Acute Abdominal Pain - Clinical Tree

Acute abdominal pain is a frequent complaint that causes patients to visit an emergency department. In 2014, 11.1 million emergency department visits in the USA were due to abdominal pain, accounting for 8% of all emergency department visits that year. Approximately 40% of these patients have nonspecific findings. Of the remainder in whom a specific diagnosis is ascertainable, most causes are surgical disorders that warrant further evaluation and intervention. In a small number, life-threatening pathologies are present. Therefore the evaluation of acute abdominal pain must be efficient and lead to an accurate diagnosis soon after presentation so that the treatment of patients who are seriously ill is not delayed and resources are not overutilized on patients with a self-limited disorder.

Anatomy and Physiology

A number of physiologic factors determine how abdominal pain in perceived. These include the nature of the stimulus, type of neuroreceptor involved, anatomy of the neural pathways from the site of injury to the CNS, and interaction of modifying influences on the transmission, interpretation, and reaction to pain messages. Pain resulting from abdominal pathology is transduced in different ways by sensory afferent fibers that travel with the autonomic and somatic nervous systems. These two systems transduce pain in different ways, leading to different nociceptive sensations. Crosstalk between the two systems can result in yet more variation in the perception of abdominal distress. This unique neuroanatomy results in three distinct types of pain: visceral, somatic-parietal, and referred. Visceral pain is usually vague in both onset and localization and perceived as a dull sensation in the abdominal midline. Somatic-parietal pain is more intense, sharp, and well localized. Referred pain is perceived at a point distant from the inciting pathology and may be perceived to be outside the abdomen entirely.

Sensory neuroreceptors in abdominal organs are located in the mucosa and muscularis of hollow viscera, on serosal structures such as the peritoneum, and within the mesentery ( Fig. 11.1 ). In addition to nociception (the perception of noxious stimuli), sensory neuroreceptors are involved in the regulation of secretion, motility, and blood flow via local and central reflex arcs. Although sensory information conveyed in this manner is not usually perceived, disordered regulation of these GI functions (secretion, motility, blood flow) can cause pain. For example, patients with IBS perceive pain as a result of heightened sensitivity of intestinal afferent neurons to normal endogenous stimuli that results in altered intestinal motility and secretion (see Chapter 122 ).

Fig. 11.1, Sensory innervation of the GI tract. The distribution of afferent sensory nerve endings in the intestinal wall is shown, as follows: (1) mesentery, (2) mesenteric blood vessels, (3) serosa, (4) intramuscular arrays (vagus nerves only), (5) intraganglionic laminar endings (vagus and pelvic nerves only), (6) mucosa. The principal contributors to nociception are 1, 2, 3, and 6.

Visceral Pain

The abdominal viscera are innervated by two systems: vagal afferent nerves and spinal visceral sensory nerves. Spinal visceral afferent nerves are further specified as splanchnic nerves that follow sympathetic efferent pathways and pelvic visceral afferent nerves that run with parasympathetic efferent pathways ( Fig. 11.2 ). Spinal visceral nerves , also known as splanchnic nerves , innervate all layers of the intestinal wall, including the serosa, and the mesentery. These nerves are composed predominantly of unmyelinated C fibers, although a small number of fine, myelinated A-delta fibers are also present. Visceral pain is transduced at its source by bare nerve endings that lack the specialized structures such as capsules found in somatic nerve endings. Neurophysiologic studies have identified four distinct types of visceral sensory nerves: chemonociceptors found in the mucosa, tonic mechanoreceptors, high-threshold mechanoreceptors, and so-called “silent” nociceptors. Mucosal chemonociceptors are sensitive to noxious luminal contents. Tonic mechanoreceptors, also known as “wide-range” receptors, have relatively high levels of resting activity and respond to rising wall tension with a linear increase in activity. High-threshold mechanoreceptors, also known as “phasic” receptors, have low resting activity and respond to excessive mechanical distention only. Silent nociceptors are activated only in the presence of inflammatory mediators.

Fig. 11.2, Pathways of visceral sensory innervation. The visceral afferent fibers that mediate pain travel with autonomic nerves to communicate with the central nervous system. In the abdomen, these fibers include the vagal and pelvic parasympathetic nerves and thoracolumbar sympathetic nerves. Sympathetic fibers (red lines) ; parasympathetics (blue lines) . Spinal cord levels: C , Cervical; L , lumbar; S , sacral; T , thoracic.

High-threshold receptors are thought to transduce pain from organs like the ureter and kidney, for which pain is the only sensation perceived consciously, whereas organs like the bladder and stomach, from which non-noxious as well as noxious sensations are perceived consciously, are innervated by both tonic and high-threshold receptors. Spinal splanchnic nerves have wide afferent distribution in the spinal cord through laminae I, II, V, and X. Four anatomic factors contribute to the poor localization of visceral pain and the phenomenon of referred pain to areas distant from its origin. First, spinal splanchnic afferents are spread across a broad range of dorsal root ganglia. The dispersal of painful input at the level of the spinal cord leads to poor anatomic discrimination. Second, spinal afferents have a more generalized and overlapping viscerotopic distribution and enter the spinal cord bilaterally. This lack of side specificity leads to localization of visceral pain in the midline ( Fig. 11.3 ). Third, the ratio of afferent fibers to cell bodies in the dorsal root ganglia is low, and fourth, there is considerable convergence, or crosstalk, between the visceral afferents and the somatic pain neurons in the dorsal horn of the spinal cord. Therefore visceral pain is often vaguely assigned to a broad topologic area. Crosstalk within the spinal cord between spinal visceral afferents fibers and somatic parietal fibers that originate in distant body areas can create the perception of pain in a distant location, or referred pain (see later). In contrast to the spinal splanchnic afferent sensory system, vagal visceral afferents primarily convey non-noxious stimuli, such as satiety.

Fig. 11.3, Localization of visceral pain. Pain arising from organ areas depicted in 1 , 2 , and 3 is felt in the epigastrium, midabdomen, and hypogastrium, respectively, as shown in A . The arrow in A indicates biliary pain that is referred to the right scapular area.

Pain from the abdominal viscera is primarily the result of stretch and distention transduced by mechanoreceptors and, in more severe situations, the presence of inflammatory mediators detected by the silent nerve endings. Cutting and burning of abdominal viscera is not perceived as noxious. These properties explain why gaseous distention during colonoscopy is frequently painful, but polypectomy is not. Once the visceral pain-sensing neurons enter the CNS, they project not only to the somatosensory cortex as part of the lateral pain system (which assigns the signal a location and intensity) but also to the cingulate gyrus as part of the medial pain system, which influences affective behavior (see Chapter 12 ).

Somatic-Parietal Pain

Somatic-parietal pain is mediated by A-δ fibers that are distributed principally to skin and muscle. Signals from this neural pathway are perceived as sharp, sudden, well-localized pain, such as that which follows an acute injury. These fibers convey pain sensations through somatic spinal nerves. Stimulation of these fibers activates local regulatory reflexes mediated by the enteric nervous system and long spinal reflexes mediated by the autonomic nervous system, in addition to transmitting pain sensation to the CNS.

Somatic-parietal pain arising from noxious stimulation of the parietal peritoneum is more intense and more precisely localized than visceral pain. An example of this difference occurs in acute appendicitis, in which early vague periumbilical visceral pain originating within the appendix is followed by localized somatic-parietal pain at McBurney’s point that is produced by inflammatory involvement of the parietal peritoneum adjacent to the appendix. Somatic-parietal abdominal pain is usually aggravated by movement or vibration. The nerve impulses that mediate such pain travel in somatic sensory spinal nerves that correspond to the cutaneous dermatomes of the skin from the sixth thoracic (T6) to first lumbar (L1) vertebral segment. Because these nerve fibers do not cross the midline at the spinal cord, lateralization of parietal pain is much more precise than in visceral pain.

Reflexive responses (e.g., involuntary guarding, abdominal rigidity) are mediated by spinal reflex arcs involving somatic-parietal pain pathways. Afferent pain impulses are modified by inhibitory mechanisms at the level of the spinal cord. Somatic A-delta fibers mediate touch, vibration, and proprioception in a dermatomal distribution that matches the visceral innervation of the injured viscera and synapse with inhibitory interneurons of the substantia gelatinosa in the spinal cord. In addition, inhibitory neurons that originate in the mesencephalon, periventricular gray matter, and caudate nucleus descend within the spinal cord to modulate afferent pain pathways. These inhibitory mechanisms allow cerebral influences to modify afferent pain impulses (see Chapter 12 ).

Referred Pain

Referred pain is felt in areas remote from the diseased organ and results when visceral afferent neurons and somatic afferent neurons from a different anatomic region converge on second-order neurons in the spinal cord at the same spinal segment. This convergence may result from the innervation, early in embryologic development, of adjacent structures that subsequently migrate away from each other. As such, referred pain can be understood to refer to an earlier developmental state (e.g., the central tendon of the diaphragm begins its development in the neck and moves craniocaudad, bringing its innervation, the phrenic nerve, with it). Fig. 11.4 shows how diaphragmatic irritation from a subphrenic hematoma or splenic rupture may be perceived as shoulder pain (Kehr sign).

Evaluation

Effective evaluation of a patient with acute abdominal pain requires careful but expeditious history taking and physical examination (often repeated serially) and, in many cases, informed use of imaging studies. When a carefully performed history and physical examination are paired with appropriate and timely imaging, an accurate diagnosis can often be determined relatively quickly. Inadequate clinical evaluation or poor selection of imaging methods leads to unnecessary delay, often resulting in a poor outcome. Common entities like appendicitis, cholecystitis, and diverticulitis can be diagnosed with almost complete accuracy; patients with other diseases require an orderly and efficient evaluation and judicious selection of imaging studies.

Approach to Acute Care

Abdominal pain can be the presenting symptom of a life-threatening abdominal catastrophe (“acute abdomen”). Therefore when approaching a patient with acute abdominal pain, the physician should begin with a rapid assessment of the patient’s overall physiologic state looking for clues that the patient is in shock or on the precipice of hemodynamic instability. Quickly identifying patients who are unstable or in shock is essential to expedite treatment and improve the likelihood of a satisfactory outcome. Shock is suggested by pallor, cyanosis, mottling, prostration, hypotension, tachycardia, or other signs of hypoperfusion, such as tachycardia, tachypnea, and presence of a metabolic acidosis. In addition to vital sign changes such as tachycardia and hypotension, the evaluation of patients with acute abdominal pain should include assessment of organ perfusion, specifically serum lactate, platelet count, serum bilirubin, Glasgow coma scale, and serum creatinine. The Sequential Organ Failure Assessment, or SOFA, score ( Table 11.1 ) is a useful tool to assess the presence of the systemic inflammatory response seen in early sepis. In the setting of acute abdominal pain, a SOFA score greater than or equal to 2, serum lactate levels of greater than 2, or a requirement for vasopressor support defines patients with septic shock. If hemodynamic instability is apparent, including clinical evidence of shock, surgical consultation should be sought immediately, and consideration should be given to endotracheal intubation and aggressive hemodynamic resuscitation early in the encounter. The adage in acute care surgery that “death begins in radiology” is a reminder that hemodynamic resuscitation should be initiated prior to diagnostic imaging.

TABLE 11.1

Sequential Organ Failure (SOFA) Score

Adapted from Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA 2016;315:801–10.

Score		1	2	3	4
Organ system	Units
Respiratory
PaO ₂ /FiO ₂	mm Hg	<400	<300	<200 ∗	<100 ∗
Coagulation
Platelets	000/mm ³	<150	<100	<50	<20
Liver
Bilirubin	mg/dL	1.2-1.9	2.0-5.9	6.0-11.9	≥12
	μmol/L	20-32	33-101	102-204	>204
CNS
Glasgow coma scale		13-14	10-12	6-9	<6
Renal
Creatinine	mg/dL	1.2-1.9	2.0-3.4	3.5-4.9	>5
	μmol/L	110-170	171-299	300-440	>440
Urine output	mL/day	—	—	<500	<200

SOFA score = sum of individual Organ System scores.

Sepsis should be suspected if the SOFA score is greater than 2 in the setting of acute abdominal pain.

Septic shock is defined as a SOFA score greater than 2 and serum lactate level greater than 2 mmol/L or if a vasopressor is required in the setting of infection.

∗ Or requiring respiratory support.

History

In the timeless treatise on abdominal pain bearing his name, first published in 1921, Sir Zachary Cope tells us, “It can be confidently asserted that a large number, if not the majority, of acute abdominal conditions could be diagnosed by considering carefully the history of onset.” Despite the advances made in clinical imaging in the century since then, history taking remains the most important component of the initial evaluation of the patient with acute abdominal pain. Characteristic features of pain associated with various common causes of acute abdominal pain are shown in Table 11.2 . Attention to these features can lead to a rapid clinical diagnosis or exclusion of important diseases in the differential diagnosis, thereby enhancing the reliability and effectiveness of subsequent diagnostic testing. For example, plain abdominal films are most efficacious when limited to patients with symptoms of intestinal obstruction.

TABLE 11.2

Comparison of Common Causes of Acute Abdominal Pain

Cause	Onset	Location	Character	Descriptor	Radiation	Intensity
Appendicitis	Gradual	Periumbilical area early; RLQ late	Diffuse early; localized later	Aching	None	++
Cholecystitis	Acute	Mid-epigastrium, RUQ, right scapula	Localized	Constricting	Scapula	++
Pancreatitis	Acute	Epigastrium, T10-L2 area of the back	Localized	Boring	Midback	++ to +++
Diverticulitis	Gradual	LLQ	Localized	Aching	None	++ to +++
Perforated peptic ulcer	Sudden	Epigastrium	Localized early, diffuse later	Burning	None	+++
SBO	Gradual	Periumbilical area	Diffuse	Cramping	None	++
Mesenteric ischemia, infarction	Sudden	Periumbilical area	Diffuse	Agonizing	None	+++
Ruptured abdominal aortic aneurysm	Sudden	Abdomen, back, flank	Diffuse	Tearing	None	+++
Gastroenteritis	Gradual	Periumbilical area	Diffuse	Spasmodic	None	+ to ++
Pelvic inflammatory disease	Gradual	Either LQ, pelvis	Localized	Aching	Upper thigh	++
Ruptured ectopic pregnancy	Sudden	Either LQ, pelvis	Localized	Sharp	None	++

+, mild; ++, moderate; +++, severe; LQ, lower quadrant.

Chronology

The time courses of several common causes of acute abdominal pain are diagrammed in Fig. 11.5 . The rapidity of onset of pain is often a measure of the severity of the underlying disorder. Pain that is sudden in onset, severe, and generalized is likely to be the result of an intra-abdominal catastrophe such as a perforated viscus, mesenteric infarction, or ruptured aneurysm. Affected patients usually recall the exact moment of onset of their pain. Progression is an important temporal factor in abdominal pain. In some disorders (e.g., gastroenteritis), pain is self-limited, whereas in others (e.g., appendicitis), pain is progressive. Pain associated with obstruction has a repeating crescendo-decrescendo pattern that may be diagnostic particularly when it occurs in association with nausea and vomiting. The duration of abdominal pain is also important. Patients who seek evaluation of abdominal pain that has been present for an extended period (e.g., weeks) are less likely to have an acute life-threatening illness than patients who present within hours to days of the onset of their symptoms.

Fig. 11.5, Patterns of acute abdominal pain. A, Many causes of abdominal pain subside spontaneously with time (e.g., gastroenteritis). B, Some pain is colicky (i.e., the pain progresses and remits over time); examples include intestinal, renal, and biliary pain (colic). The time course may vary widely from minutes in intestinal and renal pain to days, weeks, or even months in biliary pain. C, Commonly, acute abdominal pain is progressive, as in acute appendicitis or diverticulitis. D, Certain conditions have a catastrophic onset, such as a ruptured abdominal aortic aneurysm.

Location

The location of abdominal pain provides a clue to interpreting the cause. As noted earlier, a given noxious stimulus may result in a combination of visceral, somatic-parietal, and referred pain, thereby creating confusion in interpretation unless the neuroanatomic pathways are considered. For example, the pain of diaphragmatic irritation from a left-sided subphrenic abscess may be referred to the shoulder and misinterpreted as pain from ischemic heart disease (see Fig. 11.4 ). Pain radiating to the back from pancreatic or biliary pathology may be conflated with musculoskeletal processes, thereby delaying treatment. Changes in location may represent progression from visceral to localized parietal peritoneal irritation, as with appendicitis, or represent development of diffuse peritoneal irritation, as with a perforated ulcer.

Intensity and Character

Acute abdominal pain usually follows one of three patterns. Pain that is prostrating and physically incapacitates the sufferer is usually due to a severe life-threatening disease like a perforated viscus, ruptured aneurysm, or severe pancreatitis. By contrast, patients with obstruction of a hollow viscus, as in intestinal obstruction, renal colic, or biliary pain, present with gradual onset of cramping pain that follows a sinusoidal pattern of intense pain alternating with a period of relief. Nausea and vomiting are characteristic symptoms associated with this group of disorders. The obstructed viscus need not be the intestine for nausea or vomiting to occur, as in the case of a kidney stone. The third pattern is of gradually increasing discomfort, usually vague and poorly localized at the start but becoming more localized as the pain intensifies. This picture is usually due to inflammation, as with acute appendicitis or diverticulitis. Some disorders, such as acute cholecystitis, may start out as colicky pain but evolve into a constant pain as cystic duct obstruction leads to gallbladder inflammation. The clinician should be cautious in assigning too much importance to a patient’s description of the pain; exceptions are common, and a given descriptor may be attributable to a number of conditions. Symptoms in the elderly can be subtle despite the presence of life-threatening pathology, making this group particularly challenging.

Aggravating and Alleviating Factors

The relationship of pain to positional changes, meals, bowel movements, and stress may yield important diagnostic clues. Patients with peritonitis lie motionless, whereas those with renal colic may writhe in an attempt to find a comfortable position. Sometimes, certain foods exacerbate pain. A classic example is the relationship between the intake of fatty foods and development of biliary pain. Pain associated with duodenal ulcer is often alleviated by meals. By contrast, patients with gastric ulcer or chronic mesenteric ischemia may report exacerbation of pain with eating. Patients often self-medicate to alleviate symptoms. A history of chronic antacid or NSAID use, for example, may suggest the presence of PUD. This is a growing consideration as patients and physicians increasingly rely on NSAIDs as alternatives to opioids for chronic pain.

Associated Symptoms

Information regarding changes in constitutional symptoms (e.g., fever, chills, night sweats, weight loss, myalgias, arthralgias), digestive function (e.g., anorexia, nausea, vomiting, flatulence, diarrhea, constipation), jaundice, dysuria, changes in menstruation, and pregnancy should be solicited from the patient. A careful review of these symptoms may reveal important diagnostic information. Clear vomitus suggests gastric outlet obstruction, whereas feculent vomitus suggests more distal small bowel or colonic obstruction. A constellation of findings may indicate a particular disease entity.

Past Medical History

A careful review of the patient’s other medical problems often sheds light on the presentation of acute abdominal pain. Previous experience with similar symptoms suggests a recurrent problem. Patients with a history of partial SBO, renal calculi, or pelvic inflammatory disease are likely to have recurrences. A patient whose presentation suggests intestinal obstruction, and who has no prior surgical history, deserves special attention because of the likelihood of surgical pathology such as a hernia or neoplasm. Patients with a systemic illness, such as scleroderma, SLE, nephrotic syndrome, porphyria, or sickle cell disease, often have abdominal pain as a manifestation of the underlying disorder. Abdominal pain may also arise as a side effect of a medication taken for another disease.

Physical Examination

The physical examination of the patient with acute abdominal pain begins with an assessment of the patient’s appearance and assessment for signs of sepsis or shock, as described earlier. The patient’s ability to converse, breathing pattern, position in bed, posture, degree of discomfort, and facial expression should be noted. A patient lying still in bed in the fetal position and reluctant to move or speak, with a distressed facial expression, is likely to have peritonitis. A patient who writhes and frequently changes position has purely visceral pain, as in intestinal obstruction or gastroenteritis. Tachypnea may be a sign of metabolic acidosis caused by shock. Atrial fibrillation noted on physical examination or an electrocardiogram may suggest mesenteric arterial embolus. All patients should undergo a careful systematic examination regardless of the differential diagnosis suggested by the history.

Abdominal Examination

Examination of the abdomen is central to evaluating a patient with acute abdominal pain and should begin with careful inspection. The entire abdomen, from the nipple line to the thighs, should be exposed. Obese patients should be asked whether the degree of protrusion of the abdominal wall is greater than usual. Asthenic patients may feel themselves to be distended but have relatively little apparent abdominal protrusion. Assessment for the presence of bowel sounds and their character should precede any maneuvers that will disturb the abdominal contents. Before concluding that an abdomen is silent, the examiner should listen for at least 2 minutes and in more than one quadrant of the abdomen. Experienced listeners may distinguish the high-pitched churning of a mechanical SBO from the more hollow sounds of toxic megacolon (like dripping in a cavern). Nevertheless, some studies have cast doubt on the reliability of bowel sound assessment in patients with SBO and other conditions, and clinicians should avoid basing clinical decisions too heavily on assessment of bowel sounds. Auscultation may, however, be a good way to assess tenderness. When listening with the stethoscope, the astute clinician may begin to palpate the abdomen with the head of the stethoscope while carefully watching the patient’s facial expression. If tenderness is detected, an assessment for rebound tenderness should be carried out next to look for evidence of peritonitis. Rebound tenderness may be elicited by jarring the patient’s bed or stretcher or by finger percussion. Palpation is performed next. If pain is emanating from one particular region, that area should be palpated last to detect involuntary guarding and muscular rigidity. Patients with a rigid abdomen rarely reveal any additional findings (e.g., a mass) on physical examination. Because these patients usually have a surgical emergency, abdominal examination can be done more completely once the patient is under anesthesia, just before laparotomy.

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