1. Definition : arrest of downward propulsion of intestinal
content
Classification :
according to :
A)pathological cause:
1)simple intestinal obstruction
2) strangulated intestinal obstruction
B)level of obstruction:
1) high small intestinal obstruction
2) low small intestinal obstruction
3) large intestinal obstruction
C)onset and course of obstruction
1) acute
2)chronic
D) mechanical Vs Adynamic
E) complete Vs incomplete
3. Small intestinal ileus is the most common form of intestinal
obstruction; it occurs after most abdominal operations and is a
common response to acute intra abdominal inflammatory
conditions
Mechanical small bowel obstruction is somewhat less common;
such obstruction is secondary to intra-abdominal adhesions,
hernias, or cancer
Mechanical colonic obstruction most often develops in response to
obstructing carcinoma, diverticulitis,or volvulus.
Acute colonic pseudo-obstruction occurs most frequently in the
postoperative period or in response to another acute medical
illness.
4. When the bowel is occluded at a single point along the
intestinal tract, simple obstruction is present.
When a segment of bowel is occluded at two points along its
course by a single constrictive lesion that occludes both the
proximal and the distal end of the intestinal loop as well as
traps the bowel’s mesentery, closed-loop obstruction is
present.
When the blood supply to a closed-loop segment of bowel
becomes compromised, leading to ischemia and eventually
to bowel wall necrosis and perforation, strangulation is
present.
The most common causes of simple obstruction are intra-
abdominal adhesions, tumors, and strictures.
The most common causes of closed-loop obstruction are
hernias, adhesions, and volvulus.
6. Simple
distal to obstruction
proximal
peristalsis
blind loop
Strangulation
General effect
fluid and electrolyte loss
septicaemia
7. Early in the course of an obstruction, intestinal motility and contractile
activity increase in an effort to propel luminal contents past the
obstructing point. Later in the course of obstruction, the intestine
becomes fatigued and dilates, with contractions becoming less frequent
and less intense.
As the bowel dilates, water and electrolytes accumulate both
intraluminally and in the bowel wall itself. This massive third-space fluid
loss accounts for the dehydration and hypovolemia.
The metabolic effects of fluid loss depend on the site and duration of the
obstruction. With a proximal obstruction, dehydration may be
accompanied by hypochloremia, hypokalemia, and metabolic alkalosis
associated with increased vomiting. Distal obstruction of the small bowel
may result in large quantities of intestinal fluid into the bowel; however,
abnormalities in serum electrolytes are usually less dramatic.
Oliguria, azotemia, and hemoconcentration can accompany the
dehydration. Hypotension and shock can ensue. Other consequences of
bowel obstruction include increased intra-abdominal pressure,
decreased venous return, and elevation of the diaphragm, compromising
ventilation. These factors can serve to further potentiate the effects of
hypovolemia.
8. As the intraluminal pressure increases in the bowel, a
decrease in mucosal blood flow can occur. These
alterations are particularly noted in patients with a
closed-loop obstruction in which greater intraluminal
pressures are attained. A closed-loop obstruction,
produced commonly by a twist of the bowel, can
progress to arterial occlusion and ischemia if left
untreated and may potentially lead to bowel
perforation and peritonitis. Bacteria translocating to
mesenteric lymph nodes and even systemic
organs.However, the overall importance of this
bacterial translocation on the clinical course has not
been entirely defined.
9. Cardinal symptom
Pain, Distention , Vomiting, Absolute constipation
The nature of the presentation will be influenced by the site
■ In high small bowel obstruction, vomiting occurs early and is profuse with rapid
dehydration. Distension is minimal with little evidence of fluid levels on abdominal
radiography
■ In low small bowel obstruction, pain is predominant with central distension. Vomiting is
delayed. Multiple central fluid levels are seen on radiography
■ In large bowel obstruction, distension is early and pronounced. Pain is mild and vomiting
and dehydration are late. The proximal colon and caecum are distended on abdominal
radiography
The nature of the presentation will also be influenced by whether the obstruction is: • acute;•
chronic;• acute on chronic;• subacute.
Acute obstruction usually occurs in small bowel obstruction, with sudden onset of severe colicky
central abdominal pain, distensionand early vomiting and constipation
Chronic obstruction is usually seen in large bowel obstruction, with lower abdominal colic and
absolute constipation followed by distension.
In acute on chronic obstruction there is a short history of distension and vomiting against a
background of pain and constipation.
Subacute obstruction implies an incomplete obstruction.
Presentation will be further influenced by whether the obstruction is:
• simple – in which the blood supply is intact;
• strangulating/strangulated
Examination
General,
Abdominal inspection, palpation ,percussion , auscultation
10.
11. The patient with intestinal obstruction may present with tachycardia and
hypotension, demonstrating the severe dehydration that is present.
Fever suggests the possibility of strangulation.
Abdominal examination demonstrates a distended abdomen, with the
amount of distention some what dependent on the level of obstruction.
Previous surgical scars should be noted. Early in the course of bowel
obstruction, peristaltic waves can be observed, particularly in thin
patients, and auscultation of the abdomen may demonstrate hyperactive
bowel sounds with audible rushes associated with vigorous peristalsis
(i.e., borborygmi). Late in the obstructive course, minimal or no bowel
sounds are noted.
Mild abdominal tenderness may be present with or without a palpable
mass; however, localized tenderness, rebound, and guarding suggest
peritonitis and the likelihood of strangulation.
A careful examination must be performed to rule out incarcerated hernias
in the groin, the femoral triangle, and the obturator foramen.
A rectal examination should be performed to assess for intraluminal
masses and to examine the stool for occult blood, which may be an
indication of malignancy, intussusception, or infarction.
12. “Classic” picture of strangulation include tachycardia, fever, leukocytosis, and a
constant, noncramping abdominal pain. Tenderness with rigidity, Shock ,With the
cardinal signs of intestinal obstruction
• In cases of intestinal obstruction in which 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 and
irreducible, there is no expansile cough impulse and it has recently increased in
size.
Pathology
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, which has a smaller
absorptive surface.
Causes of strangulation
External:■ Hernial orifices ■ Adhesions/bands
Interrupted blood flow ■ Volvulus ■ Intussusception
Increased intraluminal pressure ■ Closed-loop obstruction
Primary ■ Mesenteric infarction
13. This occurs when the bowel is obstructed at both the proximal and
distal points.
It is present in many cases of intestinal strangulation. Unlike cases of
non-strangulating obstruction, there is no early distension of the
proximal intestine. When gangrene of the strangulated segment is
imminent, retrograde thrombosis of the mesenteric veins results in
distension on both sides of the strangulated segment.
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 (present in up to one-third of individuals). 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
14. Plain X ray of the abdomen: Radiological features of obstruction
■ The obstructed small bowel is characterised by straight segments that are
generally central and lie transversely. No 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 described 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
Blood urea and electrolyte
Blood picture
U.S.
CT scan
Endoscopy
15. The treatment is urgent relief of obstruction after preparation
Preoperative preparation ( fluid and electrolyte replacement ,antibiotics and Tube
Decompression )
Operation :exploration
Immediate operation indicated in peritonitis, incarcerated hernia, suspected or confirmed
strangulation, sigmoid volvulus with systemic toxicity or peritoneal irritation, small bowel
volvulus, colonic volvulus above sigmoid,
Conservative (with exeption)
indication 1)Adhesive
2)Ileocaecal itussusception
3)Sigmoid volvuls
4)feacal impaction
Reassess patient every 4 hr. Look for changes in pain, abdominal findings, and
volume and character of NG aspirate. Repeat abdominal x-rays, and look for changes in gas
distribution, pneumatosis cystoides intestinalis, and free intraperitoneal air.
Classify patient’s condition as improved, unchanged, or worse.
Decide whether operative treatment is necessary and, if so, whether it should be done on
urgent or elective basis.
Urgent operation Indications include: • Lack of response to 24–48 hr of nonoperative therapy
(increasing abdominal pain, distention, or tenderness; NG aspirate changing from nonfeculent
to feculent; ↑ proximal small bowel distention with ↓ distal gas).
16. Patients with intestinal obstruction are usually dehydrated and depleted
of sodium, chloride, and potassium, requiring aggressive intravenous
replacement with an isotonic saline solution such as lactated Ringer’s.
Urine output should be monitored by the placement of a Foley catheter.
After the patient has formed adequate urine, potassium chloride should
be added to the infusion if needed. Serial electrolyte measurements, as
well as hematocrit and white blood cell count, are performed to assess
the adequacy of fluid repletion.
Because of large fluid requirements, patients, particularly the elderly, may
require central venous assessment and, in some cases, the placement of a
Swan-Ganz catheter.
Broad-spectrum antibiotics are given prophylactically by some surgeons
based on the reported findings of bacterial translocation occurring even
in simple mechanical obstructions. In addition, antibiotics are
administered as a prophylaxis for possible resection or inadvertent
enterotomy at surgery.
17. Nasogastric suction empties the stomach, reducing the hazard of
pulmonary aspiration of vomitus and minimizing further intestinal
distention from preoperatively swallowed air. Patients with adhesive
simple intestinal obstruction may be treated conservatively with
resuscitation and tube decompression alone. Resolution of symptoms and
discharge without the need for surgery have been reported in 60% to
85% of patients with an adhesive simple intestinal obstruction .
Although an initial trial of nonoperative management of most patients with
partial small bowel obstruction is warranted, it should be emphasized that
clinical deterioration of the patient or increasing small bowel distention
on abdominal radiographs during tube decompression warrants prompt
operative intervention.
The decision to continue to treat a patient nonoperatively with a
presumed bowel obstruction is based on clinical judgment and requires
constant vigilance to ensure that the clinical course has not changed.
19. Causes of Ileus
Post laparotomy
Metabolic and electrolyte derangements
(e.g., hypokalemia, hyponatremia,
hypomagnesemia, uremia, diabetic coma)
Drugs (e.g., opiates, psychotropic agents,
anticholinergic agents)
Intra-abdominal inflammation
Retroperitoneal hemorrhage or inflammation
Intestinal ischemia
Systemic sepsis
20. Abdominal distention, usually without the colicky abdominal pain,
is the typical and most notable finding. Nausea and vomiting may
occur.
Plain abdominal radiographs may reveal distended small bowel
as well as large bowel loops.
The treatment of an ileus is entirely supportive with nasogastric
decompression and intravenous fluids.
The most effective treatment to correct the underlying condition
may be aggressive treatment of the sepsis, correction of any
metabolic or electrolyte abnormalities, and discontinuation of
medications that may produce an ileus. Pharmacologic agents
have been used but for the most part have been ineffective. Drugs
that block syinput (e.g., guanethidine) or stimulate
parasympathetic activity (e.g., bethanechol or neostigmine) have
been tried.
In addition, hormonal manipulation, using cholecystokinin or
motilin, has been evaluated, but the results have been
inconsistent.
21. Factors associated with pseudo-obstruction
Idiopathic
■ Metabolic Diabetes, intermittent porphyria,Acute
hypokalaemia, Uraemia,Myxodoema
■ Severe trauma (especially to the lumbar spine and
pelvis)
■ Shock
Burns
Myocardial infarction
Stroke
Septicaemia
■ Retroperitoneal irritation by : Blood,Urine,nzymes
(pancreatitis),Tumour
■ Drugs,Tricyclic
antidepressants,Phenothiazines,Laxatives
■ Secondary gastrointestinal involvement, Scleroderma
,Chagas’ disease
22. 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 the visceral vessels most likely to be affected by
embolisation or thrombosis, with the former being most common. Occlusion at the
origin of the superior mesenteric artery (SMA) is almost invariably the result of
thrombosis, whereas emboli lodge at the origin of the middle colic artery. Inferior
mesenteric involvement is usually clinically silent because of a better collateral
circulation.
Possible sources for the embolisation of the SMA include a left atrium associated with
fibrillation, a mural myocardial infarction, an atheromatous plaque from an aortic
aneurysm and a mitral valve vegetation associated with endocarditis.
Primary thrombosis is associated with atherosclerosis and thromboangitis obliterans.
Primary thrombosis of the superior mesenteric veins may occur in association with
factor V Leiden, portal hypertension, portal pyaemia and sickle cell disease and in
women taking the contraceptive pill.
Irrespective of whether the occlusion is arterial or venous, haemorrhagic infarction
occurs. The intestine and its mesentery become swollen and oedematous. Blood-
stained fluid exudes into the peritoneal cavity and bowel lumen. If the main trunk of
the SMA is involved, the infarction covers an area from just distal to the
duodenojejunal flexure to the splenic flexure. Usually, a branch of the main trunk is
implicated and the area of infarction is less.
23. The most important clue to an early diagnosis of acute
mesenteric ischaemia is the sudden onset of severe
abdominal pain in a patient with atrial fibrillation or
atherosclerosis. The pain is typically central and out of all
proportion to physical findings.
Persistent vomiting and defaecation occur early, with the
subsequent passage of altered blood. Hypovolaemic shock
rapidly ensues. Abdominal tenderness may be mild initially
with rigidity being a late feature.
Investigation will usually reveal a profound neutrophil
leucocytosis with an absence of gas in the thickened small
intestine on abdominal radiographs. The presence of gas
bubbles in the mesenteric veins is rare but pathognomonic.
24. Treatment needs to be tailored to the individual.
In conjunction with full resuscitation, embolectomy via the
ileocolic artery or revascularisation of the SMA may be
considered in early embolic cases.
The majority of cases, however, are diagnosed late.
All affected bowel should be resected.
Anti-coagulation should be implemented early in the
postoperative period.
After extensive enterectomy it is usual for patients to require
intravenous alimentation.
The young, however, may sometimes develop sufficient
intestinal digestive and absorptive function to lead relatively
normal lives.
In selected cases consideration may be given to small bowel
transplantation.
25. Infarction of the large intestine alone is relatively rare.
Involvement of the middle colic artery territory should
be treated by transverse colectomy and
exteriorisation of both ends, with an extended right
hemicolectomy in selected cases.
Ischaemic colitis describes the structural changes that
occur in the colon as a result of the deprivation of
blood. They are most common in the splenic flexure,
whose blood supply is particularly tenuous.
They have been classified by Marston into gangrenous,
transient and stricturing forms; only stricturing forms
cause obstruction and only a few such patients
require resection.
