intestinal obstruction

Intestinal obstruction

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Intestinal obstruction

Intestinal Obstruction (I.O.) may be classified into 2 types:-
1-Dynamic: peristalsis working against a mechanical obstruction either acute or chronic.
2-Adynamic; two forms:
a. peristalsis is absent(paralytic ileus)
b. non- propulsive form ( e.g. mesenteric vascular occlusion or pseudo obstruction).

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Causes of Intestinal Obstruction

Dynamic
Intraluminal:
Impaction
Foreign Body
Bezoar
Gall stones


Intramural:
Stricture
Malignancy

Extramural :

Bands/adhesions
Hernia
Volvulus
Intussusception
Adynamic
Paralytic ileus
Mesenteric vascular occlusion
Pseudo obstruction

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Relative frequency of the underlying diagnosis

Adhesions 40%
Inflammatory 15%
Obstructed hernia 12%
Fecal impaction 8%
Pseudo obstruction 5%
Miscellaneous 5%


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Strangulation

when it occurs, it affects the viability of the bowel
The venous return is compromised before the arterial supply .This will lead to Increased capillary pressurelocal distention & extravasation of fuid &RBCs intramurally & extraluminally.
When the arterial bl. Supply is impaired haemorrhagic infarction will
occur
As the viability of the bowel affected there is translocation & systemic exposure to aerobic &anaerobic m. o. &its toxins peritonitisincreased mortality &morbidity which increases by age &extent of the disease.
when the bowel involvement is extensive, the loss of blood &circulatory volume will cause peripheral circulatory failure.

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Causes of strangulation:

External
• hernial orifice
• adhesions
Primary
mesenteric infarction
Interrupted blood supply
volvulus
intussuption
Increased intramural pressure
closed loop obstruction


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Clinical features of strangulation

It is vital to distinguish strangulating from non-strangulating intestinal obstruction, as the former is a surgical emergency. The diagnosis is entirely clinical. In addition to the features outlined above, the following should be noted:
• the presence of shock indicates underlying ischaemia;
• in impending strangulation, pain is never completely absent;
• symptoms usually commence suddenly and recur regularly;
• the presence and character of any local tenderness are of great significance and, however mild, tenderness requires frequent reassessment.

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In non -strangulated obstruction there may be an area of localized tenderness at the site of the obstruction; in strangulation there is always localized tenderness associated with rigidity/rebound tenderness.
• Generalized tenderness and the presence of rigidity are indicative of the need for early laparotomy.
• In cases of intestinal obstruction where pain persists despite conservative management, even in the absence of the above signs, strangulation should be diagnosed.
• When strangulation occurs in an external hernia the lump is tense, tender, irreducible, there is no expansile cough impulse and it has recently increased in size.

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Dynamic Obstruction

The diagnosis is based on the classical quartet of:
Pain
Distention
Vomiting
absolute constipation

Obstruction may be classified clinically into two types;
Small bowel Obstruction ( high or low )
Large bowel Obstruction


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Features of Obstruction

a- small bowel obstruction
In high small bowel Obstruction
vomiting early
minimal distention,
rapid dehydration,
with little evidence of fluid level in abdominal radiography

In low small bowel Obstruction

mainly pain
central distention,
vomiting delayed,
multiple central fluid level in abdominal radiography

b-large bowel obstruction

distention early,
pain is mild,
vomiting& dehydration is late
the proximal colon & cecum are distended in abdominal radiography


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Regarding the nature of onset &timing:

Acute:- small intestine
Chronic :- large Intestine
acute on chronic :- short history of distention against background of pain &constipation
subacute :- incomplete obstruction

Presentation is also influenced by whether the obstruction:
Simple: blood supply intact
Strangulation:- blood supply interference ( by hernial rings bands, adhesions)

Clinical Features vary according to:

Location of obstruction
Duration of obstruction
Underlying pathology
Absence or presence of Intestinal ischemia

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Cardinal features:

1-pain:
small bowel : sudden \sever \ colicky \central around umbilicus
Large bowel the same + lower abdomen
Increase with the peristaltic activity
with increasing distention , the colicky pain replaced by a (mild \ constant \ diffuse ) pain
development of severe pain indicate strangulation
pain not significant in postoperative simple mechanical obstruction
Pain not occurs in paralytic ileus.

2- vomiting :
The more distal the obstruction the larger interval between onset of nausea & vomiting
As obstruction progress the vomit change from digested food  feculent material (( due to bacteria overgrowth)).


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3- distension :

In small bowel , the degree of distension is depend on site of obstruction & is greater the more distal the lesion .
visible peristalsis may be absent
Distention is delayed in colonic obstruct & may be minimal or absent in presence of mesenteric vascular occlusion.

4- Constipation :

Classified as :-
absolute (neither foeces nor flatus is passed )
relative (where only flatus is passed )
Absolute constipation is cardinal sympt. of complete I.O.

The rule that constipation is present in I.O. is not apply in
1-Richter hernia
2- Gall stone obstruction
3- Mesenteric vascular occlusion
4- Obstruct ass. with pelvic abscess.
5- Partial obstruction.(faucal impaction \ colonic neoplasm)

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Other manifestation:
1-Dehydration :
Most is seen in small bowel obstruction due to repeated vomiting & fluid sequestration. it results in dry skin& tongue , poor venous filling & sunken eye with oliguria. The blood urea & haematocrit rise giving a 2° polycythemia

2-hypokalemia :

not common feature in simple mechanical obstruction.
Increase in serum K+, amylase, LDH & may be associated with presence of strangulation, as leukocytosis or penia.

3-pyrexia :
when occur indicate:
The onset of ischemia.
Intestinal perforation.
Inflammation associated with the obstructing disease
Hypothermia indicate septicaemic shock.

4. local tenderness

Indicates impending or established ischemia
The development of peritonitis or peritonism indicates overt infarction & or perforation.

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Investigation
Laboratory &radiology

Treatment of acute Intestinal obstruction.

1.Gastro- intestinal drainage
2.fluid & electrolyt replacement
3.relief of obstruction

The first two steps are always necessary before surgical relief of obstruction& are the mainstay of post op. management
In some cases like adhesive obstruction, they may be used exclusively

the surgical treat is necessary for most of cases of I.O. but should be delay until resuscitation is complete provided there is no sign of strangulation , evidence of closed loop obstruction

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The principles of surgical intervention for obstruction:-

Management of:-
segment at site of obstruction
The distended proximal bowel
Underlying cause of obstruction

Supportive Management
Nasogastric decompression is achieved by the passage of a NG tube
The basic biochemical abnormality is sodium and water loss, and therefore the appropriate replacement is Hartmann’s solution or normal saline. The volume required varies and should be determined by clinical haematological and biochemical criteria.
Broad specturm antibiotics


Surgical treatment
The time of operation depend on
1. clinical picture
2. indication for early operation :
Obstruct or strangulation eternal hernia
Internal hernia intestinal strangulation
Acute obstruction

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The classic clinical advice that ‘the sun should not both rise and set’ on a case of unrelieved intestinal obstruction is sound and should be followed unless there are positive rea­sons for delay.
Such cases may include obstruction secondary to adhesions where there is no pain or tenderness, despite continued radiological evidence of obstruction. Under these circumstances, conservative management may be continued for up to 72 hours in the hope of spontaneous resolution.

If the site of obstruction is unknown, adequate exposure is best achieved by a midline incision. Operative assessment is directed to:
• the site of obstruction;
• the nature of the obstruction;
• the viability of the gut.

Identification and assessment of the caecum is the best initial manoeuvre. If it is collapsed, the lesion is in the small bowel and may be identified by careful retrograde assess­ment. A dilated caecum indicates large bowel obstruction.

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Operative decompression
indicated in
A- if dilatation of bowel loop prevents exposure
B- if bowel wall viability compromised
C- subsequent closure will be compromised

Its benefits should be balanced against potential risk of septic complications from spillage.

Decompression may be performed using Savage’s decompressor within a seromuscular purse-string suture.
The type of surgical procedure required will depend upon the nature of the cause — division of adhesions (enterolysis), excision, bypass or proximal decompression.
Following relief of obstruction, the viability of the involved bowel should be carefully assessed .Whilst frankly infarcted bowel is obvious, the viability status in many cases may be difficult to discern.

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If in doubt, the bowel should be wrapped in hot packs for 10 minutes with increased oxygenation and reassessed. The state of the mesenteric vessels and pulsation in adjacent arcades should be sought.

Nevertheless, non-occlusive vascular insufficiency may occur despite adequate pulsation. In doubtful cases, following resection, both ends of the bowel should be raised as stomas. This is not only safe but also allows regular assessment of the bowel. Where 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.

Whenever small bowel is resected, the exact site of resection, the length of the resected segment and that of the residual bowel should be recorded.

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Large bowel obstruction

This is usually due to underlying carcinoma or occasionally diverticular disease, and presents in an acute or chronic form.
The condition of pseudo-obstruction should always be considered and excluded by a limited contrast study or air computerised tomography (CT) scan to confirm organic obstruction.

Rx
After full resuscitation the abdomen should be opened through a midline incision.
Distension of the caecum will confirm large bowel involvement. Identification of a collapsed distal segment of the large bowel and its sequential proximal assessment will readily lead to identification of the cause.
When a removable lesion is found in the caecum, ascending colon, hepatic flexure or proximal transverse colon an emergency right hemicolectomy should be per­formed.

If the lesion is irremovable, a proximal stoma (colostomy or ileosotomy if the ileocaecal valve is incompetent) or ileotransverse bypass should be considered. Obstructing lesions at the splenic flexure should be treated by an extended right hemicolectomy with ileodescending colonic anastomosis.

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For obstructing lesions of the left colon or rectosigmoid junction, immediate resection should be considered unless there are clear contraindications such as:
• inexperienced surgeon; We prefer proximal colostomy in these circumstance
• moribund patient;
• Advanced disease.

In the absence of senior clinical staff, it is safest to bring the proximal colon to the surface as a colostomy. Where possible the distal bowel should be brought out at the same time (Paul—Mikulicz procedure) to facilitate subsequent extraperitoneal 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.

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Obstruction by adhesions and bands

May be classified into
Early fibrinous adhesions
late fibrinous adhesions
or by underlying etiology.

Bands may be:-

congenital, for example obliterated vitellointestinal duct;
• a string band following previous bacterial peritonitis;
• a portion of greater omentum usually adherent to the parietes.

Rx:-
• Initial management is based on intravenous rehydration and nasogastric decompression.

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• Rx:- ( continue )

• regular assessment is mandatory to ensure that strangulation does not occur. Conservative treatment should not be prolonged beyond 72 hours.
• Several procedures may be considered in the presence of recurrent obstruction, including:
• repeat adhesiolysis (enterolysis) alone;
• Noble’s plication operation;
• Charles—Phillips transmesenteric plication;
• intestinal intubation.


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Special types of mechanical intestinal obstruction:-

1- Internal hernia thru:-
• the foramen of Winslow;
• a hole in the mesentery;
• a hole in the transverse mesocolon;
• defects in the broad ligament;
• congenital or acquired diaphragmatic hernia;
• duodenal retroperitoneal fossae — left paraduodenal and right duodenojejunal;
• caecal/appendiceal retroperitoneal fossae — superior, inferior and retrocaecal;
• intersigmoid fossa.

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2-Obstruction from enteric strictures

Small bowel strictures usually occur secondary to
tuberculosis & Crohn’s disease.
Malignant strictures associated with lymphoma are common, whilst carcinoma and sarcoma are rare.
Standard surgical management consists of resection & anastomosis.


3- Bolus obstruction
food,
gallstones,
trichobezoar,
phytobezoar,
stercoliths and
worms(ascaris).
4- Intussusception

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Volvulus

May involve :-
small intestine- rx by reduction of twist
cecum Rx by fixation& or cecostomy
Sigmoid
Sigmoid volvulus
This is rare in Europe
The predisposing cause is summarized in figure

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Presentation :-

Abdominal distension
vomiting occurs late.
Constipation is absolute
A plain radiograph shows massive colonic distension. The classic appearance is of a dilated loop of bowel running diagonally across the abdomen from right to left with two fluid levels seen, one within each loop of bowel.

Treatment

Flexible sigmoidoscopy or rigid sigmoidoscopy and insertion of a flatus tube should be carried out to allow deflation of the gut. Success, as long as ischaemic bowel is excluded, will provide temporary cure allowing resuscitation and an elective procedure.

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Treatment ( continue)

failure results in an early laparotomy, with untwisting of the loop and per-anal decompression, When the bowel is viable, fixation of the sigmoid colon to the posterior abdominal wall may be a safer manoeuvre in inexperienced hands.
Paul—Mikulicz proceduredouble barrel colostomy.
An alternative is a sigmoid colectomy and, where anastomosis is considered unwise, a Hartmann’s procedure with subsequent reanastomosis.

Compound volvulus

This is a rare condition also known as ileo-sigmoid knotting.
The patient presents with acute intestinal obstruction, but distension is comparatively mild. Plain radiography reveals distended ileal loops in a distended sigmoid colon. At operation decompression, resection and anastomosis are required.


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Adynamic obstruction

• Paralytic ileus.
• Pseudo-obstruction
• Acute mesenteric ischemia

Paralytic ileus:-

failure of transmission of peristaltic waves secondary to neuro­muscular failure
Varieties
1-Postoperative — a degree of ileus usually occurs after any abdominal procedure and is self-limiting with a variable duration of 24—72 hours.
2- Infection — intra-abdominal sepsis
3-Reflex ileus — may occur following fractures of the spine or ribs, retroperitoneal haemorrhage or even the application of a plaster jacket.
4-Metabolic — uraemia and hypokalaemia.

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Clinical features

Abdominal distension becomes more marked and tympanitic.
Absent bowel sounds


Management :-
The essence of treatment is prevention, with the use of nasogastric suction and restriction of oral intake until bowel sounds and the passage of flatus return. Electrolyte balance must be maintained.
Conservative Rx maintained but when ileus is prolonged, lapratomy considered excluding hidden cause & facilitating bowel decompression.


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Pseudo-obstruction:-

Small intestinal pseudo-obstruction:- associated with familial visceral myopathy
Colonic pseudo-obstruction:- either acute or chronic
Acute known as Ogilvie syndrome, presents as acute large bowel obstruction.
Rx by colonoscopic decompression, if failure tube caecostomy may be required.

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Acute mesenteric ischaemia

Mesenteric vascular disease may be classified as acute intestinal ischaemia with or without occlusion venous, chronic arterial, central or peripheral. The superior mesenteric vessels are likeliest of the visceral vessels to be affected by embolisation or thrombosis, with the former being most common.

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