acute appendicitis

Acute AppendicitisAcute Appendicitis

EpidemiologyEpidemiology

• 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.

PathophysiologyPathophysiology

• 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


• 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.


• Increased pressure also leads to arterial stasis and tissue infarction

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


• 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.


• 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


• 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.


• 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


• 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

HistoryHistory

• 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

HistoryHistory

• 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

HistoryHistory

• 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 ExamPhysical 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


• 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


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


• 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


• 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

DiagnosisDiagnosis

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

DiagnosisDiagnosis

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

• Additional studies: CBC, UA, imaging studies

DiagnosisDiagnosis

• 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

DiagnosisDiagnosis

• 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

DiagnosisDiagnosis

• 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

DiagnosisDiagnosis

• 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

DiagnosisDiagnosis

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

DiagnosisDiagnosis

• 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.

DiagnosisDiagnosis

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

Special PopulationsSpecial 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

TreatmentTreatment

• 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

TreatmentTreatment

• 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

DispositionDisposition

• 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


• 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


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

Ileitis, Colitis, and Ileitis, Colitis, and DiverticulitisDiverticulitis

Crohn DiseaseCrohn 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


• 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.


• Cytokines,including IL and TNF have been implicated in perpetuating the inflammatory response.

• Anti-TNF(remicade) drugs have shown efficacy in treating 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


• 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


• 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


• 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


• Clinical course and manifestation depends of anatomic distribution.

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


• 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


• Dermatologic complications: erythema nodosum and pyoderma gangrenosum

• Ocular: episcleritis and uveitis

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


• Vascular: thromboembolic disease, vasculitis, arteritis

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


• 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


• 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


• 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.


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


• 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.


• 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


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


• 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


• 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


• 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


• 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


• 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


• 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


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


• 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


• 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.

Ulcerative ColitisUlcerative 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


• 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


• 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


• 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)


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


• 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


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


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


• 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


• Differential Dx: similar to that of Crohn disease.

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


• 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


• 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


• 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


• 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

Pseudomembranous ColitisPseudomembranous Colitis

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


• 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


• 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


• C. difficile produces

• toxin A enterotoxin

• toxin B cytotoxin

• Toxins interact and produce the colitis and associated symptoms


• 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


• Complications: severe electrolyte imbalance, hypotension, anasarca from low albumin, toxic megacolon, bowel perforation

• Onset is typically 7-10 days after starting atbx therapy


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


• 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


• 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


• Relapses occur in 10-20% of patients

• Use of anti-diarrheals should be avoided

• Surgery or steroids are rarely needed


• 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


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

DiverticulitisDiverticulitis

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

• Caused by either a micro- or macroperforation


• 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 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


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


• Pathophysiology:

• Cause is not known

• Low residue diets have been implicated

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


• 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


• 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


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


• 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,


• 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


• 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


• 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


• 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


• Differential Dx:

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


• 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)


• 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.


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

Questions: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)


• 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


• 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


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

• Answers: 1T, 2F, 3E, 4A, 5T

acute appendicitis

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occursrlq pain

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triggers somatic pain

periumbilical area

rlq localization