1. Acute Appendicitis

2. Epidemiology
The incidence of appendectomy appears to be declining due to more accurate preoperative diagnosis.
Despite newer imaging techniques, acute appendicitis can be very difficult to diagnose.

3. Pathophysiology
Acute appendicitis is thought to begin with obstruction of the lumen
Obstruction can result from food matter, adhesions, or lymphoid hyperplasia
Mucosal secretions continue to increase intraluminal pressure

4. Pathophysiology
Eventually the pressure exceeds capillary perfusion pressure and venous and lymphatic drainage are obstructed.
With vascular compromise, epithelial mucosa breaks down and bacterial invasion by bowel flora occurs.

5. Pathophysiology
Increased pressure also leads to arterial stasis and tissue infarction
End result is perforation and spillage of infected appendiceal contents into the peritoneum

6. Pathophysiology
Initial luminal distention triggers visceral afferent pain fibers, which enter at the 10th thoracic vertebral level.
This pain is generally vague and poorly localized.
Pain is typically felt in the periumbilical or epigastric area.

7. Pathophysiology
As inflammation continues, the serosa and adjacent structures become inflamed
This triggers somatic pain fibers, innervating the peritoneal structures.
Typically causing pain in the RLQ

8. Pathophysiology
The change in stimulation form visceral to somatic pain fibers explains the classic migration of pain in the periumbilical area to the RLQ seen with acute appendicitis.

9. Pathophysiology
Exceptions exist in the classic presentation due to anatomic variability of the appendix
Appendix can be retrocecal causing the pain to localize to the right flank
In pregnancy, the appendix ca be shifted and patients can present with RUQ pain

10. Pathophysiology
In some males, retroileal appendicitis can irritate the ureter and cause testicular pain.
Pelvic appendix may irritate the bladder or rectum causing suprapubic pain, pain with urination, or feeling the need to defecate
Multiple anatomic variations explain the difficulty in diagnosing appendicitis

11. History Primary symptom: abdominal pain
½ to 2/3 of patients have the classical presentation
Pain beginning in epigastrium or periumbilical area that is vague and hard to localize

12. History
Associated symptoms: indigestion, discomfort, flatus, need to defecate, anorexia, nausea, vomiting
As the illness progresses RLQ localization typically occurs
RLQ pain was 81 % sensitive and 53% specific for diagnosis

13. History
Migration of pain from initial periumbilical to RLQ was 64% sensitive and 82% specific
Anorexia is the most common of associated symptoms
Vomiting is more variable, occuring in about ½ of patients

14. Physical Exam Findings depend on duration of illness prior to exam.
Early on patients may not have localized tenderness
With progression there is tenderness to deep palpation over McBurney’s point

15. Physical Exam
McBurney’s Point: just below the middle of a line connecting the umbilicus and the ASIS
Rovsing’s: pain in RLQ with palpation to LLQ
Rectal exam: pain can be most pronounced if the patient has pelvic appendix

16. Physical Exam
Additional components that may be helpful in diagnosis: rebound tenderness, voluntary guarding, muscular rigidity, tenderness on rectal

17. Physical Exam
Psoas sign: place patient in L lateral decubitus and extend R leg at the hip. If there is pain with this movement, then the sign is positive.
Obturator sign: passively flex the R hip and knee and internally rotate the hip. If there is increased pain then the sign is positive

18. Physical Exam Fever: another late finding.
At the onset of pain fever is usually not found.
Temperatures >39 C are uncommon in first 24 h, but not uncommon after rupture

19. Diagnosis
Acute appendicitis should be suspected in anyone with epigastric, periumbilical, right flank, or right sided abd pain who has not had an appendectomy

20. Diagnosis
Women of child bearing age need a pelvic exam and a pregnancy test.
Additional studies: CBC, UA, imaging studies

21. Diagnosis CBC: the WBC is of limited value.
Sensitivity of an elevated WBC is 70-90%, but specificity is very low.
But, +predictive value of high WBC is 92% and –predictive value is 50%
CRP and ESR have been studied with mixed results

22. Diagnosis UA: abnormal UA results are found in 19-40%
Abnormalities include: pyuria, hematuria, bacteruria
Presence of >20 wbc per field should increase consideration of Urinary tract pathology

23. Diagnosis Imaging studies: include X-rays, US, CT
Xrays of abd are abnormal in 24-95%
Abnormal findings include: fecalith, appendiceal gas, localized paralytic ileus, blurred right psoas, and free air
Abdominal xrays have limited use b/c the findings are seen in multiple other processes

24. Diagnosis
Graded Compression US: reported sensitivity 94.7% and specificity 88.9%
Basis of this technique is that normal bowel and appendix can be compressed whereas an inflamed appendix can not be compressed
DX: noncompressible >6mm appendix, appendicolith, periappendiceal abscess

25. Diagnosis
Limitations of US: retrocecal appendix may not be visualized, perforations may be missed due to return to normal diameter

26. Diagnosis
CT: best choice based on availability and alternative diagnoses.
In one study, CT had greater sensitivity, accuracy, -predictive value
Even if appendix is not visualized, diagnose can be made with localized fat stranding in RLQ.

27. Diagnosis
CT appears to change management decisions and decreases unnecessary appendectomies in women, but it is not as useful for changing management in men.

28. Special Populations
Very young, very old, pregnant, and HIV patients present atypically and often have delayed diagnosis
High index of suspicion is needed in the these groups to get an accurate diagnosis

29. Treatment Appendectomy is the standard of care
Patients should be NPO, given IVF, and preoperative antibiotics
Antibiotics are most effective when given preoperatively and they decrease post-op infections and abscess formation

30. Treatment
There are multiple acceptable antibiotics to use as long there is anaerobic flora, enterococci and gram(-) intestinal flora coverage
One sample monotherapy regimen is Zosyn 3.375g or Unasyn 3g
Also, short acting narcotics should be used for pain management

31. Disposition Abdominal pain patients can be put in 4 groups
Group 1: classic presentation for Acute appendicitis- prompt surgical intervention
Group 2: suspicious, but not diagnosed appendicitis- benefit from imaging and 4-6h observation with surgical consult if serial exam changes or imaging studies confirm

32. Disposition
Group 3: remote possibility of appendicitis- observe in ED for serial exams; if no change and course remains benign patient can D/C with dx of nonspecific abd pain
Patients are given instructions to return if worsening of symptoms, and they should be seen by PCP in h
Also advised to avoid strong analgesia

33. Disposition
Group 4: high risk population(including elderly, pediatric, pregnant and immunocomprimised)- require high index of suspicion and low threshold for imaging and surgical consultation

34. Ileitis, Colitis, and Diverticulitis

35. Crohn Disease
Chronic granulomatous inflammatory disease of the GI tract.
Can involve any part of GI tract from mouth to anus
Ileum is involved in majority of cases
Confined to colon in 20%
Terms:regional enteritis, terminal ileitis, granulomatous ileocolitis

36. Crohn Disease Etiology and pathogenesis are unknown.
Infectious, genetic, environmental factors have been implicated.
Autoimmune destruction of mucosal cells as a result of cross-reactivity to antigens from enteric bacteria.

37. Crohn Disease
Cytokines,including IL and TNF have been implicated in perpetuating the inflammatory response.
Anti-TNF(remicade) drugs have shown efficacy in treating Crohn disease

38. Crohn Disease
Epidemiology: peak incidence is years old with a second peak 55-66years
20-30% increase in women
More common in European
4 times more common in Jews than non-Jews
More common in whites vs blacks
10-15% have family hx

39. Crohn Disease
Pathology: most important is the involvement of all layers of the bowel and extension into mesenteric lymph nodes
Disease has skip areas between involved areas
Longitudinal deep ulcers and cobblestoning of mucosa are characteristic
These result in fissures, fistulas, and abscesses

40. Crohn Disease Clinical features: variable and unpredictable
Abd pain, anorexia, diarrhea, and weight loss are present in most cases
1/3 of patients develop perianal fissures or fistulas, abscesses, or rectal prolapse

41. Crohn Disease Patients may present with lat complications including:
Obstruction, crampy abd pain, obstipation, intraabdominal abscess with fever
10-20% have extraabdominal features such as: arthritis, uveitis, or liver disease
Crohn’s should also be considered when evaluating FUO

42. Crohn Disease
Clinical course and manifestation depends of anatomic distribution.
30% involves only small bowel, 30% only colon, and 50% involves both

43. Crohn Disease
Recurrence rate is as high as 50% for those responding to medical management
Rate is even higher for those requiring surgery
Incidence of hematochezia and perianal disease is higher when the colon is involved

44. Crohn Disease
Dermatologic complications: erythema nodosum and pyoderma gangrenosum
Ocular: episcleritis and uveitis
Hepatobiliary: pericholangitis, chronic hepatitis, primary sclerosing cholangitis, cholangiocarcinoma, pancreatitis, gallstones

45. Crohn Disease Vascular: thromboembolic disease, vasculitis, arteritis
Other: anemia, malnutrition, hyperoxaluria leading to nephrolithiasis, myeloplastic disease, osteomyelitis, osteonecrosis

46. Crohn Disease
Complications: >75% of patients will require surgery within the first 20 years
Abscesses present with pain and tenderness, but may also have palpable masses or fever spikes
Most common fistula sites are between ileum and sigmoid colon, cecum, another ileal segment, or the skin

47. Crohn Disease
Fistulas should be suspected when there is a change in bowel movement frequency, amount of pain or weight loss
GI bleed is common, but only 1% develop life threatening hemorrhage.
Toxic megacolon occurs in 6% of patients and results massive GI bleed 50% of the time

48. Crohn Disease
Complications can also arise from the treatment of the disease
Sulfasalazine, steroids, immunosuppressive agents, and antibiotics can cause leukopenia, thrombocytopenia, fever, infection, diarrhea, pancreatitis, renal insufficiency, liver failure.

49. Crohn Disease
Incidence of malignancy is 3 times higher in Crohn disease than in general population

50. Crohn Disease
Diagnosis: history, Upper GI, air-contrast barium enema and colonoscopy
Characteristic radiologic findings in small intestine include: segmental narrowing, destruction of normal mucosal pattern, and fistulas.

51. Crohn Disease Colonoscopy is most sensitive for patients with colitis
Useful for detecting mucosal lesions, defining extent of involvement, occurrence of colon ca.
Abd CT is most useful for acute presentation

52. Crohn Disease
Findings of bowel wall thickening, mesenteric edema, local abscess formation suggest Crohn disease.

53. Crohn Disease
Differential Dx: lymphoma, ileocecal amebiasis, sarcoidosis, deep chronic mycotic infections involving GI tract, GI TB, Kaposi’s sarcoma, campylobacter, Yersinia, ulcerative colitis, C.diff, ischemic colitis.

54. Crohn Disease
Tx: relief of symptoms, induction of remission, maintenance of remission, prevention of complications, optimizing timing of surgery, and maintenance of nutrition
Since the disease is virtually incurable, emphasis should be placed of relief of symptoms and preventing complications

55. Crohn Disease
Initial ED management: focus on severity of attack, identifying possible complications such as obstruction, hemorrhage, abscess, toxic megacolon.
CBC, electrolytes, BUN/creatinine, and type and cross if appropriate
Plain films may be useful for obstruction, perforation or toxic megacolon

56. Crohn Disease
Initial Tx: NPO, IVF resuscitation and correction of electrolytes
NG decompression if indicated, broad spectrum atbx(ampicillin or a cephalosporin, aminoglycoside, and flagyl) should be used for suspected fulminant colitis or peritonitis

57. Crohn Disease
IV steroids: hydrocortisone 300mg qd, methylprednisone 48mg qd, or prednisolone 60mg qd should be used for severe disease
Sulfasalazine 3-4g qd can be effective for mild-moderate cases, although it has many toxic side effects

58. Crohn Disease
Oral steroids are reserved for severe disease-prednisone 40-60mg qd
Immunosuppressive drugs:
6-MP or azathioprine are useful for steroid alternatives, healing fistulas, or in patients with contraindications to surgery
Response to immunosuppressant agents takes 3-6 months

59. Crohn Disease
Flagyl and Cipro have been shown some improvement in perianal complications and fistulous disease.
Medically resistant or moderate cases may benefit from anti-TNF(Remicade) 5 mg/kg IV
Cellcept, etanercept, thalidomide, IL therapy may also be beneficial

60. Crohn Disease
Diarrhea can be controlled using imodium, lomotil, or questran

61. Crohn Disease
Disposition: patients with signs of fulminant colitis, peritonitis, obstruction, significant hemorrhage, dehydration, electrolyte/fluid imbalance should be hospitalized under the care of a surgeon or gastroenterologist

62. Crohn Disease
Patients with chronic disease can be discharged home as long as there are no serious complications.
Alterations in maintenance therapy should be discussed with GI
Close follow up should be secured.

63. Ulcerative Colitis Chronic inflammatory disease of the colon.
Inflammation is more severe from proximal to distal colon
Rectum is involved in nearly 100%
Characteristic symptom is bloody diarrhea
Etiology remains unknown

64. Ulcerative Colitis Epidemiology: similar to Crohn disease
More prevalent in US and northern Europe.
First degree relatives have 15 fold increase for UC and 3.5 fold increase for Crohn disease

65. Ulcerative Colitis Pathology: involves mucosa and submucosa
Mucosal inflammation and formation of crypt abscesses, epithelial necrosis, and mucosal ulceration
Early stages mucosa membrane appears finely granular and friable
Severe cases show large oozing ulcerations and pseudopolyps

66. Ulcerative Colitis Clinical features:
Mild: <4 bm per day, no systemic symptoms, and few extraintestinal manifestations. (account for 60% of all UC patients)
Severe: frequent bm’s, anemia, fever, wt loss, tachycardia, low albumin, frequent extraintestinal manifestations. (accounts for 15% of all patients and 90% of mortality)

67. Ulcerative Colitis
Moderate: manifesations are less severe and respond well to treatment. Typically have left sided colitis, but can have pancolitis.

68. Ulcerative Colitis
Characterized by: intermittent attacks of acute disease with remission between attacks
Unfavorable prognosis and increased mortality is seen with higher severity and extent of disease, short interval between attacks, and onset of disease after 60

69. Ulcerative Colitis
Extraintestinal complications: arthritis, ankylosing spondylitis, episcleritis, uveitis, pyoderma gangrenosum, erythema nodosum, liver disease(similar to that found in Crohn disease)

70. Ulcerative Colitis
Complications: hemorrhage, toxic megacolon, perirectal abscesses and fistulas, colon ca, perforation

71. Ulcerative Colitis Dx: lab findings are nonspecific.
Diagnosis is made by Hx of abd cramps and diarrhea, mucoid stools, stool negative for ova/parasites, negative stool cultures
confirmation of disease by colonoscopy showing granular, friable, ulceration of the mucosa, and sometimes pseudopolyps

72. Ulcerative Colitis Differential Dx: similar to that of Crohn disease.
Also be aware of STD’s when confined to the rectum

73. Ulcerative Colitis Treatment:
Severe UC: IV steroids, fluid replacement, electrolyte correction, broad spectrum atbx(amp and clindamycin or flagyl)
Cyclosporine has been advocated for steroid refractory cases
NG for toxic megacolon just as in crohn disease

74. Ulcerative Colitis
Mild to moderate: majority of cases can be treated as outpatient with daily prednisone 40-60mg
Active proctitis, proctosigmoiditis, and left side colitis can be treated with 5-aminosalicylic acid enemas or topical steroid preparations

75. Ulcerative Colitis Treatment is very similar to Crohn disease
Other supportive measures include metamucil or other bulking agents
Anti-diarrheals should be used with caution in case of toxic megacolon

76. Ulcerative Colitis
Disposition:Fulminant attacks should be hospitalized for aggressive IVF and elctrolyte correction.
Complications should be managed with appropriate surgical or GI consult
Mild-moderate: may be discharged with close follow up secured. Instructions on when to return should be given

77. Pseudomembranous Colitis
Inflammatory bowel disorder with membrane-like yellowish plaques of exudate overlie and replace necrotic intestinal mucosa

78. Pseudomembranous Colitis
Epidemiology:
Clostridium Difficile- spore forming obligate anaerobic bacillus
3 types: neonatal, post-operative and antibiotic associated
Risk factors: recent atbx, GI surgery, severe medical illness, advancing age
Transmission: direct contact and objects

79. Pseudomembranous Colitis
Pathophysiology: 10-25% of hospital patients are colonized
Diarrhea in recently hospitalized person should suggest C.difficile
Broad spectrum atbx such as clindamycin, cephalosporins, amp/amox- alter gut flora and allow C.difficile to flourish
However any atbx can lead to C.difficile

80. Pseudomembranous Colitis
C. difficile produces
toxin A enterotoxin
toxin B cytotoxin
Toxins interact and produce the colitis and associated symptoms

81. Pseudomembranous Colitis
Clinical features: from frequent mucoid, watery stools to profuse toxic diarrhea(>20-30 stools/day), abdominal pain, fever, leukocytosis, dehydration, hypovolemia
Stool exam may reveal fecal leukocytes

82. Pseudomembranous Colitis
Complications: severe electrolyte imbalance, hypotension, anasarca from low albumin, toxic megacolon, bowel perforation
Onset is typically 7-10 days after starting atbx therapy

83. Pseudomembranous Colitis
Extraintestinal complications are rare, but include: arthritis, visceral abscesses, cellulitis, necrotizing fasciitis, osteomyelitis, prostheitc device infection

84. Pseudomembranous Colitis
Diagnosis: hx of diarrhea that develops during or within 2 weeks of atbx treatment.
Confirmed by stool for C.difficile toxin and colonoscopy
Most labs use ELISA to detect C.difficile toxins even though there are many other modes
5-20% of patients require more than one stool to diagnose

85. Pseudomembranous Colitis
Treatment: d/c atbx, supportive IVF, electrolyte correction, flagyl 250 mg qid, or vancomycin mg po qid(alternative regimen)
25% of patients will respond to supportive measures only
Severely ill patients should hospitalized

86. Pseudomembranous Colitis
Relapses occur in 10-20% of patients
Use of anti-diarrheals should be avoided
Surgery or steroids are rarely needed

87. Pseudomembranous Colitis
Disposition:
Severe diarrhea, symptoms that persist despite outpatient management, or those with systemic response(fever, leukocytosis, severe abdominal pain) should be hospitalized
Suspected perforation, toxic megacolon or failure to respond to medical treatment need a surgical consult

88. Pseudomembranous Colitis
For patients who are discharged whom: good oral intake must be encouraged. Flagyl or vancomycin are equally effective for treatment.

89. Diverticulitis
Acute inflammation of the wall of a diverticulum and surrounding tissue
Caused by either a micro- or macroperforation

90. Diverticulitis Epidemiology:
Acquire disease of the colon has become common in industrialized nations
Approximately 1/3 of population will acquire diverticuli by age 50 and 2/3 by age 85
Rare <20 years

91. Diverticulitis
Diverticulitis is estimated in 10-25% of people with known diverticulosis
Incidence increases with age
Only 2-4 % are < 40
Diverticulitis in younger age is associated with more complications requiring surgical intervention

92. Diverticulitis
Frequency is slightly higher in men, the incidence is on the rise in women

93. Diverticulitis Pathophysiology: Cause is not known
Low residue diets have been implicated
Acute complications: Inflammation(and associated complications) and Bleeding

94. Diverticulitis
Inflammation is the most common complication of diverticulosis
Mechanism was thought to occur when fecal material was inspissated in the neck of a diverticulum, resulting in bacterial proliferation, mucous secretion, and distention

95. Diverticulitis
More commonly, it results from high pressure in the colon, erosion of diverticulum wall, microperforation, and inflammation.
Free perforation can occur with generalized peritonitis, but is uncommon

96. Diverticulitis
Other complications: obstruction and fistula formation between the bladder and diverticulum

97. Diverticulitis Clinical Features: most common symptom is pain.
Described as steady, deep discomfort in the LLQ
Other complaints: change in bowel habit, tenesmus, dysuria, frequency, UTI, distention, nausea, vomiting,

98. Diverticulitis
Presentation may be indistinguishable for acute appendicitis
Diverticulitis should always be considered in patient >50 with abdominal pain
Perforation is characterized by sudden lower abdominal pain progressing general abdominal pain

99. Diverticulitis
Physical exam: frequently fever of 38 C, localized abdominal tenderness, voluntary guarding, rebound, rectal tenderness on left side, possibly occult blood +,
As always, Pelvic should be done with female
Watch for signs of peritonitis or perforation

100. Diverticulitis Diagnosis: typically suspected by Hx and physical
Abdominal plain films can show partial SBO, free air, extraluminal air
CT is procedure of choice. Demonstrates inflammation of pericolic fat, diverticula, thickening of bowel wall, peridiverticular abscess

101. Diverticulitis
Barium enema can be done, but are insensitive and may cause perforation due to the introduction of barium at high pressures
Routine labs include: CBC, electrolytes, BUN/creatinine, UA
Sigmoidoscopy and colonoscopy are performed only after inflammation has decreased

102. Diverticulitis Differential Dx:
Similar to that of appendicititis, Crohn disease, UC, and C.difficile colitis

103. Diverticulitis Treatment:
NPO, IVF, electrolyte correction, NG for obstruction, Broad spectrum atbx, observation for complications
Outpatient management includes liquids only for 48 hours and oral antibiotics(Cipro, flagyl, bactrim, ampicillin)

104. Diverticulitis Disposition:
Patients without signs of peritonitis or systemic infection maybe treated as outpatients with careful follow up arranged. Should be instructed to return for fever, increasing pain, unable to tolerate po.

105. Diverticulitis
If patient shows signs of systemic infection, perforation or peritonitis then they should be hospitalized with a surgical consult

106. Questions:
1. With a retrocecal appendix, the pain of acute appendicitis may localize to the right flank. (True or false)
2. Outpatient antibiotics is the standard treatment of acute appendicitis. (True or False)

107. Questions:
3. Special populations of people that may have delayed diagnosis of acute appendicitis due to atypical presentation include:
A.) very young patients
B.) elderly patients
C.) AIDS patients
D.) Pregnant patients
E.) all of the above

108. Questions: 4. Crohn disease can involve:
A.) any part of the GI tract(from mouth to anus
B.) colon only
C.) esophagus only
D.) small intestine only

109. Questions:
5. Ulcerative colitis and Crohn disease are both considered types of inflammatory bowel disease. (True or False)
Answers: 1T, 2F, 3E, 4A, 5T