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
‡ 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

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

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

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

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

.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.

the appendix ca be shifted and patients can present with RUQ pain .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.

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

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

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

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 .

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 .

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 .

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

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

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

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

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

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

Diagnosis ‡ UA: abnormal UA results are found in 1940% ‡ Abnormalities include: pyuria. bacteruria ‡ Presence of >20 wbc per field should increase consideration of Urinary tract pathology . hematuria.

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

appendicolith.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. periappendiceal abscess .Diagnosis ‡ Graded Compression US: reported sensitivity 94.7% and specificity 88.

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

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

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

very old. 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 . pregnant.Special Populations ‡ Very young.

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

375g or Unasyn 3g ‡ Also. short acting narcotics should be used for pain management .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.

benefit from imaging and 46h observation with surgical consult if serial exam changes or imaging studies confirm .prompt surgical intervention ‡ Group 2: suspicious. but not diagnosed appendicitis.Disposition ‡ Abdominal pain patients can be put in 4 groups ‡ Group 1: classic presentation for Acute appendicitis.

and they should be seen by PCP in 12-24 h ‡ Also advised to avoid strong analgesia . 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.Disposition ‡ Group 3: remote possibility of appendicitisobserve in ED for serial exams.

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

and Diverticulitis .Ileitis. Colitis.

terminal ileitis. ‡ 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. granulomatous ileocolitis .Crohn Disease ‡ Chronic granulomatous inflammatory disease of the GI tract.

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

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 .

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 nonJews ‡ More common in whites vs blacks ‡ 10-15% have family hx .

and abscesses . fistulas.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.

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

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

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

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 .

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

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

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

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

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

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

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

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

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

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

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

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

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

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

or in patients with contraindications to surgery Response to immunosuppressant agents takes 3-6 months .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.

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

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

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

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

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

5 fold increase for Crohn disease .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.

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

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

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

short interval between attacks. and onset of disease after 60 .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.

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

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

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

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

Ulcerative Colitis ‡ Treatment: ‡ Severe UC: IV steroids. 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 . fluid replacement.

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

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 .

Instructions on when to return should be given .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.

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

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

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

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

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

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

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

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

supportive IVF. flagyl 250 mg qid.Pseudomembranous Colitis ‡ Treatment: d/c atbx. or vancomycin 125-250mg po qid(alternative regimen) ‡ 25% of patients will respond to supportive measures only ‡ Severely ill patients should hospitalized . electrolyte correction.

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

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

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

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

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 .

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 .

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

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

and distention . resulting in bacterial proliferation.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. mucous secretion.

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

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

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

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 .

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

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

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

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

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

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

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

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

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

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

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

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