DISSERTATION SUBMITTED FOR DNB ( GENERAL SURGERY )

A STUDY OF SURGICAL MANAGEMENT OF DUODENAL & SMALL BOWEL PERFORATION. STUDY AT WANLESS HOSPITAL MIRAJ

NAME OF INSTITUTE WANLESS HOSPITAL MIRAJ MEDICAL CENTRE MIRAJ, SANGLI MAHARASHTRA

NAME :- DR ABHIJIT ANIL WHATKAR

SUBJECT :- D.N.B. GENERAL SURGERY

DURATION : 3 YEARS 1st JULY-AUG, 2010 TO 31st JULY,2010

REGISTRATION NO :

INSTITUTE : WANLESS HOSPITAL, MIRAJ

TOPIC : STUDY OF SURGICAL MANAGEMANT OF DUODENAL & SMALL BOWEL PERFORATION. STUDY AT WANLESS HOSPITAL, MIRAJ.

NAME OF GUIDE : Dr. T.B.MORE M.S.GENERAL SURGERY.

Dr. T.B.MORE D.N.B GUIDE, GENERAL SURGERY, WANLESS HOSPITAL, MIRAJ.

Dr. D.M.KAMLE HEAD OF DEPT, SURGERY, WANLESS HOSPITAL, MIRAJ.

Dr. D.M.KAMLE DIRECTOR, WANLESS HOSPITAL, MIRAJ.

LIST OF ABBREVIATIONS

ARDS - Acute Respiratory Distress Syndrome

ATT - Anti Tubercular Treatment

C.D - Crohns disease

C.T - Computerised Tomography

DIC - Disseminated Intravascular Coagulation

G.I - Gastrointestinal

GIT - Gastro intestinal Tract

MODS - Multi Organ Dysfunction Syndrome

MOF - Multi Organ Failure

Perf - Perforation

RPM - Right Paramedian

S. Creat - Serum Creatinine

SIRS - Systemic Inflammatory Response Syndrome

T.B - Tuberculosis

W.I - Wound Infection

ABSTRACT BACKGROUND: Small bowel perforation is commonly encountered problem in surgical practice. There are different modes of presentation of cases, which can be misleading in the diagnosis of its origin. It is necessary to know the current surgical procedures for different perforations to manage such a case. An effort has been made here, to know the different modes of presentation, diagnosis and management of perforation pre operative & post operative. And a special attention has been given to the time between the operation and pre-operative time for resuscitation.

MATERIAL AND METHODS: A prospective study of 50 patients presenting to Wanless Hospital with a clinical diagnosis of Small bowel perforation between August 2010 and July 2011 is done. The clinical data, the investigations done and the surgical procedure undertaken are recorded according to the proforma decided.

OBSERVATIONS: ********************* **** Pain abdomen was the presenting complaint of all the patients, followed by Vomiting (76%), Fever (46%), and Distension (44%). Diagnosis was made clinically with guarding and rigidity being present in 84% cases and obliteration of liver dullness in 42% cases. Erect abdomen X-ray showed air under diaphragm in 70% cases. Right Para median incision was employed in 50% of cases. The most common cause of Small bowel perforation was Ileal perforation. Tubercular perforation was the most common cause of ileal perforation.

Resection and anastomosis in two layers was the commonly done procedure. Patients were followed up in the post operative period to know the post operative complications, morbidity and mortality rates. The most common complication in this series was wound infection which accounted for 17 cases (34%). Wound dehiscence was seen in 3 cases. CONCLUSIONS: Pain abdomen (100%) is the most common presenting symptom in Small bowel perforation followed by vomiting,fever, abdominal distension and constipation. Erect abdomen X-ray and USG abdomen are very useful investigation for diagnosis in perforation. Resection and anastomosis was the most common procedure employed. The most common complication in this series was wound infection. Mortality rate in our study was 10%. KEY WORDS: Small bowel; Perforation; Management; Mortality; Morbidity

CONTENTS

1.

Introduction

2. Aims and objectives 3. 4. 5. 6. Review of literature Anatomy Physiology Pathophysiology Material methods and observation 7. 8. 9. Discussion Summary Conclusions

10. Performa 11. Bibliography 12. Master chart 13. Abbreviations

INTRODUCTION ************************* Perforation of the small bowel especially terminal ileum is a common abdominal emergency faced by the general surgeon. Perforation of the small bowel from a wide variety of causes comprises the majority of emergency surgical admissions. Perforation of the small bowel is relatively uncommon in western societies except in regions where typhoid, tuberculosis and parasitic infestation are endemic.1 The preeminent complication of typhoid is perforation seen in 3rd week. The ileum is the main site of perforation. 2 The perforated viscus challenges the surgeons skill as a technician and his knowledge of pre-operative, intra-operative and post-operative care of severely ill surgical patient. 3 Majority of the patients present with sudden onset of abdominal pain. A high index of suspicion is essential to diagnose hollow viscus perforation early as significant mortality and morbidity results from diagnostic delay. Surgery plays an important role in the management of perforations. Evaluation and management of gastro intestinal perforation provide some of the most challenging experiences for a surgeon with the advent of new technology. This study is undertaken to find out the age and sex incidence, etiological factors, clinical features and various surgical procedures for gastro intestinal perforations, its complications in our setup.

AIMS & OBJECTIVES

1. 2.

To study the various causes of small bowel perforation. To study various clinical features of small bowel perforation.

3. 4. 5. 6.

To study various diagnostic modalities especially X-ray abdomen erect. To study various surgical procedures & outcomes. To study post surgical complications & management. To study outcomes after certain time of resuscitation.

REVIEW OF LITERATURE The Hippocratic facies seen in terminal stages of peritonitis was described by hippocrates in 460 B.C. 4 Aristotle was the first to discribe intestinal injury as consequence of blunt abdominal trauma. 5 Singhai et al showed that ileo-caecal region was a commonest site of involvement in abdominal tuberculosis.
6

Bhansali et al in 1968 reported that closure of tubercular perforation with or without bypass has been show to give poor results and hence resection and anastomosis recommended. 7 Das . P.Shukla in 1968 showed that abdominal tuberculosis was 2 to 3 times more common in females. 8 Nair S.K in 1981 reported maximum morbidity in the form of wound infection in 52% of the patients, followed by fecal fistula (16%), septicemia (8%), respiratory infections (4%). 9 Beniwal Uday Singh in 2003 concluded that repair of the typhoid perforation is better procedure than temporary ileostomy in enteric perforation due to its cost effectiveness and absence of complications related to ileostomy. 10 Ileostomy and ileo transverse bypass should be considered as a treatment option in patients with unhealthy gut.

GROSS ANATOMY The length of the alimentary tract in normal humans averages about 453 cm. from the nose to the anus. The duodenum is approximately 21 cm. long, and the colon is approximately 109 cm. long. The combined length of the jejunum and ileum is 261 cm., or about three fifths of the entire canal. 11 The jejunum begins at the duodenojejunal angle, supported by the ligament of Treitz. The jejunum constitutes the proximal two fifths of the small intestine, and the ileum makes up the distal three fifths; however, there is no clear demarcation between jejunum and ileum. The small intestine, which decreases in luminal diameter as it proceeds distally, is convoluted or folded upon itself to occupy the central and lower part of the abdominal cavity; it is enclosed laterally and superiorly by the colon. 12

Figure 1: Mucosa and Musculature of Jejunum

Figure 2: Mucosa and Musculature of Ileum

Mesentery: The mesentery, a large fold of peritoneum, suspends the small intestine from the posterior abdominal wall. The base of the mesentery attaches to the posterior abdominal wall to the left of the second lumbar vertebra and passes obliquely to the right and inferiorly to the right sacroiliac joint. The mesentery contains blood vessels, nerves, lymphatics, and lymph nodes, as well as considerable fat. It attaches to the small intestine along the length of one side, the mesenteric border, leaving the remainder of the surface of the bowel covered by its visceral peritoneum, the serosa. The broad-based attachment of the mesenteric base stabilizes the small bowel and prevents it from twisting upon its blood supply.

Blood Supply: The small intestine receives its blood supply from the superior mesenteric artery, the second large branch of the abdominal aorta. The superior mesenteric artery courses anterior to the uncinate process of the pancreas and the third portion of the duodenum, where it divides to supply the pancreas, duodenum, and entire small intestine, as well as the ascending and transverse colon. The intestinal arteries branch within the mesentery to unite with adjacent arteries to form a series of arterial arcades before sending small straight arteries to the small intestine. The intestinal arteries contact the small intestine on the mesenteric border, where they pass toward the antimesenteric border, sending small branches into the layers of the intestine. The veins of the small intestine drain into the superior mesenteric vein, a major tributary to the portal vein.

Lymphatics: Peyer's patches are lymph nodules aggregated in the submucosa of the small intestine. These lymphatic nodules are most abundant in the ileum, but the jejunum also contains them. The lymphatic drainage from the small intestine passes into three sets of mesenteric nodes: a first set close to the wall of the small intestine, a second set adjacent to the mesenteric arcades, and a third set along the trunk of the superior mesenteric artery. The superior mesenteric preaortic group drains into the intestinal trunk, which drains into the cisterna chyli. The lymphatic drainage of the small intestine constitutes a major route for transport of absorbed lipid into the circulation.

Mucosa: The mucosal surface of the small intestine contains numerous circular mucosal folds called the plicae circulares (valvulae conniventes, or valves of Kerckring). These folds are 3 to 10 mm. in height; they are taller and more numerous in the distal duodenum and proximal jejunum, becoming shorter and fewer distally. Intestinal villi barely visible to the naked eye resemble tiny finger-like processes projecting into the intestinal lumen.

Innervation: The parasympathetic and sympathetic divisions of the autonomic nervous system provide the efferent nerves to the small intestine. The parasympathetic preganglionic fibers pass through the vagus nerves to synapse with neurons of the intrinsic plexuses of the intestine. The sympathetic preganglionic fibers arise from the ninth and tenth thoracic segments of the spinal cord and synapse in the superior mesenteric ganglion. The postganglionic sympathetic fibers pass along the branches of the superior mesenteric artery to the intestine. Pain from the intestine is mediated through thoracic visceral afferents, not vagal afferents. Although the vagus contains large numbers of afferent fibers, thoracic visceral afferents, not vagal afferents, mediate pain from the intestine. 13

MICROSCOPIC ANATOMY The small intestine consists of four layers. From the lumen outward, they are the mucosa, the submucosa, the muscularis, and the adventitia or serosa.

Mucosa: The mucosa of the small intestine encompasses the epithelium, the lamina propria, and the muscularis mucosae. The mucosal surface has two important structural features: the villi and the crypts of Lieberkhn. The villi have a columnar epithelial surface and a cellular connective tissue core of lamina propria. Each villus contains a central lymphatic vessel called a lacteal, a small artery, a vein, and a capillary network. Human jejunal villi measure 0.5 to 1.0 mm. high and number 10 to 40 villi per square millimeter of mucosal surface. In addition to the vessels, the villi contain smooth muscle fibers extending from the muscularis mucosae, providing contractility to each villus. The crypts of Lieberkhn, or intestinal glands, reside adjacent to the bases of the villi and extend down to, but not through, the muscularis mucosae. The lamina propria between the intestinal epithelium and the muscularis mucosae contains blood and lymph vessels, nerve fibers, smooth muscle fibers, fibroblasts, macrophages, plasma cells, lymphocytes, eosinophils, and mast cells, as well as elements of connective tissue. 14 Scanning electron micrographs provide an in-depth perspective of the mucosa with excellent resolution. The villi vary in shape from circular to flattened or fingershaped. The finger-shaped villi are 0.1 to 0.25 mm. in diameter, are corrugated by deep horizontal clefts, and have holes 3 to 8 m. across on the surface, representing the

openings of the goblet cells. 23 The muscularis mucosa is a thin layer of smooth muscle separating the mucosa from the submucosa. 15 Cells of the Epithelium: Cells of the Villi. The columnar epithelial cells are responsible for absorption. These cells, 22 to 26m. tall, exhibit a striated luminal border (brush border) and a basally placed nucleus. The microvilli, which are projections 1 m. tall and 0.1 m. wide and are produced by numerous folds in the apical plasma membrane, account for the brush border appearance. The microvilli greatly increase the absorptive surface of the epithelial cell. The membrane of the microvillus is continuous, without fenestrations and it separates the lumen of the gut from the interior of the epithelial cell. The brush border contains high concentrations of digestive enzymes, particularly disaccharidases. The plasma membrane contains 80% to 90% of the disaccharidase activity of the intestinal cell. These findings indicate that the microvilli, besides increasing absorptive surface, perform an important digestive function. Goblet cells are present in both the villi and the crypts. These cells have cytoplasm filled with mucous granules between the nucleus and the apical brush border. Intestinal goblet cells secrete their mucus by merocrine secretion. 13

Cells of the Crypts: Enterochromaffin cells reside in the crypts of the small intestine and in other parts of the gastrointestinal system as well, including the esophagus, stomach, colon, gallbladder, and pancreas. These cells do not contact the intestinal lumen, and their secretory granules are usually below the nuclei away from the lumen, suggesting

secretion into the blood rather than the lumen. The enterochromaffin cells have an endocrine function. Paneth cells occur in the base of the crypts and are structurally similar to cells known to secrete large amounts of protein, such as pancreatic or parotid acinar cells. The function of Paneth cells is unknown. Undifferentiated cells, the most frequent cell in the base of the crypts, multiply and differentiate to replace lost absorptive cells.

Epithelial Renewal: The epithelium of the small intestine is a dynamic, rapidly proliferating tissue in which old dying cells are constantly replaced by newly formed cells, thus maintaining the structural integrity of the mucosa. Mitotic division of undifferentiated cells occurs in the crypts. New growth replaces the population of intestinal epithelial cells every 3 to 7 days. 13

Submucosa: The submucosa is a strong fibroelastic and areolar connective tissue layer containing vessels, nerves, and lymph nodules.

Muscular Layer and Intramural Neural Structures

Two distinct layers of smooth or nonstriated muscle, an outer longitudinal coat and an inner circular coat, form the muscular portion of the small intestine. Intestinal smooth muscle fibers are spindle-shaped structures about 250 m. long. The plasma

membrane of adjacent cells approximate at points, forming structures called nexuses. The nexuses allow electrical continuity between smooth muscle cells and permit conduction through the muscle layer. The small intestine has four identifiable neural plexuses: (1) The subserous plexus, noticeable on the mesenteric attachment, forms the transition between the mesenteric nerve fibers and the myenteric plexus. Ganglia occur in the subserous plexus. (2) The myenteric plexus is located between the longitudinal and circular muscle layers and consists of three networks linking various ganglia and ramifying within the muscle layers. (3) The submucosal plexus is a network of nerve fibers and ganglia in the submucosa. (4) The mucous plexus consists of fibers from the submucosal plexus extending into the mucosa. This plexus does not contain nerve cell bodies. 13,14,16

PHYSIOLOGY DIGESTION AND ABSORPTION Carbohydrate: The digestion of starch by amylase probably occurs predominantly in the lumen of the alimentary tract. Maltose, maltotriose, and dextrin, as well as the dietary

disaccharides lactose (glucose-galactose) and sucrose (glucose-fructose), are completely broken down to the constituent monosaccharides by the microvilli. The intestinal cells actively transport glucose and galactose against a concentration gradient. Glucose and galactose compete for transport in a manner similar to competitive inhibition in other enzyme substrate systems. The active transport of sugars requires metabolic energy as well as oxygen. Sodium ion is important in the transport of glucose and galactose. Glucose and galactose are absorbed by carriermediated active transport. The absorption of glucose and galactose depends on Na+ movement into the cell produced by the Na+K+ ATPase, located on the basolateral cell membrane. Fructose, the other significant monosaccharide, is not absorbed by active transport but probably enters the intestinal cells by facilitated diffusion. 13,16

Protein: The intestinal enzyme enterokinase converts trypsinogen to trypsin. The activation of trypsinogen is autocatalytic; that is, trypsin also activates trypsinogen. Trypsin likewise activates the other pancreatic proteolytic enzyme precursors. Amino acids are the final product of protein digestion. However, some dipeptides are also absorbed.

Amino acids are absorbed from the intestinal lumen by carrier-mediated active transport. The transport of amino acids requires oxygen and sodium. The sodium pump on the basolateral cell membrane of the intestinal epithelial cells maintains an electrical potential across the brush border. Digestion and absorption of protein are usually 80 to 90% completed in the jejunum. 13

Fat: The bile salts that occur in humansglycine or taurine conjugates of cholic acid, deoxycholic acid, or chenodeoxycholic acidare detergents; they are water-soluble at one portion of the molecule and fat-soluble at the other. In solution, substances produce polymolecular aggregates called micelles, which can dissolve fat. 17 Lecithin, a phospholipid, greatly enhances the capacity of bile salts to form micelles and dissolve fat. Bile salt and lecithin solubilize lipid in an aqueous environment to produce a micellar solution. This provides an optimal physicochemical environment for the action of pancreatic lipase. Pancreatic bicarbonate regulates the pH of the intestinal lumen to allow lipase to function optimally. An alkaline pH favors ionization of fatty acids and bile salts, which increases their solubility in micelles. An alkaline pH also increases the solubility of bile salts. Chylomicrons pass from the epithelial cells into the lacteals, where they pass through the lymphatics into the venous system. Medium-chain triglyceride (C 8 to C 10) may be absorbed without hydrolysis and pass into portal blood rather than into lymph via the formation of chylomicrons.

The jejunum absorbs most dietary fat. Although unconjugated bile acids are absorbed in the jejunum by passive diffusion, the conjugated bile acids that form micelles are absorbed in the ileum by active transport. There they are almost completely absorbed and pass via the portal venous blood to the liver, for resecretion as bile.

Water and Electrolytes: Large quantities of water enter the small intestine. Some water is ingested, but the digestive glands secrete a larger amount to provide the luminal environment for optimal digestion and absorption. Five to 10 liters of water enters the small bowel daily, whereas only about 500 ml. or less leaves the ileum and enters the colon. The small intestine, therefore, absorbs large quantities of water.18 The important factors in the movement of water across the intestinal mucosa are diffusion and osmotic filtration caused by osmotic or hydrostatic pressure differences across the membrane. Intestinal cells have a sodium pump (Na+K+ ATPase) on the basolateral cell membrane that moves Na+ out of the cell into the basolateral intercellular space. Movement of K+ into the cell accompanies the Na+ movement. The sodium pump produces a concentration gradient that moves Na+ into the cell from the lumen. This movement of Na+ by the sodium pump also transports glucose, amino acids, and oligopeptide into the intestinal epithelial cells. In the jejunum, a small portion of sodium absorption is mediated by active transport, but most of jejunal sodium absorption occurs by bulk flow along osmotic gradients. The jejunum effectively absorbs bicarbonate against steep electrochemical gradients.19

The human ileum absorbs Na+, Cl- against steep electrochemical gradients; this absorption is unaffected by water flow and is not stimulated by glucose, galactose, or HCO 3 -. Potassium is passively absorbed from the intestine according to its electrochemical gradients. Calcium is absorbed, particularly in the proximal small intestine (duodenum and jejunum), by a process of active transport. This ion is absorbed better from an acid than from an alkaline environment, which may explain the better absorption in the proximal intestine. Vitamin D and parathyroid hormone enhance calcium absorption. An important electrolyte absorbed by the small intestine is iron. One of the important functions of the small intestine is to regulate the body pool of iron.

MOTILITY13, 16 There are several types of visible small intestinal muscular activity. The segmenting contraction is a localized circumferential contraction of the circular muscle over a length of about 1 cm. of the small intestine. Segmenting contractions divide the luminal content within the area of contraction. Their rhythmic segmenting activity occurs in the proximal small intestine at about nine contractions per minute. Segmenting contractions occurring regularly and rhythmically in adjacent portions of the small intestine divide and subdivide the intestinal content, mixing it and exposing it to larger areas of mucosa, which facilitates digestion and absorption. Peristalsis consists of intestinal contractions passing aborally at a rate of 1 to 2 cm. per second through several centimeters of intestine. Peristalsis is slower in the distal than in the proximal small bowel. The major function of peristalsis is the distal movement of intestinal chyme.

The Migrating Myoelectrical Complex (MMC): During the interdigestive period, there are cyclically occurring contractions that move aborally along the intestine every 75 to 90 minutes during fasting. Most of these fronts of activity begin in the stomach or duodenum, last about 4 minutes, and pass along the gut at about 6.8 cm. per minute. The MMC is thought to sweep or cleanse the intestine during the interdigestive period. Motilin may regulate the MMC. 16, 20

Regulation of Small Intestinal Motility: .. Myogenic Factors: Two types of electrical activity can be recorded from the small intestine. Slowwave electrical activity begins in the longitudinal muscle layer of the duodenum and is propagated distally. This phenomenon, called the basic electrical rhythm (BER), is independent of the intrinsic neural plexuses, and is unrelated to motor activity. Intestinal spike potential may occur spontaneously during depolarization or from stretching of the bowel, and it is associated with motor activity.

.. Neurogenic Factors: Intrinsic neural regulation is initiated by stimulation of the mucosa, particularly by distention, which causes contraction of longitudinal and circular muscle, propelling luminal content distally. The intrinsic nerve supply regulates rather than initiates motor action. In general, sympathetic activity inhibits motor function, whereas parasympathetic

activity stimulates it. Epinephrine inhibits small intestinal motor activity, whereas

acetylcholine stimulates it. Distention of the small intestine can inhibit small intestinal motility by the intestinointestinal inhibitory reflex. Distention of the ureter, renal pelvis, or biliary system or peritoneal irritation may inhibit intestinal movements. 13

.. Hormonal Factors: Gastrointestinal hormones may be important in regulating intestinal motility. Gastrin stimulates gastric and intestinal motility and relaxes the ileocecal sphincter. Cholecystokinin-pancreozymin (CCK-PZ) also stimulates intestinal motility and may decrease intestinal transit time. Secretin and chemically similar glucagon inhibit intestinal motility.

ENDOCRINE FUNCTION The mucosa of the small intestine is an important source of peptide hormones, whose main function is to regulate the gastrointestinal tract.21

Secretin: Secretin is released from duodenal mucosal S cells in response to intraluminal H+. Secretin promotes digestion by stimulating copious secretion of water and

bicarbonate from the pancreas. This action facilitates entry of pancreatic enzymes into the intestinal lumen and provides a pH favoring digestion of fat. Secretin is also a choleretic and inhibits gastric acid secretion and gastrointestinal motility.

CCK-PZ: Cholecystokinin and pancreozymin are the same substance and are released from intestinal mucosal I cells. CCK-PZ facilitates digestion and absorption by stimulating emptying of the gallbladder as well as by increasing bile flow and relaxing the sphincter of Oddi. Another important action of CCK-PZ is stimulation of pancreatic enzyme secretion Other Gut Hormones .. Enteroglucagon is released from the EG cells, which occur predominantly in the distal small intestine. Enteroglucagon is released by carbohydrate and long-chain fatty acid and inhibits intestinal motility. .. Gastric inhibitory polypeptide: GIP is released from K cells, predominantly in the jejunum, on stimulation by carbohydrate or fat. The concentration of serum GIP increases after meals, and it is believed that its most significant action is to stimulate insulin secretion. .. Motilin is released from the EC cells of the intestine, predominantly the jejunum. Motilin inhibits gastric emptying in humans and may also alter the interdigestive myoelectrical complex and cause changes in the lower esophageal sphincter.

IMMUNOLOGIC FUNCTION OF THE INTESTINE The intestine is a source of immunoglobulin, particularly IgA.22 It is believed that this immunoglobulin arises from plasma cells in the lamina propria, and after linkage with a protein synthesized by epithelial cells, it is secreted into the lumen. Secretory IgA

contains antibody activities, the exact roles of which are not yet known. SMALL BOWEL PERFORATION CLASSIFICATION 1,23 The causes of perforation are broadly classified into Non-traumatic nflammatory bowel disease. I cute Typhoid fever. A Necrotizing entero colitis. Chronic - Tuberculosis. Crohns disease. Vascular Arterial cclusive O o Thrombosis o Atherosclerosis o Oral contraceptive pill. o Embolism. o Aortic aneurysm. o Valvular heart disease. Non occlusive o Spasm o Reflex due to systemic hypo perfusion. o Drugs: digoxin, vasopressin. o Congestive heart failure. o Arrhythmia. 19

Venous Intra-abdominal o Portal stasis o Pelvic and abdominal infections. o Tumor. o Volvulus. o Adhesions. Secondary to blood dyscrasia o Polycythemia. o Splenic anaemia. Thrombo phlebitis migrans Oral contraceptive pill. Neoplastic Leiomyosarcoma Adenocarcinoma Kaposi sarcoma. Lymphoma. Miscellaneous Meconium ileus. Diverticular disease. Foreign body. Round worm. Radiation enteritis Peptic ulcer in Z.E. syndrome. Acute intestinal obstruction of any etiology. Drugs: steroids, KCl. Traumatic External violence due to blunt or penetrating abdominal injury. Operative injury.

20 Typhoid is the commonest cause of ileal perforation in tropics. Analysis of 12 regional reports from different parts of India between 1972 and 1989 reveals that the causes of small bowel perforation in 450 cases out of 513 (87.7%) were Typhoid.24 As evidence obtained from studies in university hospitals, Ibaban, Nigeria by J.A.S. Dickson and G.J. Cole in 1964,25 the causes of perforation of terminal ileum has aroused a considerable speculation and suggested causative agents include Typhoid Tuberculosis 21

 Trauma Ascariasis Amoebiasis Archampong26 from Ghana has reported that in Tropics, perforation of Ileum is most frequently encountered complication of Typhoid fever. Other causes were Tuberculosis Trauma Ascariasis Amoebiasis Mackels Diverticulum Intussusception Crohns Disease Malignancy Non-specific ulceration S.K. Nair9 from New Delhi in a series of 50 cases of non-traumatic perforation has reported that Typhoid, Tuberculosis, Amoebiasis and Round worms were most common causes. 22

TYPHOID Typhoid Pathogenesis: Typhoid Perforation is the foremost and most dreaded complication of typhoid fever and is fairly common surgical emergency in the tropics and sub-tropics. Amongst all, the intestinal perforation is the most serious complication of typhoid fever. Typhoid fever is caused by Gram negative bacillus, Salmonella typhi and is contracted by ingestion of contaminated water or food. The ingested bacteria enter the blood stream via peyers patches, multiply in RE system during next 14 days and then spread hematogenously. This phase is corresponding with onset of clinical symptoms. Bacteria reach the gut wall via blood stream or bile and concentrate in peyers patches of terminal ileum which swell. There is an associated mesenteric adenitis. Ulceration of the payers patches in a cranio caudal access of bowel occurs and complicated by hemorrhage or perforation, which most frequently is on the anti-mesenteric border of terminal ileum. Perforation usually occurs 8 to 11 days after the onset of clinical symptom.2 Intestinal lesions, which are confined to the lymphoid tissue, are most marked in the lower part of ilum but may involve greater part of small intestine. The Peyers patches and solitary follicles are crowded with large mononuclear phagocytes, so that the lymphoid masses project above the surface. Edema associated with hyperplasia leads to vascular obstructions, necrosis and consequent death of the covering mucosa and formation of an ulcer. The typhoid ulcers are ovoid or round in shape with irregular undermined edges. The long axis of the ulcer lie along the long axis of the bowel, along which lies the peyers patches. The ulcers are usually shallow but the sub-mucosa is often perforated so 23

that the floor of the ulcer is formed by muscularis propria or the serosal layer. If extensive, may lead to erosion of the blood vessels or perforation of the gut wall. The ulcers usually heal by scaring without causing intestinal obstruction as the scar do not encircle the intestine. Sudden, acute abdominal pain followed by guarding and rigidity of the abdomen, cessation of bowel sounds; loss of liver dullness, vomiting, gas under the diaphragm is typical of small bowel perforation. The patient with typhoid fever usually respond in a few days to treatment with chloramphenicol but the condition of the intestine may not match the clinical improvement and perforation may occur after the temperature has fallen and patient seems well on the way to recovery. The incidence of perforation varies from 0.5 39 % of typhoid fever as reported various authors from different countries. Age and Sex: 25-34 There is a male predominance with second and third decades as a peak age group. Table2: Age and Year Sex Incidence of Typhoid Perforations Author Duration of illness prior to perforation25-34: Three weeks is the duration of illness prior to perforation. Table 3: Duration of illness Year prior to Typhoid Perforation Author Rowland Dickson and Cole Abdal Meneim Theodore P. Welchi Prasad et al Gandhi J.M. Eustache Incidence41 The disease is as common in men as in women and can strike persons of any age, although the peak age of onset is between the second and fourth decades of life. The disease is more common among whites than blacks or Asians. A familial tendency is noted, but the disease is not inherited in an autosomal dominant pattern. Etiology42 1961 1964 1969 1974 1975 1975 1983 ROHNS DISEASE 5 16 1 30 8 30 1 30 7 28 49 7 14 Duration (days) M:F Peak Age (Yrs)

No specific etiology of the disease has been identified. Microbiologists have long sought a specific micro-organism that might be the cause of the disease. Recent reports of the isolation of Mycobacterium paratuberculosis from segments of bowel affected with Crohn's disease excited interest, but this organism as a specific etiology for the disease has yet to be proved. Also, no virus has been identified as an etiologic agent. An immunologic origin of the disease has also been sought. Some have postulated that a childhood sensitization to milk impairs mucosal integrity and allows bacteria or bacteriologic products to enter the body. A cellular and humoral immune response to these products then ensues. The ileocolic epithelium, in particular, may be the target of a necrotizing immune response, with ensuing ulceration, tissue destruction, and the clinical appearance of the disease. Although an immunologic response certainly plays a role in the pathogenesis of the condition, its role as an etiologic agent is still unclear. Smoking may exert a stimulating effect on the disease; many patients with Crohn's disease are heavy smokers. 39

Pathology Location of Lesions: Crohn's disease is a generalized inflammatory disorder of the alimentary tract that can involve any area from the mouth to the anus. The disease, however, is discontinuous and segmental. The small intestine and the large intestine are the most frequent sites of gross, macroscopic involvement. 55% of patients had involvement of small and large intestine, 30% of small intestine alone, and 15% of large intestine alone Gross Pathologic Features: Aphthous Ulcers. One of the earliest macroscopic signs of Crohn's disease is the appearance of aphthous ulcers in the mucosa of the gastrointestinal tract. These small, flat, soft ulcers have a whitish center and a red border. They are scattered in the mucosa, with normal areas of mucosa in between. As the disease progresses, the aphthous ulcers deepen and coalesce, penetrating through the entire mucosa and forming longer ulcers that may reach 1 cm. or larger. The ulcers remain discontinuous and asymmetrical. They often appear first on the mesenteric border of the bowel and have a linear pattern along the wall of the intestine. Islands of normal mucosa can remain in between the ulcers to give the surface of the bowel a cobblestone appearance. As the ulcers grow and the inflammation spreads, the lesions extend deep into the wall of the bowel through the mucosa and muscularis, out to the serosa, to form transmural fissures and thornlike defects. The inflammatory response creates a thickening of the bowel wall and a narrowing of its lumen, the so-called rubber-hose intestine. The inflammatory response on the serosa and adjacent mesentery also thickens these structures, and the fat of the 40

mesentery creeps around the side of the bowel to add to the thickening. The intestinal lymphatic vessels are engorged, and the lymph nodes in the adjacent mesentery are enlarged. Crohns disease is characterized pathologically by Sharply demarcated and transmural involvement of the bowel by an inflammatory process with mucosal damage. Non caseating granuloma. Fissuring and Fistula. Microscopic Features: Focal Chronic Inflammation. A chronic inflammatory infiltrate appears in the mucosa and submucosa and extends transmurally through the bowel wall. The areas of inflammation are focal and scattered in between areas of uninvolved bowel. Distortion of the normal architecture of the intestinal crypts accompanies the inflammation. Granulomas. A characteristic microscopic lesion of Crohn's disease is the granuloma, which appears in the mucosa, submucosa, or elsewhere in the wall of the bowel or its adjacent lymph nodes, in association with the chronic inflammatory response. Diagnosis is based on the history, physical findings, and appropriate laboratory tests. The physical findings include the palpation of the thickened bowel wall or adjacent inflammatory response or abscesses in the abdomen. Hyperactive bowel tones are heard using auscultation, and peristaltic rushes in the small intestine may even be seen through 41

a thin abdominal wall. Abdominal distention occurs. On inspection, the perianal skin appears bluish, and perianal fissures, abscesses, and fistulas can be identified. Colonoscopy delineates the extent of the lesions in the large intestine. The hallmarks of Crohn's disease are the discontinuous and asymmetrical nature of the endoscopic findings. Biopsies taken during endoscopy show chronic inflammation and sometimes granulomas. Roentgenographic examination of the gastrointestinal tract using BaSO4 reveals the ulcerating lesions scattered in a segmental, irregular pattern along the wall of the involved intestine, producing irregular areas of ulceration, luminal narrowing, and thickened bowel wall. Proximal dilatation of the bowel accompanies obstructing lesions. Long lengths of narrowed terminal ileum may reduce the caliber of the lumen to the size of a string (the string sign). Areas of dilatation may alternate with areas of constriction. The cobblestone appearance of the mucosa may be apparent, as may the rake ulcers. Fissures, fistulas, and perienteric abscesses may be found. Computed axial tomography may help delineate thickened bowel, perienteric abscesses, and perforations. Free air in the abdomen is present with free perforation. Perforation: Acute perforation with a diffuse spreading peritonitis is rare and alarming manifestation of regional enteritis. Treatment43: Simple suture is quite inappropriate and comes with high mortality. Resection is necessary but primary endto-end anastomosis is restricted to only those patients who are 42

healthy without gross peritoneal soiling. If this is present, thorough peritoneal lavage, debridement with antibiotic lavage is given. Ileocoloecostomy with reestablishment of intestinal continuity at later date is considered. 43

SMALL INTESTINE TRAUMA44 The incidence of small bowel injury secondary to blunt trauma ranges from 5% to 15% and approaches 50% for all penetrating abdominal injuries. Injuries to the small intestine following blunt trauma may be due to three mechanisms: (1) crush injury between the vertebrae and the anterior abdominal wall; (2) sudden increase in the intraluminal pressure; and (3) tears at the junction of a mobile and a fixed segment of bowel. Motor vehicle accidents, child abuse, bicycle accidents, and assorted falls account for most of these injuries. The sudden deceleration causes the mobile portion of the bowel to move away from its point of fixation (ligament of Treitz, ileocecal junction, sites of adhesions), causing a tangential tear. Rarely, adhesions involve a portion of the bowel in such a manner that during sudden compression of the abdomen a closed-loop phenomenon is created with a resultant blow-out of the area. Occasionally, direct trauma from a blow or seat belt may be responsible for the damage that occurs at the point of impact. The association of chance-type lumbar fracture with intestinal injuries in children and adults wearing only a lap belt restraining device has now been recognized with sufficient frequency as to require its exclusion. Clinical features: Most patients with a perforated small intestine exhibit some evidence of peritoneal irritation and may have frank abdominal rigidity. Lacerations of the lower small bowel may be particularly deceptive, however, because surrounding loops may wall off the damaged area quickly and efficiently. In such cases, the patient may appear surprisingly well for days, demonstrating only mild localized tenderness. Free air may not 44

be visible radiographically, and bowel sounds may persist. Such patients may eat and have bowel movements for a week or more before fever and other signs of intraperitoneal sepsis appear. Occasionally, damage may occur to the mesentery without involving the bowel. Minor tears are of little significance, but large hematomas may ultimately compress the adjacent mesenteric vessels and cause intestinal ischemia with later perforation. Investigation: Diagnostic peritoneal lavage is 95% accurate in identifying small bowel injury. Diagnostic errors are generally due to small intestinal perforations with minimal bleeding that have developed delayed signs of peritonitis. CT scanning is less precise and requires both oral and intravenous contrast agents and careful inspection for the presence of bowel wall thickening, mesenteric hematoma, or fluid of nonblood density pooling in the pelvis. The presence of any of these signs, particularly when combined with abdominal tenderness or absent bowel sounds, warrants further emergency evaluation or surgical exploration. During any laparotomy for possible intra-abdominal injuries, the entire small bowel should be meticulously examined. Each tear, as it is encountered, should be clamped or quickly sutured to prevent further leakage and contamination of the peritoneal cavity during the remainder of the exploration. The wounds of entrance and exit on the abdominal wall cannot be used to predict the likely site of a small bowel injury because of the mobility of the small intestine and the variability of the patient's position at the time of injury. 45

Treatment: Simple lacerations of the small bowel are sutured with a single layer of interrupted nonabsorbable Lembert sutures after removal of any tissue that is even questionably nonviable. Patients who have multiple additional injuries, shock, dilated small bowel, or a coagulopathy may benefit from a two-layer closure to ensure hemostasis. Care is taken to avoid excessive narrowing of the bowel by repair. Where damage to the bowel wall is extensive or where multiple tears are situated fairly close to one another, resection of the involved segment rather than repair of the individual perforations is preferred. Removal of the extensively damaged intestine is generally safer, provided that a sufficient length of viable bowel remains to permit adequate absorption of food. 46

COMPLICATIONS: Complications of hollow viscous perforations are due to peritonitis Systemic Bacteremia /endotoxic shock. Broncho pneumonia respiratory failure. Renal failure Marrow suppression. MOF Abdomen. Wound infection. Wound dehiscence. Incisional hernia. Obstruction. Paralytic ileus. Residual/Recurrent abscess. Portal pyemia/liver abscess

INTRODUCTION

Small bowel perforation is commonly encountered in surgical practice. The different modes of presentation of cases may be misleading in the diagnosis of its origin. It is necessary to know the current surgical procedures for different perforations to manage such a case. An effort has been made here, to know the different modes of presentation, diagnosis and management of perforation. Perforation of the small bowel especially duodenum & terminal ileum is a common abdominal emergency faced by the general surgeon. Perforation of the small bowel from a wide variety of causes comprises the majority of emergency surgical admissions. Perforation of the small bowel is relatively uncommon in western societies except in regions where typhoid, tuberculosis and parasitic infestation are endemic. The preeminent complication of typhoid is perforation seen in 3rd week. The terminal ileum is the main site of perforation. The perforated viscus challenges the surgeons skill as a technician and his knowledge of pre-operative, intra-operative and post-operative care of severely ill surgical patient. Majority of the patients present with sudden onset of abdominal pain. A high index of suspicion is essential to diagnose hollow viscus perforation early as significant mortality and morbidity results from diagnostic delay. Surgery plays an important role in the management of perforations. Evaluation and management of gastro intestinal perforation provide some of the most challenging experiences for a surgeon with the advent of new technology.

This study is undertaken to find out the age and sex incidence, etiological factors clinical features and various surgical procedures for gastro intestinal perforations, its complications in our institute.

PATHOPHYSIOLOGY Small bowel perforations & duodenal perforations presents as acute pain in abdomen. There are many etiological factors that can lead to perforations..

The perforations are sequely of ulcers of gastrointestinal mucosa. Duodenal ulcers & small bowel ulcers are caused by infective or traumatic means. The foremost etiological factor comes forward is ulcers due to Acid peptic disease, Typhoid ulcers , ulcers due to intestinal tuberculosis & Crohns disease. ACID PEPTIC DISEASE Duodenal ulcers due to APD, presents as an acute emergency. Patients give history of dyspepsia, acidity, burning sensation . Most occur in the first part of the duodenum. A chronic ulcer penetrates the mucosa and into the muscle coat, leading to fibrosis. The fibrosis causes deformities such as pyloric stenosis. When an ulcer heals, a scar can be observed in the mucosa. Sometimes there may be more than one duodenal ulcer. The situation in which there is both a posterior and an anterior duodenal ulcer is referred to as kissing ulcers. Anteriorly placed ulcers tend to perforate and, in contrast, posterior duodenal ulcers tend to bleed, sometimes by eroding a large vessel such as the gastroduodenal artery. Occasionally, the ulceration may be so extensive that the entire duodenal cap is ulcerated and devoid of mucosa. With respected to the giant duodenal ulcer, malignancy in this region is so uncommon that under normal circumstances surgeons can be confident that they are dealing with benign disease, even though from external palpation it may not appear so. Acid peptic disease is major reason in duodenal perforations. In contrast to this typhoid ulcers occurs in terminal part of ileum TYPHOID Intestinal lesions, which are confined to the lymphoid tissue, are most marked in the lower part of ilum but may involve greater part of small intestine. The Peyers patches and solitary follicles are crowded with large mononuclear phagocytes, so that the lymphoid masses project above the surface. Edema associated with hyperplasia leads to vascular obstructions, necrosis and consequent death of the covering mucosa and formation of an ulcer.

The typhoid ulcers are ovoid or round in shape with irregular undermined edges. The long axis of the ulcer lie along the long axis of the bowel, along which lies the peyers patches. The ulcers are usually shallow but the sub-mucosa is often perforated so that the floor of the ulcer is formed by muscularis propria or the serosal layer. If extensive, may lead to erosion of the blood vessels or perforation of the gut wall. The ulcers usually heal by scaring without causing intestinal obstruction as the scar do not encircle the intestine. Like this there are many pathophysiological factors that can come across the study of Small bowel perforations & duodenal perforations.

METHODOLOGY This study, carried out over a span of 3 years, extending from July-Aug, 2010 to Dec, 2013, of 50 patients admitted to Wanless Hospital with a diagnosis of Small Bowel perforation with peritonitis. Only patients who will undergo surgery will be included. The data shall be collected by purposive sampling with respect to their age and sex. A detailed clinical history will be obtained for all the patients with an emphasis on the presenting complaints. A thorough physical examination will be done for all patients. Vital signs will be recorded. Presence of Guarding / Rigidity, rebound tenderness, liver dullness obliteration shall be looked for in all patients. Absence or decreased bowel sounds will also recorded. The investigations, which will be particularly asked for, are white cells counts, Blood routine. An Erect Abdomen X-ray will be done for all patients to particularly look for presence of gas under the diaphragm. All patients will be operated upon, after adequate resuscitation. Patients will be subjected for per-cutaneous intraperitoneal drainage when patients GC is not good for anaesthesia. Patients will be subjected for laparotomy with incisions depending on the probable site of perforation. The perforation shall be managed according to the protocol followed in our hospital.

The surgical procedures undertaken will be recorded. Patients will be followed up in the post operative period to know the post operative complications, morbidity and mortality rates. The data shall be analyzed to find the usefulness of clinical features and investigations for the diagnosis.

Inclusion Criteria Patients aged > 20 years Patients presenting with Small bowel perforation.

Exclusion Criteria Patients aged <20years Patients managed conservatively (non surgically).

CONCLUSION A prospective study of 50 patients admitted to Wanless Hospital with a diagnosis of Small Bowel perforation during the period of Aug2010 to July2013 was included under the study. Only patients who underwent surgery were included. The data was collected by purposive sampling with respect to their age & sex. Incidence is more in the economically productive age group 2nd 4th decade. There was a M:F ratio of 4:1 A detailed clinical history was taken for all these patients with an emphasis on the presenting complaints. A thorough physical examination was done for all patients vital signs were recorded. Pain abdomen was the presenting symptom in almost all cases under study followed by vomiting (76%), fever (46 %) and distension of abdomen (44%). Constipation accounted for only 14% of cases. Presence of Guarding / Rigidity, rebound tenderness, liver dullness obliteration was looked for in all patients. Absence or decreased bowel sounds were also recorded. Majority of cases had guarding and rigidity at presentation (84%), rebound tenderness (84%), absent bowel sounds were in 72% cases, distension of abdomen (66%), obliteration of liver dullness (42%) and per rectal tenderness (12%). 67

 An Erect Abdomen X-ray was done for all patients to particularly look for presence of gas under diaphragm. Pneumoperitoneum was detected in 70% of cases. Patients were subjected for laparotomy with incisions depending on the probable site of perforation. Right Para median incision was employed in 92% of cases. The perforations were managed according to the protocol followed in our hospital. The surgical procedures undertaken were recorded. In our study the most common cause of Small bowel perforation was Ileal perforation. Resection and anastomosis in two layers was the commonly done procedure. Patients were followed up in the post operative period to know the post operative complications, morbidity and mortality rates. The most common complication in this series was wound infection which accounted for 17 cases (34%). Wound dehiscence was seen in 3 cases. Renal failure and ARDS were also part of the complication. Mortality rate in our study was 10%. Delay in the surgery and septicemia were associated with high mortality. 68

SUMMARY Males are affected 4 times more than females. Age groups between 20 and 40 are most commonly involved. Pain abdomen is the most common presenting symptom in Small bowel perforation followed by vomiting, fever, abdominal distension and constipation. Erect abdomen X-ray and USG abdomen are very useful investigation for diagnosis in Small bowel perforation. Resection and anastomosis was the most common procedure employed. Primary closure of perforation also is done for bowel perforations. Wound infection was the most common post operative complication. 69

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PROFORMA Topic : Surgical management of duodenal & small bowel Perforation Case No: Name : Age : Address: Hospital No. : Sex:

DOA: DOD: History: Chief Complaints, Pain - Yes / No Time of onset Site Character

DOO:

Mode of onset : Degree Mild / mod / severe,

Radiation according to site of pain: Aggravating / Relieving factors: Food increase / decrease Movement increase / decrease Vomiting - Yes / No Time of onset Frequency: Contents Projectile / non projectile relation to pain incre / decre, Distension of abdomen : Yes / No Time of onset Relation to pain incre / decre,

Bowels : Last evacuated : Constipation / Diarrhoea. Fever- Yes / No DurationH/O Drug IntakePast History: H/O Haemetamesis / Malena / T.B / Previous treatment / Surgery / Hypertension / Diabetes / Asthma Family history : Personal history : Smoking / alcoholism Food habits : Regular / irregular Degree Chills / Rigors

General Examination: Consciousness : Built / Nourishment Hydration: Pulse: /min, B.P: Temp: Pallor: mm of Hg,

Systemic Examination Per Abdominal Examination: Inspection Shape : Umbilicus : Scar/s of pre surgery : Hernial orifices : Palpation : Tenderness site : Guarding / rigidity Yes / No Rebound tenderness Yes / No Organomegaly Yes / No. Mass : Percussion note over abdomen: Obliteration of liver dullness : Yes / No Shifting dullness : Yes / No. Auscultation : Bowel sounds Frequency : Character :

Per rectal :

Per vaginal : Other systems : C.V.S.: R.S. : C.N.S : PROVISIONAL DIAGNOSIS : INVESTIGATIONS Haemogram :Blood sample for cross matching. UrineBiochemistry:S. Electrolytes : Urea : BSL (R) :Serology :H.I.V. (spot): HBsAg : Hepatitis C:Radiological investigations: 1. X-rayabdomen erect Air under diaphragm : Air fluid level : S. creat :

Other findings : 2. 3. 4. CXR : Ultrasonography:Other CT scan Pre-op treatment: Antibiotics : I.V.F : Gastric aspiration : Others : Operative details: Anaesthesia:Incision: Laparotomy findings : Type of procedure / definitive surgery : Drain put/ not put Closure single layered / Layered closure. Post-op Management: I.V.F : Antibiotics : H2 blockers/ PPI : Blood transfusions:

Ryles tube aspiration:-:

Oral feeds started on : RT removed on: Drain removal: Suture removal: Complications General Pulmonary / renal / toxemia / thrombosis / others, Local Treatment of complications : Conditions on discharge :Follow up : 1st2nd3rd4th-

Mucosa & musculature of jejunum

mucosa & musculature of ileum