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

Pathophysiology
Eventually the pressure exceeds capillary
perfusion pressure and venous and
lymphatic drainage are obstructed.
With vascular compromise, epithelial
mucosa breaks down and bacterial
invasion by bowel flora occurs.
Pathophysiology
Increased pressure also leads to arterial
stasis and tissue infarction
End result is perforation and spillage of
infected appendiceal contents into the
peritoneum
Pathophysiology
Initial luminal distention triggers visceral
afferent pain fibers, which enter at the 10
th

thoracic vertebral level.
This pain is generally vague and poorly
localized.
Pain is typically felt in the periumbilical or
epigastric area.
Pathophysiology
As inflammation continues, the serosa and
adjacent structures become inflamed
This triggers somatic pain fibers,
innervating the peritoneal structures.
Typically causing pain in the RLQ

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.
Pathophysiology
Exceptions exist in the classic
presentation due to anatomic variability of
the appendix
Appendix can be retrocecal causing the
pain to localize to the right flank
In pregnancy, the appendix ca be shifted
and patients can present with RUQ pain
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
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 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 McBurneys point
Physical Exam
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
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.
Additional studies: CBC, UA, imaging
studies
Diagnosis
CBC: the WBC is of limited value.
Sensitivity of an elevated WBC is 70-90%,
but specificity is very low.
But, +predictive value of high WBC is 92%
and predictive value is 50%
CRP and ESR have been studied with
mixed results
Diagnosis
UA: abnormal UA results are found in 19-
40%
Abnormalities include: pyuria, hematuria,
bacteruria
Presence of >20 wbc per field should
increase consideration of Urinary tract
pathology
Diagnosis
Imaging studies: include X-rays, US, CT
Xrays of abd are abnormal in 24-95%
Abnormal findings include: fecalith,
appendiceal gas, localized paralytic ileus,
blurred right psoas, and free air
Abdominal xrays have limited use b/c the
findings are seen in multiple other
processes

Diagnosis
Graded Compression US: reported
sensitivity 94.7% and specificity 88.9%
Basis of this technique is that normal
bowel and appendix can be compressed
whereas an inflamed appendix can not be
compressed
DX: noncompressible >6mm appendix,
appendicolith, periappendiceal abscess
Diagnosis
Limitations of US: retrocecal appendix
may not be visualized, perforations may
be missed due to return to normal
diameter
Diagnosis
CT: best choice based on availability and
alternative diagnoses.
In one study, CT had greater sensitivity,
accuracy, -predictive value
Even if appendix is not visualized,
diagnose can be made with localized fat
stranding in RLQ.
Diagnosis
CT appears to change management
decisions and decreases unnecessary
appendectomies in women, but it is not as
useful for changing management in men.
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

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

Treatment
There are multiple acceptable antibiotics
to use as long there is anaerobic flora,
enterococci and gram(-) intestinal flora
coverage
One sample monotherapy regimen is
Zosyn 3.375g or Unasyn 3g
Also, short acting narcotics should be
used for pain management
Disposition
Abdominal pain patients can be put in 4
groups
Group 1: classic presentation for Acute
appendicitis- prompt surgical intervention
Group 2: suspicious, but not diagnosed
appendicitis- benefit from imaging and 4-
6h observation with surgical consult if
serial exam changes or imaging studies
confirm
Disposition
Group 3: remote possibility of appendicitis-
observe in ED for serial exams; if no
change and course remains benign patient
can D/C with dx of nonspecific abd pain
Patients are given instructions to return if
worsening of symptoms, and they should
be seen by PCP in 12-24 h
Also advised to avoid strong analgesia
Disposition
Group 4: high risk population(including
elderly, pediatric, pregnant and
immunocomprimised)- require high index
of suspicion and low threshold for imaging
and surgical consultation
Ileitis, Colitis, and
Diverticulitis
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
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.

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 non-
Jews
More common in whites vs blacks
10-15% have family hx
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
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
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
Crohns should also be considered when
evaluating FUO
Crohn Disease
Clinical course and manifestation depends
of anatomic distribution.
30% involves only small bowel, 30% only
colon, and 50% involves both
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
Crohn Disease
Dermatologic complications: erythema
nodosum and pyoderma gangrenosum
Ocular: episcleritis and uveitis
Hepatobiliary: pericholangitis, chronic
hepatitis, primary sclerosing cholangitis,
cholangiocarcinoma, pancreatitis,
gallstones
Crohn Disease
Vascular: thromboembolic disease,
vasculitis, arteritis
Other: anemia, malnutrition, hyperoxaluria
leading to nephrolithiasis, myeloplastic
disease, osteomyelitis, osteonecrosis
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
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
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.
Crohn Disease
Incidence of malignancy is 3 times higher
in Crohn disease than in general
population
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.

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
Crohn Disease
Findings of bowel wall thickening,
mesenteric edema, local abscess
formation suggest Crohn disease.
Crohn Disease
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.
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
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
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
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
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
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
Crohn Disease
Diarrhea can be controlled using imodium,
lomotil, or questran
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
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.
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

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
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
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 bms, anemia, fever, wt loss,
tachycardia, low albumin, frequent
extraintestinal manifestations. (accounts for 15%
of all patients and 90% of mortality)
Ulcerative Colitis
Moderate: manifesations are less severe
and respond well to treatment. Typically
have left sided colitis, but can have
pancolitis.

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
Ulcerative Colitis
Extraintestinal complications: arthritis,
ankylosing spondylitis, episcleritis, uveitis,
pyoderma gangrenosum, erythema
nodosum, liver disease(similar to that
found in Crohn disease)
Ulcerative Colitis
Complications: hemorrhage, toxic
megacolon, perirectal abscesses and
fistulas, colon ca, perforation
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
Ulcerative Colitis
Differential Dx: similar to that of Crohn
disease.
Also be aware of STDs when confined to
the rectum
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
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
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
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
Pseudomembranous Colitis
Inflammatory bowel disorder with
membrane-like yellowish plaques of
exudate overlie and replace necrotic
intestinal mucosa
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


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

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

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, 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
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
Diverticulitis
Frequency is slightly higher in men, the
incidence is on the rise in women
Diverticulitis
Pathophysiology:
Cause is not known
Low residue diets have been implicated
Acute complications: Inflammation(and
associated complications) and Bleeding

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

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

Diverticulitis
Other complications: obstruction and
fistula formation between the bladder and
diverticulum
Diverticulitis
Clinical Features: most common symptom
is pain.
Described as steady, deep discomfort in
the LLQ
Other complaints: change in bowel habit,
tenesmus, dysuria, frequency, UTI,
distention, nausea, vomiting,
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
Diverticulitis
Physical exam: frequently fever of 38 C,
localized abdominal tenderness, voluntary
guarding, rebound, rectal tenderness on
left side, possibly occult blood +,
As always, Pelvic should be done with
female
Watch for signs of peritonitis or perforation
Diverticulitis
Diagnosis: typically suspected by Hx and
physical
Abdominal plain films can show partial
SBO, free air, extraluminal air
CT is procedure of choice. Demonstrates
inflammation of pericolic fat, diverticula,
thickening of bowel wall, peridiverticular
abscess
Diverticulitis
Barium enema can be done, but are
insensitive and may cause perforation due
to the introduction of barium at high
pressures
Routine labs include: CBC, electrolytes,
BUN/creatinine, UA
Sigmoidoscopy and colonoscopy are
performed only after inflammation has
decreased
Diverticulitis
Differential Dx:
Similar to that of appendicititis, Crohn
disease, UC, and C.difficile colitis
Diverticulitis
Treatment:
NPO, IVF, electrolyte correction, NG for
obstruction, Broad spectrum atbx,
observation for complications
Outpatient management includes liquids
only for 48 hours and oral
antibiotics(Cipro, flagyl, bactrim, ampicillin)
Diverticulitis
Disposition:
Patients without signs of peritonitis or
systemic infection maybe treated as
outpatients with careful follow up
arranged. Should be instructed to return
for fever, increasing pain, unable to
tolerate po.

Diverticulitis
If patient shows signs of systemic
infection, perforation or peritonitis then
they should be hospitalized with a surgical
consult
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)
Questions:
3. Special populations of people that may have
delayed diagnosis of acute appendicitis due to
atypical presentation include:
A.) very young patients
B.) elderly patients
C.) AIDS patients
D.) Pregnant patients
E.) all of the above
Questions:
4. Crohn disease can involve:
A.) any part of the GI tract(from mouth to
anus
B.) colon only
C.) esophagus only
D.) small intestine only

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

Answers: 1T, 2F, 3E, 4A, 5T