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Acute abdominal pain represents the cardinal symptom of a large number of intra-abdominal pathologies. Because of multiple organ systems, varied pathology from life threatening to benign, and differences in presentation related to sex and age, identifying a final diagnosis is a challenge. The clinician's goal for patients with acute abdominal pain is to rapidly identify whether the underlying cause requires an urgent or immediate surgical intervention. By developing a systematic approach to evaluating patients with abdominal pain, clinicians can generate a differential diagnosis to ensure appropriate treatment and improved patient outcomes. The purpose of this article is to provide clinicians with a framework for evaluating the complaint of acute abdominal pain and recognizing patients who require expedited evaluation.
Abdominal pain is cited as the most common reason for going to the emergency department in the 18- to 64-year age group and is the third most common reason in the population older than 65 years.1 Approximately 8% of chief complaints are specifically for abdominal pain or include abdominal pain as a component of a constellation of symptoms resulting in the perceived need to access emergent health care services.2 The admission rate for abdominal pain in the adult population is approximately 18%; however, in the population older than 65 years, the admission rate increases to 50%.3,4 Most individuals (65%-75%) with acute abdominal pain have a nonsurgical problem.3 A life-threatening cause for abdominal pain is identified in 10% of patients, with most requiring surgery.3 Even in today's era of advanced diagnostic testing, approximately 20% to 40% of patients will not have a definitive diagnosis for their abdominal pain at the conclusion of their evaluation and discharge.4
The abdomen, like a "mysterious black box," contains multiple distinct, yet interrelated organ systems. Specific pathology can develop in each organ, and each organ can be affected by systemic disease. The spectrum and acuity of disease is quite large, with benign abdominal processes and acute life-threatening events having considerable overlap in presentation. Common causes of intra-abdominal pathology frequently lack the signs and symptoms of the classic presentation, which can vary with age, sex, and comorbidities.3
Confounding the evaluation of abdominal pain is the potential for a nonabdominal source to manifest as an intra-abdominal process.3 Providing care for patients with acute abdominal pain requires familiarity with the epidemiology, prevalence, and presentation of abdominal pathology, as well as a working knowledge of the differential diagnoses. The evaluation and management of this population require a thorough history, complete physical examination, and selected diagnostic testing to pinpoint a specific diagnosis.5
The problem of abdominal pain is not unique to the emergency department. Acute abdominal pain is a complication that can occur across the continuum of care, from primary care to the acute care inpatient setting. Acute gastrointestinal (GI) pathology occurring in the acutely and critically ill inpatient population frequently has an atypical presentation. Classic signs and symptoms are absent or diminished, delaying diagnosis and surgical evaluation of the patient, which increases morbidity and mortality rates. Patients at greatest risk for a delay in diagnosis are those admitted with an initial presentation not involving the GI system.6
The approach to evaluating patients experiencing abdominal pain as a symptom of an acute intra-abdominal process is the same in all locations of presentation. This article reviews the key components of a diagnostic process used to develop a differential diagnosis. It focuses on the rapid recognition of patients with severe or life-threatening conditions and identification of high-risk populations.
The initial step in evaluating patients with acute abdominal pain is to determine the acuity of the problem. Clues that the pain is of a serious nature include rapidity of onset of the pain, severity of the pain, and an ill appearance of the patient. Assessing the onset, quality, character, and severity of the pain is essential to developing an initial differential diagnosis for the patient's abdominal pain5 (Table 1).
A rapid onset of severe pain raises the concern for an acute process such as peritonitis, perforation, obstruction, torsion, or vascular pathology, such as mesenteric ischemia, aortic rupture, or aortic dissection.5 Assessing the patient for temperature abnormalities, tachycardia, tachypnea, and alteration in blood pressure will assist in triaging the acuity of the situation. Performing a focused assessment of the GI, genitourinary, cardiovascular, and pulmonary systems helps the clinician identify an acute surgical abdomen requiring expedient diagnosis and urgent surgical consultation. Diagnostic studies that may support the acuity of the presentation include leukocytosis with bandemia, metabolic acidosis, azotemia, positive focused assessment with sonography for trauma examination, or plain radiograph of the chest or abdomen noting obstruction or free intraperitoneal air. Early recognition of a patient with an acute surgical abdomen or life-threatening intra-abdominal process allows the clinician to rapidly initiate interventions to stabilize and resuscitate the patient. These interventions should include intravenous administration of fluids, initiating appropriate empiric antibiotic therapy, analgesia, and early surgical consultation. The judicious administration of analgesia may produce some alteration in the physical examination, but recent studies, including meta-analyses of the use of analgesic drugs in patients with acute abdominal pain, conclude that analgesia does not compromise the physical assessment sufficiently to result in diagnostic error.7-10 The conclusion is that treating pain and relieving anxiety related to pain are appropriate interventions that may enhance the patient's cooperation to undergo serial abdominal examinations.7-10 Early surgical consultation for any patient thought to have an acute surgical abdomen reduces morbidity and mortality rates, including inpatients who are suspected to have developed GI complications.6 Once appropriate stabilizing interventions for the acutely ill patient or for the patient with life-threatening acuity have been initiated, the differential diagnosis and identification of the problem can be addressed.
A second triage technique in evaluating and developing a differential diagnosis for patients with abdominal pain is outlined in Figure 1. Sex, age, and race are important epidemiological factors to consider when developing a differential diagnosis. For example, inflammatory bowel disease is more prevalent in females than males, more common in whites compared with other ethnicities, and risk increases with age.11 The differential diagnosis to consider in an older adult varies significantly from that of a younger individual11,12,13 (Table 2).
Many of the sex-specific pathologies for abdominal pain have a genitourinary cause. Two life-altering pathologies can occur in females of reproductive age: ectopic pregnancy and ovarian torsion. In a patient with a ruptured ectopic pregnancy, hypovolemic shock as a result of blood loss requires immediate resuscitation and surgery. In the female patient with an undiagnosed ischemic ovary as a result of torsion, a systemic inflammatory response can cause hypotension. In both situations, delay in diagnosis can affect future fertility. In female patients of reproductive age, clinicians must determine pregnancy status. In early ectopic pregnancy, the patient can present with amenorrhea, lower abdominal pain, vaginal bleeding, or all 3 symptoms. However, until the human chorionic gonadotropin (hCG) hormone test is performed, and pregnancy is confirmed or excluded, the differential diagnosis is quite broad, including gynecological, urinary, and bowel pathology. In a situation where the hCG is 2000 IU/L or less and a transvaginal ultrasound does not confirm an intrauterine pregancy with fetal pole, the patient is still at risk for an ectopic pregnancy. In this situation, a repeat hCG must be obtained in 48 hours to document hormonal progression.14 Despite improved diagnostic modalities, including sensitive hCG tests and transvaginal ultrasound, ectopic pregnancy remains a life-threatening complication of early pregnancy and a leading cause of mortality in female patients.14
In the patient experiencing ovarian torsion, the pain is sudden in onset, moderate to severe, intensifying, and often associated with vomiting.15 Time is of the essence in making this diagnosis; the longer the delay, the greater the risk for necrosis of the ovary, requiring oophorectomy. Ovarian torsion can occur in pregnant or nonpregnant female patients, with ovarian mass or cyst being a significant risk factor.15 Other pathology that can mimic ovarian torsion includes tubo-ovarian abscess, rupture of hemorrhagic ovarian cyst, and appendicitis. A diagnostic dilemma encountered by clinicians evaluating female patients with lower abdominal pain in the initial stages of either ectopic pregnancy or ovarian torsion is that minimal or no clinical findings may be present on examination. The only clues to the diagnosis would be in the subjective data collection.
To continue the diagnostic process, the clinician should investigate information about the character, location, quality, and associated symptoms. By carefully elucidating the history, the clinician can identify contextual clues about the specifics of each patient's presentation, which may assist in identifying the symptom cluster, which can help refine the diagnosis.
Abdominal pain may be characterized as visceral or somatic. Visceral discomfort occurs with noxious stimulation of afferent nerves in visceral organs.16 The precipitator of the sensory stimuli may be due to mechanical forces seen in obstruction; chemical irritation and inflammation as a result of blood, bile, urine, stool, or pus in the abdomen; acute inflammation of an organ as seen in pancreatitis; or ischemia seen in torsion or incarceration of an organ.17 Afferent pain fibers located in the abdominal organs transmit impulses via the spinal nerves and autonomic nervous system that terminate in the brain stem.16 An overlapping network of the afferent nerve fibers from the abdominal viscera transmit impulses to the spinal cord via more than 1 dorsal spinal nerve root.16 These fibers synapse in the dorsal ganglion of the spinal cord with afferent fibers from adjacent visceral structures as well as somatic afferent fibers, a process known as convergence.5,16 The pain produced by this process is poorly localized, described as dull, aching, gnawing, or colicky, and is typically perceived to be located in the midline.5,17 Clinically, the patient may be unable to find a comfortable position, pacing or frequently changing positions.18
The convergence of pain fibers gives rise to the referral or radiation patterns associated with abdominal pain.5,16 These regions of radiation generate a pain pattern described as aching near the surface of the body and are located away from the organ causing the pathology. For example, ureteral colic can produce referred pain to the testicles or vagina, an impacted stone in the common bile duct can produce pain in the right shoulder, and pancreatic disease or splenic injury can cause pain in the left shoulder. Clinicians caring for patients with abdominal pain should recognize and correlate reports of referred pain with the visceral organ causing the pathology.
Somatic or parietal pain is well localized, often described as sharp or stabbing.5,16 It typically results from irritation to the parietal peritoneum or mesodermal structures of the abdominal wall. An acute inflammatory process of solid or hollow organs initially will cause a visceral sensation of pain caused by inflammation of the visceral peritoneum. As the disease process progresses, the inflammatory markers will cause a chemical irritation and inflammation of the parietal peritoneum, which stimulates the somatic pain fibers, increasing the severity of the pain with localization in the area of the culprit organ.5,16 Clinically, patients experiencing somatic or parietal pain do not want to move, as the pain can be provoked by coughing, walking, or a jostling motion. As the pathology producing visceral pain extends beyond the involved organ, the quality of the pain changes from visceral to somatic.18 The classic example of this progression of pain symptoms occurs with appendicitis. Initially described as an aching periumbilical discomfort, as the appendix becomes distended and inflamed with impaired lymphatic drainage and wall ischemia, the parietal peritoneum and surrounding fat and mesentery become inflamed, which results in the localized, sharp pain at McBurney's point. The transition from visceral pain to somatic pain is a key assessment feature that the clinician should look for when obtaining the patient's history. The involvement of the parietal peritoneum can be an indication of progression of the disease due to peritonitis, abscess formation, or perforation.5
Nociceptive fibers stimulated by pathology of the foregut, stomach, proximal duodenum, biliary system, liver, or pancreas produce visceral pain in the epigastric and lower sternal area.5 The remainder of the small bowel and proximal one-third of the colon are midgut structures. Involvement of these structures produces visceral discomfort in the periumbilical region of the abdomen.5 The genitourinary structures and distal two-thirds of the colon are considered hindgut structures, with the visceral pain perceived in the suprapubic area.5 Pathology of retroperitoneal structures such as the kidneys and aorta can produce back pain.
In addition to the patient ascribing visceral pain to a localized area of the abdomen, he or she may report referred pain. Information on localization of visceral pain should be interpreted carefully by the clinician and in context with other data, such as quality, severity, duration, onset, and provoking and relieving features of the pain. Because of the overlap of afferent nociceptive fibers of the gut, attributing a patient's symptoms to a specific organ or location solely based on the patient's identified site of visceral pain can increase the risk for diagnostic error.5,18
As a clinical tool, sudden onset of severe pain should always raise a concern for potentially catastrophic pathology. The evaluator must remember, however, that significant pathology can evolve over time and present in a less-dramatic fashion. A patient with sudden onset of maximal intensity of abdominal pain should trigger prompt concerns for vascular emergencies, including ruptured aortic aneurysm, aortic dissection, or mesenteric ischemia. Bowel pathology, such as perforation, intestinal volvulus, and torsion, frequently will cause an acute onset of pain requiring emergent surgical intervention to limit morbidity. However, these pathologies also may have an insidious onset, which does not diminish the risk that the process is serious and potentially life threatening.18 An increased risk exists for a delay in presentation due to a gradual onset of pain in patients who are elderly or immunocompromised.
Typically, inflammatory or infectious pathology has a gradual onset.5 As the inflammatory process progresses with increased release of inflammatory markers, the pain will intensify and become more localized. With the development of somatic pain, the patient frequently will access emergent care. The patient with an inflammatory process that presents early in the course of the disease with diffuse vague abdominal pain is difficult to diagnose. A technique to avoid missing an infectious process or misdiagnosing the patient is serial examinations over a period of time.
Establishing the time of onset of symptoms provides a timeline for comparing current symptoms with the natural progression of intra-abdominal pathology that produces abdominal pain.5 Temporal progression can help the clinician narrow the differential diagnosis.5
A final red flag related to onset is pain or discomfort that wakes a patient from sleep, which should always be considered an ominous sign until proven otherwise.18 The ominous symptoms related to acute abdominal pain that increase the suspicion for an acute surgical abdomen are listed in Table 3.
Continuous and intensifying abdominal pain is indicative of disease progression. Recognizing patterns of disease progression can facilitate diagnosis. The inflammatory process of diverticulitis initially may cause a vague aching discomfort in the left abdomen. As the inflammation of the bowel wall progresses, involving the adjacent parietal peritoneum, the pain frequently localizes to the left lower quadrant, which results in peritoneal signs including rebound tenderness and guarding on palpation of the abdomen. A similar pattern occurs with appendicitis, with initial periumbilical pain that migrates to the right lower quadrant over the course of hours to 1 to 2 days. The colicky pain seen in the passage of a stone in cholelithiasis is described as constant and nonparoxysmal, and lasts 4 to 6 hours; it rarely lasts less than 1 hour.19 The pain of intestinal obstruction also has a colic quality, progressing from intermittent discomfort to constant pain as the bowel becomes more distended. The development of somatic pain in bowel obstruction is a late ominous finding, raising concern for transmural wall ischemia due to complete obstruction or perforation.5
Pain reported as severe, unremitting, or intensifying increases the suspicion for a serious underlying cause.5 Situations that produce this finding include infectious processes leading to abscess formation and peritonitis, perforated viscus, ischemia progressing to infarction as seen in torsion, complete bowel obstruction, and mesenteric ischemia. However, a report of milder pain does not exclude serious illness.
Identifying factors that can intensify, trigger, or relieve the pain helps clinicians refine the differential diagnosis.5 Movement accentuates the pain in acute inflammatory or infectious processes; therefore, the patient prefers to remain quiet and still. Pain that increases with coughing, walking, or jarring motions suggests peritoneal irritation.5,18 Patients with acute pancreatitis typically prefer to be sitting upright, leaning slightly forward, thus shifting the organs anterior to the pancreas forward, relieving some of the discomfort.
Determining whether the pain is provoked or diminished with the consumption of food provides additional data to narrow the differential diagnosis. Ingestion of food will increase the pain of gastritis, gastric ulcer disease, and pancreatitis, and potentially trigger biliary colic. A decrease in upper abdominal pain following eating occurs in duodenal disease. Mesenteric ischemia or "abdominal angina" caused by celiac artery compromise frequently occurs after ingestion of a meal. Individuals experiencing mesenteric ischemia induced by eating may avoid eating and experience weight loss. Consider mesenteric ischemia in the differential diagnosis of a patient with severe coronary artery disease, peripheral vascular disease, heart failure, or dysrhythmia.
An important part of the patient's history is self-treatment with over-the-counter or prior prescription medications. The use of these medications may diminish or mask pain severity and therefore delay the diagnosis of a potentially life-threatening process.
Abdominal pain can be a component of a constellation of symptoms the patient is experiencing. In addition to pain, the individual may report nausea, vomiting, diarrhea, constipation, dysuria, and anorexia. Assessing for systemic symptoms, such as fever, myalgias, arthralgias, headache, and dizziness as well as symptoms involving the cardiopulmonary system, including chest pain, dyspnea, cough, and syncope, is necessary. In developing the differential diagnosis for a patient with abdominal pain, clinicians must consider systemic and extra-abdominal causes for the abdominal pain. Epigastric pain with vomiting or accompanied by indigestion could be a symptom of an inferior wall myocardial infarction. Pathology of the lower lobes of the lungs, such as pneumonia, pleural effusions, or pulmonary embolus, can present as right or left upper abdominal pain. Severe flank pain could be ureteral colic but also could be the harbinger of an aortic dissection or ruptured abdominal aneurysm.
Vomiting frequently occurs in response to visceral pain.18 Typically, vomiting occurs after the onset of the pain.19(pp18-27) The exception to this axiom is esophageal rupture from forceful regurgitation.19 Vomiting associated with a small bowel obstruction can progress from gastric content to bilious to feculent emesis as the obstruction progresses. An individual with a large bowel obstruction may experience no vomiting. Hematemesis raises concern for gastritis, peptic ulcer disease, and liver disease.
Determining a change in bowel habit, change in consistency of the stool, and the presence of hematochezia or melena, can be indicators for specific pathology.18 Melenic stools indicate a bleeding source in the upper portion of the GI tract. Bleeding from the lower GI tract typically produces bright red bleeding. Blood in the stool should raise a concern for inflammatory disease, infection, ischemia, diverticulosis, and malignancy. In a bowel obstruction where increased peristalsis occurs in an attempt to move intestinal contents past the obstruction, the stool distal to the obstruction will be expelled.5 The expelled stool is frequently in the form of diarrhea. An important question to ask the patient with suspected bowel obstruction is the passage of flatus. In a bowel obstruction, the patient will expel gas faster than fluid.5 The gas is not replaced while intestinal fluid will continue to be secreted from the mucosal membrane.5 Thus, the patient may continue to produce stool but no flatus. A report of change in bowel habit, consistency and caliber of the stool, development of constipation, or blood in the stool should raise the suspicion of a tumor as the cause of bowel obstruction.
Pathology of the genitourinary system can produce lower abdominal pain. Associated symptoms include dysuria, hematuria, abnormal vaginal bleeding, or vaginal or penile discharge. A ruptured ovarian cyst can produce peritoneal signs similar to those for appendicitis, increasing the difficulty in distinguishing the cause of the right lower quadrant pain. Women with endometriosis or pelvic inflammatory disease frequently experience GI symptoms in addition to pelvic pain. A young patient with an ectopic pregnancy may experience no pain at all, only amenorrhea or vaginal bleeding.14 In the reproductive female patient, an unexplained syncope event may be the only indication of a ruptured ectopic pregnancy with bleeding into the pelvis.14
The patient's medical and surgical history assists the clinician to identify risk factors for specific pathology that can cause acute abdominal pain. Prior abdominal surgery heightens the suspicion for an intestinal obstruction and excludes pathology in the absence of the surgically removed organ. A higher probability of mesenteric ischemia is found in patients with a history of heart failure, low cardiac output states, atrial fibrillation, or peripheral vascular disease. Malignancy, particularly with metastasis to the bones, can produce hypercalcemia, causing abdominal pain. Endocrine pathology such as diabetic ketoacidosis and acute adrenal insufficiency frequently causes abdominal pain. The immunosuppressed patient with abdominal pain (Table 4) raises concerns for serious sequela due to an impaired immune response. These patients can have a less-dramatic presentation of life-threatening disease. The medications the patient is taking can alter abdominal assessment findings, rendering the physical examination less reliable. Frequently, medications that suppress inflammation or perception of pain create a risk for delay in presentation to the health care system. This delay can increase morbidity and mortality rates. On review of the patient's medication profile, if the drug profile includes narcotics, nonsteroidal anti-inflammatory drugs, steroids, and immune modulating agents, be suspicious for serious pathology causing the pain. In this population, it may be necessary to use advanced diagnostic studies such as ultrasound, CT scanning, or MRI earlier in the diagnostic process, because of the masking of symptoms by the medications resulting in delay in diagnosis.
As the history is obtained, the clinician should integrate the patient's epidemiological factors of age, sex, race, and ethnicity with the presenting signs and symptoms to develop a differential diagnosis. Recognition of disease-specific risk factors and symptoms or symptom clusters may increase the probability of a correct diagnosis. As the physical examination is performed, the clinician is looking for objective data that will increase or decrease the likelihood of the diagnosis.
The physical examination should contain all of the components of an abdominal examination, but palpation will probably produce the most significant findings. The purpose of palpation is to localize areas of tenderness and identify signs of peritonitis. It is recommended to start with percussion followed by gentle palpation to identify areas of abdominal tenderness.17 Palpation should begin in a nontender area of the abdomen and progress to the area in which the patient subjectively reports discomfort.17 By observing facial expressions, body posture, and placing hands on the abdomen, the clinician is able to determine areas of greatest discomfort, in addition to the patient's report of tenderness. The abdominal organs in the area where pain is elicited on percussion or palpation should generate a differential diagnosis. For example, pain on palpation of the epigastric area suggests gastric, duodenal, pancreatic, small bowel, or transverse colon as possible sources of pathology. Each quadrant or region of the abdomen should generate a list of differential diagnoses specific to the organs located in that area. Localization of pain on examination is correlated with the subjective data collected in the history. These data are analyzed to support or refute the differential diagnosis of highest suspicion or generate a new diagnosis. A problem arises when the pain is not localized but diffuse, with minimal discomfort reported on examination. These individuals may have a benign problem causing their symptoms or be in the early stages of a serious inflammatory or infectious process. In these situations, observation over a period of time, repeat examinations, and close follow-up are mandatory.
As percussion and palpation are being performed, the clinician should be observant for signs of peritoneal irritation. Guarding is an increase in abdominal wall muscle tone, an involuntary reflex to minimize the movement of the abdominal structures.5 Abdominal wall rigidity is the extreme manifestation of guarding and indicative of an acute surgical abdomen.5 Rebound tenderness is elicited when the abdominal wall is gently compressed for 15 to 30 seconds and then suddenly released. Positive rebound tenderness occurs when the patient reports more pain with the release of the downward pressure than the initial steady compression.5 Testing for rebound in this manner has a sensitivity of approximately 80% for peritonitis, with a specificity of 40% to 50%.5 Other methods to elicit rebound include having the patient cough, jarring the bed, or striking the patient's heel.
Unfortunately, not all abdominal pathology presents with easily recognizable symptom clusters or localization of pain on examination. The clinician must approach the patient with acute abdominal pain without bias to avoid committing a cognitive error, such as premature diagnostic closure, resulting in the misdiagnosis of the patient's problem. Reevaluating the differential diagnosis if investigative studies do not support the diagnosis or if treatment is unsuccessful is essential.3 In situations in which the cause of the acute abdominal pain remains unclear after adequate evaluation, the clinician should consider uncommon pathology that can cause acute abdominal pain. Uncommon pathologies that should be considered include metabolic derangements, endocrine disorders, heavy metal toxicities, rheumatological diseases, and adverse effects from medications (see Table 5).
The recognition of individuals at risk for atypical presentations of abdominal disease is important. The elderly, psychiatric patients, pregnant patients, postbariatric surgery patients, and patients who are immunosuppressed are vulnerable to a delay in diagnosis3 (Table 4). A recommendation for any at-risk patient with one of these comorbidities is to always consider an atypical presentation of common intra-abdominal pathology. Serial examinations of the abdomen performed over a period of observation, while diagnostic studies are being obtained, can assist in identifying progression of the disease process and localization of pain. Anticipate the need for the increased use of resources including laboratory data, radiographic imaging, and medications.20 These patients benefit from a prolonged evaluation time and may require admission to the hospital.20
In specialized populations, notably the elderly and the immunocompromised, determining the cause of abdominal pain has additional challenges. Although the same abdominal processes occur, they may be more difficult to diagnose because of an uncharacteristic presentation, including a suppressed immune response. Age, medications, and disease processes can decrease the body's immune and inflammatory response, which can blunt the severity of pain and limit febrile and white blood cell response.21,22,23
Clinicians should recognize situations in which a response to pain is altered. In patients who are immunocompromised, including those receiving chemotherapy or immunomodulating drugs, an equivalent inflammatory response is not generated. In these situations, a delay in presentation of a potentially life-threatening process is possible. At-risk populations for compromised immune response are summarized in Table 4. The elderly population can underreport the intensity of the pain as a result of physiological changes of aging or regular use of anti-inflammatory medications.
For older patients, abdominal pain is the third most common reason for seeking medical help.2 Because the immune response decreases with age, changes in temperature and white blood cell count are unreliable when trying to determine the severity of an abdominal process. History taking, which is paramount to determine the cause of any abdominal process, also can be circumspect in elderly patients. Any level of underlying dementia can hinder being able to get an accurate history. Further confounding the development of a diagnosis is that elderly patients frequently present with an altered mental status, which can delay evaluation of the abdomen.22 In patients older than 65 years, knowing the likely causative pathology, which is different from that in the younger adult population, is helpful (Table 2).
Biliary tract disorders are the most common cause of abdominal pain in the older population. By the age of 70 years, 33% of patients will have gallstones.21,24 Diseases of the biliary system, including cholecystitis and potentially life-threatening ascending cholangitis, will cause some degree of epigastric or right upper quadrant pain in most older patients.22 However, only 50% of patients older than 65 years who are ultimately diagnosed with acute cholecystitis present with classic symptoms of acute onset colicky epigastric or right upper quadrant pain with nausea and Murphy sign.22 Elderly patients with acute cholecystitis are less likely to experience back or flank pain; in fact, 5% may not experience any pain.22 Clinicians should have a high index of suspicion that vague abdominal pain is caused by biliary disease, as many elderly patients will not develop fever and have little to no change in white blood cell count, despite the presence of severe disease.24
Pancreatitis is the most common nonsurgical cause of abdominal pain in the older population. A patient may present with classic signs of upper abdominal pain radiating to the back but are just as likely to experience diffuse abdominal, back, or chest pain with nausea and vomiting.24 The diagnosis should be considered in elderly patients who present with a vague complaint of upper abdominal pain.22 The cause of pancreatitis in the elderly population is more likely related to the presence of gallstones as opposed to hyperlipidemia or alcohol ingestion.24
Although the presentation of bowel obstruction in the elderly is similar to that of younger patients, it is more common and should be high on the list of differential diagnoses. Small bowel obstruction occurs most frequently, with the leading causes being adhesions, hernias, and tumors.24 Obstruction of the large bowel is less common across all age groups; it occurs in the elderly as a result of the increased incidence of malignancy.24 Tumor is the most common cause of a large bowel obstruction, and the incidence of tumor increases with age.24
Ischemic bowel disease and bowel infarction can be very difficult to diagnose in elderly patients, and a degree of suspicion is necessary, particularly in those patients who have other vascular disorders. The classic presentation of acute mesenteric ischemia, abdominal pain, fever, and blood in the stool may occur in only 30% of elderly patients.24 Pain out of proportion to clinical assessment findings should always raise the suspicion of mesenteric ischemia or ischemic colitis in this patient population.
When evaluating abdominal pain in patients who are immunocompromised, note that the level of pain, change in white blood cell count, and elevation in temperature are unreliable in determining the severity of the process. Although these patients have similar abdominal processes as immunocompetent patients, the presentation may be dramatically different. For example, patients who are immunocompromised may not develop peritoneal signs typically associated with appendicitis, which can delay appropriate medical or surgical intervention.
In addition, these patients have unique processes that need to be considered during the evaluation process. This patient population, depending on the level of immunosuppression, is at risk for the development of cytomegalovirus infections, intra-abdominal abscesses, and neutropenic enterocolitis, which, because of right lower quadrant pain, may initially lead to a diagnosis of appendicitis.23
Another specialized population that poses a challenge in evaluating and diagnosing the cause of abdominal pain includes patients admitted to intensive care units (ICUs). Abdominal complications can increase ICU length of stay and morbidity and mortality rates.6 Clinicians need to identify problems when they arise, so that definitive medical or surgical treatment can be provided as soon as possible to improve survival. However, the critically ill patient with abdominal pain presents additional challenges for the clinician. Although identifying any abdominal process that might complicate the patient's recovery is important, identifying abnormalities that may be present is difficult.
Gastrointestinal and abdominal complications can occur in up to 50% of patients being treated with mechanical ventilation.25 These complications range from a decrease in bowel sounds to intolerance of enteral feedings caused by delayed gastric emptying to diarrhea, which can lead to complications associated with volume status and skin integrity.25 Recognizing these changes during daily patient assessment is important in identifying potentially life-threatening complications, as critically ill patients tend not to display the expected signs and symptoms related to an abdominal process.
Critically ill patients may have difficulty communicating pain that they are experiencing, which can be due to an alteration in mental status related to the underlying disease process, the presence of sedative and analgesic medications, or an inability to communicate while intubated.6 Furthermore, continuous infusions of analgesic medication may mask the pain of a developing abdominal complication.6 At the same time, patients who are very uncomfortable might overemphasize pain as "everything hurts," and they grimace or complain of discomfort at any touch. Alternative methods for abdominal pain assessment should be considered in all critically ill patients.
Subtle changes in the patient's clinical status, such as fever, tachycardia, altered bowel sounds, abdominal distention, new onset of enteral feeding intolerance, diarrhea, or constipation, could be the initial indication of an intra-abdominal complication. Recognizing these signs should lower the threshold for evaluation of the so-called silent offenders; these are abdominal complications that in alert and oriented patients would be evident with abdominal pain and peritoneal signs.6 The silent offenders include cholecysitis, pancreatitis, colitis due to inflammation or ischemia, and bowel obstruction. If not recognized and treated early and aggressively, these complications result in increase in ICU length of stay with worsening morbidity and mortality rates.6 A greater delay may occur in diagnosing patients who are mechanically ventilated, have altered mental status, or are receiving antibiotic or opioid medications.6
Acalculous cholecystitis (AC) should be considered in any critically ill patient with right upper quadrant pain, especially associated with persistent fever and leukocytosis.26 Critically ill patients are at an increased risk of developing acute AC. Many patients in the ICU require treatment with mechanical ventilation and continuous infusions of pain and sedating medications, experience episodes of dehydration or shock, and require multiple transfusions. These factors can contribute to ischemia or inflammation of the gallbladder, which can lead to the development of acute AC.27 If undetected, and without timely medical or surgical intervention, gangrene and perforation can occur, with associated mortality rates as high as 40% to 65%.26,28
Because the biliary tree is not blocked, aside from an abnormal white blood cell count, laboratory results may provide no indication of gallbladder abnormalities. Evidence indicates that ultrasound is sensitive and specific in diagnosing AC.27,29,30 The advantage of this modality is that it can be performed at the bedside. Aggressive medical management is necessary to maintain hemodynamic stability; however, early inclusion of gastroenterology and surgery is imperative if the gallbladder needs to be decompressed or removed.
Patients in the ICU who experience centralized, upper abdominal pain should be evaluated for acute pancreatitis. Although mechanical causes such as biliary duct obstruction can cause acute pancreatitis, other causes, more common in the ICU patient, also can lead to the development of acute pancreatitis. Medications such as diuretics and antiepileptics, hypertriglyceridemia, and shock states, all common in critically ill patients, can increase the risk of acute pancreatitis.29 Perforation of the posterior wall of the stomach causes a chemical exposure to the pancreas.6 This exposure to gastric contents results in an inflammation of the pancreas with the risk of abscess formation.6
Diagnosis can frequently be made on the basis of epigastric abdominal pain, and laboratory findings of increased amylase and lipase levels. However, if the diagnosis is unclear, an abdominal computed tomography scan can be used to identify characteristic changes associated with acute pancreatitis.28
Inflammation of the bowel from various causes can develop in patients in the ICU. A common cause in the ICU is Clostridium difficile infection (CDI), which develops in up to 20% of hospitalized patients receiving antibiotic therapy.28 Any ICU patient who has an elevated white blood cell count, fever, and diarrhea should be suspected of having CDI.26 In severe cases of CDI, patients complain of diffuse abdominal discomfort with the development of colitis and ileus. These patients develop sepsis, becoming tachycardic and hypotensive, causing hypovolemia from excessive diarrhea, or systemic inflammation. Any unexplained increase in white blood cell count, regardless of the presence or absence of diarrhea, should elicit a suspicion for CDI.28 In situations in which an ileus-complicating CDI develops, diarrhea may not be present.28Clostridium difficile infection can occur in any ICU patient, even in those who have not received antibiotics.28
Radiographic changes on an abdominal x-ray, obtained to evaluate abdominal pain or taken for another purpose such as identification of appropriate enteral tube placement, can be the first indication of colitis.28 Dilation of the colon, if seen, should lead to further evaluation to determine the cause. Although an ileus can occur related to narcotic administration or severity of illness, an infectious cause needs to be suspected and appropriately treated. A colonoscopy can be helpful in aiding diagnosis if no stool output is available for evaluation, although this procedure is not without risk. If significant dilation of the colon is present, a surgical consult may be obtained because of the risk of perforation.6,28
The underlying cause of abdominal pain can be difficult to diagnose in any patient. Many factors can interfere with the diagnostic process of abdominal pain in both patients who present to the emergency department and acute care patients who experience abdominal pain during hospitalization. Rapid evaluation is important. Immediate, life-threatening causes, as well as those that will increase morbidity and mortality rates, must be identified to ensure a positive outcome. A thorough history and physical examination are the clinician's most important tools to identify the appropriate laboratory and radiographic tests needed to aid in diagnosis. Appropriate management, whether medical, surgical, or some combination of both, must be started early and aggressively to give patients the best chance for a positive outcome. For a summary of the diagnostic framework, please refer to Figure 2.
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acute abdominal pain; differential diagnosis; surgical abdomen
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