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Intestinal obstruction

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Title: Intestinal obstruction


1
Intestinal obstruction
  • 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

2
Causes of intestinal obstruction
  • Dynamic
  • Intraluminal
  • Impaction
  • Foreign bodies
  • Bezoars
  • Gallstones
  • Intramural
  • Stricture
  • Malignancy
  • Extramural
  • Bands/adhesions
  • Hernia( internal /external )
  • Volvulus
  • Intussusception
  • Adynamic
  • Paralytic ileus
  • Mesenteric vascular occlusion
  • Pseudo-obstruct

3
Intestinal obstruction
  • 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
    bowels 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.

5
Etiology according to age
  • Neonates congenital atresia , volvulus
    neonatorum, anorectal malformation ,mechonium
    ileus and Hirschsprungs disease
  • infant ileocaecal intussusception ,
    Hirschsprungs disease and strangulated hernia
  • Adult adhesion, strangulated hernia
  • Elderly colon carcinoma, adhesion and
    strangulated hernia

6
Pathology
  • Simple
  • distal to obstruction
  • proximal
  • peristalsis
  • blind loop
  • Strangulation
  • General effect
  • fluid and electrolyte loss
  • septicaemia

7
Pathophysiology
  • 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
Pathophysiology
  • 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
Clinical picture
  • 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
History
  • The typical crampy abdominal pain associated with
    intestinal obstruction occurs in paroxysms at 4-
    to 5-minute intervals and occurs less frequently
    with distal obstruction. It is usually centred on
    the umbilicus (small bowel) or lower abdomen
    (large bowel). With increasing distension, the
    colicky pain is replaced by a mild constant
    diffuse pain.
  • The development of severe persistant pain is
    indicative of the presence of strangulation. Pain
    may not be a significant feature in postoperative
    simple mechanical obstruction and does not
    usually occur in paralytic ileus.
  • Nausea and vomiting are more common with a higher
    obstruction and may be the only symptoms in
    patients with gastric outlet or high intestinal
    obstruction. An obstruction located distally is
    associated with less emesis, and the initial and
    most prominent symptom is the cramping abdominal
    pain. As obstruction progresses the character of
    the vomitus alters from digested food to
    faeculent material, as a result of the presence
    of enteric bacterial overgrowth.
  • In the small bowel the degree of distension is
    dependent on the site of the obstruction and is
    greater the more distal the lesion. Visible
    peristalsis may be present. Distension is delayed
    in colonic obstruction and may be minimal or
    absent in the presence of mesenteric vascular
    occlusion.
  • Constipation may be classified as absolute (i.e.
    neither faeces nor flatus is passed) or relative
    (where only flatus is passed). Absolute
    constipation is a cardinal feature of complete
    intestinal obstruction. Some patients may pass
    flatus or faeces after the onset of obstruction
    as a result of the evacuation of the distal bowel
    contents. The rule that constipation is present
    in intestinal obstruction does not apply in
    Richters hernia gallstone obturation
    mesenteric vascular occlusion obstruction
    associated with pelvic abscess partial
    obstruction (faecal impaction/colonic neoplasm)
    in which diarrhoea may often occur.

11
Physical Examination
  • 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
Strangulation
  • 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
Closed-loop obstruction
  • 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
Investigations
  • 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
Treatment
  • 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 patients 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 2448 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
TreatmentFluid Resuscitation and Antibiotics
  • 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 Ringers.
  • 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
TreatmentTube Decompression and follow-up
  • 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.

18
Special forms
  • Intussusceptions
  • Volvulus
  • Paralytic illeus
  • mesenteric vascular occlusion
  • Pseudo-intestinal obstruction

19
Paralytic illeus
  • 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
pseudo-obstruction
  • 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,L
    axatives
  • Secondary gastrointestinal involvement,
    Scleroderma ,Chagas disease

22
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
    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
Clinical features
  • 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
  • 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
Ischaemic colitis
  • 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.
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