Plena Ri
Transcript of Plena Ri
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PLENARY DISCUSSION
BLOCK OF TROPICAL MEDICINE
DISUSUN OLEH:
TUTORIAL 1
ADIL HIJRI MUHAMMAD
AINAL FADLY
AJENG TITI
ARDILA WARADUHITA
ARYANTI AMBARSARI
DINAR SANDI AJI
DONNI TEGAR PAMBUDI
ESTIANNA KHOIRUNNISA
FATIMATUZZAROH
INDAH KURNIAWATY
MICHAEL WIJAYA
MIFTAKURROHMAH
PRIBADI MUSLIM
UNIVERSITAS MUHAMMADIYAH YOGYAKARTA
2012
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KASUS PLENARY DISCUSSION
A 28 year old man had acute onset of fever, chill, nausea, vomiting, dizzy,
malaise, myalgia, and jaundice that started five days before admission to a
hospital. He also complain about his urine, less volume and looks like a tea water.
He is a farmer and reported that rats were common in his neighborhood and that
he was eposed to floodwaters one week prior to symptoms. !ast medical history
was unremarkable.
!hysical eamination
"ital sign
H# $ %&& times'minute
## $ 2& times.minute
( )ailla* $ +8, degrees celcius-! $ %&&'& mmHg
He was alert, jaundiced, lungs were clear to auscultation, hepar palpable 2 cm
below arcus costarum, gastrocnemius sign '.
-- $ & kg
(- $ %/ cm
0aboratory eamination
-lood counts showed %2&&& leukocytes'mm+. (he hematocrit was 21 and theplatelet count was 3+&&& cells'mm+. He had the following laboratory test values.
4erum creatinine $ /,5 mg'dl
4erum ureum $ %8& mg'dl
(otal bilirubin $ %% mg'dl
467( $ %/& 9'0
46!( $ %53 9'0
9rinalysis showed urine density $ %,&5&
!rotein level $ , bilirubin $ trace )*
9rine output was /&& ml in the first 25 hours
:9;4(7hat are differential diagnoses that relevant with the case= >hy=
+. >hat is the etiology of the disease and how the pathogenesis=
5. >hat is the treatment for the case=
/. >hat is the prognosis of the patient=
. >hat are complications that may arise in the patient=3. >hat are the preventions of the disease=
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A;#4
%. (he interpretations of the physical eamination and lab results
!hysical eamination
"ital sign
H# $ increase
## $ normal
( )ailla* $ increase
-! $ decrease
He was alert, means there is no neurological deficits and the disease has
not influence the central nervous system. ?aundiced, means there is
increasing of bilirubin in the blood. Hepar palpable 2 cm below arcus
costarum, means the hepar is enlarged. 6astrocnemius sign ' is very
patognomonic in leptospirosis.
-- $ & kg
(- $ %/ cm, means the -@ is normal.
0aboratory eamination
-lood counts showed %2&&& leukocytes'mm+, means the leukocytes
increase, or there is infection. (he platelet count was 3+&&& cells'mm+,
means platelet decreases.
4erum creatinine $ /,5 mg'dl )decrease*4erum ureum $ %8& mg'dl )increase*
(otal bilirubin $ %% mg'dl, means increase )normal &,2/ %,&*
467( $ %/& 9'0, means increase )normal B2%*
46!( $ %53 9'0, means increase )normal B2+*
9rinalysis showed urine density $ %,&5& )increase*
!rotein level $ , bilirubin $ trace )* )increase*
9rine output was /&& ml in the first 25 hours )decrease*
t means that there is disturbance of hepar and renal functions. Also there
is infection in the body.
(his picture below shows the stage of leptospirosis considering the time
and it determine the clinical manifestations too. t can help us to
establishing diagnoses from the eamination based on the time scale.
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2. Cifferential diagnoses from anamnesis and physical eaminations$
a. nfluenza$fever, chill, malaise, myalgia,dizzy. n influenza, there is no
specific'particular muscle pain )myalgia*. -esides that, the fever is
usually shorter on duration.
b. Hepatitis viral $ fever, jaundice, hepatomegali. 7( !( increased, urine
can be darker because of increasing in urobilin.
c. @alaria$ fever,chill, malaise, myalgia, dizzy, jaundice, hepatomegaly.
n malaria, there is intermitten fever, and history of travelling to
endemic area.d. 0eptospira$ same as malaria gastrocnemius pain
+. ;tiology and pathogenesis
0eptospires enter the host through abrasions in the skin or through intact
mucous membranes, especially the conjunctiva and the lining of the oroD
and nasopharyn. Crinking of contaminated water may introduce
leptospires through the mouth, throat, or esophagus. After entry of the
organisms, leptospiremia develops, with subseEuent spread to all organs.
@ultiplication takes place in blood and in tissues, and leptospires can beisolated from blood and cerebrospinal fluid )F4G* during the first 5%&
days of illness. F4G eamination during this period documents pleocytosis
in the majority of instances, but only a minority of patients develop
symptoms and signs of meningitis at this point. All forms of leptospires
can damage the wall of small blood vessels this damage leads to vasculitis
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with leakage and etravasation of cells, including hemorrhages. (he most
important known pathogenic properties of leptospires are adhesion to cell
surfaces and cellular toicity.
Although leptospires mainly infect the kidneys and liver, any organ may
be affected. n the kidney, leptospires migrate to the interstitium, renaltubules, and tubular lumen, causing interstitial nephritis and tubular
necrosis. Hypovolemia due to dehydration or altered capillary
permeability may contribute to the development of renal failure. n the
liver, centrilobular necrosis with proliferation of Iupffer cells may be
found. However, severe hepatocellular necrosis is not a feature of
leptospirosis. !ulmonary involvement is the result of hemorrhage and not
of inflammation. nvasion of skeletal muscle by leptospires results in
swelling, vacuolation of the myofibrils, and focal necrosis. n severe
leptospirosis, vasculitis may ultimately impair the microcirculation and
increase capillary permeability, resulting in fluid leakage and
hypovolemia.>hen antibodies are formed, leptospires are eliminated from all sites in
the host ecept the eye, the proimal renal tubules, and perhaps the brain,
where they may persist for weeks or months. (he persistence of
leptospires in the aEueous humor occasionally causes chronic or recurrent
uveitis. (he systemic immune response is effective in eliminating the
organism but may also produce symptomatic inflammatory reactions. A
rise in antibody titer coincides with the development of meningitis this
association suggests that an immunologic mechanism is responsible.
5. (reatment and @anagement for the patient
(ough having jaundice, but other clinical symptoms of him showed us that
this patient still in the mi! "#$m #" %&'#(&i$#(i(. Hence, we offer these
antibiotics doycycline, ampicillin or amoicillin. Among these three, we
would like to give him doycycline. t can be taken twice a day only )the
other two taken four times a day* so we epect that the patient would get
easier way also more pursuance to have it. -eside, doycycline could be
taken with empty or full stomach.
(he dosage is 2%&& mg !7 and be administered for 3 days. (he patient
shouldnJt have it with antacid or iron product. >e should tell the patient
that he may have these as adverse effect$ dizziness, vertigo, nausea andeven vomit, so we suggest him to rest.
7ther symptoms such renal dysfunction will be back to normal when the
microbes killed. >e advise patient to take more drink in order to avoid
dehydration. 0ater, we can give him and people around the neighborhood
chemoprophylais because of their high population of rat to prevent them
from leptospirosis.
n easy way, this is the resume of the treatments and chemoprophylais for
leptospirosis
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/. !rognoses
@ost patients with leptospirosis recover. @ortality rates are highest among
patients who are elderly and those who have >eilKs syndrome.
0eptospirosis during pregnancy is associated with high rates of fetal
mortality. 0ongDterm followDup of patients with renal failure and hepatic
dysfunction has documented good recovery of renal and hepatic function.
. Fomplications
4evere 0eptospirosis )>eilKs 4yndrome*
>eilKs syndrome, the most severe form of leptospirosis and also the
complication of leptospirosis, is characterized by jaundice, renal
dysfunction, and hemorrhagic diathesis by pulmonary involvement in
many cases and by mortality rates of /%/. n ;urope, this syndrome is
freEuently but not eclusively associated with infection due to serovar
cterohaemorrhagiae'Fopenhageni. (he onset of illness is no different
from that of less severe leptospirosis however, after 51 days, jaundice as
well as renal and vascular dysfunction generally develop. Although some
degree of defervescence may be noted after the first week of illness, abiphasic disease pattern like that seen in anicteric leptospirosis is lacking.
(he jaundice of >eilKs syndrome, which can be profound and give an
orange cast to the skin, is usually not associated with severe hepatic
necrosis. Ceath is rarely due to liver failure. Hepatomegaly and tenderness
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in the right upper Euadrant are usually detected. 4plenomegaly is found in
2& of cases.
#enal failure may develop, often during the second week of illness.
Hypovolemia and decreased renal perfusion contribute to the development
of acute tubular necrosis with oliguria or anuria. Cialysis is sometimes
reEuired, although a fair number of cases can be managed without dialysis.
#enal function may be completely regained.
!ulmonary involvement occurs freEuently in some clusters of cases, it is a
major manifestation, resulting in cough, dyspnea, chest pain, and bloodD
stained sputum and sometimes in hemoptysis or even respiratory failure.
Hemorrhagic manifestations are seen in >eilKs syndrome$ epistais,
petechiae, purpura, and ecchymoses are found commonly, while severe
gastrointestinal bleeding and adrenal or subarachnoid hemorrhage are
detected rarely.#habdomyolysis, hemolysis, myocarditis, pericarditis, congestive heart
failure, cardiogenic shock, adult respiratory distress syndrome, necrotizing
pancreatitis, and multiorgan failure have all been described during severe
leptospirosis.
3. (he preventions$
a. Ieep clean the environment especially in stall, farm, swimming pool,
and houseb. mmunization for the high risk occupation for eample farmer or labor
c. mmunization for the animals, pets, but the successful rate depends on
antigenic potential that belongs to vaccines.
d. Avoid any skin damage or torture because it can be the port dJentry
)entrance* of the spirochaeta )leptospira* to get inside the body.
--076#A!HL
%. HarrisonJs !rinciple of nternal @edicine
2. -uku Ajar lmu !enyakit Calam GI9
+. @odul -lock of (ropical @edicine
5. IatzungJs -asic of !harmacology