Classify Intestinal Obstruction. Discuss the D\D and
management of AIO in a 70 yr old male.
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Describe the c\f ,diagnosis and management of AIO.
Enumerate causes of dynamic IO. Discuss the
diagnosis and management of acute small bowel
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obstruction.
The common Scenario
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A 50 year old gentleman presents
with abdominal pain, distension and
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absolute constipation. Withrepeated episodes of vomiting.
His vital sign were stable, abdomen
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distended with diffuse tenderness
but minimal peritonism. Bowel
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Sounds are hyperactive.The plain abdominal xray was taken
on admission.
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What are your objectives?
You should be able to address the following questions
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1. Is this bowel obstruction or ileus?2. Is this a small or large bowel obstruction?
3. Is this proximal or distal obstruction?
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4. What is the cause of this obstruction?
5. Is this a complex or simple obstruction?
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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?
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9. What are the indications for surgery?
10. What are the medico-legal and ethical issues that I
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should address?Definition
Any condition that interferes with normal propulsion
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and passage of intestinal contents.Can involve the small bowel, colon or both.
TYPES
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Dynamic: where peristalsis is working against a
mechanical obstruction.
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Adynamic: mechanical element is absent- Peristalsis may be absent(paralytic ileus)
-May be present in non propulsive form. (mesenteric
vascular occlusion or pseudo-obstruction)
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Mechanical ObstructionAcute vs Chronic
Partial vs Complete
Simple vs Closed loop
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Gangrenous vs NongangrenousPATHOPHYSIOLOGY
Small Intestine Function
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Transport - Distension stimulates contractionsMixing and peristalsis
Absorption
Colon Function
Water Absorption
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TransportStorage
PATHOPHYSIOLOGY
Dependent Upon:
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Degree of ObstructionDuration of Obstruction
Presence and Severity of Ischemia
Results in:
Accumulation of fluid and air
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Bacterial overgrowthMaximal by 24 hrs after obstruction
Gut translocation to nodes and portal system
Once Distended :
Impaired fluid and nutrient absorption
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Secretion of isotonic fluid (intravascular to intraluminal)PATHOPHYSIOLOGY
Systemic symptoms are secondary to:
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HypovolemiaBacterial translocation (typically E. coli)
Ischemia worsens general inflammatory state,
bacterial translocation, and fluid requirements
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Large Bowel Obstruction
Ileocecal valve plays prominent role in
pathophysiology of LBO
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If competent valve = closed loop obstruction
Caecal ischemia around 10-13 cm
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Causes- SBO
Luminal
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Mural
Extraluminal
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F.BodyNeoplasims
Postoperative
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Bezoars
lipoma
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adhesionsGallstone
polyps
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FoodParticles
leiyomayoma
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Congenitaladhesions
A.lumbricoides
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hematomalymphoma
Hernia
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carcimoidcarinoma
Volvulus
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secondaryTumorsCrohns
TB
Stricture
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IntussusceptionCongenital
Intussusception
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Gall stone IleusIBD
Large Bowel Obstruction
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?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
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?Perforation results in the release of formed feaces with heavy
bacterial contamination
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Aetiology:1. Carcinoma: The commonest cause, 18% of colonic ca. present
with obstruction
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2. Benign stricture: Due to Diverticular disease, Ischemia,
Inflammatory bowel disease.
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3. Volvulus: 1. Sigmoid Volvulus: Results from long redundant,faecaly loaded colon with a narrow pedicle
2. Caecal Volvulus
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4. Hernia.
5. Congenital : Hirschusbrung, anal stenosis and agenesis
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Colonic ObstructionSigmoid Volvulus
COMMON CAUSES:
Adhesions- 40%
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Tumors -15%Inflamatory- 15%
Obstructed hernia-12%
Intraluminal-10%
Miscellaneous -8%
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SYMPTOMS
The four cardinal features of intestinal obstruction:
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-abdominal pain-vomiting
-distension
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-constipation
Vary according to:-
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location of obstructionDuration of obstruction
underlying pathology
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intestinal ischemia
HISTORY
Did this ever happen before?
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Change in bowel habits (acute vs chronic)Progressive vs acute abd. distention
Weight loss
Flatus?
Prior Surgeries
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Hx of abdominal CA?Hx of Inflammatory Bowel Dz
Prior abdominal XRT?
Meds: Anticoagulants, Anticholinergics, Opioids,
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Antihistamines, Alpha-agonists, CatecholaminesSYMPTOMS
Abdominal pain:
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- colicky in nature, around the umbilicus in SBO while in
the lower abdomen in LBO
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- if it becomes continuous, think about perforation orstrangulation.
- does not usually occurs in paralytic ileus.
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Vomiting-starts early in SBO and late in LBO
-As obstruction progresses vomitus alters from digested food
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to faeculent due to enteric bacterial overgrowth
Distension
-more with lower obstruction
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SYMPTOMS
Constipation
-more with lower or complete obstruction
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- constipation is either absolute (no feces or flatus)
or relative (flatus passed).
-diarrhea may be present with partial obstruction
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SYMPTOMS
Dehydration
More common in small bowel obstruction, due to repeated
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vomiting.
Secondary polycythemia due to raised B.urea & hematocrit.
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PyrexiaOnset of ischemia.
Intestinal perforation.
Inflammation associated with int. obst.
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SYMPTOMSIn strangulation:
severe constant abdominal pain
fever
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tachycardiatenderness with rigidity/rebound
tenderness.
shock
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CLINICAL EXAMINATIONGeneral examination-
Vital signs
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Signs of dehydration ?tachycardia, hypotension
dry mucus membrane, decreased skin turgor, decreased urine output
Inspection
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distension, scars, peristalsis, masses, hernial orifices
Palpation
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tenderness, masses, rigidityPercussion
tympanitic abdomen
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Auscultationhigh pitched bowel sound or silent abdomen
*Examine rectum for mass, blood, feces or it may be empty in case of
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complete obstructionINVESTIGATIONS
Hemogram - WBC (neutrophilia-strangulation)
Hyper kalemia, hyperamylasemia & raised LDH may
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be associated with strangulation.
Plain AXR
Sigmoidoscopy (carcinoma, volvulus)
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Contrast x-rayCT abdomen.
The most helpful diagnostic radiographic procedure
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in suspected SBO is:A. CT of Abdomen and Pelvis
B. UGI gastrograffin contrast study
C. Supine and Erect plain films of abdomen
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D. U/S of the abdomenImaging ? Plain Films
Dilated loops, SB dilation? AFLs?
Are AFL's and bowel loops in same place on supine and upright
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films?
Is there gas throughout the entire colon? Ileus or pSBO
Paucity of distal colonic gas or abrupt cutoff of colonic gas
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w/proximal distention and/or AFLs? Suggesting complete or
near-complete LBO
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Massive dilation of colon, especially of the cecum or sigmoid?Suggestive of volvulus or pseudoobstruction
Evidence of strangulation? Thickened SB loops, mucosal
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thumb printing, pneumatosis cystoides intestinalis, or free air
Are there biliary calculi? Pneumobilia? GS ileus?
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AXRWhen distended by gas:
Jejunum is characterized by valvulae conniventes.
Ileum is featureless.
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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
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and distal site in smal bowel.
The Difference between small and
large bowel obstruction
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Large bowel
Small Bowel
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?Peripheral ( diameter 8 cm max)?Central ( diameter 5 cm max)
?Presence of haustration
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?Vulvulae coniventae
?Ileum: may appear tubeless
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Adjunctive TestsSigmoidoscopy
When large amounts of air extend down to the rectum
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Flex or Rigid wil exclude rectal or distal sigmoidobstruction ?
CT Scan or U/S
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When normal plain films but history and exam areconsistent with obstruction
Plain films in SBO wil be nondiagnostic approximately
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30% of the time
Role of CT
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Used with iv contrast, oral and
rectal contrast (triple contrast).
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Able to demonstrateabnormality in the bowel wall,
mesentery, mesenteric vessels
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and peritoneum.
It can define
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the level of obstructionThe degree of obstruction
The cause: volvulus,
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hernia, luminal and mural
causes
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The degree of ischaemiaFree fluid and gas
Ensure: patient vitally stable
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with no renal failure and no
previous allergy to iodine
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Role of barium gastrografinstudies
Barium should not be used in
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a patient with peritonitis
As: fol ow through, enema
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Limited use in the acutesetting
Gastrografin is used in
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acute abdomen but is
diluted
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Useful in recurrent andchronic obstruction
May able to define the level
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and mural causes.
Can be used to distinguish
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adynamic and mechanicalobstruction
TREATMENT
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Three main measures-- GI drainage
- Fluid &Electrolyte replacement
- Relief of obstruction, usually surgical
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Treatment
Conservative:
-Nasogastric aspiration by Ryles tube
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-IV fluids- volume varies depending on dehydration
-NPO
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-urinary catheter-check temp. and pulse 2 hourly
-abdominal examination 8 hourly
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-Broad spectrum antibiotics initiated early- reducebacterial overgrowth.
? Some cases wil settle by using this conservative regimen, other
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need surgical intervention.? Surgery should be delayed til resuscitation is complete unless signs
of strangulation and evidence of closed-loop obstruction.
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? Cases that show reasons for delay should be monitored
continuously for 72 hours in hope of spontaneous resolution e.g.
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adhesions with radiological findings but no pain or tenderness? "The sun should not both rise and set" in cases of unrelieved
obstruction.
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Indication for surgery:
- failure of conservative management
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- tender, irreducible hernia
- strangulation
If the site of obstruction is unknown; laparotomy
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assessment is directed to-
-The site of obstruction.
-The nature of obstruction.
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-The viability of gut.Surgical treatment
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Operative decompression required-ifdilatation of bowel loops prevent exposure,
bowel wall viability is compromised,
or if subsequent closure will be compromised.
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Savage's decompressor used within
seromuscular purse-string suture.
Or large-bore NG tube maybe used for milking
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intestinal contents into stomach.
SURGERY
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The type of surgical procedure depend upon the cause ofobstruction viz division of bands,adhesiolysis, excision ,or
bypass
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*Once obstruction relieved, the bowel is inspected for
viability, and if non-viable, resection is required.
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Indicators of non-viability1.absent peristalsis
2.loss of normal shine
3.loss of pulsation in mesentry
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4.green or black color of bowel
SURGERY
If in doubt of viability, bowel is wrapped in hot packs
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for 10 minutes with increased oxygen and reassessed
for viability.
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Resection of non viable gut should be done followedby stoma.
Sometimes a second look laprotomy is required in 24-
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48 hours e.g. multiple ischemic areas.
Adhesions
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Most common cause of intestinal obstruction.Peritoneal irritation results in local fibrin production,
which produce adhesions.
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BANDSCongenital : obliterated vitellointestinal duct.
A string band following previous bacterial peritonitis.
A portion of greater omentum adherent to parietes.
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Causes of adhesions :Abdominal operation : anastomosis, raw peritoneal surfaces
Foreign material: talc, starch, gauze, silk
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Infection: peritonitis, T.B.
Inflammatory conditions: crohn's disease.
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Radiation entritis.Prevention
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Good surgical technique.Washing the peritoneal cavity with saline to remove the clots.
Minimizing contact with gauze.
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Covering the anastomosis & raw peritoneal surfaces.
TREATMENT
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Usually conservative treatment is curative.(i.v. rehydration & nasogastric decompression)
It should not be prolonged beyond 72 hrs.
Surgery
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Division of band.Minimal adhesiolysis.
Tt. Of recurrent obstruction due to
adhesions
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Repeat adhesiolysis alone.
Noble's plication : adjacent intestinal coils (15-20
cms) are sutured with serosal sutures.
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Charles-Phillips trans-mesenetric plication.
Intestinal intubation : initraluminal tube insertion via
a WITZEL jejunostomy or gastrostomy.
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INTERNAL HERNIA
When a portion of small intestine is entrapped in one
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of retropritoneal fossae or in a congenital mesentricdefect.
Sites of internal herniation:
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Foramen of winslow.A hole in mesentry / transverse mesocolon.
Defects in broad ligaments.
Congenital/ acquired diaphragmatic hernia.
Duodenal retroperitoneal fossae- Lt. paraduodenal &
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rt. Duodenoojejunal.
intersigmoid fossae.
It is uncommon in the absence of adhesions.
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Treatment : to release the constricting agent bydivision.
Gal stone ileus
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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.
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-may show a radio opaque gall stone.Treatment : laparotomy & removal /crushing of stone.
FOOD
After partial /total gastrectomy.
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Unchewed food can cause obstruction.Treatment similar to gall stone.
BEZOARS
Trichobezoars
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PhytobezoarsWORMS
Ascaris lumbricoides
Frequently follows initiation of antihelminthic
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therapy.
Eosinophilia/worm with in gas filled bowel loops.
Laparotomy.
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INTUSSUSCEPTION
One portion of gut becomes invaginated with in
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adjacent segment.Most common in children(3-9 months.)
Idiopathic-70%
Associated gastroenteritis/UTI- 30%
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Hyperlpasia of Peyer's patches in terminal ileum canbe initiating factor.
In older children intussusception is usually associated with
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a lead point ? meckel's diverticulum, polyp, & appendix.Adults: always with a lead point.- polyp, submucosal
lipoma/ tumor.
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It is composed of three parts:
-Entering/ inner tube(Intussusceptum)
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- Returning/ middle tube-Sheath/ outer tube(intussuscipiens)
It is an example of strangulating obstruction with
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impaired blood supply of inner layer.It may be ileoileal(5%); ileocolic(77%); ileo-ileo-colic(12%);
colocolic (2%) & multiple.
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CLINICAL FEATURES
Severe colic pain.
vomitting as time progress
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blood & mucus (the `redcurrent' jelly stool).Abdominal lump(sausage shaped)
Emptiness in RIF(the sign of Dance).
Death may occur from bowel obstruction or
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peritonitis secondary to gangrene.RADIOGRAPHY
Plain X-ray Abd.: Bowel obstruction with absent caecal
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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.
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(small bowel mass may be revealed)Differential Diagnosis
Acute enterocolitis: faecal matter/ bile is always present.
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Henoch-schoenlein purpura.Rectal prolapse: projecting mucosa can be felt in
continuity with perianal skin
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TREATMENTTheraputic Ba-enema : -in infants.
- unlikely to succeed in lead points.
- contrindications: peritonism, prolonged
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history (> 48 hrs.).Operative
After resuscitation ;Laparotmy with reduction.
Cope's method.
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Irreducible/ gangrenous intussusception: excision ofmass & anastomosis.
Volvulus of the Colon
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Sigmoid most commonly involved
180? or > counterclockwise twist
Cecal volvulus next most common
Transverse colon volvulus is rare 4% of colonic
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volvulus
Splenic flexure volvulus VERY rare
Sigmoid Volvulus
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Predisposing Factors
Long and highly-mobile sigmoid
Lengthy mesosigmoid, Narrow at its base
Adhesions between proximal sigmoid and
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rectosigmoid with long loop of colon in between
Chronic constipation and high-fiber diet
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Sigmoid Volvulus - PathogenesisClosed-loop type obstruction
Proximal colon dilates- Extent depends on ileocecal
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valve competenceSimple or Strangulated
Venous then arterial obstruction
With simple form takes a few days for vascular
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compromise to develop
In acute fulminating variant much more rapid
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course seenSigmoid Volvulus - Varieties
Acute Fulminating Type- Mortality 37-80% ,
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Younger patient, sudden onset, rapid course Earlyvomiting, severe pain, peritonitis, and gangrene
Minimal distension often, hard to diagnose
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Subacute Progressive Type- Generally older pt.,
more gradual onset, Hx prior attacks, chronic
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constipation, Abdominal distension often extremeLate vomiting, pain is minimal, no peritonitis
Sigmoid Volvulus - Diagnosis
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Plain films of Abdomen-- Massively dilated and
distended bowel loop
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Both ends in pelvis,Bow of loop cephalad
"Bent inner tube" sign
Air/fluid level within loop
Proximal colon & SB may be dilated
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Barium enema-- "Birds beak"Sigmoid Volvulus - Treatment
Rigid sigmoidoscopic detorsion--decompression,
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& placement of rectal tubeRT inserted past obstruction point
Successful 77 - 90% of time
Mortality rate 1.2 - 5.5%
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Preferred initial treatmentColonoscopic decompression
Surgery if:
Decompression not successful
Ischemic or necrotic bowel encountered
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Sigmoid Volvulus ? Surgical
Treatment
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Recurrence rate is high (33 - 60%)Some advise elective op after 1st episode
Elective: Resection of redundant colon Small
transverse LLQ incision
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Sigmoid fixation another option
Emergent: Resection +/- stoma
Ogilvie's Syndrome
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Acute Colonic Pseudo obstructionMassive dilation of cecum, right, and transverse colon
(non-mechanical), to splenic flexure
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Dilated SB loops in > 50%Symptoms: Distension,Nausea and vomiting,
Abdominal pain in 80% ,Bowel sounds may be normal
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or increasedConditions associated with
Ogilvie's syndrome
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Non-operative Trauma
Non-GI surgery (Gyn, Ortho, Cardiac)
Pancreatitis, Cholecystitis
Diabetes, Malignancy
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Narcotics, antidepressants, anticholinergicsNeurologic or Respiratory disease
Electrolyte (hypo K+, Ca+2), Acid / Base disorder
Radiation in past
Ogilvie's Syndrome: DDx and Dx
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Plain abdominal films to diagnose and follow cecal
diameter (Q12-24 hrs)
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Normal is < 9 cmIf 14 cm - perforation in 23% ?
Differential Includes: Fecal impaction, Cecal or
Sigmoid Volvulus, IschemicBowel,Mechanical
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Obstruction
Ogilvie's Treatment :
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Correct electrolyte problems and underlyingcondition
D/C narcotics and anticholinergics
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NPO with NGT, +/- Rectal TubeColonoscopic decompression difficult but often
successful, May need 2nd decompression
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Long colonic drains can be placed via colonoscope(old)
Neostygmine is the treatment of choice now
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If signs of perforation then ORSTRANGULATION
The viability of the bowel is threatened.
Causes of strangulation
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ExternalHernial orifices
Adhesions/bands
Interrupted blood flow
Volvulus
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IntussusceptionIncreased intraluminal pressure
Closed-loop obstruction
Primary
Mesenteric infarction
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The venous return is compromised before the arterial
supply.
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The resultant increase in capillary pressure leads to localmural distension with loss of intravascular fluid and red
blood cells intramurally and extraluminally.
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Once the arterial supply is impaired, haemorrhagic
infarction occurs.
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As the viability of the bowel is compromised there ismarked translocation and systemic exposure to anaerobic
organisms with their associated toxins.
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The morbidity of intraperitoneal strangulation is far
greater than with an external hernia?
Closed-loop obstruction
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This occurs when the bowel is obstructed at both the
proximal and distal points.
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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
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competent ileocaecal valveThe inability of the distended colon to decompress itself
into the small bowel results in an increase in luminal
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pressure, which is greatest at the caecum, with subsequent
impairment of blood supply.
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Unrelieved, this results in necrosis and perforation.