European Journal of Cardiovascular Medicine

Peritonitis due to hollow viscus perforation is one of the most common emergencies encountered following acute appendicitis in the emergency department. About 30-40% of overall instances of acute abdomen presenting to the emergency department have been because of hollow viscus perforation. Among them, Duodenal and Gastric perforations have been the most common accounting for 60%- 80% in a few studies, followed by Ileal, appendicular, and large bowel. The incidence of perforation is increasing due to gastritis and the use of over-the counter NSAIDs. The increased incidence of ileal perforation is due to the increased number of people presenting to the emergency department at an early and better diagnosis and improved reporting of cases. Of all cases of hollow viscus perforation, ileal perforation accounts for about 20%3. Among the different causes of ileal perforations, Typhoid fever causing ileal perforation is the commonest etiology followed by Tuberculosis and others including inflammatory bowel disease, trauma, non-specific causes 4.  

Typhoid fever is a fatal febrile multisystemic illness caused by Salmonella enterica serotype Typhi and to a lesser extent by S.enterica serotypes paratyphi A, B, and C18.

Typhoid fever has a varied presentation with mild fever to multisystem involvement. The classical presentation is fever, malaise, lethargy, abdominal pain, constipation. When untreated typhoid fever may progress to the stage of complications like delirium, intestinal hemorrhage, bowel perforation, and death may ensue within 1 month of onset19.

Salmonella is a gram-negative bacillus, peritrich flagellates, aerobic and facultative anaerobic organisms. They resist the heat of 55 degrees for one hr and 60 degrees for 15 mins. They have H, O, Vi antigens.

Pathophysiology:

Salmonella typhi and paratyphi invade the host cells via the distal part of the ileum.These bacilli are carried to the macrophages in the lamina propria by phagocytic cells. Adhere to the Peyer’s patches in the distal ileum, which acts as a relay station for macrophages entering the lymphatic system from the gut. The bacteria then induce their host macrophages to attract more macrophages.

Salmonella typhi has Vi capsular polysaccharide antigen, LPS antigen and, flagellar antigen. The importance of Vi capsular antigen is that masks PAMPs, avoiding neutrophil-based inflammation, causing higher infectivity of typhi. Salmonella typhi co-opt the macrophages for their reproduction and are carried to the mesenteric lymph nodes to the thoracic duct and then to the reticuloendothelial tissues of the liver, spleen, bone marrow, and lymph nodes. 

The bacilli proliferate in the reticuloendothelial system and induce macrophage apoptosis and are released into the bloodstream and invade the others parts of the body. The released bacteria then infect the gallbladder via either bacteremia or direct extension of infected bile and thus re-enters the gastrointestinal tract and reinfect Peyer patches. Bacteria that do not reinfect the typically shed in the stool and are then available to infect other hosts. The course of untreated typhoid fever is divided into four individual stages, each lasting approximately one week.

In the first week, notorious gastrointestinal manifestations like diffuse abdominal pain, vomiting, constipation, etc. Inflammation of Peyer’s patches lead to narrowing of the bowel lumen causing bowel obstruction. The individual then develops a dry cough, frontal headache, delirium.

During the first week, fever along with rose spots which are often due to bacterial emboli to the dermis22 are seen. These rose spots are 1-4 CMS in width and usually less than 5 in number. The fever plateaus at 103-104°F (39-40°C). During the second week, progression of symptoms occurs which includes abdominal distension and soft splenomegaly. Relative bradycardia and dicrotic pulse may develop. 

By the third week, the patient becomes toxic and weight loss ensues. The patient becomes tachypnoeic, thready pulse and respiratory complications develop. Abdominal distension is severe. Foul-smelling, green-yellow, liquid diarrhoea (pea soup diarrhoea) may be seen in some patients.  Necrosis of Peyer’s patches may lead to bowel perforation and peritonitis causing toxaemia or intestinal haemorrhage that may cause death.

By the end of the 3^rd week, as the symptoms progress, the patient will land on intestinal perforation and present to the emergency department. Another set of people, where the symptoms are less severe but ongoing pathology occurs and eventually land on complications of typhoid.

Enteric Perforation:

Occurs in the 3^rd week of the infection. Incidence of typhoid perforation is 2% of total cases. About 75-80 percent of perforations are single, 20-25 percent are multiple.

Infection is acquired when 10 ⁶ bacilli are ingested. In the gut, the bacilli attach to the ileal mucosa, penetrate the lamina propria and submucosa, escape the host immune system, and multiply within the Peyer’s patch. Through the circulation, it reaches the mesenteric lymph nodes, multiplies, and via the thoracic duct enters the bloodstream. Transient bacteraemia occurs. Then bacilli are seeded in the liver, gall bladder, spleen, bone marrow, lymph nodes, lungs, and kidneys.

Bile is a good culture medium for the bacillus and multiplies abundantly in the gall bladder and is shredded into the intestines and again involves the Peyer’s patch of the ileum and lands on the intestinal phase of the disease which is a complication of the enteric fever. Due to vigorous inflammation of the Peyer’s patch in the ileum, occurs edema, necrosis, and sloughs off, leaving behind the characteristic typhoid ulcers. Typhoid ulcers are transverse. The ulceration of the bowel leads to perforation and haemorrhage of the ileum. These perforations may be single or multiple. They may be located on any length of the ileum but usually present in the terminal ileum because of the presence of numerous Peyer’s patches and ileocecal valve which delays emptying of the ileal contents into the colon thus by favouring the bacteria by increasing the contact time in the terminal ileum.

In 80% of cases, perforation of ileum occurs. In the rest of 20% of cases, the inflamed Peyer’s patch is ulcerated producing intestinal hemorrhage. The most common complication is the paralytic ileus.

Diagnosis:

Diagnosis of enteric fever consists of,

1. Isolation of the bacteria from the patient.
2. Demonstration of the antibodies in his serum.
3. Demonstration of the bacterial antigen in blood, urine, CSF, feces, etc.

Blood Culture:

Bacteraemia occurs early in the disease and blood cultures are 90% positive in the first week of fever, 75% in the second week, 60 % in the third week, and 25% thereafter till the subsidence of pyrexia. Blood culture becomes rapidly negative after taking antibiotics.

Clot Culture 

An alternative method to blood culture. Here 5ml of patient blood is taken and allowed to clot, and serum is pipetted out. This serum can be used for Widal tests. 

Stool Culture

Bacteria is shredded in the feces throughout the disease. Hence fecal cultures are almost as valuable as blood cultures. Fecal culture is particularly valuable in patients on antibiotics as that drug does not eliminate the bacilli from the gut as rapidly as it does from blood. Other sources like urine, bone marrow, bile, CSF, sputum can be used.

Widal Reaction

 In the patient’s sera, the H and O agglutinins for typhoid and paratyphoid bacilli are present. The antigens used in the test are H and O Antigen of salmonella typhi and H antigen of paratyphi. These react with the patient’s agglutinins and yields results.

Demonstration Of Circulating Antigen: Typhoid antigens are consistently present in the blood and urine in the early phase of the disease. This test is rapid, sensitive, and specific but is not positive after the first week of the disease.

Edge Biopsy: Edge biopsy of the ulcer can be sent intraoperatively.

Differential Diagnosis of Enteric Perforation

1. Typhoid Fever
2. Tuberculosis
3. Radiation Enteritis
4. Obstruction
5. Crohn’s Disease
6. Non-Specific Inflammation.

Medical Management

Initial resuscitation of the patient followed by treating the patient with antibiotics is necessary. Chloramphenicol was the drug used earlier. But it does not diminish the chance of a person becoming a carrier but it cures an active form of the disease. It has got the side effect of aplastic anemia. Ampicillin, amoxicillin, and co-trimaxozole reduce the carrier stage with fewer side effects. Later ciprofloxacin, azithromycin, and ceftriaxone are used which got a good response with less bacterial resistance. 

Surgical Management: Patients with Ileal perforation are managed by resuscitation and surgery is taken up. Based on the condition of the bowel different procedures like simple primary closure, ileostomy, resection, and anastomosis were performed accordingly.

This study was conducted after approval from the institutional scientific and ethical committee approval and consent from the participants. This is a prospective observational study done in the Department of General Surgery at S. V. R. R. G. G. Hospital, S. V. medical college, Tirupathi, during the year after the approval of the ethical committee. A total of 30 patients were included in the study.

Study design: Prospective cross-sectional study

Study duration: One year

Source of data: Cases that are admitted in general surgery wards in S.V.R.R.G.G. Hospital, Tirupati.

Sample size:  30 cases.

Inclusion Criteria:

1. Patients with age above 18 years present with features of hollow viscus perforation.
2. Patients with an intraoperative finding of ileal perforation. 3. Patients who gave consent for emergency exploratory laparotomy.

Exclusion Criteria:

1. Patients with intraoperative findings of hollow viscus perforation other than ileal perforation.
2. Patients with cardiopulmonary diseases, critically ill patients.

Sources Of Data:

All patients were admitted to the Department of surgery, S.V.R.R.G.G. Hospital, S.V. Medical college with signs and symptoms of hollow viscus perforation.

 Method Of Data Collection

The patients presenting with clinical features of peritonitis due to hollow viscus perforation were taken into study. Totally 102 cases were presented to the emergency department with perforation peritonitis out of which 36 patients had ileal perforation. 30 patients had typhoid ileal perforation. 30 cases were taken up for the study and patients were subjected to detailed history and thorough physical examination. Patients were subjected to necessary investigations. Serum widal, blood culture, complete blood picture, renal function tests, liver function tests, serum electrolytes, serology for HIV, HBsAg, HCV, Covid tests. USG abdomen and pelvis, chest x-ray, abdominal x-ray, CT abdomen, and CT chest. 

After stabilizing the patient hemodynamically, all cases were operated by exploratory laparotomy under General anaesthesia.

After exploring the abdomen, Ileal perforations were identified and a biopsy of the ulcer edge was sent for histopathological examination and bacterial culture. Based on the site, size of perforation and level of contamination, and bowel condition, the cases were managed.

Cases with less contamination, small perforation with good bowel condition were operated by Primary closure of the perforation and peritoneal lavage with warm normal saline. Simple primary closure done in transverse axis, the first layer was taken with absorbable suture material (Polyglactin) and the second layer with interrupted Lembert sutures burying the first layer. A proximal loop ileostomy is done in cases with higher peritoneal contamination and perforation close to the ileocecal junction.

Cases with large perforation and poor bowel condition were managed by resection of involved segment and anastomosis by four layers The fourth layer is taken in continuous interlocking with 2-0 silk and the third layer is taken which is continued with the second layer and completed by taking Connell sutures with absorbable material. The first layer is continued with the fourth layer. The mesenteric gap is closed to prevent herniations.

Peritoneal lavage is given in all cases with normal saline until the fluid becomes clear. Two abdominal drains of size 32F size were kept in the pelvis and Morrison’s pouch each respectively. For all the cases, the ulcer edge is biopsied and sent for bacterial culture and histopathological examination. The abdomen was closed 1-0 Polypropylene and the skin closed in nonabsorbable 2-0 Nylon sutures. All the patients were tested for Widal positivity and were started on ant Salmonella treatment were started in positive and suspicious cases based on intraoperative or histopathological findings. Patients were discharged after recovery if the postoperative period was uneventful. All patients were followed up for 3 months.

TABLE 1: SHOWING SITE OF PERFORATION

In the present study, Table 1 shows the common anatomical site for perforation was Duodenum with (40%) followed by Ileum (35%), followed by Stomach (13%), Appendix (5%), Colonic (3%), Caecum (2%) Jejunum (1%) and Meckel’s diverticulum (1%).

TABLE 2: ETIOLOGY OF ILEAL PERFORATION

Table 2 shows the etiology of ileal perforation in the present study. Enteric (typhoid) fever 30 cases (83%), followed by Tuberculosis 3 cases (8%), followed by Crohn’s disease 2 cases (6%), followed by trauma 1 case (3%).

TABLE 3: SHOWS AGE-GENDER DISTRIBUTION

Table 3 shows the Age Gender distribution of typhoid ileal perforation. The present study shows between 20 to 29 years of age group, 9 males and 4 females, betwee6 males and 1 female, between 40 to 49 years 3 males and 2 females, between 50 to 59 years 2 males and 1 female and above 60 years 1 male and 1 female noted.

TABLE 4: DURATION OF SYMPTOMS BEFORE ADMISSION:

Table 4 shows the duration of illness before admission. There were no cases noted in 1 to 2week, followed by 13 cases (44%) during 2-3 weeks, followed by 16 cases (53%) in 3-4 weeks, followed by 1 case (3%) during the 4^th week.

TABLE 5: SHOWS SYMPTOMS AND SIGNS

Table 5 shows symptoms and signs of the typhoid ileal perforation. Pain abdomen (100%), vomiting (93%), abdominal distension (73%), fever (70%), diarrhoea (20%), temperature (50%), tachycardia (83%), hypotension (20%), coated tongue (20%), tachypnoea (30%), dyspnoea (20%), abdominal tenderness (100%), guarding (100%), ileus (80%) and clinical jaundice (20%).

TABLE 6: SEROLOGY AND IMAGING

Table 6 shows serology and imaging findings. Air under the diaphragm in x-ray (100%), US Abdomen positive in 26 cases (87%). Biopsy culture positive in 22 cases (73%) and negative in 8 cases (32%), serum widal test positive in 11 cases (37%) and negative in 19 cases (63%), blood culture positive in 5 cases (17%) and negative in 25 cases (83%).

TABLE 7: SITE OF PERFORATION FROM ILEOCECAL JUNCTION

TABLE 8: OPERATIVE PROCEDURE DONE

Table 8 shows the operative procedure executed in the present study. Primary closure and peritoneal lavage were done in 21 cases (70%) followed by primary closure and ileostomy in 6 cases (20%), followed by resection and anastomosis in 3 cases (10%). From this study, the majority of typhoid ileal perforation was managed by primary closure

TABLE 9: POST OPERATIVE COMPLICATIONS

Table 9 shows postoperative complications. Wound infection is seen in 9 cases (30%), followed by pneumonitis in 8 cases (27%), followed by burst abdomen in 2 cases (7%), followed by fecal fistula in 2 cases (7%).This shows that the most common complication was wound infection. Wound infections were managed with intravenous antibiotics according to culture and sensitivity.

TABLE 10: SHOWS RE-EXPLORATION AND OUTCOME OF PATIENT

2 patients were re-explored for burst abdomen and re-do surgery was performed but patients were expired due to pneumonitis. Another 2 patients with fecal fistula were followed up and it was closed spontaneously without requiring re-exploration. The overall mortality was 6.6%.

Typhoid fever is a common infection that has remained a public health problem in developing countries. Terminal ileal perforation must be suspected in all cases of hollow viscus perforation. The enteric perforation is a strong possibility. The typhoid perforation still carries high morbidity and mortality. Early diagnosis and treatment reduce morbidity and mortality. The overall mortality was 6.66% in the present study.

The typhoid ileal perforation should always be treated surgically. There are many surgical procedures to deal with but none is proven to be better than the other. Regardless of the type of procedure executed, surgery in early presentation with good resuscitation is a way to decrease morbidity and mortality.

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