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Intestinal Obstruction
Presenter : Dr. Naresh Shrestha
Moderator : Dr. Ajay KC
Department of Surgery
Pokhara Academy of Health Sciences
2079-7-27
Objectives
• Introduction
• Types
• Investigations
• Management
Intestinal obstruction
• Bowel obstruction is defined by the lack of aborad transit of intestinal contents,
regardless of etiology
• Bowel obstruction one of the most common intraabdominal problems faced by
general surgeons
• In a 2010 global burden of disease study
• bowel obstruction and ileus were responsible for 2.1 deaths
• 54 years of life lost
• 54 disability-adjusted life-years per 100,000 population.
• Independent of the underlying etiology, bowel obstruction remains a major
cause of morbidity and mortality
• Maingots Abdominal Operations 13th Edition
• Incidence in patients who present to the emergency department : estimated at
2% to 8%
• Ten Broek RP et al. Burden of adhesions in abdominal and pelvic surgery: systematic review and
meta-analysis. BMJ. 2013
• May involve only the small intestine (small bowel obstruction), the
large intestine (large bowel obstruction), or both via systemic
alterations in metabolism, electrolyte balance, or neuroregulatory
mechanisms (generalized ileus)
• In 90% of cases, small bowel obstruction -caused by adhesions,
hernias, and neoplasms
• Adhesive small bowel obstruction represents 55–75% of small bowel
obstruction cases while hernias and small bowel tumors account for
the remainder
• Large bowel obstruction is provoked by cancer in about 60% of cases
volvulus and diverticular disease are responsible of other 30%
(Bowel obstruction: a narrative review for all physicians)
Causes of obstruction
Sabiston Textbook of Surgery Bailey and Love
Classification
• peristalsis is working against a mechanical obstruction.
• It may occur in an acute or a chronic form
Dynamic
• no mechanical obstruction
• peristalsis is absent or inadequate (e.g. paralytic ileus or pseudo-
obstruction)
Adynamic
Mechanical
Partial
Complete
Simple
Closed loop
Strangulated
Mechanical bowel obstruction
No vascular compromise and intestine
can be decompressed proximally
Both ends of the involved intestinal
segment are obstructed
Increases intraluminal pressure
Blood supply to affected segment
compromised focal or segmental
transmural necrosis
Lumen narrowed and some
intestinal content can transit
distally
Lumen obliterated and no
content can pass beyond
point of obstruction
Narrowing or
physical
occlusion of
intestinal
lumen
Causes MBO
• Mechanical SBO can be divided
into three main categories
• Extrinsic
• Intramural
• Intraluminal
Functional
Caused by local or
systemic stimuli
Post op ileus –M/C type
Transient
Pseudoobstruction
Irreversible
Aim -palliation
a group of rare, chronic,
progressive,
gastrointestinal (GI)
functional obstruction
Functional Bowel Obstruction/Adynamic
FUNCTIONAL BOWEL
OBSTRUCTION, ILEUS, AND
PSEUDOOBSTRUCTION
Etiology
Pathophysiology
1. Bowel distension, decreased absorption, intraluminal hypersecretion
2. Alterations in motility are found universally, but the mechanisms -
unclear
3. Accompanied by considerable disruption of mechanisms of neural and
hormonal control, the type and quantity of endogenous bacterial flora,
and the innate immunity of the gut
Distension, Absorption, and Secretion
• Bowel distension is a characteristic
• swallowed air –leads to small bowel distention in the early
phases .
• other sources in early phase -Fermentation of sugars,
production of carbon dioxide by interaction of gastric acid and
bicarbonates , and diffusion of oxygen and carbon dioxide from
the blood are of gas in early obstruction.
• Dilation and inflammation of the bowel wall -cause
accumulation of activated neutrophils and
macrophages
• Decrease in the absorptive capacity and increase in
secretion lead to important fluid losses
(enterosecretion) may result in profound
dehydration
first 12 hours
of SBO-secondary decrease in net
absorption -water and electrolytes into
the lumen
In 24 hrs
further increase in net intestinal secretion
(secretory flux).-by increased
permeability due to secondary mucosal
injury resulting in intraluminal leakage
With a more chronic obstruction, bacterial
proliferation - disrupting absorption, secretion,
and mucosal integrity
proliferation reaches a plateau of 10^9to 10^10
colonies/mL after 12 to 48 hours
Intestinal Motility
• Initially increases in the early phase of bowel obstruction
• Later decreases - likely secondary to a relative hypoxia of the intestinal wall and
enhanced intramural inflammation.
• The exact mechanisms have not been described adequately,
• More recent investigative of attention - opioid administration postoperatively.
• The μ-receptor antagonist alvimopan appears to inhibit opioid-induced intestinal
impairment and enhance motility.
Circulatory Changes
• Bowel wall ischemia may occur through several mechanisms such as
• extrinsic compression of the mesenteric arcades by adhesions or an axial twist of
the mesentery in a hernia defect.
• progressive distention in closed-loop bowel obstruction cause vascular
compromise
• Rarely, extensive mesenteric venous thrombosis - compromised arterial inflow
and ischemia.
• COLON - especially susceptible to vascular compromise because
watershed areas of colonic perfusion, represent end organ blood supply.
• Colonic ischemia is further exacerbated by bacterial proliferation and
generation of luminal gas. -compromise blood flow -most commonly in
the ascending colon Clinical implication :
This pathophysiology
increases the
urgency for large
bowel obstruction
Microbiology and Bacterial Translocation
• Rapid proliferation of bacteria proximal to
obstruction, predominantly of fecal-type
organisms.
• The proliferation reaches a plateau of 109 to 1010
colonies/ml after 12 to 48 hours
• Toxins play an important role –the loss of mucosal
integrity allows luminal bacteria to
• both translocate as well as to invade the
submucosa
• enter the systemic circulation via the portal venous
and lymphatic systems
The resident and transient flora of the
upper small intestine gram-positive,
facultative, anaerobic organisms in
small concentrations: less than 106
colonies/mL.
The bacterial count increases distally to
about 108 colonies/mL in the distal
ileum.
Early in the course of an obstruction intestinal motility and contractile
activity increase in an effort to propel luminal contents past the
obstructing point
The increase in peristalsis that occurs early  present above and below
the point of obstructioncausing diarrhea that may accompany partial
or even complete small bowel obstruction in the early period
Later the intestine becomes fatigued and dilates, with contractions
becoming less frequent and less intense
As the bowel dilates, water and electrolytes accumulate intraluminally
and in the bowel wall itself massive third-space fluid lossresulting
in dehydration and hypovolemia
metabolic effects of fluid loss depend on the site and duration of the
obstruction
Pathophysiology
Other consequences of bowel obstruction
• Increased intra-abdominal pressure, decreased venous return, and elevation
of the diaphragm, compromising ventilation.
Increased Intraluminal pressure decreases in mucosal blood flow
A closed loop obstruction, produced commonly by a twist of the bowel,
can progress to arterial occlusion and ischemia if it is left untreated and
may potentially lead to bowel perforation and peritonitis.
In the absence of intestinal obstruction, the jejunum and proximal ileum
are almost sterile.
With obstructionthe flora of the small intestine changes
• Type (most commonly Escherichia coli, Streptococcus faecalis, and
Klebsiella spp.)
• Quantity, with organisms reaching concentrations of 10^9 to 10^10/mL.
Clinical presentation
• Coliky abdominal pain
• crampy abdominal pain associated with intestinal
obstruction occurs in paroxysms at 4- to 5-minute intervals
and occurs less frequently with distal obstruction
• Pain –common with proximal than distal obstruction
• Nausea /Vomiting
• Obstipation
• Abdominal distension
• degree of distension is dependent on the site of the
obstruction
• greater more distal the lesion
• Vomitting is more prominent with
proximal obstruction than distal
• Character of vomitus is important
–more feculent with more
established obstruction
• Continued passage of flatus /stool
beyond 6 -12 hrs after onset of
symptoms is characteristic of
partial obstruction rather than
complete
• Distension is more pronounced if
obstruction is in distal ileum
On examination
• May present with
• tachycardia and hypotension
• dehydration
• Fever (suggests the possibility of
strangulation)
• Per Rectal Examinations:
• To rule out fecal impaction or locate a
low-lying rectal cancer as a cause of
obstruction
Abdominal Examination
• Abdominal distension, Scars of
previous surgery, Visible peristalsis
• Swelling in case of Hernia
• Abdominal tenderness , Guarding ,
Rebound tenderness
• hyperactive bowel sounds with
audible rushes associated with
vigorous peristalsis (borborygmi)
Diagnosis
• Should focus on
1. Distinguishing mechanical obstruction from ileus
2. Determine etiology of obstruction
3. Determine partial from complete obstruction
4. Discriminate simple from strangulating obstruction
Laborotary parameters
• CBC( leukocytosis may be present in strangulation, Sepsis)
• Electrolyte panel
• Blood urea nitrogen
• Creatinine
• Arterial blood pH, serum lactate concentrations, and amylase and lactate
dehydrogenase to exclude the presence of strangulation or underlying bowel
necrosis
An increase in serum lactate
concentrations should raise the
suspicion of intestinal ischemia:
however, it is often a late finding
Radiologic Findings
• Diagnosis is usually confirmed with radiographic examination
• Initial imaging modality
• Abdominal series consists of –abdominal x-ray erect , supine ,
CXR
• Radiographs are usually diagnostic in ~60% of cases
• Remaining 20-30%, additional modality required
3-6-9 rule
Normal caliber of
Small bowel <3cm
Large bowel <6 cm
Appendix<6mm
Caecum<9cm
Findings in xray:
• distended loops of bowel greater than 3-6-9 cm
• collapsed colon
• differential air–fluid levels, and thickened bowel wall
• The string-of pearls sign may also be identified
• Strangulation may be indicated by edematous folds, pneumatosis intestinalis
Imaging
Adhesional small-bowel obstruction
shows multiple dilated loops of small
bowel
Valvulae conniventes appear
prominent
Multiple air–fluid levels (arrows)
and string-of-pearls sign
Erect
Pneumatosis intestinalis( Intramural gas)
Ultrasonography
• Sonography sensitivity of 89% compared with 71% for conventional abdominal radiography
in diagnosing small-bowel obstruction
• superior in its ability to
• Identify features of strangulation
• predict the location and cause of obstruction
• Schmutz GR, Benko A, Fournier L, et al. Small bowel obstruction: role and contribution of
sonography. Eur Raddiol
Findings suggestive of intestinal obstruction:
 multiple dilated (> 3 cm)
 fluid filled loops
 The obstructing cause can occasionally be visualized if it is a tumor or hernia.
 The presence of aperistalsis, fluid-filled bowel distention and wall thickening supports
infarction
 Bowel wall perfusion can also be assessed by Doppler sonography
Useful in
Critically ill
Pregnant
Computed Tomography
• Contrast enhanced CT  advocated as diagnostic imaging
modality of choice
• Diagnostic accuracy of greater than 90%
The presence of two or
more beak signs, a whirl
sign, a C- or U-shaped
appearance of the
bowel loop, and a high
degree of obstruction
were associated with
nonsurgical treatment
failure
Findings in small-bowel obstruction:
 dilated loops of bowel proximally with normal-caliber or collapsed loops distally (>2.5cm –
small bowel considered dilated)
 Transition point the diagnosis is more certain
 The transition point often resembles a beak (the beak sign  present in 60% of simple
small-bowel obstruction)
 the string-of-pearls sign
 small-bowel feces sign The small-bowel feces sign is a result of stasis and mixing of small-
bowel contents present in 82% of cases of small bowel obstruction
CECT features of strangulation
• thickening of bowel wall
• pneumatosis intestinalis
• portal venous gas
• mesenteric haziness
• poor uptake of IV
contrast into bowel
wall/lack of bowel wall
enhancement
MAGNETIC RESONANCE ENTEROGRAPHY
• Magnetic resonance enterography (MRE) has not been utilized
frequently performance of this examination is more time
consuming and requires substantial expertise in interpretation
• In contrast, in centers that use MRE frequently, diagnostic accuracy
exceeding 90% is achievable.
• Advantage of distinguishing benign from malignant bowel strictures in
patients with suspected malignant bowel obstruction
Approach to
bowel
obstruction
Algorithm for management of
bowel obstruction
Ashwini k.Decision Making in Bowel Obstruction: A Review.
Journal of Clinical and Diagnostic Research. 2016
Management
Resuscitate the patient
IV crystalloids 0.9% NS
CVP lines if required
Foleys catherisation
Broad spectrum antibiotics
NG- decompression
Correction of electrolyte imbalance
Non-operative management
• Nonoperative management of intestinal obstruction should be
considered only in patients with uncomplicated intestinal obstruction
in the absence of:
• peritonitis
• a progressive leukocytosis
• impaired bowel wall perfusion on imaging.
• When indicatedthis approach is reported to be successful in 62% to
85% of patients
Water soluble contrast in Non operative management
Gastrograffin(GG- diatrizoate meglumine and diatrizoate sodium)
• A Hyperosmolar contrast agent
• Advocated for diagnostic and therapeutic tool for SBO management
The appearance of contrast in the colon 4–24 hours after administration had a
sensitivity of 96% and a specificity of 98% in predicting resolution of small bowel
obstruction
 If contrast does not reach the colon, surgery required in about 90% of patients
Dual purpose of GG
1st- Visualised on X-ray – contrast in colon i.e point of obstruction passed and no need
for operative exploration
2nd – Hyperosmolar property- draws edema present in obstructed bowel into bowel
lumen and helps reverse obstruction
Bologna guidelines
for ASBO
For suspected adhesive small
bowel obstruction
Operative Management
• When to Convert to Operative Management ??
• Prompt operative intervention is mandatory in patients who develop
signs and symptoms suggestive of a strangulation obstruction
• Parameters include:
 fever
Tachycardia
 leukocytosis
 localized tenderness
continuous abdominal pain
 peritonitis
 presence of any three of these signs has an 82% predictive value for
strangulation obstruction
 presence of any four of the above signs has a near 100% predictive value for
strangulation obstruction
Surgical management
• Depends upon the etiology of the obstruction
• If the site of obstruction is unknown adequate exposure is best
achieved by a midline incision
• Assessment is directed to:
● the site of the obstruction
● the nature of the obstruction
● the viability of the gut
Etiology Management Remarks
Adhesions Adhesionolysis Only divide the causative adhesion and
leave rest of adhesions
When obstruction is caused by an area
of multiple adhesions, the adhesions
should be freed by sharp dissection
from the duodenojejunal junction to
the caecum
Intussuception Pneumatic or hydrostatic reduction
Successful in 70% (85-90% in Literature)
Recurrence 11% and usually within 24 hours
If recurs 2nd enema reduction
3rd recurrence  Operative management
• Transverse incision
• Reduction achieved by gently compressing
the most distal part of the intussusception
toward its origin making sure not to pull
• The last part of the reduction is the most
difficult
An irreducible intussusception or one
complicated by infarction or a
pathological lead point requires
resection and primary anastomosis
Appendectomy –essential component
irrespective of bowel
resection(Sabiston)
Laparoscopic surgery in SBO
• Candidates for laparoscopic management
• Patients who have:
• mild abdominal distention allowing adequate
visualization
• proximal obstruction
• partial obstruction
• anticipated single-band obstruction
Candidates for Laparotomy
Patients who have :
• Advanced
• complete
• distal small bowel
• matted adhesions or carcinomatosis
• those who remain distended after
nasogastric intubation
laparoscopic treatment  found to be of greatest benefit in patients who have
• undergone <3 previous operations
• Early presentation after the onset of symptoms
• Anticipation of adhesive bands as the cause
Surgical management of Large bowel obstruction
• Large bowel obstruction  usually caused by an underlying carcinoma or
occasionally diverticular disease
• Presents in an acute or chronic form
• Removable lesion 
• in the caecum, ascending colon, hepatic flexure or proximal transverse colon emergency
right hemicolectomy
• A primary anastomosis is safe if the patient’s general condition is reasonable
• Irremovable (Rare) 
• a proximal stoma (colostomy or ileosotomy if the ileocaecal valve is incompetent) or
ileotransverse bypass should be considered
• Obstructing lesions at the splenic flexure An extended right hemicolectomy with
ileodescending colonic anastomosis
• Obstructing lesions of the left colon or rectosigmoid junctionimmediate
resection (unless there are clear contraindications)
• If caecal perforation is imminent additional time to improve the
patient’s clinical condition can be bought by performing an emergency
caecostomy (or ileosotomy in the presence of an incompetent ileocaecal
valve)
• Self-expanding metal stent (SEMS) : Palliation or Bridge
Palliative situation Bridge to surgery
Incurable disease or Patient unfit for surgery or both
Reduces mortality and morbidity a/w stoma
formation
potentially curative disease  stenting as a bridge to
surgery (usually performed 1–4 weeks post stenting)
Reduce stoma formation but doesn’t reduce
postoperative mortality
long-term oncological effects of stenting are still
uncertain
success rates for stenting  80–90% current recommendation  stenting as a bridge to
surgery in patients with potentially curative disease
should only be used in patients with a high risk of
postoperative morbidity and mortality
SEMS
Volvulus
• Treatment of caecal volvulus :
• At operation the volvulus usually found to be ischaemic and needs
resection
• If viable the volvulus should be reduced(sometimes requires
decompression of the caecum using a needle)
• Further management  fixation of the caecum to the right iliac fossa
(caecopexy) and/or a caecostomy
• Recurrence of volvulus after caecopexy has been reported in up to
40% of cases.
Treatment of sigmoid volvulus
• Flexible sigmoidoscopy or rigid sigmoidoscopy and insertion of a flatus
tube to decompress the gut
• Successful (as long as ischaemic bowel is excluded)  resolves the acute
problem
• In young patientsan elective sigmoid colectomy
• In Elderlyno further treatment following successful endoscopic
decompression as there is a high death rate (~80% at two years) from
causes other than recurrent volvulus
• In elderly patients with co-morbidities and recurrent episodes of volvulus
• Resection or two-point fixation with combined endoscopic/percutaneous tube
insertion
• Failure results in an early laparotomy, with untwisting of the loop and per anum
decompression (
• If bowel viablefixation of the sigmoid colon to the
posterior abdominal wall  a safer manoeuvre in
inexperienced hands
• Resection preferable if it can be achieved safely
• A Paul–Mikulicz procedure is useful if there is
suspicion of impending gangrene
• Alternative procedure  a sigmoid colectomy +if
anastomosis considered unwise a Hartmann’s
procedure with subsequent reanastomosis can be
carried out
Post operative ileus
• POI is described as a transient impairment of bowel motility that may occur
after major surgery
• A Comprehensive Review of Evidence-Based Strategies to Prevent and Treat Postoperative Ileus Sara K.
Story a Ronald S. Chamberlain
• Paralytic ileus is a condition of transport disturbances from intestinal
contents due to decreased activity of smooth muscle in the small intestine or
colon
• Recent Pathophysiology and Therapy for Paralytic Ileus .Putu Surya Pridanta et al.
• Postoperative ileus is divided into two: immediate postoperative ileus after
surgery and diminishing with flatus and bowel, and prolonged postoperative
ileus
• Postoperative ileus is an ileus occurring in 4 or more days after surgery
• The underlying pathology of POI is best described as a lack of coordinated
bowel activity
Post op ileus
• The duration of postoperative ileus
may correlate with the degree of
surgical trauma and might even be
considered a “physiologic” response.
• A prolonged duration- in pts
operated for radiation enteropathy,
chronic obstruction, or severe
peritonitis.
• Recovery from ileus -differs among
anatomic segments
Organ (characteristic
sequence )
Time to regain
Intestine Hours,within first 24 hrs
Stomach within 48 hrs
Colon 3-5 days
Listening bowel sound is not
a reliable indicator that ileus
has fully resolved
Flatus or bowel movement is
more useful indicator of
coordinated action of
resumed bowel
Mechanism of Post operative ileus(POI)
Prevention of POI A Comprehensive Review of
Evidence-Based Strategies to
Prevent and Treat Postoperative
Ileus Sara K. Story a Ronald S.
Chamberlain
RECURRENT SMALL BOWEL OBSTRUCTION
• 4% - 34% of patients will experience
recurrent small bowel obstruction
regardless of management modality
• Recurrent obstruction more common in
patients with
• multiple adhesions
• matted adhesions
• previous admissions for small bowel
obstruction
• previous pelvic, colonic, and rectal surgery
Recurrent BO in unscarred
abdomen/virgin abdomen:
• mostly due to internal hernia,
• keep resolving on conservative
management.
• A CT scan with oral contrast and
even a barium study of small bowel is
usually diagnostic.
• Para-duodenal hernia constitute
50% of internal herniation
• Includes
the gentle handling of the bowel to reduce serosal trauma
avoidance of unnecessary dissection
 exclusion of foreign material from the peritoneal cavity (the use of absorbable
suture material when possible, the avoidance of excessive use of gauze sponges, and
the removal of starch from gloves)
adequate irrigation
 removal of infectious and ischemic debris
 preservation and use of the omentum around the site of surgery or in the denuded
pelvis
To date, the most effective means of limiting the number of
adhesions is a good surgical technique
Acute post operative bowel obstruction
• BO occurring within 6 weeks of the original operation
• Diagnosis is often difficult because the primary symptoms of abdominal pain and
nausea or emesis may be attributed to a postoperative ileus
• Electrolyte deficiencies hypokalemia  cause ileus correct
• Plain abdominal films are usually not helpful in distinguishing an ileus from
obstruction
• More than 90% of early postoperative obstructions are partial and will resolve
spontaneously, given ample time.
CECT abdomen(with oral contrast) helps in determining whether
 an obstruction exists
 the level of the obstruction.
• Conservative management ( bowel rest, fluid resuscitation, electrolyte replacement,
and parenteral nutrition  routinely successful.
• Obstructions caused by extrinsic bowel compression amenable to percutaneous
correction fluid collections, abscesses, and hematomas treated by percutaneous
drainage
• Development of complete obstruction or signs of strangulation mandates reoperative
intervention
• Postoperative bowel obstruction after laparoscopic surgery  more commonly
associated with a definitive obstruction point such as a port site hernia or an
internal hernia  requires a high index of suspicion for the need for operative
intervention
Pseudo-Obsstruction
• An obstruction, usually of the colon, that
occurs in the absence of a mechanical
cause or acute intra-abdominal disease
• A/w a variety of syndromes with
• an underlying neuropathy and/or myopathy
and a range of other factors
• Small intestinal pseudo-obstruction
• may be primary (i.e. idiopathic or associated with familial visceral
myopathy) or secondary.
• Clinical manifestation of recurrent subacute obstruction
• Diagnosis made by the exclusion of a mechanical cause
• Treatment
• correction of any underlying disorder
• Metoclopramide and erythromycin may be of use
Colonic – pseudo obstruction
• occur in an acute or a chronic form.
• Ogilvie’s syndromepresents as acute large bowel
obstruction
• Abdominal radiographs show signs of colonic
obstruction, with marked caecal distension ( common
finding)
• caecal perforation well recognised complication
• Absence of a mechanical cause requires urgent
confirmation by colonoscopy or a single contrast
water-soluble barium enema or CT
Treatment:
• Treat any identifiable cause
• If this is ineffective, give iv neostigmine 1mg  1 mg given iv within a few
minutes if the first dose is ineffective.
• During this procedure, it is best to sit the patient on commode
• Electrocardiograph (ECG) monitoring + atropine should be available
• Neostigmine ineffective perform colonoscopic decompression
• Surgery is associated with high morbidity and mortality
• reserved for those with impending perforation when other treatments have failed
or perforation has occurred
•Thank You
References
• Schwartz’s Principles of Surgery 11th edition
• Sabistons Text book of surgery 21th edition
• Bailey and love short practice of Surgery 27th edition
• Maingots Abdominal operations 13th edition
• Bologna guidelines for diagnosis and management of adhesive small bowel
obstruction (ASBO): 2017 update of the evidence-based guidelines from the
world society of emergency surgery ASBO working group
• Imaging of Acute Small-Bowel Obstruction, Savvas Nicolaou et al,AJR
• Ashwini k.Decision Making in Bowel Obstruction: A Review. Journal of Clinical
and Diagnostic Research. 2016
• Sara K. Story et. al .A Comprehensive Review of Evidence-Based Strategies to
Prevent and Treat Postoperative Ileus 2009
Intestinal Obstruction

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Intestinal Obstruction

  • 1. Intestinal Obstruction Presenter : Dr. Naresh Shrestha Moderator : Dr. Ajay KC Department of Surgery Pokhara Academy of Health Sciences 2079-7-27
  • 2. Objectives • Introduction • Types • Investigations • Management
  • 3. Intestinal obstruction • Bowel obstruction is defined by the lack of aborad transit of intestinal contents, regardless of etiology • Bowel obstruction one of the most common intraabdominal problems faced by general surgeons • In a 2010 global burden of disease study • bowel obstruction and ileus were responsible for 2.1 deaths • 54 years of life lost • 54 disability-adjusted life-years per 100,000 population. • Independent of the underlying etiology, bowel obstruction remains a major cause of morbidity and mortality • Maingots Abdominal Operations 13th Edition • Incidence in patients who present to the emergency department : estimated at 2% to 8% • Ten Broek RP et al. Burden of adhesions in abdominal and pelvic surgery: systematic review and meta-analysis. BMJ. 2013
  • 4. • May involve only the small intestine (small bowel obstruction), the large intestine (large bowel obstruction), or both via systemic alterations in metabolism, electrolyte balance, or neuroregulatory mechanisms (generalized ileus) • In 90% of cases, small bowel obstruction -caused by adhesions, hernias, and neoplasms • Adhesive small bowel obstruction represents 55–75% of small bowel obstruction cases while hernias and small bowel tumors account for the remainder • Large bowel obstruction is provoked by cancer in about 60% of cases volvulus and diverticular disease are responsible of other 30% (Bowel obstruction: a narrative review for all physicians)
  • 5. Causes of obstruction Sabiston Textbook of Surgery Bailey and Love
  • 6. Classification • peristalsis is working against a mechanical obstruction. • It may occur in an acute or a chronic form Dynamic • no mechanical obstruction • peristalsis is absent or inadequate (e.g. paralytic ileus or pseudo- obstruction) Adynamic
  • 7. Mechanical Partial Complete Simple Closed loop Strangulated Mechanical bowel obstruction No vascular compromise and intestine can be decompressed proximally Both ends of the involved intestinal segment are obstructed Increases intraluminal pressure Blood supply to affected segment compromised focal or segmental transmural necrosis Lumen narrowed and some intestinal content can transit distally Lumen obliterated and no content can pass beyond point of obstruction Narrowing or physical occlusion of intestinal lumen
  • 8. Causes MBO • Mechanical SBO can be divided into three main categories • Extrinsic • Intramural • Intraluminal
  • 9. Functional Caused by local or systemic stimuli Post op ileus –M/C type Transient Pseudoobstruction Irreversible Aim -palliation a group of rare, chronic, progressive, gastrointestinal (GI) functional obstruction Functional Bowel Obstruction/Adynamic
  • 10. FUNCTIONAL BOWEL OBSTRUCTION, ILEUS, AND PSEUDOOBSTRUCTION Etiology
  • 11.
  • 12. Pathophysiology 1. Bowel distension, decreased absorption, intraluminal hypersecretion 2. Alterations in motility are found universally, but the mechanisms - unclear 3. Accompanied by considerable disruption of mechanisms of neural and hormonal control, the type and quantity of endogenous bacterial flora, and the innate immunity of the gut
  • 13. Distension, Absorption, and Secretion • Bowel distension is a characteristic • swallowed air –leads to small bowel distention in the early phases . • other sources in early phase -Fermentation of sugars, production of carbon dioxide by interaction of gastric acid and bicarbonates , and diffusion of oxygen and carbon dioxide from the blood are of gas in early obstruction. • Dilation and inflammation of the bowel wall -cause accumulation of activated neutrophils and macrophages • Decrease in the absorptive capacity and increase in secretion lead to important fluid losses (enterosecretion) may result in profound dehydration first 12 hours of SBO-secondary decrease in net absorption -water and electrolytes into the lumen In 24 hrs further increase in net intestinal secretion (secretory flux).-by increased permeability due to secondary mucosal injury resulting in intraluminal leakage With a more chronic obstruction, bacterial proliferation - disrupting absorption, secretion, and mucosal integrity proliferation reaches a plateau of 10^9to 10^10 colonies/mL after 12 to 48 hours
  • 14. Intestinal Motility • Initially increases in the early phase of bowel obstruction • Later decreases - likely secondary to a relative hypoxia of the intestinal wall and enhanced intramural inflammation. • The exact mechanisms have not been described adequately, • More recent investigative of attention - opioid administration postoperatively. • The μ-receptor antagonist alvimopan appears to inhibit opioid-induced intestinal impairment and enhance motility.
  • 15. Circulatory Changes • Bowel wall ischemia may occur through several mechanisms such as • extrinsic compression of the mesenteric arcades by adhesions or an axial twist of the mesentery in a hernia defect. • progressive distention in closed-loop bowel obstruction cause vascular compromise • Rarely, extensive mesenteric venous thrombosis - compromised arterial inflow and ischemia. • COLON - especially susceptible to vascular compromise because watershed areas of colonic perfusion, represent end organ blood supply. • Colonic ischemia is further exacerbated by bacterial proliferation and generation of luminal gas. -compromise blood flow -most commonly in the ascending colon Clinical implication : This pathophysiology increases the urgency for large bowel obstruction
  • 16. Microbiology and Bacterial Translocation • Rapid proliferation of bacteria proximal to obstruction, predominantly of fecal-type organisms. • The proliferation reaches a plateau of 109 to 1010 colonies/ml after 12 to 48 hours • Toxins play an important role –the loss of mucosal integrity allows luminal bacteria to • both translocate as well as to invade the submucosa • enter the systemic circulation via the portal venous and lymphatic systems The resident and transient flora of the upper small intestine gram-positive, facultative, anaerobic organisms in small concentrations: less than 106 colonies/mL. The bacterial count increases distally to about 108 colonies/mL in the distal ileum.
  • 17. Early in the course of an obstruction intestinal motility and contractile activity increase in an effort to propel luminal contents past the obstructing point The increase in peristalsis that occurs early  present above and below the point of obstructioncausing diarrhea that may accompany partial or even complete small bowel obstruction in the early period Later the intestine becomes fatigued and dilates, with contractions becoming less frequent and less intense As the bowel dilates, water and electrolytes accumulate intraluminally and in the bowel wall itself massive third-space fluid lossresulting in dehydration and hypovolemia metabolic effects of fluid loss depend on the site and duration of the obstruction Pathophysiology
  • 18. Other consequences of bowel obstruction • Increased intra-abdominal pressure, decreased venous return, and elevation of the diaphragm, compromising ventilation. Increased Intraluminal pressure decreases in mucosal blood flow A closed loop obstruction, produced commonly by a twist of the bowel, can progress to arterial occlusion and ischemia if it is left untreated and may potentially lead to bowel perforation and peritonitis. In the absence of intestinal obstruction, the jejunum and proximal ileum are almost sterile. With obstructionthe flora of the small intestine changes • Type (most commonly Escherichia coli, Streptococcus faecalis, and Klebsiella spp.) • Quantity, with organisms reaching concentrations of 10^9 to 10^10/mL.
  • 19. Clinical presentation • Coliky abdominal pain • crampy abdominal pain associated with intestinal obstruction occurs in paroxysms at 4- to 5-minute intervals and occurs less frequently with distal obstruction • Pain –common with proximal than distal obstruction • Nausea /Vomiting • Obstipation • Abdominal distension • degree of distension is dependent on the site of the obstruction • greater more distal the lesion • Vomitting is more prominent with proximal obstruction than distal • Character of vomitus is important –more feculent with more established obstruction • Continued passage of flatus /stool beyond 6 -12 hrs after onset of symptoms is characteristic of partial obstruction rather than complete • Distension is more pronounced if obstruction is in distal ileum
  • 20. On examination • May present with • tachycardia and hypotension • dehydration • Fever (suggests the possibility of strangulation) • Per Rectal Examinations: • To rule out fecal impaction or locate a low-lying rectal cancer as a cause of obstruction Abdominal Examination • Abdominal distension, Scars of previous surgery, Visible peristalsis • Swelling in case of Hernia • Abdominal tenderness , Guarding , Rebound tenderness • hyperactive bowel sounds with audible rushes associated with vigorous peristalsis (borborygmi)
  • 21. Diagnosis • Should focus on 1. Distinguishing mechanical obstruction from ileus 2. Determine etiology of obstruction 3. Determine partial from complete obstruction 4. Discriminate simple from strangulating obstruction
  • 22. Laborotary parameters • CBC( leukocytosis may be present in strangulation, Sepsis) • Electrolyte panel • Blood urea nitrogen • Creatinine • Arterial blood pH, serum lactate concentrations, and amylase and lactate dehydrogenase to exclude the presence of strangulation or underlying bowel necrosis An increase in serum lactate concentrations should raise the suspicion of intestinal ischemia: however, it is often a late finding
  • 23. Radiologic Findings • Diagnosis is usually confirmed with radiographic examination • Initial imaging modality • Abdominal series consists of –abdominal x-ray erect , supine , CXR • Radiographs are usually diagnostic in ~60% of cases • Remaining 20-30%, additional modality required 3-6-9 rule Normal caliber of Small bowel <3cm Large bowel <6 cm Appendix<6mm Caecum<9cm Findings in xray: • distended loops of bowel greater than 3-6-9 cm • collapsed colon • differential air–fluid levels, and thickened bowel wall • The string-of pearls sign may also be identified • Strangulation may be indicated by edematous folds, pneumatosis intestinalis
  • 24. Imaging Adhesional small-bowel obstruction shows multiple dilated loops of small bowel Valvulae conniventes appear prominent Multiple air–fluid levels (arrows) and string-of-pearls sign Erect Pneumatosis intestinalis( Intramural gas)
  • 25. Ultrasonography • Sonography sensitivity of 89% compared with 71% for conventional abdominal radiography in diagnosing small-bowel obstruction • superior in its ability to • Identify features of strangulation • predict the location and cause of obstruction • Schmutz GR, Benko A, Fournier L, et al. Small bowel obstruction: role and contribution of sonography. Eur Raddiol Findings suggestive of intestinal obstruction:  multiple dilated (> 3 cm)  fluid filled loops  The obstructing cause can occasionally be visualized if it is a tumor or hernia.  The presence of aperistalsis, fluid-filled bowel distention and wall thickening supports infarction  Bowel wall perfusion can also be assessed by Doppler sonography
  • 27. Computed Tomography • Contrast enhanced CT  advocated as diagnostic imaging modality of choice • Diagnostic accuracy of greater than 90% The presence of two or more beak signs, a whirl sign, a C- or U-shaped appearance of the bowel loop, and a high degree of obstruction were associated with nonsurgical treatment failure Findings in small-bowel obstruction:  dilated loops of bowel proximally with normal-caliber or collapsed loops distally (>2.5cm – small bowel considered dilated)  Transition point the diagnosis is more certain  The transition point often resembles a beak (the beak sign  present in 60% of simple small-bowel obstruction)  the string-of-pearls sign  small-bowel feces sign The small-bowel feces sign is a result of stasis and mixing of small- bowel contents present in 82% of cases of small bowel obstruction
  • 28. CECT features of strangulation • thickening of bowel wall • pneumatosis intestinalis • portal venous gas • mesenteric haziness • poor uptake of IV contrast into bowel wall/lack of bowel wall enhancement
  • 29. MAGNETIC RESONANCE ENTEROGRAPHY • Magnetic resonance enterography (MRE) has not been utilized frequently performance of this examination is more time consuming and requires substantial expertise in interpretation • In contrast, in centers that use MRE frequently, diagnostic accuracy exceeding 90% is achievable. • Advantage of distinguishing benign from malignant bowel strictures in patients with suspected malignant bowel obstruction
  • 31. Algorithm for management of bowel obstruction Ashwini k.Decision Making in Bowel Obstruction: A Review. Journal of Clinical and Diagnostic Research. 2016
  • 32. Management Resuscitate the patient IV crystalloids 0.9% NS CVP lines if required Foleys catherisation Broad spectrum antibiotics NG- decompression Correction of electrolyte imbalance
  • 33. Non-operative management • Nonoperative management of intestinal obstruction should be considered only in patients with uncomplicated intestinal obstruction in the absence of: • peritonitis • a progressive leukocytosis • impaired bowel wall perfusion on imaging. • When indicatedthis approach is reported to be successful in 62% to 85% of patients
  • 34. Water soluble contrast in Non operative management Gastrograffin(GG- diatrizoate meglumine and diatrizoate sodium) • A Hyperosmolar contrast agent • Advocated for diagnostic and therapeutic tool for SBO management The appearance of contrast in the colon 4–24 hours after administration had a sensitivity of 96% and a specificity of 98% in predicting resolution of small bowel obstruction  If contrast does not reach the colon, surgery required in about 90% of patients Dual purpose of GG 1st- Visualised on X-ray – contrast in colon i.e point of obstruction passed and no need for operative exploration 2nd – Hyperosmolar property- draws edema present in obstructed bowel into bowel lumen and helps reverse obstruction
  • 35. Bologna guidelines for ASBO For suspected adhesive small bowel obstruction
  • 36. Operative Management • When to Convert to Operative Management ?? • Prompt operative intervention is mandatory in patients who develop signs and symptoms suggestive of a strangulation obstruction • Parameters include:  fever Tachycardia  leukocytosis  localized tenderness continuous abdominal pain  peritonitis  presence of any three of these signs has an 82% predictive value for strangulation obstruction  presence of any four of the above signs has a near 100% predictive value for strangulation obstruction
  • 37. Surgical management • Depends upon the etiology of the obstruction • If the site of obstruction is unknown adequate exposure is best achieved by a midline incision • Assessment is directed to: ● the site of the obstruction ● the nature of the obstruction ● the viability of the gut
  • 38. Etiology Management Remarks Adhesions Adhesionolysis Only divide the causative adhesion and leave rest of adhesions When obstruction is caused by an area of multiple adhesions, the adhesions should be freed by sharp dissection from the duodenojejunal junction to the caecum Intussuception Pneumatic or hydrostatic reduction Successful in 70% (85-90% in Literature) Recurrence 11% and usually within 24 hours If recurs 2nd enema reduction 3rd recurrence  Operative management • Transverse incision • Reduction achieved by gently compressing the most distal part of the intussusception toward its origin making sure not to pull • The last part of the reduction is the most difficult An irreducible intussusception or one complicated by infarction or a pathological lead point requires resection and primary anastomosis Appendectomy –essential component irrespective of bowel resection(Sabiston)
  • 39. Laparoscopic surgery in SBO • Candidates for laparoscopic management • Patients who have: • mild abdominal distention allowing adequate visualization • proximal obstruction • partial obstruction • anticipated single-band obstruction Candidates for Laparotomy Patients who have : • Advanced • complete • distal small bowel • matted adhesions or carcinomatosis • those who remain distended after nasogastric intubation laparoscopic treatment  found to be of greatest benefit in patients who have • undergone <3 previous operations • Early presentation after the onset of symptoms • Anticipation of adhesive bands as the cause
  • 40. Surgical management of Large bowel obstruction • Large bowel obstruction  usually caused by an underlying carcinoma or occasionally diverticular disease • Presents in an acute or chronic form • Removable lesion  • in the caecum, ascending colon, hepatic flexure or proximal transverse colon emergency right hemicolectomy • A primary anastomosis is safe if the patient’s general condition is reasonable • Irremovable (Rare)  • a proximal stoma (colostomy or ileosotomy if the ileocaecal valve is incompetent) or ileotransverse bypass should be considered • Obstructing lesions at the splenic flexure An extended right hemicolectomy with ileodescending colonic anastomosis • Obstructing lesions of the left colon or rectosigmoid junctionimmediate resection (unless there are clear contraindications)
  • 41. • If caecal perforation is imminent additional time to improve the patient’s clinical condition can be bought by performing an emergency caecostomy (or ileosotomy in the presence of an incompetent ileocaecal valve) • Self-expanding metal stent (SEMS) : Palliation or Bridge Palliative situation Bridge to surgery Incurable disease or Patient unfit for surgery or both Reduces mortality and morbidity a/w stoma formation potentially curative disease  stenting as a bridge to surgery (usually performed 1–4 weeks post stenting) Reduce stoma formation but doesn’t reduce postoperative mortality long-term oncological effects of stenting are still uncertain success rates for stenting  80–90% current recommendation  stenting as a bridge to surgery in patients with potentially curative disease should only be used in patients with a high risk of postoperative morbidity and mortality
  • 42. SEMS
  • 43. Volvulus • Treatment of caecal volvulus : • At operation the volvulus usually found to be ischaemic and needs resection • If viable the volvulus should be reduced(sometimes requires decompression of the caecum using a needle) • Further management  fixation of the caecum to the right iliac fossa (caecopexy) and/or a caecostomy • Recurrence of volvulus after caecopexy has been reported in up to 40% of cases.
  • 44. Treatment of sigmoid volvulus • Flexible sigmoidoscopy or rigid sigmoidoscopy and insertion of a flatus tube to decompress the gut • Successful (as long as ischaemic bowel is excluded)  resolves the acute problem • In young patientsan elective sigmoid colectomy • In Elderlyno further treatment following successful endoscopic decompression as there is a high death rate (~80% at two years) from causes other than recurrent volvulus • In elderly patients with co-morbidities and recurrent episodes of volvulus • Resection or two-point fixation with combined endoscopic/percutaneous tube insertion • Failure results in an early laparotomy, with untwisting of the loop and per anum decompression (
  • 45. • If bowel viablefixation of the sigmoid colon to the posterior abdominal wall  a safer manoeuvre in inexperienced hands • Resection preferable if it can be achieved safely • A Paul–Mikulicz procedure is useful if there is suspicion of impending gangrene • Alternative procedure  a sigmoid colectomy +if anastomosis considered unwise a Hartmann’s procedure with subsequent reanastomosis can be carried out
  • 46. Post operative ileus • POI is described as a transient impairment of bowel motility that may occur after major surgery • A Comprehensive Review of Evidence-Based Strategies to Prevent and Treat Postoperative Ileus Sara K. Story a Ronald S. Chamberlain • Paralytic ileus is a condition of transport disturbances from intestinal contents due to decreased activity of smooth muscle in the small intestine or colon • Recent Pathophysiology and Therapy for Paralytic Ileus .Putu Surya Pridanta et al. • Postoperative ileus is divided into two: immediate postoperative ileus after surgery and diminishing with flatus and bowel, and prolonged postoperative ileus • Postoperative ileus is an ileus occurring in 4 or more days after surgery • The underlying pathology of POI is best described as a lack of coordinated bowel activity
  • 47. Post op ileus • The duration of postoperative ileus may correlate with the degree of surgical trauma and might even be considered a “physiologic” response. • A prolonged duration- in pts operated for radiation enteropathy, chronic obstruction, or severe peritonitis. • Recovery from ileus -differs among anatomic segments Organ (characteristic sequence ) Time to regain Intestine Hours,within first 24 hrs Stomach within 48 hrs Colon 3-5 days Listening bowel sound is not a reliable indicator that ileus has fully resolved Flatus or bowel movement is more useful indicator of coordinated action of resumed bowel
  • 48. Mechanism of Post operative ileus(POI)
  • 49.
  • 50. Prevention of POI A Comprehensive Review of Evidence-Based Strategies to Prevent and Treat Postoperative Ileus Sara K. Story a Ronald S. Chamberlain
  • 51. RECURRENT SMALL BOWEL OBSTRUCTION • 4% - 34% of patients will experience recurrent small bowel obstruction regardless of management modality • Recurrent obstruction more common in patients with • multiple adhesions • matted adhesions • previous admissions for small bowel obstruction • previous pelvic, colonic, and rectal surgery Recurrent BO in unscarred abdomen/virgin abdomen: • mostly due to internal hernia, • keep resolving on conservative management. • A CT scan with oral contrast and even a barium study of small bowel is usually diagnostic. • Para-duodenal hernia constitute 50% of internal herniation
  • 52. • Includes the gentle handling of the bowel to reduce serosal trauma avoidance of unnecessary dissection  exclusion of foreign material from the peritoneal cavity (the use of absorbable suture material when possible, the avoidance of excessive use of gauze sponges, and the removal of starch from gloves) adequate irrigation  removal of infectious and ischemic debris  preservation and use of the omentum around the site of surgery or in the denuded pelvis To date, the most effective means of limiting the number of adhesions is a good surgical technique
  • 53. Acute post operative bowel obstruction • BO occurring within 6 weeks of the original operation • Diagnosis is often difficult because the primary symptoms of abdominal pain and nausea or emesis may be attributed to a postoperative ileus • Electrolyte deficiencies hypokalemia  cause ileus correct • Plain abdominal films are usually not helpful in distinguishing an ileus from obstruction • More than 90% of early postoperative obstructions are partial and will resolve spontaneously, given ample time. CECT abdomen(with oral contrast) helps in determining whether  an obstruction exists  the level of the obstruction.
  • 54. • Conservative management ( bowel rest, fluid resuscitation, electrolyte replacement, and parenteral nutrition  routinely successful. • Obstructions caused by extrinsic bowel compression amenable to percutaneous correction fluid collections, abscesses, and hematomas treated by percutaneous drainage • Development of complete obstruction or signs of strangulation mandates reoperative intervention • Postoperative bowel obstruction after laparoscopic surgery  more commonly associated with a definitive obstruction point such as a port site hernia or an internal hernia  requires a high index of suspicion for the need for operative intervention
  • 55. Pseudo-Obsstruction • An obstruction, usually of the colon, that occurs in the absence of a mechanical cause or acute intra-abdominal disease • A/w a variety of syndromes with • an underlying neuropathy and/or myopathy and a range of other factors
  • 56. • Small intestinal pseudo-obstruction • may be primary (i.e. idiopathic or associated with familial visceral myopathy) or secondary. • Clinical manifestation of recurrent subacute obstruction • Diagnosis made by the exclusion of a mechanical cause • Treatment • correction of any underlying disorder • Metoclopramide and erythromycin may be of use
  • 57. Colonic – pseudo obstruction • occur in an acute or a chronic form. • Ogilvie’s syndromepresents as acute large bowel obstruction • Abdominal radiographs show signs of colonic obstruction, with marked caecal distension ( common finding) • caecal perforation well recognised complication • Absence of a mechanical cause requires urgent confirmation by colonoscopy or a single contrast water-soluble barium enema or CT
  • 58. Treatment: • Treat any identifiable cause • If this is ineffective, give iv neostigmine 1mg  1 mg given iv within a few minutes if the first dose is ineffective. • During this procedure, it is best to sit the patient on commode • Electrocardiograph (ECG) monitoring + atropine should be available • Neostigmine ineffective perform colonoscopic decompression • Surgery is associated with high morbidity and mortality • reserved for those with impending perforation when other treatments have failed or perforation has occurred
  • 60. References • Schwartz’s Principles of Surgery 11th edition • Sabistons Text book of surgery 21th edition • Bailey and love short practice of Surgery 27th edition • Maingots Abdominal operations 13th edition • Bologna guidelines for diagnosis and management of adhesive small bowel obstruction (ASBO): 2017 update of the evidence-based guidelines from the world society of emergency surgery ASBO working group • Imaging of Acute Small-Bowel Obstruction, Savvas Nicolaou et al,AJR • Ashwini k.Decision Making in Bowel Obstruction: A Review. Journal of Clinical and Diagnostic Research. 2016 • Sara K. Story et. al .A Comprehensive Review of Evidence-Based Strategies to Prevent and Treat Postoperative Ileus 2009

Notas do Editor

  1. intestinal obstruction can be classified based on duration of presence (acute vs chronic obstruction), extent (partial vs complete), type of obstruction (simple vs closed-loop), and risk of bowel compromise (incarcerated vs strangulated) Bowel obstruction may involve only the small intestine (small bowel obstruction), the large intestine (large bowel obstruction), or both via systemic alterations in metabolism, electrolyte balance, or neuroregulatory mechanisms (generalized ileus). In 90% of cases, small bowel obstruction is caused by adhesions, hernias, and neoplasms [5]. Adhesive small bowel obstruction represents 55–75% of small bowel obstruction cases [6] while hernias and small bowel tumors account for the remainder [2]. Large bowel obstruction is provoked by cancer in about 60% of cases [7]; volvulus and diverticular disease are responsible of other 30 (Bowel obstruction: a narrative review for all physicians)
  2. intestinal obstruction can be classified based on duration of presence (acute vs chronic obstruction), extent (partial vs complete), type of obstruction (simple vs closed-loop), and risk of bowel compromise (incarcerated vs strangulated)
  3. Partial obstruction implies that the intestinal lumen is narrowed, and some intestinal content can transit distally. In the presence of a complete obstruction, the lumen is obliterated, and no intestinal content can pass beyond the point of obstruction A simple obstruction has no associated vascular compromise, and the intestine can be decompressed proximally. Closed-loop obstruction occurs when both ends of the involved intestinal segment are obstructed (eg, volvulus or compressive adhesive bands), and results in increased intraluminal pressure secondary to increased intestinal secretion and accumulation of fluid in the involved intestinal segment Closed-loop obstruction carries a substantial risk of vascular compromise and irreversible intestinal ischemia of the involved bowel, and thus requires emergent operative attention. Finally, strangulation occurs when the blood supply to the affected intestinal segment is compromised, leading to focal or segmental transmural necrosis. The affected segment may involve only a portion of the bowel wall compressed by a tight adhesive band or an entire intestinal segment as occurs with a strangulated hernia or a closed loop. If viability of the bowel is maintained after relief of the obstruction, strangulation can be reversed (reversible strangulation obstruction). In contrast, irreversible strangulation occurs if the vascular compromise has caused irreversible transmural necrosis whether or not the strangulation is relieved. All irreversible strangulated obstructions start as reversible strangulated obstructions, and thus early diagnosis is paramount to rescuing compromised intestine
  4. Strangulation pathophysiology(bailey):Distension of the obstructed segment of bowel results in high pressure within the bowel wall. This can happen when only part of the bowel wall is obstructed as seen in Richter’s hernias. Venous return is compromised before the arterial supply. The resultant increase in capillary pressure leads to impaired local perfusion and once the arterial supply is impaired, haemorrhagic infarction occurs. As the viability of the bowel is compromised, translocation and systemic exposure to anaerobic organisms and endotoxin occurs.
  5. Functional obstruction or ileus occurs when the bowel, small or large, fails to propel content distally in the absence of a mechanical obstruction Pathophysiology involves electrolyte disturbances, impaired neuroregulatory innervation, imbalanced hormonal input, etc Pseudoobstruction -related either to hereditary or acquired visceral myopathies, visceral neuropathies, or a poorly understood disruption of myoneural coordination of organized contractile activity.
  6. The older, classic literature addressing the pathophysiology of bowel obstruction considered a decrease in blood flow as the sentinel event leading to most of the observed pathophysiologic changes. More recent experimental work, however, suggests that an increase in blood flow in association with an intense intramural inflammatory reaction and subsequent mucosal production of reactive oxygen species mediate many of the pathophysiologic changes observed in the early phase of bowel obstruction
  7. in the ascending colon where the luminal diameter and resulting wall tension are the greatest. Progressive distention of the bowel lumen with a concomitant increase in intraluminal pressure results in increased transmural pressure on capillary blood flow within the bowel wall. The possibility of intestinal wall ischemia presents a real concern in a closed-loop small bowel obstruction, especially in large bowel obstruction when the ileocecal valve is competent and the distended colon cannot decompress retrograde into the small bowel. The resultant increase in intraluminal pressure may compromise blood flow by exceeding venous pressure. This scenario occurs most commonly in the ascending colon where the luminal diameter and resulting wall tension are the greatest. This pathophysiology increases the urgency of treatment response for large bowel obstruction since vascular compromise may occur quickly
  8. . In the enterocyte, the endoplasmic reticulum dilates as early as 4 hours after onset of bowel obstruction. Mitochondrial swelling, focal epithelial necrosis, intracellular ballooning, and degenerative changes in the nucleus of epithelial cells (apoptosis) have been demonstrated as early as 6 to 12 hours after the onset of obstruction in this experimental model. The mucosal defense is compromised further by a decrease in perfusion of the intestinal wall. The loss of mucosal integrity allows luminal bacteria to both translocate as well as to invade the submucosa and enter the systemic circulation via the portal venous and lymphatic systems.
  9. Fluid: this is made up of the various digestive juices. (saliva 500mL, bile 500mL, pancreatic secretions 500mL, gastric secretions 1 litre – all per 24 hours). This accumulates in the gut lumen as absorption by the obstucted gut is retarded. Dehydration and electrolyte loss are therefore due to: ● reduced oral intake; ● defective intestinal absorption; ● losses as a result of vomiting; ● sequestration in the bowel lumen; ● transudation of fluid into the peritoneal cavity
  10. Oliguria, azotemia, and hemoconcentration can accompany the dehydration. Hypotension and shock can ensue
  11. severe or complete constipation Features of Strangulation Pain often disproportionate to findings 6 parameters include fever, tachycardia, leukocytosis, localized tenderness, continuous abdominal pain, and peritonitis. any three of these = 82% predictive value for strangulation obstruction any four =near 100% any three of these = 82% predictive value for strangulation obstruction.84 of article decision to make
  12. The presence of a succussion splash is not normal in a patient who has not eaten or ingested liquids in the previous 1 to 2 hours and should be regarded as an important, abnormal, and often underappreciated sign of bowel obstruction.
  13. Radiological features of obstruction (on plain x-ray) ● The obstructed small bowel is characterised by straight segments that are generally central and lie transversely. No/ minimal 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 piquantly described by Wangensteen 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
  14. Even though the reported specificity is 82%, sensitivity is 95%, and overall accuracy is 81%, this modality is highly operatordependent, and the results are unlikely to be reproduced consistently in many institutions( Maingots)
  15. Diagnostic accuracy >90% CT not only provides information about the presence or absence of a luminal obstruction but it can also define both the site of obstruction and the existence of extraluminal processes, a small bowel transition point,associated inflammation, fluid collections, masses, abdominal wall or internal hernias, and free intraperitoneal fluid Further, CT can expedite the diagnosis of strangulation obstruction if findings including mesenteric edema, free peritoneal fluid, intestinal wall thickness, and the absence of fecalization of the small bowel content are present. Among studies utilizing IV contrast, reduced bowel wall enhancement had a 95% specificity in determining ischemia, and absence of mesenteric fluid had an 89% sensitivity in ruling out strangulation. 53 O’Daly and colleagues found the association of peritoneal fluid with small bowel obstruction to be a strong predictor for the need for operative treatment. 54 In settings where iodinated contrast is contraindicated, the finding of increased bowel-wall attenuation on unenhanced images is concerning for bowel ischemia, with a 100% specificity and 56% sensitivity. The sensitivity of contrast-enhanced CT for intestinal ischemia has been reported to be as high as 90%
  16. A recent study by Zielinski et al. suggested that CT findings of free peritoneal fluid, thickened bowel, and mesenteric edema, combined with vomiting, were predictive of the need for eventual operative management, but though relatively sensitive for ischemia, CT was not very specific. 47
  17. Early postoperative bowel obstruction is defined as bowel obstruction occurring within the first 6 weeks postoperatively.
  18. The appearance of contrast in the colon 4–24 hours after administration had a sensitivity of 96% and a specificity of 98% in predicting resolution of small bowel obstruction. If contrast does not reach the colon, sugery is required in about 90% of patients from maingots The presence of contrast material within the colonic lumen within 8 hours of oral administration had an accuracy of 93% for predicting which patients would benefit from nonoperative therapy Following WSCA, abdominal plain films were taken at 8 hours 80,81 after WSCA or 1, 2, 4, and 8 hours 82 after administration, depending on the study. Patients passed WSCA challenge if contrast reached the right colon by times ranging from 8 hours 80,81 to 24 hours 82 after WSCA. Patients who developed worsening signs and symptoms consistent with peritonitis underwent exploratory laparotomy. Among the patients who failed WSCA challenge but did not have a worsening exam, time from WSCA administration to operative management varied from 24 hours 82 to 4 to 5 days. 8
  19. From maingots Obviously, patients who develop free air, signs of a closed-loop obstruction on abdominal radiograph, or gross peritonitis require emergent operative exploration. If CT demonstrates evidence of ischemia, such as pneumatosis intestinalis, bowel wall thickening, portal venous gas, generalized ascites, or nonenhancement of the bowel wall, operative intervention should be strongly considered.
  20. Operative decompression should be performed whenever possible. This reduces pressure on the abdominal wound, reducing pain and improving diaphragmatic movement. The simplest and safest method is to insert a large-bore orogastric tube and to milk the small bowel contents in a retrograde manner to the stomach for aspiration. All volumes of fluid removed should be accurately measured and appropriately replaced. It is important to ensure that the stomach is empty at the end of the procedure to prevent postoperative aspiration Following relief of obstruction, the viability of the involved bowel should be carefully assessed (Table 71.3). Although frankly infarcted bowel is obvious, the viability status in many cases may be difficult to discern. If in doubt, the bowel should be wrapped in hot packs for 10 minutes with increased oxygenation and then reassessed. The state of the mesenteric vessels and pulsation in adjacent arcades should be sought. Viability is also confirmed by colour, sheen and peristalsis. If, at the end of this period, there is still uncertainty about gut viability, the gut should be resected if this does not result in short bowel syndrome Intestinal ischaemia/reperfusion injury has been described following reperfusion of ischaemic bowel with remote lung injury resulting from the release of inflammatory mediators. For example if there is a volvulus with established infarction, detorsion should be avoided until the affected mesentery has been clamped and thus reperfusion injury prevented. When no resection has been undertaken or there are multiple ischaemic areas (mesenteric vascular occlusion), a second-look laparotomy at 24–48 hours may be required.
  21. Treatment of recurrent intestinal obstruction caused by adhesions Several procedures may be considered in the presence of recurrent obstruction including: ● repeat adhesiolysis (enterolysis) alone; ● Noble’s plication operation; ● Child–Phillips transmesenteric plication; ● intestinal intubation
  22. In particular, laparoscopic treatment has been found to be of greatest benefit in patients who have undergone fewer than three previous operations, were seen early after the onset of symptoms, and were thought to have adhesive bands as the cause Sabiston
  23. Colorectal cancer presents as an emergency with LBO in up to 29% of cases
  24. In rare instances, or when caecal perforation is imminent, additional time to improve the patient’s clinical condition can be bought by performing an emergency caecostomy (or ileosotomy in the presence of an incompetent ileocaecal valve). In the absence of senior clinical staff it is safest to bring the proximal colon to the surface as a colostomy. When possible the distal bowel should be brought out at the same time (Paul–Mikulicz procedure) to facilitate subsequent closure. In the majority of cases, the distal bowel will not reach and is closed and returned to the abdomen (Hartmann’s procedure). A second-stage colorectal anastomosis can be planned when the patient is fit. If an anastomosis is to be considered using the proximal colon, in the presence of obstruction, it must be decompressed and cleaned by an on-table colonic lavage. In the absence of senior clinical staff it is safest to bring the proximal colon to the surface as a colostomy. When possible the distal bowel should be brought out at the same time (Paul–Mikulicz procedure) to facilitate subsequent closure. In the majority of cases, the distal bowel will not reach and is closed and returned to the abdomen (Hartmann’s procedure). A second-stage colorectal anastomosis can be planned when the patient is fit. If an anastomosis is to be considered using the proximal colon, in the presence of obstruction, it must be decompressed and cleaned by an on-table colonic lavage
  25. Flexible sigmoidoscopy or rigid sigmoidoscopy and insertion of a flatus tube to decompress the gut Tube secured in place with tape for 24 hours  repeat x-ray to ensure decompression of gut When the bowel is viable, fixation of the sigmoid colon to the posterior abdominal wall may be a safer manoeuvre in inexperienced hands. Resection is preferable if it can be achieved safely. A Paul–Mikulicz procedure is useful, particularly if there is suspicion of impending gangrene (Figure 71.22); an alternative procedure is a sigmoid colectomy and, when anastomosis is considered unwise, a Hartmann’s procedure with subsequent reanastomosis can be carried
  26. ] . Inhibited motility in the small intestine is usually transient, recovering within several hours of surgery [12, 14, 15] . Gastric motility typically recovers within 24–48 h after surgery [5, 9] , whereas the colon, the final portion of the GI tract to return to normal, usually recovers 48–72 h postsurgery [12–16] . Recovery of colonic motility is usually the limiting factor in resolving POI An ileus is defined as intestinal distention and the slowing or absence of passage of luminal contents without a demonstrable mechanical obstruction(sabiston) Postoperative hypomotility affects all segments of the gastrointestinal (GI) tract and recovery differs by segment
  27. Differentiation of postoperative ileus from early postoperative mechanical bowel obstruction is important, because these anomalies are caused by different pathophysiologic mechanisms.3 Paralytic ileus This may be defined as a state in which there is failure of transmission of peristaltic waves secondary to neuromuscular failure (i.e. in the myenteric (Auerbach’s) and submucous (Meissner’s) plexuses). The resultant stasis leads to accumulation of fluid and gas within the bowel, with associated distension, vomiting, absence of bowel sounds and absolute constipation. Varieties The following varieties are recognised: ● Postoperative: a degree of ileus usually occurs after any abdominal procedure and is self-limiting, with a variable duration of 24–72 hours. Postoperative ileus may be prolonged in the presence of hypoproteinaemia or metabolic abnormality (see below). ● Infection: intra-abdominal sepsis may give rise to localised or generalised ileus. ● Reflex ileus: this may occur following fractures of the spine or ribs, retroperitoneal haemorrhage or even the application of a plaster jacket. ● Metabolic: uraemia and hypokalaemia are the most common contributory factors. Clinical features Paralytic ileus takes on a clinical significance if, 72 hours after laparotomy: ● there has been no return of bowel sounds on auscultation; ● there has been no passage of flatus. Abdominal distension becomes more marked and tympanitic. Colicky pain is not a feature. Distension increases pain from the abdominal wound. In the absence of gastric aspiration, effortless vomiting may occur. Radiologically, the abdomen shows gas-filled loops of intestine with multiple fluid levels (if an erect film is felt necessary Specific treatment is directed towards the cause, but the following general principles apply: ● If a primary cause is identified this must be treated. ● Gastrointestinal distension must be relieved by decompression. ● Close attention to fluid and electrolyte balance is essential. ● There is no convincing evidence for the use of prokinetic drugs to treat postoperative adynamic ileus. ● If paralytic ileus is prolonged CT scanning is the most effective investigation; it will demonstrate any intraabdominal sepsis or mechanical obstruction and therefore guide any requirement for laparotomy. Otherwise the decision to take a patient back to theatre in these circumstances is always difficult. The need for a laparotomy becomes increasingly likely the longer the bowel inactivity persists, particularly if it lasts for more than seven days or if bowel activity recommences following surgery and then stops again.
  28. 1.Preoperative Bowel Preparation: Perioperative mechanical bowel preparation has been a cornerstone of colon surgery for decades; however, recent studies suggest it may be unnecessary and even deleterious. A systemic review of 9 RCTs including over 1,500 patients by Guenaga et al.[25] also found that mechanical bowel preparation did not decrease the incidence of anastomotic leaks, but actually increased the rate at which they occur as well as increasing the rate of wound infections 2.Preoperative carbohydrate loading: More recently, studies have shown that using carbohydrate-rich liquids within hours prior to surgery shortens bowel recovery time postoperatively 3.Epidural Local Anesthetics : As outlined earlier ( fig. 1 ), several inhibitory reflexes in the GI tract have been proposed to play a role in POI, including activation of inhibitory reflexes originating from the incision and/or manipulation of the intestines [7, 21] . It has been hypothesized that epidural local anesthetics may decrease POI by blocking these afferent sympathetic inhibitory reflexes, as well as efferent sympathetics with a concomitant increase in splanchnic blood flow. Systemic absorption of local anesthetics may also have anti-inflammatory effects 4. COX-2 Inhibitors Because of the role of prostaglandins in the inflammatory response, it has been suggested that NSAIDs or COX2 inhibitors might be used to increase GI motility as well as to reduce opioid use postoperatively [21] . Perioperative administration of COX-2 inhibitors has been found to reduce opioid administration, pain and vomiting after joint replacement surgery 5. Gastric ‘Decompression’ via Nasogastric Tube (NGT) and the Use of Intraoperative Drains Nasogastric decompression and the practice of advancing postoperative feeding only after the presence of bowel sounds and/or flatus has been a routine in surgery for decades. However, experience with laparoscopic surgery has taught us much about the archaic nature of this practice. Cheatham et al.[50] published a meta-analysis of all clinical trials comparing selective versus routine nasogastric decompression after elective laparotomy and found that routine insertion of an NGT resulted in increased adverse events including fever, pneumonia and atelectasis. They concluded that only 5% of patients stood to benefit from NGT decompression, and that it should not be routinely utilized 6. Opioids and Opioid Antagonists Opioids are freely used as methods of pain control following abdominal and other surgeries. With repeated opioid administration for pain relief, tolerance to the analgesic effect subsequently develops; however, tolerance to the GI adverse effects does not [21, 53] . Therefore, limiting opioid use postoperatively has been associated with a significant decrease in POI and remains a mainstay of POI prevention and treatment approaches 7. Early Ambulation It has long been believed that early ambulation increases GI motility and therefore reduces POI. In an effort to discern whether ambulation hastens recovery from ileus following laparotomy. However, despite this well-designed study, early ambulation is still important to patients in other ways, and remains a major component of most multimodal fast-track approaches to reducing POI. 8. Postoperative Feeding Early feeding following intra-abdominal surgery has recently gained favor based on emerging clinical studies [64, 65] . Jeffery et al. [64] found no difference in recovery of patients receiving a clear liquid diet, compared with those receiving a regular diet beginning with the first oral intake after surgery. However, Stewart et al. [65] found that patients in an early oral feeding group passed flatus and moved their bowels much sooner than the control group thus reducing the duration of POI and hospital stay. Though these results are mixed, there is no increase in occurrence of associated complications, leading to a growing popularity of early feeding as a potential strategy to prevent POI 9. Gum Chewing Gum chewing has been proposed to assist in postoperative recovery of GI function by serving as a ‘sham feeding’, thereby stimulating associated neuronal pathways. Although a recent meta-analysis of 5 randomized, controlled studies showed that gum chewing shortened mean time to flatus by 20 h and time to defecation by 29 h, there was a nonsignificant trend toward shorter hospital stay
  29. This “conservative” approach may allow the acute inflammatory process to resolve or regress (often 3-6 months); should the obstruction not resolve by 6 months, the plan should be to reoperate at a time when the adhesions have matured, allowing a more controllable and much safer adhesiolysis
  30. The most effective method to date has been the application of a sheet of bioresorbable hyaluronate membrane Other materials to prevent adhesions: These include gel and liquid preparations such as hyaluronic acid and carboxymethylcellulose, hydrogel, fibrin sealant, and protein polymers. Other adhesion barriers include oxidized regenerated cellulose (ORC).
  31. After a thorough physical examination and the decision that emergent intervention is not indicated, a search for the cause of obstruction should be undertaken. CT can be helpful in determining the etiology of an obstruction but is notoriously unreliable at differentiating ileus versus partial obstruction. Obstructions caused by extrinsic bowel compression amenable to percutaneous correction, including fluid collections, abscesses, and hematomas, may be diagnosed and treated by percutaneous drainage. CT may be able to detect those causes of obstruction that will likely require operative intervention, such as internal hernia, fascial dehiscence, and uncontrolled anastomotic leak. Early CT may be warranted in patients who had a laparoscopic operation and have signs of early obstruction, because a port site hernia may be evident and would require prompt operation.
  32. Caecal perforation can occur in pseudo-obstruction Abdominal examination should pay attention to tenderness and peritonism over the caecum and as with mechanical obstruction, caecal perforation is more likely if the caecal diameter is 14cm or greater.