Download MBBS (Bachelor of Medicine, Bachelor of Surgery) 1st Year, 2nd Year, 3rd Year and Final year Surgery 30 Intestinal Obstruction PPT-Powerpoint Presentations and lecture notes
INTESTINAL
OBSTRUCTION
Classify Intestinal Obstruction. Discuss the D\D and
management of AIO in a 70 yr old male.
Describe the c\f ,diagnosis and management of AIO.
Enumerate causes of dynamic IO. Discuss the
diagnosis and management of acute small bowel
obstruction.
The common Scenario
A 50 year old gentleman presents
with abdominal pain, distension and
absolute constipation. With
repeated episodes of vomiting.
His vital sign were stable, abdomen
distended with diffuse tenderness
but minimal peritonism. Bowel
Sounds are hyperactive.
The plain abdominal xray was taken
on admission.
What are your objectives?
You should be able to address the following questions
1. Is this bowel obstruction or ileus?
2. Is this a small or large bowel obstruction?
3. Is this proximal or distal obstruction?
4. What is the cause of this obstruction?
5. Is this a complex or simple obstruction?
6. How should I start investigating my patient?
7. What is the role of other supportive investigations?
8. What is my immediate/ intermediate treatment plan?
9. What are the indications for surgery?
10. What are the medico-legal and ethical issues that I
should address?
Definition
Any condition that interferes with normal propulsion
and passage of intestinal contents.
Can involve the small bowel, colon or both.
TYPES
Dynamic: where peristalsis is working against a
mechanical obstruction.
Adynamic: mechanical element is absent
- Peristalsis may be absent(paralytic ileus)
-May be present in non propulsive form. (mesenteric
vascular occlusion or pseudo-obstruction)
Mechanical Obstruction
Acute vs Chronic
Partial vs Complete
Simple vs Closed loop
Gangrenous vs Nongangrenous
PATHOPHYSIOLOGY
Small Intestine Function
Transport - Distension stimulates contractions
Mixing and peristalsis
Absorption
Colon Function
Water Absorption
Transport
Storage
PATHOPHYSIOLOGY
Dependent Upon:
Degree of Obstruction
Duration of Obstruction
Presence and Severity of Ischemia
Results in:
Accumulation of fluid and air
Bacterial overgrowth
Maximal by 24 hrs after obstruction
Gut translocation to nodes and portal system
Once Distended :
Impaired fluid and nutrient absorption
Secretion of isotonic fluid (intravascular to intraluminal)
PATHOPHYSIOLOGY
Systemic symptoms are secondary to:
Hypovolemia
Bacterial translocation (typically E. coli)
Ischemia worsens general inflammatory state,
bacterial translocation, and fluid requirements
Large Bowel Obstruction
Ileocecal valve plays prominent role in
pathophysiology of LBO
If competent valve = closed loop obstruction
Caecal ischemia around 10-13 cm
Causes- SBO
Luminal
Mural
Extraluminal
F.Body
Neoplasims
Postoperative
Bezoars
lipoma
adhesions
Gallstone
polyps
FoodParticles
leiyomayoma
Congenital
adhesions
A.lumbricoides
hematoma
lymphoma
Hernia
carcimoid
carinoma
Volvulus
secondaryTumors
Crohns
TB
Stricture
Intussusception
Congenital
Intussusception
Gall stone Ileus
IBD
Large Bowel Obstruction
?Distinguishing ileus from mechanical obstruction is challenging
?According to Laplace's law: maximum pressure is at the it's
maximum diameter. Cecum is at the greatest risk of perforation
?Perforation results in the release of formed feaces with heavy
bacterial contamination
Aetiology:
1. Carcinoma: The commonest cause, 18% of colonic ca. present
with obstruction
2. Benign stricture: Due to Diverticular disease, Ischemia,
Inflammatory bowel disease.
3. Volvulus: 1. Sigmoid Volvulus: Results from long redundant,
faecaly loaded colon with a narrow pedicle
2. Caecal Volvulus
4. Hernia.
5. Congenital : Hirschusbrung, anal stenosis and agenesis
Colonic Obstruction
Sigmoid Volvulus
COMMON CAUSES:
Adhesions- 40%
Tumors -15%
Inflamatory- 15%
Obstructed hernia-12%
Intraluminal-10%
Miscellaneous -8%
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
HISTORY
Did this ever happen before?
Change in bowel habits (acute vs chronic)
Progressive vs acute abd. distention
Weight loss
Flatus?
Prior Surgeries
Hx of abdominal CA?
Hx of Inflammatory Bowel Dz
Prior abdominal XRT?
Meds: Anticoagulants, Anticholinergics, Opioids,
Antihistamines, Alpha-agonists, Catecholamines
SYMPTOMS
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
SYMPTOMS
Constipation
-more with lower or complete obstruction
- constipation is either absolute (no feces or flatus)
or relative (flatus passed).
-diarrhea may be present with partial obstruction
SYMPTOMS
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.
Inflammation 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
tympanitic 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
INVESTIGATIONS
Hemogram - WBC (neutrophilia-strangulation)
Hyper kalemia, hyperamylasemia & raised LDH may
be associated with strangulation.
Plain AXR
Sigmoidoscopy (carcinoma, volvulus)
Contrast x-ray
CT abdomen.
The most helpful diagnostic radiographic procedure
in suspected SBO is:
A. CT of Abdomen and Pelvis
B. UGI gastrograffin contrast study
C. Supine and Erect plain films of abdomen
D. U/S of the abdomen
Imaging ? Plain Films
Dilated loops, SB dilation? AFLs?
Are AFL's and bowel loops in same place on supine and upright
films?
Is there gas throughout the entire colon? Ileus or pSBO
Paucity of distal colonic gas or abrupt cutoff of colonic gas
w/proximal distention and/or AFLs? Suggesting complete or
near-complete LBO
Massive dilation of colon, especially of the cecum or sigmoid?
Suggestive of volvulus or pseudoobstruction
Evidence of strangulation? Thickened SB loops, mucosal
thumb printing, pneumatosis cystoides intestinalis, or free air
Are there biliary calculi? Pneumobilia? GS ileus?
AXR
When distended by gas:
Jejunum is characterized by valvulae conniventes.
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 smal bowel considered normal.
No. of fluid level is proportional to degree of obstruction
and distal site in smal bowel.
The Difference between small and
large bowel obstruction
Large bowel
Small Bowel
?Peripheral ( diameter 8 cm max)
?Central ( diameter 5 cm max)
?Presence of haustration
?Vulvulae coniventae
?Ileum: may appear tubeless
Adjunctive Tests
Sigmoidoscopy
When large amounts of air extend down to the rectum
Flex or Rigid wil exclude rectal or distal sigmoid
obstruction ?
CT Scan or U/S
When normal plain films but history and exam are
consistent with obstruction
Plain films in SBO wil be nondiagnostic approximately
30% of the time
Role of CT
Used with iv contrast, oral and
rectal contrast (triple contrast).
Able to demonstrate
abnormality in the bowel wall,
mesentery, mesenteric vessels
and peritoneum.
It can define
the level of obstruction
The degree of obstruction
The cause: volvulus,
hernia, luminal and mural
causes
The degree of ischaemia
Free fluid and gas
Ensure: patient vitally stable
with no renal failure and no
previous allergy to iodine
Role of barium gastrografin
studies
Barium should not be used in
a patient with peritonitis
As: fol ow through, enema
Limited use in the acute
setting
Gastrografin is used in
acute abdomen but is
diluted
Useful in recurrent and
chronic obstruction
May able to define the level
and mural causes.
Can be used to distinguish
adynamic and mechanical
obstruction
TREATMENT
Three main measures-
- GI drainage
- Fluid &Electrolyte replacement
- Relief of obstruction, usually surgical
Treatment
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 wil settle by using this conservative regimen, other
need surgical intervention.
? Surgery should be delayed til 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.
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.
SURGERY
The type of surgical procedure depend upon the cause of
obstruction viz division of bands,adhesiolysis, excision ,or
bypass
*Once obstruction relieved, the bowel is inspected for
viability, and if non-viable, resection is required.
Indicators of non-viability
1.absent peristalsis
2.loss of normal shine
3.loss of pulsation in mesentry
4.green or black color of bowel
SURGERY
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 laprotomy is required in 24-
48 hours e.g. multiple ischemic areas.
Adhesions
Most common cause of intestinal obstruction.
Peritoneal irritation results in local fibrin production,
which produce adhesions.
BANDS
Congenital : obliterated vitellointestinal duct.
A string band following previous bacterial peritonitis.
A portion of greater omentum adherent to parietes.
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 entritis.
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.
Tt. Of recurrent obstruction due to
adhesions
Repeat adhesiolysis alone.
Noble's plication : adjacent intestinal coils (15-20
cms) are sutured with serosal sutures.
Charles-Phillips trans-mesenetric plication.
Intestinal intubation : initraluminal tube insertion via
a WITZEL jejunostomy or gastrostomy.
INTERNAL HERNIA
When a portion of small intestine is entrapped in one
of retropritoneal 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.
Gal stone ileus
It tends to occur in elderly.
Erosion of large gallstone into duodenum.
Present with recurrent obstruction.
X-ray: small bowel obstruction with air in billiary 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.
INTUSSUSCEPTION
One portion of gut becomes invaginated with in
adjacent segment.
Most common in children(3-9 months.)
Idiopathic-70%
Associated gastroenteritis/UTI- 30%
Hyperlpasia of Peyer's patches in terminal ileum can
be initiating factor.
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.
Volvulus of the Colon
Sigmoid most commonly involved
180? or > counterclockwise twist
Cecal volvulus next most common
Transverse colon volvulus is rare 4% of colonic
volvulus
Splenic flexure volvulus VERY rare
Sigmoid Volvulus
Predisposing Factors
Long and highly-mobile sigmoid
Lengthy mesosigmoid, Narrow at its base
Adhesions between proximal sigmoid and
rectosigmoid with long loop of colon in between
Chronic constipation and high-fiber diet
Sigmoid Volvulus - Pathogenesis
Closed-loop type obstruction
Proximal colon dilates- Extent depends on ileocecal
valve competence
Simple or Strangulated
Venous then arterial obstruction
With simple form takes a few days for vascular
compromise to develop
In acute fulminating variant much more rapid
course seen
Sigmoid Volvulus - Varieties
Acute Fulminating Type- Mortality 37-80% ,
Younger patient, sudden onset, rapid course Early
vomiting, severe pain, peritonitis, and gangrene
Minimal distension often, hard to diagnose
Subacute Progressive Type- Generally older pt.,
more gradual onset, Hx prior attacks, chronic
constipation, Abdominal distension often extreme
Late vomiting, pain is minimal, no peritonitis
Sigmoid Volvulus - Diagnosis
Plain films of Abdomen-- Massively dilated and
distended bowel loop
Both ends in pelvis,
Bow of loop cephalad
"Bent inner tube" sign
Air/fluid level within loop
Proximal colon & SB may be dilated
Barium enema-- "Birds beak"
Sigmoid Volvulus - Treatment
Rigid sigmoidoscopic detorsion--decompression,
& placement of rectal tube
RT inserted past obstruction point
Successful 77 - 90% of time
Mortality rate 1.2 - 5.5%
Preferred initial treatment
Colonoscopic decompression
Surgery if:
Decompression not successful
Ischemic or necrotic bowel encountered
Sigmoid Volvulus ? Surgical
Treatment
Recurrence rate is high (33 - 60%)
Some advise elective op after 1st episode
Elective: Resection of redundant colon Small
transverse LLQ incision
Sigmoid fixation another option
Emergent: Resection +/- stoma
Ogilvie's Syndrome
Acute Colonic Pseudo obstruction
Massive dilation of cecum, right, and transverse colon
(non-mechanical), to splenic flexure
Dilated SB loops in > 50%
Symptoms: Distension,Nausea and vomiting,
Abdominal pain in 80% ,Bowel sounds may be normal
or increased
Conditions associated with
Ogilvie's syndrome
Non-operative Trauma
Non-GI surgery (Gyn, Ortho, Cardiac)
Pancreatitis, Cholecystitis
Diabetes, Malignancy
Narcotics, antidepressants, anticholinergics
Neurologic or Respiratory disease
Electrolyte (hypo K+, Ca+2), Acid / Base disorder
Radiation in past
Ogilvie's Syndrome: DDx and Dx
Plain abdominal films to diagnose and follow cecal
diameter (Q12-24 hrs)
Normal is < 9 cm
If 14 cm - perforation in 23% ?
Differential Includes: Fecal impaction, Cecal or
Sigmoid Volvulus, IschemicBowel,Mechanical
Obstruction
Ogilvie's Treatment :
Correct electrolyte problems and underlying
condition
D/C narcotics and anticholinergics
NPO with NGT, +/- Rectal Tube
Colonoscopic decompression difficult but often
successful, May need 2nd decompression
Long colonic drains can be placed via colonoscope
(old)
Neostygmine is the treatment of choice now
If signs of perforation then OR
STRANGULATION
The viability of the bowel is threatened.
Causes of strangulation
External
Hernial orifices
Adhesions/bands
Interrupted blood flow
Volvulus
Intussusception
Increased intraluminal pressure
Closed-loop obstruction
Primary
Mesenteric infarction
The venous return is compromised before the arterial
supply.
The resultant increase in capillary pressure leads to local
mural distension with loss of intravascular fluid and red
blood cells intramurally and extraluminally.
Once the arterial supply is impaired, haemorrhagic
infarction occurs.
As the viability of the bowel is compromised there is
marked translocation and systemic exposure to anaerobic
organisms with their associated toxins.
The morbidity of intraperitoneal strangulation is far
greater than with an external hernia?
Closed-loop obstruction
This occurs when the bowel is obstructed at both the
proximal and distal points.
There is no early distension of the proximal intestine.
A classic form of closed-loop obstruction is seen in the
presence of a malignant stricture of the right colon with a
competent ileocaecal valve
The inability of the distended colon to decompress itself
into the small bowel results in an increase in luminal
pressure, which is greatest at the caecum, with subsequent
impairment of blood supply.
Unrelieved, this results in necrosis and perforation.
This post was last modified on 08 April 2022