# 04 - 16 Abdominal Pain

### 16 Abdominal Pain

positron emission tomography offers advantages of improved diag­
nostic performance and fewer nondiagnostic studies than singlephoton emission CT. 
EXERCISE ELECTROCARDIOGRAPHY
Exercise electrocardiography has historically been commonly 
employed for completion of risk stratification of patients who have 
undergone an initial evaluation that has not revealed a specific 
cause of chest discomfort and has identified a low risk of ACS. 
Early exercise testing is safe in patients without ongoing chest pain 
or high-risk findings and may assist in refining their prognostic 
assessment. However, for patients with chest pain for whom both 
cardiac troponin and clinical risk stratification have determined the 
patient to have low probability of ACS, there is insufficient evidence 
that stress testing or cardiac imaging improves their outcomes. 
This evolution in evidence supports a change from past practice in 
which stress testing within 72 hours was broadly used for patients 
with acute chest pain. Exercise ECG is an alternative for patients 
without known coronary artery disease who remain eligible for 
additional testing based on intermediate risk of ACS but should be 
performed with cardiac imaging in patients with known coronary 
atherosclerosis. 
OTHER NONINVASIVE STUDIES
Other noninvasive imaging studies of the chest can be used selec­
tively to provide additional diagnostic and prognostic information 
in patients with chest discomfort. 
Echocardiography  Echocardiography (nonstress) is not routinely 
necessarily in patients with chest discomfort. However, in patients 
with an uncertain diagnosis, particularly those with nondiagnos­
tic ST elevation, ongoing symptoms, or hemodynamic instability, 
detection of abnormal regional wall motion provides evidence of 
possible ischemic dysfunction. Echocardiography is diagnostic in 
patients with mechanical complications of MI or in patients with 
pericardial tamponade. Transthoracic echocardiography is poorly 
sensitive for aortic dissection, although an intimal flap may some­
times be detected in the ascending aorta. 
MRI (See Chap. 248)  Cardiac magnetic resonance (CMR) imaging 
is a versatile technique for structural and functional evaluation of 
the heart and the vasculature of the chest. CMR can be performed 
as a modality for pharmacologic stress perfusion imaging and is an 
alternative for completing risk assessment in patients with interme­
diate risk of ACS. Gadolinium-enhanced CMR can provide early 
detection of MI, defining areas of myocardial necrosis accurately, 
and can delineate patterns of myocardial disease that are often 
useful in discriminating ischemic from nonischemic myocardial 
injury. Although not practical in some institutions for the urgent 
evaluation of acute chest discomfort, CMR can be a useful modality 
for cardiac structural evaluation of patients with elevated cardiac 
troponin levels in the absence of definite coronary artery disease. 
CMR coronary angiography is in its early stages. MRI also permits 
highly accurate assessment for aortic dissection but is infrequently 
used as the first test because CT and transesophageal echocardiog­
raphy are usually more practical.
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■OUTPATIENT EVALUATION OF 

CHEST DISCOMFORT
Chest pain is common in outpatient practice, with a lifetime preva­
lence of 20–40% in the general population. More than 25% of patients 
with MI have had a related visit with a primary care physician in the 
previous month. The diagnostic principles are the same as in the ED. 
However, the pretest probability of acute cardiopulmonary cause is 
significantly lower. Therefore, testing paradigms are less intense, with 
an emphasis on the history, physical examination, and ECG. Moreover, 
decision-aids developed for settings with a high prevalence of sig­
nificant cardiopulmonary disease have lower positive predictive value 
when applied in the practitioner’s office. However, in general, if the 

level of clinical suspicion of ACS is sufficiently high to consider tro­
ponin testing, the patient should be referred to the ED for evaluation.

■
■FURTHER READING
Anand A et al: High-sensitivity cardiac troponin on presentation to 
rule out myocardial infarction: A stepped-wedge cluster randomized 
controlled trial. Circulation 153:2215, 2021.
Fanaroff AC et al: Does this patient with chest pain have acute coro­
nary syndrome? JAMA 315:1955, 2015.
Gulati M et al: 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR 
guideline for the evaluation and diagnosis of chest pain: A report 
of the American College of Cardiology/American Heart Asso­
ciation Joint Committee on Clinical Practice Guidelines. Circulation 
154:e368, 2021.
Hsia RY et al: A national study of the prevalence of life-threatening 
Abdominal Pain
CHAPTER 16
diagnoses in patients with chest pain. JAMA Intern Med 176:1029, 
2016.
Kontos MC et al: 2022 ACC expert consensus decision pathway on 
the evaluation and disposition of acute chest pain in the emergency 
department. J Am Coll Cardiol 80:1925, 2022.
Mahler SA et al: Safely identifying emergency department patients 
with acute chest pain for early discharge: HEART pathway acceler­
ated diagnostic protocol. Circulation 138:2456, 2018.
Danny O. Jacobs

Abdominal Pain
Correctly diagnosing acute abdominal pain can be quite challenging. 
Few clinical situations require greater judgment, because the most 
catastrophic of events may be heralded by the subtlest of symptoms and 
signs. In every instance, the clinician must distinguish those conditions 
that require urgent intervention from those that do not and are best 
managed nonoperatively. A meticulously executed, detailed history 
and physical examination are critically important for focusing the dif­
ferential diagnosis and allowing the diagnostic evaluation to proceed 
expeditiously (Table 16-1).
The etiologic classification in Table 16-2, although not complete, 
provides a useful framework for evaluating patients with abdominal 
pain.
Any patient with abdominal pain of recent onset requires an early 
and thorough evaluation. The most common causes of abdominal pain 
on admission are nonspecific abdominal pain, acute appendicitis, pain 
of urologic origin, and intestinal obstruction. A diagnosis of “acute 
or surgical abdomen” is not acceptable because of its often mislead­
ing and erroneous connotations. Although most patients who present 
with acute abdominal pain will have self-limited disease processes, 
it is important to remember that pain severity does not necessarily 
TABLE 16-1  Some Key Components of the Patient’s History
Age
Time and mode of onset of the pain
Pain characteristics
Duration of symptoms
Location of pain and sites of radiation
Associated symptoms and their relationship to the pain
Nausea, emesis, and anorexia
Diarrhea, constipation, or other changes in bowel habits
Menstrual history

TABLE 16-2  Some Important Causes of Abdominal Pain
Pain Originating in the Abdomen
Parietal peritoneal inflammation
  Bacterial contamination
    Perforated appendix or other 
Vascular disturbances
  Embolism or thrombosis
  Vascular rupture
  Pressure or torsional occlusion
  Sickle cell anemia
Abdominal wall
  Distortion or traction of mesentery
  Trauma or infection of muscles
Distension of visceral surfaces, e.g., by 
hemorrhage
  Hepatic or renal capsules
Inflammation
  Appendicitis
  Typhoid fever
  Neutropenic enterocolitis or 
perforated viscus
    Pelvic inflammatory disease
  Chemical irritation
    Perforated ulcer
    Pancreatitis
    Mittelschmerz
Mechanical obstruction of hollow 
viscera
  Obstruction of the small or large 
PART 2
Cardinal Manifestations and Presentation of Diseases
intestine
  Obstruction of the biliary tree
  Obstruction of the ureter
“typhlitis”
Pain Referred from Extraabdominal Source
Cardiothoracic
  Acute myocardial infarction
  Myocarditis, endocarditis, 
  Pleurodynia
  Pneumothorax
  Empyema
  Esophageal disease, including 
pericarditis
  Congestive heart failure
  Pneumonia (especially lower lobes)
  Pulmonary embolus
spasm, rupture, or inflammation
Genitalia
  Torsion of the testis
Metabolic Causes
Diabetes
Uremia
Hyperlipidemia
Hyperparathyroidism
Acute adrenal insufficiency
Familial Mediterranean fever
Porphyria
C1 esterase inhibitor deficiency 
(angioneurotic edema)
Neurologic/Psychiatric Causes
Herpes zoster
Tabes dorsalis
Causalgia
Radiculitis from infection or arthritis
Spinal cord or nerve root compression
Functional disorders
Psychiatric disorders
Toxic Causes
Lead poisoning
Insect or animal envenomation
  Black widow spider bites
  Snake bites
 
Uncertain Mechanisms
Narcotic withdrawal
Heat stroke
 
correlate with the severity of the underlying condition. In addition, 
the presence or absence of various degrees of “hunger” is unreliable 
as a sole indicator of the severity of intraabdominal disease. The most 
obvious of “acute abdomens” may not require operative intervention, 
but the mildest of abdominal pain could.
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■SOME MECHANISMS OF PAIN ORIGINATING IN 
THE ABDOMEN
Inflammation of the Parietal Peritoneum 
The pain of pari­
etal peritoneal inflammation is steady and aching in character and is 
located directly over the inflamed area and is transmitted by somatic 
nerves. The intensity of the pain is dependent on the type and amount 
of material to which the peritoneal surfaces are exposed in a given 
time period. For example, the sudden release of a small quantity of 
sterile acidic gastric juice into the peritoneal cavity causes much more 
pain than the same amount of grossly contaminated pH neutral feces. 

Enzymatically active pancreatic juice incites more pain and inflamma­
tion than does the same amount of sterile bile containing no potent 
enzymes. Because blood is normally only a mild irritant, and the 
response to urine is also typically bland, exposure of blood and urine to 
the peritoneal cavity may go unnoticed unless it is sudden and massive. 
Bacterial contamination, such as may occur with pelvic inflammatory 
disease or perforated distal intestine, causes low-intensity pain until 
multiplication causes significant amounts of inflammatory mediators 
to be released. Patients with perforated upper gastrointestinal ulcers 
may present entirely differently depending on how quickly gastric 
juices enter the peritoneal cavity and their pH. Thus, the rate at which 
any inflammatory material irritates the peritoneum is important.
The pain of peritoneal inflammation is invariably accentuated by 
pressure or changes in tension of the peritoneum, whether produced 
by palpation or by movement such as with coughing or sneezing. The 
patient with peritonitis characteristically lies quietly in bed, preferring 
to avoid motion, in contrast to the patient with colic, who may be 
thrashing in discomfort.
Another characteristic feature of peritoneal irritation is tonic reflex 
spasm of the abdominal musculature, localized to the involved body 
segment. Its intensity depends on the integrity of the nervous system, 
the location of the inflammatory process, and the rate at which it devel­
oped. Spasm over a perforated retrocecal appendix or perforation into 
the lesser peritoneal sac may be minimal or absent because of the pro­
tective effect of overlying viscera. Catastrophic abdominal emergencies 
may be associated with minimal or no detectable pain or muscle spasm 
in obtunded, seriously ill, debilitated, immunosuppressed, or psychotic 
patients. A slowly developing process also often greatly attenuates the 
degree of muscle spasm.
Obstruction of Hollow Viscera 
Intraluminal obstruction clas­
sically elicits intermittent or colicky abdominal pain that is not as well 
localized as the pain of parietal peritoneal irritation. However, the 
absence of cramping discomfort can be misleading because distention of 
a hollow viscus may also produce steady pain with only rare paroxysms.
Small-bowel obstruction often presents as poorly localized, inter­
mittent periumbilical or supraumbilical pain. As the intestine progres­
sively dilates and loses muscular tone, the colicky nature of the pain 
may diminish. With superimposed strangulating obstruction, pain 
may spread to the lower lumbar region if there is traction on the root 
of the mesentery. The colicky pain of colonic obstruction is of lesser 
intensity, is commonly located in the infraumbilical area, and may 
often radiate to the lumbar region.
Sudden distention of the biliary tree produces a steady rather than 
colicky type of pain; hence, the term biliary colic is misleading. Acute 
distention of the gallbladder typically causes pain in the right upper 
quadrant with radiation to the right posterior region of the thorax or 
to the tip of the right scapula, but discomfort is also not uncommonly 
found near the midline. Distention of the common bile duct often 
causes epigastric pain that may radiate to the upper lumbar region. 
Considerable variation is common, however, so that differentiation 
between gallbladder or disease affecting the common bile duct may be 
impossible.
Gradual dilatation of the biliary tree, as can occur with carcinoma of 
the head of the pancreas, may cause no pain or only a mild aching sen­
sation in the epigastrium or right upper quadrant. The pain of disten­
tion of the pancreatic ducts is similar to that described for distention of 
the common bile duct but, in addition, is very frequently accentuated 
by recumbency and relieved by the upright position.
Obstruction of the urinary bladder usually causes dull, low-

intensity pain in the suprapubic region. Restlessness, without a specific 
complaint of pain, may be the only sign of a distended bladder in an 
obtunded patient. In contrast, acute obstruction of the intravesicular 
portion of the ureter is characterized by severe suprapubic and flank 
pain that radiates to the penis, scrotum, or inner aspect of the upper 
thigh. Obstruction of the ureteropelvic junction manifests as pain near 
the costovertebral angle, whereas obstruction of the remainder of the 
ureter is associated with flank pain that often extends into the same 
side of the abdomen.

Vascular Disturbances 
A frequent misconception is that pain due 
to intraabdominal vascular disturbances is sudden and catastrophic in 
nature. Certain disease processes, such as embolism or thrombosis of 
the superior mesenteric artery or impending rupture of an abdominal 
aortic aneurysm, can certainly be associated with diffuse, severe pain. 
Yet, just as frequently, the patient with occlusion of the superior mes­
enteric artery only has mild continuous or cramping diffuse pain for 2 
or 3 days before vascular collapse or findings of peritoneal inflamma­
tion appear. The early, seemingly insignificant discomfort is caused by 
hyperperistalsis rather than peritoneal inflammation. Indeed, absence 
of tenderness and rigidity in the presence of continuous, diffuse pain 
(e.g., “pain out of proportion to physical findings”) in a patient likely to 
have vascular disease is quite characteristic of occlusion of the superior 
mesenteric artery. Abdominal pain with radiation to the sacral region, 
flank, or genitalia should always signal the possible presence of a rup­
turing abdominal aortic aneurysm. This pain may persist over a period 
of several days before rupture and collapse occur.
Abdominal Wall 
Pain arising from the abdominal wall is usually 
constant and aching. Movement, prolonged standing, and pressure 
accentuate the discomfort and associated muscle spasm. In the rela­
tively rare case of hematoma of the rectus sheath, now most frequently 
encountered in association with anticoagulant therapy, a mass may be 
present in the lower quadrants of the abdomen. Simultaneous involve­
ment of muscles in other parts of the body usually serves to differenti­
ate myositis of the abdominal wall from other processes that might 
cause pain in the same region.
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■REFERRED PAIN IN ABDOMINAL DISEASE
Pain referred to the abdomen from the thorax, spine, or genitalia may 
present a diagnostic challenge because diseases of the upper part of the 
abdominal cavity such as acute cholecystitis or perforated ulcer may 
be associated with intrathoracic complications. A most important, yet 
often forgotten, dictum is that the possibility of intrathoracic disease 
must be considered in every patient with abdominal pain, especially if 
the pain is in the upper abdomen.
Systematic questioning and examination directed toward detect­
ing myocardial or pulmonary infarction, pneumonia, pericarditis, or 
esophageal disease (the intrathoracic diseases that most often mas­
querade as abdominal emergencies) will often provide sufficient clues 
to establish the proper diagnosis. Diaphragmatic pleuritis resulting 
from pneumonia or pulmonary infarction may cause pain in the right 
upper quadrant and pain in the supraclavicular area, the latter radia­
tion to be distinguished from the referred subscapular pain caused by 
acute distention of the extrahepatic biliary tree. The ultimate decision 
as to the origin of abdominal pain may require deliberate and planned 
observation over a period of several hours, during which repeated 
questioning and examination will provide the diagnosis or suggest the 
appropriate studies.
Referred pain of thoracic origin is often accompanied by splinting of 
the involved hemithorax with respiratory lag and a decrease in excur­
sion more marked than that seen in the presence of intraabdominal 
disease. In addition, apparent abdominal muscle spasm caused by 
referred pain will diminish during inspiration, whereas it persists 
throughout both respiratory phases if it is of abdominal origin. Palpa­
tion over the area of referred pain in the abdomen also does not usually 
accentuate the pain and, in many instances, actually seems to relieve it.
Thoracic disease and abdominal disease frequently coexist and may 
be difficult or impossible to differentiate. For example, the patient with 
known biliary tract disease often has epigastric pain during myocardial 
infarction, or biliary colic may be referred to the precordium or left 
shoulder in a patient who has suffered previously from angina pectoris. 
For an explanation of the radiation of pain to a previously diseased 
area, see Chap. 14.
Referred pain from the spine, which usually involves compression 
or irritation of nerve roots, is characteristically intensified by certain 
motions such as cough, sneeze, or strain and is associated with hyper­
esthesia over the involved dermatomes. Pain referred to the abdomen 
from the testes or seminal vesicles is generally accentuated by the 

slightest pressure on either of these organs. The abdominal discomfort 
experienced is of dull, aching character and is poorly localized.

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■METABOLIC ABDOMINAL CRISES
Pain of metabolic origin may simulate almost any other type of 
intraabdominal disease. Several mechanisms may be at work. In cer­
tain instances, such as hyperlipidemia, the metabolic disease itself may 
be accompanied by an intraabdominal process such as pancreatitis, 
which can lead to unnecessary laparotomy unless recognized. C1 
esterase deficiency associated with angioneurotic edema is often asso­
ciated with episodes of severe abdominal pain. Whenever the cause of 
abdominal pain is obscure, a metabolic origin always must be consid­
ered. Abdominal pain is also the hallmark of familial Mediterranean 
fever (Chap. 381). Rarely, some patients with COVID-19 may present 
with severe abdominal pain in the absence of pulmonary symptoms.
Abdominal Pain
CHAPTER 16
The pain of porphyria and of lead colic is usually difficult to dis­
tinguish from that of intestinal obstruction because severe hyperperi­
stalsis is a prominent feature of both. The pain of uremia or diabetes 
is nonspecific, and the pain and tenderness frequently shift in location 
and intensity. Diabetic acidosis may be precipitated by acute appendi­
citis or intestinal obstruction, so if prompt resolution of the abdominal 
pain does not result from correction of the metabolic abnormalities, an 
underlying organic problem should be suspected. Black widow spider 
bites produce intense pain and rigidity of the abdominal muscles and 
back, an area infrequently involved in intraabdominal disease.
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■IMMUNOCOMPROMISE
Evaluating and diagnosing causes of abdominal pain in immunosup­
pressed or otherwise immunocompromised patients is very difficult. 
This includes those who have undergone organ transplantation; who 
are receiving immunosuppressive treatments for autoimmune dis­
eases, chemotherapy, or glucocorticoids; who have AIDS; and who 
are very old. In these circumstances, normal physiologic responses 
may be absent or masked. In addition, unusual infections may cause 
abdominal pain where the etiologic agents include cytomegalovirus, 
mycobacteria, protozoa, and fungi. These pathogens may affect all 
gastrointestinal organs, including the gallbladder, liver, and pancreas, 
as well as the gastrointestinal tract, causing occult or overtly symp­
tomatic perforations of the latter. Splenic abscesses due to Candida or 
Salmonella infection should also be considered, especially when evalu­
ating patients with left upper quadrant or left flank pain. Acalculous 
cholecystitis may be observed in immunocompromised patients or 
those with AIDS, where it is often associated with cryptosporidiosis or 
cytomegalovirus infection.
Neutropenic enterocolitis (typhlitis) is often identified as a cause 
of abdominal pain and fever in some patients with bone marrow sup­
pression due to chemotherapy. Acute graft-versus-host disease should 
be considered in this circumstance. Optimal management of these 
patients requires meticulous follow-up including serial examinations 
to assess the need for more surgical intervention, for example, to 
address perforation.
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■NEUROGENIC CAUSES
Diseases that injure sensory nerves may cause causalgic pain. This pain 
has a burning character and is usually limited to the distribution of a 
given peripheral nerve. Stimuli that are normally not painful such as 
touch or a change in temperature may be causalgic and are often pres­
ent even at rest. The demonstration of irregularly spaced cutaneous 
“pain spots” may be the only indication that an old nerve injury exists. 
Even though the pain may be precipitated by gentle palpation, rigidity 
of the abdominal muscles is absent, and the respirations are not usually 
disturbed. Distention of the abdomen is uncommon, and the pain has 
no relationship to food intake.
Pain arising from spinal nerves or roots comes and goes suddenly 
and is of a lancinating type (Chap. 18). It may be caused by herpes 
zoster, impingement by arthritis, tumors, a herniated nucleus pulposus, 
diabetes, or syphilis. It is not associated with food intake, abdominal 
distention, or changes in respiration. Severe muscle spasms, when pres­
ent, may be relieved by, but are usually not accentuated by, abdominal

palpation. The pain is made worse by movement of the spine and is 
usually confined to a few dermatomes. Hyperesthesia is very common.

Pain due to functional causes conforms to none of the aforemen­
tioned patterns. Here mechanisms of disease are not as clearly estab­
lished. For example, irritable bowel syndrome (IBS) is a functional 
gastrointestinal disorder characterized by abdominal pain and altered 
bowel habits. The diagnosis is made on the basis of clinical criteria 
(Chap. 338) and after exclusion of demonstrable structural abnormali­
ties. The episodes of abdominal pain may be brought on by stress, and 
the pain varies considerably in type and location. Nausea and vomiting 
are rare. Localized tenderness and muscle spasm are inconsistent or 
absent. The causes of IBS or related functional disorders are not yet 
fully understood, although proinflammatory cells and lipotoxic lipids 
likely play a role.
PART 2
Cardinal Manifestations and Presentation of Diseases
APPROACH TO THE PATIENT
Abdominal Pain
Few abdominal conditions require such urgent operative interven­
tion that an orderly approach needs to be abandoned, no matter 
how ill the patient is. Only patients with exsanguinating intraab­
dominal hemorrhage (e.g., ruptured aneurysm) must be rushed 
to the operating room immediately, but in such instances, only a 
few minutes are required to assess the critical nature of the prob­
lem. Under these circumstances, all obstacles must be swept aside, 
adequate venous access for fluid replacement obtained, and the 
operation begun. Unfortunately, many of these patients may die in 
the radiology department or the emergency room while awaiting 
unnecessary examinations. There are no absolute contraindications 
to operation when massive intraabdominal hemorrhage is present. 
Fortunately, this situation is relatively rare. This statement does 
not necessarily apply to patients with intraluminal gastrointestinal 
hemorrhage, who can often be managed by other means (Chap. 51). 
In these patients, obtaining a detailed history when possible can be 
extremely helpful even though it can be laborious and timeconsuming. Decision-making regarding next steps is facilitated and 
a reasonably accurate diagnosis can be made before any further 
diagnostic testing is undertaken.
In cases of acute abdominal pain, a diagnosis can be readily 
established in most instances, whereas success is not so frequent in 
patients with chronic pain. IBS is one of the most common causes of 
abdominal pain and must always be kept in mind (Chap. 338). The 
location of the pain can assist in narrowing the differential diagno­
sis (Table 16-3); however, the chronological sequence of events in the 
patient’s history is often more important than the pain’s location. 
Careful attention should be paid to the extraabdominal regions. 
Narcotics or analgesics should not be withheld until a definitive 
diagnosis or a definitive plan has been formulated; obfuscation of 
the diagnosis by adequate analgesia is unlikely.
An accurate menstrual history in a female patient is essential. It 
is important to remember that normal anatomic relationships can 
be significantly altered by the gravid uterus. Abdominal and pelvic 
pain may occur during pregnancy due to conditions that do not 
require operation. Lastly, some otherwise noteworthy laboratory 
values (e.g., leukocytosis) may represent the normal physiologic 
changes of pregnancy.
In the examination, simple critical inspection of the patient, for 
example, of facies, position in bed, and respiratory activity, provides 
valuable clues. The amount of information to be gleaned is directly 
proportional to the gentleness and thoroughness of the examiner. 
Once a patient with peritoneal inflammation has been examined 
brusquely, accurate assessment by the next examiner becomes 
almost impossible. Eliciting rebound tenderness by sudden release 
of a deeply palpating hand in a patient with suspected peritonitis is 
cruel and unnecessary. The same information can be obtained by 
gentle percussion of the abdomen (rebound tenderness on a minia­
ture scale), a maneuver that can be far more precise and localizing. 
Asking the patient to cough will elicit true rebound tenderness 

TABLE 16-3  Differential Diagnoses of Abdominal Pain by Usual Location
Right Upper Quadrant
Epigastric
Left Upper Quadrant
Cholecystitis
Cholangitis
Pancreatitis
Pneumonia/empyema
Pleurisy/pleurodynia
Subdiaphragmatic abscess
Hepatitis
Budd-Chiari syndrome
Peptic ulcer disease
Gastritis
GERD
Pancreatitis
Myocardial infarction
Pericarditis
Ruptured aortic 
aneurysm
Esophagitis
Splenic infarct
Splenic rupture
Splenic abscess
Gastritis
Gastric ulcer
Pancreatitis
Subdiaphragmatic 
abscess
Right Lower Quadrant
Periumbilical
Left Lower Quadrant
Appendicitis
Salpingitis
Inguinal hernia
Ectopic pregnancy
Nephrolithiasis
Inflammatory bowel disease
Mesenteric lymphadenitis
Typhlitis
Early appendicitis
Gastroenteritis
Bowel obstruction
Ruptured aortic 
aneurysm
Diverticulitis
Salpingitis
Inguinal hernia
Ectopic pregnancy
Nephrolithiasis
Irritable bowel syndrome
Inflammatory bowel 
disease
Diffuse Nonlocalized Pain
Gastroenteritis
Mesenteric ischemia
Bowel obstruction
Irritable bowel syndrome
Peritonitis
Diabetes
Malaria
Familial 
Mediterranean fever
Metabolic diseases
Psychiatric disease
 
Abbreviation: GERD, gastroesophageal reflux disease.
without the need for placing a hand on the abdomen. Furthermore, 
the forceful demonstration of rebound tenderness will startle and 
induce protective spasm in a nervous or worried patient in whom 
true rebound tenderness is not present. A palpable gallbladder will 
be missed if palpation is so aggressive that voluntary muscle spasm 
becomes superimposed on involuntary muscular rigidity.
As with history taking, sufficient time should be spent in the 
examination. Abdominal signs may be minimal but, nevertheless, 
if accompanied by consistent symptoms, may be exceptionally 
meaningful. Abdominal signs may be virtually or totally absent in 
cases of pelvic peritonitis, so careful pelvic and rectal examinations 
are mandatory in every patient with abdominal pain. Tenderness 
on pelvic or rectal examination in the absence of other abdominal 
signs can be caused by operative indications such as perforated 
appendicitis, diverticulitis, twisted ovarian cyst, and many oth­
ers. Much attention has been paid to the presence or absence of 
peristaltic sounds, their quality, and their frequency. Auscultation 
of the abdomen is one of the least revealing aspects of the physi­
cal examination of a patient with abdominal pain. Catastrophes 
such as a strangulating small-intestinal obstruction or perforated 
appendicitis may occur in the presence of normal peristaltic 
sounds. Conversely, when the proximal part of the intestine above 
obstruction becomes markedly distended and edematous, peristal­
tic sounds may lose the characteristics of borborygmi and become 
weak or absent, even when peritonitis is not present. It is usually 
the severe chemical peritonitis of sudden onset that is associated 
with the truly silent abdomen.
Laboratory examinations may be valuable in assessing the patient 
with abdominal pain, yet, with few exceptions, they rarely establish 
a diagnosis. Leukocytosis should never be the single deciding fac­
tor as to whether or not operation is indicated. A white blood cell 
count >20,000/μL may be observed with perforation of a viscus, 
but pancreatitis, acute cholecystitis, pelvic inflammatory disease, 
and intestinal infarction may also be associated with marked leu­
kocytosis. A normal white blood cell count is not rare in cases of