Presentation on theme: " Definition : arrest of downward propulsion of intestinal content Classification : according to : A)pathological cause: 1)simple intestinal obstruction."— Presentation transcript:
Definition : arrest of downward propulsion of intestinal content Classification : according to : A)pathological cause: 1)simple intestinal obstruction 2) strangulated intestinal obstruction 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 ;
Small intestinal ileus is the most common form of intestinal obstruction; it occurs after most abdominal operations and is a common response to acute intra abdominal inflammatory conditions Mechanical small bowel obstruction is somewhat less common; such obstruction is secondary to intra-abdominal adhesions, hernias, or cancer Mechanical colonic obstruction most often develops in response to obstructing carcinoma, diverticulitis,or volvulus. Acute colonic pseudo-obstruction occurs most frequently in the postoperative period or in response to another acute medical illness.
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 bowel’s 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.
Simple distal to obstruction proximal peristalsis blind loop Strangulation General effect fluid and electrolyte loss septicaemia
Early in the course of an obstruction, intestinal motility and contractile activity increase in an effort to propel luminal contents past the obstructing point. Later in the course of obstruction, the intestine becomes fatigued and dilates, with contractions becoming less frequent and less intense. As the bowel dilates, water and electrolytes accumulate both intraluminally and in the bowel wall itself. This massive third-space fluid loss accounts for the dehydration and hypovolemia. 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. Oliguria, azotemia, and hemoconcentration can accompany the dehydration. Hypotension and shock can ensue. Other consequences of bowel obstruction include increased intra-abdominal pressure, decreased venous return, and elevation of the diaphragm, compromising ventilation. These factors can serve to further potentiate the effects of hypovolemia.
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.
Cardinal symptom Pain, Distention, Vomiting, Absolute constipation The nature of the presentation will be influenced by the site ■ In high small bowel obstruction, vomiting occurs early and is profuse with rapid dehydration. Distension is minimal with little evidence of fluid levels on abdominal radiography ■ In low small bowel obstruction, pain is predominant with central distension. Vomiting is delayed. Multiple central fluid levels are seen on radiography ■ In large bowel obstruction, distension is early and pronounced. Pain is mild and vomiting and dehydration are late. The proximal colon and caecum are distended on abdominal radiography The nature of the presentation will also be influenced by whether the obstruction is: acute; chronic; acute on chronic; subacute. Acute obstruction usually occurs in small bowel obstruction, with sudden onset of severe colicky central abdominal pain, distensionand early vomiting and constipation Chronic obstruction is usually seen in large bowel obstruction, with lower abdominal colic and absolute constipation followed by distension. In acute on chronic obstruction there is a short history of distension and vomiting against a background of pain and constipation. Subacute obstruction implies an incomplete obstruction. Presentation will be further influenced by whether the obstruction is: simple – in which the blood supply is intact; strangulating/strangulated Examination General, Abdominal inspection, palpation,percussion, auscultation
The typical crampy abdominal pain associated with intestinal obstruction occurs in paroxysms at 4- to 5-minute intervals and occurs less frequently with distal obstruction. It is usually centred on the umbilicus (small bowel) or lower abdomen (large bowel). With increasing distension, the colicky pain is replaced by a mild constant diffuse pain. The development of severe persistant pain is indicative of the presence of strangulation. Pain may not be a significant feature in postoperative simple mechanical obstruction and does not usually occur in paralytic ileus. Nausea and vomiting are more common with a higher obstruction and may be the only symptoms in patients with gastric outlet or high intestinal obstruction. An obstruction located distally is associated with less emesis, and the initial and most prominent symptom is the cramping abdominal pain. As obstruction progresses the character of the vomitus alters from digested food to faeculent material, as a result of the presence of enteric bacterial overgrowth. In the small bowel the degree of distension is dependent on the site of the obstruction and is greater the more distal the lesion. Visible peristalsis may be present. Distension is delayed in colonic obstruction and may be minimal or absent in the presence of mesenteric vascular occlusion. Constipation may be classified as absolute (i.e. neither faeces nor flatus is passed) or relative (where only flatus is passed). Absolute constipation is a cardinal feature of complete intestinal obstruction. Some patients may pass flatus or faeces after the onset of obstruction as a result of the evacuation of the distal bowel contents. The rule that constipation is present in intestinal obstruction does not apply in: Richter’s hernia; gallstone obturation; mesenteric vascular occlusion; obstruction associated with pelvic abscess; partial obstruction (faecal impaction/colonic neoplasm) in which diarrhoea may often occur.
The patient with intestinal obstruction may present with tachycardia and hypotension, demonstrating the severe dehydration that is present. Fever suggests the possibility of strangulation. Abdominal examination demonstrates a distended abdomen, with the amount of distention some what dependent on the level of obstruction. Previous surgical scars should be noted. Early in the course of bowel obstruction, peristaltic waves can be observed, particularly in thin patients, and auscultation of the abdomen may demonstrate hyperactive bowel sounds with audible rushes associated with vigorous peristalsis (i.e., borborygmi). Late in the obstructive course, minimal or no bowel sounds are noted. Mild abdominal tenderness may be present with or without a palpable mass; however, localized tenderness, rebound, and guarding suggest peritonitis and the likelihood of strangulation. A careful examination must be performed to rule out incarcerated hernias in the groin, the femoral triangle, and the obturator foramen. A rectal examination should be performed to assess for intraluminal masses and to examine the stool for occult blood, which may be an indication of malignancy, intussusception, or infarction.
“Classic” picture of strangulation include tachycardia, fever, leukocytosis, and a constant, noncramping abdominal pain. Tenderness with rigidity, Shock,With the cardinal signs of intestinal obstruction In cases of intestinal obstruction in which pain persists despite conservative management, even in the absence of the above signs, strangulation should be diagnosed. When strangulation occurs in an external hernia, the lump is tense, tender and irreducible, there is no expansile cough impulse and it has recently increased in size. Pathology 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, which has a smaller absorptive surface. Causes of strangulation External: ■ Hernial orifices ■ Adhesions/bands Interrupted blood flow ■ Volvulus ■ Intussusception Increased intraluminal pressure ■ Closed-loop obstruction Primary ■ Mesenteric infarction
This occurs when the bowel is obstructed at both the proximal and distal points. It is present in many cases of intestinal strangulation. Unlike cases of non-strangulating obstruction, there is no early distension of the proximal intestine. When gangrene of the strangulated segment is imminent, retrograde thrombosis of the mesenteric veins results in distension on both sides of the strangulated segment. 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 (present in up to one-third of individuals). The inability of the distended colon to decompress itself into the small bowel results in an increase in luminal pressure, which is greatest at the caecum, with subsequent impairment of blood supply. Unrelieved, this results in necrosis and perforation
Plain X ray of the abdomen: Radiological features of obstruction ■ 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 Blood urea and electrolyte Blood picture U.S. CT scan Endoscopy
The treatment is urgent relief of obstruction after preparation Preoperative preparation ( fluid and electrolyte replacement,antibiotics and Tube Decompression ) Operation :exploration Immediate operation indicated in peritonitis, incarcerated hernia, suspected or confirmed strangulation, sigmoid volvulus with systemic toxicity or peritoneal irritation, small bowel volvulus, colonic volvulus above sigmoid, Conservative (with exeption) indication 1)Adhesive 2)Ileocaecal itussusception 3)Sigmoid volvuls 4)feacal impaction Reassess patient every 4 hr. Look for changes in pain, abdominal findings, and volume and character of NG aspirate. Repeat abdominal x-rays, and look for changes in gas distribution, pneumatosis cystoides intestinalis, and free intraperitoneal air. Classify patient’s condition as improved, unchanged, or worse. Decide whether operative treatment is necessary and, if so, whether it should be done on urgent or elective basis. Urgent operation Indications include: Lack of response to 24–48 hr of nonoperative therapy (increasing abdominal pain, distention, or tenderness; NG aspirate changing from nonfeculent to feculent; ↑ proximal small bowel distention with ↓ distal gas).
Patients with intestinal obstruction are usually dehydrated and depleted of sodium, chloride, and potassium, requiring aggressive intravenous replacement with an isotonic saline solution such as lactated Ringer’s. Urine output should be monitored by the placement of a Foley catheter. After the patient has formed adequate urine, potassium chloride should be added to the infusion if needed. Serial electrolyte measurements, as well as hematocrit and white blood cell count, are performed to assess the adequacy of fluid repletion. Because of large fluid requirements, patients, particularly the elderly, may require central venous assessment and, in some cases, the placement of a Swan-Ganz catheter. Broad-spectrum antibiotics are given prophylactically by some surgeons based on the reported findings of bacterial translocation occurring even in simple mechanical obstructions. In addition, antibiotics are administered as a prophylaxis for possible resection or inadvertent enterotomy at surgery.
Nasogastric suction empties the stomach, reducing the hazard of pulmonary aspiration of vomitus and minimizing further intestinal distention from preoperatively swallowed air. Patients with adhesive simple intestinal obstruction may be treated conservatively with resuscitation and tube decompression alone. Resolution of symptoms and discharge without the need for surgery have been reported in 60% to 85% of patients with an adhesive simple intestinal obstruction. Although an initial trial of nonoperative management of most patients with partial small bowel obstruction is warranted, it should be emphasized that clinical deterioration of the patient or increasing small bowel distention on abdominal radiographs during tube decompression warrants prompt operative intervention. The decision to continue to treat a patient nonoperatively with a presumed bowel obstruction is based on clinical judgment and requires constant vigilance to ensure that the clinical course has not changed.
Causes of Ileus Post laparotomy Metabolic and electrolyte derangements (e.g., hypokalemia, hyponatremia, hypomagnesemia, uremia, diabetic coma) Drugs (e.g., opiates, psychotropic agents, anticholinergic agents) Intra-abdominal inflammation Retroperitoneal hemorrhage or inflammation Intestinal ischemia Systemic sepsis
Abdominal distention, usually without the colicky abdominal pain, is the typical and most notable finding. Nausea and vomiting may occur. Plain abdominal radiographs may reveal distended small bowel as well as large bowel loops. The treatment of an ileus is entirely supportive with nasogastric decompression and intravenous fluids. The most effective treatment to correct the underlying condition may be aggressive treatment of the sepsis, correction of any metabolic or electrolyte abnormalities, and discontinuation of medications that may produce an ileus. Pharmacologic agents have been used but for the most part have been ineffective. Drugs that block syinput (e.g., guanethidine) or stimulate parasympathetic activity (e.g., bethanechol or neostigmine) have been tried. In addition, hormonal manipulation, using cholecystokinin or motilin, has been evaluated, but the results have been inconsistent.
Factors associated with pseudo-obstruction Idiopathic ■ Metabolic Diabetes, intermittent porphyria,Acute hypokalaemia, Uraemia,Myxodoema ■ Severe trauma (especially to the lumbar spine and pelvis) ■ Shock Burns Myocardial infarction Stroke Septicaemia ■ Retroperitoneal irritation by : Blood,Urine,nzymes (pancreatitis),Tumour ■ Drugs,Tricyclic antidepressants,Phenothiazines,Laxatives ■ Secondary gastrointestinal involvement, Scleroderma,Chagas’ disease
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.
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 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.
Infarction of the large intestine alone is relatively rare. Involvement of the middle colic artery territory should be treated by transverse colectomy and exteriorisation of both ends, with an extended right hemicolectomy in selected cases. Ischaemic colitis describes the structural changes that occur in the colon as a result of the deprivation of blood. They are most common in the splenic flexure, whose blood supply is particularly tenuous. They have been classified by Marston into gangrenous, transient and stricturing forms; only stricturing forms cause obstruction and only a few such patients require resection.