a cute appendic its

8/6/2019 A Cute Appendic Its

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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.


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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


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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 ofinfected 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 orrectum 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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HistoryHistory

Primary symptom: abdominal pain

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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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


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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 of patients


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Physical ExamPhysical Exam

Findings depend on duration of illness

prior to exam.

E

arly on patients may not have localizedtenderness

With progression there is tenderness to

deep palpation over McBurneys point


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McBurneys Point: just below the middle of

a line connecting the umbilicus and the

ASIS

Rovsings: pain in RLQ with palpation to

LLQ

Rectal exam: pain can be most

pronounced if the patient has pelvic

appendix


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Additional components that may be helpful

in diagnosis: rebound tenderness,

voluntary guarding, muscular rigidity,

tenderness on rectal


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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 ispositive


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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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DiagnosisDiagnosis

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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DiagnosisDiagnosis

Women of child bearing age need a pelvic

exam and a pregnancy test.

Additional studies: CBC, UA, imagingstudies


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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

andE

SR have been studied withmixed results


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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


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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 thefindings are seen in multiple other

processes


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DiagnosisDiagnosis

Graded Compression US: reported

sensitivity 94.7% and specificity 88.9%

Basis of this technique is that normalbowel and appendix can be compressed

whereas an inflamed appendix can not be

compressed

DX: noncompressible >6mm appendix,

appendicolith, periappendiceal abscess


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DiagnosisDiagnosis

Limitations of US: retrocecal appendix

may not be visualized, perforations may

be missed due to return to normal

diameter


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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.


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DiagnosisDiagnosis

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 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


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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


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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


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DispositionDisposition

Abdominal pain patients can be put in 4groups

Group 1: classic presentation for Acute

appendicitis- prompt surgical intervention

Group 2: suspicious, but not diagnosedappendicitis- benefit from imaging and 4-

6h observation with surgical consult ifserial exam changes or imaging studiesconfirm


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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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Ileitis, Colitis, andIleitis, Colitis, and

DiverticulitisDiverticulitis


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Crohn DiseaseCrohn Disease

Chronic granulomatous inflammatory

disease of the GI tract.

Can involve any part of GI tract frommouth 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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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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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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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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Pathology: most important is theinvolvement of all layers of the bowel andextension into mesenteric lymph nodes

Disease has skip areas between involvedareas

Longitudinal deep ulcers and

cobblestoning of mucosa are characteristic These result in fissures, fistulas, and

abscesses


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Clinical features: variable and

unpredictable

Abd pain, anorexia, diarrhea, and weightloss are present in most cases

1/3 of patients develop perianal fissures or

fistulas, abscesses, or rectal prolapse


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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

Crohns should also be considered when

evaluating FUO


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Clinical course and manifestation depends

of anatomic distribution.

30% involves only small bowel, 30% onlycolon, and 50% involves both


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Recurrence rate is as high as 50% for

those responding to medical management

Rate is even higher for those requiringsurgery

Incidence of hematochezia and perianal

disease is higher when the colon is

involved


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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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Vascular: thromboembolic disease,

vasculitis, arteritis

Other: anemia, malnutrition, hyperoxalurialeading to nephrolithiasis, myeloplastic

disease, osteomyelitis, osteonecrosis


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Complications: >75% of patients will

require surgery within the first 20 years

Abscesses present with pain andtenderness, 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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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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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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Incidence of malignancy is 3 times higher

in Crohn disease than in general

population


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Diagnosis: history, Upper GI, air-contrast

barium enema and colonoscopy

Characteristic radiologic findings in smallintestine include: segmental narrowing,

destruction of normal mucosal pattern, and

fistulas.


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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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Findings of bowel wall thickening,

mesenteric edema, local abscess

formation suggest Crohn disease.


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Differential Dx: lymphoma, ileocecal

amebiasis, sarcoidosis, deep chronic

mycotic infections involving GI tract, GI

TB, Kaposis sarcoma, campylobacter,

Yersinia, ulcerative colitis, C.diff, ischemic

colitis.


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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 ofsymptoms and preventing complications


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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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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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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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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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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, ILtherapy may also be beneficial


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Diarrhea can be controlled using imodium,

lomotil, or questran


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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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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 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

E

tiology remains unknown


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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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Pathology: involves mucosa andsubmucosa

Mucosal inflammation and formation of

crypt abscesses, epithelial necrosis, andmucosal ulceration

Early stages mucosa membrane appears

finely granular and friable Severe cases show large oozingulcerations and pseudopolyps


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Clinical features:

Mild:


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Moderate: manifesations are less severe

and respond well to treatment. Typically

have left sided colitis, but can have

pancolitis.


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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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Extraintestinal complications: arthritis,

ankylosing spondylitis, episcleritis, uveitis,

pyoderma gangrenosum, erythema

nodosum, liver disease(similar to thatfound in Crohn disease)


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Complications: hemorrhage, toxic

megacolon, perirectal abscesses and

fistulas, colon ca, perforation


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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 themucosa, and sometimes pseudopolyps


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Differential Dx: similar to that of Crohn

disease.

Also be aware of STDs when confined to

the rectum


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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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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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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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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 onwhen to return should be given


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Pseudomembranous ColitisPseudomembranous Colitis

Inflammatory bowel disorder with

membrane-like yellowish plaques of

exudate overlie and replace necrotic

intestinal mucosa


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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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C. difficile produces

toxin A enterotoxin

toxin B cytotoxin Toxins interact and produce the colitis and

associated symptoms


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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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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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Extraintestinal complications are rare, but

include: arthritis, visceral abscesses,

cellulitis, necrotizing fasciitis,

osteomyelitis, prostheitc device infection


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Diagnosis: hx of diarrhea that developsduring 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 othermodes

5-20% of patients require more than onestool to diagnose


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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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Relapses occur in 10-20% of patients

Use of anti-diarrheals should be avoided

Surgery or steroids are rarely needed


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Disposition:

Severe diarrhea, symptoms that persistdespite outpatient management, or those

with systemic response(fever,leukocytosis, severe abdominal pain)should be hospitalized

Suspected perforation, toxic megacolon orfailure to respond to medical treatmentneed a surgical consult


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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


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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

Di i li iDi i li i


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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,

Di ti litiDi ti liti


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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, peridiverticularabscess



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Barium enema can be done, but areinsensitive and may cause perforation dueto the introduction of barium at high

pressures Routine labs include: CBC, electrolytes,

BUN/creatinine, UA

Sigmoidoscopy and colonoscopy areperformed only after inflammation hasdecreased



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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

Q tiQ ti


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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)

Q tiQ ti


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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

Q estionsQ estions


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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

a cute appendic its

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