Embryology determines where a patient feels visceral pain, which is generally perceived in the midline because afferent impulses from visceral organs are poorly localized. Pain fibers travel to the central nervous system via both autonomic nerves and spinal afferents. The latter fibers tend to synapse with second-order neurons in the posterior horns that are shared with afferent fibers from other visceral structures as well as somatic afferents (convergence). This arrangement with projections extending over several spinal cord levels results in poorly localized pain that may be referred to musculoskeletal structures as well as other visceral organs.^5,6 To further complicate the situation, numerous studies have indicated that patients with chronic painful or inflammatory conditions have heightened sensitivity to pain in anatomically remote visceral and somatic structures.^7,8

Visceral nociceptors can be stimulated by distention, stretching, vigorous contraction, and ischemia. Pain from foregut structures, which include the stomach, pancreas, liver, biliary system, and the proximal duodenum, is typically localized to the epigastric region. The rest of the small bowel and the proximal third of colon, including the appendix, are midgut structures, and visceral pain associated with these organs is perceived in the periumbilical region. Hindgut structures, such as the bladder, distal two-thirds of the colon, and pelvic genitourinary (GU) organs, usually cause pain in the suprapubic region. Pain is often reported in the back for retroperitoneal structures, such as the aorta and kidneys.^9,10 The implications of the visceral innervation of the gallbladder are frequently overlooked by clinicians who exclude gallstone disease if patients do not have localized right upper quadrant pain. The gallbladder is innervated by visceral fibers, and studies consistently show that biliary colic is extremely poorly localized, with pain being perceived almost anywhere in the epigastrium or lower chest, and several investigators finding that it is less likely to be perceived in the right upper quadrant than in the epigastrium.^11,12 In summary, with afferent sensory pathways under active scientific investigation, the prudent clinician will be cautious in ascribing a patient’s symptoms to a specific organ or location based solely on a patient’s localization of his or her symptoms.

Clinicians should seek to distinguish between the dull, poorly localized, aching or gnawing pain generated by viscerally innervated organs, compared with the characteristically sharp, more defined, and localized somatic pain caused by irritation of the parietal peritoneum or other somatically innervated structures. Somatic pain is transmitted via the spinal nerves from the parietal peritoneum or mesodermal structures of the abdominal wall. Noxious stimuli to the parietal peritoneum may be inflammatory or chemical in nature (eg, blood, infected peritoneal fluid, gastric contents).^9,13

Acute onset pain, especially if severe, should prompt immediate concern about an intra-abdominal complication. The foremost consideration would be a vascular emergency, such as a ruptured abdominal aortic aneurysm (AAA) or aortic dissection. Other considerations for pain of acute onset include a perforated ulcer, volvulus, mesenteric ischemia, and torsion; however, these conditions may also occur without an acute onset. For example, only 47% of elderly patients with a proven perforated ulcer report the acute onset of pain.¹⁴ Likewise, volvulus, particularly of the sigmoid colon, can present with a gradual onset of pain.¹⁵ Other serious vascular issues, such as mesenteric ischemia, may present with a gradual onset of pain. Conversely, a gradual onset in the setting of an infectious or inflammatory process may be expected. Pain that awakens the patient from sleep should be considered serious until proven otherwise.¹⁶ The time of onset establishes the duration of pain and allows the physician to interpret the current findings in relation to the expected temporal progression of the various causes of abdominal pain.

Pain that is severe should heighten the concern for a serious underlying cause; however descriptions of milder pain cannot be relied on to exclude serious illness, especially in older patients who may underreport symptoms.

The previous discussion of afferent neural pathways and convergence gives rise to predictable patterns of referred pain and radiation. Kehr sign is a classic example in which diaphragmatic irritation, usually from free intraperitoneal blood, causes shoulder pain.¹⁷ Any other inflammatory process or organ contiguous to the diaphragm can also cause referred shoulder pain. Another well-described example is ipsilateral scapular pain caused by biliary disease. Radiation may also reflect progression of disease such as with continued aortic dissection or ongoing passage of a ureteral stone. While considering referred pain, it is important to remember that deep musculoskeletal structures (especially of the back) are innervated by visceral sensory fibers with similar qualities to those arising from intra-abdominal organs. These fibers converge in the spinal cord, giving rise to scleratomes, which are regions of referral in the abdomen and flanks. Thus, in cases in which the patients’ perceived location of symptoms seems to be completely unrevealing on physical examination, a careful assessment of musculoskeletal structures should be made.¹⁸

Persistent worsening pain is worrisome, whereas pain that is improving is typically favorable. Serious causes of abdominal pain may present early in their course, allowing opportunity for intervention if promptly diagnosed. However, delays in onset of symptoms or in presentation frequently occur, especially in the elderly. Certain patterns of progression can be diagnostic, such as the migration of pain in appendicitis where the initial distention of the appendix causes a periumbilical visceral pain that shifts to the right lower quadrant once the inflammatory process is detected by the somatic sensors of the parietal peritoneum. It should be noted that in contrast to other forms of colic, gallbladder pain caused by an affected stone is not waxing and waning in quality. It is steady, almost never lasts less than 1 hour, and with an average of 5 to 16 hours duration, ranges up to 24 hours.^11,19 Small bowel obstruction typically progresses from an intermittent (colicky) pain to more constant pain when distention occurs. One would only expect somatic pain (arising from transmural ischemia or perforation contiguous to the parietal peritoneum) very late in the course.

The clinician needs to ask what, if anything, worsens and improves the pain. It is important to establish whether jarring motions, such as coughing or walking, exacerbate the pain, suggesting peritoneal irritation.¹³ Patients with peritonitis often remark on increased pain with jolts or bumps in the road. With upper abdominal pain, the clinician should specifically determine if it is pleuritic because this may signify chest disease. Peptic ulcer disease may be exacerbated (gastric) or relieved (duodenal) by eating. Mesenteric ischemia may be precipitated by eating, as can the pain of intermittently symptomatic gallstones, often associated with fatty meals. The patient should be questioned about any self-treatment, particularly analgesics and antacids, and the response to these measures.

Recurrent episodes generally point to a medical cause with the exceptions of mesenteric ischemia (intestinal angina), gallstones, ureterolithiasis, diverticulitis, or partial bowel obstruction.

With appendicitis most physicians expect the patient to report anorexia. However, pooling of the literature indicates that, although anorexia is a discriminatory symptom, it is only present in 68% of patients with appendicitis.²⁰ The report of this symptom decreases to 20% to 44% in elderly patients with appendicitis.²¹

Vomiting may occur in almost any abdominal disease. Pain generally precedes vomiting in surgical conditions, with the important exception of esophageal rupture from forceful emesis.^16,22 It is usually present in small bowel obstruction unless the obstruction is partial or the patient is presenting early in the course. Many other serious entities, including large bowel obstruction, frequently present without vomiting. The nature of the vomiting may be diagnostically helpful. With small bowel obstruction, a progression from gastric contents to bilious to feculent emesis is anticipated as the duration of the illness increases. Frequent nonproductive retching can point to gastric volvulus,²³ whereas repetitive nonbilious vomiting may indicate gastric outlet obstruction. The presence of blood or bile should be noted. Bilious vomiting in an infant is always considered a harbinger of serious abdominal illness such as malrotation.²⁴ Blood or coffee-ground emeses is usually caused by gastric diseases or complications of liver disease. Hematemesis caused by aortoenteric fistula is bright red, massive, and usually catastrophic and should be suspected with a history of a prior AAA repair.²⁵ The key feature of vomiting from more benign causes, such as viral or food-borne illness, is that it is self-limited.

Although diarrhea is a frequent accompaniment of more benign abdominal conditions, its presence alone should never rule out serious disease. For example, diarrhea is common with mesenteric ischemia and is frequently reported in conditions such as appendicitis.^20,26 In one series of 1000 ED patients presenting with abdominal pain, 18% presented with diarrhea. No patient younger than 40 years with diarrhea and continuous pain was found to have a surgical cause for their symptoms.²⁷ Conversely, diarrhea can occur in up to one-fifth of patients with colonic obstruction.²⁸ Diarrhea also occurs in early small bowel obstruction as the reflexively hyperactive bowel distal to the obstruction clears itself, and with partial obstruction, diarrhea may be ongoing. Absence of flatus is a more reliable sign than constipation in bowel obstruction because the bowel clears gas more rapidly than fluid. In addition, gas, in contrast to fluid, cannot be replaced by intestinal secretory mechanisms distal to an obstruction. Bloody stool in the presence of significant abdominal pain should raise the suspicion for mucosal compromise from ischemia. Melena suggests an upper source of bleeding, whereas frank blood can indicate a lower source or a massive upper bleed with rapid transit time. In a patient with acute abdominal pain, the urge to defecate has been described as a harbinger of serious disease, including a ruptured aneurysm in the older patient or ruptured ectopic pregnancy in the young.²⁹

Many GU tract diseases can present with abdominal pain. Conversely, any inflammatory process contiguous to the GU tract (including appendicitis, cholecystitis, pancreatitis, or any inflammatory process involving bowel) may result in both pyuria and dysuria. This condition can lead to misdiagnosis of both GI and GU conditions. In men, testicular torsion may present as abdominal pain with nausea and vomiting, and chronic prostatitis may cause nonspecific symptoms. In women, pelvic inflammatory disease, endometriosis, and ovarian pathologic condition frequently cause abdominal or GI symptoms.⁶ The enlarging uterus of pregnancy can itself cause discomfort and displace abdominal organs in such a way as to further complicate the diagnosis of many abdominal conditions, especially appendicitis. For these reasons a menstrual (where applicable), sexual, and GU history should be obtained in most patients with abdominal pain. The report of normal regular menses should not preclude consideration of current pregnancy.³⁰ Cardiopulmonary symptoms, such as cough and dyspnea, can point to a nonabdominal cause of abdominal pain. Syncope may indicate disease originating in the chest (pulmonary embolism, dissection) or abdomen (acute aortic aneurysm, ectopic pregnancy).