Seminar presentation by 5th-year medical students under the supervision of in house lecturer. He was previously working as a consultant surgeon in Syria. Reference as mentioned in the slides.
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PRESENTED BY NURUL HIDAYU AUDI RAHMAN AFFAN SYAFIQI MANAGEMENT OF INTESTINAL OBSTRUCTION
Introduction Classification of Intestinal Obstruction 3. Pathophysiology 4. Clinical Presentation 5. Investigation – Imaging Study 6. Management OUTLINE Location Degree of obstruction Causes Vascular Compromise
INTRODUCTION Bowel obstruction occur when there is any form of impedance of the normal flow of material through a hollow viscous (Garden, 6 th edition) Lead to dilatation of bowel proximally and disrupts peristalsis Obstruction can be functional (due to abnormal intestinal physiology) or due to a mechanical obstruction, which can be acute or chronic.
INTRODUCTION
RISK FACTOR Factors that may lead to increase risk developing IO : Abdominal or pelvic surgery which may cause adhesion Previous history of obstruction Crohn’s disease – cause intestinal walls to be thicken, narrowing the passageway Cancer within abdomen especially history of removal abdominal tumor History of constipation – impacted faeces Malrotation – congenital
INTRODUCTION
PRESENTED BY NURUL HIDAYU CLASSIFICATION OF INTESTINAL OBSTRUCTION
A. LOCATION SMALL BOWEL LARGE BOWEL PROXIMAL DISTAL Bilious vomiting Shorter onset Abdominal distension Fecaloid vomitus Longer onset Common Causes :
A. LOCATION
A. LOCATION Prognosis GOOD PROGNOSIS (proper diagnosis and treatment of the obstruction) Complete obstructions treated successfully non-operatively have a higher incidence of recurrence than do those treated surgically. Morbidity/mortality Morbidity and mortality are dependent on the early recognition and correct diagnosis of obstruction. If untreated, strangulated obstructions cause death in 100% of patients . If surgery is performed within 36 hours , the mortality rate decreases to 8% . The mortality rate is 25% if the surgery is postponed beyond 36 hours in these patients. Some factors associated with death and postoperative complications include age, comorbidity, and treatment delay. Small Bowel Obstruction
A. LOCATION Mortality & Prognosis Mortality is determined by the patient's overall medical condition and the presence of any comorbidities that may influence the patient's surgical risk. If large bowel obstruction is treated early , the outcome is generally good . Mortality is higher in patients who have developed bowel ischemia or perforation . After surgical decompression, the prognosis is determined by the underlying disease. In general, overall mortality for large-bowel obstruction is 20%, which increases to 40% if there is colonic perforation . Mortality for acute colonic pseudo-obstruction (ACPO; Ogilvie syndrome) is 15% with early care ; it increases to 36% if colonic ischemia or perforation develops . Large Bowel Obstruction
B. DEGREE OF OBSTRUCTION DEGREE OF OBSTRUCTION PARTIAL COMPLETE Lumen narrowed but allow transit some content Abdominal distension Presence of flatus Presence of bowel movement Lumen totally obstructed Complete obstipation Closed loop (both ends are obstructed) Simple obstruction (no vascular impairment) Strangulation
B. DEGREE OF OBSTRUCTION Degree of obstruction is based on degree of collapse and amount of residual contents distal to obstruction. OGILVIE SYNDROME
C. CAUSES EXTRAMURAL MECHANICAL / DYNAMIC FUNCTIONAL / ADYNAMIC CAUSES INTRAMURAL INTRALUMINAL Adhesions Hernias Congenital bands Tumors volvulus Strictures : inflammatory (Crohn , TB ) Tumors Intussusception Lymphomas Impacted faeces Gallstones Bezoar Foreign bodies Paralytic ileus Post op : 24-72 hour Infection Metabolic – uremic / hypokalemia Pseudo-obstruction Peristalsis against a mechanical obstruction Absent peristalsis due to intestinal atony in absence of mechanical cause
INTESTINAL OBSTRUCTION
CAUSES INTUSSUSCEPTION
INTESTINAL OBSTRUCTION TRICHOBEZOARS AND PHYTOBEZOARS Trichobezoars (Undigested hair ball): Due to persistent hair chewing or sucking, and may be associated with underlying psychiatric abnormality. Phytobezoars (Fruit/vegetable fibre): Due to high fibre intake, inadequate chewing, previous gastric surgery and loss of the gastric pump mechanism. Preoperative diagnosis is difficult even with high resolution CT scanning. WORMS Ascaris lumbricoides may cause low small bowel obstruction, particularly in children . Diagnosis by: Worms in the stool or vomitus, eosinophilia or the sight of worms within gas-filled small bowel loops on a plain radiograph. Occasionally, worms may cause a perforation and peritonitis, especially if the enteric wall is weakened by such conditions as ameobiasis .
ADHESION Most commonly occurs due to previous abdominal surgery. Risk of acquiring adhesion subsequent to abdominal surgery is 4% and that after laparotomy is 2% Adhesions start to form within hours of abdominal surgery. Classified into 2 types: early (fibrinous) and late (fibrous)
BAND Usually only one band is culpable. This maybe: Congenital, eg . Obliterated vitellointestinal duct A string band following previous bacterial peritonitis A portion of greater omentum usually adherent to the parietals
OBLITERATED VITELLOINTESTINAL DUCT Embryologically vitellointestinal tract comprises of three structures: the vitelline duct, artery, and vein. During early phases of development, the yolk sac acts as a prime source of nutrition for the quickly growing fetus . The vitellointestinal duct is the developing structure joining the primary yolk sac to the developing midgut during fetal enlargement. Typically, at the 5th-10th week of gestation , it turns out to be a thin fibrous band that spontaneously obliterates and separates from the intestine . Source : NCBI
OBLITERATED VITELLOINTESTINAL DUCT Partial or complete failure of abolition of vitellointestinal duct may lead to diverse type of congenital intestinal malformations comprising; Meckel's diverticulum , vitelline cord, umbilical sinus, enteric fistula and haemorrhagic umbilical granuloma . Though rare, intestinal obstruction is one of the complications of vitellointestinal duct, occurs due to numerous mechanisms including intussusceptions of the diverticulum , internal herniation or volvulus from a patent band. It is very challenging to know the reasons of the intestinal obstruction without diagnostic laparotomy or laparoscopy. Source : NCBI
HERNIA Most common cause of small bowel obstruction in patients with no prior history of surgery is hernia. Careful search for inguinal, femoral and umbilical hernia must be made. Consider internal hernia too. Internal herniation occurs when a portion of the small intestine becomes trapped in one of the retroperitoneal fossae or in a congenital mesenteric defect
HERNIA
HERNIA
D. VASCULAR COMPROMISE STRANGULATED NON-STRANGULATED Absence of signs and symptoms strangulation Life threatening condition “Hemodynamic instability” Peritoneal signs Direct pressure on the bowel wall Interrupted mesenteric blood flow Increased intraluminal pressure Hernial orifices Adhesion/bands Volvulus Intussusception Closed – loop obstruction
CLOSED LOOP IO This occur when the bowel is obstructed at both the proximal and distal points Its is present in many cases of intestinal strangulation When gangrene of the strangulated segment is imminent, retrograde thrombosis of the mesenteric vein result in distension of both sides of the strangulated segment
STRANGULATED IO Strangulation occurs in nearly 25% of people with small bowel obstruction. Usually, strangulation results when part of the intestinal becomes trapped in an abnormal opening such in diagram above. Gangrene can develop in as few as 6 hours . Mortality rate : 10-35% Gangrene the intestinal wall dies usually causing rupture peritonitis , shock and if untreated, death
PRESENTED BY AFFAN SYAFIQI PATHOPHYSIOLOGY AND CLINICAL FEATURES
Irrespective of aetiology or acuteness of onset, in dynamic (mechanical) obstruction the bowel proximal to the obstruction dilates and the bowel below the obstruction exhibits normal peristalsis and absorption until it becomes empty and collapse. Initially, proximal peristalsis is increased in an attempt to overcome the obstruction. If the obstruction is not relieved, the bowel continue to dilate , ultimately there is a reduction in peristaltic strength , resulting in flaccidity and paralysis . PATHOPHYSIOLOGY
The distension of proximal to an obstruction is caused by two factors: Gas : there is significant overgrowth of both aerobic and anerobic organism , resulting in considerable gas production. Following the reabsorption of oxygen and carbon dioxide, the majority is made up of nitrogen (90%) and hydrogen sulphide . Fluid : this is made up of the various digestive juice (Saliva 500mL, bile 500mL, pancreatic secretion 500mL, gastric secretion 1Litre- in all per 24 hours.) this accumulate in the guts lumen as absorption by the obstructed gut is retarded . Dehydration and electrolyte loss are therefore due to: - reduced oral intake - defective intestinal absorption - sequestration in the bowel lumen - transudation of fluid into the peritoneal cavity PATHOPHYSIOLOGY
Cardinal features Colicky pain Vomiting Abdominal distension Constipation Other features Dehydration Hypokalemia Pyrexia Abdominal tenderness CLINICAL FEATURES
Supine (Most of diagnosis made by this position) Erect (May be requested when in doubt) (3/6/9 rule) : 3cm for the small bowel, 6cm for the colon and 9cm for the caecum ABDOMINAL X-RAY
O BSTRUCTED SMALL BOWEL Characterized by straight segments that are generally central and lie transversely No/minimal gas is seen in the colon J EJUNUM Characterized by its valvulae conniventes , which completely pass across the width of the bowel and are regularly spaced, giving a ‘concertina’ or ladder effect RADIOLOGICAL FEATURES OF IO
ILEUM The distal ileum has been described by wangensteen as featureless CAECUM A distended caecum is shown by a rounded gas shadow in the right iliac fossa LARGE BOWE L Except for the caecum, shows haustral folds, which are spaced irregularly & do not cross the whole diameter of the bowel . RADIOLOGICAL FEATURES OF IO
RADIOLOGICAL FEATURES OF IO
LARGE BOWEL OBS. SMALL BOWEL OBS.
In intestinal obstruction, fluid levels appear later than gas shadows as it takes time for gas and fluid to separate . (M ost prominent on an erect film ) When fluid levels are pronounced, the obstruction is advanced. In the small bowel, the number of fluid levels is directly proportional to the degree of obstruction and to its site, the number increasing the more distal the lesion.
BARIUM STUDIES Done in patients without evidence of strngulation Adhesive small bowel obstruction Predicts resolution of small bowel obstruction Contraindicated in acute obstruction CONTRAST ABD X-RAY
Widely used nowadays Highly accurate Limitation : cannot diagnose ischemia CT SCAN
1. Plain X-ray : evidence of small or large bowel obstruction with an absent caecal shadow in ileocecal cases 2. Barium enema : shows claw sign in ileocolic intussusception 3. CT scan : shows a target or sausage-shaped soft tissue mass with a layering effect ( mesenteric vessels within bowel lumen ) 4. Ultrasound : shows a doughnut appearance of concentric rings in transverse section IMAGING IN INTUSSUSCEPTION
CAECAL VOLVOLUS Characterised with Caecal dilatation ( 98-100% ), Single air-fluid level (72–88 % ), Small bowel dilatation (42–55 % ) Absence of gas in distal colon (82 % ) IMAGING IN VOLVULUS
SIGMOID VOLVULUS Shows massive colonic distension. The classic appearance: two twisted loops with a central doubled wall component. ( On plain xray ) Coffee bean sign IMAGING IN VOLVULUS
Rigler’s triad Pneumobilia Small bowel obstruction Atypical mineral shadow 2 of these 3 signs are pathognomic of gallstone ileus. GALLSTONES ILEUS
PRESENTED BY AUDI RAHMAN MANAGEMENT
DANGEROUS SIGNS Constant pain Absent bowel sounds Tenderness with rigidity Leukocytosis Fever and tachycardia Shock
ACUTE INTESTINAL OBSTRUCTION It involves: Conservative management Surgical management Some cases will settle by using conservative regimen, other need surgical intervention Surgery should be delayed till resuscitation is complete unless signs of strangulation and evidence of closed-loop obstruction Cases that show reason for delay should be monitored continuously for 72 hours in hope of spontaneous resolution
ACUTE INTESTINAL OBSTRUCTION SUPPORTIVE MANAGEMENT Nasogastric aspiration by Ryle's tube IV fluid NPO Urinary catheter Check temperature and pulse 2 hourly Abdominal temperature 8 hourly Broad spectrum antibiotics initiated early
ACUTE INTESTINAL OBSTRUCTION SURGICAL MANAGEMENT Principles: Management of segment at site of obstruction Management of distended proximal bowel Management of underlying cause of obstruction
ACUTE INTESTINAL OBSTRUCTION INDICATION FOR SURGERY Failure of conservative management Tender and irreducible hernia Strangulation Virgin abdomen If the site of obstruction is unknown, laparotomy assessment is directed to: The site of obstruction The nature of obstruction The viability of gut
The type of surgical procedure depend upon the cause of obstruction via division of bands, adhesiolysis , excision, or bypass Once obstruction relieved, the bowel is inspected for viability, and if non-viable, resection is required SURGICAL TREATMENT Absent peristalsis Loss of normal shine Loss of pulsation in mesentery Green or black color of bowel Absent mesenteric pulsations INDICATION FOR NON-VIABILITY
SURGICAL TREATMENT VIABLE NON-VIABLE CIRCULATION Dark color becomes lighter Dark color remain Visible pulsation in mesenteric arteries No detectable pulsation GENERAL APPEARANCE Shiny Dull and lusterless INTESTINAL MUSCULATURE Firm Flabby, thin and friable Peristalsis may be observed No peristalsis
IN CASE OF SMALL BOWEL OBSTRUCTION SURGICAL TREATMENT The first maneuver is to deliver the distended small bowel into the wound The small bowel should be covered with moist swabs and the weight of the fluid filled bowel supported so that the blood supply to the mesentery is not impaired Operative decompression should be performed whenever possible. This reduces pressure on the abdominal wound, reducing pain and improving diaphragmatic movement This is done via large bore orogastric tube and milking the bowel content in retrograde manner to the stomach for aspiration All volumes of fluid removed should be accurately measured and appropriately replaced Following relief of obstruction, the viability of the involved bowel should be carefully assessed
PLAN IV fluids and electrolytes resuscitation for all NG tube if repeated vomiting Antibiotics for all Hernia –> Operation Adhesions –> Conservative first Obstruction –> Remove Volvulus –> Derotate and/or operate Mesenteric ischemia –> Operate Abscess or peritonitis –> Drain and treat Intussusception –> Pneumatic or barium reduction or operate
IN CASE OF ACUTE LARGE BOWEL OBSTRUCTION SURGICAL TREATMENT After full resuscitation the abdomen should be opened through a midline incision Distension of caecum will confirm large bowel involvement. Identification of a collapsed distal segment of large bowel and its sequential proximal assessment will readily lead to identification of the cause When a removable lesion is found in the caecum, ascending colon, hepatic flexure or proximal transverse colon, an emergency right hemicolectomy should be performed If the lesion is irremovable, a proximal stoma or ileotransverse bypass should be considered
IN CASE OF ACUTE LARGE BOWEL OBSTRUCTION SURGICAL TREATMENT Obstructing lesions at the splenic flexure should be treated by an extended right hemicolectomy with ileodescending colonic anastomosis For obstructing lesions of left colon or rectosigmoid junction, immediate resection should be considered unless there are clear contraindications CONTRAINDICATIONS TO IMMEDIATE RESECTION INCLUDE: Inexperienced surgeon Moribund patient Advanced disease
IN CASE OF CHRONIC LARGE BOWEL OBSTRUCTION SURGICAL TREATMENT Arise from 2 sources – the cause and the subsequent obstruction The cause can be organic or functional Organic disease requires decompression Stomal stenosis can be managed at abdominal level Functional disease requires colonoscopic decompression and conservative management
MANAGEMENT DYNAMIC VS ADYNAMIC SMALL INTESTINE VS LARGE INTESTINE SIMPLE VS COMPLICATED
DYNAMIC VS ADYNAMIC DYNAMIC ADYNAMIC Peristalsis is working against a mechanical obstruction May be in acute and chronic form Peristalsis is absent or inadequate where there is no obstruction Causes: Intraluminal Intramural Extramural Causes: Paralytic ileus Pseudo-obstruction Abdominal pain Abdominal distension Vomiting Absolute constipation Paralytic ileus: Clinical significance after 72 hours Absence of bowel sound and no passing out flatus Abdominal distension becomes more marked and tympanic Effortless vomiting
DYNAMIC OBSTRUCTION ADHESIVE OBSTRUCTION CONSERVATIVE MANAGEMENT NG decompression and rehydration Not prolonged beyond 72 hours SURGICAL MANAGEMENT Divide the causative adhesion(s ) and limit the dissection Repair serosal tears , resect areas of doubtful viability Laparoscopic adhesiolysis in expert surgeon’s hands
DYNAMIC OBSTRUCTION INTUSSUSCEPTION CONSERVATIVE MANAGEMENT NG drainage, resuscitation with IV fluids, antibiotics NON OPERATIVE MANAGEMENT Air OR barium enema performed if there are no signs of peritonitis, perforation OPERATIVE MANAGEMENT Reducible intussusception Irreducible intussusception – resection with primary anastomosis
DYNAMIC OBSTRUCTION VOLVULUS CAECAL VOLVULUS If viable, volvulus should be reduced achieved after decompression of caecum using needle Further management consists of fixation of caecum to right iliac fossa ( caecopexy ) or caecostomy
DYNAMIC OBSTRUCTION VOLVULUS SIGMOID VOLVULUS Flexible sigmoidoscopy or rigid sigmoidoscopy & insertion of a flatus tube should be carried out to allow deflation of gut The tube should be secured in place with tape for 24 hours and a repeat X-Ray taken to ensure that decompression has occurred This will resolve the acute problem
DYNAMIC OBSTRUCTION VOLVULUS SIGMOID VOLVULUS FURTHER TREATMENT YOUNG: Elective sigmoid colectomy is required ELDERLY: If endoscopic decompression is successful, it is reasonable to not offer further treatment as 80% death rate If it’s recurrent, the options available are: Resection Two point fixation with combine endoscopic / percutaneous tube insertion Failure results in an early laparotomy with untwisting of the loop and per anum decompression
ADYNAMIC OBSTRUCTION Failure of transmission of peristaltic waves secondary to neuromuscular failure PARALYTIC ILEUS CAUSES Post operative, infection, reflex ileus, metabolic MANAGEMENT NG suction, fluid replacement Use prokinetics (domperidone/erythromycin) in resistant case Laparotomy – if inactivity persists > 7 days, only after confirmation of abdominal sepsis / mechanical obstruction
ADYNAMIC OBSTRUCTION Obstruction in absence of mechanical cause or acute intra-abdominal disease PSEUDO-OBSTRUCTION ASSOCIATIONS Metabolic, severe trauma, shock, retroperitoneal irritation Radiographs show colon obstruction and distension If no obstruction, confirm by colonoscopy & barium enema MANAGEMENT Treat the identifiable cause IV Neostigmine 1mg Repeat with second dose after few minutes if first dose is ineffective Colonoscopic decompression Surgery is associated with high mortality and morbidity
SBO VS LBO HIGH SMALL BOWEL LOW SMALL BOWEL LARGE BOWEL Vomiting occurs early and profuse Vomitus contain undigested food Rapid dehydration Minimal distension Upper abdominal discomfort Little evidence of dilated small bowel loops Pain is predominant with central distension Vomiting is delayed Vomitus may contain feaculant material Multiple small bowel loops is dilated Distension is early and pronounced Less severe pain Vomiting and dehydration present later Obstipation indicates complete obstruction History of constipation The proximal colon and caecum are distended on abdominal radiography Presence of haustral folds The small bowel is dilated if ileocecal valve is incompetant
SIMPLE VS COMPLICATED OBSTRUCTION SIMPLE OBSTRUCTION COMPLICATED OBSTRUCTION Blood supply is intact The obstruction occludes the lumen only Strangulation occurs when there is interference with the blood flow Obstruction with strangulation impairs the blood flow leading to necrosis to intestinal wall CLINICAL FEATURES Vomiting Abdominal distension Abdominal pain Constipation CLINICAL FEATURES Fever Constant severe pain Generalized tenderness with rigidity Shock PLAIN X RAY Dilated small bowel loops with air fluid levels CT SCAN Shows a discrepancy in the caliber between distended proximal bowel and collapsed distal intestine CT SCAN Thickening of bowel wall Air in the bowel wall / portovenous system Absence of mesenteric fluid Intrapertoneal free air indicated perforation
Bailey and Love 26 th Edition UpToDate MedTube.Net MSDManuals REFERENCE