History taking by an experienced physician is an active process
whereby a cluster of diagnostic possibilities is considered in order
to systematically eliminate less likely conditions. Pain is the
most common and predominant presenting feature of an acute abdomen. Careful
consideration of the location, the mode of onset and progression,
and the character of the pain will suggest a preliminary list of
Because of the complex dual visceral and parietal sensory network
innervating the abdominal area, pain is not as precisely localized
as in the extremities. Fortunately, some general patterns do emerge
that provide clues to diagnosis. Visceral sensation is mediated
primarily by afferent C fibers located in the walls of hollow viscera
and in the capsules of solid organs. Unlike cutaneous pain, visceral
pain is elicited by distention, by inflammation or ischemia
stimulating the receptor neurons, or by direct involvement (eg,
malignant infiltration) of sensory nerves. The centrally perceived sensation
is generally slow in onset, dull, poorly localized, and protracted.
Different visceral structures are associated with different sensory
levels in the spine (Table 21–2).
Because of this, increased wall tension due to luminal distention
or forceful smooth muscle contraction (colic) produces diffuse,
deep-seated pain felt in the midepigastrium, periumbilical area, lower
abdomen, or flank areas (Figure 21–1).
Visceral pain is most often felt in the midline
because of the bilateral sensory supply to the spinal cord.
Table 21–2. Sensory Levels Associated with Visceral Structures. |Favorite Table|Download (.pdf)
Table 21–2. Sensory Levels Associated with Visceral Structures.
|Structures||Nervous System Pathways||Sensory Level|
|Liver, spleen, and central part of diaphragm||Phrenic nerve||C3–5|
|Peripheral diaphragm, stomach, pancreas, gallbladder, and
small bowel||Celiac plexus and greater splanchnic nerve||T6–9|
|Appendix, colon, and pelvic viscera||Mesenteric plexus and lesser splanchnic nerve||T10–11|
|Sigmoid colon, rectum, kidney, ureters, and testes||Lowest splanchnic nerve||T11–L1|
|Bladder and rectosigmoid||Hypogastric plexus||S2–4|
By contrast, parietal pain is mediated by both C
and A delta nerve fibers, the latter being responsible for the transmission
of more acute, sharper, better-localized pain sensation. Direct
irritation of the somatically innervated parietal peritoneum (especially
the anterior and upper parts) by pus, bile, urine, or gastrointestinal
secretions leads to more precisely localized pain. The cutaneous distribution
of parietal pain corresponds to the T6–L1 areas. Parietal
pain is more easily localized than visceral pain because the somatic
afferent fibers are directed to only one side of the nervous system.
Abdominal parietal pain is conventionally described as occurring
in one of the four abdominal quadrants or in the epigastric or central
Abdominal pain may be referred or may shift to sites far removed
from the primarily affected organs (Figure 21–2). Referred
pain denotes noxious (usually cutaneous)
sensations perceived at a site distant from that of a strong primary
stimulus. Distorted central perception of the site of pain is due
to the confluence of afferent nerve fibers from widely disparate
areas within the posterior horn of the spinal cord. For example, pain due to subdiaphragmatic irritation
by air, peritoneal fluid, blood, or a mass lesion is referred to
the shoulder via the C4-mediated (phrenic) nerve. Pain may also
be referred to the shoulder from supradiaphragmatic lesions such
as pleurisy or lower lobe pneumonia, especially in young patients. Although
more often perceived in the right scapular region, referred biliary
pain may mimic angina pectoris if it is perceived in the anterior
chest or left shoulder areas. Posterolateral right flank pain may
be seen in retrocecal appendicitis.
Referred pain and shifting pain in the acute abdomen.
Solid circles indicate the site of maximum pain; dashed circles indicate
sites of lesser pain.
Spreading or shifting pain parallels the course
of the underlying condition. The site of pain at onset should be
distinguished from the site at presentation. Beginning classically
in the epigastric or periumbilical region, the incipient visceral pain
of acute appendicitis (due to distention of the appendix) later
shifts to become sharper parietal pain localized in the right lower
quadrant when the overlying peritoneum becomes directly inflamed
(Figure 21–2). In perforated peptic ulcer, pain almost always begins in the epigastrium,
but as the leaked gastric contents track down the right paracolic gutter,
pain may descend to the right lower quadrant with even diminution
of the epigastric pain.
The location of pain serves only as a rough guide to the diagnosis—“typical” descriptions
are reported in only two thirds of cases. This great variability
is due to atypical pain patterns, a shift of maximum intensity away
from the primary site, or advanced or severe disease. In cases presenting
late with diffuse peritonitis, generalized pain may completely obscure
the precipitating event. Pain confined to either upper quadrant
may be evaluated by anatomic consideration of acute conditions that
affect the underlying organs.
Mode of Onset
and Progression of Pain
The mode of onset of pain reflects the nature and severity of
the inciting process. Onset may be explosive (within seconds), rapidly
progressive (within 1–2 hours), or gradual (over several
hours). Unheralded, excruciating generalized pain suggests an intra-abdominal
catastrophe such as a perforated viscus or rupture of an aneurysm,
ectopic pregnancy, or abscess. Accompanying systemic signs (tachycardia,
sweating, tachypnea, shock) soon supersede the abdominal disturbances
and underscore the need for prompt resuscitation and laparotomy.
A less dramatic clinical picture is steady, mild pain becoming
intensely centered in a well-defined area within 1–2 hours. Any
of the above conditions may present in this manner, but this mode
of onset is more typical of acute cholecystitis, acute pancreatitis,
strangulated bowel, mesenteric infarction, renal or ureteral colic,
and high (proximal) small
Finally, some patients initially have slight—at times
only vague—abdominal discomfort that is fleetingly present
diffusely throughout the abdomen. It may be unclear whether these
patients even have an acute abdomen or whether the illness is likely
to be a matter for medical rather than surgical attention. Associated
gastrointestinal symptoms are infrequent at first, and systemic
symptoms are absent. Eventually, the pain and abdominal findings
become more pronounced and steady and are localized to a smaller
area. This pattern may reflect a slowly developing condition or
the body’s defensive efforts to cordon off an acute process.
This broad category includes acute appendicitis (especially retrocecal
or retroileal), incarcerated hernias, low (distal) small bowel and large
bowel obstructions, uncomplicated peptic ulcer disease, walled-off
(often malignant) visceral perforations, some genitourinary and
gynecologic conditions, and milder forms of the rapid-onset group
mentioned in the first paragraph.
The nature, severity, and periodicity of pain provide useful clues
to the underlying cause (Figure 21–3).
Steady pain is most common. Sharp superficial
constant pain due to severe peritoneal irritation is typical of
perforated ulcer or a ruptured appendix, ovarian cyst, or ectopic
pregnancy. The gripping, mounting pain of small bowel obstruction
(and occasionally early pancreatitis) is usually intermittent, vague,
deep-seated, and crescendo at first but soon becomes sharper, unremitting,
and better localized. Unlike the disquieting but bearable pain associated
with bowel obstruction, pain caused by lesions occluding smaller conduits
(bile ducts, uterine tubes, and ureters) rapidly becomes unbearably intense.
Pain is appropriately referred to as colic if there
are pain-free intervals that reflect intermittent smooth muscle
contractions, as in ureteral colic. In the strict sense, the term “biliary
colic” is a misnomer because biliary pain does not remit.
The reason is that the gallbladder and bile duct, in contrast to
the ureters and intestine, do not have peristaltic movements. The “aching
discomfort” of ulcer pain, the “stabbing, breathtaking” pain
of acute pancreatitis and mesenteric infarction, and the “searing” pain
of ruptured aortic aneurysm remain apt descriptions. Despite the
use of such descriptive terms, the quality of visceral pain is not
a reliable clue to its cause.
The location and character of pain are helpful in the
differential diagnosis of the acute abdomen.
Agonizing pain denotes serious or advanced disease. Colicky pain
is usually promptly alleviated by analgesics. Ischemic pain due
to strangulated bowel or mesenteric thrombosis is only slightly assuaged
even by narcotics. Nonspecific abdominal pain is usually mild, but
mild pain may also be found with perforated ulcers that have become
localized and in mild acute pancreatitis. An occasional patient
will deny pain but complain of a vague feeling of abdominal fullness
that feels as though it might be relieved by a bowel movement. This
visceral sensation (gas stoppage sign) is due to reflex
ileus induced by
an inflammatory lesion walled off from the free peritoneal cavity,
as in retrocecal or retroileal appendicitis.
Past episodes of pain and factors that aggravate or relieve pain
should be noted. Pain caused by localized peritonitis, especially
when it affects upper abdominal organs, tends to be exacerbated
by movement or deep breathing.
The clinician should be familiar with the pathophysiology and
salient features of the common causes of acute abdomen. The location,
character, and severity of the pain in relation to its duration
of onset along with the presence or absence of systemic symptoms
help to differentiate rapidly progressive (and usually more serious)
surgical conditions (eg, intestinal ischemia) from more indolent
or medical causes (eg, ruptured ovarian cysts).
Associated with Abdominal Pain
Anorexia, nausea and vomiting, constipation, or diarrhea often
accompanies abdominal pain, but since these are nonspecific symptoms,
they do not have much diagnostic value.
When sufficiently stimulated by secondary visceral afferent fibers,
the medullary vomiting centers activate efferent fibers to induce
reflex vomiting. Hence, pain in the acute surgical abdomen usually
precedes vomiting, whereas the reverse holds true in medical conditions.
Vomiting is a prominent symptom in upper gastrointestinal diseases
such as Boerhaave syndrome, Mallory-Weiss syndrome, acute gastritis,
and acute pancreatitis. Severe, uncontrollable retching provides
temporary pain relief in moderate attacks of pancreatitis. The absence
of bile in the vomitus is a feature of pyloric stenosis. Where associated
findings suggest bowel obstruction, the onset and character of vomiting
may indicate the level of the lesion. Recurrent vomiting of bile-stained
fluid is a typical early sign of proximal small bowel obstruction.
In distal small or large bowel obstruction, prolonged nausea precedes vomiting,
which may become feculent in late cases. Disorders that induce vomiting
in younger patients may give rise only to anorexia or nausea in
older patients. Although vomiting may present in either acute appendicitis
or nonspecific abdominal pain, coexisting nausea and anorexia are
more suggestive of the former condition.
Reflex ileus is often induced by visceral afferent fibers stimulating
efferent fibers of the sympathetic autonomic nervous system (splanchnic
nerves) to reduce intestinal peristalsis. Hence, paralytic ileus
undermines the value of constipation in the differential diagnosis
of an acute abdomen. Constipation itself is hardly an absolute indicator
of intestinal obstruction. However, obstipation (the
absence of passage of both stool and flatus) strongly suggests mechanical bowel
obstruction if there is progressive painful abdominal distention
or repeated vomiting.
Copious watery diarrhea is characteristic of gastroenteritis
and other medical causes of an acute abdomen. Blood-stained diarrhea
suggests ulcerative colitis, Crohn disease, or bacillary or amebic dysentery.
It is also common with ischemic colitis but often absent in intestinal
infarction due to superior mesenteric artery occlusion.
These are extremely helpful if present. Jaundice suggests
hepatobiliary disorders; hematochezia or hematemesis, a gastroduodenal
lesion or Mallory-Weiss syndrome; or hematuria, ureteral
colic or cystitis. The passage of blood clots or necrotic mucosal
debris may be the sole evidence of advanced intestinal ischemia.
Aspects of the History
The menstrual history is crucial to the diagnosis of ectopic
pregnancy, mittelschmerz (due to a ruptured ovarian follicle), and
endometriosis. A history of vaginal discharge or dysmenorrhea may denote
pelvic inflammatory disease.
Anticoagulants have been implicated in retroperitoneal and intramural
duodenal and jejunal hematomas; oral contraceptives have been implicated
in the formation of benign hepatic adenomas and in mesenteric venous
infarction. Corticosteroids, in particular, may mask the clinical
signs of even advanced peritonitis. Pyloric perforation has been
caused by “crack” smoking.
Family history often provides the best information about medical
causes of an acute abdomen.
Travel history may raise the possibility of amebic liver abscess
or hydatid cyst, malarial spleen, tuberculosis, Salmonella
typhi infection of the ileocecal area, or dysentery.
Any history of a previous abdominal, groin, vascular, or thoracic
operation may be relevant to the current illness. Particular attention
to the mode of operation (laparoscopic, open, endovascular) and
any anatomic reconstructions may clarify aspects of the current
complaint. If possible within the time constraints imposed by the
urgency of the current problem, operative notes and pathology reports
should be obtained and reviewed.