Lower GI - Toronto Notes Flashcards

1
Q

What are the most common sites for the tumours of the small intestine?

A
  • Terminal ileum
  • Proximal jejunum
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2
Q

Outline the types of polyp disease

A
  • Adenomas
  • Hamartomas
  • Familial adenomatous polyposis (FAP)
  • Juvenile polyps
  • Other
    • leiomyomas
    • lipomas
    • hemangiomas
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3
Q

What are the risk factors for adenocarcinoma?

A
  • FAP
  • History of colorectal cancer
  • HNPCC
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4
Q

What are the clinical features of an adenocarcinoma?

A
  • Early metastasis to lymph nodes
  • 80% metastatic at time of operation
  • Common - abdominal pain - general
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5
Q

What are the clinical features of a carcinoid tumour?

A
  • Nausea
  • Vomiting
  • Anaemia
  • GI bleeding
  • Jaundice
  • Slow growing - usually asymptomatic, incidental finding
  • Obstruction, bleeding, crampy abdominal pain, intussusception
  • Specifically:
    • hot flashes, hypotension, diarrhea, bronchoconstriction, right heart failure
    • requires liver involvement - lesion secretes serotonin, kinins and vasoactive peptides directly to systemic circulation (normally inactivated by liver)
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6
Q

What are the risk factors for small bowel lymphoma?

A
  • Crohn’s
  • Celiac
  • Autoimmune disease
  • Immunosuppression
  • Radiation therapy
  • Nodular lymphoid hyperplasia
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7
Q

What are the clinical features of a small bowel lymphoma?

A
  • Fatigue, weight loss, fever, malabsorption, abdominal pain
  • Anorexia, vomiting ,constipation and mass
  • Rarely:
    • perforation
    • obstruction
    • bleeding
    • intussusception
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8
Q

What are the risk factors for metastatic disease in the small bowel?

A
  • Melanoma
  • Breast cancer
  • Lung cancer
  • Ovarian cancer
  • Colon cancer
  • Cervical cancer
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9
Q

What are the key clinical features of metastatic disease in the small bowel?

A
  • Obstruction
  • Bleeding
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10
Q

What are your investigations of choice for an adenocarcinoma?

A
  • CT abdomen and pelvis
  • Endoscopy
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11
Q

What are your investigations of choice for a carcinoid tumour?

A
  • Most are found incidentally at surgery for obstruction or appendectomy
  • Chest thorax/abdo/pelvis CT
  • Consider small bowel enteroclysis to look for primary
  • Elevated 5-HIAA (break down product of serotonin) in urine or increased 5-HT in blood
  • Radiolabelled octreotide or MIBG scans to locate tumour
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12
Q

What are your investigations of choice for a lymphoma of the small bowel?

A
  • CT abdo/pelvis
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13
Q

What are your investigations of choice for metastatic disease of the small bowel?

A
  • CT abdo/pelvis
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14
Q

Outline brief plans for treatment of each of the four malignant pathologies the small intestine discussed so far.

A
  • Adenocarcinoma
    • Surgical resection and chemotherapy
  • Carcinoid
    • Surgical resection and chemotherapy
    • Carcinoid syndrome treated witih steroids, histamine, octreotide
  • Lymphoma
    • Low grade - chemotherapy with cyclophosphamide
    • High grade - surgical resection, radiation
    • Palliative - somatostatin and doxorubicin
  • Metastatic
    • Paliation
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15
Q

Simply define a hernia.

A
  • It is a fascial defect - in which there is a protrusion of a viscus into an area in which it is not normally contained.
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16
Q

What are the risk factors for a hernia?

A
  • Activities which increased intra-abdominal pressure
    • Obesity
    • Chronic cough
    • Pregnancy
    • Constipation
    • Straining on urination or defecation
    • Ascites
    • Heavy lifting
  • Congenital abnormality
  • Previous hernia repair
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17
Q

What are the clinical features of a hernia?

A
  • It is a mass of variable size
  • Tenderness worse at end of the day, relieved by supine position or with reduction
  • Abdominal fullness, vomiting and constipation
  • Transmits palpable impulse with coughing or straining
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18
Q

Outline some investigations for a hernia.

A
  • Physical examination usually sufficient
  • Ultrasound
    • With or without a CT
      • A CT is usually required for obturator hernias, internal abdominal hernias and Spigelian femoral hernias in obese patients
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19
Q

What are the borders of Hesselbach’s Triangle?

A
  • Lateral - inferior epigastric artery
  • Inferior - inguinal ligament
  • Medial - lateral margin of rectus sheath
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20
Q

Outline a classification system for hernias.

A
  • Complete
    • hernia sac and contents protrude through defect
  • Incomplete
    • Partial protrusion through the defect
  • Internal hernia
    • Sac herniating into or involving intra-abdominal structure
  • External hernia
    • Sac protrudes completely through the abdominal wall
  • Strangulated hernia
    • Vascular supply of protruded viscus is compromised ( ischemia)
      • Requires emergency repair
  • Incarcerated hernia
    • Irreducible hernia, not necessarily strangulated
  • Richter’s hernia
    • Only part of bowel circumference (usually anti-mesenteric border) is incarcerated or strangulated so may not be obstructed
      • A strangulated Richter’s hernia may self-reduce and thus be overlooked, leaving a gangrenous segment at risk of perforation
  • Sliding hernia
    • Part of wall of hernia formed by protruding viscus (usually cecum)
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21
Q

What are the different anatomical types of hernias?

A
  • Groin
    • Indirect and direct inguinal, femoral
    • Pantaloon - combined direct and indirect hernias - peritoneum draped over epigastric vessels
  • Epigastric
    • Defect in linea alba above umbilicus
  • Incisional
    • Ventral hernia at site of wound closure - may be secondary to wound infection
  • Other
    • Littre’s (involving Meckel’s diverticulum)
    • Amyand’s (containing appendix)
    • Lumbar
    • Obturator
    • Parastomal
    • Umbilical
    • Spigelian (ventral hernia through linea semilunaris)
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22
Q

What are the complications of hernias?

A
  • Incarceration - irreducible hernias
  • Strangulation
    • irreducible with resulting ischemia
      • Small - new hernias more likely to strangulate
      • Femoral >>, indirect iinguinal > direct inguinal
      • Intense pain followed by tenderness
      • Intestinal obstruction, gangrenous bowel and sepsis
      • Surgical emergency
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23
Q

What treatment options are available for a hernia?

A
  • Surgical treatment (herniorrhaphy) is only to prevent strangulation and evisceration for symptomatic relief, for cosmesis - if asymptomatic can delay surgery
  • Repair may be done open or laproscopic and may use mesh for tension free closure
  • Most repairs are now done using tension-free techniques - a plug in the hernial defect and a patch over it or patch alone
  • Observation is acceptable for small asymptomatic inguinal hernias
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24
Q

What are the postoperative complications for hernia repair?

A
  • Recurrence
    • Risk factors
      • Age greater than 50
      • BM greater than 25
      • Poor pre-op functional status
      • Associated medical conditions:
        • Type II DM
        • Hyperlipidemia
        • Immunosuppression
        • Any comorbid conditions increasing intra-abdominal pressure
        • Less common with mesh/tension free repair
  • Scrotal hematoma
    • Painful scrotal swelling from compromised venous return of testes
    • Deep bleeding - may enter retroperitoneal space and not be initially apparent
    • Difficulty voiding
  • Nerve entrapment
    • Ilioinguinal (causes numbness of inner thigh or lateral scrotum)
    • Genital branch of genitofemoral (spermatic cord)
  • Stenosis/occlusion of femoral vein
    • Acute leg swelling
  • Ischaemic colitis
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25
Q

What are the contents of the spermatic cord?

A
  • Vas deferens
  • Testicular artery/veins
  • Genital branch of gentiofemoral nerve
  • Lymphatics
  • Cremaster muscle
  • Hernia sac
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26
Q

Describe the anatomical location of an inguinal hernia

A

MD’s Don’t LIe

MD: Medial to: the inferior epigastric artery = Direct inguinal hernia

LIe: Lateral to the inferior epigastric artery = Indirect inguinal hernia

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27
Q

Describe the etiology of groin hernias.

A
  • Direct inguinal
    • Acquired weakness of trasvrsalis fascia
    • Wear and tear
    • Increased abdominal pressure
  • Indirect inguinal
    • Congenital persistence of processus vaginalis in 20% of adults
  • Femoral
    • Pregnancy - weakness of pelvic floor musculature
    • Increased intra-abdominal pressure
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28
Q

What is the anatomy of direct inguinal hernias?

A
  • Through Hessellbach’s triangle
  • Medial to inferior epigastric artery - usually does not descend into scrotal sac
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29
Q

What is the anatomy of an indirect inguinal hernia?

A
  • Originates in deep inguinal ring
  • Lateral to inferior epigastric artery
  • Often descends into scrotal sac (or labia majora)
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30
Q

What is the anatomy of a femoral hernia?

A
  • Into femoral canal, below inguinal ligament but may override it
  • Medial to femoral vein within femoral canal
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31
Q

Describe the anatomy of the superficial inguinal ring.

A
  • Opening in external abdominal aponeurosis; palpable superior and lateral to pubic tubercle
  • Medial border:
    • Medial crus of external abdominal aponeurosis
  • Lateral border
    • Lateral crus of external oblique aponeurosis
  • Roof
    • Intercrural fibres
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32
Q

Describe the anatomy of the deep inguinal ring

A
  • Opening in transversalis fascia - palpable superior to mid-inguinal ligament
  • Medial border:
    • Inferior epigastric vessels
  • Superior-lateral border:
    • Internal oblique and transversus abdominis muscles
  • Inferior:
    • Inguinal ligament
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33
Q

Define the term ‘‘bowel obstruction’’

A
  • Partial or complete blockage of the bowel resulting in failure of intestinal contents to pass through the lumen
34
Q

What is the pathogenesis of bowel obstruction?

A
  • Disruption of the normal flow of intestinal contents - proximal dilatation + distal decompression
  • May tak 12-24 h to decompress, therefore passage of feces and flatus may occur after the onset of obstruction
  • Bowel ischaemia may occur if blood supply is strangulated or bowel wall inflammation leads to venous congestion
  • bowel wall edema and disrupton of normal bowel absorptive function - increased intraluminal fluid - transudative fluid loss into the peritoneal cavity - leading to electrolyte disturbances
35
Q

What are the clinical features of bowel obstruction?

A
  • Must differentiate between obstruction and ileus - characterise obstruction as acute vs chronic, partial vs complete (constipation vs obstipation), small vs large bowel, strangulating vs non-strangulating, and with vs without perforation.
36
Q

What are the clinical features of a small bowel obstruction?

A
  • Nausea, vomiting
    • Early, may be bilious
  • Abdominal pain
    • Colicky
  • Constipation
    • +
  • Other
    • May have visible peristalsis
  • Bowel sounds
    • Normal - increased
    • Absent if secondary ileus
  • AXR findings
    • Air-fluid levels
    • ‘Ladder’ pattern plicae circularis
    • Proximal distention (>3cm) with no colonic gas
37
Q

What are the clinical features of a large bowel obstruction?

A
  • Nausea, vomiting
    • Late and may be feculent
  • Abdominal pain
    • Colicky
  • Abdominal distention
    • ++
  • Other
    • May present with visible peristalsis
  • Bowel sounds
    • Normal, increased (borborygmi)
    • Absent if secondary ileus present
  • AXR findings
    • Air-fluid levels
    • ‘Picture frame’ appearance
    • Proximal distention and distal decompression
    • No small bowel air if competent ileocecal valve
    • Coffee bean sign
38
Q

What are the clinical features of a paralytic ileus?

A
  • Nausea and vomiting
    • Present
  • Abdominal pain
    • Minimal or absent
  • Abdominal distention
    • +
  • Constipation
    • +
  • Bowel sounds
    • Decreased or absent
  • AXR findings
    • Air throughout small bowel and colon
39
Q

What are the complications of total obstruction?

A
  • Strangulating obstruction (10% of bowel obstructions) = surgical emergency
    • Cramping pain turns to continuous ache, hematemesis, melena (if infarction)
    • Fever, leukocytosis and tachycardia
    • Peritoneal signs, early shock
  • Other
    • Perforation - secondary to ischaemia and luminal distention
    • Septicemia
    • Hypovolemia (due to third spacing)
40
Q

What investigations will you consider in bowel obstruction?

A
  • Radiological
    • Upright CXR or left lateral decubitus (LLD) to rule out free air; usually seen under the right hemidiaphragm
    • Abdominal x-ray (3 views) to determine SBO vs LBO vs ileus
      • If ischaemc bowel look for:
        • free air
        • pneumatosis
        • thickened bowel wall
        • air in portal vein
        • dilated small and large bowels
        • thickened or hose like haustra (normally finger like projections)
    • Other
      • Most used - CT provides information on level of obstruction, severity and cause
        • important to r/o closed loop obstruction - especially in the elderly
      • Less used - upper GI series/small bowel series for SBO (if no cause apparaent i.e. no pervious hernias or surgeries)
      • If suspect LBO - consider a rectal water soluble enema rather than a barium enema (can thicken and cause complete obstruction)
      • May consider ultrasound or MRI in pregnany patients
  • Laboratory studies
    • May be normal early in disease course
    • BUN, creatinine, hematocrt (hemoconcentration) to assess degree of hydration
    • fluid, electrolyte abnormalities
    • amylase elevated
    • metabolic alkalosis due to frequent emesis
    • if strangulation - leukocytosis with left shift, lactic acidosis, elevated LDH (late signs)
41
Q

What are the causes of SBO?

A

SHAVING

Stricture

Hernia

Adhesions

Volvulus

Intussusception/IBD

Neoplasm

Gallstones

42
Q

What is the management plan for bowel obstruction?

A
  • Stabilize vitals, fluids and electrolyte resuscitation (with normal saline/Ringer’s first, then with added potassium after fluid deficits are corrected)
  • NG tube to relieve vomiting, prevent aspiration and decompress small bowel by prevention of further distention by swalloed air
  • Foley catheter to monitor in and outs
43
Q

What is the etiology of a small bowel obstruction?

A
  • Intraluminal
    • Intussuscpetion
    • Gallstones
  • Intramural
    • Crohn’s
    • Radiation stricture
    • Adenocarcinoma
  • Extramural
    • Adhesions
    • Incarcerated hernia
    • Peritoneal carcinomatosis
44
Q

What is the tratment of a small bowel obstruction?

A
  • Consider whether complete or partial obstruction, ongoing or impending strangulation location and cause:
    • SBO with history of previous abdo/pelvic surgery - likely to resolve with conservative management - surgery if no resolution in 48-72 hours or complications
    • Complete SBO, strangulation - urgent surgery after stabilizing patient with fluid resuscitation
    • SBO with no previous surgery and no evidence of carcinomatosis - operate
    • Trial of medical management may be indicated with Crohn’s, recurrent SBO, carcinomatosis
      • NGT decompression
      • GI rest
      • Serial abdominal exams
    • Special case:
      • Early postoperative SBO (within 30 days of abdominal surgery) - prolonged trial of conservative therapy may be appropriate, surgery is reserved for complications such as strangulation
45
Q

What is the etiology of large bowel obstruction?

A
  • Intraluminal
    • constipation
  • Intramural
    • Adenocarcinoma
    • Diverticultis
    • IBD stricture
    • Radiation stricture
  • Extramural
    • Volvulus
    • Adhesions
46
Q

What are the clinical features of a large bowel obstruction?

A
  • Open loop (10-20%) (safer):
    • Incompetent ileocecal valve allows relief of colonic pressure as contents reflux into the ileum, therefore clinical presentation similar to SBO
  • Closed loop (80-90%) (dangerous)
    • Competent ileocecal valve, resulting in proximal and distal occlusions
    • Massive colonic distention
      • Increased pressure in the cecum - leading to bowel ischaemia - necrosis and ultimately perforation
47
Q

What is the treatment of a LBO?

A
  • Surgical correction of obstruction (usually requires resection and temporary diverting colostomy)
  • Volvulus requires sigmoidoscopic or endoscopic decompression followed by operative reduction if unsuccessful
    • If successful, consider sigmoid resection on same admission
  • Cecal volvulus can be a true volvulus or a cecal ‘bascule’ - both need surgical treatment
48
Q

What is the defintion of a colonic pseudo-obstruction?

A
  • Condition with symptoms of intestinal blockage without any physical signs of blockage
49
Q

What is the differential diagnosis of a colonic pseudo-obstruction?

A
  • Acute
    • toxic megacolon
    • trauama
    • postoperative (especially post orthopedic procedures with prolonged immoblization)
    • neurological disease
    • retroperitnoeal disease
    • medications (narcotic and psychiatric)
  • Chronic
    • Neurologic disease (enteric, central, peripheral nervous system)
    • Scleroderma
50
Q

What is the pathogenesis of toxic megacolon?

A
  • Extension of inflammation into smooth muscle layer causing paralysis
  • Damage to myenteric plexus and electrolyte abnormalities are not consistently found
51
Q

What is the etiology of toxic megacolon?

A
  • IBD
  • Infectious colitis
    • bacterial (c.diff, salmonella, shigella, campylobacter)
    • viral (cytomegalovirus)
    • parasitic (E.histolytica)
  • Volvulus
  • Diverticulitis
  • Ischaemic colitis
  • Obstructing colon cancer are rare causes
52
Q

What are the clinical features of toxic megacolon?

A

• infectious colitis usually present for >1 wk before colonic dilatation
• diarrhea ± blood (but improvement of diarrhea may portend onset of megacolon)
• abdominal distention, tenderness, ± local/general peritoneal signs (suggest perforation)
• triggers: hypokalemia, constipating agents (opioids, antidepressants, loperamide,
anticholinergics), barium enema, colonoscopy

53
Q

What is the diagnostic criteria for toxic megacolon?

A
  • Must have both colitis and sytemic manifestations for diagnosis
  • Radiologic evidence of dilated colon
  • Three of:
    • Fever
    • Hear rate (greater than 120)
    • WBC (greater than 10.5)
    • Anaemia
  • One of:
    • Fluid and electrolyte disturbances
    • Hypotension
    • Altered LOC
      *
54
Q

What are the investigations that form part of the work up for toxic megacolon?

A
  • FBC
    • Look for leukocytosis
    • Anaemia from bloody diarrhea
    • Electrolytes
    • Elevated CRP and ESR
  • ABG
    • Metabolic alkalosis - due to volume contraction and hypokalemia
    • Hypoalbuminaemia
    • Although these are late findings
  • AXR
    • Dilated colon (greater than 6cm) (right>transverse>left), loss of haustra
  • CT
    • Useful in assessing underlying disease
55
Q

What is your management plan for a patient with toxic megacolon?

A
  • NBM
  • NG Tube
  • Stop constipating agents
  • Correct fluid and electrolyte abnormalities and transfusion
  • Serial AXRs
  • Broad-spectrum antibiotics
    • reduce sepsis
    • anticipate perforation
  • Aggressive treatment of underlying disease
    • (steroids in IBD or metronidazole for C.difficile)
56
Q

What are the indications for surgery in a patient with toxic megacolon?

A
  • Worsening or persisting toxicity or dilatation after 48-72 hours
  • Severe haemorrhage and perforation
  • High lactate and WBC specifically for C.difficile
57
Q

What is the surgical procedure indicated for toxic megacolon?

A
  • Subtotal colectomy and end ileostomy (may be temporary, with second operation for re-anastamosis later)
58
Q

Briefly, what is the pathogenesis for paralytic ileus?

A
  • Temporary paralysis of the myenteric plexus
59
Q

What are the associations with paralytic ileus?

A
  • Postoperative
  • Intra-abdominal sepsis
  • Medications
    • Opiates
    • Anesthetics
    • Psychotropics
  • Electrolyte disturbances
    • Sodium
    • Potassium
    • Calcium
  • Microbiology
    • C.difficile
  • Inactivity
60
Q

What is the treatment for paralytic ileus?

A
  • NG decompression
  • NBM
  • Fluid resuscitation
  • Correct causative abnormalities
    • Sepsis
    • Medications
    • Electrolytes
  • Consider TPN for prolonged ileus
  • Post-operatively - gastric and small bowel motility returns by 24-48 hours, colonic motility by day 3-5.
61
Q

What is the etiology of intestinal ischaemia?

A
  • Acute
    • Arterio-occlusive mesenteric ischemia (AOMI)
      • thrombotic
      • embolic
      • extrinsic compression (e.g. strangulating hernia)
    • Non-occlusive mesenteric ischaemia (NOMI)
      • mesenteric vasoconstriction secondary to systemic hypoperfusion (preserves supply to vital organs)
    • Mesenteric venous thrombosis (MVT)
      • consider hypercoagulable state (ruling out malignancy)
      • DVT (prevents venous outflow)
  • Chronic
    • Usually due to atherosclerotic disease - look for CVD risk factors
62
Q

What are the clinical features of intestinal ischaemia?

A
  • Acute
    • Severe abdominal pain out of proportion to physical findings
    • Vomiting
    • Bloody diarrhea
    • Bloating
    • Minimal peritoneal signs early in course
    • Hypotensive shock and sepsis
  • Chronic
    • Postprandial pain
    • Fear of eating
    • Weight loss
  • Common sites:
    • Superior mesenteric artery (SMA) supplied territory
  • ‘Watershed’ areas of the colon:
    • splenic flexure
    • left colon
    • sigmoid colon
63
Q

What are the investigations to be considered when diagnosing intestinal ischaemia?

A
  • FBC
    • Leukocytosis
  • Bloods
    • Lactic acidosis (late finding)
    • Amylase
    • LDH
    • CK
    • ALP
    • Hypercoagulability workup if suspect venous thrombosis
  • AXR
    • Portal venous gas
    • Intestinal pneumatosis
    • Free air, if perforation
  • Contrast CT
    • thickened bowel wall
    • luminal dilatation
    • SMA or SMV thrombus, mesenteric/portal venous gas
    • pneumatosis
  • CT angiography is the gold standard for acute arterial ischaemia
64
Q

What is your management and treatment plan for intestinal ischaemia?

A
  • Fluid resuscitation
  • Correct metabolic acidosis
  • NBM
  • NG decompression of stomach
  • Prophylactic broad spectrum antibiotics, avoid vasoconstrictors and digitalis
  • Exploratory laparotomy
  • Angiogram, embolectomy/thrombectomy, bypass graft and mesentric endarterectomy, anticoagulation therapy, percutaneous transluminal angioplasty with or without stent
  • Segmental resection of necrotic intestine:
    • assess extent of viability; if extent of bowel viability is uncertain, a second look laparotomy 12-24 hours later is mandatory.
65
Q

What is the modified Alvarado score for acute appendicitis?

A

1 point per:

• Migratory right Iliac fossa pain
(1 point)
• Anorexia (1 point)
• Nausea/vomiting (1 point)

• Tenderness in right Iliac fossa
(2 points)

• Rebound tenderness in right Iliac
fossa (1 point)

  • Fever >37.5°C (1 point)
  • Leukocytosis (2 points)

• 0-3 = low risk, discharge to return if
no improvement
• 4-6 = moderate risk, admit, observe,
repeat examinations

• Male 7-9 = appendectomy
• Female (not pregnant) 7-9 = diagnostic
laparoscopy ± appendectomy

66
Q

What is McBurney’s sign?

A

Tenderness 1/3 the distance from the ASIS to the umbilicus on the right side

67
Q

What is the pathogensis of appendicitis?

A
  • Luminal obstruction - bacterial overgrowth - inflammation/swellling - increased pressure - localised ischaemia - gangrene/perforation - localised abscess (walled off by omentum) or peritonitis
68
Q

What is the etiology of appendicitis?

A
  • Children or young adult:
    • Hyperplasia of lymphoid follicces
    • Initiated by infection
  • Adult
    • Fibrosis/stricture
    • Fecolith
    • Obstructing neoplasm
  • Other causes:
    • parasites and foreign body
69
Q

What are the clinical features of appendicitis?

A
  • Most reliable feature is progression of signs and symptoms
  • Low grade fever, rises with perforation
  • Abdominal pain then anorexia, nausea and vomiting
  • Classic pattern:
    • Pain initially periumbilical; constant, dull, poorly localised, then well localised pain over McBurney’s point
      • Due to progression of disease from visceral irritation (causing referred pain from structures of the embryologic midgut - including the appendix) to irritation of parietal structures
      • McBurney’s sign
  • Signs:
    • Inferior appendix - McBurney’s sign, Rosving’s sign (palpation presure to left abdomen causes McBurney’s point tenderness)
    • Retrocecal appendix:
      • Psoas sign (pain on flexion of hip against resistance or passive hyperextension of hip)
    • Pelvic appendix:
      • Obturator sign (flexion then external or internal rotation about right hip causes pain)
  • Complications
    • Perforation
    • Abscess, phlegmon
70
Q

What investigations would you order for a case of appendicitis?

A
  • Labs/Bloods:
    • Mild leukocytosis with left shift (normal WBC counts)
    • Higher leukoctye count with perforation
    • beta hCG to rule out pregnancy
    • urinalysis
  • Imaging:
    • upright CXR, AXR - usually nonspecific - free air if perforated (rarely), calcified fecolith, loss of psoas shadow, RLQ ileus
    • Ultrasound - may visualise appendix but also helps rule out gynecological causes
    • CT scan - thick wall, appendicolith, inflammatory changes
71
Q

What is your treatment plan for appendicitis?

A
  • Hydration and correct electrolyte abnormalities
  • Surgery (gold standard, 20% mortality with perforation especially in the elderly) + antibiotic coverage
  • If localised abscess (palpable masses or large phlegmon on imaging and often pain >4-5 days)
  • consider radiological drainage and antibiotics x 14 days + or - interval appendectomy in 6 weeks
  • Appendectomy
    • Laparoscopic or open
    • Complications
      • Spillage of bowel contents
      • Pelvic abscess
      • Enterocutaneous fistula
    • Perioperative antibiotics
      • cefazolin + metronidazole (no post-op antibiotics unless perforated)
      • other choices - 2nd or 3rd generation cephalosporin for aerobic gut organisms
    • Colonoscopy in the eldery to rule out other etiology (neoplasm)
72
Q

Compare laparoscopic and open appendectomy

A
  • Laparoscopic
    • Wound infection less likely
    • Intra-abdominal abscesses 2 times more likely
    • Reduced pain on post-operative day 1
    • Reduced hospital stay
    • Sooner return to normal activity, work and sport
    • Costs outside outside hospital are reduced
  • Open
    • Shorter duration of surgery
    • Lower operation costs
73
Q

What is:

  • A diverticulum
  • Diverticulosis
  • Diverticulitis
  • True diverticuli
  • False diverticuli
A
  • Abnormal sac like protrusion from the wall of a hollow organ
  • Presence of multiple diverticula
  • Inflammation of diverticula
  • Contain all layers of the colonic wall, often right sided
  • False diverticuli - contain mucosa and submucosa - often left sided
74
Q

What is the pathogenesis of diverticulosis?

A
  • Risk factors:
    • Lifestyle
      • Low fibre diet
        • Predispose to motility abnormalities and higher intraluminal pressure, inactivity and obesity
        • muscle wall weakness from aging and illness (Ehler-Danlos, Marfan’s)
      • high intraluminal pressure causes outpouching to occur at point of greatest weakness, most commonly where vasa recta penetrates the circular muscle layer - therefore increasing the risk of haemorrhage.
75
Q

What are the clinical features of diverticulosis?

A
  • Uncomplicated diverticulosis - asymptomatic
  • Episodic abdominal pain (often LLQ), bloating, flatulence, constipation and diarrhea
  • Absence of fever and leukocytosis
  • No physical exam findings or poorly controlled LLQ tenderness
  • Complicatoins
    • Diverticulitis
      • 25% of which are complicated (i.e. abscess, obstruction, perforation and fistula)
      • Bleeding (5-15%) - painless rectal bleeding, 30-50% of massive lower GI bleeds
      • Diverticular colitis (rare) - diarrhea, hematochezia, tenesmus, abdominal pain
76
Q

What is the treatment for diverticulosis?

A
  • Uncomplicated diverticulosis: high fibre and education
  • Diverticular bleed
    • Initially work up and treat as any lower GI bleed
    • If haemorrhage does not stop, resect involved region
77
Q

What is the pathogenesis of diverticulitis ?

A
  • erosion of the wall by increased intraluminal pressure or inspissated food particles leading to…
  • inflammation and focal necrosis gmicro or macroscopic perforation usually mild inflammation with perforation walled off by pericolic fat and mesentery; abscess,
  • fistula or obstruction can ensue
  • poor containment results in free perforation and peritonitis
78
Q

What are the clinical features of diverticulitis?

A
  • depend on severity of inflammation and whether or not complications are present; hence ranges from asymptomatic to generalized peritonitis
  • LLQ pain/tenderness (2/3 of patients) often for several days before admission
  • constipation, diarrhea, nausea, vomiting, urinary symptoms (with adjacent inflammation)
  • complications (25% of cases):
    • ƒabscess: palpable tender abdominal mass
    • ƒfistula: colovesical (most common), coloenteric, colovaginal, colocutaneous
    • ƒcolonic obstruction: due to scarring from repeated inflammation
    • ƒperforation: generalized peritonitis (feculent vs. purulent)
      • Šrecurrent attacks rarely lead to peritonitis
  • low-grade fever, mild leukocytosis common,
  • occult or gross blood in stool rarely coexist with acute diverticulitis
79
Q

What are the investigations for diverticulitis?

A
  • AXR, upright CXR
    • Localized diverticulitis (ileus, thickened wall, SBO, partial colonic obstruction)
    • Free air may be seen in 30% with perforation and generalized peritonitis
  • CT scan (test of choice) - very useful for assessment of severity and prognosis
    • 97%, sensitive; 99% specific
    • Increased soft tissue density within pericolic fat secondary to inflammation, diverticula secondary to inflammation, bowel wall thickening, soft tissue mass (pericolic fluid, abscesses), fistula
    • 10% of diverticulitis cannot be distinguished from carcinoma
  • Hypaque (water soluble) enema - safe (under low pressure)
    • Saw tooth pattern (colonic spasm)
    • May show site of perforation, abscess cavities or sinus tracts, fistulas
  • Elective evaluations: establish extent of disease and rule out other diagnoses (polyps, malignancies) after resolution of acute episode
    • Colonoscopy or barium enema and flexible sigmoidoscopy
80
Q

What are your treatment options for diverticulosis?

A
  • Uncomplicated:
    • Conservative management
  • Outpatient:
    • Clear fluids only until improvement and antibiotics (e.g. ciproflxacin and metronidazole) 7-10 days to cover gram negative rods and anaerobes (e.g. B fragilis)
  • Hospitalize: if severe presentation, inability to tolerate oral intake, significant comorbidities, fail to improve outpatient management
  • Treat with NBM, IV fluids, IV antibiotics, (e.g. IV ceftriaxone + metronidazole, ampicillin, gentamicin)
  • Indications for surgery:
    • Unstable patient with peritonitis
    • Hinchey stage 3-4
    • After 1 attack if:
      • Immunosuppressed
      • Abscess needing percutaneous