Transcript Acute Appendicitis

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 10th
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
• 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.
• 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 1940%
• 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 46h observation with surgical consult if
serial exam changes or imaging studies
confirm
Disposition
• Group 3: remote possibility of appendicitisobserve 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 nonJews
• 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
• Crohn’s 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, Kaposi’s 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 bm’s, 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 STD’s 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 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
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
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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
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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