Abdominal pain is an unpleasant experience commonlyassociated with tissue injury . The sensation of pain repre-sents an interplay of pathophysiologic and psychosocial fac-tors. Physiologic determinants of pain include the nature ofthe stimuli, the type of receptor involved, the organization ofthe neuroanatomic pathways from the site of injury to thecentral nervous system, and a complex interaction of modi-fying influences on the transmission, interpretation, and reac-tion to pain messages.', 2 Psychosocial factors modifying thesensation of pain include personality, ethnic and culturalbackground, and circumstances surrounding the injury . Thus,pain represents a complex sensation with different manifesta-tions in different individuals . It is the clinician's responsibil-ity to interpret the patient's complaint of pain with completeunderstanding of factors modifying its sensation and mani-festations .

ANATOMIC BASIS OF PAIN

Sensory neuroreceptors in abdominal organs are locatedwithin the mucosa and muscularis of hollow viscera, onserosal structures such as the peritoneum, and within themesentery. 3 In addition to nociception (the perception ofnoxious stimuli), sensory neuroreceptors are involved in theregulation of secretion, motility, and blood flow via localand central reflex arcs . 4 Although sensory information con-veyed in this manner is usually not perceived, disorderedregulation of these gastrointestinal functions can cause pain .For example, patients with irritable bowel syndrome perceivepain related to a heightened sensitivity of gut afferent neu-rons to normal endogenous stimuli, resulting in altered gutmotility and secretions (see Chapter 91) .

The neuroreceptors involved in nociception are the pe-ripheral ends of two distinct types of afferent nerve fibers :myelinated A-delta fibers and unmyelinated C fibers . A-deltafibers are distributed principally to skin and muscle and

ABDOMINAL PAINNCLUDING THE ACUTE

ABDOMEN

Robert E. Glasgow and Sean J. Mulvihill

mediate the sharp, sudden, well-localized pain that followsan acute injury. These fibers convey somatoparietal painsensations through spinal nerves . C fibers are found in mus-cle, periosteum, mesentery, peritoneum, and viscera. Mostnociception from abdominal viscera is conveyed by this typeof fiber and tends to be dull, burning, poorly localized, moregradual in onset, and longer in duration . These C fibersutilize substance P and calcitonin gene-related peptide asneurotransmitters . Stimulation of these fibers activates localregulatory reflexes mediated by the enteric nervous systemand long spinal reflexes mediated by the autonomic nervoussystem, in addition to the transmission of pain sensation tothe central nervous system .'

The visceral afferent fibers mediating painful stimuli fromthe abdominal viscera follow the distribution of the auto-nomic nervous system, as summarized in Figure 4-1 . Thecell bodies for these fibers are located in the dorsal rootganglia of spinal afferent nerves . On entering the spinalcord, these fibers branch into the dorsal horn and to Lis-sauer's tract cranially and caudally over several spinal seg-ments before terminating on dorsal horn cells in laminae Iand V. From the dorsal horn, second-order neurons transmitnociceptive impulses via fibers that cross through the ante-rior commissure and ascend the spinal cord in the contralat-eral spinothalamic tract . These fibers project to the thalamicnuclei and the reticular formation nuclei of the pons andmedulla. The former sends third-order neurons to the soma-tosensory cortex, where the discriminative aspects of painare perceived . The latter sends neurons to the limbic systemand frontal cortex, where the emotional aspects of pain areinterpreted .'' a

Afferent pain impulses are modified by inhibitory mecha-nisms at the level of the spinal cord . Somatic A-delta fibersmediating touch, vibration, and proprioception from a der-matomal distribution matching the visceral innervation of theinjured viscera synapse with inhibitory interneurons of the

71

ANATOMIC BASIS OF PAIN, 71 Extra-abdominal Causes of Acute Abdomi- APPROACH TO THE PATIENT WITHSTIMULANTS OF PAIN, 72 nal Pain, 78 CHRONIC ABDOMINAL PAIN, 80

TYPES OF PAIN, 72 Special Circumstances, 78 Clinical Evaluation, 80

APPROACH TO THE PATIENT WITH Pharmacologic Management of the Acute Diagnosable Causes, 81ACUTE ABDOMINAL PAIN, 73 Abdomen, 80 Treatment, 81Clinical Evaluation, 73Intra-abdominal Causes of the Acute Abdo-men, 77

'H'SYMOCIMS AND St(,NS

substantia gelatinosa in the spinal cord . In addition, inhibi-tory neurons originating in the mesencephalon, periventricu-lar gray matter, and caudate nucleus descend within the cordto modulate afferent pain pathways . These inhibitory mecha-nisms allow cerebral influences to modify afferent pain im-pulses .s • 9

STIMULANTS OF PAIN

Abdominal visceral nociceptors respond to mechanical andchemical stimuli . The principal mechanical signal to whichvisceral nociceptors are sensitive is stretch . Unlike for soma-toparietal nociceptors, cutting, tearing, or crushing of visceradoes not result in pain. Visceral stretch receptors are locatedin the muscular layers of the hollow viscera, between themuscularis mucosa and submucosa, in the serosa of solidorgans, and in the mesentery (especially adjacent to largevessels) .' , 10 Mechanoreceptor stimulation can result fromrapid distention of a hollow viscus (e.g ., intestinal obstruc-tion), forceful muscular contractions (e .g ., biliary or renalcolic), and rapid stretching of solid organ serosa or capsule(e .g ., hepatic congestion) . Similarly, torsion of the mesentery(e .g ., cecal volvulus) or tension from traction on the mesen-tery or mesenteric vessels (e .g ., retroperitoneal or pancreatictumor) results in stimulation of mesenteric stretch receptors .

Abdominal visceral nociceptors also respond to variouschemical stimuli. Chemical nociceptors are contained mainly

Figure 4-1 . Pathways of visceral sensory innervation,ceral afferent fibers that mediate pain travel with anerves to communicate with the central nervous systeabdomen, these nerves include both vagal and pelvicpathetic nerves and thoracolumbar sympathetic newlines, sympathetic fibers; dashed lines, parasympathetic

within the mucosa and submucosa of the hollow viThese receptors are directly activated by substances relin response to local mechanical injury, inflammation,ischemia and necrosis, and noxious thermal or radiaticjury. Such substances include H+ and K+ ions, histaiserotoinin, bradykinin and other vasoactive amines,stance P, calcitonin gene-related peptide, prostaglandinsleukotrienes ." • 12 Accumulation of nocireactive subst .may change the microenvironment of the injured tissuesuiting in a reduction of the pain threshold. This incrthe sensation of pain to a given stimulus and makes (wise innocuous stimuli painful . For example, the u!chemical irritants or pressure on normal gastric mutenot painful, whereas the application of the same stimiinflamed or injured mucosa causes pain .

TYPES OF PAIN

Abdominal pain may be classified into three categoriesceral pain, somatoparietal pain, and referred pain .

Visceral pain is experienced when noxious stimuli tivisceral nociceptors. The pain is usually dull and plocalized in the midline epigastrium, periumbilical regi(lower midabdomen because abdominal organs transmitsory afferents to both sides of the spinal cord (Fig .The site where the pain is felt corresponds roughly tdermatomes appropriate to the diseased organ's innerv

I

The pain is not well localized because the innervation ofmost viscera is multisegmental and the number of nerveendings in viscera is lower than that in highly sensitiveorgans such as the skin . The pain is generally described ascramping, burning, or gnawing . Secondary autonomic effectssuch as sweating, restlessness, nausea, vomiting, perspira-tion, and pallor often accompany visceral pain . The patientmay move about in an effort to relieve the discomfort .

Somatoparietal pain arises from noxious stimulation ofthe parietal peritoneum and is generally more intense andmore precisely localized than visceral pain. An example ofthis difference is the early vague periumbilical visceral painin acute appendicitis, which is followed by the localizedsomatoparietal pain at McBumey's point produced by in-flammatory involvement of the parietal peritoneum . Parietalpain is usually aggravated by movement or coughing . Thenerve impulses mediating parietal pain travel within somaticsensory spinal nerves. The fibers reach the spinal cord in theperipheral nerves corresponding to the cutaneous derma-tomes from the sixth thoracic (T6) to the first lumbar (LI)region. Lateralization of the discomfort of parietal pain ispossible because only one side of the nervous system inner-vates a given part of the parietal peritoneum .

Referred pain is felt in areas remote to the diseased or-gan. It is a result of convergence of visceral afferent neuronswith somatic afferent neurons from different anatomic

Figure 4-2. Visceral pain localization . Pain arising from the organsshown in 1, 2, and 3 is felt in the epigastrium, midabdomen, andhypogastrium, respectively .

Aftprr.,t:r-f .At PAPN . -1i,4`t ;

To Brain

Visceral Afferent First Order Neuron - ASpinal Cord Second Order Neuron - BSomatic Afferent First Order Neuron - C

Figure 4-3 . Demonstration of the neuroanatomic basis of referred pain .Visceral afferent fibers innervating the diaphragm are stimulated bylocal irritation (e .g ., subdiaphragmatic abscess) . These visceral afferentfibers (A) synapse with second-order neurons in the spinal cord (B) atthe same level as somatic afferent fibers (C) arising from the shoulderarea (cervical roots 3 to 5) . The brain interprets the pain to be somaticin origin and localizes it to the shoulder .

regions on second-order neurons in the spinal cord at thesame spinal segment. Referred pain may be felt in skin ordeeper tissues but is usually well localized . Generally, re-ferred pain appears as the noxious visceral stimulus becomesmore intense . An example is illustrated in Figure 4-3, inwhich diaphragmatic irritation from a subphrenic hematomaor abscess results in shoulder pains

APPROACH TO THE PATIENT WITHACUTE ABDOMINAL PAIN

The goal of the evaluation of the patient with acute abdomi-nal pain is an early, efficient, and accurate diagnosis . Whenevaluating a patient with acute abdominal pain, the mostimportant elements in making an accurate early diagnosis arethe history and physical examination . A careful descriptionof the chronology, location, intensity, and character of thepain as well as aggravating and alleviating factors, othersymptoms, and other medical history usually allows an accu-rate diagnosis to be made. A thorough physical examinationcan confirm a diagnosis that was suspected during the his-tory. Finally, selective use of appropriate laboratory and ra-diographic examinations provides further objective evidencein support of a specific diagnosis .

In some cases, the diagnosis is obscure despite an ex-haustive evaluation . In most settings in which the patient'sclinical status is stable, repetitive examination over timeeliminates diagnostic uncertainty . In this situation, admissionto the hospital for serial abdominal examinations or closetelephone or office follow-up is necessary . When the pa-tient's clinical status is deteriorating and diagnostic uncer-tainty remains, surgical exploration may be necessary .

Clinical Evaluation

History

The most important part of the evaluation of a patient withabdominal pain is the history (Table 4-1) .' 3 ~ 14

M :ww- SMPTOMS AND SIGNS

Table 4-1 1 Comparison of Common Causes of Acute Abdominal Pain

RLQ, right lower quadrant ; LLQ, left lower quadrant; RUQ, right upper quadrant; +, mild; ++, moderate; +++, severe .

CHRONOLOGY . Temporal considerations in the evaluationof a patient with acute abdominal pain include the rapidityof onset and the progression and duration of symptoms (Fig .4-4) . The rapidity of onset of pain is often a measure of itssignificance. Pain that is sudden in onset, severe, and welllocalized is likely to be the result of an intra-abdominalcatastrophe such as a perforated viscus, mesenteric infarc-tion, or ruptured aneurysm . Such patients usually recall theexact moment of onset of their pain . A second importanttemporal factor in abdominal pain is its progression . Pain insome disorders, such as gastroenteritis, is self-limited,whereas in others, such as appendicitis, it is progressive .Colicky pain has a crescendo-decrescendo pattern that maybe diagnostic, such as in renal colic. The duration of abdom-inal pain is also important . Patients who seek evaluation ofabdominal pain that has been present for an extended period(e .g ., weeks) are less likely to have an acutely threatening

I-a,

a,N t

TimeFigure 4-4. Patterns of acute abdominal pain . A, Many causes of ab-dominal 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 colic . The time coursemay vary widely from minutes in intestinal and renal colic to days,weeks, or even months in biliary colic . C, Commonly, abdominal painis progressive, as with appendicitis or diverticulitis . D, Certain condi-tions have a catastrophic onset, such as ruptured aortic aneurysm .

illness than are those who do so within hours to days of theonset of symptoms .

LOCATION. The location of abdominal pain provides clueswhen interpreting the cause . As previously discussed, agiven noxious stimulus may result in a combination of vis-ceral, somatoparietal, and referred pain . This may createconfusion in interpretation unless the neuroanatomic path-ways are considered . For example, the pain of diaphragmaticirritation from a left-sided subphrenic abscess may be re-ferred to the shoulder and misinterpreted as the pain fromischemic heart disease. Changes in location may representprogression from visceral to parietal irritation, as in appendi-citis, or represent the development of diffuse peritoneal irri-tation, as with a perforated ulcer.

INTENSITY AND CHARACTER . The intensity of pain is diffi-cult to measure. Perception of intensity is dependent uponthe point of reference from which the patient is describingthe pain . This point of reference varies among individualsand depends on the setting in which the pain is occurring,past experience with various types of pain, personality, andcultural differences . For these reasons, estimates of pain se-verity are not uniformly reliable diagnostic clues . However,the severity of the pain is loosely related to the magnitudeof the noxious stimulus. Several classic descriptors havebeen assigned to certain acute abdominal conditions (seeTable 4-1) . The clinician should be cautious, however, toprevent assigning too much importance to descriptions ofpain. It must be recognized that the exceptions may outnum-ber the rule and a given description may be applied to anumber of conditions .

AGGRAVATING AND ALLEVIATING FACTORS . The settingin which pain occurs or is exacerbated may yield importantdiagnostic information . The relationship to positionalchanges, meals, bowel movements, and stress may be signif-icant . Patients with peritonitis, for example, lie motionless,whereas those with renal colic may writhe in an attempt tofind a comfortable position. Sometimes, certain foods exac-erbate pain . A classic example is the relationship betweenfatty foods and the development of biliary colic . Pain associ-

CONDITION ONSET LOCATION CHARACTER DESCRIPTOR RADIATION INTENSITY

Appendicitis Gradual Periumbilical early;RLQ late

Diffuse early, localizedlate

Ache RLQ ++

CholecystitisPancreatitisDiverticulitis

RapidRapidGradual

RUQEpigastric, backLLQ

LocalizedLocalizedLocalized

ConstrictingBoringAche

ScapulaMidbackNone

++++ to ++++ to ++

Perforated peptic ulcer Sudden Epigastric Localized early, diffuselate

Burning None +++

Small bowel obstruction Gradual Periumbilical Diffuse Crampy None ++Mesenteric ischemia/in-

farctionSudden Periumbilical Diffuse Agonizing None +++

Ruptured abdominal aor-tic aneurysm

Gastroenteritis

Sudden

Gradual

Abdominal, back, flank

Periumbilical

Diffuse

Diffuse

Tearing

Spasmodic

Back, flank

None

+++

+ to ++Pelvic inflammatory dis-

easeGradual Either LQ, pelvic Localized Ache Upper thigh ++

Ruptured ectopic preg-nancy

Sudden Either LQ, pelvic Localized Light-headed None ++

ated with duodenal ulcer is often alleviated by meals . Incontrast, patients with gastric ulcer or chronic mesentericischemia may report exacerbation of pain with eating . Pa-tients often self-medicate to alleviate symptoms . A history ofchronic antacid use, for example, may suggest the presenceof peptic ulcer disease.

ASSOCIATED SYMPTOMS AND REVIEW OF SYSTEMS. Acareful history of other symptoms coexisting with the pre-sentation of abdominal pain should be elicited . Informationregarding changes in constitutional symptoms (e.g ., fever,chills, night sweats, weight loss, myalgias, arthralgias), di-gestive function (e.g., anorexia, nausea, vomiting, flatus, di-arrhea, and constipation), jaundice, dysuria, menstruation,and pregnancy should be solicited . A careful review of thesesymptoms may reveal important diagnostic information . Forexample, vomitus that is clear suggests gastric outlet ob-struction, whereas feculent vomitus suggests more distalsmall bowel or colonic obstruction . A constellation of find-ings may indicate a particular disease entity .

PAST MEDICAL HISTORY . A careful review of the patient'sother medical problems often sheds light on the currentpresentation of acute abdominal pain . Previous experiencewith similar symptoms suggests a recurrent problem . Patientswith a history of partial small bowel obstructions, renalcalculi, or pelvic inflammatory disease are likely to haverecurrences. Systemic illnesses such as scleroderma, lupus,nephrotic syndrome, porphyrias, and sickle cell disease oftenhave abdominal pain as a manifestation of their illness. Ab-dominal pain may also arise as a side effect of medicationtaken for other illness .

FAMILY AND SOCIAL HISTORY. A careful review of thepatient's family history may yield information relevant to thediagnosis. This is especially true in the pediatric population .Sickle cell disease in black patients and familial Mediterra-nean fever in patients of Armenian or Sephardic Jewishheritage are examples . Likewise, the patient's social history,including habits or history of substance abuse, occupationalhistory, travel history, and history of contact with animals orother ill people, may provide useful diagnostic information .

Physical Examination

The physical examination must be pursued systematically totest specific hypotheses formed while eliciting the historyand to uncover unsuspected abnormalities . When examininga patient, the clinician must interpret his or her findings inthe context of the patient's history . For example, the elderly,immunocompromised, or long-term diabetic patient is lesslikely to show signs of peritoneal irritation, even in thepresence of a perforated viscus . When the source of the painis intra-abdominal, many important clues are derived from acomplete physical examination . Therefore, a careful systemicexamination must be performed, in addition to a thoroughabdominal examination .

SYSTEMIC EXAMINATION . The physical examination beginswith an assessment of the patient's appearance, ability toconverse, breathing pattern, position in bed, posture, degreeof discomfort, and facial expression . A patient lying still inbed, in the fetal position, reluctant to move or speak, with a

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distressed facial expression is likely to have peritonitis . Onthe other hand, patients who writhe with frequent positionchanges likely have pure visceral pain, such as in bowelobstruction or gastroenteritis . Vital signs should be obtainedto exclude conditions such as hypovolemia, tachypnea re-lated to metabolic acidosis, or atrial fibrillation as a cause ofmesenteric arterial embolus . Careful lung examination mayyield findings suggestive of pneumonia . Examination of theextremities may provide evidence for inadequate perfusion,as in shock, or the presence of chronic vascular disease .

ABDOMINAL EXAMINATION . An assessment of the degreeof tenderness and its location must be made in each patientwith abdominal pain . Severe diffuse tenderness with rigiditysuggests generalized peritonitis . Mild tenderness withoutsigns of peritoneal irritation is more characteristic of condi-tions that do not require surgical treatment (e.g ., salpingitisand gastroenteritis) . The abdomen should be inspected fordistention, scars, hernias, muscle rigidity, splinting duringrespiration, ecchymoses, and visible hyperperistalsis . Hyper-peristalsis may be detected by auscultation in patients withintestinal obstruction or enteritis . Generalized peritonitis usu-ally causes diminished peristalsis. Bruits may point to avascular stenosis. Abdominal percussion may elicit tympanyfrom excess abdominal gas, whether it is intraluminal (asoccurs with intestinal obstruction) or extraluminal (as occurswith perforated viscus) . Light, gentle palpation is superior todeep palpation in the identification of peritoneal irritation .Peritonitis may also be detected through innocuous measuressuch as gently shaking the bed or asking the patient tobreathe deeply or cough. Palpation should begin at the pointof least tenderness and proceed to the point of greatesttenderness . The degree of tenderness, guarding, and rigidityshould be determined. Enlargement of a diseased organ, tu-mor, or inflammation may produce a palpable mass . Poten-tial hernia orifices should be examined .

GENITAL, RECTAL, AND PELVIC EXAMINATION . The pelvicorgans and external genitalia should be examined in everypatient with abdominal pain. The rectum and vagina provideadditional avenues for gentle palpation of pelvic viscera. Thepresence of gynecologic abnormality should be excluded inall women with abdominal pain .

Laboratory Data

Laboratory tests ordered should reflect the clinical suspicionraised during the history and physical examination . Unneces-sary laboratory testing is costly and often clouds the diag-nostic picture . All patients with acute abdominal pain shouldhave a complete blood count with differential count andurinalysis . The determination of serum electrolyte, bloodurea nitrogen, creatinine, and glucose concentrations is use-ful in ascertaining fluid status, acid-base status, renal func-tion, and metabolic state but is not necessary for everypatient. Urine or serum pregnancy testing should be per-formed in all women of reproductive age with lower abdom-inal pain. Liver function tests and serum amylase determina-tion should be ordered in patients with upper abdominalpain. Other tests are obtained on the basis of clinical history(e .g ., prothrombin time and a blood albumin in patients withsuspected liver disease) .

tJ/f fiYi.iP O v15 AND SIGNS

Figure 4-5 . This upright chest radiograph of an 80-year-old womanwith acute onset of severe epigastric pain demonstrates free intra-ab-dominal air, which is most evident under the right hemidiaphragm . Thepatient has pneumoperitoneum as a result of a perforated duodenalulcer . At surgery, an anterior duodenal ulcer perforation was found .

Radiographic Evaluation

As is the case with laboratory tests, diagnostic imaging mustbe tailored to answer specific questions arising from a care-fully derived differential diagnosis based on history, physicalexamination, and laboratory testing. A patient who has aclinical picture suggestive of a bowel obstruction, for exam-ple, is best served by obtaining plain radiographs of theabdomen, whereas a patient with suspected acute cholecysti-tis is best evaluated via ultrasonography .

The most common imaging examination ordered in theevaluation of the patient with acute abdominal pain is theplain abdominal series . This should include two views ofthe abdomen: one in the supine and one in the uprightposition. In patients unable to sit upright, a lateral decubitusfilm with the left side down may identify abnormal gaspatterns . In addition, an upright chest radiograph should beperformed to exclude intrathoracic causes of abdominal pain(e .g ., lower lobe pneumonia) and pneumoperitoneum (Fig .4-5) . Only 10% of abdominal radiographs reveal findingsdiagnostic of abdominal abnormality . Even so, the examina-tion is readily available and inexpensive and should be ob-tained in most circumstances . 15

Ultrasonography can provide rapid, accurate, and inex-pensive anatomic information about the liver, biliary tree,spleen, pancreas, kidneys, and pelvic organs . In some cases(e .g ., biliary colic, cholecystitis, ectopic pregnancy, ovariancyst, or tubo-ovarian abscess), ultrasonography is the pre-ferred initial imaging test . Endovaginal and endorectal ultra-sonography can be useful in identifying pelvic abnormalitiesnot seen by other imaging modalities. Doppler technologypermits evaluation of vascular lesions such as aortic or vis-ceral aneurysms, venous thrombi, and anomalies . 16

The most versatile imaging tool in the evaluation of acute

abdominal pain is computed tomography (CT) . CT of theabdomen and pelvis provides information about the presenceof pneumoperitoneum, abnormal bowel gas patterns, and cal-cifications similar to that obtained with plain radiographs . Inaddition, CT permits detection of inflammatory lesions (e .g .,appendicitis, diverticulitis, pancreatitis, and abscess), neo-plastic lesions (e .g ., obstructing colon cancer, pancreatic tu-mors), and trauma (e .g ., spleen, liver, and kidney injury). CTalso provides information about vascular lesions (e.g ., portalvein thrombosis, pylephlebitis, aneurysm disease) and intra-abdominal or retroperitoneal hemorrhage (e .g ., trauma, adre-nal hemorrhage, ruptured hepatoma) . 16 • "

Recent improvements in CT technology have enhancedimage resolution and expanded its utility . Helical CT exami-nations generate high-resolution images rapidly and havelargely replaced previous techniques . These improvements inCT technology include focused or organ-specific examina-tions and CT angiography . An example of a focused exami-nation is the focused helical CT of the appendix. In a 1998study of 100 patients with clinically suspected appendicitis,treatment plans were altered in over half of the patients andunnecessary appendectomy was prevented in 13 patients . Inthis study, the savings realized exceeded the cost of thescans by $447 per patient, making the focused examinationhighly cost-effective ." Other examples of focused helical CTexaminations include the use of organ-specific protocols inwhich timing of contrast ingestion or injection is coordinatedwith image acquisition to optimize visualization of specificorgans. Examples of these techniques include CT of theesophagus or upper abdomen with oral contrast medium toevaluate perforated viscera and CT of the pancreas or liverin which the image acquisition is coordinated with the arte-rial and/or venous phase to evaluate for perfusion defectsfrom ischemia, trauma, or neoplasia . CT arteriography isuseful in evaluating the aorta and visceral vasculature . Theseimprovements in technology make CT the most versatileadjunct to the clinical history and physical examination inthe evaluation of the acute abdomen .

Other imaging modalities are occasionally useful in theevaluation of the patient with acute abdominal pain . Theseinclude magnetic resonance imaging (MRI) angiography andendoscopy. The former is a useful, noninvasive method toevaluate the visceral vasculature . Endoscopy can be useful inthe evaluation of the stomach, duodenum, and colon mucosafor ulceration, neoplasia, ischemia, and inflammation .

Other Diagnostic Tests

Other diagnostic tests occasionally useful in evaluating thepatient with acute abdominal pain include peritoneal lavage,laparoscopy, and exploratory laparotomy . Peritoneal lavageis useful in detecting the presence of hemoperitoneum afterblunt or penetrating trauma and of purulent or feculent mate-rial after hollow viscus injuries, ischemia, or perforation .

Diagnostic laparoscopy is useful when diagnostic uncer-tainty exists and the patient's clinical condition demandsintervention. Recent improvements in minimally invasivetechnology and techniques have increased the utility of lapa-roscopy in the evaluation and treatment of the acute abdo-men. Refinements and miniaturization of instruments, the useof laparoscopic ultrasonography, and increased experience

with advanced laparoscopic techniques have led to a widerapplication of minimally invasive surgery to the evaluationand treatment of almost all intra-abdominal diseases, includ-ing most causes of the acute abdomen. For example, in afemale patient of reproductive years with obvious peritonitislocalized to the right lower quadrant, diagnostic laparoscopypermits differentiation between adnexal disease and acuteappendicitis. In addition to its diagnostic usefulness, laparos-copy can be used in the treatment of these disorders . Sincethe late 1990s, the addition of laparoscopic ultrasonographytechnology has improved the evaluation of the solid visceralorgans and retroperitoneum . The diagnostic accuracy of lapa-roscopy in patients with acute nontraumatic abdominal painis 93% to 98% . In various series, 57% to 77% of patientswho underwent diagnostic laparoscopy for acute abdominalpain were successfully treated by laparoscopic or laparoscop-ically assisted methods . 19-21

Exploratory laparotomy is reserved for patients with intra-abdominal catastrophe whose diagnosis is obvious from theclinical history and examination (e .g ., ruptured spleen fromblunt trauma, ruptured abdominal aortic aneurysm) or pa-tients in extremis in whom delay in therapy would be life-threatening .

Intra-abdominal Causes of the AcuteAbdomen

Acute abdominal pain is pain of less than 24 hours' dura-tion. It has many causes, and only after a careful history,physical examination, and appropriate laboratory and radio-graphic examination can the clinician differentiate betweenthose conditions that require surgery and those that can betreated nonoperatively . Acute abdomen, therefore, does notmandate surgery. If, after the initial evaluation, the diagnosisis unclear, periodic physical and laboratory re-examinationcan often eliminate any uncertainty . The list of intra-abdomi-nal causes of the acute abdomen is exhaustive . In this chap-ter, the most common causes are discussed; for more de-tailed information, refer to the corresponding organ systemchapters .

ACUTE APPENDICITIS . Acute appendicitis begins with pro-dromal symptoms of anorexia, nausea, and vague periumbili-cal pain. Within 6 to 8 hours, the pain migrates to the rightlower quadrant and peritoneal signs develop . In uncompli-cated appendicitis, a low-grade fever to 38°C and mild leu-kocytosis are usually present. Higher temperatures and whiteblood cell counts are associated with perforation and abscessformation. The mnemonic PANT can help the novice re-member the classic progression of symptoms in appendicitis(pain followed by anorexia followed by nausea followed bytemperature elevation) . Plain abdominal radiographs are notdiagnostic, but suggestive findings include a localized rightlower quadrant ileus, an appendicolith, or spasm of the rightpsoas muscle . Ultrasonography and CT are useful diagnosticadjuncts in selected patients . Treatment of uncomplicatedcases is via appendectomy (see Chapter 107) .

ACUTE CHOLECYSTITIS . Acute cholecystitis is caused bygallstone obstruction of the cystic duct, except in acalculouscholecystitis, which may be a result of gallbladder ischemia,stasis, or viral infection . Acute cholecystitis causes pain that

AW)0&i cAt VMN,

is almost indistinguishable from the pain of biliary colic .The pain is usually a persistent, dull ache . It is usuallylocalized to the right upper quadrant or epigastrium but mayradiate around the back to the right scapula . The pain usu-ally subsides within 6 hours of onset in biliary colic butpersists in acute cholecystitis . Nausea, vomiting, and low-grade fever are commonly present . On examination, rightupper quadrant tenderness, guarding, and Murphy's sign arediagnostic of acute cholecystitis . The white blood cell countis usually mildly elevated, although it may be normal . Mildelevations in total bilirubin and alkaline phosphatase concen-trations are typical . More marked liver function test resultabnormalities are associated with choledocholithiasis, Mir-izzi's syndrome, or hepatitis . Acute cholecystitis may bedifferentiated from cholangitis by the high fevers (especiallywith chills), jaundice, and leukocytosis observed in the lat-ter. Treatment of acute cholecystitis includes intravenousfluid replacement, antibiotics, bowel rest, and early laparo-scopic cholecystectomy (see Chapters 55 to 58) .

ACUTE PANCREATITIS . Pancreatitis typically begins with theacute onset of epigastric and upper abdominal pain, whichrapidly increases in severity . The pain may bore through tothe back or be referred to the left scapular region . The painis constant and unrelenting. Fever, anorexia, nausea, andvomiting are typical. Physical examination reveals an acutelyill patient in considerable distress . Patients are usually tachy-cardic and tachypneic. Hypotension is a late finding, relatedto extravasation of intravascular fluid and/or hemorrhage .Abdominal examination reveals hypoactive bowel soundsand marked tenderness to percussion and palpation in theepigastrium . Abdominal rigidity is a variable finding. In rarecases flank or periumbilical ecchymoses (Turner's and Cul-len's signs) develop in the setting of hemorrhagic pancreati-tis . Extremities are often cool and cyanotic, reflecting under-perfusion. White blood cell counts of 12,000 to 20,000/µLare common. Elevated serum and urine amylase levels areusually present within the first few hours. Other useful labo-ratory tests include concentrations of serum electrolytes, in-cluding calcium, liver function tests ; levels of blood glucose ;and arterial blood gas evaluation . Plain abdominal films mayshow a "cutoff sign" or sentinel loop and may exclude othercauses of pain, including perforated peptic ulcer. Ultrasonog-raphy is useful in identifying gallstones as the cause ofpancreatitis . Computed tomography is reserved for compli-cated pancreatitis (see Chapter 48) .

ACUTE DIVERTICULITIS. Acute diverticulitis is a diseasecommon in the older population. Although the entire colonmay be involved with diverticula, diverticulitis most oftenoccurs in the sigmoid colon . Symptoms relate to inflamma-tion or obstruction. Early in the course of diverticulitis, pa-tients describe mild anorexia, nausea, vomiting, and a vis-ceral-type pain located in the hypogastrium. Later, with theonset of somatoparietal irritation, the pain shifts to the leftlower quadrant. Obstipation or diarrhea may be present. Fe-ver is common. Abdominal examination reveals slight dis-tention with left lower quadrant tenderness and guarding . Amass is sometimes palpable . Leukocytosis is present. Ab-dominal radiography may exclude perforation or obstruction .CT is useful to define the extent of inflammation and ex-clude the presence of abscess or underlying perforated can-cer. Barium enema and colonoscopy are contraindicated dur-

"tW WITH SYMPTCJMS AiND SIGNS

ing the acute illness. Colonoscopy performed 4 to 6 weekslater is recommended, however, to define the extent of di-verticula and exclude other colonic abnormalities, especiallyneoplasm. Treatment is supportive with bowel rest and anti-biotics . Surgery is reserved for patients with obstruction,failure of conservative therapy, or recurrent episodes (seeChapter 108) .

PERFORATED DUODENAL ULCER. Perforation due to duode-nal ulcer usually occurs in the anterior portion of the firstpart of the duodenum. The pain is sudden, sharp, and severe .At first, it is located in the epigastrium, but it quicklyspreads over the entire abdomen, especially along the rightside, as the chemical peritonitis descends down the rightpericolic gutter, where it can mimic appendicitis (Valentino'ssyndrome) . Nausea is common . The patient typically liesmotionless, but in obvious distress . Tachypnea and tachycar-dia are present early. Hypotension and fever develop 4 to 6hours into the illness . Examination reveals diffuse peritonitis,with a characteristic "board-like" abdomen caused by invol-untary guarding . Laboratory study findings reveal leukocyto-sis and volume depletion . Pneumoperitoneum is identified onabdominal radiographs in 75% of patients . In equivocalcases, water-soluble contrast studies or computed tomogra-phy reveals localized perforation . Most patients require im-mediate surgery (see Chapters 40 and 42) .

SMALL BOWEL OBSTRUCTION . Intestinal obstruction occursin patients of all ages . In pediatric patients, intussusception,atresia, and meconium ileus are the most common causes . Inadults, about 70% of cases are caused by postoperative ad-hesions. Incarcerated hernias make up the majority of theremainder . Small bowel obstruction is characterized by sud-den, sharp periumbilical abdominal pain . Nausea and vomit-ing occur soon after the onset of pain and provide temporaryrelief of discomfort. Frequent bilious emesis with epigastricpain is suggestive of high intestinal obstruction . In contrast,crampy periumbilical pain with infrequent feculent emesis ismore typical of distal obstruction . Examination reveals anacutely ill, restless patient . Fever, tachycardia, and ortho-static hypotension are common . Abdominal distention is usu-ally present with hyperactive bowel sounds and audiblerushes. Diffuse tenderness to percussion and palpation ispresent, but peritoneal signs are absent, unless a complica-tion such as ischemia or perforation has occurred . Leukocy-tosis suggests the presence of ischemia . Plain radiographsare diagnostic when they reveal dilated loops of small bowelwith air-fluid levels and decompressed distal small boweland colon . Plain films can be misleading in patients withproximal jejunal obstruction, as dilated bowel loops and air-fluid levels may be absent . Treatment is surgical (see Chap-ter 109) .

ACUTE MESENTERIC ISCHEMIA . Acute ischemic syndromesinclude embolic arterial occlusion, thrombotic arterial occlu-sion, nonocclusive mesenteric ischemia, and venous throm-bosis . 22 An antecedent history of "intestinal angina," weightloss, diarrhea, abdominal bruit, cardiac arrhythmias, coronaryor peripheral vascular disease, and valvular heart disease iscommon. The hallmark of the diagnosis is acute onset ofcrampy epigastric and periumbilical pain out of proportion tothe physical findings. Other symptoms include diarrhea,vomiting, bloating, and melena. On examination, most pa-

tients appear acutely ill ; however, the presentation may besubtle. Shock is present in about 25% of cases. Peritonealsigns usually denote intestinal infarction . Leukocytosis andhemoconcentration are present . Metabolic acidosis is a latefinding . CT is the best initial diagnostic test . Visceral angi-ography may be useful to differentiate the causes of intesti-nal ischemia and define the extent of disease . Immediatesurgery is mandated except in nonocclusive mesenteric is-chemia (see Chapter 119) .

ABDOMINAL AORTIC ANEURYSM . Rupture or dissection ofan abdominal aortic aneurysm is heralded by acute, sudden-onset, severe abdominal pain localized to the midabdomen,paravertebral, or flank area . The pain is tearing in nature andassociated with light-headedness, diaphoresis, and nausea . Ifthe patient survives transit to the hospital, shock is the mostcommon presentation . Physical examination reveals a pulsa-tile, tender abdominal mass in about 90% of cases . Theclassic triad of hypotension, a pulsatile mass, and abdominalpain is present in 75% of cases . Once the clinical diagnosisis made, emergency surgery is required . 23

OTHER CAUSES. Other intra-abdominal causes of acute ab-dominal pain include gynecologic conditions such as endo-metritis, acute salpingitis with or without tubo-ovarian ab-scess, ovarian cysts or torsion, and ectopic pregnancy 24 ;spontaneous bacterial peritonitis (see Chapter 78) ; peptic ul-cer disease and nonulcer dyspepsia (see Chapters 7 and 40) ;gastroenteritis (see Chapters 96 and 97) ; viral hepatitis andliver infections (see Chapters 68 and 69) ; pyelonephritis ;cystitis ; mesenteric lymphadenitis ; inflammatory bowel dis-ease (see Chapters 103 and 104) ; and functional abnormali-ties such as irritable bowel syndrome (see Chapter 91) andintestinal pseudo-obstruction (see Chapter 111) .

Extra-abdominal Causes of AcuteAbdominal Pain

Acute abdominal pain may arise from disorders involvingextra-abdominal organs and systemic illnesses . 25 Examplesare summarized in Table 4-2 . Surgical intervention in pa-tients with acute abdominal pain arising from extra-abdomi-nal or systemic illnesses is seldom required . Instances inwhich surgery is required include pneumothorax, empyema,and esophageal perforation . The latter may be iatrogenic,result from blunt or penetrating trauma, or occur spontane-ously (Boerhaave's syndrome) (see Chapter 34) .

Special Circumstances

EXTREMES OF AGE. Evaluation of acute abdominal pain inpatients at the extremes of age is a challenge. Historicalinformation and physical examination findings are often dif-ficult to elicit and/or unreliable . Similarly, laboratory find-ings may be misleadingly normal in the face of significantintra-abdominal abnormality . For these reasons, patients atthe extremes of age are often diagnosed late in their diseasecourse and have higher rates of morbidity. For example, theperforation rate for appendicitis in the general populationaverages 10%, but it exceeds 50% in infants . A carefulhistory, thorough physical examination, and high level of

Table 4-2 1 Extra-abdominal Causes of Acute AbdominalPain

CardiacMyocardial ischemia and infarctionMyocarditisEndocarditisCongestive heart failure

MetabolicUremiaDiabetes mellitusPorphyriaAcute adrenal insufficiency (Addison's disease)HyperlipidemiaHyperparathyroidism

ThoracicPneumonitisPleurodynia (Bornholm's disease)Pulmonary embolism and infarctionPneumothoraxEmpyemaEsophagitisEsophageal spasmEsophageal rupture (Boerhaave's syndrome)

HematologicSickle cell anemiaHemolytic anemiaHenoch-Schonlein purpuraAcute leukemia

ToxinsHypersensitivity reactions, insect bites, reptile venomsLead poisoning

InfectionsHerpes zosterOsteomyelitisTyphoid fever

NeurologicRadiculitis: spinal cord or peripheral nerve tumors, degenerative ar-

thritis of the spineAbdominal epilepsyTabes dorsalis

MiscellaneousMuscular contusion, hematoma, or tumorNarcotic withdrawalFamilial Mediterranean feverPsychiatric disordersHeat stroke

suspicion are the most useful tools in aiding diagnosis. Thepresentation of acute abdominal conditions is highly variablein these populations and alert observation is required .

In the pediatric population, the causes of acute abdominalpain vary with age. In infancy, intussusception, pyelonephri-tis, gastroesophageal reflux, Meckel's diverticulitis, and bac-terial or viral enteritis are common . In children, Meckel'sdiverticulitis, cystitis, pneumonitis, enteritis, mesentericlymphadenitis, and inflammatory bowel disease are preva-lent. In adolescents, pelvic inflammatory disease, inflamma-tory bowel disease, and the common adult causes of acuteabdominal pain prevail . In children of all ages, two of themost common causes of pain are acute appendicitis andabdominal trauma secondary to child abuse .26, 27

In the geriatric population, biliary tract disease accountsfor nearly 25% of cases of acute abdominal pain, followedby nonspecific pain, malignancy, bowel obstruction, compli-cated peptic ulcer disease, and incarcerated hernias . Appen-dicitis, although rare in elderly patients, usually becomesapparent late in its course with high morbidity and mortalityrates . 13, 21

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PREGNANCY . Pregnancy poses unique problems in the eval-uation of the patient with acute abdominal pain . In preg-nancy, the enlarged uterus displaces lower abdominal organsfrom their usual position, compromises abdominal examina-tion, alters clinical manifestations, and interferes with naturalmechanisms that localize infection . Acute abdominal pain inpregnant patients results from diseases similar to those thataffect age-matched nonpregnant counterparts and with equalfrequency. The most common causes of acute abdominalpain in pregnancy are appendicitis, cholecystitis, pyelone-phritis, and adnexal problems, including ovarian torsion andovarian cyst rupture. The rate of fetal loss in intra-abdominaldisease is related more to the severity of the disease than tothe treatment, including surgery . Therefore, early diagnosisand therapy are indicated . Appendicitis, for example, occursin about 7 of every 10,000 pregnant women . Appendectomyfor uncomplicated appendicitis results in a 3% fetal loss rate,which increases to 20% in perforated appendicitis . Aftercholecystectomy, the rate of preterm labor is about 7% andthe rate of fetal loss is 8% . 29, 30

IMMUNOCOMPROMISED HOST. The immunocompromisedpatient population includes patients undergoing organ trans-plantation, chemotherapy for cancer, and immunosuppressivetherapy for autoimmune disease and those with congenital oracquired immunodeficiency syndromes (see Chapters 27 and28). As in the elderly population, immunocompromised hostsoften demonstrate few abdominal signs and symptoms, mini-mal systemic manifestations of peritonitis, and little changein laboratory data in the face of acute abdominal pathologicconditions. Therefore, a thoughtful approach to diagnosis isnecessary .

Two categories of disease cause acute abdominal pain inthese patients : (1) diseases that occur in the general popula-tion independently of immune function (e.g ., appendicitis,cholecystitis), and (2) diseases unique to the immunocom-promised host (e.g ., neutropenic enterocolitis, drug-inducedpancreatitis, graft-versus-host disease, pneumatosis intesti-nalis, cytomegalovirus [CMV], and fungal infections) . Intes-tinal obstruction or perforation is the most common indica-tion for surgery and may occur in the setting of Kaposi'ssarcoma of the intestine, lymphoma or leukemia afterchemotherapy, atypical mycobacterial infections, CMV infec-tions, iatrogenic perforations, and neutropenic enterocoli-tiS. 31-34

ACUTE ABDOMEN IN THE INTENSIVE CARE UNIT PATIENT .The gastroenterologist or surgeon is occasionally asked toevaluate patients in the intensive care unit for acute abdomi-nal pain or intra-abdominal causes of sepsis . Critical carepatients often have altered sensorium as a result of medica-tion, injury, or metabolic disorders . Often one cannot obtaina thorough history and physical examination in these pa-tients . In this situation, a greater reliance on helical CT anddiagnostic laparoscopy is necessary . In the intensive careunit an acute abdominal condition unrelated to the mainreason for hospitalization may develop . In addition, thesepatients are at risk for unusual illness related to their hospi-talization or underlying condition . Examples of causes ofacute abdominal pain in the intensive care unit patient in-clude overlooked trauma injuries ; postoperative complica-tions, such as anastomotic leak and obstruction ; and compli-cations of critical illness, including acalculous cholecystitisand stress ulcer.

FATi'FNTS'Vt''tTt - { SYMf'[OMM qND ti](IdS

Pharmacologic Management of the AcuteAbdomen

Early in the course of the evaluation of the patient withacute abdominal pain, the clinician must consider the impor-tant role of analgesics and antibiotics in both the evaluationand the early treatment of the underlying problem . Patientswith acute abdominal pain are often in great distress, whichoften obviates their ability to participate in the history andphysical examination . Despite data from well-designed stud-ies showing that the administration of analgesics to patientswith acute abdominal pain does not adversely affect theclinician's ability to make a timely and accurate diagnosis,75% of emergency room physicians withhold analgesicspending evaluation of the patient by a surgeon .35-37 Thisdelay results in unnecessary suffering and is not warranted .Patients with moderate to severe abdominal pain should re-ceive analgesics during their evaluation .

Similarly, patients with acute abdominal pain from pri-mary or secondary bacterial peritonitis should receive antibi-otics empirically directed against the likely offending orga-nisms. Primary bacterial peritonitis has an extra-abdominalsource, often hematogenous, of transmitted bacterial infec-tion to the peritoneal fluid. Examples include spontaneousbacterial peritonitis, tuberculosis peritonitis, and peritonitisassociated with chronic ambulatory peritoneal dialysis . Incontrast, secondary bacterial peritonitis arises as a conse-quence of an intra-abdominal process . Causes include appen-dicitis, diverticulitis, perforated viscus, intestinal ischemia,biliary tract disease, and pelvic inflammatory disease . Al-though the treatment for secondary peritonitis is usually sur-gical, appropriate antibiotics should be started soon after thediagnosis is made (see Chapter 121) .

APPROACH TO THE PATIENT WITHCHRONIC ABDOMINAL PAIN

Chronic abdominal pain is common . A survey of more than1 million Americans revealed that 13% experienced "stom-ach pain" and 15% experienced "pain in the lower abdo-men."38 Most of these are minor discomforts, but some re-flect genuine disease. Causes of chronic abdominal pain maybe divided into those that are diagnosable, either intermittentor constant and unrelenting, and those that are undiagnosa-ble. Patients with chronic abdominal pain are plagued notonly by their symptoms, but also by the disruption of theirlives, including increased dependency, altered self-image,and interference with work, family, and social relationships .Often psychologic disturbances, including affective disorders(see Chapters 5 and 122),8 result.

Chronic intractable abdominal pain or chronic undiag-nosed abdominal pain is defined as abdominal pain that ispresent for at least 6 months without diagnosis despite ap-propriate evaluation. Women are more likely to be afflictedthan men. A history of sexual or physical abuse is common .The pain is described in vague, peculiar terms ; is exacer-bated by psychologic stresses ; and is associated with multi-ple somatic complaints . It is unresponsive to standard treat-ment and often provokes multiple unnecessary procedures .The pain is disruptive to the patient's relationships and work

and often leads to depression, anxiety, illness behavior, andsomatoform disorders or traits . 39 40 (See Chapter 5more detailed discussion .)

The remainder of this chapter focuses on the evaluationof diagnosable causes of chronic abdominal pain .

Clinical Evaluation

History

The pattern of chronic diagnosable abdominal pain may beintermittent or constant. Pain that is intermittent is character-ized by episodes that last minutes or hours to several daysseparated by pain-free periods . In these patients, a carefulhistory of the chronology, location, character, and aggravat-ing and alleviating factors often narrows the differential di-agnosis. Description of associated symptoms, a careful pastmedical history, and review of systems are also necessary .Pain stimulated by eating suggests chronic mesenteric ische-mia. Pain associated with abnormal bowel habits or bloatingmay be due to irritable bowel syndrome or recurrent intesti-nal obstruction. Ulcer-like pain may represent nonulcer dys-pepsia or recurrent pancreatitis . Pelvic pain at monthly inter-vals suggests endometriosis . 41 Pain that is constant andunrelenting suggests other causes . In these patients, historyof weight loss, fever, and medical and surgical histories areparticularly important. Weight loss suggests malignancy ormalabsorption . The latter may result from intestinal or pan-creatic disorders (e .g., sprue and chronic pancreatitis) . Feveris common in occult intra-abdominal abscesses, autoimmunedisorders, and hematologic malignancies such as lymphoma .

Physical Examination

The physical examination should include both a careful ab-dominal examination and a systemic examination for extra-abdominal manifestations of the underlying disease . For ex-ample, jaundice may be associated with chronic hepatitis,choledocholithiasis, or hepatic or biliary cancer . Perianal le-sions may suggest the presence of inflammatory bowel dis-ease .

Laboratory Data

As in the patient with acute abdominal pain, laboratory test-ing should reflect the differential diagnosis generated by thehistory and physical examination . Anemia may reflectchronic blood loss from a gastrointestinal source . An ele-vated sedimentation rate may signify an inflammatory dis-ease or autoimmune disease .

Diagnostic Studies

Diagnostic imaging, including abdominal radiography, ultra-sonography, and computed tomography, is valuable in estab-lishing a diagnosis. In addition, upper and lower endoscopyand laparoscopy should be considered . For many patientswith chronic abdominal pain diagnosis requires extensiveevaluation .

for a

MiscellaneousIrritable bowel syndromeNonulcer dyspepsiaChronic mesenteric ischemiaMittelschmerz

Diagnosable Causes

Table 4-3 lists some commonly overlooked causes ofchronic abdominal pain . For further discussion, refer to theappropriate chapter within the text .

Treatment

The goals of treatment of patients with chronic abdominalpain are identification and cure of the responsible underlyingdisease . Cure, however, is often not possible; in these pa-tients, palliation of symptoms may be worthwhile . Palliativecare may involve medications, surgery, or psychologic sup-port. For example, a patient with metastatic colon cancermay benefit from excision of the primary lesion to alleviatepain caused by local invasion or obstruction . Similarly, pa-tients with advanced malignancy and biliary obstruction mayexperience significant relief of symptoms through surgical,endoscopic, or percutaneous biliary decompression . Palliationmay also be achieved by pharmacologic and mechanicalmeans. Analgesics, antidepressants, antiemetics, and anxio-lytics are often useful tools in palliative care . In addition,chemical and surgical nerve ablation or transcutaneous elec-trical nerve stimulation may be useful in relieving pain .

The treatment strategy pursued must also address thephysical and psychologic symptoms associated with chronicpain. This is often the most difficult aspect of treatmentfacing the clinician. A multidisciplinary approach, includingpsychiatrists, physiotherapists, pharmacists, and social work-ers, may help the patient and the clinician cope with chronicabdominal pain and its associated physical and psychologicmanifestations. Where these resources are not available,however, the presence of a caring physician with an unhur-

Sensation . New York, Elsevier, 1986, p 189 .8 . Fields H : Pain . New York, McGraw-Hill, 1987 .9 . Basbaum AI, Fields HL : Endogenous pain control systems : Brainstem

spinal pathways and endorphin circuitry . Annu Rev Neurosci 7 :309,1984 .

10 . Janig W, Morrison JFB : Functional properties of spinal visceral affer-ents supplying abdominal and pelvic organs, with special emphasis onvisceral nociception . In Cervero F, Morrison JFB (eds) : Visceral Sensa-tion . New York, Elsevier, 1986, p 87 .

It . Bonica J : The Management of Pain . Philadelphia, Lea & Febiger, 1990.12 . Higashi H : Pharmacological aspects of visceral sensory receptors . In

Cervero F, Morrison JFB (eds) : Visceral Sensation. Amsterdam, Else-vier, 1986, p 21 .

13 . Bender J : Approach to the acute abdomen . Med Clin North Am 73 :1413, 1989 .

14 . Silen W : Cope's Early Diagnosis of the Acute Abdomen . New York,Oxford University Press, 1991 .

15 . Eisenberg R, Heineken P, Hedgcock MW, et al : Evaluation of plainabdominal radiographs in the diagnosis of abdominal pain. Ann InternMed 97:257, 1982 .

16 . Jeffrey RJ : CT and Sonography of the Acute Abdomen. New York,Raven Press, 1989 .

17 . Shaff MI, Tarr RW, Partain CL, et al : Computed tomography andmagnetic resonance imaging of the acute abdomen . Surg Clin NorthAm 68 :233, 1988 .

18 . Rao PM, Rhea JT, Novelline RA, et al : Effect of computerized tomog-raphy of the appendix on treatment of patients and use of hospitalresources . N Engl J Med 338 :141, 1998 .

19 . Poulin EC, Schlachta CM, Mamazza J : Early laparoscopy to help diag-nose acute non-specific abdominal pain . Lancet 355 :861, 2000 .

20. Salky BA, Edye MB : The role of laparoscopy in the diagnosis andtreatment of abdominal pain syndromes . Surg Endosc 12 :911, 1998 .

21 . Navez B, d'Udekem Y, Cambier E, et al : Laparoscopy for managementof nontraumatic acute abdomen. World J Surg 19 :382, 1995 .

22. Williams L : Mesenteric ischemia . Surg Clin North Am 68 :331, 1988 .23. Mannick JA, Whetlemore AO : Management of ruptured or sympto-

matic abdominal aortic aneurysms . Surg Clin North Am 68 :377, 1988 .24. Burnett L : Gynecologic causes of the acute abdomen . Surg Clin North

Am 68:385, 1988 .25. Purcell T : Nonsurgical and extraperitoneal causes of abdominal pain .

Emery Med Clin North Am 7 :721, 1989 .26 . Hatch E : The acute abdomen in children . Pediatr Clin North Am 32 :

1151, 1985 .27. Neblett WW, Pietsch JB, Holcomb GW : Acute abdominal conditions in

children and adolescents . Surg Clin North Am 68 :415, 1988 .28. Bugliosi TF, Meloy TD, Vukov LF: Acute abdominal pain in the

elderly . Ann Emerg Med 19 :1383, 1990 .29. Howard F : Laparoscopic surgery in pregnancy . Chir Int 2 :16, 1995 .30 . Glasgow RE, Visser BC, Harris HW, et al : Changing management of

gallstone disease during pregnancy . Surg Endosc 12 :241, 1998.

ABU()r;tlNAL P?,t^t INC] t €INU 4'HEAt`

Table 4-3 1 Causes of Chronic Abdominal Pain ried attitude can provide significant reassurance and comfortto an afflicted patient .

CHRONIC INTERMITTENT CHRONIC CONSTANTPAIN PAIN

Mechanical Malignancy (primary or meta- REFERENCESIntermittent intestinal obstruc- static)

tion (hernia, intussusception, Abscess I . Melzack R, Wall PD : Pain mechanisms : A new theory . Science 150 :adhesions, volvulus) Chronic pancreatitis 971, 1965 .

Gallstones Psychiatric (depression, somato- 2. Melzack R, Torgerson WS : On the language of pain . AnesthesiologyAmpullary stenosis form disorder) 34:50, 1971 .

Inexplicable (chronic intractable 3. Leek B : Abdominal visceral receptors. In Neil E (ed) : Enteroceptors :Inflammatory abdominal pain) Handbook of Sensory Physiology, vol 3 . New York, Springer-Verlag,Inflammatory bowel diseaseEndometriosis/endometritis 1972, p 113 .Acute relapsing pancreatitis 4. Gershon MD, Kirchgessner AL, Wade PR : Functional anatomy of the

Familial Mediterranean fever enteric nervous system . In Johnson LR, et al (eds) : Physiology of theGastrointestinal Tract, vol 1 . New York, Raven Press, 1994, p 381 .

Neurologic and metabolic 5. Mayer EA, Raybould HE : Role of visceral afferent mechanisms inPorphryia functional bowel disorders. Gastroenterology 99 :1688, 1990 .Abdominal epilepsy 6 . Sengupta JN, Gebhart GF : Gastrointestinal afferent fibers and sensation .Diabetic radiculopathy In Johnson LR, et al (eds) : Physiology of the Gastrointestinal Tract, volNerve root compression or en- 1 . New York, Raven Press, 1994, p 483 .trapment 7. Cervero F, Tattersall JEH : Somatic and visceral sensory integration in

Uremia the thoracic spinal cord. In Cervero F, Morrison JFB (eds) : Visceral