The Problem of Pain
Approach to Abdominal Pain
Jason Phillips, MD
ER approach
to abdominal pain
Chief complaint: abd pain
 Labs: CBC, chem, LFTs, lipase
 CT abdomen
 History
 Possible PE
How do you approach a
workup for abdominal pain
What are the most likely possibilities?
How do you organize your thoughts?
The Problem of Pain
 Neurologic basis of pain
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Why is it difficult to localize?
Why does the intensity of the pain vary?
 General overview of approaching a
patient with abdominal pain
 Pain syndromes
Neurologic basis of abdominal
pain
 Pain receptors respond to
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Mechanical stimuli
Chemical stimuli
 Nociception mechanical receptors are
located on serosa, within the mesentery,
in the GI tract wall in the
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myenteric plexus (Auerbach plexus)
submucosal plexus (Meissner plexus)
Neurologic basis of abdominal
pain
 Mucosal receptors respond to chemical
stimuli
 Substance P, serotonin, histamine, and
prostaglandins
 Chemical stimuli are released in
response to inflammation or ischemia
Two basic problems with
abdominal pain
 Localization of visceral pain
 Intensity of pain response
Localization of visceral pain
 Visceral pain localizes to midline
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Bilateral, symmetric innervation
Afferent fibers  celiac, superior
mesenteric, or inferior mesenteric ganglion
Localizes: epigastrium, periumbilical, and
lower abdomen
Localization of visceral pain
 Exceptions to the bilateral rule
 Gallbladder
 Ascending and descending colon
 Although bilaterally innervated, they
have predominant ipsilateral innervation
Localization of visceral pain
 Referred pain
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Somatic fiber “cross-talk”
Activate same spinothalamic pathways 
referred pain as the cutaneous dermatome
sharing the same spinal cord level
(Gallbladder – scapula)
Results in aching pain with skin
hyperalgesia and rigidity
Intensity of pain response
 Threshold for perceiving pain from
visceral stimuli has marked individual
variability
 Balloon distension experiment in IBS
History
 MOST IMPORTANT CLUE to the
source of abdominal pain
 Type of pain
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Visceral = dull, aching, poorly localized
Parietal = sharp, well localized
Referred pain
History
 General location

Generalized, RUQ, epigastric, LUQ,
periumbilical, RLQ, LLQ, and ‘migratory’

General region localizes organs/structures
to include in the DDX

Radiation of pain (e.g., acute pancreatitis)
History
 Onset of pain
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Most gradual, steady crescendo (e.g., cholecystitis)
Abrupt, “10/10” – suggestive of perforation
 Quality of pain
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Colicky (comes and goes) – e.g., gastroenteritis
Steady – (e.g., acute pancreatitis; biliary colic is a
misnomer)
Burning
History
 Severity of pain

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Generally corresponds to severity of illness
However, marked patient variability (“12/10
pain” is often functional or has functional
overlay)
 Aggravating or Relieving factors
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Eating (mesenteric ischemia vs PUD)
Position changes (acute pancreatitis,
peritonitis)
History
 Associated symptoms
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Nausea/vomiting
Weight loss
Changes in bowel habits
Physical exam:
Acute abdomen or not?
 General appearance and Vital signs
 Abdominal exam

Auscultation
 Bowel
sounds present?
 High pitched sounds of obstruction
 Stethoscope palpation

Percussion
 Tympany
= distended bowel
 Most humane test for rebound tenderness
Physical exam:
Acute abdomen or not?
 Palpation:
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Acute abdomen or not? Peritoneal signs
Rebound tenderness
Mass? Hernia
 Abdominal wall maneuvers
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Leg lift maneuvers (Carnett’s sign)
Abdominal crunch
Further evaluation
 Directed at pain syndromes
 Labs
 Imaging
Is the pain functional
or not?
Functional abdominal pain
 Can be difficult to distinguish from
organic pain
 Can only be labeled as functional when
organic causes are excluded
 Can superimpose on organic pain
 Should not cause

Weight loss, Anemia, GI bleeding, Fever,
Night sweats
Is it functional or not?
 Clues that are suggestive of functional

Atypical history
 RUQ
that lasts 20 sec is not biliary colic
 Dyspesia that worsens with a PPI

Overly dramatic descriptions of pain
 “It
feels like a knife stabbing me over and
over and then something is pushing inside
out”

Hyperbolic intensity
 “11/10
exam
epigastric pain” with a benign abd
Is it functional or not?
 Clues that are suggestive of functional

Absence of nocturnal symptoms
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Exacerbated by stress
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Distractible exam
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“Gut feeling”
Pain syndromes
Irritable Bowel Syndrome

Prevalence: 10-15% of overall
population

Only ~15% of patients seek medical
care

25-50% of gastroenterology visits

Annual healthcare cost: $1.7 billion
Irritable Bowel Syndrome
ROME criteria:
 12 weeks or more of abdominal
pain/discomfort in the last 12 months
(does not have to be consecutive)

Two or more features:
1.
2.
3.
Relieved with defecation
Change in frequency of stool
Change in appearance of stool
Irritable Bowel Syndrome
3 types of IBS patients
 Constipation-predominant

Diarrhea-predominant

Alternating
Irritable Bowel Syndrome
What is the normal range for frequency of bowel
movements?
Rule of 3s:
- Normal = Anywhere from 3x per week to up
to 3x per day
Irritable Bowel Syndrome
Pathophysiology
Alterations in motility
Visceral hyperalgesia
Postinfectious IBS – lymphocytic infiltration of
myenteric plexus?
Irritable Bowel Syndrome
How do you prove its only IBS?
Rome criteria positive for IBS 

No alarm features and mild symptoms,
reassurance and treatment of symptoms

Alarm features or severe symptoms, consider
referral to GI
Upper abdominal pain
 Biliary disease
 Dyspepsia
 Pancreatitis
 Gastroparesis
 Other
Upper abdominal pain:
Biliary disease
1.
2.
3.
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Most common location – epigastric NOT
RUQ
Steady onset; last hours (not minutes or
seconds)
Can radiate to right scapula
Biliary colic
Cholecystitis
Acute cholangitis
Upper abdominal pain:
Biliary disease
 Workup:

Labs: When are liver tests abnormal?
Imaging: What is the most sensitive
imaging study for biliary tract disease?

What are its limitations?

Upper abdominal pain:
Biliary disease
 Labs: LFTs increase with choledocholithiasis
(first transaminases, then AP/T Bili)
 Ultrasound:
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Sensitivity
Cholecystitis
 HIDA
Gallstones
Biliary dilation
Choledocholithiasis
dilated CBD)
Specificity
88%
89%
97%
90%
84%
99%
55-91%
50 vs 75% (nondilated vs
Upper abdominal pain:
Dyspepsia
 Dyspepsia = “persistent or recurrent
abdominal pain or discomfort in the
upper abdomen.”
 Vague diagnosis that includes a long
DDX
Upper abdominal pain:
Dyspepsia
 80-100% of ‘dyspepsia’ is a acid-related
phenomenon or functional
 Usually an outpatient problem
 Peptic ulcer pain = epigastric, burning or
hunger-like, worse between meals,
relieved with food, nocturnal pain,
associated nausea
Upper abdominal pain:
Dyspepsia
 GERD = heartburn (retrosternal
burning), water brash (acid taste in
mouth), regurgitation, and sensation of
dysphagia
Upper abdominal pain:
Dyspepsia
 Functional dyspepsia = same symptoms
but no organic etiology can be found
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12 weeks over last 12 months
Not relieved with BM or associated with
alterations in BMs (i.e., NOT IBS)
Upper abdominal pain:
Dyspepsia
 Best test?
 3 strategies
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Empiric PPI
H pylori – test and treat
EGD
Gastroparesis
 Often overlooked as a cause for
epigastric pain
 Gastroparesis symptoms
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Nausea 93%
Abdominal pain 90%
 Epigastric
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burning, vague, cramping
Early satiety 86%
Vomiting 68%
Gastroparesis
 60% report pain is worse after eating
 80% reports pain interrupted sleep
 Vomiting food hours later
 Look for important historical clues
 Diabetes
 Meds (narcotics, anticholinergics)
 Recent viral gastroenteritis
 CNS disease
 Amyloid, scleroderma
Gastroparesis
 Workup

EGD or UGI – rule out GOO

Gastric emptying scan
Upper abdominal pain:
Pancreatitis
 Acute Pancreatitis = acute epigastric
pain that radiates to back, constant,
severe, rapid onset within 1 hour, lasts
days, associated nausea/vomiting,
relieved with sitting forward; assoc
restlessness
 Rarely diffuse pain, RUQ, or LUQ
Upper abdominal pain:
Pancreatitis
Diagnosis is made when you have at least
2 of the 3 criteria:
- Typical pancreatitic pain
- Elevation in amylase and lipase
- Abnormal imaging
Upper abdominal pain:
Pancreatitis
 Chronic pancreatitis = similar pain, less
severe and onset 20-30 minutes after a
meal, can be episodic (early in disease
course) or constant (late finding)
 Associated malabsorption (pancreatic
exocrine insufficiency) and diabetes
(endocrine insufficiency)

Steatorrhea does not occur until 90% or
more of pancreatic function is lost
Upper abdominal pain:
Other causes
 Acute MI
 Pneumonia
 Splenic abscess or infarct
Lower abdominal pain
 Appendicitis
 Diverticular disease
 IBS
 Crohn’s disease
 Hernia
 Other
Lower abdominal pain
 Appendicitis = begins as periumbilical pain
that localizes to RLQ (McBurney’s point)
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Initially visceral pain (superior mesenteric ganglion)
RLQ when inflammation extends to peritoneal
surface (parietal pain)
 Pain evolves over hours
 Exam: peritoneal irritation (rebound) + fever
 Labs: Elevated WBC
Lower abdominal pain
Diverticulitis = usually LLQ abdominal
pain
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Constant w insidious onset
Worsening over days
Associated symptoms of fever and
worsening constipation
Lower abdominal pain
 Exam: spectrum of severity
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Mild  LLQ tenderness
Severe  LLQ rebound
 Labs: Elevated WBC
 Imaging
Lower abdominal pain
 70% of diverticulitis in Western countries
in left sided. What group of patients
usually have right sided diverticultitis
(~75%)?
 Do seeds cause diverticulitis and should
they be avoided?
Lower abdominal pain
 IBD can give lower abdominal pain with
diarrhea, weight loss, hematochezia,
fever

These clues are more obvious
 However, 10% of patients with Crohn’s
disease will NOT have diarrhea and can
present with abdominal pain
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RLQ  ileocecal
CT, colonoscopy, SBFT
Lower abdominal pain
 Hernia = weakness or disruption of the
abdominal wall
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Indirect: at the internal ring
Direct: Hesselbach’s triangle
Umbilical
Epigastric
Incisional
Lower abdominal pain
 Groin hernias  pain or dull pressure
with lifting, straining, or increasing
intrabdominal pressure; worse with
prolonged standing and at end of day

Physical exam is crucial
 Outright pain at rest is concerning for
strangulation
Lower abdominal pain
 If in doubt, consult surgery for an opinion
 If a hernia is bright red and impossible to
reduce, call a surgeon immediately
Lower abdominal pain:
Non-GI causes
 Nephrolithiasis
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Colicky pain (spasms lasting 20-60 mins)
Site depends on location of stone
(flankgroin)
UA: hematuria (neg in 20-30% of cases)
CT renal stone protocol
Lower abdominal pain:
Non-GI causes
 Pelvic inflammatory disease
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Pelvic pain during menses or coitus
Onset during of shortly after menses
Bilateral
Usually less than 2 weeks
Exam critical: speculum and bimanual
exam
Diffuse abdominal pain
 Gastroenteritis
 IBS
 Obstruction
 Mesenteric ischemia
Diffuse abdominal pain
 Viral gastroenteritis = colicky abdominal
cramps, watery diarrhea, and
nausea/vomiting
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Incubation 24-48 hours
Symptoms begin with abdominal cramps
and/or nauseamost have vomiting and
watery diarrhea
Mild fever, myalgias
Lasts 48-72 hrs
Diffuse abdominal pain
 Obstruction
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Periumbilical pain with paroxysms of
cramps occurring every 4-5 minutes
Abdominal distension
Nausea
Obstipation may be delayed up to 24 hours
History of abdominal surgery or
malignancy
Diffuse abdominal pain
 Obstruction

Exam: distended appearance, tympanic,
high pitched tinkle or large bowel sounds
NGT decompression
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Abdominal x-rays – supine and upright
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Ischemia
 Acute mesenteric ischemia
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Embolism
Thrombosis
Vasospasm
 Chronic mesenteric ischemia
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Intestinal angina
 Can be difficult to diagnose
Acute mesenteric ischemia
 Embolic  sudden onset of severe,
diffuse pain
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Writhing in pain
Abdominal exam feels benign - :pain out of
proportion to exam”
Be suspicious in the right patient: atrial
fibrillation, mechanical heart valves, age
Acute mesenteric ischemia
 Thrombotic and non-occlusive 
insidious onset of pain
 Labs: nonspecific until late in the course
 Imaging: mesenteric angiogram
Questions?