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INTESTINAL OBSTRUCTION



  Acute intestinal obstruction.
 Definition of the concept.
 Classification (by origin, pathogenesis, anatomical localization, clinical course).
 Methods of diagnostics.

Intestinal obstruction
The impedance to the normal passage of the bowel contents through the small or large intestine. It is a common cause of acute abdominal pain.



CAUSES OF OBSTRUCTION
A.  DYNAMIC (mechanical obstruction)
1.Intraluminal: impacted faeces, foreign bodies, gallstones, Bezoars.
 2.Intramural: tumors, inflammatory strictures,
  3.Extramural: adhesion, hernias, volvulus, intussusception, tumors
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According to site of obstruction its classified as:

B. Adynamic: (functional obstruction)
     1. (paralytic ileus) small bowel obstruction (SBO)
          -high ->early perfuse vomiting, rapid dehydration
          -low->predominant pain, and central distention; vomiting delayed; multiple central air-fluid levels seen on AXR
    2.  Pseudo-obstruction -large bowel obstruction (LBO)
          early pronounced distension, mild pain, vomiting, dehydration late    e.g. -carcinoma
            -diverticulitis or volvulus
3.  Mesenteric vascular occlusion.

  
OBSTRUCTION CAN ALSO BE DIVIDED INTO:

Simple: blockage without interfering with vascular supply
 Strangulation: significant impairment of blood supply most commonly associated with hernia, volvulus, intussusception, mesenteric infarction, adhesions/Bands
          -surgical emergency
   Closed loop obstruction: bowel is obstructed at both the proximal and distal end

  

  


Pathophysiology.
Irrespective of etiology or acuteness of onset:
Proximal to obstruction
Increased fluid secretion à abdominal distention
Accumulation of gas à abdominal distention
Increased intraluminal pressure
Vomiting
Dehydration
Dilatation of bowel
Reflex contraction of smooth muscle à colicky pain
Increased peristalsis to overcome obstruction à increased bowel sounds
If obstruction not overcome à bowel atony
Decreased reabsorption with time and flaccidity to prevent vascular damage from high pressure
Distal to obstruction:  nothing is passed & bowel collapse à constipation.
   
Symptoms
The four cardinal features of intestinal obstruction:
    -abdominal pain
     -vomiting
     -distension
     -constipation
Vary according to: -
          location of obstruction
          Duration of obstruction
          underlying pathology
          intestinal ischemia

Abdominal pain
   -  colicky in nature, around the umbilicus in SBO while in the lower abdomen in LBO
    - if it becomes continuous, think about perforation or strangulation.
   - does not usually occurs in paralytic ileus.
Vomiting
     -starts early in SBO and late in LBO
     -As obstruction progresses vomitus alters from digested food to faeculent due to enteric bacterial overgrowth
Distension
     -more with lower obstruction

Constipation
   -more with lower or complete obstruction
          - constipation is either absolute (no feces or flatus)
        cardinal feature of complete Int.obst.
     or relative (flatus passed).
¨  it does not apply in
    -Richter’s Hernia
    -Gallstone obstruction.
    -mesenteric vascular occlusion.
    - obstruction associated with pelvic abscess.
     -diarrhea may be present with partial obstruction

    Dehydration
¨ More common in small bowel obstruction.due to repeated vomiting .
¨ Secondary polycythemia due to raised B.urea & hematocrit.

       Pyrexia
¨ Onset of ischemia.
¨ Intestinal perforation.
¨ Inflamation associated with int. obst.

Symptoms.
In strangulation:
¨      severe constant abdominal pain
¨      fever
¨      tachycardia
¨      tenderness with rigidity/rebound
         tenderness.
¨      Shock
  

Clinical examination.
General examination-
          Vital signs
          Signs of dehydration –tachycardia, hypotension
          dry mucus membrane, decreased skin turgor, decreased urine output
Inspection
          distension, scars, peristalsis, masses, hernial orifices
Palpation
          tenderness, masses, rigidity
Percussion
      tympanic abdomen
Auscultation
     high pitched bowel sound or silent abdomen
*Examine rectum for mass, blood, feces or it may be empty in case of complete obstruction

Investigation
¨ Hemogram - WBC (neutrophilia-strangulation)
¨ Hyper kalemia, hyperamylasemia & raised LDH may be associated with strangulation.
¨ Plain AXR
¨ Sigmoidoscopy (carcinoma, volvulus)
¨  Contrast x-ray
¨ CT abdomen.


X-ray abdomen

    When distended by gas:
¨ Jejunum is characterized by valvulae conniventes (completely pass across the width & regularly placed)
¨ Ileum is featureless.
¨ Caecum is shown by rounded gas shadow in RIF.
¨ Colon shows haustral folds.
¨ Fluid level appears later than gas shadow
¨ Two fluid level in small bowel considered normal.
¨ No. of fluid level is proportional to degree of obstruction and distal site in small bowel.
¨ Colonic obstruction does not commonly give rise to small bowel fluid level unless advanced.
¨ Associated with large ammount of gas in  caecum.
¨ Ba-follow through is contraindicated in acute intestinal obstruction.




Treatments
¨ Three main measures-
- GI drainage
- Fluid &Electrolyte replacement
- Relief of obstruction, usually surgical

Conservative:
    -Nasogastric aspiration by Ryles tube
     -IV fluids- volume varies depending on dehydration
     -NPO    
          -urinary catheter
     -check temp. and pulse 2 hourly
     -abdominal examination 8 hourly
          -Broad spectrum antibiotics initiated early- reduce bacterial overgrowth.
  Some cases will settle by using this 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 reasons for delay should be monitored continuously for 72 hours in hope of spontaneous resolution e.g. adhesions with radiological findings but no pain or tenderness
  “The sun should not both rise and set” in cases of unrelieved obstruction.

Indication for surgery:
    
         - failure of conservative management
     - tender, irreducible hernia
     - strangulation
¨ 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 site of obstruction can be determined by caecum

Surgical treatment

Operative decompression required-if
*  dilatation of bowel loops prevent exposure,
*   bowel wall viability is compromised,
*  or if subsequent closure will be compromised.
          Savage’s decompressor used within seromuscular purse-string suture.
          Or large-bore NG tube maybe used for milking intestinal contents into stomach.
 The type of surgical procedure depends upon the cause of obstruction vs division of bands, adhesiolysis, excision, or bypass
*Once obstruction relieved, the bowel is inspected for viability, and if non-viable, resection is required.
 Indication of non-viability
     1.absent peristalsis
     2.loss of normal shine
          3.loss of pulsation in mesentery
     4.green or black color of bowel

¨ If in doubt of viability, bowel is wrapped in hot packs for 10 minutes with increased oxygen and reassessed for viability.
¨ Resection of non-viable gut should be done followed by stoma.
¨ Sometimes a second look laparotomy is required in 24-48 hours e.g. multiple ischemic areas.
  
OBSTRUCTION BY ADHESION AND BAND
¨ Most common cause of intestinal obstruction.
¨ Peritoneal irritation results in local fibrin production, which produce adhesions.
                              BANDS
¨ Congenital: obliterated vitelli intestinal duct.
¨ A string band following previous bacterial peritonitis.
¨ A portion of greater omentum   adherent to parietals.

  Causes of adhesions:
¨ Abdominal operation: anastomosis, raw peritoneal surfaces
¨ Foreign material:    talc, starch, gauze, silk
¨ Infection:  peritonitis, T.B.
¨ Inflammatory conditions: crohn’s disease.
¨ Radiation enteritis.             
                                            Prevention 
¨ Good surgical technique.
¨ Washing the peritoneal cavity with saline to remove the clots.
¨ Minimizing contact with gauze.
¨ Covering the anastomosis & raw peritoneal surfaces. 

Treatment

¨ Usually conservative treatment is curative.
  (i.v. rehydration & nasogastric decompression)
¨ It should not be prolonged beyond 72 hrs.
                     Surgery
¨ Division of band.
¨ Minimal adhesiolysis.

Treatment of recurrent obstructions due to adhesions.
¨ Repeat adhesiolysis alone.
¨ Noble’s plication: adjacent intestinal coils (15-20 cm) are sutured with serosal sutures.
¨ Charles-Phillips trans-mesenteric plication.
¨ Intestinal intubation: intraluminal tube insertion via a WITZEL jejunostomy or gastrostomy.

 Internal hernias

¨ When a portion of small intestine is entrapped in one of retroperitoneal fossae or in a congenital mesentric defect.
        Sites of internal herniation:
¨ Foramen of Winslow.
¨ A hole in mesentry / transverse mesocolon.
¨ Defects in broad ligaments.
¨ Congenital/ acquired diaphragmatic hernia.
¨ Duodenal retroperitoneal fossae- Lt. paraduodenal & rt. Duodenoojejunal.
¨  intersigmoid fossae.
¨ It is uncommon in the absence of adhesions.
¨ Treatment: to release the constricting agent by division.

Intramural obstruction by gallstone stones
¨ It tends to occur in elderly.
¨ Erosion of large gallstone into duodenum.
¨ Present with recurrent obstruction.
¨ X-ray: small bowel obstruction with air in biliary tree.
     -may show a radio opaque gall stone.
¨ Treatment: laparotomy & removal /crushing of stone.

Food

¨ After partial /total gastrectomy.
¨ Unchewed food  can cause obstruction.
¨ Treatment similar to gall stone.
                                          BEZOARS
¨ Trichobezoars
¨ Phytobezoars
                                           WORMS
¨ Ascaris lumbricoides
¨ Frequently follows initiation of antihelminthic therapy.
¨ Eosinophilia/worm with in  gas filled bowel loops.
¨ Laparotomy.

¨ In older children intussusception is usually associated with  a lead point – meckel’s  diverticulum, polyp, & appendix.
¨ Adults: always  with a lead point.- polyp, submucosal lipoma/ tumor.
¨ It is composed of three  parts:
    -Entering/ inner tube(Intussusceptum)
   - Returning/ middle  tube
    -Sheath/ outer tube(intussuscipiens)
¨ It is an example of strangulating  obstruction with impaired blood supply of inner layer.
¨ It may be ileoileal(5%); ileocolic(77%); ileo-ileo-colic(12%); colocolic (2%) & multiple.

Clinical features
¨ Severe colic  pain.
¨  vomitting as time progress
¨  blood & mucus (the ‘redcurrent’ jelly stool).
¨ Abdominal lump(sausage shaped)
¨  Emptiness in RIF(the sign of Dance).
¨ Death may occur from bowel obstruction or peritonitis  secondary to gangrene.

Radiography
¨ Plain X-ray Abd.: Bowel obstruction with absent caecal shadow gas in ileo-ileal & ileo-colic cases.
¨ Ba-enema: the claw sign in ileocolic & colocolic cases.
¨ CT scan in equivocal cases of ileo-ileal  intussusception. (small bowel mass may be revealed)
                  
                               Differential Diagnosis
¨ Acute enterocolitis:  faecal matter/ bile is always present.
¨ Henoch-schoenlein purpura.
¨ Rectal prolapse: projecting mucosa can be felt in continuity with perianal skin

Treatment

¨ Theraputic Ba-enema :  -in infants.
     - unlikely to succeed in lead points.
     - contrindications: peritonism, prolonged  
        history (> 48 hrs.).
      
                                   Operative
¨ After resuscitation ;Laparotmy with reduction.
¨ Cope’s method.
¨ Irreducible/ gangrenous intussusception: excision of mass & anastomosis.


Duodenal atresia

         Occurs in 1 in 10,000 live births
        Site of obstruction is most commonly in 2nd part of duodenum
        Proximal duodenum become hypertrophied
        50% are associated with polyhydramnios
        60% of such pregnancies are complicated or end prematurely
        Can often be diagnosed with antenatal ultrasound
        30% of babies with duodenal atresia have Down's syndrome
        Other associated abnormalities are cardiac anomalies, malrotation and biliary atresia
        Postnatally presents with bilious or non-bile stained vomiting
        X-ray may show a 'double-bubble' and no gas within the bowel




Management
        A nasogastric tube should be passed
        Intravenous fluid resuscitation should be given
        Major cardiac and other defects should be excluded
        Duodenoduodenostomy should be performed when resuscitated


Other atresias
         Atresias of the small bowel and colon are less common
        Often associated with polyhydramnios
        Bilious vomiting and distension are key features
        x-ray will show dilated bowel and a gas-free rectum
        A nasogastric tube should be passed
        Intravenous fluid resuscitation should be given
        At operation, dilated proximal bowel should be resected or tapered
        A primary anastomosis may be possible

Hirschsprung,s Disease
        Due to absence of autonomic ganglion cells in Auerbach's plexus of distal large intestine
        Commences at internal sphincter and progresses for variable distance proximally
        Affects 1 in 5000 live births
        Male : female ratio 4:1
        Some appear to be due to autosomal dominant inheritance
        75% cases confined to recto-sigmoid
        10% cases have total colonic involvement

Clinical features
        80% present in neonatal period with delayed passage of meconium
        Followed by increasing abdominal distension and vomiting
        Accounts for 10% of neonatal intestinal obstruction
        Child is at increased risk of enterocolitis and perforation
        Occasionally presents with chronic constipation in infancy

  
Diagnosis
        Barium enema - Contracted rectum, cone shaped transitional zone and proximal dilatation
        Anorectal manometry - No recto-sphincteric inhibition reflex on rectal distension
        Rectal biopsy shows:
      Absent ganglion cells in submucosa
      Increased acetylcholinesterase cells in muscularis mucosa
      Increased unmyelinated nerves in bowel wall  




Treatment
        Initial defunctioning stoma to relieve obstruction
        Bypass of affected segment - Duhamal or Soave bypass
        Excision of aganglionic segment - Swenson procedure

Meconium ileus
        Commonest cause of neonatal intraluminal intestinal obstruction
        80% cases are associated with cystic fibrosis
        Cystic fibrosis occurs in 1 in 2000 live births
        Inherited as an autosomal recessive trait
        Viscid pancreatic secretions cause autodigestion of pancreatic acinar cells
        Resulting meconium is abnormal and putty-like in consistency
        Meconium becomes inspissated in the lower ileum
        There is a microcolon
        Presents with bilious vomiting and distension usually on first day of life
        Passage of meconium is delayed
        Meconium filled loops of bowel may be palpable
        X-ray may show a 'ground-glass' appearance, especially in the right upper quadrant
Management
        Gastrografin enemas may be successful in 50% of patients
        If unsuccessful, surgery will be required
        Limited resection and stomas may be required


complications
        Peritonitis from bowel perforation secondary to over-strenuous attempts at reduction of volvulus or intussusception
        Misdiagnosis of an ileus secondary to intra-abdominal infection as large bowel obstruction, with consequent delay in treatment
        Intra-abdominal abscess from anastomotic leakage
        Pneumonia from aspiration during emesis
        Dehydration
        Electrolyte disturbance

Sigmoid Volvulus

        Twisting of loop of intestine around its mesenteric attachment site may occur at various sites in the GI tract
        Most commonly: sigmoid & cecum
        Rarely: stomach, small intestine, transverse colon
        Results in partial or complete obstruction
        May also compromise bowel circulation resulting in ischemia
        Sigmoid volvulus most common form of GI tract volvulus
        Accounts for up to 8% of all intestinal obstructions
        Most common in elderly persons (often neurologically impaired)
        Patients almost always have a history of chronic constipation

Pathophysiology
        Redundant sigmoid colon that has a narrow mesenteric attachment to posterior abdominal wall allows close approximation of 2 limbs of sigmoid colon à twisting of sigmoid colon around mesenteric axis
        Other predisposing factors
      Chronic constipation
      High-roughage diet (may cause a long, redundant sigmoid colon)
      Roundworm infestation
      Megacolon (often due to Chagas dz)
       Peak age > 50 yrs.
      Second largest group à children
        Torsion usually counterclockwise ranging from 180 – 540 degrees
        Luminal obstruction generally at 180 degrees
        Venous occlusion generally at 360 degrees à gangrene & perforation

Signs and symptoms

May present as abdominal emergency
        Acute distension
        Colicky pain (often LLQ)
        Failure to pass flatus or stool (constipation is prevailing feature)
        Vomiting is late sign

Physical examination
        Tympanitic abdomen
        Abdominal distention
        +/- palpable mass

Diagnosis


        Abdominal plain films usually diagnostic
      Inverted U-shaped appearance of distended sigmoid loop
        Largest  and most dilated loops of bowel are seen with volvulus
      Loss of haustra
      Coffee-bean sign à midline crease corresponding to mesenteric root in a greatly distended sigmoid
        Sigmoid volvulus – bowel loop points to RUQ
        Cecal volvulus – bowel loop points to LUQ
      Dilated cecum comes to rest in left upper quadrant
      Bird’s-beak or bird-of-prey sign à seen on barium enema as it encounters the volvulated loop
        CT scan useful in assessing mural wall ischemia






Differential Diagnosis

        Large bowel obstruction due to other causes à sigmoid colon CA
        Giant sigmoid diverticulum
        Pseudoobstruction


Complications
1.   Colonic ischaemia
2.   Perforation
3.   Sepsis

Treatment

         Derotation & decompression by barium enema or with rectal tube, colonoscope, or sigmoidoscope if no signs of bowel ischemia or perforation
      Laparoscopic derotation or laparotomy +/- bowel resection
      Cecopexy à suture fixation of bowel to parietal peritoneum may prevent recurrence
      Recurrence rate after decompression alone à 50%

Intestinal Pseudo-obstruction
        The term intestinal pseudo-obstruction is used to indicate a syndrome characterized by a clinical picture suggestive of mechanical obstruction in the absence of any demonstrable evidence of such an obstruction in the intestine
        Based on clinical presentation, pseudo-obstruction syndromes can be divided into acute and chronic forms
        Acute colonic pseudo-obstruction is a clinical condition that appears with symptoms, signs, and radiological findings similar to those of acute large bowel obstruction, without any apparent mechanical cause
        Frequency: Recent studies involving more than 13,000 orthopedic and burn patients documented the prevalence of acute colonic pseudo-obstruction to be 0.29%
        Acute colonic pseudo-obstruction generally develops in hospitalized patients and is associated with a variety of medical and surgical conditions
        The most commonly associated conditions include trauma, pregnancy, cesarean delivery, severe infections, and cardiothoracic, pelvic, or orthopedic surgery
        Most recent reports now indicate the mean age to be in the seventh and eighth decades of life
        the male-to-female ratio (1.5-4:1)
         The mortality rate in medically treated patients has been documented to be 14%; in surgically treated patients, 30%.
        The most serious complication of colonic pseudo-obstruction is perforation of the cecum. The reported incidence of cecal perforation is 3-40%, and the associated mortality rate is 40-50%.
        Pathophysiology remains unknown






















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