TUTORIAL KLINIK HIV – REZA

1. Apa saja differential diagnosis pasien dengan nyeri perut kanan atas?
Visceral pain occurs when hollow abdominal organs such as the intestine or
biliary tree contract unusually forcefully or are distended or stretched. Solid organs
such as the liver can also become painful when their capsules are stretched. Visceral
pain may be diffcult to localize. It is typically palpable near the midline at levels that
vary according to the structure involved, as illustrated on the next page. Ischemia also
stimulates visceral pain fbers.
Parietal pain originates from inflammation in the parietal peritoneum. It is a
steady, aching pain that is usually more severe than visceral pain and more precisely
localized over the involved structure. It is typically aggravated by movement or
coughing. Patients with this type of pain usually prefer to lie still.
Referred pain is felt in more distant sites, which are innervated at
approximately the same spinal levels as the disordered structures. Referred pain often
develops as the initial pain becomes more intense and thus seems to radiate or travel
from the initial site. It may be felt superfcially or deeply but is usually localized.
 A specific cause may be difficult to find, but the nature and location of a pain-
provoking lesion can usually be determined from the clinical description. Two types
of nerve fibers transmit painful stimuli in the abdomen. In skin and muscle, A fibers
mediate sharp localized pain; and C fibers from viscera, peritoneum, and muscle
transmit poorly localized, dull pain. These afferent fibers have cell bodies in the
dorsal root ganglia, and some axons cross the midline and ascend to the medulla,
midbrain, and thalamus. Pain is perceived in the cortex of the postcentral gyrus, which
can receive impulses arising from both sides of the body.
Visceral pain tends to be experienced in the dermatome from which the
affected organ receives innervation. Painful stimuli originating in the liver, pancreas,
biliary tree, stomach, or upper bowel are felt in the epigastrium; pain from the distal
small bowel, cecum, appendix, or proximal colon is felt at the umbilicus; and pain
from the distal large bowel, urinary tract, or pelvic organs is usually suprapubic.
When pain is referred to remote areas supplied by the same neurologic segment as the
diseased organ, the phenomenon usually means an increased intensity of the
provoking stimuli. Parietal pain impulses travel in C fibers of nerves corresponding to
dermatomes T6–L1; such pain tends to be more localized and intense than visceral
pain. (Nelson)

Gastrointestinal (GI) manifestations of HIV disease include diarrhea,

dysphagia and odynophagia, nausea, vomiting, weight loss, abdominal pain, anorectal
disease, jaundice and hepatomegaly, GI bleeding, interactions of HIV and
hepatotropic viruses, and GI tumors (Kaposi's sarcoma and non-Hodgkin's
lymphoma). The evaluation of specific gastrointestinal complaints must be based on
an assessment of the degree of immunosuppression. Progressive immunocompromise
 is associated with increasing prevalence of GI symptoms(3) and remains the common
endpoint for most individuals infected with HIV.

he patient's history is important in identifying the origin of abdominal pain. In general, the
associated symptoms and signs should help identify the particular organ involved. The
specific work-up is similar to that for a patient without HIV infection. An exception is that
abdominal sonography and computed tomography scanning are useful early in the assessment
of abdominal pain in HIV-infected patients and may highlight regions of disease not usually
suspected clinically.(87) Unsuspected findings have often included thickening of the
gallbladder or colonic wall, focal hepatic lesions, biliary ductal dilatation, pancreatic
infiltration, adenopathy, and peritoneal thickening. Abnormal bowel wall thickening in
patients with HIV infection should be pursued with endoscopic biopsies. Rockey et al.
reported a specific diagnosis in 7 of 15 patients (64%), including CMV, lymphoma, and
MAC.(88)

The quality and duration of the abdominal pain may implicate specific diseases. In general,
perforation results most often from CMV infection and occurs frequently in the distal small
bowel or colon. Lymphoma or KS may also perforate, either spontaneously if the tumor is
bulky or due to tumor lysis following chemotherapy or radiation. Obstruction is most likely
to develop from an intestinal neoplasm but may also develop from an inflammatory mass or
stricture. Intussusception may be an unusual form of lymphomatous obstruction. Infectious
enteritis may lead to dull, intermittent abdominal pain in the absence of obstruction or
perforation. This is particularly true of infection by Cryptosporidium and Mycobacterium
avium-intracellulare complex (MAC) but may also occur in infections from other protozoa, as
well as from enteric bacteria including Salmonella, Shigella, and Campylobacter.

Infectious or nonspecific peritonitis in the absence of bowel perforation is increasingly

recognized. Infectious etiologies may include histoplasmosis,(89) tuberculosis,(82)
MAC, Vibrio vulnificus,(90) toxoplasmosis,(91) and Cryptococcus,(92) in addition to
lymphoma.(93) High-protein ascites of uncertain etiology has also been reported and may
necessitate laparoscopy to identify a cause.(92)

Pancreatitis can cause abdominal pain in patients with advanced HIV disease and may arise
for a variety of reasons. Affected patients usually have elevations of amylase and lipase,
unless acute inflammation occurs in a patient with pre-existing underlying chronic
pancreatitis. Amylase elevations in the absence of pancreatic disease may indicate
macroamylasemia, which occurs in patients with and without HIV disease.(94) Medications
are the most common cause of pancreatitis in HIV, particularly pentamidine,(95,96,97)
dideoxyinosine (ddI),(98,99) and trimethoprim-sulfamethoxazole.(100) Pentamidine-induced
pancreatitis may develop following either inhaled(96) or parenteral administration,(97) and it
is associated with the typical clinical features of pancreatitis.(95) The clinical course may be
mild, severe, or fatal; it is often accompanied by dysregulation of glucose
metabolism.(101,102,95)

Potential infectious causes of pancreatitis in HIV disease are multiple. Most common is
CMV,(103) followed by M. tuberculosis,(104) M. avium,(105) Cryptococcus,(106) and
herpes simplex (HSV).(107) Infectious pancreatitis may not always be clinically obvious; it
should be suspected in any patient with abdominal pain and elevated amylase.(103) In CMV-
induced pancreatitis, inclusions may be demonstrable either in ductal epithelium or acinar
cells. Fine-needle aspiration may be able to uncover these findings antemortem in patients in
whom this infection is suspected. Pancreatic infiltration by lymphoma(108) and KS(109)
occurs occasionally, manifested either by mass effect on adjacent duodenum or exocrine
insufficiency if the pancreatic duct is obstructed.

Table 5 defines abdominal pain in terms of the four most common pain syndromes, likely
causes, and diagnostic methods. The duration and severity of symptoms dictate the urgency
of evaluation. For example, patients with dull, insidious abdominal pain can be evaluated
with less urgency than patients who develop acute, severe abdominal pain with evidence of
peritonitis.

Treatment of Abdominal Pain

Managing abdominal pain begins with deciding if the patient requires surgery.(101) In
general, the indications for surgical intervention in HIV-infected patients are similar to those
in patients without HIV infection. Intestinal perforation or obstruction almost always requires
surgical management, despite the increased perioperative and postoperative risk for patients
with advanced HIV disease. Clinicians must submit all tissue specimens for viral and fungal
culture and for pathologic examination, and mesenteric nodes should be biopsied.(110)
Laparoscopic surgery may provide a less invasive alternative in select patients, such as those
with cholecystitis. The main goal of any surgical procedure should be the palliation of
symptoms. Prolonged anesthesia and extensive tissue resection should be avoided if possible.

The morbidity and mortality in early reports of surgical procedures in patients with advanced
HIV disease have been exceedingly high.(83,86) This is due partly to the underlying poor
health of patients with advanced HIV disease who require laparotomy; most have CMV
infection, which tends to occur in late-stage HIV disease. Complications and mortality are far
less likely in patients with asymptomatic HIV infection,(111) although the exact frequency
relative to comparable non-HIV-infected persons has not been reported.(83) The result of
clinical evaluation determines the nonsurgical management of abdominal pain. Any treatable
infection contributing to the symptoms should be managed appropriately. Symptoms due to
lymphoma or KS may respond to chemotherapy or radiation therapy. Symptomatic treatment
with analgesics may be indicated in addition to specific antibiotic or antineoplastic regimens.
HIV-related conditions and chronic opportunistic infections may improve with HAART.
(Jurnal, Gastrointestinal manifestation of HIV)
(Abdominal Pain on HIV Infection, Douglas Yoshida, 2002)
 (Acute Abdomen on HIV Infection, Intech, 2011)

2. Mengapa diberikan sukralfat dan ranitidin pada pasien ini?

Sukralfat : Sukralfat adalah suatu kompleks yang dibentuk dari sukrosa oktasulfat
dan polialuminum hidroksida. Aktivitas sukralfat sebagai anti ulkus merupakan hasil
dari pembentukan kompleks sukralfat dengan protein yang membentuk apisan
pelindung menutupi ulkus serta melindungi dari serangan asam lambung,pepsin dan
garam empedu. Percobaan laboratorium dan klinis menunjukkan bahwa sukralfat
menyembuhkan tukak dengan tiga cara :
1. Membentuk kompleks kimiawi yang terikat pada pusat ulkus sehingga merupakan
lapisan pelindung.
2. Menghambat aksi asam,pepsin dan garam empedu.
3. Menghambat difusi asam lambung menembus lapisan film sukralfat-albumin.

Penelitian menunjukkan bahwa sukralfat dapat berada dalam jangka waktu

lama dalam saluran cerna sehingga menghasilkan efek obat yang panjang. Sukralfat
sangat sedikit terabsorpsi di saluran pencemaan sehingga menghasilkan efek samping
sistemik yang minimal.
Ranitidin : Menghambat secara kompetitif histamin pada reseptor H2 sel-sel
parietal lambung, yang menghambat sekresi asam lambung; volume lambung dan
konsentrasi ion hidrogen berkurang. Tidak mempengaruhi sekresi pepsin, sekresi
faktor intrinsik yang distimulasi oleh penta-gastrin, atau serum gastrin.
H2 antagonis adalah inhibitor kompetitif histamin pada reseptor H2 sel parietal.
Mereka menekan sekresi asam normal (alami) oleh sel parietal dan sekresi
asam yang dirangsang makan. Mereka melakukannya dengan dua
mekanisme: histamin yang dilepaskan oleh sel-sel ECL dalam perut diblokir dari
pengikatan dengan reseptor H2 sel parietal yang merangsang sekresi asam, dan zat
lain yang meningkatkan sekresi asam (seperti gastrin dan asetilkolin) efek yang
dimiliki pada sel parietal dikurangi ketika reseptor H2 diblokir.
Penghambatan kompetitif histamin pada H2-reseptor sel parietal lambung,
yang menghambat sekresi asam lambung, Volume lambung, dan konsentrasi ion
hidrogen berkurang. Tidak mempengaruhi sekresi pepsin, faktor intrinsik stimulasi
sekresi pentagastrin, atau serum gastrin

3. Batuk pilek berasal dari TB atau infeksi lain?

Anamnesis
What are the previous illnesses of the patient?
Someone who has suffered from a PCP once is at a higher risk of having another
one. A patient with hyperlipidaemia and carotid stenosis might have coronary heart
disease.
What medication does the patient take?
Taking cotrimoxazol regularly makes a PCP unlikely, and the risk of bacterial
pneumonia may also be reduced (Beck 2001). In the case of PCP prophylaxis with
Pentamidine inhalation, however, atypical, often apically pronounced manifestations
of a PCP are to be expected.
Has the patient recently started HAART?
Particularly HAART can induce pulmonary problems:
During a newly begun course of treatment with abacavir, asthma could also be due
to hypersensitivity. Dyspnea (13 %), cough (27 %) and pharyngitis (13 %) are
common symptoms (Keiser 2003). Some patients even develop pulmonary infiltrates.
T-20 seems to increase the risk of bacterial pneumonia, at least among smokers.
Dyspnea and tachypnea are also seen in lactic acidosis secondary to nuke therapy.
In addition, pulmonary symptoms after institution of HAART might result from the
Immune Reconstitution and Inflammatory Syndrome (IRIS). The list of etiologies
includes a number of infective and non-infective causes (Grubb 2006). Low CD4+
T-cell count and high viral load are risk factors. In a retrospective analysis, IRIS
was seen in 30 % of patients with TB, atypical mycobacteriosis and cryptococcosis
(Shelburn 2005).
Does the patient smoke?
Although smoking is more harmful to HIV-positive than to HIV-negative persons,
it is still more common among HIV-positives (Royce 1990). All HIV-associated
and HIV-independent pulmonary diseases are more common in smokers than in
non-smokers. This starts with bacterial pneumonia and PCP, but also applies to
asthma, COPD and pulmonary carcinomas (Hirschtick 1996). Smoking promotes
the formation of a local immune deficit in the pulmonary compartment: it reduces
the number of alveolar CD4+ cells and the production of important proinflammatory
cytokines such as IL-1 and TNF-α (Wewers 1998). Furthermore,
smoking suppresses the phagocytosis capacity of alveolar macrophages. This effect
is more pronounced in HIV patients than in HIV-negative patients. HIV infection
itself, however, does not seem to have any direct influence on the capability for
bacterial killing (Elssner 2004).
Motivating the patient to restrict nicotine intake is thus an important medical task,
particularly in HIV consultation. Strategies which promise success and are supported
by the evidence of studies include participation in motivational groups,
nicotine substitutes and taking Buproprion, whereby interactions, particularly with
Ritonavir, should be taken into consideration.
Where does the patient come from?
Another important question is that of the travelling history and/or the origin of the
patient. There are places where disease such as histoplasmosis and coccidiomycosis
occur endemically. Histoplasmosis, for example, is more widespread in certain
parts of the USA and in Puerto Rico than PCP, while it is rare in Europe.
Tuberculosis plays a greater role among immigrants.
How did the patient become infected with HIV?
Intravenous drug users suffer more often from bacterial pneumonia or tuberculosis
(Hirschtick 1995). Pulmonary Kaposi’s sarcomas are almost exclusively found in
MSM (men who have sex with men).
What are the symptoms?
Occasionally, some valuable information can be gained above the more uniform
symptoms such as coughing and shortness of breath, which might be useful for
differentiation between PCP and bacterial pneumonia. Thus, for example, it is typical
for the onset of bacterial pneumonia to be more acute. Patients usually go to the
doctor after only 3-5 days of discomfort, whereas patients with PCP suffer from
symptoms for an average of 28 days (Kovasc 1984). PCP patients typically have
dyspnea and a non-productive cough. A large quantity of discoloured sputum is
more likely to indicate a bacterial cause or a combination of infections.
The most important question: What is the immune status?
The number of CD4+ T-cells provides an excellent indication of the individual risk
of a patient to suffer from specific opportunistic infections. More important than the
nadir is the current CD4+ T-cell count. In patients with more than 200/µl, infection
with typical opportunistic HIV-associated diseases is very unlikely. Here, as with
HIV-negative patients, one generally tends to expect more „normal“ problems like
acute bronchitis and bacterial pneumonia. However, tuberculosis should always be
considered. Although the risk of becoming infected with tuberculosis grows along
with increasing immunodeficiency, more than half of all tuberculosis infections in
HIV patients occur at a CD4+ T-cell count of above 200/µl (Lange 2004, Wood
2000).
At less than 200 CD4+ T-cells/µl, PCP and, more rarely, pneumonia/pneumonitis
with cryptococci, occurs. At this stage too, however, bacterial pneumonia is the
most common pulmonary disease overall.
Below 100 CD4+ T-cells/µl, there is an increase in the number of pulmonary Kaposi
sarcomas and toxoplasma gondii infections. At a cell count of under 50/µl,
infections with endemic fungi (histoplasma capsulatum, Coccidioides immitis),
non-endemic fungi (Aspergillus, Candida species), atypical mycobacteria and
different viruses (mostly CMV) occur. Especially in patients with advanced
immunodeficiency, it must be remembered that pulmonary illness may only represent
an
organ manifestation of a systemic infection. Rapid, invasive diagnostic procedure is
thus advisable in such patients.
(HIV and Pulmonary Disease, Sven Philips)
4. Bagaimana membedakan BRPN, TB, ISPA, batuk pilek pada anak?
5. Bagaimana memperkirakan pemberian PRC pada anak dengan anemia?
Secara umum, transfusi PRC hampir selalu diindikasikan pada kadar Hb <7,0
g/dL, terutama pada keadaan anemia akut. Transfusi juga dapat dilakukan pada kadar
Hb 7,0-10,0 g/dL, apaapabila ditemukan hipoksia atau hipoksemia yang bermakna
secara klinis dan laboratorium. Transfusi jarang dilakukan pada kadar Hb >10,0 g/dL
kecuali terdapat indikasi tertentu, seperti penyakit yang membutuhkan kapasitas
transpor oksigen lebih tinggi. Sebagai contoh, pada anak dengan anemia defisiensi
besi, transfusi pada umumnya tidak dilakukan jika tidak terdapat keluhan dan anak
dalam kondisi klinis baik. Sebaliknya, pada pasien anak yang membutuhkan transfusi
rutin, transfusi diberikan pada kadar Hb pra-tansfusi 9,0-10,0 g/dL, untuk
mempertahankan tumbuh kembang mendekati tumbuh kembang pada anak normal.1

Pada bayi prematur, transfusi PRC diindikasikan apaapabila kadar Hb <7,0

g/dL. Pada keadaan infant respiratory distress syndrome (IRDS), transfusi diberikan
pada kadar Hb <12,0 g/dL untuk bayi yang membutuhkan oksigen, atau < 10.0 g/dL
untuk bayi yang tidak membutuhkan oksigen. Pada bayi prematur dengan tanda dan
gejala anemia ringan seperti takikardia atau peningkatan berat badan yang tidak
adekuat, transfusi diberikan apaapabila kadar Hb <10,0 g/dL. Namun, apabila terjadi
tanda dan gejala anemia berat seperti apnea, hipotensi, atau asidosis, transfusi PRC
dapat diberikan pada kadar Hb <12,0 g/dL.5,6

Pada bayi aterm di bawah usia 4 bulan, transfusi diberikan apabila terdapat
manifestasi klinis anemia seperti apnea, takikardia, atau peningkatan berat badan yang
tidak adekuat apabila kadar Hb <7,0 g/dL. Transfusi PRC juga dapat diberikan pada
bayi dengan anemia perioperatif yang memiliki kadar Hb < 10.0 g/dL, atau pada
kondisi perdarahan akut yang melebihi 10% dari volume darah total yang tidak
menunjukkan respon terhadap terapi lain. Transfusi PRC juga dapat diberikan pada
pasien pasca operasi dengan tanda dan gejala anemia dan kadar Hb <10,0 g/dL, serta
pasien yang menderita penyakit kardiopulmonal berat dengan kadar Hb <12,0 g/dL.5-
7
Dosis yang digunakan untuk transfusi PRC pada anak adalah 10-15
mL/kgBB/hari apabila Hb >6,0 g/dL, sedangkan pada Hb <5,0 g/dL, transfusi PRC
dapat dilakukan dengan dosis 5 mL/kgBB dalam 1 jam pertama. Pada keadaan darurat
sisa darah yang masih ada pada kantong dihabiskan dalam 2-3 jam selanjutnya,
asalkan total darah yang diberikan tidak melebihi 10-15 mL/kgBB/hari. Namun,
apabila jumlah transfusi yang dibutuhkan hanya sedikit, dianjurkan untuk
menggunakan kantong kecil/ pediatrik. Dosis transfusi PRC pada neonatus 20
mL/kgBB, dan disarankan untuk menggunakan kantong pediatrik dengan kapasitas
±50 mL/kantong.Pada anak, pemberian PRC 4 mL/kgBB dapat meningkatkan kadar
Hb sekitar 1 g/dL. Rumus untuk menghitung kebutuhan PRC adalah [DHb (target Hb
– Hb saat ini) x berat badan x 4], sementara kebutuhan per hari adalah 10-15
kg/BB/hari. (sari pediatri)