LARGE BOWEL OBSTRUCTION TYPES OF INTESTINAL OBSTRUCTION DYNAMIC

LARGE BOWEL OBSTRUCTION

TYPES OF INTESTINAL OBSTRUCTION DYNAMIC – where peristalsis is working against a mechanical obstruction. ADYNAMIC – where mechanical element is absent. 1. Peristalsis may be absent; eg: paralytic ileus 2. Peristalsis present in a non propulsive form.

CLASSIFICATION (Contd. . ) ACUTE OBSTRUCTION CHRONIC OBSTRUCTION ACUTE ON CHRONIC OBSTRUCTION SUBACUTE OBSTRUCTION

CAUSES OF LARGE BOWEL OBSTRUCTION

DYNAMIC INTRALUMINAL impaction foreign bodies bezoar gall stones INTRAMURAL strictures malignancy EXTRAMURAL bands/adhesions hernia volvulus intussusception ADYNAMIC paralytic ileus pseudo obstruction

PATHOPHYSIOLOGY ABOVE THE LEVEL OF OBSTRUCTION Obstruction proximal peristalsis is increased proportional to the distance of obstruction Obstruction not relieved bowel begins to dilate reduction in peristaltic strength flaccidity & paralysis

PATHO PHYSIOLOGY Distension proximal to obstruction -GAS (nitrogen & hydrogen sulphide) -FLUID (digestive juices) BELOW THE LEVEL OF OBSTRUCTION Normal peristalsis & absorption till empty then bowel contracts and becomes immobile

STRANGULATION Venous return is compromised increase in capillary pressure local mural distension loss of intravascular fluid & RBCs occurs Once the arterial supply is impaired, hemorrhagic infarction occurs viability of the bowel wall is compromised translocation & systemic exposure to aerobic & anaerobic organisms with their toxins.

CAUSES OF STRANGULATION EXTERNAL hernial orifices adhesions/bands INTERRUPTED BLOOD SUPPLY volvulus, intussusception INCREASED INTRALUMINAL PRESSURE closed loop obstruction PRIMARY mesenteric infarction

CLINICAL FEATURES The signs & symptoms depend on the site of location of obstruction Cancers arising in the left colon & rectum are more likely to obstruct than the more capacious proximal colon The symptoms are : 1. 2. 3. Failure to pass stools or flatus(constipation/opstipation) Abdominal distention Cramping abdominal pain

OTHER MANIFESTATIONS DEHYDRATION HYPOKALAEMIA PYREXIA – may indicate 1. onset of ischemia 2. intestinal perforation 3. associated inflammation HYPOTHERMIA ABDOMINAL TENDERNESS

Clinical features of strangulation Presence of shock indicates underlying ischemia Constant pain Symptoms usually commence suddenly & recur regularly Localised tenderness will always be present associated with rigidity/rebound tenderness

CLOSED LOOP OBSTRUCTION Occurs when the bowel is obstructed at both the proximal & distal points. There is no early distension of the proximal intestine. When gangrene of the strangulated segment occurs, retrograde thrombosis of mesentric veins results in distension on both sides.

INTERNAL HERNIA SITES OF INTERNAL HERNIA Defect in the mesentery Defect in the transverse colon Congenital or acquired diaphragmatic hernias, Caecal/ appendiceal retroperitoneal fossae Inter sigmoid fossa

OBSTRUCTION FROM ENTERIC STRICTURES Occurs secondary to TB or Crohn’s disease Malignant strictures lymphoma Presentation is sub a/c or c/c Standard surgical management is resection& anastomosis Strictureplasty for Crohn’s

BOLUS OBSTRUCTION FOOD GALL STONES TRICHO BEZOARS PHYTO BEZOARS STERCOLITHS WORMS

TRICHO BEZOAR STERCOLITH FABRIC BEZOAR

CHRONIC INTESTINAL OBSTRUCTION The causes of obstruction may be ORGANIC Intramural - faecal impaction Mural - diverticulitis, strictures, anastomotic stenosis Extramural -adhesion , metastatic deposits, endometriosis FUNCTIONAL - pseudo-obstruction. FUNCTIONAL

Constipation appears first. It is initially relative and then absolute Associated with distension and pain Vomiting is a late feature

Plain abdominal radiography may be useful. Contrast water-soluble enema study to rule out functional disease. Organic disease requires a laparotomy Functional disease requires colonoscopic decompression and conservative management

ADYNAMIC OBSTRUCTION

PARALYTIC ILEUS It is a state in which there is failure of peristaltic waves secondary to neuromuscular failure Stasis accumulation of fluid and gas within the bowel with associated distension, vomiting, absence of bowel sounds and absolute constipation

TYPES OF PARALYTIC ILEUS Postoperative — self-limiting with a duration of 24— 72 hours. Infection — intra-abdominal sepsis Reflex ileus — fractures of the spine or ribs, retroperitoneal haemorrhage or application of a plaster jacket. Metabolic — uraemia and hypokalaemia.

CLINICAL FEATURES Occurs 72 hours after laparotomy No bowel sounds on auscultation No passage of flatus. Abdominal distension becomes more marked and tympanitic. Pain is not a feature. Radiologically, the abdomen shows gas-filled loops of intestine with multiple fluid levels

MANAGEMENT Prevention by Nasogastric suction Restriction of oral intake Electrolyte balance must be maintained

General principles of specific treatment are The primary cause must be removed GI distension must be relieved by decompression Close attention to fluid and electrolyte balance Catchpole regime with neostigmine may be used in resistant cases If prolonged and threatens life laparotomy

TREATMENT OF LARGE BOWEL OBSTRUCTION HISTORY PHYSICAL EXAMINATION ABDOMEN SHOULD BE PALPATED FOR MASSES GROIN PALPATED FOR HERNIAS DIGITAL RECTAL EXAMINATION TO EXCLUDE RECTAL CANCERS

PRINCIPLES OF TREATMENT OF ACUTE INTESTINAL OBSTRUCTION GASTROINTESTINAL DRAINAGE FLUID & ELECTROLYTE REPLACEMENT RELIEF OF OBSTRUCTION

SUPPORTIVE MANAGEMENT NASOGASTRIC DECOMPRESSION 4 th hourly aspiration by Ryle’s or Salem tube.

REPLACEMENT OF SODIUM AND WATER LOSS with Hartmann’s solution or normal saline. The volume required is determined by clinical, haematological & biochemical criteria. ANTIBIOTICS

SURGERY 1. 2. 3. Surgical options in case of sigmoid colon cancer include: Hartmann’s Operation – simoidectomy with descending colostomy & closure of rectal stump Sigmoidectomy with primary colorectal anastamosis Abdominal colectomy with ileorectal anastamosis

Right sided colonic obstruction whether caused by cancer or volvulus is generally treated by resection & primary anastamosis

PSEUDO OBSTRUCTION Pseudo-obstruction of the colon (also called Ogilvie's syndrome, after its description by Sir Heneage Ogilvie in 1948) describes the condition of distention of the colon, with signs and symptoms of colonic obstruction, in the absence of an actual physical cause of the obstruction. Ogilvie described two patients with clinical features of colonic obstruction despite a normal barium enema. Both patients underwent laparotomy for the condition; neither had mechanical obstruction, but both had unsuspected malignant disease involving the area of the celiac axis and semilunar ganglion.

Contd…. . The cause of the dilation was attributed to the malignant infiltration of the sympathetic ganglia. Subsequently there have been numerous descriptions of cases of colonic distention in the absence of mechanical obstruction and without malignant involvement of the visceral autonomic nerves. Very few cases of pseudo-obstruction have malignant infiltration of the autonomic nerves as the cause; in fact, the exact pathogenesis of the syndrome remains unknown, and it has been associated with a heterogeneous group of conditions.

PRIMARY PSEUDO OBSTRUCTION Primary pseudo-obstruction is a motility disorder that is either a familial visceral myopathy (hollow visceral myopathy syndrome) or a diffuse motility disorder involving the autonomic innervation of the intestinal wall. The latter may be modified by a disturbance of intestinal hormones or may be principally due to disordered autonomic innervation.

SECONDARY PSEUDOOBSTRUCTION Secondary pseudo-obstruction is more common and has been associated with neuroleptic medications, opiates, severe metabolic illness, myxedema, diabetes mellitus, uremia, hyperparathyroidism, lupus, scleroderma, Parkinson's disease, and traumatic retroperitoneal hematomas. One mechanism thought to play a role in the pathogenesis is sympathetic overactivity overriding the parasympathetic system. Indirect support for this theory has been derived from the success in treating the syndrome with neostigmine, a parasympathomimetic agent. Further support comes from reports of immediate resolution of the syndrome after administration of an epidural anesthetic that provides sympathetic blockade.

Pseudo-obstruction may present in acute or chronic forms. The acute variety most commonly affects patients with chronic renal, respiratory, cerebral, or cardiovascular disease. It usually involves only the colon, whereas the chronic form affects other parts of the gastrointestinal tract, usually presents as bouts of subacute and partial intestinal obstruction, and tends to recur periodically.

Acute colonic pseudo-obstruction should be suspected when a medically ill patient suddenly develops abdominal distention. The abdomen is tympanitic, usually nontender, and bowel sounds are usually present. Plain abdominal radiographs reveal a distended colon, with the right and transverse segments tending to be most dramatically affected. The radiologic appearance is one of large bowel obstruction.

The most useful investigation is a watersoluble contrast enema, which should be performed in all patients in whom the diagnosis is suspected, provided their condition is stable enough to warrant the procedure. The contrast enema can reliably differentiate between mechanical obstruction and pseudoobstruction, a differentiation that is essential to guide appropriate therapy.

Colonoscopy is the alternative diagnostic investigation for pseudo-obstruction and has the attractive advantage that it can be used for treatment. However, at the present time, the water-soluble contrast enema is generally the preferred initial test.

TREATMENT When the diagnosis of acute pseudo-obstruction is suspected, treatment should accompany the diagnostic evaluation. Initial treatment includes nasogastric decompression, replacement of extracellular fluid deficits, and correction of electrolyte abnormalities. All medications that inhibit bowel motility, such as opiates, should be discontinued. Patient response is monitored by serial abdominal examinations and radiographs. Most patients improve with this regimen.

Until the mid-1990 s, the treatment usually used when the colonic distention failed to resolve with supportive measures was colonoscopic decompression. Although this approach was generally successful, it required skilled personnel and equipment and carried the risk for colonic perforation from both instrument trauma and insufflation. In addition, the procedure often had to be repeated because of recurrence of the colonic distention.

At the present time, the trend has been to treat this condition with neostigmine, a parasympathomimetic agent. It is obviously imperative that mechanical obstruction be excluded (either by watersoluble contrast enema or colonoscopy) before the administration of neostigmine because the subsequent high pressures generated in the colon against a distal obstruction could cause colonic perforation.

Neostigmine enhances parasympathetic activity by competing with acetylcholine for acetylcholinesterase binding sites. In the treatment of colonic pseudoobstruction, 2. 5 mg of neostigmine is given intravenously over 3 minutes. The resolution of the condition is indicated within less than 10 minutes of administration of the drug, by the passage of stool and flatus by the patient. The recurrence rates following the administration of neostigmine appear to be far lower than those associated with colonoscopic decompression, with satisfactory decompression being achieved in about 90% of patients after a single administration of the medication.

A significant side effect of neostigmine is bradycardia, and all patients must be monitored by telemetry during administration of the drug. Atropine must be immediately available, and patients with significant cardiac disease are not candidates for this treatment.