Typhoid ileal perforation


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  • Those organisms that survive the acidity of the stomach
  • Some organisms pass into the gall bladder, where they multiply and remain. Invasion of the wall of the gall bladder lead to cholecystitis. Bacteria are also excreted in the stool at this phase. Note separation of slough from ulcers may lead to severe heamorrhage or perforation.
  • Diarrhea may set in the early stage of the disease but constipation sets in later the course of the illness.
  • Generalised tenderness with guarding is present; this finding, however, may not be remarkable, especially in patients who perforateunder medical treatment
  • platelet count is ascertained, particularly in patients with evidence of coagulopathyleucopaenia is a more common finding inpatients with uncomplicated typhoid fever
  • . May be as high as 96% in those with typhoid colonic perforation. The extent ofpneumoperitoneum is important as it may be necessary to vent theair to improve respiration and reduce hypoxia. Pulmonaryconsolidation may be present in those with chest infection.
  • Frequently, all that can be seen is a diffuse opacity in most of the abdomen, particularly in those presenting late with intraperitoneal collection. The shadowof a distended gallbladder may be obvious, suggesting cholecystitis.
  • Correction of fluid and electrolyte deficits: Care needs to betaken to achieve adequate correction. A common cause of death isinadequate replacement of fluid and electrolyte deficits. Four to sixhours may be needed to achieve adequate correction.• Dextrose: Intravenous dextrose in 0.18-0.45% N saline is used inchildren younger than 5 years of age (the amount of saline usedwill depend on the serum level of Na+). In older children, dextrosein 0.9% N saline is used. Large volumes of fluid may be required:20 ml/kg by bolus infusion is given initially in severely dehydratedpatients and those presenting in shock. Ten ml/kg may be repeatedafter 1 hour if urine output is not satisfactory (never give bolusinfusion of any potassium-containing fluid). Thereafter, adjustinfusion to maintain a urine output of 1.5–2 ml/kg/hr.• Potassium (K+): Once the child is making adequate urine, give atleast a daily requirement of K+ (1–2 mmol/kg/day) until a serumbiochemistry result is available. Thereafter, any calculated deficitis added to the daily requirement. The amount of potassiumrequired is added to the intravenous fluid and administered over18 to 24 hours (do not give more than 10 mmol of K+ in an hourunless the child is in the intensive care unit (ICU) and is beingmonitored using an electrocardiogram (ECG)).2. Nasogastric decompression: An appropriate size nasogastric tubeis inserted and the stomach decompressed by low pressure suction orintermittent aspiration. This will also help in reducing the pressure onthe diaphragm and improve respiration.3. Urethral catheter: An indwelling urethral catheter is left in placeto ensure adequate monitoring of urine output.4. Reversal of hypoxia: Hypoxia is a common problem that mayaffect the integrity of intestinal anastomosis as well as survival.Respiration may be impaired by abdominal distention, peritonitis, andpresence of a large pneumoperitoneum. If the pneumoperitoneum islarge (see Figure 17.3), insert a size 16G–18G intravenous cannulain the right or left upper quadrant (depending on the site of maximalair collection) to vent the collected gas (avoid the lower borderof the liver, if enlarged). The cannula is removed after adequateventing. This manoeuvre often helps to improve respiration and reducehypoxia. Administer 100% oxygen by nasal catheter until surgery.Oxygen administration may need to be continued for up to 6 hourspostoperatively in very ill children.5. Blood transfusion: This is necessary to correct anaemia if thehaemogram is <8 gm/dl (packed cell volume of <24%). Anaemia isalways corrected before surgery to minimise hypoxia. A rough estimatefor blood transfusion is 20 ml/kg body weight to attempt to correct theanaemia before surgery.6. Correction of coagulopathy: A vitamin K injection, 10 mg daily,is given and maintained for at least 5 days.7. Antibiotic therapy: Intravenous, broad-spectrum antibiotics arecommenced immediately when the diagnosis of typhoid is suspected.The antibiotics may need to be changed later if there is no improvementand culture results become available. A commonly used effectiveantibiotic combination is one of the following:• Chloramphenicol (50–75 mg/kg/24 hours in 6-hour dosing) + gentamicin(3–5 mg/kg/24 hours in 8-hour dosing) + metronidazole(7.5 mg/kg/dose given in 8-hour dosing).• Amoxicillin [50–75 mg/kg/24 hours in 8-hour dosing (or ampicillin,50–75 mg/kg/24 hours in 6-hour dosing)] + gentamicin (3–5mg/kg/24 hours in 8-hour dosing) + metronidazole (7.5 mg/kg/dose given in 8-hour dosing).• Third-generation cephalosporin + metronidazole.
  • The resected length of intestine is always measured and documented. Then intestinalcontinuity is restored by end-to-end anastomosis. The resectedsegment is sent to the lab for histopathology.
  • complication rate maybe significantly higher in children younger than 5 years of age.Mortality is<15% in those presenting within 24hrs and >80% in those presenting more than 4days
  • Typhoid ileal perforation

    2. 2. INTRODUCTION The most common surgical complication of typhoid fever. Remains a problem in developing countries due to gross defect in sanitation and lack of portable water. It is associated with significant morbidity and mortality due to late presentation. The diagnosis is mainly clinical. Surgery remains the gold standard of treatment after adequate resuscitation. 9/1/2013
    3. 3. EPIDEMIOLOGY Global incidence of typhoid fever is 21million cases annually with 1-4% mortality predominantly in 5-15years. Children account for >50% of all cases of typhoid ileal perforation with peak age of 5-9years. Has equal M:F ratio in children in contrary to adult with higher male prevalence. Perforation rate is about 10% in children which increase with age reaching a high of 30% by the age of 12years. Has higher incidence in rainy season. 9/1/2013
    4. 4. PATHOGENESIS  The infection is caused by the bacteria, Salmonella typhi (a gram-negative rod found only in humans), and rarely by Salmonella paratyphi A,B and C  Transmission is by feco-oral due to fecal contamination of food and water  1st week bacteremia; the organisms multiply the intestine, passes through the peyer’s patches into the circulation.(reaches various organs). There is sensitization of the lymphoid tissue. 9/1/2013
    5. 5. PATHO… CT  By the 2nd week, organisms are mopped up from the circulation by the reticuloendothelial system esp. the kuffer cells of the liver. There is multiplication of the organism, necrosis of the RE cells, release into the circulation leading to the septicemic phase of the illness. 9/1/2013
    6. 6. PATHO….CT  The organisms are also released into the bile through which they reach the intestine. Invade the previously sensitized peyer’s patches and multiply there. Hypersensitivity reaction occurs with swelling of the peyer’s patches and congestion of the submucosal and muscular layers. Blockage of the capillaries lead to necrosis and ulceration and subsequent bleeding or perforation usu at the 3rd week. 9/1/2013
    7. 7. 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. 9/1/2013
    8. 8. CLINICAL FEATURES  History of fever, 2-3weeks preceding the onset of abdominal pain.  Abdominal pain  ± hematochezia prior to onset of pain  Diarrhea or constipation.  ± jaundice may be a complaint. 9/1/2013
    9. 9. GENERAL EX  Depending on the stage of the illness  Very ill patient  Dehydrated  Pale  Pyrexia  Wasted 9/1/2013
    10. 10. CVS  Tachypnea  Hypotension  shock 9/1/2013
    11. 11. 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 9/1/2013
    12. 12. 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.  Blood may be seen on the examining finger in patients with bleeding. 9/1/2013
    13. 13. INVESTIGATIONS The diagnosis of is often clinical, based on Hx, features of peritonitis and investigations are done to  support the diagnosis  identify deficits, as well as to  ascertain the fitness of the patient for surgery  NOTE THAT RESUSCITATION TAKES PRECEDENCE OVER INVESTIGATIONS, WHICH SHOULD NOT DELAY INTERVENTION AFTER RESUSCITATION IS COMPLETE. 9/1/2013
    14. 14.  Serum electrolytes, urea, and creatinine: ↓K⁺ (Hypokalaemia is a troublesome problem), ↓Na⁺,↓Cl⁻,↓HCO₃⁻,↑Urea  Complete blood count: anaemia. , leucocytosis and neutrophilia  Blood grouping and cross matching: For correcting anaemia or intraoperative use. 9/1/2013
    15. 15. Plain radiography:  Chest and upper abdomen (erect film): Some patients with intestinal perforation present evidence of air under the diaphragm. This is present in about 55% of children. Absence of air under the diaphragm, however, does not exclude perforation. 9/1/2013
    16. 16.  Full abdomen (erect and supine): The intestines may show dilatation and oedematous walls. Patients who are too sick for erect film should have a lateral decubitus film to identify pneumoperitoneum. 9/1/2013
    17. 17.  Microbiological cultures: Blood and urine, as well as an operative specimen of intraperitoneal fluid/pus, are cultured to identify the Salmonella organism and any superimposed infections. 9/1/2013
    18. 18. RESUSCITATION  Correction of fluid and electrolyte deficits:  Nasogastric decompression  Urethral catheter:  Reversal of hypoxia  Blood transfusion:  Antibiotic therapy: 9/1/2013
    19. 19. 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 9/1/2013
    20. 20. 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). Then simple closure is achieved by a single layer OR double layer 9/1/2013
    21. 21. RESECTION & ANASTOMOSIS  Large solitary perforation  Multiple perforation in close vicinity to each other.  Adjacent bowel is friable/ near perforation  The resection margin should be healthy and free of evidence of inflammation such as oedema.  A limited right hemicolectomy may be necessary if the most distal perforation is too close to the ileocaecal junction for safe anastomosis ( <3 cm). 9/1/2013
    22. 22. 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. 9/1/2013
    23. 23. POST OP MGT  Strict fluid and electrolyte mgt  The chosen antibiotic regime(base on result of culture) is continued postoperatively until the temperature returns to normal. Thereafter, the drugs are continued orally (if an oral form is available) for 7–14 days.  Correction of aneamia  Close monitoring of vital signs  Daily monitoring for intra-abdominal collection  Nutritional rehabilitation  Wound dressing 9/1/2013
    24. 24. POST OPERATIVE COMPLICATIONS  Prolonged ileus  Surgical site infection  Abdominal wound dehiscence  Anastomotic leakage or complete breakdown of the anastomosis  Enterocutaneous fistula  Intraperitoneal abscess  Adhesion intestinal obstruction 9/1/2013
    25. 25.  Reperforation  Hypoproteinaemia  Pleural effusion  Transient psychosis 9/1/2013
    26. 26. PROGNOSIS  Age of patient  Duration of perforation before surgery  Degree of fluid and electrolyte correction  GI hemorrhage  Number of perforation 9/1/2013
    27. 27. CONCLUSION Typhoid perforation is a challenging surgical condition especially in developing countries. Prompt diagnosis, aggressive resuscitation, and proper choice of surgical procedure is necessary to reduce its morbidity and mortality. 9/1/2013
    28. 28. REFERENCES  Emmanuel .A Ameh., Paediatric Surgery;A comprehensive text for Africa.  E.A Badoe.,Principle and practice of surgery; Including pathology in the tropics. 4th Ed.  Indian journal of clinical practice, Vol.12,No.10, March 2002.  Nelson Awori., Primay surgery Vol. 1online ed. 9/1/2013