Transcript GI_1_-_Abd_Pain_2015x

Nursing 870
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Approach to Abdominal Pain
Appendicitis
Acute Hepatitis
Diverticulitis
 Abdominal
pain
 Diarrhea
 Constipation
 Focus on common conditions
 Begin by ruling out the red flags
surgical problems
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and
AAA
Mesenteric ischemia
Appendicitis
Cholecystitis
Perforated ulcer
Peritonitis
Mesenteric vascular occlusion
 Begin the work-up
 Let the location drive
the evaluation
RUQ
Biliary: Cholecystitis, cholelithiasis,
cholangitis
Colonic: Colitis, diverticulitis
Hepatic: abscess, hepatitis, mass
Pulmonary: pneumonia, embolus
Renal: nephrolithiasis, pyelonephritis
Epigastric
Biliary: cholecystitis, cholelithiasis, cholangitis
Cardiac: myocardial infarction, pericarditis
Gastric: esophagitis, gastritis, peptic ulcer
Pancreatic: mass, pancreatitis
Vascular: aortic dissection, mesenteric
ischemia
LUQ
Cardiac: angina, myocardial infarction,
pericarditis
Gastric: esophagitis, gastritis, peptic ulcer
Pancreatic: mass, pancreatitis
Renal: nephrolithiasis, pyelonephri
Vascular: aortic dissection, mesenteric ischemia
Periumbilical
Colonic: early appendicitis
Gastric: esophagitis, gastritis, peptic ulcer, small-bowel
mass or obstruction
Vascular: aortic dissection, mesenteric ischemia
RLQ
Colonic: appendicitis, colitis, diverticulitis, IBD, IBS
Gynecologic: ectopic pregnancy, fibroids, ovarian
mass, torsion, PID
Renal: nephrolithiasis, pyelonephritis
Suprapubic
Colonic: appendicitis, colitis, diverticulitis, IBD,
IBS
Gynecologic: ectopic pregnancy, fibroids, ovarian
mass, torsion, PID
Renal: cystitis, nephrolithiasis, pyelonephritis
LLQ
Colonic: colitis, diverticulitis, IBD, IBS
Gynecologic: ectopic pregnancy, fibroids, ovarian
mass, torsion, PID
Renal: nephrolithiasis, pyelonephritis
Any location
Abdominal wall: herpes zoster, muscle strain, hernia
Other: bowel obstruction, mesenteric ischemia,
peritonitis, narcotic withdrawal, sickle cell crisis,
porphyria, IBD, heavy metal poisoning
 Fever
 Protracted
vomiting
 Syncope or presyncope
 GI blood loss
 Can
help to narrow the dx
 General appearance
 Vital signs: any orthostatic changes,
tachycardia, fever
 Focus on the location of pain
• Attention to Resp/CV status with upper abd pain
 Murphy’s
sign
• Cholecystitis
• Not reliable in older adults
 Psoas
sign
• AP
 Rectal
exam warranted
 Pelvic exam often in females
 CBC
• 25% pt with acute AP have no WBC elevation
 Amylase/lipase
(epigastric pain)
• Lipase more specific for pancreatitis, both
elevated
 Liver
function testing
 Urine
 Urine
pregnancy
Location of Pain
Imaging
RUQ
US
LUQ
CT
RLQ
CT with IV contrast
LLQ
CT with oral and IV contrast
Suprapublic
US
 Inflammation
of the inner lining of the
vermiform appendix
 Common cause of acute abdominal pain
 Obstruction of appendiceal lumen
 Increased lumen pressure
 Intestinal bacteria multiply, recruitment
of
WBCs
 Formation of pus and higher lumen pressure
 If obstruction persists, intraluminal pressure
rises above the appendiceal veins
 Venous outflow obstruction
 Appendiceal wall ischemia
 Bacterial invasion of appendiceal wall
 Localized condition may lead to perforation
and gangrene OR peritonitis OR abscess
 Obstruction
related to
• Lymphoid hyperplasia sec. to IBD
• Infections
• Fecal stasis and fecaliths
• Parasites (Eastern countries)
• Foreign bodies and neoplasms (rare)
 Common
surgical emergency
 Higher incidence in US due to dietary
habits
 Current incidence 10 cases/100,000
population
 Some predisposition to families
 Slightly higher in males
 Peaks late teens and declines in older
adults
 Complication
rate of 4-15%
 Delayed diagnosis increases morbidity
and mortality
• Overall mortality 0.2-0.8%
 Perforation
 Peritonitis
 Wound infections
 Misdiagnosed
in up to 20% of cases
 Classic symptoms (duration of symptoms
< 48 hrs)
• Abdominal pain
 Periumbilical or epigastric migrating to RLQ
(sensitivity 80%)
 Nausea, anorexia, vomiting
 With or without fever
 Rebound
tenderness
 Pain on percussion
 Rigidity
 Guarding
 RLQ tenderness up to 96%; is nonspecific
• LLQ pain may also occur
 Evaluate
the GI, GU, Resp systems
 Pelvic exam in women
 Rectal exam
Characteristic
Score
M= Migration of pain to RLQ
1
A= Anorexia
1
N = Nausea and vomiting
1
T = Tenderness in RLQ
2
R = Rebound pain
1
E = Elevated temperature
1
L = Leukocytosis
2
S = Shift of WBCs to the left
1
Total
10
 Scores:
• 0-3: Discharge without scanning (3.6%
incidence)
• 4-7: CT scan (32% incidence)
• >7: Surgical consult (78% incidence)
• Not highly reliable
• Not likely to improve clinician's judgment
 Nonpregnant
women
• In up to 33% of nonpregnant women
• Seen as PID, UTI, gastroenteritis
 Older
adults
• May see symptoms > 48 hrs
• Diagnostic delay increases morbidity and
mortality
 CBC
• >80 % patients with AP have WBC >10,500
• Neutrophilia < 75%
• Not reliable in infants, pregnancy, and older adults
 Others if suspect other cause
• Amylase
• Lipase
• UA
• Liver functions
• Urine pregnancy
 CT with oral contrast
 Surgical
consult
 Appendectomy: only curative treatment
 May need antiemetics
 Analgesics
• Usually Morphine sulfate
 Antibiotics
• All patients should receive prior to surgery
• Need aerobic and anaerobic coverage
 Penicillins
 Beta lactams
 Cephalosporins
 Cefotetan and cefoxitin are good choices
 Aminoglycosides
• If PCN allergy: cabapenems good option
 Other
signs (seen in minority of patients)
• Rosvsing sign
• Obturation sign
• Psoas sign
• Dunphy sign
• Markle sign
Type
Transmission
Incubation
Chronic Vaccine
Infection
Hep A
Fecal-oral
Contaminated food/water
Contaminated hand to
mouth
2-7 wks (mean = No
28 day )
Yes
Hep B
Sexual contact
Blood to blood
Mother with virus to
newborn
6wk-6mo
Yes
Yes
Hep C
Blood to blood
Mother to baby low risk
2-26 wks
Yes
No
Hep D
In people with Hep B
Percutaneous or mucosal
contact
3-7 wks
Yes
No
Hep E
Fecal oral
Water contamination
3-8 wks
No
No
 Acute
or Viral Hepatitis
 Defintion (CDC, 2011)
• Discrete onset of symptoms
 Nausea
 Anorexia
 Fever
 Malaise and/or
 Abdominal pain AND
• Jaundice
• Dark urine
• Elevated ALT (aminotransferase) >200IU/L
 Person
to person through fecal-oral route
• Ingestion of contaminated feces of infected
person
• Most infections in US from close personal contact
or through sexual partner
 Water
in undeveloped countries
 Contaminated/undercooked foods
 Travelers
to countries with high
endemicity of HAV
 Men who have sex with men
 Drug use
 Persons with clotting disorders
 Persons working with nonhuman
primates susceptible to HAV
 Vaccination: 2 dose series
 Recommended for
• All children at age 1
• Ages 2-18 (for those not vaccinated)
• Persons traveling or working in countries with high
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rates
Men who have sex with men
Users of illegal injection and noninjection drugs
(methamphetamines)
Occupational risk
Persons with chronic liver disease
Persons with clotting factor disorders
 For
patient or close personal contacts
 Immune globulin (0.02 mL/kg) OR
 Hepatitis A vaccine (as of 2007)
• Single dose of single-antigen Hep A vaccine
 Look
for source of exposure
• Overseas travel
• Lack of immunization
• IV or other drug use
 Other
possible causes
• Acetaminophen overdose
 Prodrome
• Mild flu-like symptoms
 Anorexia
 Nausea and vomiting
 Malaise
 Low grade fever
 Myalgia
 Mild headache
 Icteric
phase
• Dark urine (bilirubinuria) usually first
• Pale stool
• Jaundice (70-80%)
 Less likely in children
• Abdominal pain (40%)
• Pruritis
• Arthralgia
• Skin rash
 Jaundice
 Fever
 Hepatomegaly
 Prolonged cholestasis
• Pruritis
• Fever
• Diarrhea
• Weight loss
• Bilirubin > 10mg/dL
 Increases with age
 Prolonged
jaundice (> 3 mo.)
 Corticosteroids and usodoxycholic acid
may shorten duration
 Acute renal failure
 Interstitial nephritis
 Pancreatitis
 RBC aplasia
 Agranulocytosis
 Bone marrow aplasia
 Heart block
 Guillian-Barre syndrome
 Acute arthritis
 Lupus like syndrome
 Sjogren syndrome
• These are all uncommon
 Relapsing
HAV
• In 3-20% of patients with acute HAV
• Initial recovery followed by return of symptoms
 Hepatitis
E
 Alcoholic hepatitis
 Autoimmune hepatitis
 Hepatitis B, C, D
 Drug induced liver disease
 Acute HIV
 Drug induced hypersensitivity
 Budd-Chiari syndrome
 CMV
 Fever
 Fatigue
 Loss
of appetite
 Nausea
 Vomiting
 Abdominal pain
 Dark urine
 Clay-colored bowel movements
 Joint pain
 Jaundice
 Usually
last < 2 months
• Up to 15% of patients can have prolonged
symptoms or relapse for up to 6 months
 Incubation: average
is 28 days (15-50
days)
 Once symptoms resolve; cannot get the
disease again r/t development of IgG
antibodies
 Lab
Criteria for Diagnosis
• Immunoglobulin M (IgM) antibody to hep A
virus (anti-HAV) positive OR
• Clinical presentation in person with
epidemiologic link to a person with lab
confirmation (household or sexual contact with
infected person during 15-50 days prior to
onset) (CDC, 2011)
 CBC
• May see mild lymphocytosis
• May see low grade hemolysis
• Rarely RBC aplasia
 Pro-Time
• Usually remain near normal
• Significant increases warrant close monitoring
• If associated with hepatic encephalopathy; may
have hepatic failure
 ALT
 IgM antibody (anti-HAV IgM)
• Remains positive for 3-6 mo after primary infection
• May remain positive up to 12 mo
• False positives are not common
 IgG (anti-HAV IgG)
• Positive after IgM
• Persists for years
• Presence of anti-HAV IgG without IgM indicates past
infection or prior immunization
• Shows protective immunity
 Liver
Enzymes
• ALT
• AST
 Return to normal over 5-20 weeks
 Bilirubin
• Follows rise in ALT/AST
• Can remain elevated for several months
• If elevated > 3 mo indicates cholestatic HAV
 Imaging
studies not usually required
 May need US to r/o other disorders or
chronic liver disease or liver failure
 Liver biopsy
• Not usually required
• May be considered with relapse or uncertain
diagnosis
 Supportive
Care
• May be only requirement if uncomplicated
• Prevent transmission
• Bed rest
• Antiemetics
• Fluids if dehydration
 Diet
• Adequate diet
• No alcohol
• Cautious with meds
 If giving acetaminophen: strict dose <4 g/day
 Return
to work
• With resolution of symptoms
• Minimum of 10 days after onset of jaundice
 May
occur sec. to hepatitis/other causes
 Symptoms and/or diagnosis of liver
disease and development of
• Hepatic encephalopathy
 Mental disorientation
 Changes in LOC
 Coma
• Coagulopathy
 INR > 1.5
 May
occur with Hepatitis A
 More common with Hepatitis E in
pregnant women Or Hepatitis B
 Mortality up to 80% without transplant
 Jaundice
 Abdominal
 Liver
tenderness
span
• May be increased or decreased (r/t hepatic
necrosis and loss of volume)
 Cerebral
edema
• Papilledema
• Hypertension
• Bradycardia
 Ascities
 Hematemesis
or melena
 May be hypotensive and tachycardic
 Seizures
 Portal hypertension
• Hemorrhage
 Esophageal
 Gastric
 Infection
 Renal
failure
 Metabolic alterations
• Hypoglycemia
• Alkalosis and acidosis
 Serum
ammonia
 Glucose
 Creatinine
 Phosphate
 ABG
 US
 CT: abdomen and/or head
 EEG
 Liver biopsy
 Defined
as an inflammation of one or
more diverticula, which are small
pouches created by herniation of mucosa
into the wall of the colon
Diverticula are small mucosal herniations
protruding through the intestinal layers and the
smooth muscle along the natural openings
created by the vasa recta or nutrient vessels in
the wall of the colon.
 These herniations create small pouches lined
solely by mucosa.
 The sigmoid colon has the highest intraluminal
pressures and is most commonly affected.
 The cause of diverticulosis is not yet conclusive,
but it appears to be associated with a low-fiber
diet, constipation, and obesity.
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Fecal material or undigested food particles may collect in a
diverticulum causing obstruction.
This obstruction may result in distension of the diverticula a
secondary to mucous secretion and overgrowth of normal
colonic bacteria
Vascular compromise and subsequent microperforation or
macroperforation then ensue
Some believe that increased intraluminal pressure or food
particles cause erosion of the diverticular wall, resulting in
inflammation, focal necrosis, and perforation
The disease is frequently mild when pericolic fat and
mesentery wall off a small perforation
Larger perforations and more extensive disease lead to
abscess formation and, rarely, intestinal rupture or
peritonitis.
Diverticulosis occurs more frequently in Western
countries and industrialized societies
 Diverticulosis increases with age,

• Less than 5% before age 40 years to greater than 65% by
age 85
• As many as 20% of patients with diverticulitis are younger
than 50 years
• Younger patients have a higher diverticulitis incidence
per year of life compared with older patients,

More common in patients with the largest
number of diverticula;
• 15-20% of those with diverticulosis develop diverticulitis
 Of
patients with diverticulosis
• 80-85% remain asymptomatic
• Approximately 5% develop diverticulitis
 15-25% of those with diverticulitis develop
complications leading to surgery.
 Complications include abscess formation, intestinal
rupture, peritonitis, and fistula formation.
 Diverticulitis
may be more severe illness
in patients immunocompromised, with
significant comorbid conditions, and if
taking anti-inflammatory medications
 In Patients who are managed
conservatively, a recurrence rate of 2035%.
 LLQ
pain is the most common presenting
complaint
• Occurs in 70% of patients
• Pain is often described as crampy and may be
associated with a change in bowel habits
 Nausea
and vomiting
 Constipation,
 Diarrhea
 Flatulence,
 Bloating
A
microperforation may present with no
systemic signs of illness or infection
 Disease may progress from a localized
and walled-off process to one with
peridiverticular inflammatory and
localized abscess
• Systemic signs of infection (eg, fever) then
develop

More severe diverticulitis is often accompanied
by
• anorexia, nausea, and vomiting.
• Typically, the pain is localized and severe and present for
several days prior to presentation.
• Altered bowel habits, especially constipation, are
reported by most patients.
• A small percentage of patients may complain of urinary
symptoms, such as dysuria, urgency, and frequency, due
to inflammation adjacent to urinary tract structures.
• Macroperforation with spillage of colonic contents into
the peritoneum leads to generalized abdominal pain and
peritonitis
 Simple
diverticulitis, localized abdominal
tenderness in the area of the affected
diverticula and fever are common
findings
 LLQ tenderness is the most common
physical finding
 RLQ tenderness, mimicking acute
appendicitis, can occur in right-sided
diverticulitis
 Complicated
formation
diverticulitis with abscess
• A tender palpable mass may be felt on physical
examination
 20% of cases present with a palpable mass on abdominal,
pelvic, or rectal examination
• Peritonitis due to free perforation results in
generalized tenderness with rebound and guarding
on abdominal examination.
 The abdomen may be distended and tympanic to
percussion
 Bowel sounds can be diminished or absent

Elderly patients and some patients taking
corticosteroids may have unremarkable findings
on physical examination even in the presence of
severe diverticulitis
• Must be approached with a high index of suspicion to
avoid a delay in establishing the correct diagnosis

If a fistula forms, the findings vary depending on
the type of fistula
• Colovesicular fistulas may present with urinary tract
symptoms, such as suprapubic, flank, or costovertebral
angle tenderness
• Fecaluria can also be observed.
• Female patients with colovaginal fistulas may present with
a purulent vaginal discharge.
 Appendicitis
 Biliary Colic/Biliary Disease/Obstruction
 Colon obstruction
 Constipation
 Gastric Ulcers
 Gastroenteritis
 Gyn pain
 Inflammatory Disease
 IBS
 Mesenteric ischemia
 Many others
 Diagnosis
can usually be made on the basis
of the H&P
 Laboratory tests may be of help when the
diagnosis is in question
 CBC: may reveal leukocytosis and a left
shift, indicating infection
 Chemistries may be helpful in the patient
who is vomiting or has diarrhea to assess
electrolyte abnormalities
 Renal function is assessed prior to the
administration of most intravenous contrast
material
 Liver
tests and lipase may help to exclude
other causes of abdominal pain
 UA: if a colovesicular fistula is suspected,
may reveal RBCs or WBCs
 UA c&s: may confirm sterile pyuria due to
inflammation versus polymicrobial infection
in the case of a fistula.
 Blood cultures: prior to the administration of
empiric parenteral antimicrobial therapy in
patients who are severely ill or in those with
complicated disease
 Pregnancy
test: performed in any female
of childbearing age who presents with
abdominal pain to rule out ectopic
pregnancy, as well as prior to radiologic
studies or medications
 CT scan of the abdomen is considered
the best imaging method to confirm the
diagnosis (but not always needed)
 Simplest
Method
• Symptomatic diverticulosis
• Uncomplicated diverticulitis
• Complicated diverticulitis
 Clinical
staging by Hinchey's
classification is geared toward choosing
the proper surgical procedure when
diverticulitis is complicated
Acute uncomplicated diverticulitis is successfully
treated in 70-100% of patients with conservative
management
 Mild diverticulitis, typically with Hinchey stage I

• Outpatient treatment regimen
 Clear liquid diet; advance the diet slowly as tolerated after
clinical improvement (usually in 2-3 days)
 After resolution; a high fiber, low fat diet
 7-10 days of oral broad-spectrum antimicrobial therapy
 Oral antibiotics can includea combination of ciprofloxacin (or
trimethoprim-sulfamethoxazole) and metronidazole
 Moxifloxacin is appropriate monotherapy for outpatient treatment of
uncomplicated diverticulitis
 Amoxicillin/clavulanic acid monotherapy is acceptable
 Hospitalization
is required if
• Evidence of severe diverticulitis, such as
•
•
•
•
systemic signs of infection or peritonitis.
Unable to tolerate oral hydration
Fail outpatient therapy (persistent or increasing
fever, pain, or leukocytosis after 2-3 d)
Immunocompromised, or who have
comorbidities may also require hospitalization
Pain severe enough to require parenteral
narcotic analgesia
 Once
the acute episode has resolved, the
patient may advance diet as tolerated
and then maintain a lifelong high-fiber
diet
 Colonoscopy or, alternatively, barium
enema with flexible sigmoidoscopy
• Performed after resolution of an initial episode
(typically 2-6 wk after recovery) to exclude
other diagnoses, such as cancer, ischemia, and
inflammatory bowel disease
 Studies
have reported the efficacy of
different regimens of anti-inflammatory
agents, including mesalamine,
nonabsorbable antibiotics such as
rifaximin, and probiotics alone or in
combination in the management of
diverticulitis

The surgical indications include some features
characteristic of Hinchey stage III or IV disease
and are:
Free-air perforation with fecal peritonitis
Suppurative peritonitis secondary to a ruptured abscess
Uncontrolled sepsis
Abdominal or pelvic abscess (unless CT-guided
aspiration is possible)
• Fistula formation
• Inability to rule out carcinoma
•
•
•
•
 Intestinal obstruction
 Failing medical therapy
• Immunocompromised status
• Extremes of age
A
2-stage surgical approach is the most
common surgical procedure performed
today for the emergency treatment of acute
diverticulitis.
• A traditional Hartmann procedure which involves
resection of the diseased segment of bowel, an endcolostomy, and closure of the rectal stump
• Typically, 3 months later, a second procedure can be
performed to close the rectal stump; however, this
second operation can be technically difficult and is
not performed in many patients.
• This is the preferred approach in patients with fecal
peritonitis and in most cases of purulent peritonitis
 An
alternative to the Hartmann procedure
includes resection of the diseased colon,
primary anastomosis (with or without
intraoperative colonic lavage), and proximal
diverting stoma, either colostomy or
ileostomy
 The second procedure in this course would
be to close the stoma. This approach is
primarily used when there are relative
contraindications to primary anastomosis
but no purulent or feculent peritonitis and
there is nonedematous bowel
 Performed
at least 6 weeks after recovery
from acute diverticulitis
 A 1-stage surgical approach with
resection and primary anastomosis is
often possible since the disease is well
localized and/or significantly resolved
 Recurrent
episodes of acute diverticulitis:
Elective surgery was previously
recommended in any patient who had 2
or more episodes of diverticulitis that
were successfully treated medically; data
have since called this practice into
question when the patient is otherwise
healthy.
 GI
 Surgery
 Monitor
at 24-72 hours for improvement;
if outpatient care
 After recovery from acute diverticulitis
• Colonoscopy to rule out malignancy
 Diet
instruction: high fiber, low fat

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
Anderson, J., Bundgaard, L., et al. (2012). Danish national guidelines for
treatment of diverticular disease. Danish Medical Journal, 59, 5, C4453.
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