Acute appendicitis
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Acute Appendicitis - PowerPoint PPT Presentation

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Acute Appendicitis. 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. . Pathophysiology.

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Epidemiology l.jpg

  • 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.

Pathophysiology l.jpg

  • 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

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  • 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.

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  • Increased pressure also leads to arterial stasis and tissue infarction

  • End result is perforation and spillage of infected appendiceal contents into the peritoneum

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  • 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.

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  • 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

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  • 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.

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  • 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

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  • 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

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  • 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

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  • 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

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  • 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

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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

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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

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Physical Exam

  • Additional components that may be helpful in diagnosis: rebound tenderness, voluntary guarding, muscular rigidity, tenderness on rectal

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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

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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

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

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  • Women of child bearing age need a pelvic exam and a pregnancy test.

  • Additional studies: CBC, UA, imaging studies

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  • 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

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  • 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

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  • 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

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  • 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

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

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  • 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.

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

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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

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  • 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

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  • 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

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  • 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

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  • 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 12-24 h

  • Also advised to avoid strong analgesia

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

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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

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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.

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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

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Crohn Disease

  • Epidemiology: peak incidence is 15-22 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

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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

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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

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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

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Crohn Disease

  • Clinical course and manifestation depends of anatomic distribution.

  • 30% involves only small bowel, 30% only colon, and 50% involves both

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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

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Crohn Disease

  • Dermatologic complications: erythema nodosum and pyoderma gangrenosum

  • Ocular: episcleritis and uveitis

  • Hepatobiliary: pericholangitis, chronic hepatitis, primary sclerosing cholangitis, cholangiocarcinoma, pancreatitis, gallstones

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Crohn Disease

  • Vascular: thromboembolic disease, vasculitis, arteritis

  • Other: anemia, malnutrition, hyperoxaluria leading to nephrolithiasis, myeloplastic disease, osteomyelitis, osteonecrosis

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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

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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

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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.

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Crohn Disease

  • Incidence of malignancy is 3 times higher in Crohn disease than in general population

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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.

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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

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Crohn Disease

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

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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.

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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

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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

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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

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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

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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

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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

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Crohn Disease

  • Diarrhea can be controlled using imodium, lomotil, or questran

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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

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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.

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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

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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

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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

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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)

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Ulcerative Colitis

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

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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

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Ulcerative Colitis

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

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Ulcerative Colitis

  • Complications: hemorrhage, toxic megacolon, perirectal abscesses and fistulas, colon ca, perforation

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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

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Ulcerative Colitis

  • Differential Dx: similar to that of Crohn disease.

  • Also be aware of STD’s when confined to the rectum

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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

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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

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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

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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

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Pseudomembranous Colitis

  • Inflammatory bowel disorder with membrane-like yellowish plaques of exudate overlie and replace necrotic intestinal mucosa

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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

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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

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Pseudomembranous Colitis

  • C. difficile produces

  • toxin A enterotoxin

  • toxin B cytotoxin

  • Toxins interact and produce the colitis and associated symptoms

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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

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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

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Pseudomembranous Colitis

  • Extraintestinal complications are rare, but include: arthritis, visceral abscesses, cellulitis, necrotizing fasciitis, osteomyelitis, prostheitc device infection

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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

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Pseudomembranous Colitis

  • Treatment: d/c atbx, supportive IVF, electrolyte correction, flagyl 250 mg qid, or vancomycin 125-250mg po qid(alternative regimen)

  • 25% of patients will respond to supportive measures only

  • Severely ill patients should hospitalized

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Pseudomembranous Colitis

  • Relapses occur in 10-20% of patients

  • Use of anti-diarrheals should be avoided

  • Surgery or steroids are rarely needed

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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

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Pseudomembranous Colitis

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

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  • Acute inflammation of the wall of a diverticulum and surrounding tissue

  • Caused by either a micro- or macroperforation

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  • 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

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  • 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

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  • Frequency is slightly higher in men, the incidence is on the rise in women

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  • Pathophysiology:

  • Cause is not known

  • Low residue diets have been implicated

  • Acute complications: Inflammation(and associated complications) and Bleeding

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  • 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

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  • 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

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  • Other complications: obstruction and fistula formation between the bladder and diverticulum

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  • 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,

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  • 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

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  • 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

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  • 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

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  • 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

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  • Differential Dx:

  • Similar to that of appendicititis, Crohn disease, UC, and C.difficile colitis

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  • 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)

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  • 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.

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

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  • 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)

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  • 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

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  • 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

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  • 5. Ulcerative colitis and Crohn disease are both considered types of inflammatory bowel disease. (True or False)

  • Answers: 1T, 2F, 3E, 4A, 5T