The clinician should try to obtain as complete a history as possible as this is generally the cornerstone of an accurate diagnosis. The history should include a complete description of the patient’s pain and associated symptoms. Medical, surgical, and social history should also be sought as this may provide important information.
Assessment of the patient’s pain
The classic PQRST mnemonic for a complete pain history is as follows:
- P3 – Positional, palliating, and provoking factors
- Q – Quality
- R3 – Region, radiation, referral
- S – Severity
- T3 – Temporal factors (time and mode of onset, progression, previous episodes)
This mnemonic will help to ensure a thorough history, but rigidly following the above sequence does not allow for a smooth patient interview, so the authors prefer to ask the patient where they feel the pain (location), what kind of pain it is (character), when and how it began (onset), how bad it is (intensity), and where else they feel it, what makes it worse or better, how it has changed over time, and whether they have ever had it before.
Embryology determines where a patient will “feel” visceral pain, which is generally perceived in the midline because afferent impulses from visceral organs are poorly localized. Visceral nociceptors can be stimulated by distention, stretch, vigorous contraction, and ischemia. Pain from foregut structures, which include the stomach, pancreas, liver, biliary system, and the proximal duodenum, will be typically localized to the epigastric region. The rest of the small bowel and the proximal third of the 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, and distal two-thirds of the colon, as well as pelvic genitourinary organs usually cause pain in the suprapubic region. Pain is usually reported in the back for retroperitoneal structures such as the aorta and kidneys.5
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, and gastric contents).5
Acute-onset pain, especially if severe, should prompt immediate concern about a potential intra-abdominal catastrophe. 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.8
Likewise, volvulus, particularly of the sigmoid colon, can present with a gradual onset of pain.9
Serious vascular issues such as mesenteric ischemia may present with a gradual onset of pain. Conversely, one would expect a gradual onset in the setting of an infectious or inflammatory process. Pain that awakens the patient from sleep should be considered serious until proven otherwise.10
The time of onset establishes the duration of the 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 under-report symptoms.
Patterns of radiation and referral of pain
The neural pathways give rise to predictable patterns of referred pain and radiation. Kehr’s sign is a classic example where diaphragmatic irritation, usually from free intraperitoneal blood, causes shoulder pain.11
Any other inflammatory process or organ contiguous to the diaphragm can also cause referred shoulder pain. Another well described example is ipsilateral scapula 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”: regions of referral in the abdomen and flanks. Thus, in cases where a patient’s perceived location of symptoms appears to be completely unrevealing on physical exam, a careful assessment of musculoskeletal structures should be made.12
Duration and progression
Persistent worsening pain is worrisome, while pain that is improving is typically favorable. Serious causes of abdominal pain generally present early in their course; however, delays in presentation can 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. Although labeled “colic,” gallbladder pain is generally not paroxysmal, and it almost never lasts less than 1 hour, with an average of 5–16 hours’ duration, and ranging up to 24 hours.13
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) late in the course of a bowel obstruction.
Provocative and palliating factors
The clinician needs to ask what, if anything, makes the pain worse and what improves the pain. It is important to establish whether jarring motions such as coughing or walking exacerbate the pain, suggesting peritoneal irritation.14
Patients with peritonitis often remark on increased pain with jolts or bumps in the road. A recommended interview sequence would be “how did you get here today? Tell me about the ambulance/car ride.” With upper abdominal pain one should specifically ask whether it is pleuritic as 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 treatments, 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, or partial bowel obstruction.
Assessment of the associated symptoms
Gastrointestinal and urinary symptoms are the primary focus; however, it is important to ask about fever and cardiopulmonary symptoms. Associated symptoms should be placed in the clinical context, including the patient’s age and the current point in the course of the illness.
With appendicitis, most physicians expect the patient to report anorexia. However, pooling of the literature indicates that, while this is a discriminatory symptom, it is only present in 68% of patients with appendicitis.15
The report of this symptom decreases to 20%–44% in elderly patients with appendicitis.16
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.10
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, one anticipates a progression from gastric contents to bilious to feculent emesis as the duration of the illness increases. Frequent nonproductive retching can point to gastric volvulus,18
while 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 intestinal malrotation.19
Blood or coffee ground emeses are usually caused by gastric diseases or complications of liver disease. Massive hematemesis in a patient with a prior abdominal aortic aneurysm repair may be due to aorto-enteric fistula.20
The key feature of vomiting from more benign causes such as viral or food-borne illness is that it is self-limited.
While 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.15
In one series of 1000 ED patients presenting with abdominal pain, 18% presented with diarrhea. No patient aged less than 40 with diarrhea and continuous pain was found to have a surgical cause for their symptoms.22
Conversely, diarrhea can be reported in up to one-fifth of patients with colonic obstruction.23
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, since the bowel clears gas more rapidly than fluid. 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, while frank blood can indicate a lower source or a massive upper bleed with rapid transit time. The urge to defecate in a patient with acute abdominal pain has been described as a harbinger of serious disease including a ruptured aneurysm in the older patient or ruptured ectopic pregnancy in the young.24
Many genitourinary tract diseases can present with abdominal pain. Conversely, any inflammatory process contiguous to the genitourinary tract (including appendicitis, cholecystitis, pancreatitis, or any inflammatory process involving bowel) may result in both pyuria and dysuria. This can lead to misdiagnosis of both gastrointestinal and genitourinary conditions. In men, testicular torsion may present as abdominal pain, nausea, and vomiting. In women, 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 genitourinary history should be obtained in most patients with abdominal pain. The report of normal, regular menses should not preclude consideration of current pregnancy.25
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).
Past medical and surgical history, current medications
A history of prior abdominal surgery can rule out a condition or raise the suspicion for a complication such as obstruction from adhesions. Many medical conditions cause acute abdominal pain, including diabetic ketoacidosis, hypercalcemia, Addison’s disease, and sickle cell crisis. Other less common metabolic causes of acute abdominal pain include uremia, lead poisoning, methanol intoxication, hereditary angioedema, and porphyria. The patient’s current medications should be reviewed with attention to those affecting the integrity of the gastric mucosa (steroids and nonsteroidal anti-inflammatory drugs), immunosuppressive agents (impair host defenses and the generation of an inflammatory response), and any that can impair nociception (narcotics may also be a cause of pain due to constipation).
The patient’s use of drugs and alcohol may have important diagnostic implications. Cocaine use may cause intestinal as well as cardiac ischemia. Gastrointestinal complications of alcohol abuse are extensive and well known. Direct questions regarding domestic violence may reveal a traumatic source of pain.