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Surgery Clerkship- Amboss Study Plan > Abdominal Surgery- Intestines Part B > Flashcards

Abdominal Surgery- Intestines Part B Flashcards

1
Q

Diverticular Disease

A
  • encompasses a set of colonic pathologies that result from abnormal outpouchings of the colonic mucosa (diverticula).
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2
Q

Diverticula

A

blind pouches that protrude from the gastrointestinal wall and communicate with the lumen

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3
Q

Diverticulosis

A

the presence of multiple colonic diverticula without evidence of infection

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4
Q

Diverticulitis

A

inflammation or infection of colonic diverticula

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5
Q

Diverticular Disease

Epidimeology

A

∼ 50% of individuals > 60 years have diverticulosis

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6
Q

Diverticular Disease Etiology

A

Caused mainly by lifestyle and environmental factors

  • Diet (low-fiber, rich in fat and red meat)
  • Obesity
  • Low physical activity
  • Increasing age
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7
Q

Diverticulitis Pathophysiology

A

Most commonly:

  1. chronic inflammation and increased intraluminal pressure →
  2. erosion of diverticula wall →
  3. inflammation and bacterial translocation

Rarely:

  1. stool becomes lodged in diverticula →
  2. obstruction of intestinal lumen → inflammation
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8
Q

Diverticulosis Clinical Features

A
  • Usually asymptomatic
  • may have abdomincal discomfort
  • chronic constipation
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9
Q

Diverticulitis Clinical Features

A
  • Low-grade fever
  • Sigmoid colon most commonly affected → left lower quadrant pain
  • Possibly tender, palpable mass (pericolonic inflammation)
  • Change in bowel habits
    • (constipation in ∼ 50% of cases and diarrhea in 25–35% of cases)
  • Nausea and vomiting

Elderly or immunocompromised milder symptoms

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10
Q

Symptomatic Diverticulosis Diagnosis

A

Colonoscopy- modality of choice

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11
Q

Diverticulitis Diagnotics

A

Laboratory studies

  • leukocytosis; possible anemia

Imaging

  • CT abdomen and pelvis with IV contrast
    • Preferred initial imaging modality
    • Bowel wall thickening > 3 mm
  • Screening colonoscopy
    • 6–8 weeks after acute episode to assess and rule out malignancy
    • Contraindicated during an acute episode because of the increased risk of perforation.
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12
Q

Diverticulitis Tx Aproach

A

Uncomplicated diverticulitis

  • Conservative management
  • Consider broad-spectrum oral antibiotics (e.g., ciprofloxacin PLUS metronidazole)

Complicated diverticulitis

  • broad-spectrum IV antibiotics
  • CT-guided percutaneous drainage for abscesses > 4 cm
  • Emergency colectomy in patients with generalized peritonitis
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13
Q

Uncomplicated vs Complicated Diverticulitis

A

Uncomplicated diverticulitis: localized inflammation of a colonic diverticulum with no evidence of complications

Complicated diverticulitis: inflammation of a colonic diverticulum associated with

  • perforation,
  • abscess,
  • fecal peritonitis,
  • bowel obstruction,
  • fistula formation
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14
Q

Uncomplicated DIverticulitis Tx

A

Mild diverticulitis is more likely to be an inflammatory process rather than an infectious one. The selective administration of antibiotics is a conditional recommendation.

  • MetronidazolePLUS one of the following
    • Ciprofloxacin
    • Levofloxacin
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15
Q

Complicated Diverticulitis Tx

A

Antibiotic therapy: broad-spectrum IV antibiotics

  • Metronidazole PLUS one of the following
    • Ciprofloxacin
    • Levofloxacin

Management of complications

  • Abscess Size ≥ 4 cm
    • Ultrasound- or CT-guided percutaneous drainage
  • Perforation with generalized peritonitis;
    • emergency surgery

Elective colectomy

  • Routinely recommended 6–8 weeks after resolution of complicated diverticulitis
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16
Q

Prevention of Diverticulitis

A
  • High-fiber diet
  • Fluid hydration
  • Vigorous physical activity
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17
Q

Complications of Diverticular Disease

A
  • GI Bleeding
  • Fistulas
  • Inflammtions (diverticulitis)
  • Abscess
  • Perforation
  • Intestinal Obstruction
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18
Q

Diverticular Disease Fistulas

A

Colovesical (most common)

Symptoms : Pneumaturia and fecaluria

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19
Q

Volvulus

A

twisting of a loop of bowel on its mesentery

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20
Q

Volvulus Epidimiology

A

Incidence

  • Volvulus: 3rd most common cause (∼ 10–15%) of intestinal obstruction in the United States
  • Sigmoid volvulus (most common, 80%)

Age and sex

  • Sigmoid volvulus: ∼ 70 years
  • Cecal volvulus: 40–60 years
  • Intestinal malrotation and midgut volvulus: neonates and infants
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21
Q

Vovulus Risk Factors

A
  • Long mesentery
    • Acquired (sigmoid volvulus): chronic constipation
    • Congenital (cecal volvulus): abnormally mobile cecum
  • Intestinal malrotation
  • Megacolon
  • Intestinal bands/adhesions
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22
Q

Sigmoid Volvulus Clinical Features

A
  • abdominal pain, which decreased after explosive passage of stool/gas
  • Slowly (most common) or rapidly progressive symptoms of bowel obstruction
  • peritonitis
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23
Q

Sigmoid Volvulus Tx

A
  1. IV fluids; NPO; placement of a nasogastric tube
  2. Evaluation
    • No signs of peritonitis: rigid/flexible sigmoidoscopic detorsion of the volvulus
    • Signs of peritonitis→ broad-spectrum IV antibiotics and emergency surgery
  3. Surgery
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24
Q

Sigmoid Vovlus Surgery

A

Sigmoid colectomy and primary anastomosis :

  • indicated in hemodynamically stable patients with viable bowel

Hartmann procedure:

  • resection of the rectosigmoid colon followed by creation of an end colostomy with closure of the rectal stump
  • indicated in hemodynamically unstable patients (faster)
  • those with ischemic/gangrenous bowel (risk of anastomosis leak)
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25
Q

Cecal Volvus Clinical Features

A
  • Acute presentation: features of small bowel obstruction
  • Insidious onset: recurrent episodes of right lower abdominal pain
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26
Q

Cecal Volvus Tx

A
  1. IV fluids; NPO; placement of a nasogastric tube
  2. Surgery
    • Stable patients: ileocecal resection or right colectomy with ileocolic anastomosis
    • Hemodynamically unstable patients
      • Cecostomy
      • Detorsion with cecopexy
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27
Q

Midgut Volvulus

A

torsion of a malrotated midgut causing mechanical bowel obstruction, mostly in neonates and infants

28
Q

Midgut Volvulous Clinical Presentation

A
  • Bilious vomiting with abdominal distension in a neonate/infant
  • Signs of bowel ischemia: hematochezia
  • older children/adults: recurrent episodes of abdominal pain and vomiting; failure to gain weight; malabsorption
29
Q

MIdgut Volvulus Tx

A
  • Initial resuscitation: NPO; nasogastric tube insertion; IV fluids
  • broad-spectrum IV antibiotics
  • Emergency surgery- Ladd Proceddure

Incidentally detected/asymptomatic intestinal malrotation: elective surgery

30
Q

Volvulus Diagnostics

A

Abdominal x-ray (erect and supine)

  • Sigmoid volvulus: coffee bean sign
  • Cecal volvulus: kidney bean sign
  • Bowel perforation: air under diaphragm

CT scan

  • Whirl sign/ Whrilpool sign: pathognomonic for volvulus

Barium enema

  • bird’s beak sign
31
Q

Whril Sign

A
  • characterized by a whorled appearance created by the twisting of one structure around another
  • Twisted loops of bowel are seen on the axial plane of the CT scan.
  • Twisted mesentry and vascular pedicle lies at the center of the whirl.
32
Q

Megacolon

A

Loss of intestinal peristalsis and subsequent dilation of the colon in the abscence of a mechanical obstruction

  • Acute megacolon
  • Chronic megacolon
  • Toxic megacolon
33
Q

Acute Mega Colon

(Acute Colonic Pseudo-Obstruction/Olgivie’s Syndrome)

A

Acute dilation of the colon in the absence of a mechanical obstruction; characteristically seen in severely ill or postoperative patients

34
Q

Acute Mega Colon

Etiology

A
  • Occurs in seriously ill patients or those who have undergone a major surgical procedure
  • Idiopathic; possible factors include:
    • Electrolyte imbalance
    • Drugs (anticholinergic drugs, opioid analgesics, antipsychotics, calcium channel blockers)
35
Q

Acute Mega Colon

Pathophysiology

A
  1. Etiological factors →
  2. impairment/destruction of the autonomic nervous system →
  3. imbalance between sympathetic and parasympathetic control of intestinal motility
36
Q

Acute Mega Colon

Clinical Features

A
  • Gradual abdominal distention
  • Abdominal pain
  • Constipation/diarrhea
  • Tympanitic abdominal percussion
  • Decreased frequency of bowel sounds
  • Signs of colonic ischemia or impending perforation: Fever, tachycardia, and peritoneal signs
37
Q

Acute Megacolon

Treatment

A

Conservative management

  • IV fluids and bowel rest (NPO)
  • Bowel decompression
    • Nasogastric tube
    • Rectal tube
  • Pharmacologic management: NeostigmineIndications
    • No improvement > 24–48 hours

Surgery

  • Signs of impending or actual colonic ischemia/perforation or peritonitis
  • Failure of conservative therapy
38
Q

Acute Megacolon

Diagnostics

A
  • Abdominal x-ray: dilation of the cecum and right colon (occasionally up to the rectum) with/without multiple air-fluid levels; haustrae are preserved
  • Contrast enhanced CT scan (oral and IV contrast)
    • Confirms x-ray findings
39
Q

Chronic Megacolon

Chronic colonic pseudo-obstruction

A

Permanent dilation of the colon caused by congenital/acquired colonic dysmotility in the absence of a mechanical obstruction

40
Q

Chronic Megacolon

Etiology

A
  • Congenital
    • Hirschsprung disease
  • Acquired
    • Neuropathies (diabetic)
    • Myopathies (Duchenne’s muscular dystrophy)
    • Chronic Chagas disease
41
Q

Chronic Megacolon

Clinical Features

A

Recurrent episodes of:

  • Constipation
  • Abdominal pain and distention
  • Anorexia, early satiety, and nausea

Examination findings:

  • Abdominal distention; mild abdominal tenderness
42
Q

Chronic Megacolon

Diagnostics

A
  • Abdominal x-ray: dilation of the cecum and right colon (occasionally up to the rectum) with/without multiple air-fluid levels; haustrae are preserved
  • The cecum, ascending, and transverse colonare the first to dilate, followed by the splenic flexure, descending, and sigmoid colon.
43
Q

Chronic Megacolon

Tx

A

Conservative management

  • Dietary modifications
  • Osmotic laxatives and enemas
  • Prokinetic drugs

Surgery:

  • patients who do not improve/worsen on conservative therapy
  • colectomy with ileorectal anastomosis
    • partia colectomy high chance of recurrance
44
Q

Toxic Megacolon

A

A life-threatening, acute dilation of the colon associated with systemic toxicity

45
Q

Toxic Megacolon

Etiology

A

Infectious colitis

  • Bacterial: C. difficile (pseudomembranous colitis), Salmonella, Shigella, Campylobacterinfections

Inflammatory colitis:

  • Ulcerative colitis, Crohn’s disease
46
Q

Toxic Megacolon

Clinical Features

A
  • (Bloody) diarrhea and vomiting
  • Abdominal distention and pain
  • Signs of sepsis (fever, tachycardia, hypotension) and dehydration
47
Q

Toxic Megacolon

Diagnostics

A

Labs:

  • neutrophilic leukocytosis, anemia, ↑ ESR/CRP, hypokalemia

Abdominal x-ray findings

  • Dilation of the colon (transverse colon diameter > 6 cm)
  • Loss of haustration
  • Multiple air-fluid levels
48
Q

Toxic Megacolon

Treatment

A

Conservative treatment

  • Admission to intensive care unit
  • Complete bowel rest: NPO
  • Nasogastric tube insertion
  • IV fluids
  • Correction of fluid and electrolyte imbalances

Surgery

  • No response to medical management within 24–72 hours; development of complications
  • Subtotal colectomy and end ileostomy
    • anastamosis contraindicated due to inflamed and friable bowel wall
49
Q

Colonic Polyps

A

Abnormal colonic mucosal overgrowths.

  • Pendunculated
  • Sessile
50
Q

Colonic Polyps

Epidemiology

A

∼ 30% of individuals > 50 years

Male> female

∼ 70% are adenomatous polyps

51
Q

Colonic Polyp

Highest Malignancy Potential

A

Adenomatous polyps. Villous adenoma Histology: finger-like projections lined by dysplastic epithelium. Risk of malignancy: ∼ 50%. Frequency: 5–15%

52
Q

Colonic Polyps

Clinical Features

A

Mostly asymptomatic

If symptomatic

  • Blood in stool (hematochezia) is the most common symptom
  • Change in bowel habits (constipation/diarrhea)
  • Mucus in stool
53
Q

Hereditary Polyposis Syndrome

A
  1. Adenomatous Polyposis Syndromes (Familial Adenomatous Polyposis)
  2. Hamartomatous Polyposis Syndromes
54
Q

Familial Adenomatous Polyposis

Inheritance

A
  • Mutation of the tumor suppressor gene APC (adenomatous polyposis coli)
  • Autosomal dominant;
  • positive family history
55
Q

Familial Adenomatous Polyposis

Epidemiology

A

Develops during 3rd dacade of life

56
Q

FAP

Clinical Features

A
  • initially asymptomatic until progressing to colon cancer
  • Altered bowel habits (constipation/diarrhea), blood in stool, and abdominal pain
  • Congenital hypertrophy of the retinal pigment epithelium
57
Q

FAP

Diagnosis

A

Colonoscopy: >100 polyps

gentic testing: APC mutations

58
Q

FAP

Treatment

A
  • Screening beginning at 10 years of age
  • Prophylactic proctocolectomy + ileoanal anastomosis; diagnosis
  • Screening upper endoscopy beginning at 25 years of age
  • Celecoxib; sulindac
59
Q

Gardner Syndrome

A
  • FAP + extracolonic bony and/or soft tissue tumors (e.g., osteomas, desmoid tumors, sebaceous cysts, lipomas, fibromas)
60
Q

Turcot Syndrome

A

Adenomatous colonic polyps + brain tumors

61
Q

Hamartomatous Polyposis Syndromes

A
  • Peutz-Jeghers Syndrome
  • Juvenile Polyposis Syndrome
  • Cowden Syndrome
  • Cronkhite- Canada Syndrome
62
Q

Peutz-Jeghers Syndrome

A
  • 95% of patients have mucocutaneous hyperpigmentation
  • Autosomal Dominant
  • Enteroscopy: hamartomatous polyps throughout the gastrointerstinal tract
  • Prognosis
    • The lifetime risk of colorectal cancer is ∼40%.
    • Increased risk of ovarian, breast, and pancreatic cancer
63
Q

Juvenile Polyposis Syndrome

A

Etiology: autosomal dominant with incomplete penetrance

Clinical features: Onset is within the first decade of life, often with gastrointestinal bleedingand anemia

64
Q

Cronkhite- Canada Syndrome

A
  • Etiology: probably immune-mediated (rare, nonfamilial disorder)
  • Clinical features: GI polyposis with alopecia and cutaneous hyperpigmentation
65
Q

Colorectal Rectal

A

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