A PERFORATED GANGRENOUS APPENDICITIS

FOLLOWING TYPHOID FEVER IN CHILD

Case Report

Presented by:
Rizka Arifani, dr.

Consultants:
Prof. Dr. Ismoedijanto, dr.,DTM&H, Sp.A(K)
Prof. Parwati Setiono, dr., M.Sc., DTM&H., Sp.A(K)
Dr. Dominicus Husada., dr, DTM&H,MCTM(TP),Sp.A(K)
Dwiyanti Puspitasari., dr.,DTM&H,MCTM(TP),Sp.A(K)
Leny Kartina, dr., Sp.A(K)
Fendy Matulatan, dr. Sp.B, Sp.BA(K)
Prof. Dr. Eddy Bagus Wasito, dr. MS., Sp.MK(K)

Department of Child Health

Faculty of Medicine Airlangga University
Dr. Soetomo Hospital Surabaya
2018
 INTRODUCTION

One of common systemic infection in children is typhoid fever which

caused by bacterium Salmonella enterica serotype typhi. There are at least 16
million new cases of typhoid fever each year, with 600,000 deaths.1 Salmonella
organisms are able to survive and multiply within the mononuclear phagocytic
cells of the lymphoid follicles, liver, and spleen. The most common sites of
secondary infection are the liver, spleen, bone marrow, gallbladder, and Peyer’s
patches of the terminal ileum.2
Salmonellas infections can be particularly challenging when they manifest
as acute abdominal problems and lead to emergency surgery. Examples of such
serious conditions are related intestinal perforation, gallbladder involvement,
salpingitis, and peritonitis. In some case, it leads to appendix or mesenteric lymph
involvement.1
An acute abdominal problem from salmonella infection can happen
because of complication such as another organ involvement or misdiagnosis
another caused of acute abdomen as a typhoid fever such as acute appendicitis.
Acute appendicitis can frequently have symptoms, commonly fever and pain in
the right lower abdominal quadrant, similar to those observed in infectious
enteritis from Salmonella typhi. Mesenteric lymphadenitis associated with
Salmonella mimics acute appendicitis and can make it difficult to establish a
timely and definitive diagnosis in children who present with right lower
abdominal pain.3 It more difficult to diagnose in child who present with general
abdominal pain, whether the cause is intestinal perforation or appendicitis or
mesenteric lymphadenitis.4
Among those difficulties, an early intervention is crucial, and mortality
rates increase as the delay between perforation and surgery lengthens. In acute
abdomen cases in which Salmonella is suspected, stool culture may help establish
the diagnosis, but it should be kept in mind that even repeat cultures are negative
in a significant number of infected patients. Definitive diagnosis usually is based
on blood culture and serologic testing, but the time delay in getting these results
can be problematic when a patient’s condition is serious. The combination of

2
USG and stool culture may help reduce the number of needless surgeries done in
cases of suspected appendicitis. However, in cases in which the diagnosis cannot
be pinned down, surgical intervention is the appropriate step to take in light of the
high morbidity and mortality rates associated with untreated appendicitis and
intestinal perforations.3
According to the explanation above, the purpose of this paper is to report
a case of typhoid fever in 6 years child with acute abdomen and got surgical
intervention in case of suspected peritonitis, focusing on the diagnosis and the
relation with acute appendicitis.

3
CASE REPORT
A 6 years old boy came to Emergency Department, referred from Haji
Hospital on November 12nd 2017 with fever more than 7 days. His parents
complained fever since 10 days before admission, sub febrile for 3 days continued
higher with high fever 2 days before admission. The fever was not decreased by
antipyretic. The patient also complained with nausea which was getting worse for
2 days before admission. There was no vomit. He had dyspepsia and a mushy
stool 2-3 times a day for 3 days before admission. The last defecation was 1 day
before admission. His appetite decreased with the dried tongue for a week before.
There was no cough, no watery nose, no odynophagia, no sign of bleeding and no
loss of body weight.
Patient was born as term baby, spontaneously in house, with 2500 grams
birth weight and 49 centimeters height, 34 centimeters head circumference from
30 years old mother, from 3rd pregnancy without any pregnancy or delivery
complication. This boy was crying soon after birth. She was healthy and did not
take any traditional herbs nor vitamins during pregnancy. Before pregnancy, his
mother also in good nutritional state and within normal range body mass index.
Her weight during pregnancy raised about 14 kg. The baby was breastfed along
with formula milk until now, the feeding process was fine. There was no history
of tuberculosis in the families.
From the physical examination, he was conscious, pulse was 101 beats per
minute, respiratory rate was 25 times per minute adequately, the axillary
temperature was 390C, and the oxygen saturation was 99%. On inspection of the
head revealed no pale, no icterus, no cyanosis. Physical examination on the neck
there were multiple lymph nodes enlargement, mobile, no pain of the nodes. The
chest showed symmetric chest wall movement. Percussion examination was sonor
in all thoracic area. Palpation revealed no tenderness on the both of thoracic area.
Auscultation sound revealed no rales in both lungs, no wheezing, no ronchi, and
the heart sounds was regular, with no splitting, no murmur and no gallop.
Abdomen was flat, no prominent veins, bowel sound was normal with
enlargement of the liver 4x4x4cm and no enlargement of spleen. Upper and lower

4
extremities have sufficient perfusion, with a capillary refill time of less than two
seconds and no cyanosis of the extremities was found.
From the history of vaccination, patient never got immunization. He was
already able to lift her head up at the age of 3 months old. From neurological
examination revealed glasgow coma scale 456, round isokor pupils with each
diameter 3 milimeters and the light reflex on her eyes was positive. Physiological
and patological reflexes were normal limit.
His anthropometric status was body weight 14.5 kg and body height 108
cm. His ideal body weight was 19 kg and his ideal body weight score was 73%.
The nutritional status was moderate malnutrition.

5
Figure 1. CDC Growth Chart of 2-20 years old boy

6
 Based on history taking, clinical manifestation and physical examination,
we assesed this patient as typhoid fever. We did laboratory test on November 12nd
2017, hemoglobin 10.5 g/dL, haematocrit 33.4%, red blood cell 4.42 x 106 /uL,
platelet count 66000/uL, white blood cell count was 5960/uL, eosinophil 1.52%,
basophil 0.9 %, neutrophil 77.3%, lymphocyte 18.9 %, monocyte 1.7 %, SGOT
161/uL, SGPT 33/uL blood glucose 108mg/dl, albumin 3,5mg/dL, BUN
13mg/dL, CS 0.57mg/dL, GFR 101, urinalisis in a normal limit, CRP 73.7mg/dl,
IgM salmonella tubex 10. We also did chest x-ray on November 12nd 2017, cor
and pulmo in a normal limit.
November 14th patient still fever, with abdominal pain in all region. Patient
has no defecation for 2 days, nausea, loss of appetite with no vomit. From
physical examination we found axillary temperature 38 oC, heart rate 124bpm,
respiratory rate 32tpm, blood pressure 90/50mmHg. We found abdominal
distended 51cm, decreased of abdominal sound. We did abdominal
decompression by opened NGT.
November 14th evening, there were hematin from NGT equal to
0,2ml/kgbw/hour. Patient looked pale, clammy extrimities, lethargia, Heart rate
126bpm, respiratory rate 32tpm, blood pressure 80/40mmHg, axillary temperature
38.5oC. Abdomen distended, decreased of abdominal sound, pain in every region
of abdomen. From laboratory test we found Hb 7.8mg/dL, platelet count
34000/uL, Haematocrit 23.3%, white blood cell count was 2320/uL, Natrium
131mg/dl, Kalium 2.5mg/dl, Cl 100mg/dl, Ca 7mg/dL, PPT 12.3 (11.3), APTT
37.6 (24.3). Electrocardiography sinus tachycardia. Blood gas analisis: pH 7.41,
Pco2 26mmHg, pO2 185mmHg, TCO2 18.5mmol/L, BEecf -6.5mmol/L, SO2c
100%, A-aDO2 75mmHg, FiO2 41%, HCO3 17.7mmol/L. Advise from ERIA
division indication moved to PICU, Advice from hematology division planed for
PRC and WB transfusion, omeprazole injection, sucralfate, thermoregulation,
ceftriaxone injection, SE correction. We assessed this patient as typhoid fever
suspicious of intestinal perforation and consulted to pediatric surgeon.

7
 November 15th patient still fever, agitated. Blood pressure 90/50mmHg,
heart rate 118bpm, respiratory rate 24tpm, axillary temperature 38oC. From BOF
we found intestinal dilatated, LLD we found multiple step ladder, no
pneumoperitoneum. Patient prepared for laparotomy exploration with TC
transfusion durante operation.
November 15th laparotomy exploration by paediatric surgeon. We found
minimal pus in pole appendix + 5 cc with fibrin, hyperemic omentum with no
walling off and adhesion, inflamed appendix, height 6 cm Ø 1,5 cm, peritoneum
fluid + 150 cc, enlargement of mesenteric lymph in appendix region sized 9-11
mm, no perforation of another hollow and solid organ. There were multiple
lymphadenopathy in mesenteric lymph in small intestine region, size <8mm no
hyperemic and pus.
November 16th patient compos mentis, has no fever, no abdominal pain.
Vital sign blood pressure 95/50mmHg, heart rate 112bpm, respiratory rate 22tpm,
axillary temperature 37.4oC. Abdomen sounds 10tpm, soepel, no bloody seep in
bandage, drain production equal to 0,1ml/kgbw/hour yellowish. From laboratory
test we found Hb 12.7mg/dL, platelet count 64000/uL, Haematocrit 36.7%, white
blood cell count was 7970/uL, Natrium 136mg/dl, Potassium 3.8mg/dl, Cl
106mg/dl, Ca 6.5mg/dL, PPT 14 (11.3), APTT 30 (24.3), SGOT 166, SGPT 38,
Alb 2.29mg/dL, BUN 6mg/dL, CS 0.37mg/dl, Glucose 119mg/dL, we assessed
this patient as typhoid fever and peritonitis et causa perforated gangrenous
appendicitis. We continued the ceftriaxone injection, albumin transfusion, and SE
correction.
November 17th patient compos mentis, has no fever, no abdominal pain.
Vital sign blood pressure 95/50mmHg, heart rate 112bpm, respiratory rate 22tpm,
axillary temperature 37.4oC. Abdomen sounds 10tpm, soepel, no bloody seep in
bandage, drain production equal to 0,03ml/kgbw/hour still yellowish. Peritoneal
dialysate culture was Staphylococcus epidermidis. Blood culture sterile. We
continued ceftriaxone injection and gave metronidazole injection.
November 20th patient compos mentis, has no fever, no abdominal pain.
Vital sign blood pressure 100/50mmHg, heart rate 110bpm, respiratory rate
23tpm, axillary temperature 37.0oC. Abdomen sounds 10tpm, soepel, no bloody

8
seep in bandage, no drain production. Pathology anatomy from the appendix
tissue: inflammation with lymphocyte and hystiocyte infiltration in submucous to
serosa without specific sign of tuberculosis infection. Pathology anatomy from
mesenteric: reactive lymphoid hyperplasia without specific sign of tuberculosis
infection. From laboratory test we found Hb 10.5mg/dL, platelet count
107000/uL, Haematocrit 32.5%, white blood cell count was 7390/uL,
procalcitonin 0.12mg/dL, Natrium 141mg/dl, Potassium 3.2mg/dl, Cl 103mg/dl,
Ca 7,8mg/dL, albumin 3.4mg/dL.
November 21st patient compos mentis, has no fever, no abdominal pain.
Normal defecation. Vital sign blood pressure 95/50mmHg, heart rate 114bpm,
respiratory rate 22tpm, axillary temperature 37.2oC. Abdomen sounds 10tpm,
soepel, no bloody seep in bandage. Plan for outpatient from paediatric surgeon
and paediatric division.

9
DISCUSSION
In this case, a 6 years old boy came to Emergency Department, with chief
complained fever since 10 days before admission, sub febrile for 3 days continued
higher with the highest fever 2 days before admission. The fever was not
decreased by paracetamol and continued >380C for the last 7 days before
admission. A temperature above 38°C by mouth or above 38.4°C by rectum is a
practical definition of fever.5 It is an adaptive response that is well regulated by
the body and is not dangerous in and of itself (although the cause of the fever may
be quite serious). Body temperature is a dynamic balance between heat production
and heat loss.6 In the case of infections, fever is probably produced both by
vasoconstriction and by increased heat production. These functions are controlled
by the thermoregulatory center in the hypothalamus, which responds to
stimulation by pyrogens.7

Table 1. The difference features between viral and bacterial infection

Source: El-Radhi, A. Sahib; Carroll, James; Klein N. Clinical Manual of Fever in

Children. london: springer; 20097

In this case, there was no cough, no watery nose, no odynophagia, no sign

of bleeding, so we classified this patient has a fever without localizing sign. Fever
without localizing signs is defined as a fever of less than or equal to 10 days

10
duration, with no signs of the source of the infection. It is a tentative diagnosis
and we can sharpen the diagnosis with the type of fever.8

Figure 2. Pattern of fever and the most common cause.

Source: Fisher A, Randall G, Thomas G, Barrett KB. Moffet’s Pediatric Infectious
Diseases: A Problem-Oriented Approach, 4th Edition. 4th ed. Lippincott Williams
& Wilkins; 20058

In this case, this patient has a continuous fever with a stepwise pattern. A
continuous fever is characterized by a persistent elevation of body temperature
with a maximal fluctuation of 0.4°C during a 24hour period. Normal diurnal
fluctuation temperature is usually absent or insignificant. Examples of this pattern
of fever are typhoid fever, malaria, and FUO.7

Figure 3. continuous step ladder pattern of fever classical of typhoid fever.

Source: Fisher A, Randall G, Thomas G, Barrett KB. Moffet’s Pediatric Infectious
Diseases: A Problem-Oriented Approach, 4th Edition. 4th ed. Lippincott Williams
& Wilkins; 2005

11
 The patient in this case, also complained with nausea which was getting
worse for 2 days before admission but no vomit. In 3 days before admission, he
got diarrhea, he had a mushy stool 2-3 times a day, no blood. In diarrhea caused
by Salmonella species, occasionally blood or mucus is present in the stool
(dysentery-like diarrhea). Often, however, the clinical pattern is that of a subacute
diarrhea, which does not have an explosive onset but is somewhat persistent and
may lead to moderate dehydration after several days.9
In this case, the last defecation was 1 day before admission. His appetite
decreased with the dried tongue for a week before. Fever with abdominal
discomfort in tropical developing countries commonly refers to typhoid fever.
Symptoms then gradually increase over 2–3 days. The child often constipated
following diarrhea, nausea, and anorexia.10
From vital sign from this patient, we found heart rate 101 bpm and
respiratory rate 25 tpm when the temperature was 39oC. Heart rate and respiratory
rate include in signs of fever, with the pulse rate rising 10 beats per minute for
every 1°C temperature elevation. Tachypnoea during fever is an increase of
respiratory rate by approximately 2.5 breaths per minute for each 1°C elevation of
body temperature, occasionally associated with grunting (arousing the suspicion
of pneumonia). An occasionally encountered sign during fever is relative
bradycardia, which is a pulse rate disproportionately low for the degree of fever.
Normally, for every 1°C (1.8°F) rise in fever, the pulse rate increases by 10bpm.7
The normal heart rate for 6 years old boy is 70-110bpm.5 Relative
bradycardia is one of typhoid important sign, but we can’t evaluate in this patient.
Criteria for using relative bradycardia in clinical diagnosis is age of patient ≥ 13
years, temperature ≥ 102°F and ≤ 106°F which the pulse is taken simultaneously
with the temperature, the patient has normal sinus rhythm with no arrhythmias,
second or third degree heart block, or pacemaker.11
From laboratory we found haemoglobin 10.5 g/dL, haematocrit 33.4%, red
blood cell 4.42 x 106 /uL, platelet count 66000/uL, white blood cell count was
5960/uL, eosinophil 1.52%, basophil 0.9 %, neutrophil 77.3%, lymphocyte 18.9
%, monocyte 1.7 %. A marked leucocytosis (greater than 25,000/μL) with a
predominance of neutrophils is often taken as presumptive evidence for a bacterial

12
infection. The most widely used screening values (in conjunction with high fever)
are a count of 15,000/μL or more and total segmented neutrophils of 10,000/μL or
more. Otherwise, bacterial infection can cause leucopenia.12 Leukopenia is an
absolute decrease in the number of circulating leukocytes below 4300/μl.
Leukopenia may be caused by decrease in numbers of one or more specific
leukocyte subgroups as a result of various causes. Leucopenia caused by bacterial
infection is typhoid fever, paratyphoid fever, and brucellosis.13

Table 2. Cause of leucocytosis and leukopenia

Leucocytosis
• Most Bacterial infections
• Sepsis
• Surgical procedures
• Multiple trauma/burns
• Tissue infarction (e.g.,
myocardial, pulmonary, intestine)
• Acute haemorrhage
Source: Birk-Urovitz E. Overview of Lekopenia. Toronto M. 2013;2:1–312
Leukopenia
• Viral infections
• Some of Bacterial infections:
typhoid fever, tuberculosis
• Parasyte infection: malaria
• Sepsis/septic shock
• Chemotherapeutic agents
• Medications
(e.g., antibiotics, anti-epileptics,
diuretics)
• Vitamin deficiency
(e.g., B12 and folate)
• Autoimmune disease
(e.g., lupus)

In this case, white blood cell count was 5960/uL, eosinophil 1.52%,
basophil 0.9 %, neutrophil 77.3%, lymphocyte 18.9 %, monocyte 1.7 %, CRP
73.7mg/dl. In typhoid fever, laboratory findings include leukopenia, anemia,
thrombocytopenia, and increased serum aspartate transaminase (SGOT).
Leukopenia in typhoid fever usually still >3000mg/dL.10 Elevated agglutination
titers of O and H antigens at 1:160 in widal test are significant.2 But the blood
culture test was found to be more sensitive than the widal test in endemic area
with 5% level difference of significance.14
In this case, we didn’t take blood culture in a first day of admission and
IgM salmonella TUBEX was ten. The definitive diagnosis is based on isolation of

13
Salmonella typhi or other salmonella strains from blood or bone marrow culture.15
Even though an array of specimens including whole blood, bone marrow, stool,
duodenal fluid, urine and skin (rose spots) have historically been shown to harbor
cultivable bacteria, blood is the most common specimen submitted for culture of
S. Typhi. Between 45 and 70% of patients with typhoid fever may be diagnosed
by blood culture. The sensitivity of culture from blood is dependent on a variety
of factors including the volume of blood taken (and its ratio to enrichment broth),
pre-treatment with antibiotics and delay in transportation of the sample to the
laboratory.16 All of those factors making the sensitivity diagnosis by culture of
blood is about 60–80% and bone marrow is about 80–95%. Stool cultures are only
positive in about 30% of patients. For the conventional method, typhoid fever can
only diagnosed by blood culture.17
In ASIA, gold standard to diagnose typhoid fever is immunoassay TUBEX
with sensitivity 95% and specificity 97%.18 A hundred percent of patient with
positive blood culture of Salmonella typhi has a positive TUBEX test in east
ASIA.19 So in this case, in the first day of admission, we assessed this patient as
typhoid fever.
Typhoid fever is an enteric infection caused by Salmonella typhi, chiefly
involving the lymphoid follicles of the ileum. Typhoid fever includes infection
with Salmonella typhi and Salmonella paratyphi A, B and C, and rarely
Salmonella choleraesuis, Salmonella heidlberg, and Salmonella typhimurium.20
The incidence of typhoid fever in the world is 17 million new cases each
year, with a case fatality rate of 1.3%. In Indonesia, incidence is 810 / 100.000
case.21 Characteristic features are fever, which gradually rises during the first
week, relative bradycardia, headache, abdominal distension, splenomegaly, and
maculopapular rash. Initially, influenza-like symptoms develop with fever,
malaise, headache, dry cough, and myalgia. Poorly localized abdominal
discomfort and nausea are common.22 Fever rises progressively, until by the
second week it is high grade and sustained. On physical examination, abdominal
tenderness and hepatosplenomegaly are common. Occasionally, there is a faint
maculopapular truncal rash (referred to as rose spots).23

14
 In this case, in the 3rd day of admission, patient got abdominal pain in all
the region. He has no vomit, no diarrhea, no constipation, and still fever.
Abdominal pain in this case was severely increased and felt in each abdominal
region. Acute abdominal pain is a severe sudden pain in the abdomen. It can be
caused by a wide range of underlying surgical and non-surgical conditions. which
varies with age, associated symptoms, and pain location.24
Acute abdominal pain may be classified as visceral, somato-parietal, and
referred pain, according to the nature of the pain receptors involved. Interestingly,
most acute abdominal pain is associated with visceral pain receptors. Visceral
pain receptors are located on the serosal surface, in the mesentery, within the
intestinal muscle, and the mucosa of hollow organs. These pain receptors respond
to mechanical and chemical stimuli, such as stretching, tension, and ischemia.
Because visceral pain fibers are unmyelinated C-fibers, and enter the spinal cord
bilaterally at several levels, visceral pain is usually dull, poorly localized, and
perceived in the midline. In addition, there are three broad pain areas with
anatomic associations. Pain emanating from foregut structures (e.g., lower
esophagus, stomach) is felt in the epigastric area, pain from midgut structures
(e.g., small intestine) is felt in the periumbilical area, and pain from hindgut
structures (e.g., colon) is felt in the lower abdomen.25

Table 3. Different diagnosis of acute abdominal pain by predominant age

Source: Kim JS. Acute abdominal pain in children. Pediatr Gastroenterol Hepatol
Nutr. 2013;16:219–24

Many infectious diseases can resemble acute abdominal pain. In a boy 6

years old, the most common disease are gastroenteritis, appendicitis, pneumonia,
and urinary tract infections.26 In this case, patient got acute abdomen in the third
day of admission, which is has been diagnosed with typhoid fever. Acute

15
abdominal pain happen in 15% of typhoid fever.3 Acute abdominal pain in
typhoid fever can refer to:
a. Peritonitis
Peritonitis in patient with typhoid fever led by ileum perforation. By the
end of 2 weeks, perforation, in about 5%, may occur owing to typhoid ulceration
and defects in coagulation. This serious complication is associated with 50%
mortality.9
b. Acute Mesenteric Lymphadenitis
The syndrome of acute mesenteric lymphadenitis is characterized by
abdominal pain, tenderness, fever, and vomiting, which leads the surgeon to
operate on the patient for possible appendicitis. The appendix is normal, but large
mesenteric nodes are found, sized >8mm for child.27 Cultures of these nodes have
revealed a variety of pathogens, including beta Haemolytic streptococcus,
Meningococcus, Yersinia enterocolitica, and Yersinia pseudotuberculosis. In
some case the organisms escape the small intestine through the lymphatics and
may cause hyperplasia in the Peyer’s patches, as well as mesenteric
lymphadenopathy, splenomegaly, and changes in the liver parenchyma. This type
of infection also can manifest as acute abdomen.4
c. Appendicitis
Appendix may become the risk factor of typhoid fever, beside typhoid fever
can be trigger of appendicitis.28 The mechanism of those too still abroad.29 Acute
appendicitis or acute on chronic appendicitis can be the cause of acute abdomen in
typhoid fever with the incidence <0,1%.30 The appendix is inflamed, with or
without pus and adhesion of appendix wall. It can followed by enlargement of
mesenteric lymph in a local region of appendix.31

In this case, in the 3rd day of admission, in a 2nd weeks of typhoid fever,
there was a haematine from NGT beside the acute abdomen. By the end of 2
weeks of typhoid fever, perforation or haemorrhage (in about 5%) may occur
owing to typhoid ulceration and defects in coagulation.32 This serious
complication is associated with 50% mortality. Complications, such as
gastrointestinal bleeding, intestinal perforation, and typhoid encephalopathy,

16
occur in 10–15% of patients which is need surgical intervention.10 Surgical
interventions for Salmonella related to small bowel perforation, gallbladder
involvement, salpingitis, and peritonitis all have been documented in the
literature.3
Decision to decide whether the condition need surgery or not, is the most
important thing in acute abdomen case. The physician has to decide whether the
condition need surgery or not, while the diagnosis procedure should be continued
to pin down the diagnosis.26

Table 4. Diagnostic imaging strategies and treatment options for common causes
of acute abdominal pain in children/ young adult

Source: Hardy A, Butler B, Crandall M. The Evaluation of the Acute Abdomen.

acute care Surg. 2013;20:19–32.

The definitive caused of acute abdomen can be pinned down by

laboratories and most of all by laparotomy exploration. There are several
approach for determine the cause of acute abdomen in child.24

17
 Figure 4. Algorithmic approach to the children with acute abdominal pain
requiring urgent management.
Source: Kim JS. Acute abdominal pain in children. Pediatr Gastroenterol Hepatol
Nutr. 2013;16:219–24

The possible cause of acute abdomen in typhoid fever are peritonitis

caused by intestinal perforation, mesenteric lymphadenitis, and acute appendicitis.
Not all of them need a surgical intervention.27
The first approach is radiology studies, which can define is it need to get
surgical intervention as soon as possible or not.26 In this case, we did BOF and
LLD x-ray. We found intestinal dilatated from BOF and multiple step ladder from
LLD.

18
Figure 4. Step ladder appearance from this patient

Figure 6. Intestinal dilated from this patient

19
 Step ladder appearance and intestinal dilated can be sign of bowel
obstruction. The most common cause of acquired bowel obstruction in child are
adhesion following inflammation, paralytic ileus, or worm obstruction.33 In
children with typhoid fever, bowel obstruction possible happen by inflammation
(by organ perforation) or in a small case caused of electrolyte imbalance. The
most common cause of acute abdomen in typhoid fever is ileum perforation which
is need surgical intervention immediately.3
In this case, we did laparotomy exploration even though the diagnosed
was not fully confirmed. We did laparotomy exploration to diagnosed whether
acute abdomen caused by ileum perforation or acute appendicitis.

Table 5. Sign indicating the possible need for surgery in patient

with acute abdominal pain

Source: Jones J. Acute Abdominal Pain in Children. Am Fam Physician.

2016;2:830–6

In this case, from laparotomy exploration of this patient, we found no

ileum perforation. All the intestinal wall was intact. There was an inflamed
appendix with pus in pole appendix + 5 cc. The pus was with fibrin, hyperemic
omentum with no walling off and adhesion. The inflamed appendix, height 6 cm
Ø 1,5 cm, peritoneum fluid + 150 cc, enlargement of mesenteric lymph in
appendix region sized 6-9mm, no perforation of another hollow and solid organ.

20
 Figure 7. Inflamed appendicitis in this patient.

From the laparotomy exploration from this case, we found that acute
abdomen in this child caused by acute appendicitis, not because of the ileum
perforation, with mesenteric lymphadenopathy. Common cause of acute abdomen
in typhoid fever were peritonitis cause by ileum perforation, acute mesenteric
lymphadenitis, and acute appendicitis.3

Table 6. Stratified disease approach to acute appendicitis

Source: Bhangu A, Søreide K, Di Saverio S, Assarsson JH, Drake FT. Acute

appendicitis: Modern understanding of pathogenesis, diagnosis, and management.
Lancet. 2015;386:1278–87

In this case, acute appendicitis happened in the third day admission of

typhoid fever patient. Although several infectious agents are known to trigger or
be associated with appendicitis, the full range of specific causes remains

21
unknown. Recent theories focus on genetic factors, environmental influences, and
infections.34 A debated theory divides acute appendicitis into separate forms of
acute inflammation processes with different fates. One is the simple inflamed
appendicitis without gangrene or necrosis that does not proceed to perforation.
This so-called reversible form can present as phlegmonous (pus-producing) or
advanced inflammation (but without gangrene or perforation) that might need
surgery, or alternatively as a mild inflammation that can settle, either
spontaneously or with antibiotic therapy. By contrast, the more severe
inflammatory type proceeds rapidly to gangrene, perforation, or both.31
Each and every clinical sign for appendicitis alone has a poor predictive
value. The most widely used score so far is the Alvarado score.35 A systematic
review and pooled diagnostic accuracy study showed that the score has good
sensitivity (especially in men or boy) but low specificity, limiting its clinical
impact and meaning that few surgeons rely on it to guide management above and
beyond their own clinical opinion. Recently, the appendicitis inflammatory
response score has been developed, and seems to outperform the Alvarado score
in terms of accuracy.36

22
 Figure 8. Clinical risk scoring for suspected acute appendicitis.
Source : Ohle R, O’Reilly F, O’Brien KK et al. The Alvarado score for predicting
acute appendicitis: a systematic review. BMC Med. 2011;9:139. 23

In this case, we scored the patient with Alvarado score 4 and AIR score 7.
Base on the table we can conclude this patient as an intermediate risk. But it can’t
be definitive counting because it possible triggered by typhoid fever.
Modern diagnosis aims to first confirm or eliminate a diagnosis of
appendicitis, and second to stratify simple and complex disease when appendicitis
is suspected. The optimum strategy that limits harm (eg, radiation from imaging)
while maintaining a high degree of accuracy has still not achieved consensus,
representing the difficulty faced by patients and surgeons.37

23
 Biomarkers are used to supplement patient history and clinical
examination, especially in children, when diagnosis is difficult. No inflammatory
marker alone, such as white blood cell count, C-reactive protein, or other novel
tests, including procalcitonin, can identify appendicitis with high specificity and
sensitivity. However, white blood cell count is obtained in virtually all patients
who are assessed for appendicitis, when available. A range of novel biomarkers
has been suggested during the past decade, including bilirubin, but these do not
have external validity and repeatedly from low sensitivity, which means they are
unlikely to come into clinical practice. In this patient white blood cell count was
2320/uL and CRP 73.3mg/dl. Both were not specific to identify appendicitis.
Initial reliance on ultrasound has become more guarded recently because
of moderate sensitivity (86%, 95% CI 83–88) and specificity (81%, CI 78–84) as
shown through pooled diagnostic accuracy of 14 studies, 27 limiting its diagnostic
ability. Its first-line investigative role is greatest in children, who typically have
thinner musculature, less abdominal fat, and a greater need for radiation
avoidance than adult patients.38

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 Figure 9. Flowchart of guidelines for a stratified approach to preoperative
management of suspected appendicitis.
Source : Bhangu A, Søreide K, Di Saverio S, Assarsson JH, Drake FT. Acute
appendicitis: Modern understanding of pathogenesis, diagnosis, and management.
Lancet. 2015;386:1278–87

It often is hard to differentiate whether mesenteric lymphadenitis or acute

appendicitis from Salmonella infection in the lower ileum. Reports state that
Salmonella infection mimicking appendicitis usually occurs in the first 2 decades
of life.39 Corbeira et al found that patients who have mesenteric lymphadenitis and
a clinical picture of an appendicitis like syndrome often have enlarged and
erythematous lymph nodes at the root of mesentery and a normal appendix. They
noted that histopathologic examination of these nodes typically shows reactive

25
lymphadenitis or follicular hyperplasia. In cases of mesenteric adenitis caused by
Salmonella, the combination of clinical presentation and radiologic and laboratory
assessment may not always show the extent of the underlying pathology.
In this case, from laparotomy exploration we found acute appendicitis by
found an inflamed appendix, height 6 cm Ø 1,5 cm.

Figure 10. Inflamed appendicitis in this patient.

Figure 11. Mesenteric lymph in this patient

26
 Figure 12. Macroscopic pathological features of appendicitis.
(A) Macroscopically normal appendix. (B) Simple inflamed appendicitis.
(C) Complex appendicitis showing perforation with pus formation
Sumber: Bhangu A, Søreide K, Di Saverio S, Assarsson JH, Drake FT. Acute
appendicitis: Modern understanding of pathogenesis, diagnosis, and management.
Lancet. 2015;386:1278–87

Enteric infection always should be on the list of differential diagnoses

when a child presents with the atypical combination of right lower quadrant
abdominal pain and enlarged lymph nodes in the ileocecal region. Complete
intestinal obstruction is a very rare manifestation of Salmonella infection. In acute
abdomen cases in which Salmonella is suspected, stool culture may help establish
the diagnosis, but it should be kept in mind that even repeat cultures are negative
in a significant number of infected patients.4
In this case, peritoneal fluid culture was Staphylococcus epidermidis and
blood culture when acute abdomen happen was sterile. Staphylococcus
epidermidis is an integral part of the commensal microbial communities on human
skin but also acts as an important opportunistic pathogen, particularly in relation
to in-dwelling medical device-related infections.40 When it found, the first thing to
do is make sure it wasn’t a contaminant. Staphylococcus epidermidis can be a
pathogen if it found in both blood and fluid with a related clinical appearance. It is
the cause of a significant number of peritonitis episodes if it becomes an
opportunistic pathogen.

27
 Definitive diagnosis usually is based on blood culture and serologic
testing, but the time delay in getting these results can be problematic when a
patient’s condition is serious. Often, the physician is forced to take a patient to the
operating room before these findings are known. It seems logical that the
combination of USG and stool culture may help reduce the number of needless
surgeries done in cases of suspected appendicitis.29
However, in cases in which the diagnosis cannot be pinned down, surgical
intervention is the appropriate step to take in light of the high morbidity and
mortality rates associated with untreated appendicitis and intestinal perforation.28
The surgeon will determine the techniques in the operation, but the primary care
physician can dose the preoperative and postoperative antibiotics.
In this case, we could not diagnose the definitive cause of acute abdomen
in typhoid fever until the surgical intervention has been done. The clinical and
laboratory appearance look similar between acute abdomen in typhoid fever
caused by ileum perforation, or appendicitis, or mesenteric lymphadenitis. We can
differentiate from the macroscopic and microscopic view of all.

In this case there was inflamed appendix, height 6 cm Ø 1,5 cm,

peritoneum fluid + 150 cc, enlargement of mesenteric lymph in appendix region
sized 9-11 mm. There was multiple lymphadenopathy in mesenteric lymph in
small intestine region, size <8mm no hyperemic and pus. In mesenteric
lymphadenitis, the enlargement of mesenteric lymph happened in all region, with
sized >8mm and inflame.27 In peritonitis caused by intestine perforation, will
found a defect in intestine wall, usually sized 1-3mm, with thickness of another
intestine wall. In case of typhoid fever, over 80% case has an enlargement of
mesenteric lymph with sized 5-8mm with no sign of inflamed.41 In this case,
pathology anatomy from the appendix tissue: inflammation with lymphocyte and
hystiocyte infiltration in submucous to serosa without specific sign of tuberculosis
infection. Pathology anatomy from mesenteric was a reactive lymphoid
hyperplasia without specific sign of tuberculosis infection. So after the surgery
intervention, we diagnosed this case is acute appendicitis following typhoid fever.

28
 Salmonella sp. can cause true appendicitis or appendicitis like symptoms.
Overall, the spectrum of associated pathology is broad, ranging from lymphoid
hyperplasia of the appendix to lymphadenitis of adjacent nodes, and from ileitis
with or without appendicitis to suppurative appendicitis. There were 3 hypothesis
about the pathogenesis. First, Salmonella sp. go further to appendix by blood
stream, which is sign by positive blood culture in both blood and appendix swab.
Second, Salmonella sp. go further to appendix by lymphatic system. Third,
lymphadenopathy happen in typhoid fever can press and obstruct lymphatic and
blood stream around the appendix which is the risk of appendix infection. But
none of the mechanism has been clarified in literature.3,28,42

29
SUMMARY
A case of perforated gangrenous appendicitis following typhoid fever in
child already presented. We diagnosed this patient as typhoid fever in the first day
of admission based on the anamnesis, physical examination, and laboratory test.
From anamnesis we got fever for 10 days, upgrading stepwise pattern for three
days and continued fever for 7 days with no specific focal infection complain.
From the physical examination we got fever, relative bradycardia, typhoid tongue,
and hepatomegaly. From laboratory we found TUBEX was 10. In the 3rd day of
admission, the patient got acute abdomen and got emergency laparotomy. From
laparotomy exploration we found perforated gangrenous appendicitis.
It is important to identify the cause of acute abdomen in typhoid fever
whether it is because of ileum perforation, mesenteric lymphadenitis, or
appendicitis. Definitive diagnosis usually is based on blood culture and serologic
testing, but the time delay in getting these results can be problematic when a
patient’s condition is serious. In cases in which the diagnosis cannot be pinned
down, surgical intervention is the appropriate step to take in light of the high
morbidity and mortality rates.
This case can be a warning for physician that ±2% of typhoid fever has a
connected with acute appendicitis although the spectrum of associated pathology
is still unclear. Typhoid fever can be a comorbid of appendicitis and appendicitis
can be a complication of typhoid fever with an unclear mechanism.

30
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