Onset

Abdominal pain may be of sudden, rapid, or gradual onset. Pain of sudden onset occurs within a second. The patient will relate the time of onset at a precise moment, usually stating exactly what activity was going on at the time the pain began. Sudden onset of pain is commonly associated with perforation of the gastrointestinal tract from a gastric or duodenal ulcer, a colonic diverticulum, or a foreign body. Other common causes include a ruptured ectopic pregnancy, mesenteric infarction, ruptured aortic aneurysm, and embolism of an abdominal vessel.

Pain of rapid onset begins with a few seconds and steadily increases in severity over the next several minutes. The patient will recall the time of onset in general but without the precision noted in pain of sudden onset. Pain of rapid onset is associated with cholecystitis, pancreatitis, intestinal obstruction, diverticulitis, appendicitis, ureteral stone, and penetrating gastric or duodenal ulcer.

Pain of gradual onset is pain that slowly becomes more severe only after a number of hours or even days have elapsed. The patient's memory as to the time of onset of the pain is vague; he or she can pinpoint only the day or possibly the week of onset. Pain of gradual onset is commonly associated with neoplasms, chronic inflammatory processes, and large bowel obstruction. Many other intra-abdominal conditions are associated with pain of gradual onset, making an accurate diagnosis from the history more difficult with this symptom than in pain of sudden or rapid onset.

Progression

It is of real diagnostic significance to determine the progression of the pain over the interval from the time of onset until the patient seeks medical attention. Has the pain abated, or has it increased? Have there been intervals of total absence of the pain, or has the pain always been present, changing only in character? From this information the clinician may be able, for example, to identify a perforated ulcer that has produced pain of sudden onset that subsequently abates dramatically if the perforation seals and no further leak occurs.

Intermittent attacks of abdominal pain that progress to a steady, constant ache suggest a small bowel obstruction with vascular compromise that will lead to the grave complication of necrosis of the involved incarcerated bowel.

Migration

Pain that "shifts" from the original site of onset to another location in the abdomen is most often associated with acute appendicitis where periumbilical or epigastric pain (visceral) that is present early in the course of the disease is replaced with right lower quadrant (somatic) pain later in the illness when the parietal peritoneum becomes involved with the inflammatory process.

Pain produced by irritation of the parietal peritoneum by duodenal contents leaking from a perforated duodenal ulcer may begin in the epigastrum and may migrate to the lower quadrants of the abdomen or pelvis depending on the pathway that the leaking material takes through the abdominal cavity.

Character

Determining the character, or what kind of pain the patient is experiencing, is of prime importance in discovering the pathologic process responsible for it. Since the patient's description of the pain must be purely subjective, it is essential that the clinician and the patient communicate clearly so that the precise character of the pain can be identified. The patient will usually need help from the doctor in describing the pain by suggesting similarities or comparisons, such as hunger pain, burning pain, sticking pain. It is especially important that the presence or absence of cramping pain be established. The term cramp has many interpretations, so the patient will need to have an example of a cramplike pain that leaves no room for misinterpretation. One such example is to liken the pain to the wringing out of a washcloth with intense pain corresponding to wringing of the washcloth and abating when the washcloth is untwisted.

Abdominal pain can be characterized as cramping, dull, or aching and as either constant or intermittent.

Cramping abdominal pain is characterized by pain that increases in intensity in short waves to a maximum and then abruptly ceases for a period of complete absence of pain. Repetition of the pain occurs at intervals. This type of pain is associated with mechanical small bowel obstruction, and when clearly present, it is pathognomonic of that condition. The interval between cramping pain helps locate the site of the obstruction with short pain-free intervals in more proximal obstructions and longer pain-free intervals in more distal obstruction.

Constant dull or aching abdominal pain is usually caused by distention or edema of the wall of a hollow viscus. Pain from stretch of the capsule of the liver and the spleen may also be perceived as dull or aching pain.

When a hollow viscus such as the gall bladder is distended, as is most common, from obstruction of the cystic duct, constant, dull, aching pain is experienced. When the gall bladder contracts against the obstruction, the stretch of the gall bladder wall is suddenly intensified, producing a crescendo of pain in addition to the constant dull ache already present (gall bladder colic).

Intensity

Each individual perceives pain intensity differently. The intensity of pain in an individual patient can often be assessed by the way in which the patient physically responds to it. Patients with peritonitis (somatic pain) invariably lie still, perhaps on one side or the other with the knees and hips flexed, whereas patients with pain arising from the hollow or solid viscera (visceral pain) do not lie still but constantly change position or move about.

Take, for example, a patient with the sudden onset of chemical peritonitis secondary to a perforated duodenal ulcer. The patient will immediately stop whatever activity he or she was doing at the moment of perforation, quickly sit or lie down, and remain as still as possible.

By contrast, a patient who has the onset of abdominal pain caused by acute distention of the gall bladder will not be able to find comfort by lying down in any position, but will move from chair to bed to the bathroom, where numerous attempts to relieve the pain by enemas, cathartics, self-induced vomiting, antacids, or other home remedies for "gas" pains are characteristic responses to visceral pain.

Localization

Visceral pain resulting from stretch of smooth muscle is localized in one of the three midline zones of the abdomen: epigastric, midabdominal, and lower abdominal. This midline zone pain, the sum of pain from the right and left splachnic pathways, is poorly localized, covers several body segments and, depending on its cause, varies from dull, aching, constant pain to cramping pain. Nausea, vomiting, pallor, and sweating are commonly associated with visceral pain.

Somatic pain is well localized. It is located asymmetrically and is intensified by jarring, deep inspiration or pressure on the abdominal wall.

One of the most useful physical examination procedures to identify the presence of abdominal pain of somatic origin is to ask the patient to distend his abdomen alternately by "pushing out" his umbilicus to touch the examiner's hand (held a few inches above the abdomen) and then to "suck in" his umbilicus to touch his spine. These subjective parietal peritoneum stretching procedures often identify the site of somatic pain by simple observation. It is especially useful in examination of children, as the subjective location of the pain without actual palpation of the abdomen by the physician may obviate misinterpretation from the child's anxiety. Since the cerebrospinal nerves that supply sensation to the anterior and lateral peritoneal surfaces are unilateral, any stimulation of the parietal peritoneal surfaces are lateralized quite well. Nausea, vomiting, pallor, and sweating are seldom associated with somatic pain.

It is well to have the patient indicate the site of the pain while standing and in the prone position to be certain of the true location.

Referred Pain and Accompanying Symptoms

Three cerebrospinal nerves, the phrenic, obturator and genitofemoral, are of particular importance because of the characteristic referred pain carried over these pathways in certain intra-abdominal conditions. Irritation, stretch, or injury of the dorsal or ventral aspects of the dome of the diaphragm produces referred pain in the supraclavicular fossa (Kehr's sign) corresponding to the sensory branches of the phrenic nerve (C3 through C5). Irritation of the genitofemoral nerve from such retroperitoneal inflammatory processes as retrocecal appendicitis or retroperitoneal perforation of the duodenum produces pain in the labia, testicle, or shaft of the penis on the involved side.

Irritation of the obturator nerve in the obturator fossa, usually from an incarcerated obturator hernia, produces pain along the medial aspect of the thigh to the knee (Howship–Romberg's sign).

Clearly, symptoms that accompany abdominal pain are important in making an accurate diagnosis. Among the most important are nausea, vomiting, abdominal distention, diarrhea, constipation, obstipation, tarry stools, chills, fever, urinary frequency, hematuria, and jaundice.

Other Structures That Can Cause Pain

Upper abdominal organs have anatomic features that make pain patterns emanating from them far more complex than those of the appendix. Painful lesions of the gastroesophageal junction, the fundus and lesser curvature of the stomach, the biliary tract, and proximal portions of the duodenum commonly produce pain in the interscapular zone corresponding to the sixth thoracic segment, since the somatic innervation of the lesser omentum is supplied by that thoracic nerve. Pancreatic pain is often perceived in the same location one segment lower.

The stomach is so situated that portions of its surface are in contact with the diaphragm, the gastrohepatic ligament, the lesser sac, the pancreas, the parietal peritoneum, the splenic hilus, the gastrocolic ligament, the transverse mesocolon, and the transverse colon. Inflammatory or neoplastic lesions of the stomach that involve any of these surfaces may irritate somatic nerves from several different spinal segments. Accordingly, pain may be localized by the patient to the supraclavicular fossa from phrenic nerve stimuli, the interscapular region from irritation of T6 through T8, or even the lumbar region from involvement of the T12 through L1 spinal cord segments.

Similarly to the stomach, the duodenum is in anatomic relationship to a number of somatic cerebrospinal nerve roots. As a result, perforating ulcer pain can be appreciated in the interscapular zone, the right subcostal region, and the right lower quadrant depending on which somatic nerves are involved in the pathologic process. Retroperitoneal perforation of the duodenum from blunt abdominal trauma may cause irritation of the genitofemoral nerve from leaking duodenal contents resulting in pain in the right testicle or labia.

Pain from the gall bladder and biliary tract may have bilateral localization because they arise from outbudding of the midline gut and have bilateral splanchnic innervation. If the inflammatory process of acute suppurative cholecystitis involves the parietal peritoneum of the right upper quadrant, somatic pain with its usual local manifestations and referred pain along the involved cerebrospinal nerve to the tip of the scapula (T8) may be present. Involvement of the parietal peritoneum in the right upper quadrant from suppuration of the gall bladder is not a very common event, as the greater omentum (which has no somatic sensory innervation) often surrounds the inflamed gall bladder as a buffer between the inflammatory process and the parietes.

Pathologic conditions that arise from the pancreas are responsible for a broad spectrum of pain-producing syndromes. In addition, extrinsic lesions (e.g., penetrating duodenal ulcer) are frequently involved in the production of pain from the pancreas. Further, disruption of the integrity of the gland by pancreatitis permits the extravasation of enzymes that spread to many different intra-abdominal locations that may involve somatic spinal pathways from the phrenic nerve to the lumbosacral plexus.

The small intestine, like the rest of the midgut, produces upper midline, periumbilical visceral pain in response to distention or stretch. The foregut and hindgut are far less sensitive to stretch or distention. Pain from these portions of the intestinal tract, the stomach and duodenum from the former and the descending colon and rectum from the latter, is more often initiated by inflammatory lesions than from distention.

Experimental studies of the production of pain from the gastrointestinal tract in humans by inflation of balloons at various locations within the lumen of the gut should be interpreted very cautiously, as they bear little or no resemblance to actual pathologic conditions that produce pain in humans. The most valid observations concerning the origins of abdominal pain come from surgeons who have the advantage of prompt inspection of the site of pathology within the abdomen and the opportunity to compare these findings on the spot with the patient's perception of the abdominal pain.

The skin, subcutaneous tissues, fascia, muscle, and parietal peritoneum of the abdominal wall are richly supplied with somatic nerves from T6 through T12. Pain in the abdominal wall can result from neuromas in scars from previous laparotomies, such medical conditions as acute porphyria, or from herpes zoster. In addition, pain from trauma to the abdominal wall from blunt injury must be carefully identified to rule out abdominal pain originating from an intraperitoneal injury.

The ureters are second only to the pancreas as a source of abdominal pain caused by structures in the retroperitoneum. The renal pelvis is sensitive to distention, and the ureters are richly supplied with nerves from T10 through T12. Ureteral pain is ipsilateral, severe, and cramping in nature (renal colic). It is usually of such severity and located in the flank that the diagnosis is difficult to confuse with other abdominal catastrophies. Pain in the testicle or labia (T10) may on occasion confuse the diagnosis of renal colic with retrocecal appendicitis. The presence of red blood cells in the urinalysis may help solve this diagnostic dilemma.

Since the lower intercostal nerves also provide the parietal pleura and periphery of the diaphragm with sensory (somatic) innervation, as well as the abdominal wall and anterior peritoneal parietes, it is understandable that inflammatory processes that involve the parietal pleura innervated by these nerves may also be manifested by abdominal pain. Needless to say, an appendectomy is poor therapy for right lower lobar pneumonia that has produced reflex abdominal wall pain in the right lower quadrant.

Pericarditis, myocardial infarction, and pulmonary infarction may also cause inflammatory lesions that involve the parietal diaphragmatic or thoracic pleura, producing referred abdominal pain that may be misdiagnosed as a primary intraperitoneal disorder.