Typhoid intestinal perforation is a serious complication of typhoid fever caused by the bacterium Salmonella typhi. It occurs when the bacteria invade and damage the intestinal wall, usually in the terminal ileum, causing it to perforate. Risk factors include children and young adults in areas with poor sanitation and overcrowding. Symptoms include severe abdominal pain and tenderness. Diagnosis involves blood/stool cultures and imaging. Treatment requires correcting fluid/electrolyte deficits, antibiotics, and surgical closure of perforations with options like simple closure, resection, or temporary ileostomy.

1. Typhoid Perforation
By:
Muhammad Wasil Khan & Ramsha Mazhar

2. Cause + Transmission +Risk Factors
• Cause: Gram Negative bacteria
1. Salmonella typhi
2. Salmonella paratyphi (A,B or C)
• Transmission: Humans are the only reservoir thus
spread via:
1. Direct Contact
2. Contaminated food/water
Risk Factors:
1. Children and Young
Adults
2. Poor Sanitation
3. Over Crowding

3. ClinicalFeatures
Fever (Step-wise) temperature goes up, plateaus and
then goes up again.
Abdominal Pain
Diarrhea or Constipation
Headache
Rose spots (1-5mm balnchable papules)
Intestinal Bleeding
Hepatospleenomegaly
Intestinal Perforations
Typhoid Encephalopathy

5. Diagnosisand
Treatment
• Diagnosis:
 Clinical– 3 days or more of fever and Gi
symptoms + Endemic Area
 Blood culture
 Stool Culture
• Treatment:
1. First Line– Floroquinolones,
Azithromycin, Ceftriaxone or
Carbapenems
2. Severe illness– Dexamethasone

6. Typhoid
Intestinal
Perforation
• The bacterium lives in the intestines and
bloodstream of humans. It spreads
between individuals by direct contact with
the faeces of an infected person.
S. typhi enters through the mouth and
spends 1 to 3 weeks in the intestine.
After this, it makes its way through the
intestinal wall and into the bloodstream.
• From the bloodstream, it spreads into
other tissues and organs. The immune
system of the host can do little to fight
back because S. typhi can live within the
host’s cells, safe from the immune
system.

7. Pathophysiology
• The virulence of Salmonella is determined by typhoid toxin, Vi antigen
(polysaccharide capsule), liposaccharide O antigen, and flagellar H antigen.
• The main role of the Vi antigen is to act as an antiphagocytic agent preventing the action of
macrophages, thus shielding the O antigen from antibodies that confer the serum
resistance.
• The flagellar H antigen provides bacterial mobility and adherence upon the gut wall
mucosa.
• Invasion of the gut wall is assisted by flagella, and the type III secretion system is capable
of transferring bacterial protein into enterocytes and M cells (specialized epithelial cells that
serve as antigen-presenting cells in gut mucosa or lymphoid tissue) or by direct penetration
of mucosa.
• Bacteria attached to M cells are absorbed by pinched off cytoplasm containing bacteria
and extruded into the luminal space. In this process, M cells are damaged, and the basal
lamina is exposed. It provides easy access to pathogens for the invasion, which worsens
the condition

8. • Bacteria induce proliferation of Payer patches via recruitment of lymphocytes and
mononuclear cells and induce necrosis and eventually, ulceration that complicates
the symptoms.
• In general, hemorrhage and perforation occur in the terminal ileum secondary to
necrosis of Peyer's patches at 2-3 weeks after the onset of the disease.
• Perforation of terminal ileum is a cause for acute obscure peritonitis, heralded
by exacerbation of abdominal pain associated with tenderness, rigidity and
guarding, most pronounced over right iliac fossa.

9. Typhoid
perforations
• Intestinal perforation is a serious complication of
typhoid fever and remains a significant surgical
problem in developing countries, where it is
associated with high mortality and morbidity,
due to lack of clean drinking water, poor
sanitation and lack of medical facilities in
remote areas and delay in hospitalization
• The high incidence of perforation in most
developing countries has been attributed
to late diagnosis and the emergence of
multi-drug resistant and virulent strains
of Salmonella typhi.
• The disease affects mostly young adults who
contribute enormously to the economy of third
world countries .It also affects children and it is
most common in people in the low socio-
economic strata.

10. PATHOLOGY
 ULCERS; shallow irregular oval ulcers disposed
longitudinally on the antimesenteric border of
the ileum esp. terminal ileum.
 Perforation may be small or wide up to 2.5cm.
Most within 45cm from the ileocecal junction.
They are multiple in 20% of patients.
 Histologically, tissue around perforation shows
infiltration by lymphocyte ,macrophages and few
neutrophils. The macrophages may ingest
RBCs to produce typhoid cells.

11. CVS
 Tachypnea
 Hypotension
 Shock

12. CHEST
 Respiratory function is compromised by chest infection, which
is worsened by the marked abdominal distention(if present).
 Crepitation may be heard, sometimes bilaterally, indicating
that pneumonia has set in and is worsening the condition

13. ABDOMEN
 Generalized tenderness
 Rebound tenderness
 Guarding
 Rigidity
 Diminish or absent bowel sounds
 Tenderness and fullness in the recto-vesical or recto-
uterine pouch, suggesting a pelvic collection of pus.

14. DIAGNOSIS
Work up: CBC, LFT,
UCE
Erect chest
radiograph or a
lateral decubitus film
(if ill) -- free gas in
the peritoneal cavity.
Abdominal X ray
Ultrasound
CT scan (if X ray
shows any
obstruction)
Blood C/S

15. MULTIPLE ILEUM
PERFORATION
ILEAL
PERFORATION

17. Correction of Fluid and Electrolyte Deficits
Nasogastric Decompression
Urethral Catheter
Reversal of Hypoxia
Blood Transfusion
Antibiotic Therapy

18. DEFINITIVE TREATMENT
The definitive treatment for intestinal perforation is operative
to evacuate faecal contamination and prevent further
contamination.
LAPAROTOMY + SURGICAL OPTIONS;
Simple closure of perforations
Segmental resection of affected intestine
Enterostomy

19. SIMPLE CLOSURE
• Single perforation,
• If perforations are far apart
• If the number of perforations are so numerous
that resection may result in a short gut.
• The edge of the perforation is excised
circumferentially (the excised edge is sent to the
lab for histopathology).

20. RESECTION & ANASTOMOSIS
Large solitary perforation
Multiple perforation in close vicinity to each
other.
Adjacent bowel is friable/ near perforation
A limited right hemicolectomy may be necessary
if the most distal perforation is too close to the
ileocaecal junction for safe anastomosis ( <3 cm).

21. ILEOSTOMY
• The perforation (if single) or the
proximal and distal ends (following
segmental resection) of the intestine
are exteriorised as stoma, to be
closed at a later date when oedema
has subsided and the patient is fit(8-
12weeks).
• An enterostomy is performed if the
child is too sick or intestinal oedema is
too extensive for safe anastomosis or
simple closure

22. Prolonged ileus
Surgical site infection
Anastomotic leakage
Enterocutaneous fistula
Intraperitoneal abscess
Adhesion intestinal obstruction
Reperforation
Pleural effusion

23. Differential
Diagnosis
Acute Cholecystitis and Biliary Colic
Acute Pancreatitis
Constipation
Crohn Disease
Endometriosis
Inflammatory Bowel Disease
Peptic Ulcer Disease
Pelvic Inflammatory Disease

24. THANK YOU!