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APPENDICITIS ACUTA
Counsellor :
Presented by :
DEPARTMENT OF PEDIATRIC
FACULTY OF MEDICINE MARANATHA CHRISTIAN UNIVERSITY
IMMANUEL HOSPITAL - MARANATHA TEACHING HOSPITAL
BANDUNG
2005
I. PATIENT IDENTITY
Father :
Name : Mr. Iwan Raharja Age : 48 years old
Education : Senior High School
Occupation : Entrepreneur
Salary : Rp.-
Address : Jl Sadang no. 16 RT/RW : 1/3
Kelurahan Margahayu-Kecamatan Margahayu
Bandung
Mother :
Name : Mrs. Siti Fauziah Age : 44 years old
Education : Senior High School
Occupation : Entrepreneur
Salary : Rp. -
Address : Jl Sadang no. 16 RT/RW : 1/3
Kelurahan Margahayu-Kecamatan Margahayu
Bandung
II. ANAMNESIS
Teeth
First eruption : 6 month. Now : complete permanent
teeth
Family Members
Immunizations
Past Illness
Family History
1. General appearance
2. Vital signs
3. Anthropometric
4. Systematic examinations
4.4 Thorax :
Lungs :
Inspection : shape and movement symmetric between right and left,
no retraction, no intercostals widening
Palpation : vocal fremitus normal - equal between right and left,
no intercostals widening
Percussion : sonor – equal between right and left and not found dullness
Auscultation : vocal resonance normal – equal between right and left,
vesicular breath sounds positive without ronchi and
wheezing
Heart :
Inspection : ictus cordis wasn’t seen
Palpation : ictus cordis was palpable at ICS 5 linea midclavicularis
sinistra, no thrill
Percussion : border on top : ICS 2 linea parasternalis sinistra
border on left : ICS 5 linea midclavicularis sinistra
border on right : ICS 4 linea sternalis dextra
Auscultation : regular heart sounds, no murmur
4.5 Abdomen :
Inspection : dome-shape, no darm contour or darm steifung
Palpation : soepel; liver 3 cm BAC 2 cm BPX spleen and ren
unpalpable; no abdominal tenderness
Percussion : tympani, traube’s space : tympani
Auscultation : bowl sound positive normal with frequency 2 – 4 x per
minutes
Blood :
Sysmex :??????????????
Ht ???? 39 29 26 26 37 – 47 gr/dl
Leko 20,000 - - 5500 - 5000 – 10000/mm3
15/9/05 Normal
BT 1' 45" 1 – 3 minutes
CT 8' 30" 5 – 11 minutes
Serologic :
7 years and 6 months old boy, with 19 kg body weight, nutritional status
Protein and Energy Malnutrition Moderate, came to Immanuel Hospital on 14 th
September 2005 with febris as chief complain.
Febris suddenly high [39 oC] and continuous, happened at night. Rigoris
(+) Febris convulsion (-), myalgia (+), cephalgia (+), petechiae (+). His Lips had
dry and bleeding,Epistaksis (+), trauma on nose (-), vomit & nausea (+), history
of otitis media denied, history of URTI denied. Dyspnea (-), cough (-).
Past history : -
Urinate : no hemorrhage
Defecate : no bleeding
Medical effort :
To the doctor on the second day of fever, gave drugs for fever and cold but
didn’t improved.
From physical examination:
Vital sign :
Pulse : 110 X per minutes / regular / strong /equal
Temperature : axiller, 37 oC
Respiration : type abdominothoracal / 28 X per minutes
Blood pressure : 110/80 mmHg.
Rumple leede test : positive
Systematic examination :
Head :
Eyes : hyperemic conjunctiva +/+
Ear, nose & throat : epistaksis positive, tonsil normal/no hyperemic
Mouth : wet mouth mucosa, dry lips mucosa and bleeding,
no
gums bleeding, coated tongue negative
Neck : no enlargement palpable of lymph node
Thorax : Shape & movement symmetric between left & right
Lung : VBS +/+, Rh -/-, Wh -/-
Heart : regular heart sounds, no murmur
Abdomen : flat-shape, soepel, no abdominal tenderness,
liver 3 cm under BAC 2 cm BPX,spleen no palpable, bowl sound
(+) normal
Extremities : petechiae positive both upper and lower extremities
Laboratory :
Blood :
Sysmex : ??????????????
Ht ???? 39 29 26 26 37 – 47 gr/dl
Leko 20,000 - - 5500 - 5000 – 10000/mm3
15/9/05 Normal
BT 1' 45" 1 – 3 minutes
CT 8' 30" 5 – 11 minutes
Serologic :
15/9/05 – Denque Blot Result
Anti dengue IgM Negative
Anti dengue IgG Positive
VI. Diagnose
1. Roentgen Thorax
2. Virus isolation
3. Widal/Gall Culture
4. Hb, Ht, Leukocyt, Tc, interval 4 hours
5. Diff count
6. Clotting time, Bleeding time, Clot retraction
- Non Medicamentose :
1. O2 1 – 2 L/min, up to 2 – 3 L/min
2. Fluid :
- Ringer Asetat for 20 gtt/min [14/9/05] change
- Ringer Laktat 500 cc + Adona [50 mg/bottle] 15 gtt/ Mnt
3. Transfusion :
1. FFP [Fresh Frozen Plasma]
2. TC [Trombocyte Concentrate]
3. FWB [ Fresh Whole Blood]
4. Diet :
1. D II [15/9/05] 2000 kalori/day
- Medicamentose :
1. Kalmoxillin 3 x 1/3 vial
2. Vitacimin 3 x 1 tab
3. Dapyrin 3 x 2 Cth
IX. Prognosis
INTRODUCTION
Dengue is an acute mosquito-transmitted viral disease characterized by fever, headache, muscle
and joint pain, rash, nausea and vomiting. Some infections result in dengue haemorrhagic fever
(DHF), a syndrome that in its most severe form can threaten the patient’s life, primarily through
increased vascular permeability and shock. The case fatality in patients with dengue shock
syndrome can be as high as 44%.[1]
EPIDEMIOLOGY
Epidemics of an illness compatible with DF (dengue fever) were first reported in medical literature
in 1779 in Batavia (present-day Jakarta) and in 1780 in Philadelphia. Since then, epidemics have
been reported in Calcutta (1824, 1853, 1871 and 1905), the West Indies (1827), Hong Kong
(1901), Greece (1927-1928), Australia (1925-1926, 1942), the United States (1922), and Japan
(1942-1945).2
Dengue is predominant in tropical areas mostly in South-east Asia, Africa and Southern parts of
the US (Fig. 1). The first large epidemic of DHF (dengue haemorrhagic fever) occurred in Cuba in
1981 with 24,000 cases of DHF and 10,000 cases of DSS (dengue shock syndrome). In 1986
and 1987 massive outbreaks of dengue were reported in Brazil. In 1988, an epidemic of DF was
reported at 1700m above sea level in Guerrero State, Mexico3 and in 1990 almost one-fourth of
3,00,000 people living in lquitos, Peru contracted DF.4
TRANSMISSION
The known natural hosts for dengue viruses are man, lower primates, and mosquitoes. The
arthropod vectors are members of the genus Aedes that thrive both in urban and rural areas. The
predominant species implicated in disease transmission are A. aegypti and A. albopictus.
Aedes aegypti, considered the most effective vector, originated in the forests of Africa and is
found in Between 30 degrees north and 20 degrees south latitude.[11-14] The female mosquito
feeds during the daytime, with peak activity in the mornings and late afternoons. After feeding on
a viraemic individual, the mosquito may transmit the virus directly by change of host, or after 8 to
10 days during the time the virus multiplies in the salivary glands. The infected mosquito then
remains capable of transmission for its entire life. Transovarian transmission of dengue viruses
has been documented and A. aegypti eggs are highly resistant to desiccation and can survive for
extended periods.
Aedes albopictus is indigenous to Southeast Asia, feeds during the day, and has been shown to
have a higher biting frequency than A. aegypti. Recently, it has been introduced into Nigeria,
Europe, and the United States, apparently by shipments of used automobile tires. In the US
Aedes albopictus has spread as far north as Chicago. With the spread of adaptable cold-resistant
strains, the chances for a major outbreak in Europe have increased.
THE VIRUS
Dengue viruses are members of the family Flaviviridae, which include the Japanese encephalitis
virus and the yellow fever virus. Four dengue virus serotypes 1, 2, 3 and 4 and various biotypes
can be differentiated. The four serotypes are closely related antigenically.
Infection with one serotype provides life-long immunity to that virus but not to the others.
Mature Dengue virus consists of a single stranded ribonucleic acid genome (ssRNA), which has a
positive polarity. The genome is surrounded by an icosahedral nucleocapsid with a diameter of 30
nm. The nucleocapsid is covered by a lipid envelope of 10 nm thickness derived from host cell
membranes and contains the envelope and membrane proteins.
The viral genome is 11kb. The 5’end of the RNA has a type I cap structure but lacks a poly A tail
at the 3’ end. It contains a single open reading frame of about 10,000 nucleotides encoding three
structural and seven nonstructural proteins. The proteins are synthesized as a polyprotein of
about 3000 amino acids that is processed cotranslationally and posttranslationally by viral and
host proteases.
The structural proteins include a capsid protein rich in arginine and lysine residues and a
nonglycosylated prM protein. The major structural envelope protein is involved in the main
biologic functions of the virus particle such as cell tropism, acid catalyzed membrane fusion and
the induction of haemagglutination-inhibiting, neutralizing, and protective antibodies.
NS1, a glycoprotein is detected in high titers in patients with secondary dengue infections but its
function is unknown.
NS2 region, codes for two proteins (NS2A and NS2B), which are thought to be implicated in
polyprotein processing.
NS3 is the viral proteinase that functions that functions in the cytosol.
NS4 region codes for two small hydrophobic proteins that seem to be involved in the
establishment of the membrane bound RNA replication complex.
NS5 codes for a protein with a molecular weight of 105,000 and is the most conserved flavivirus
protein. This protein is believed to be the virus encoded RNA dependent RNA polymerase.
CLINICAL FEATURES
The clinical features of dengue virus infection vary from an asymptomatic infection to a febrile flu
like infection (DF-dengue fever) to more severe form like DHF (dengue haemorrhagic fever),
which can lead to DSS (dengue shock syndrome). The clinical variability is poorly understood and
seems to be related to the age, sex and the immunologic and nutritional status of the patient.
DHF is most likely to develop in immune-competent, well-nourihed girls between the ages of 7
and 12 years. DHF is most common in children between ages 5 and 15 years.
The fever in severe cases can rise up to 39 degrees Celsius or higher. It persists for 5 to 6 days.
Fever is characteristically biphasic and returns to almost normal in the middle of the febrile period
giving rise to the saddleback temperature chart. It reaches its highest level during the last 24
hours before abatement. Symptoms include headache, usually frontal, and retroorbital pain,
particularly when pressure is applied to the eyes. ("Fire is coming out of my eyes"). Arthralgias,
myalgias and a maculopapular rash may appear at the onset. Some patients report severe
backache (back-break fever), sore throat, or abdominal pain, which can be severe enough to be
confused with appendicitis. The febrile period usually lasts up to 6 days during which time the
rash may become diffusely erythematous with clear areas scattered in between, the so-called
"islands of white in sea of red". These patients are lethargic with accompanying anorexia and
nausea. Hepatomegaly can be present although splenomegaly is uncommon. Patients can have
nausea and vomiting. Thrombocytopenia is characteristic with and serum hepatic enzymes may
be elevated.
PATHOGENESIS
DHF is almost always found in individuals who had a previous experience with at least one of the
four serotypes of dengue virus. This leads to the hypothesis of heterotypic antibodies from a
previous dengue infection promoting the viral replication within the mononuclear leucocytes-the
phenomenon of antibody-dependent enhancement. Furthermore, the immunologic processes
aimed at eliminating dengue virus infected cells can result in release of histamine and substances
with vasoactive and procoagulant properties, the release of interferon-gamma, and the activation
of complement.
DHF results from an infection by a more virulent biotype of the virus or even from unfavourable
host factors such as concomitant bacterial infections. DHF is known to be more common in
Southeast Asia compared to Africa and America. Black individuals are relatively resistant to
DHF/DSS due to a speculated "resistant gene".
DIAGNOSIS
The clinical criteria for diagnosis are as follows: (1) fever; (2) haemorrhagic manifestations,
including at least a positive tourniquet test result and a major or minor bleeding phenomenon; (3)
hepatic enlargement; (4) shock (high pulse rate and narrowing of the pulse pressure to 20 mmHg
or less, or hypotension). The laboratory criteria include (5) thrombocytopenia (â 100,000/mm3),
and (6) haemoconcentration (haematocrit increase ô 20%). Thrombocytopenia with concurrent
high haematocrit levels differentiates DHF from classic DF.
Currently routine laboratory diagnosis of dengue infections depends on virus isolation or the
detection of dengue virus-specific antibodies. The isolation of viruses from clinical specimens can
be carried out in cultured mosquito cells, such as AP-61 or C6/36 cells cultures. When dengue
virus serotype-specific monoclonal antibodies are used, virus identification by indirect
immunofluorescence can be achieved within 2 weeks. The development of mosquito inoculation
techniques has not only improved the sensitivity but also reduced the time required for virus
isolation and identification. Parenteral inoculation of adult. A. albopictus yields results in 7 days.
Virus isolation by intracerebral inoculation of Toxorhychitis splendens mosquito or its fourth instar
larvae can even be achieved within 2 to 5 days.
The serologic identification of the various types of dengue virus infection is complicated by the
occurrence of cross-reactive antibodies to antigenic determinants shared by all four dengue
viruses and other members of the flavivirus family. The commonly used serologic test is the
haemagglutination inhibition test. In a primary infection dengue haemagglutination inhibition
antibody titer is generally less than 1:20 in a sample collected within the first 4 days after the
onset of symptoms. In the convalescent phase sample (collected 1 to 4 weeks after the onset of
symptoms) a fourfold or greater rise in antibody titer is detected, with antibody titer â 1:1280.
Recently commercial kits for the detection of specific IgG as well as IgM antibodies have become
available. They are based on a dot enzyme assay or a nitrocellulose membrane-based capture
format, respectively, and should be suitable for field research.
An alternative to virus isolation is the detection of viral RNA by reverse transcription polymerase
chain reaction. Reverse transcription polymerase chain reaction is a highly sensitive technique of
particular value in the early diagnosis of dengue infection, but at present is only available in
research settings.
TREATMENT
Patients with DF require rest, oral fluids to compensate for losses via diarrhoea or vomiting,
analgesics, and antipyretics for high fever (acetaminophen) but not aspirin, so that platelet
function will not be impaired. Steroids in DSS are not helpful. With the earliest suspicion of
threatened severe illness, an intravenous line should be placed so that fluids can be provided.
Monitoring of blood pressure, haematocrit, platelet count, haemorrhagic manifestations, urinary
output, and level of consciousness is important. Plasma leakage in DHF is very rapid and the
haematocrit may continue to rise even while intravenous fluids are being administered; however,
the "leaky capillary" period is short and intravenous fluids are usually required for only 1-2 days.
There is great variability from patient to patient, and the physician must adjust treatment using
serial haematocrit, blood pressure, and urinary output data. Insufficient volume replacement will
allow worsening shock, acidosis, and disseminated intravascular coagulation, while fluid overload
will produce massive effusions, respiratory compromise, and congestive heart failure. Because
patients have loss of plasma (through increased vascular permeability into the serous spaces)
they must be given isotonic solutions and plasma expanders, such as Ringer’s acetate or
Ringer’s lactate, plasma protein fraction, and Dextran. The recommended amount of total fluid
replacement in 24 h is approximately the volume required for maintenance, plus replacement of
5% of bodyweight deficit, but this volume is not administered uniformly throughout the 24 h. A
bolus of 10-20 ml of an isotonic solution per kg bodyweight is given in case of shock, and
repeated every 30 min until circulation improves and urinary output is adequate. Vital signs
should be measured every 30-60 min and haematocrit every 2-4 h, then less frequently as the
patient’s condition stabilizes.
Placement of a central-venous-pressure line is hazardous in patients with haemorrhagic
tendencies but may be necessary, especially when more than 60 ml/kg of fluids has been given
without improvement. An expert in a special care area should insert the line. It is used to estimate
filling pressures and to guide further intravenous fluid administration. An arterial line will help in
the assessment of arterial blood gases, acidbase status, coagulation profiles, and electrolytes in
the haemodynamically unstable patient, helping to identify early respiratory compromise.
Monitoring should be continued for at least a day after defervescence. Once the patient begins to
recover, extravasated fluid is rapidly reabsorbed, causing a drop in haematocrit. Before
discharge, the patient should meet the following criteria: absence of fever for 24 h (without
antipyretics) and a return of appetite; improvement in the clinical picture; hospital care for at least
3 days after recovery from shock; no respiratory distress from pleural effusion or ascites; stable
haematocrit; and platelet count greater than 50,000/ml76 Because convalescent-phase
diagnostic samples are often difficult to obtain, a second blood sample should always be taken on
the day of discharge.
Vaccine development
An effective vaccine will have to be tetravalent because pre-existing heterotypic dengue antibody
is a risk factor for DHF. Candidate attenuated vaccine viruses have been evaluated in phase I and
II trials in Thailand, and a tetravalent formulation is currently undergoing repeat phase I and II
trials. Advances have also been made with second generation recombinant dengue vaccines. A
cDNA infectious clone of the DEN-2 PDK-53 vaccine candidate virus has been constructed, and
work is in progress to construct chimeric viruses by inserting the capsid, premembrane, and
envelope genes of DEN 1, 3 and 4 into the DEN-2 PDK-53 backbone. These recombinants,
through genetic manipulation, may be made to replicate faster, be more immunogenic and safer.
However, an effective, safe and affordable vaccine is not an immediate prospect.
Vector control
At present dengue transmission can only be reduced by mosquito control. The task might seem a
simple matter of the treatment or elimination of infested containers. Source (container) reduction
campaigns have been very successful but they are hard to sustain, mainly because they are
labour intensive, require discipline and diligence, and are plagued by diminishing returns.
Emphasis has shifted first to organochloride insecticides and later to organophosphorus
larvicides, and aerosols targeted at adult mosquitoes and mostly applied outdoors as ultra-low
volume (ULV) concentrates. The aerosols are principally recommended for emergency control
during epidemic transmission as part of an integrated vector elimination effort, including
environmental management, source reduction and larvicides. Nevertheless, their routine use as
the principal response even before and after dengue epidemics has become widespread. This is
regrettable, because ULV aerosols have very limited surprisingly, therefore, there is no well-
documented example of interruption of a dengue epidemic by outdoor ULV treatments. Indoor
treatments are probably much more effective but are very labour-intensive and intrusive.
Dengue Haemorrhagic Fever Grade III & IV
15/9/05 Patient still get gum and lips bleeding - Therapy : continue
06.30 and somnolent - Infus RL 12 gtt/ mnt
- whoole blood (-)
- Tc (-)
- FFP transfusion 1 Bag
- Konsul to dr Tisna
- Dapyrin 3 x 2 tea
spoons
15/9/05 Patient still had fever - Transfusion :
12:30 Thrombosit 10.000 - FFP 3 bags and Tc 4
Bags
- Infus RL500cc + Adona
drip 50 mg for 15
gtt/mnt
Therapy
- Dapyrin 3 x 2 tea
spoons
- Vitacimin 3 x 1 tab
- Diet DI
-Observation BP, N,R, T
and manifestation
bleeding
15/9/05 Lab results reported to dr.Tisna, advice :
- Infus RL500cc + Adona
15.25 BP= 80/60 mmHg drip 50 mg release until
N= 100x/Mnt BP normal
R= 24x/mnt - Next infus RL + Adona
T= 380C 50
mg for 60 cc/hours
- 6 hours pos tranfusi
Check
Hb, Ht , Tc
Observation
15/9/05 Lab results reported to dr.Tisna post - Transfusion FFP 4 bags
23.30 transfusion, advice - Kalmethazone 3 x 2 mg
BP = 100/59 mmHg - RL release until BP
Tc = 8000 Stable
Consciousness = Somnolent - Check again after 4
Bleeding from lips still continuous hours
Hb, Ht, Tc
15/9/05 Patient had febris - Kalmetason 3 x 2 mg
23.35 Patient had bleeding continuous - RL release untul BP
stable
- Cool Compress
- more intake fluid
15/9/05 His familly are motivated, patient to enter ICU, but his familly
23.45 denied