INTESTINAL OBSTRUCTION

Under guidance of Dr.S.B.Deshmukh sir Dr.N.U.Jambhulkar sir Dr.M.P. Pote sir

Intestinal obstruction is defined as partial or complete blockage of the bowel that results in failure of intestinal contents to pass. Classification according to : A)pathological cause: 1)simple 2) strangulated B)level of obstruction: 1) high small intestinal obstruction 2) low small intestinal obstruction 3) large intestinal obstruction C)onset and course of obstruction 1) acute 2)chronic D) mechanical Vs Adynamic E) complete Vs incomplete

Dynamic Adynamic Intraluminal Paralytic ileus Impaction Mesenteric vascular Foreign bodies occlusion Bezoars Pseudo-obstruct Gallstones Intramural Stricture Malignancy Extramural Bands/adhesions Hernia( internal /external ) Volvulus Intussusception

Etiology according to age

Neonates: congenital atresia , volvulus neonatorum, anorectal malformation ,mechonium ileus and Hirschsprung`s disease infant : ileocaecal intussusception , Hirschsprung`s disease and strangulated hernia Adult: adhesion, strangulated hernia Elderly : colon carcinoma, adhesion and strangulated hernia

 Adhesion (80-90% of SBO in pts with prior abdominal surgery) Hernia Tumor Abscess Hematoma Annular pancreas SMA syndrome Congenital lesions Gallstone ileus Intussusception Foreign body (bezoars, worms, etc) Meconium ileus Malrotation

SMALL BOWEL OBSTRUCTION: CAUSES

LARGE BOWEL BOSTRUCTION:CAUSES

Cancer (60%) Volvulus (sigmoid > cecum) Adhesions Hernia UC Diverticulitis Congenital lesions Fecal impaction Adynamic ileus Hirschsprungs Meconium ileus Foreign body

 When the bowel is occluded at a single point along the intestinal tract, simple obstruction is present. When a segment of bowel is occluded at two points along its course by a single constrictive lesion that occludes both the proximal and the distal end of the intestinal loop as well as traps the bowels mesentery, closed-loop obstruction is present. When the blood supply to a closed-loop segment of bowel becomes compromised, leading to ischemia and eventually to bowel wall necrosis and perforation, strangulation is present. The most common causes of simple obstruction are intra-abdominal adhesions, tumors, and strictures. The most common causes of closed-loop obstruction are hernias, adhesions, and volvulus.

Pathophysiology
In obstruction, regardless of the cause of obstruction or its acuteness of onset, the proximal bowel dilates and develops an altered motility. Below the obstruction, the bowel exhibits normal peristalsis and absorption until it becomes empty, when it contracts and becomes immobile. Initially, proximal peristalsis is increased to overcome the obstruction, If the obstruction is not relieved the bowel begins to dilate causing a reduction in peristaltic strength, ultimately resulting in flaccidity and paralysis.

 The metabolic effects of fluid loss depend on the site and duration of the obstruction. With a proximal obstruction, dehydration may be accompanied by hypochloremia, hypokalemia, and metabolic alkalosis associated with increased vomiting. Distal obstruction of the small bowel may result in large quantities of intestinal fluid into the bowel; however, abnormalities in serum electrolytes are usually less dramatic.

 As the intraluminal pressure increases in the bowel, a decrease in mucosal blood flow can occur. These alterations are particularly noted in patients with a closed-loop obstruction in which greater intraluminal pressures are attained. A closed-loop obstruction, produced commonly by a twist of the bowel, can progress to arterial occlusion and ischemia if left untreated and may potentially lead to bowel perforation and peritonitis. Bacteria translocating to mesenteric lymph nodes and even systemic organs.However, the overall importance of this bacterial translocation on the clinical course has not been entirely defined.

The distension proximal to an obstruction is produced by two factors: Gas -Most of the gas that accumulates originates from swallowed air, although some is produced within the intestine. there is a significant overgrowth of both aerobic and anaerobic organisms resulting in considerable gas production. Fluid -The fluid consists of swallowed liquids and gastrointestinal secretions Following obstruction

Dehydration is therefore due to 1. 2. 3. 4. Reduced oral intake Defective intestinal absorption Losses due to vomiting Sequestration in the bowel lumen

STRANGULATION:Causes External Hernial orifices Adhesions/bands Interrupted blood flow Volvulus Intussusception Increased intraluminal pressure Closed-loop obstruction Primary Mesenteric infarction

 The venous return is compromised before the arterial supply. The resultant increase in capillary pressure leads to local mural distension with loss of intravascular fluid and red blood cells intramurally and extraluminally. Once the arterial supply is impaired, haemorrhagic infarction occurs. As the viability of the bowel is compromised there is marked translocation and systemic exposure to anaerobic organisms with their associated toxins. The morbidity of intraperitoneal strangulation is far greater than with an external hernia

 With partial small-bowel obstruction, only a portion of the intestinallumen is occluded, allowing passage of some gas and fluid.

The progression of pathophysiologic events described above tends to occur more slowly than with complete small-bowel obstruction, and development of strangulation is less likely.

Closed-loop obstruction
This occurs when the bowel is obstructed at both the proximal and distal points. A classic form of closed-loop obstruction is seen in the presence of a malignant stricture of the right colon with a competent ileocaecal valve. Unrelieved, this results in necrosis and perforation.

Clinical Presentation
The symptoms : colicky abdominal pain, nausea, vomiting, obstipation.

DURATION - Nature of Presentation of Obstruction will be influenced by whether the presentation is I. Acute Obstruction usually occurs in small bowel obstruction with sudden onsets of severe colicky central abdominal pain, distension, with early vomiting and constipation. II. Chronic obstruction is usually seen in large bowel obstruction with lower abdominal colic and absolute constipation, followed by distension. III. In Acute on Chronic Obstruction there is a short history of distention and vomiting against a background of pain and constipation. IV. Subacute Obstruction implies an incomplete obstruction. Presentation will be further influenced by whether the obstruction simple (With blood supply is intact) or strangulated (there is interference to blood flow)

PAIN - The Pain of intestinal obstruction is true colic, and it is the first symptom encountered. SiteOnsite- Sudden Character - Colicky i.e. pain caused by spasm, intermittent. Radiation - No Radiation. Associated SymptomsTiming- Small Bowel colic occurs every 2-20 minutes. Large Bowel Colic occurs about every 30 minutes or more. Exacerbating and Relieving Factors- Corresponds with Peristalsis Severity- Sever.

VOMITING - Frequent vomiting, nature of Vomitus depends on the level of obstruction.

I. Pyloric Obstruction vomitus is watery and acidic. II. High Small Bowel Obstruction vomitus is GreenishBlue and Bile-Stained. III. Lower Small Bowel Obstruction vomitus is foul smelling and Brown (Faeculent Vomit) IV. Large Bowel Obstruction vomitus is usually a late symptom.

DISTENTION - The lower the site of obstruction the more bowel there is available to distend.
Higher up Bowel Obstruction is NOT associated with distension. Colon Obstruction causes the colon to distend around the periphery of the abdomen and might extend into the small bowel if the ileocaecal valve is incompetent.

ABSOLUTE CONSTIPATION - Develops once the block becomes complete and the bowel below is empty, so that neither feces nor flatus are passed.
Occurs Early in lower Large Bowel Obstruction. Occurs Late in High Small Bowel Obstruction.

Late Manifestations Pyrexia Respiratory Distress Dehydration Hypovolemic Shock Peritonism

Physical examination
The patient with intestinal obstruction may present with tachycardia and hypotension, demonstrating the severe dehydration that is present. Fever suggests the possibility of strangulation.

1) INSPECTION - Look For i. Surgical Scars ii. Hernias iii. Distention iv. Visible Peristalsis 2) PALPATION Palpate for i. Masses ii. Hernias iii. Tenderness Perform Rectal Exam.

3) PERCUSSION Percuss to hear any Dullness or Resonance related to site of obstruction.

4) AUSCULTATION Bowel Sounds are Initially Loud and frequent Then as bowel distends the sounds become more resonant and high pitched Eventually becoming Amphoric

Investigations
CBC Blood urea and electrolyte X-Ray abdomen and chest Ultrasonography CT scan

Plain X ray of the abdomen:

The obstructed small bowel is characterised by straight segments that are generally central and lie transversely. No gas is seen in the colon The jejunum is characterised by its valvulae conniventes, which completely pass across the width of the bowel and are regularly spaced, giving a concertina or ladder effect Ileum the distal ileum has been described as featureless Caecum a distended caecum is shown by a rounded gas shadow in the right iliac fossa

 Large bowel, except for the caecum, shows haustral folds, which, unlike valvulae conniventes, are spaced irregularly, do not cross the whole diameter of the bowel and do not have indentations placed opposite one another The sensitivity of abdominal radiographs in the detection of small-bowel obstruction ranges from 70 to 80%. Specificity is low, because ileus and colonic obstruction can be associated with findings that mimic those observed with small-bowel obstruction.

The diagnostic evaluation should focus on the following goals; 1. distinguishing mechanical obstruction from ileus; 2. Determining the etiology of the obstruction; discriminating partial from complete obstruction; 3. Discriminating simple from strangulating obstruction.

Features of strangulated obstruction include:

tachycardia, localized abdominal tenderness fever marked leukocytosis acidosis. Serum levels of amylase, lipase, lactate dehydrogenase, phosphate, and potassium may be elevated.

Treatment
The stomach should be continuously evacuated of air and fluid using a nasogastric (NG) tube. Effective gastric decompression decreases nausea, distention, and the risk of vomiting and aspiration Small-bowel obstruction is usually associated with a marked depletion of intravascular volume caused by decreased oral intake, vomiting, and sequestration of fluid in bowel lumen and wall. Therefore, fluid resuscitation is integral. Isotonic fluid should be given intravenously and bladder catheter placed to monitor urine output.

 Central venous or pulmonary artery catheter monitoring may be necessary to assist with fluid management, particularly in patients with underlying cardiac disease. Broad-spectrum antibiotics are commonly administered because of concerns that bacterial translocation may occur in the setting of small-bowel obstruction; however, there are no controlled data to support or refute this approach.

 The classic clinical advice that the sun should not both rise andset on a case of unrelieved acute intestinal obstruction is soundand should be followed unless there are positive reasons for delay The operative procedure performed varies according to the etiology of the obstruction: For example, adhesions are lysed, tumors are resected, and hernias are reduced and repaired. Regardless of the etiology, the affected intestine should be examined, and nonviable bowel resected.

Adhesions
Most common cause of obstruction in the west. Any site of peritoneal irritation results in fibrin production, which results in adhesions between apposed surfaces. Only ONE adhesion may be causative of obstruction. There are many causes of intraperitoneal adhesions such as Ischemic Areas, Foreign Material, Infection, Inflammatory Conditions, and Radiation Enteritis. Adhesions may he classified into various types whether they are early (fibrinous), late (fibrous) or by the underlying etiology. From a practical perspective, there are only two types easy weak ones and difficult dense ones. Postoperative adhesions giving rise to intestinal obstruction usually involve the lower small bowel. Operations for appendicitis and gynecological procedures are the most common; and are an indication for early intervention.

The following factors may limit adhesion formation:

I. Good surgical technique II. Washing of the peritoneal cavity with saline to remove clots, etc. III. Minimize contact with gauze; IV. Cover anastomosis and raw peritoneal surfaces. V. Numerous substances have been instilled in the peritoneal cavity to prevent adhesion formation, no single agent has been shown to be safe and effective, and their use is not recommended.

Treatment
Treatment of adhesions is initially Conservative, but should not be prolonged beyond 72hrs. In such cases Laparotomy is required, only causative adhesion should be removed; removal of other adhesion will only cause more adhesion formation.

If multiple adhesions must be removed the bare area should be covered with omental grafts.

Volvulus A twisting or axial rotation of a portion of bowel about its mesentery. When complete it forms a closed loop of obstruction with resultant ischemia secondary to vascular occlusion. May be primary or secondary. The primary form occurs secondary to congenital malrotation of the gut, abnormal mesenteric attachments or congenital bands. A secondary Volvulus, which is the more common variety, is due to actual rotation of a piece of bowel around an acquired adhesion or stoma.

1) Volvulus Neonatorum Due to arrest gut rotation and narrow mesentery of small bowel and Caecum . Symptoms include catastrophic onset of repeated vomiting, rapid dehydration and abdominal distension 2) Volvulus of Small Intestine Primary or secondary and usually in the lower ileum Spontaneously or secondary Treatment consists of reduction of the twist and directed to the underlying cause .

3) Cecal Volvulus Primary or as a part of Volvulus Neonatorum . A clockwise twist F>M . Acute features of obstruction . 25% has tympanic swelling in the midline or left side of the abdomen . 4) Sigmoid Volvulus An anticlockwise twist . Most Common spontaneous Volvulus in Adults. Chronic constipation is a predisposing factor.

Bolus Obstruction.

Accumulation Compaction

I. II.

Gallstones: Gallstone Ileus (stones enter the intestine through a fistulous communication between the bile duct and the GI tract) Food: Bolus obstruction may occur after partial or total gastrectomy when unchewed articles can pass directly into small bowel Bezoars: Trichobezoars (Hair Balls) and Phytobezoar (Fruit/Vegetable Fibre).

III.

IV. Worms: Ascaris lumbricoides may cause low small bowel obstruction particularly in children, the institutionalized and those near the tropics.

Internal Hernia
Occurs where a portion of the small intestine becomes entrapped in one of the retroperitoneal fossae or into a congenital mesenteric defect. In the absence of adhesions hernia is uncommon to cause obstruction and a preoperative diagnosis is unusual.

The standard treatment for a hernia is to release the constricting agent by division.

Obstruction from Enteric Strictures

Small bowel strictures usually occur secondary to Tuberculosis or Crohns disease. Malignant strictures associated with lymphoma are common, whilst carcinoma and sarcoma are rare. Presentation is usually Subacute or Chronic.

Standard surgical management consists of resection and anastomosis.

Neonatal intestinal obstruction

Colon atresia Meconium plug Meconium ileus Anorectal malformation Small left colon syndrome Megacystic-microcolon-intestinal hypoperstalsis syndrome

Intussusception
most common cause of intestinal obstruction between 3 month and 6 yr of age 60% per cent of patients are younger than 1 yr 80% of the cases occur before 24 month rare in neonates incidence 1-4/1,000 live births male:female ratio is 4:1

Pathopysiology Intussusceptions are most often ileocolic and ileoileocolic, less commonly cecocolic, and rarely exclusively ileal The upper portion of bowel, the intussusceptum, invaginates into the lower, the intussuscipiens, dragging its mesentery along with it into the enveloping loop. Constriction of the mesentery obstructs venous return; engorgement of the intussusceptum follows, with edema, and bleeding from the mucosa leads to a bloody stool, sometimes containing mucus

 The apex of the intussusception may extend into the transverse, descending, or sigmoid colon--even to and through the anus in neglected cases. This presentation must be distinguished from rectal prolapse Most intussusceptions do not strangulate the bowel within the first 24 hr but may later eventuate in intestinal gangrene and shock

Clinical Presentation
sudden onset, in a previously well child, of severe paroxysmal colicky pain that recurs at frequent intervals and is accompanied by straining efforts with legs and knees flexed and loud cries Vomiting in most cases and is usually more frequent early. In the later phase, the vomitus becomes bile stained

Clinical Presentation
Stools of normal appearance may occur during the first few hours of symptoms then fecal excretions are small or more often do not occur, and little or no flatus is passed 60% of infants pass a stool containing red blood and mucus, the currant jelly stool Some patients have only irritability and alternating or progressive lethargy Eventually a shock-like state may develop, with an elevation of body temperature.

Clinical Presentation
palpation usually reveals a slightly tender sausage-shaped mass often in the right upper quadrant about 30% of patients do not have a palpable mass presence of bloody mucus on the finger after DRE supports the diagnosis abdominal distention and tenderness develop as intestinal obstruction becomes more acute

Radiographic signs of Intussusception

1. target sign 2. crescent sign 3. absent liver edge sign (also called absence of the subhepatic angle) 4. bowel obstruction

Treatment
Reduction of an acute intussusception is an emergency procedure and performed immediately after diagnosis. In patients with prolonged intussusception with signs of shock, peritoneal irritation, intestinal perforation, or pneumatosis intestinalis, hydrostatic reduction should not be attempted success rate of hydrostatic reduction under fluoroscopic or ultrasonic guidance is approximately 7580% if reduction is done within the first 48 hrand 50% if symptoms are present longer than 48 hr. Bowel perforations occur in 0.5-2.5% of attempted barium reductions. The perforation rate with air reduction ranges from 0.1-0.2%

 characterized by compression of the third portion of the duodenum by the superior mesenteric artery as it crosses over this portion of the duodenum. This condition should be considered in young asthenic individuals who have chronic symptoms suggestive of proximal small-bowel obstruction.

superior mesenteric artery syndrome

MESENTERIC ISCHAEMIA
Mesenteric vascular disease may be classified as acute intestinal ischaemia with or without occlusion venous, chronic arterial, central or peripheral. The superior mesenteric vessels are the visceral vessels most likely to be affected by embolisation or thrombosis, with the former being most common. Occlusion at the origin of the superior mesenteric artery (SMA) is almost invariably the result of thrombosis, whereas emboli lodge at the origin of the middle colic artery. Inferior mesenteric involvement is usually clinically silent because of a better collateral circulation. Possible sources for the embolisation of the SMA include a left atrium associated with fibrillation, a mural myocardial infarction, an atheromatous plaque from an aortic aneurysm and a mitral valve vegetation associated with endocarditis. Primary thrombosis is associated with atherosclerosis and thromboangitis obliterans. Primary thrombosis of the superior mesenteric veins may occur in association with factor V Leiden, portal hypertension, portal pyaemia and sickle cell disease and in women taking the contraceptive pill. Irrespective of whether the occlusion is arterial or venous, haemorrhagic infarction occurs. The intestine and its mesentery become swollen and oedematous. Blood-stained fluid exudes into the peritoneal cavity and bowel lumen. If the main trunk of the SMA is involved, the infarction covers an area from just distal to the duodenojejunal flexure to the splenic flexure. Usually, a branch of the main trunk is implicated and the area of infarction is less.

Clinical features
The most important clue to an early diagnosis of acute mesenteric ischaemia is the sudden onset of severe abdominal pain in a patient with atrial fibrillation or atherosclerosis. The pain is typically central and out of all proportion to physical findings. Persistent vomiting and defaecation occur early, with the subsequent passage of altered blood. Hypovolaemic shock rapidly ensues. Abdominal tenderness may be mild initially with rigidity being a late feature. Investigation will usually reveal a profound neutrophil leucocytosis with an absence of gas in the thickened small intestine on abdominal radiographs. The presence of gas bubbles in the mesenteric veins is rare but pathognomonic.

Treatment
Treatment needs to be tailored to the individual. In conjunction with full resuscitation, embolectomy via the ileocolic artery or revascularisation of the SMA may be considered in early embolic cases. The majority of cases, however, are diagnosed late. All affected bowel should be resected. Anti-coagulation should be implemented early in the postoperative period. After extensive enterectomy it is usual for patients to require intravenous alimentation. The young, however, may sometimes develop sufficient intestinal digestive and absorptive function to lead relatively normal lives. In selected cases consideration may be given to small bowel transplantation.

Hirschsprungs disease
Abnormal innervation of the bowel . Most common cause of lower intestinal obstruction in neonates .
Usually begin at birth with the delayed passage of meconium. Some infants pass meconium normally but subsequently present with a history of chronic constipation.

Hirschsprungs disease
Failure to thrive, with hypoproteinemia from a protein-losing enteropathy, is a less common presentation.
Rectal examination demonstrates normal anal tone and is usually followed by an explosive discharge of foul-smelling feces and gas.

Hirschsprungs disease
Rectal manometry and rectal suction biopsy are the easiest and most reliable indicators of Hirschsprung disease. Barium enema examination is useful in determining the extent of aganglionosis.
Sonography may also help in determining the dynamic or adynamic state of fluid-filled or solid-filled bowel loops.

Ileus: Common Etiologies

Abdominal surgery Infection
Sepsis Intra-abdominal abscess Peritonitis Pneumonia

Electrolyte abnormalities Hypokalemia Hypomagnesemia Hypermagnesemia Hyponatremia

Medications

Anticholinergics Opiates Phenothiazines Calcium channel blockers Tricyclic antidepressants

Hypothyroidism Ureteral colic Retroperitoneal hemorrhage Spinal cord injury Myocardial infarction Mesenteric ischemia

 Following most abdominal operations or injuries, the motility of the gastrointestinal tract is transiently impaired. Among the proposed mechanisms responsible for this dysmotility are surgical stress-induced sympathetic reflexes, inflammatory responsemediator release, and anesthetic/analgesic effects; each of which can inhibit intestinal motility.

 The return of normal motility generally follows a characteristic temporal sequence, with small intestinal motility returning to normal within the first 24 hours after laparotomy and gastric and colonic motility returning to normal by 48 hours and 3 to 5 days, respectively. Resolution of ileus may be delayed in the presence of other factors capable of inciting ileus such as the presence of intra-abdominal abscesses or electrolyte abnormalities.

The management of ileus consists of :

1. 2. 3. limiting oral intake correcting the underlying inciting factor If vomiting or abdominal distention are prominent, the stomach should be decompressed using a nasogastric tube.

4. Fluid and electrolytes should be administered intravenously until ileus resolves. 5. If the duration of ileus is prolonged, TPN may be required

Pseudo-Obstruction
This condition describes an obstruction, usually of the colon, in the absence of a mechanical cause or acute intra-abdominal disease. It is associated with a variety of syndromes where there is an underlying neuropathy and/or myopathy.

1) Small intestinal pseudo-obstruction This condition may be primary or secondary. The clinical picture consists of recurrent subacute obstruction. The diagnosis is made by the exclusion of a mechanical cause. Treatment consists of initial correction of any underlying disorder.

2) Colonic pseudo-obstruction. This may occur in an acute or a chronic form. The acute form is known as Ogilvie syndrome, presents as acute large bowel obstruction. Abdominal radiographs show evidence of colonic obstruction with marked caecal distension being a common feature Perforation is a common complication. Treated by colonoscopic decompression

Adynamic ileus
I.
A.

Pathophysiology
Paralysis of intestinal motility

Adynamic ileus
II. Causes A. Abdominal trauma B. Abdominal surgery (i.e. laparatomy) C. Serum electrolyte abnormality 1. Hypokalemia 2. Hyponatremia 3. Hypomagnesemia 4. Hypermagensemia

Adynamic ileus
D. Infectious, Inflammatory or irritation (bile, blood) 1. Intrathoracic a. Pneumonia b. Lower lobe rib fractures c. Myocardial Infarction 2. Intrapelvic e.g. Pelvic Inflammatory Disease

Adynamic ileus
3. Intraabdominal
a. Appendicitis b. Diverticulitis

c. Nephrolithiasis
d. Cholecystitis e. Pancreatitis

f. Perforated Duodenal Ulcer

Adynamic ileus
E. Intestinal Ischemia
1.

Mesenteric embolism, ischemia or thrombosis Rib fracture Vertebral fracture (e.g. lumbar compression fracture)

F. Skeletal injury
1. 2.

Adynamic ileus
G. Medications
1. 2.

3.
4. 5.

Narcotics Phenothiazines Diltiazem or Verapamil Clozapine Anticholinergic Medications

Adynamic ileus
III. Symptoms
A. B. C.

Abdominal distention Nausea and Vomiting are variably present Generalized abdominal discomfort 1. Colicky pain of Mechanical Ileus is usually absent Flatus and Diarrhea may still be passed

D.

Adynamic ileus
IV. Signs
A. B.

Quiet bowel sounds Abdominal distention Mechanical Ileus Bowel Pseudoobstruction

V. Differential Diagnosis
A. B.

Adynamic ileus
VI. Radiology: Refractory ileus course
A. B.

Indicated to evaluate for Mechanical Ileus Upper GI series and small bowel follow through 1. May be diagnostic and therepeutic 2. Use gastrograffin instead of barium
3. 4.

Barium may further obstruct bowel lumen Gastrograffin may stimulate bowel motility

C.

D.

Decompress stomach with Nasogastric Tube Instill gastrograffin via Nasogastric Tube

Adynamic ileus
D. Contrast with Mechanical Ileus
1. Less prominent air fluid levels 2. Generalized involvement of entire GI tract 3. Air filled bowel loops tend not to be distended

Adynamic ileus
VII. Management
A.

B.

Initial 1. Limit or eliminate oral intake 2. Intravascular fluid replacement 3. Correct electrolyte abnormalities (e.g. Hypokalemia) 4. Consider Nasogastric Tube placement Refractory Management 1. Consider Prokinatics 2. Consider lower bowel stimulation (e.g. Enema)

Adynamic ileus
VIII. Course A. Post-operative ileus resolves within 24-48 hours

Small bowel obstruction secondary to intraperitoneal fibrous band adhesion

GIT 3

Index 85

SMALL BOWEL OBSTRUCTION

Ng tube

ERECT

Note dilated small bowel centrally placed with air/fluid levels on upright exam.

 GIT 3

Index 87

Intestinal Obstruction Small Bowel Infarction secondary to intraperitoneal fibrous band (Late presentation
irreversible intestinal ischemia)

The commonest cause of inrtaperitoneal bands is previous inrtaperitoneal operation. e.g. :

appendectomy, exploration,..
GIT 3

Index 88

Foreign body
Phyto-bezoar in the jejunum

GIT 3

Index 89

 GIT 3

Index 90

Meckels diverticulum

Inflamed

Remember the complications of Meckels diverticulum

Infection & obstruction (as the appendix) May contain gastric, colonic or pancreatic tissue usually at the diverticulum mouth Peptic ulceration with severe bleeding

Intussusception

GIT 3

91

Index