Download MBBS Surgery Presentations 30 Intestinal Obstruction Lecture Notes

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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