Management of Typhoid Intestinal Perforation which is a common and the most dreaded surgical complication of Typhoid fever. This menace is still on the rise in low and medium income countries where we still battle with lack of potable water and open defecation. This presentation is especially targeted at trainee surgeons in Nigeria and Medical Students also who may find it worthwhile.

1. MANAGEMENT OF TYPHOID
INTESTINAL PERFORATION
PRESENTER : DR. ITANKA, UBONG COLUMBA
PGY2, SURGERY DEPARTMENT, UNIVERSITY OF ILORIN TEACHING HOSPITAL
SUPERVISING SENIOR REGISTRAR: DR. ADEPOJU
Saturday 5th November, 2022

2. Outline
• Introduction
• Epidemiology
• Historical Perspective
• Functional Anatomy
• Bacteriology
• Risk factors
• Pathogenesis
• Pathology
• Management
• Prognosis
• Prevention
• Local challenges
• Current Trends
• Conclusion

3. Introduction
• Typhoid fever is a common,potentially fatal multisystemic infection that
has continued to be a public health problem in many developing countries .
• The surgical complications of typhoid fever are a cause of significant
morbidity and mortality.
• The management of Typhoid intestinal perforation TIP has posed a difficult
challenge due to its high morbidity and mortality.
• The management is multidisciplinary with surgery playing a major role.

4. Statement of Surgical Importance
• Being a common complication of Typhoid fever, the trainee surgeon
must have the basic knowledge of proper diagnosis, management and
prevention of this menace in the society.

5. Epidemiology
• According to WHO, incidence of Typhoid fever is between 20 and
30million cases with 1-4% mortality.
• 10% of patients with Typhoid fever will develop TIP
• Predominantly affects school age children 5-15yrs of age
• Children account for >50%.
• Commoner in low socio-economic age groups and also said to be
commoner during the rainy season.
• Sex M:F 1 in children, while in adults, M>F
• Children account for >50% of cases of TIP with a peak age of 5 to 9
years.

6. Historical Perspective
• The term typhoid derived
from the ancient Greek word
for cloud, was chosen to
emphasize the severity and
long lasting neuropsychiatric
effects among the untreated.

7. Historical Perspective

8. Historical Perspective
Damon Elder Salmon

9. Historical Perspective
• Mary Mallon (September 23, 1869
– November 11, 1938),was
an American cook believed to have
infected between 51 and 122
people with typhoid fever.
• The infections caused three
confirmed deaths, with
unconfirmed estimates of up to 50.
• She was the first person in the
United States identified as
an asymptomatic carrier of the
pathogenic bacteria Salmonella
typhi.

10. Relevant Anatomy • Larger aggregations of lymphoid
tissue, each consisting of 10 to 200
follicles are present in the small
intestine called aggregated lymphatic
follicles or Peyer’s patches.
• Peyer’s patches always lie along the
antimesenteric border of the
intestine.
• They are most numerous and largest
in the terminal ileum.

11. Aetiology - Bacteriology
• Caused by the bacteria Salmonella
typhi and rarely by Salmonella
paratyphi
• Salmonella typhi, a gram negative,
flagellated, glucose fermenting,
aerobic bacilli that can also exist in
facultative anaerobic conditions
• S. typhi infects only humans
• S. paratyphi infects both humans and cattle
(serotype B). Can cause colonic perforation
• Possesses three major antigens: H or
flagellar antigen; O or somatic
antigen; and Vi antigen (possessed by
only a few serovars).

12. Aetiology – Risk factors
Bacterial Factors
• Infective dose: 105 for
salmonella typhi, more for s.
paratyphi
• Virulence: O, H and Vi antigens.
• Quorum sensing: Ability to
coordinate swarming and
biofilm production.
Host Factors
• Achlohydria
• Previous gastrectomy
• Antacids
• Immunosuppresion
• Cystic Fibrosis – Protective.

13. Pathogenesis – Natural History
i. Incubation: 10 to 14 days
ii. Active invasion
iii. Fastigium
iv. Lysis
v. Convalescence

14. Pathogenesis
Week 1
• Ingestion of contaminated food/water; bacilli evade stomach acidity
• Bacteria in small intestine; recognized by antigen presenting cells in
terminal ileum.
• Pass through Peyer's patches into blood stream (initial bacteremia;
detectable in blood – active invasion phase) then spreads to organs.
• Sensitization of the lymphoid tissue.

15. Pathogenesis
Week 2:
• Bacilli taken from circulation into the reticuloendothelial system
especially liver Kuffer cells; multiply; apoptosis of macrophages in RE
cells and release of the bacteria, PAMPS and lysozomal contents into
circulation and bile heralding the Fastigium phase.
• Bacteria secreted in bile; gall bladder wall: cholecystitis, empyema,
rupture, chronic carrier state.
• Invasion Payer's patches (previously sensitized); multiply; passed in
stool

16. Pathogenesis
• Week 3:
• Hypersensitivity in Peyer's patches; swelling , mucosal/
submucosal/muscular layers congestion – LYTIC PHASE.
• Blockage of capillaries; necrosis; ulceration; bleeding/perforation.
• Salmonella bacilli may be detectable in urine.

17. Pathogenesis - Summary
• Typhoid infection is faeco-oral in
nature and is due to faecal
contamination of food and
water.

18. Pathology – GROSS PATHOLOGY
• ULCERS: Shallow, irregular, oval
shaped, longitudinally oriented
on the antimesenteric border.
The base of the ulcers is black
due to sloughed mucosa.
Margins are slightly raised.
• Fibrosis not significant
• PERFORATION: Small or wide;
most are single and within 45cm
of terminal ileum.

19. Pathology – MICROSCOPIC PATHOLOGY
• hyperaemia,
• oedema
• cellular proliferation consisting of phagocytic histiocytes ,
lymphocytes and plasma cells.

20. Other Organs/Tissues of affectation
i)Mesenteric lymph nodes—haemorrhagic lymphadenitis.
ii) Liver—foci of parenchymal necrosis.
iii) Gallbladder—typhoid cholecystitis.
iv) Spleen—splenomegaly with reactive hyperplasia.
v) Kidneys—nephritis.
vi) Abdominal muscles—Zenker’s degeneration.
vii) Joints—arthritis.
viii) Bones—osteitis.
ix) Meninges—Meningitis.
x) Testis—Orchitis

21. Management
• Principles of management are
• Brief general assessment and SIMULTANEOUS resuscitation
• Appropriate investigations
• Source control: control of perforation & peritoneal
irrigation/toileting
• Eradicate the offending organism from the body
• Confirm absence of chronic carrier state before discharge
• Follow-up
• Prevention

22. Resuscitation
• Nil per os
• IV canula: fluids to correct dehydration and hemodynamic instability
• Intranasal Oxygen
• Nasogastric decompression
• Urethral catheter: 1 -2mls/kg/hr in children,0.5mls-1mls/kg/hr
• Fluid and electrolyte deficit correction + maintenance K
• Correction of anemia
• Analgesics
• Antibiotics therapy: Quinolone and metronidazole.
• Counsel on diagnosis, management options and prognosis
• Informed consent.

23. History
• Biodata: Age, sex, occupation of parents
• Presenting complaints: Fever and generalized body weakness
• Abdominal pain
• Abdominal distension
• Diarrhoea/Constipation
• Vomiting
• Melena
• Complications – Altered level of consciousness
• Source of drinking water/ Method of sewage disposal
• Review of other systems: N/B Typhoid is multisystemic.

24. Examination
• General Physical Examination – Toxic, dehydration, pyrexia, pallor, wasting.
• Vitals: Tachypnoeic, Tachycardic (more commonly relative bradycardia), in
shock
• Abdominal Examination :
- Abdominal distension
- minimal movement with respiration
- Tenderness
- Adeniran’s sign
- Hepatosplenomegaly
- Diminished or absent bowel sound
- DRE: Rectovesical/rectouterine pouch fullness, tenderness

25. Investigations
• Diagnosis can be made clinically with a high degree of accuracy.
Diagnosis of perforation may be difficult in
(a) a small group of patients who perforate under medical care and
(b) patients with protracted illness reaching hospital several days after
perforation.

26. Investigations
• Investigations done to
- Identify derangements and Ascertain fitness for surgery
- Support Diagnosis

27. Investigations
• Serum Electrolyte Urea and Creatinine: Hypokalemia, acidosis, ↑urea
• Full blood count: Anemia, lymphocytosis, neutropenia
• Plasma Total protein and albumin
• Group and crossmatch

28. Investigations – Support Diagnosis
• Microbiological Culture and Sensitivity: Blood, stool and urine.
• Gold standard: Bone Marrow aspirate.
• Widal Test: Depends on antibody response to O and H antigen. Not
specific, not sensitive.
• Others: TyphiDot, antiVi test

29. Investigations - Imaging
1. Chest Xray : Air under the diaphragm
2. Abdominal Xray(suppine and erect):
Dilated bowel loops, signs of
pneumoperitoneum – double bowel
sign, football sign, cupola sign,
falciform ligament sign
3. Abdominopelvic Ultrasound: Free
intraperitoneal fluid. Also to rule out
Appendicitis.
4. Computed Tomography abdomen:
early detection of pneumoperitoneum.

30. Source Control – Definitive Treatment
• The surgery done depends on the clinical state of the patient, number
of perforations, distance between perforations (if multiple) and from
the Ileocecal Junction and degree of peritoneal contamination.

31. Definitive Treatment
Options – Laparotomy + surgical options
1. Simple repair
2. Segmental resection and anastomosis
3. Limited Right Hemicolectomy
4. Enterostomy: In patients not fit, those with severe peritoneal
soilage or intestinal edema too extensive for safe anastomosis or
simple closure.

32. Laparotomy
• Anaesthesia: GA
• Position: Supine
• Pre-incision Antibiotics
• Routine skin preparation and draping
• Incision: Transverse supraumbilical in children. In older children and
adults, midline incision

33. • Access gained into peritoneal cavity
• Suction out the pus and debris
• Do quick exploration
• Identify the perforation(s). What is done depends on the number of
perforations, distance from ICJ and condition of neighbouring bowel

34. • Single perforation, > 10-15cm from ileocecal juncion:
Wedge resection with simple repair

35. • Multiple perforations far apart, none < 10-15cm from ICJ
- Close each perforation individually
• Multiple perforations, close together, none <10-15cm from ICJ
- Segmental ileal resection + ileo-ileal anastomosis

36. • Perforation (single or multiple) <
10-15cm from ICJ (this part is a
high pressure zone, prone to
leakage from closure of
perforations
- Limited Right hemicolectomy +
end-end (or end-side) ileo-
transverse anastomosis

37. • Do copious peritoneal lavage using 10-12L of N/S
• Fascia is closed.
• The skin is also closed at surgery using interrupted non-absorbable
sutures.
• Some surgeons leave the subcut and skin open, for delayed closure
(due to the risk of SSI)

38. Post-op
• Patient nursed in Intensive Care
• Fluid and Electrolyte balance
• Continue antibiotics
• Wound care
• Nutritional rehabilitation

39. Post-op Complications
• Prolonged Ileus: may last for several days and manifest as increasing
or persistent nasogastric drainage. Usually managed conservatively.
• Surgical site infection is one of the most common complications
occurring in 49–59% of patients with TIP.
• Anastomotic leakage
• Enterocutaneous fistula
• Intraperitoneal abscess: (7–9%) usually manifests as a return of fever
in a patient who had started to improve.

40. Post-op complications
• Adhesion intestinal obstruction
• Reperforation may occur at a new site in 7–9% of children with TIP. It
may be the result of an unidentified impending perforation or
progression of ongoing infection.

41. Prognosis
• Of the children treated for TIP, more than half develop one or more
complications.
• The single most important significant predictor of death in patients
with TIP is the duration of abdominal pain after 7 days.
• Delayed operation
• multiple perforations
• severe peritoneal contamination

43. Follow up
• Do microscopy, culture and sensitivity of stool at follow up to confirm
absence of carrier state.
- If positive, health education and commencement of Quinolones ,
Septrin, Ampicillin
- Failed Medical Therapy? Cholecystectomy .
• Nutritional assessment

44. Prevention
• Primary Prevention:
1. General health promotion through health education, sanitation, Personal and
food hygiene, adequate potable water and curbing open defecation
2. Specific prophylaxis: Vaccination
• Secondary Prevention: Early diagnosis and treatment to prevent further
damage and spread.
• Tertiary Prevention: Limiting damage and rehabilitation .

45. Differential Diagnosis
• Ruptured Appendix
• Gastric perforation
• TB peritonitis

46. Locoregional Challenges
• Poor sanitation
• Late presentation of patients
• Limited theatre space
• Shortage of manpower

47. Current Trends
• Typhoid conjugate vaccines: introduced to the Indian Market in 2018
and approved by the WHO.

48. Conclusion
• Typhoid Intestinal Perforation, most dreaded surgical complication of
typhoid infection.
• It is diagnosed clinically based on fever, abdominal pain/distension
and demonstrable peritonitis.
• Gold standard investigation is Bone aspirate.
• Surgery is the definitive treatment after adequate resuscitation and
appropriate antibiotics cover.