas discharged with the following medications: ibuprofen
600mg- 600mg-400mg po, cotrimoxazole 960mg/day po, colchicine
0.5mg/ day po, and fixed dose combination (FDC) of antiretroviral
therapy (Tenofovir/TDF 300mg, Lamivudine/3TC 150mg
efavirenz/EFV 600mg) 1tab/day po.
Three days after being discharged, the patient had no complaints.
He was told to continue his medications, withibuprofen tapered
downfor 200mg every week. The patient chose to continue his
treatment at Karang Tembok Hospital.
Discussion
AIDS is a syndrome caused by decrease of immunity caused
by infection of human immunodeficiency virus (HIV) belonging to
the family of retroviridae, in which AIDS is the final stage of HIV
infection.6 Classification of HIV/AIDS stage by WHO can be seen in
table 1-4.

Primary HIV infection

Asymptomatic
Acute retroviral syndrome

Clinical Stadium I

Asymptomatic
Persistent generalized lymphadenopathy (PGL)

Clinical Stadium II

Angular cheilitis
Symptomatic
Recurrent oral ulcerations
Moderate unexplained weight loss (<10%)
Papular pruritic eruptions
Recurrent respiratory tract infections
Seborrhoeic dermatitis
Herpes zoster
Fungal nail infections of fingers

Clinical Stadium III

Severe weight loss (>10%)

Unexplained chronic diarrhea>1 month
Unexplained persistent fever>1 month
Oral candidiasis
Pulmonary Tuberculosis (TB) diagnosed in last
two years
Severe presumed bacterial infections
Acute necrotizing ulcerative stomatitis, gingivitis or periodontitis
Unexplained anaemia < 8g/dl,neutropenia<500/mm3 , thrombocytopenia <50000/
mm3 >1 month

Clinical Stage IV

HIV wasting syndrome

Extra pulmonary cryptococcosis
Pneumocystis pneumonia
Disseminated non-tuberculous mycobacterial infection
Recurrent severe or radiological bacterial pneumonia
Chronic cryptosporidiosis
Chronic herpes simplex infection >1month
CMV infection
Oesophageal candidiasis
Any disseminated mycosis
Extr pulmonary TB
Invasive cervical
Kaposi's sarcoma
carcinoma Visceral
CNS toxoplasmosis
leismaniasis
HIV encephalopathy
Cardiomyopathy and nephropathy assosiated HIV
Citation: Triyono EA, Fonda T. A case report an HIV patient with acute perikarditis. J Dermat Cosmetol . 2019;3(5):132‒136. DOI: 10.15406/jdc.2019.03.00130
Copyright:
A case report an HIV patient with acute ©2019 Triyono et al. 134
perikarditis

Table 2 Treatment of acute pericarditis.8

Duration of
Drugs Usual dosing therapy Tapering

Aspirin 750-1000mg every 8 hours 1-2 weeks Decreased doses by 250-500mg every 1-2weeks

Ibuprofen 600mg every 8 hours 1-2 weeks Decreased doses by 200-400mg every 1-2weeks

0.5mg once daily (<70kg) or 0.5mg Not mandatory, alternatively 0.5mg every 48 hours (<70 kg) or
Colchicine 3 months
every 12 hours (≥70kg) 0.5mg every 24 hours (≥70kg) in the last weeks

Table 3 Options for recurrent pericarditis.11

Therapy Initial dosing Duration

Azathioprine Started at 1mg/kg/day, then gradually increased to 2-3mg/kg/day At least 6 months
Human immunoglobulin 400-500mg/kg/day (iv) for 5 days 5 days
Anakinra 1-2mg/kg / day up to 100mg/day At least 6 months
Pericardiectomy Not applicable Not applicable

Table 4 Causes of Pericarditis. 16

Infection
Gram positive and Gram negative species (streptococci, staphylococcus, pneumococcus), Mycobacterium tuberculosis. Less
Bacterial common - Legionella, Norcardia, Actinobacillus, Rickettsia, Borrelia burgdoferi (Lyme disease), Listeria, Laptospira,
Chlamydophila psittaci,Treponema pallidum (syphilis), Coxiella burnettii, Meningococcusspecies, Hemophilusspecies,
Mycoplasma
Fungal infection Histoplasma, blastomyces, coccidiosis, aspergillus, candida

Parasitic infection Toxoplasma, entomoeba, echinococcus

Coxsackie viruses, echoviruses, adenoviruses, influenza A & B viruses, enteroviruses, mumps viruses, Epstein-Barr viruses,
Viral /
HIV, herpes simplex viruses, type I varicella zoster virus (VZV), measles, influenza viruses type II, RSV, CMV, hepatitis A,
idiopathic
B & C, parvovirus B 19
causes
Non-Infection
Systemic lupus erythematous, Sjogren's syndrome, rheumatoid arthritis, scleroderma, vasculitides-eosinophilic
granulomatosis (Churg-Strauss syndrome),Takayasu disease, Behcet syndrome, scarcoidosis, familial Mediterranean fever,
Autoimmune
inflammatory bowel disease, Still disease, mixed connective tissue disorder, Reiter Wegners granulomatosis, ankylosing
spondylitis, giant cell arteritis, dermatomyocitis, serum sickness
Neoplastic causes Primary (mesothelioma), secondary (lung, breast, etc.)

Metabolic causes Uremia, myxoedema, cholesterol pericarditis

Daunorubicin, doxorubicin, cyclophosphamide, 5 flurouracil, amiodarone, cyclosporine, mesalazine, clozapine,

methysergide, anti-tumor necrosis factor, hydralazine, procainamide, methyldopa, phenytoin, Isoniazine, clozapine,
Drugs
methysergide, anti- tumor necrosis factor, hydralazine, procainamide, methyldopa, phenytoin, Isoniazide, clozapine,
methysergide, anti-tumor necrosis factor, hydralazine, procainamide, methyldopa, phenytoin, Isoniazide,
Coronary interventions, permanent pacemaker / ICD implantation , radiofrequency ablation , translucent / impermeable
Trauma, iatrogenic
trauma, esophageal perforation / rupture

This patient was diagnosed with HIV infection by antibody

testing, and he also complained severe unexplained weight loss >
10%, unexplained persistent fever > 1 month, sohe was diagnosed
with HIV stage 3
Pericarditis is categorized according to the duration of symptoms:
acute,incessant, recurrent, and chronic pericarditis. Acutepericarditis
is an inflammatory pericardial syndrome with orwithout pericardial
effusion. Incessant pericarditis is a pericarditis which lasts for more
than 4–6 weeks but less than 3 months without remission.. Recurrent
pericarditis is diagnosed with a documented first episode of acute
pericarditis, a symptom-free interval of 4–6 weeks or longer and
evidence of subsequent recurrence of pericarditis. Pericarditis is
considered chronic if it is persistent for more than 3 months.
Pericarditis is often the initial manifestation of a systemic disease.7,8
Pericarditis can be caused by either an infectious etiology
through pathogen-associated molecular patterns (PAMPs) and non-
infectious etiology through the damage-associated molecular
patterns (DAMPs). This stimulus will be recognized by receptors
of innate immunityboth intracellular (nucleotide-binding
oligomerization domain-like receptors, NLRs) and extracellular (toll
like receptors, TLRs; and P2X2/P2X7. NLRs will be integrated into
the inflammatorystructure into nucleotide-binding oligomerization
domain-like pyrin domain-containing 3 receptors (NLRP3) which
will trigger the release of interleukin 1 (IL-1). IL-1, a pro-
inflammatory cytokine, will cause inflammation of the pericardium.9
The differential diagnosis of acute pericarditis includes acute
gastritis, angina, acute myocardial infarction, aortic dissection,
pulmonary embolism, and oesophageal disorders (esophagitis,

Citation: Triyono EA, Fonda T. A case report an HIV patient with acute perikarditis. J Dermat Cosmetol . 2019;3(5):132‒136. DOI: 10.15406/jdc.2019.03.00130
A case report an HIV
patient with acute perikarditis Copyright:
©2019 Triyono et al. 135

esophageal rupture, esophageal spasms, GERD). According to

the 2015 European Society of Cardiology Guidelines for the
diagnosis and management of pericardial diseases, the diagnosis of
acute pericarditis can be established if two of 4 criteria are found:
pericarditic chest pain, pericardial frition rub , new widespread ST
elevation or PR depression on ECG examination, and pericardial
effusion (new or worsening). Pericarditic chest pain is a sharp and
pleuritic painwhich improves with sitting and bending positions.
Other tests that support the diagnosis are an increase in inflammatory
markers such as CRP, LED or leukocytosis and evidence of
pericardial inflammation from radiological examinations such as
cardiac magnetic resonance and cardiac CT scans.8,10

Figure 3 Emerging options for the therapy for recurrent pericarditis with their
mechanism of action.11

Figure 1 Pathogenesis of pericarditis.9

This patient presented with a chest pain typical of pericarditis

for 3 days, pericardial friction rub,widespread ST elevation on ECG
examination, and increase in CRP (197.16mg/L). Thus, he was
diagnosed with acute pericarditis .
Acute pericaditis are managed according to the severity;patients
are said to be high risk if they meet one of the major or minor
criteria. Major criteria include fever>38 0C, subacute onset, massive
pericardial effusion, cardiac tamponade, lack of response to aspirin
or NSAIDsafter at least 1 week of therapy. Minor criteria include
myopericarditis, immunosuppression, trauma, and anticoagulant
therapy. Patients who are classified as high risk conditions require
hospitalization and thorough search for etiology. Patients who are
not included in the high risk group can be treated as outpatient by
giving NSAIDs for 1 week. Patients who respond poorly to NSAID
are considered moderate risk group and require hospitalization and
etiology search, similar with the high risk group. The flow of triage for
the pericarditis can be seen in Figure 2-4 .8
Figure 2 Pericarditis triage.8
Figure 4 Complications of acute pericarditis.9
The treatment for acute pericarditis is the administration of
NSAIDs or aspirin. Several other literatures recommend the
administration of NSAIDs and colchicine. Corticosteroids can be
considered a second choice if there are contraindications or failure
with aspirin or NSAID treatment. Therapy is given for 1-2 weeks
followed bydose tapering after clinical, laboratory, and ECG
improvement.8,11
The NSAID of choice for acute viral or idiopathic pericarditis is
ibuprofen with an efficacy of 70-80% (Task et al., 2015). 8 In patients
with acute pericarditis with a history of acute myocardial infarction,
aspirin is the first choice, and NSAIDs must be avoided because they
interfere with the healing process. Aspirin is also preferred in
patients who need anti-platelet therapy. Colchicine is preferred in
recurrent pericarditis or lack of improvement with NSAIDs. Proton
pump inhibitors can be given to patients with a history of gastric
ulcer who require high dose NSAIDs or long-term NSAIDs use.
Corticosteroids are used as a second-line therapy with low-moderate
doses (prednisone 0.2-0.5mg/kgBB/day) tapered down slowly
(2.5mg/2weeks) after remission and CRP improvement.11-14
Several therapeutic options for recurrent pericarditis
areazathioprine, immunoglobulins, and anakinra (anti- interleukin-
1). These therapiesare still controversial and have not been widely
applied.11

Citation: Triyono EA, Fonda T. A case report an HIV patient with acute perikarditis. J Dermat Cosmetol . 2019;3(5):132‒136. DOI: 10.15406/jdc.2019.03.00130
Copyright:
A case report an HIV patient with acute ©2019 Triyono et al. 136
perikarditis
 NSAIDs work by inhibitingcyclo-oxygenase (COX) enzyme,
thereby preventing the formation of prostaglandins. Ibuprofen
possess both anti-inflammatory properties by inhibiting the COX-1
and COX- 2 enzymes and capturing free radicals, and analgetic
properties by binding to cannabinoid receptors. Aspirin works by
exerting its anti- inflammatory properties, inhibiting COX-1 and
COX-2 and regulating neutrophils.Colchicine works on white blood
cells, especially granulocytes, by inhibiting tubulin and microtubule
polymers that interfere with the function of inflammation and
migration. Colchicine also works directly on inhibiting the formation
of inflammation by inhibiting the activation of P2X2/P2X7. 9,11,15
This patientwas immunosuppressive related to HIV infection,
thus he required hospitalization and further examination of the
etiology of pericarditis. He was given 600mg ibuprofen therapy
every 8 hours orally and colchicine 0,5mg daily orally for acute
pericarditis. The etiologies of pericarditis can be divided into
infectious and non-infectious cause. Infections that can cause
pericarditis include bacterial, fungal, parasitic or viral infections.
Non-infectious causes include autoimmune, malignancy, metabolic,
drug and trauma. Viral infections are also termed idiopathic due to
the difficulty in determining the exact pathogen.10
There was no sign of infection other than HIV in this patient, no
sign of autoimmune disease, trauma, use of causative drugs,
malignancy, nor metabolic causes. He responded well to treatment
with ibuprofen and colchicine, so the most likely cause of his acute
pericarditis is of viral origin. Most patients with acute pericarditis,
especially those with idiopathic or viral causes, have a good
prognosis. Cardiac tamponade occurs mainly in patients with
specific causes such as malignancy, tuberculosis or bacterial
infection. Constrictive pericarditis occurs in about 1% of patients
with acute viral / idiopathic pericarditis. The risk for constrictive
pericarditis is divided into low risk (1%) for viral / idiopathic
pericarditis, intermediate (2-5%) for autoimmune and malignant
causes, and high risk (20-30%) for those caused by bacteria,
especially M. tuberculosis.8,9,16
10.
Summary
Acute pericarditis must be considered in an HIV/AIDS
patients presenting with typical chest pain. Hospitalization for
immunocompromised patients such as HIV/AIDS is mandatory, due
to its poor prognosis and to thoroughly search for etiology. This
patient was given ibuprofen 600mg every 8 hours and colchicine
0,5mg daily for 1 week and showed a good response. The cause of
acute pericaditis in this patient was most likely idiopathic/viral
origin.Following satisfactory improvement, he continued treatment
on outpatient basis with tapered dose of ibuprofen, colchicine, and
antiretroviral therapy.
Acknowledgment
None.
Funding
None.
Citation: Triyono EA, Fonda T. A case report an HIV patient with acute perikarditis. J Dermat Cosmetol . 2019;3(5):132‒136. DOI: 10.15406/jdc.2019.03.00130
Conflicts of interest
The authors report no conflicts of interest.
References
1. WHO. Global Health Research (GHO) data: HIV/AIDS. 2017.
2. Lind A1, Reinsch N, Neuhaus K et al. Pericardial effusion of HIV–
Infected Patients – Re of these results of a Prospective Multicenter
Cohort Study in the Era of Antiretroviral Therapy. Eur J Med Res.
2011;16(11):480–483.
3. Bammo M, Lawson ATD, Leye MM, et al. Treatment if pericarditis
in HIV–Infected Patients in a Regional Hospital in Thies (Senegal).
2018;1–4.
4. Gopal M, Bhaskaran A, Khalife WI, et al. Heart Disease in Patients
with HIV/AIDS–An Emerging Clinical Problem. Curr Cardiol Rev.
2009;5(2):149–154.
5. Nyssen A , Melon P, Garweg C , et al. Le cas clinique dumois:
Péricardite purulente chez un patient atteint de sarcoïdose pulmonaire.
Rev Med Liège. 2011;66 (7–8):411–416.
6. Djoerban Z , Djauzi S . HIV / AIDS in Indonesia. In: Siti S, Idrus A,
Aru WS, editors. Internal Medicine Teaching Volume III Ed VI .
Jakarta: Interna Publishing. 2014;887–897.
7. Awan A, T iruneh F, Wessly P, et al. Acute Pericarditis: Descriptive
Study and Etiology Determination in a Predominantly African
American Population. 2017;9:(7).e1431.
8. Task A, Members F, Adler Y, et al. 2015 ESC Guidelines for the
diagnosis and management of pericardial diseases The Task Force for
the Diagnosis and Management of Pericardial Diseases of the European
Society of Car Diology (ESC) Endorsed by: The European Association
for Cardio–Thoracic Surgery. European Heart Journal. 2015;2921–
2964.
9. Cremer PC, KumarA, Kontzias A, et al. Complicated Pericarditis.
Journal of the American College of Cardiology.2016; 68(21):2311–
2328.
Doctor NS, Shah AB, Coplan N, et al. ScienceDirect Acute
Pericarditis. Progress in Cardiovascular Diseases. 2017;59(4):349–359.
11. Imazio M, Gaita F. Acute and Recurrent Pericarditis. Cardiol Clin.
2017;35(4):505–513.
12. Hammerman H, Alker KJ, Schoen FJ, et al. Morphologic and
Functional Effects of Piroxicam on Myocardial Scar Formation After
Coronary Occlusion in Dogs. The American Journal of Cardiology.
1984;53(4):604–607.
13. Khandaker MH , Espinosa RE, Nishimura RA, et al. Pericardial
Disease: Diagnosis and Management. Mayo Clinic Proceedings.
2010;85(6):572– 593.
14. Imazio M, Bobbio M, Cecchi E, et al. Colchicine as first-choice
therapy for recurrent pericarditis: results of the CORE (COlchicine for
REcurrent pericarditis) trial. Arch Intern Med. 2005;165(17): 1987–
1991.
15. Mazaleuskayaa L , Thekena K, Gong L , et al. Pharm GKB summary:
ibuprofen pathways. Pharmacogenet Genomics. 2015;25(2):96–106.
16. Nasronudin. HIV infection. In: Askandar T, Poernomo BS, et al.
Textbook of Internal Medicine, 2nd edn . Surabaya: Airlangga
University Press. 2014;667–685.