A Clinical Perspective on Abdominal Pain

SUMMARY

The diagnosis of abdominal pain, a challenging task that physicians often face, ranges from life-threatening conditions to chronic functional disorders with little mortality but significant impact on health-related quality of life. Although acute abdominal pain of organic etiology is generally caused by an easily identifiable noxious stimulus, chronic pain occurs most commonly in the absence of detectable nociceptive causes and is referred to as functional gastrointestinal pain. Key criteria that aid the physician in arriving at an accurate diagnosis are discussed in this chapter.

Functional gastrointestinal disorders (FGIDs) make up the majority of diagnoses that a physician makes in the assessment of abdominal pain. Enhanced perception of visceral stimuli appears to be the key pathophysiological mechanism shared by most FGIDs, and this visceral hypersensitivity appears to be predominantly due to central rather than peripheral mechanisms of pain modulation. Enhanced responsiveness of central pain modulation networks to physical and psychological stressors may account for the clinical observations in patients with FGIDs. Even though treatment of acute nociceptive abdominal pain by medical or surgical means is highly effective, treatment of functional gastrointestinal pain remains less than satisfactory. The use of pharmacological and psychological treatment is reviewed in this chapter.

Introduction

Abdominal pain is a frequent symptom in both children and adults, and it is one of the most common reasons why patients consult the health care system. Abdominal pain can be a warning sign signaling acute or chronic tissue injury or damage to intra-abdominal organs (nociceptive pain), or it can be a chronically recurring condition without any detectable pathology (functional or neuropathic pain). In the former case, rapid diagnosis and treatment of the underlying pathology will generally result in prompt relief of the pain, whereas in the latter case, the diagnosis is usually made by exclusion of other causes and conditions, and treatment is currently unsatisfactory.

Pain of visceral origin makes up the majority of the clinical manifestations of abdominal pain, even though other non-visceral causes have to be considered as well. Although the physiology and pathophysiology of visceral and somatic pain share many similarities, it is important to keep the different functional significance of these two types of pain in mind. Somatic pain in general allows the organism to quickly identify, localize, appraise, and respond to a nociceptive stimulus in a purposeful manner. In the case of acute pain, this means withdrawing from the source of the stimulus or removing the stimulus. In the case of chronic pain, it means keeping the injured body part immobile and protected from further activity to allow healing and recovery.

Visceral pain, however, does not give the individual many voluntary response options. In contrast, tissue injury to the viscera generally results in autonomic reflex responses, which are beyond the control of the affected individual, and the conscious experience of visceral pain may be considered an epiphenomenon. For example, acute inflammation of the gastrointestinal (GI) tract will result in the activation of autonomic reflex responses aimed at expelling the offending infectious organism or toxin (vomiting or diarrhea), acute obstruction of a viscus will generate powerful peristaltic waves aimed at overcoming the obstruction, and perforation of a viscus will result in a pattern of motor inhibition (ileus) aimed at minimizing further spillage of intestinal contents into the abdominal cavity. For the same reasons, chronic inflammation or irritation of the viscera in general does not produce abdominal pain, presumably because of activation of endogenous pain inhibition mechanisms.

This chapter discusses key features useful in making the diagnosis of acute and chronic causes of abdominal pain and then focuses on important characteristics of and treatment options for common functional gastrointestinal disorders (FGIDs). Detailed discussion of the basic mechanisms of visceral pain, non-cardiac chest pain, and pelvic pain is presented in Chapter 51, Chapter 52, Chapter 54, Chapter 55 .

Differential Diagnosis Of Abdominal Pain

Abdominal pain can arise from a multitude of different causes and mechanisms ( Tables 53-1 and 53-2 and Box 53-1 ), yet in the majority of cases the clinician is able to rapidly narrow the differential diagnosis to a few plausible possibilities. Thus, rather than going through lengthy, all-encompassing lists of differential diagnoses, the decision-making process is focused on key categories based on acute versus chronic pain, the temporal characteristics and quality of the pain, modulating factors, and associated features.

Table 53-1

Causes of Acute Abdominal Pain and Associated Features

DIAGNOSIS	LOCATION	ONSET	CHRONOLOGY	AGGRAVATING AND RELIEVING FACTORS	ASSOCIATED FEATURES
Parietal Inflammation
Acute cholecystitis	Right upper quadrant, sometimes epigastric; localized; radiates to the shoulder or scapula	Rapid	Constant	Aggravated by food and deep inspiration	Fever, leukocytosis
Acute cholangitis	Right upper quadrant or epigastric, localized, radiates to the scapula or back	Rapid	Constant; pain may be colicky if no parietal involvement	Aggravated by food	Fever, shaking chills; jaundice; leukocytosis; hyperbilirubinemia; abnormal liver function test results (cholestatic or mixed pattern)
Acute pancreatitis	Epigastric or periumbilical, localized, radiates directly through to the midback region	Rapid	Constant	Aggravated by the supine position, relieved by sitting up and adopting a fetal position	May have a history of heavy alcohol intake, previous pancreatitis, hyperlipidemia, or certain drugs; fever; vomiting prominent; leukocytosis; hyperamylasemia
Acute appendicitis	Periumbilical initially, then right lower quadrant; diffuse pain initially, then localized	Gradual	Usually constant, may be colicky initially	When localized to the right lower quadrant, aggravated by movements, coughing	Fever, leukocytosis
Acute diverticulitis	Usually left lower quadrant, may be right lower quadrant with right-sided disease; localized	Gradual	Constant if severe	Aggravated by movement	Bloody stools, fever, leukocytosis
Perforated viscus	Generalized pain	Sudden	Constant	Aggravated by movement	Fever, rigid abdomen, rebound tenderness, absent bowel sounds, leukocytosis
Spontaneous bacterial peritonitis	Generalized, but some patients do not have pain	Gradual	Constant	None	Significant ascites; stigmata of chronic liver disease; may have fever, but this may be low grade or absent in patients with chronic liver disease; leukocytosis (may be normal with advanced liver disease) Peritoneal fluid: increased cell count, low albumin
Visceral Inflammation
Infectious enterocolitis	Variable, usually below the umbilicus; diffuse	Rapid	Colicky	Aggravated by food, may be partially relieved by defecation	Diarrhea (may be bloody, depending on pathogen); tenesmus; leukocytosis; stool tests for bacteria, parasites, or Clostridium difficile may be positive
Vascular
Acute ischemic colitis	Periumbilical or lower abdomen, diffuse	Sudden (if caused by an embolus) or rapid	May be constant or colicky	Aggravated by food	Bloody stools, pain out of proportion to findings on physical examination, atrial fibrillation, left-sided cardiac murmurs, leukocytosis
Dissecting aortic aneurysm	Epigastric or periumbilical, diffuse	Sudden	Constant	None	Described as tearing pain, radiates to the back, unequal femoral pulses, expansile abdominal mass, bruit over the abdomen, hypotensive
Splenic infarct	Left upper quadrant	Sudden	Constant	None	Rub may be auscultated over the spleen; risk factors for embolic events
Visceral Obstruction
Intestinal obstruction (volvulus, intussusception, adhesions, cancer, strangulated hernia)	Central, may be generalized; diffuse	Gradual or rapid, depending on etiology	Colicky	Aggravated by food	Vomiting is prominent; tinkling bowel sounds
Choledocholithiasis	Epigastric or right upper quadrant, diffuse	Rapid	Colicky, episodes usually last hours	Aggravated by food	Jaundice, increased bilirubin, abnormal liver function test results (cholestatic or mixed pattern)
Ureteric stones	Either flank, diffuse	Rapid	Colicky	None	Hematuria; radiates to the testes or to the inner thigh or groin
Acute urinary retention	Suprapubic, localized	Rapid	Constant	Aggravated by movements or coughing	Palpable bladder; prostatomegaly or fecal impaction may be present
Capsule Distention
Liver congestion (heart failure, Budd–Chiari syndrome, alcoholic hepatitis)	Right upper quadrant, localized	Gradual	Constant	None	Heavy alcohol intake, jaundice, hepatomegaly, features of heart failure, absent hepatojugular reflux in Budd–Chiari syndrome, abnormal liver function test results; may have exquisite tenderness with palpation over the liver
Pyelonephritis	Either flank, localized	Gradual	Constant	None	Fever, hematuria, increased cell count in urine
Ectopic pregnancy	Right or left lower quadrant, localized	Gradual (sudden if ruptured)	Constant	None	Amenorrhea, non-menstrual vaginal bleeding, adnexal mass, pregnancy test positive
Tubo-ovarian abscess	Right or left lower quadrant, localized	Gradual	Constant	None	Fever, adnexal mass, leukocytosis

Table 53-2

Causes of Chronic Abdominal Pain and Associated Features

DIAGNOSIS	LOCATION	CHRONOLOGY	AGGRAVATING OR RELIEVING FACTORS	ASSOCIATED FEATURES	PSYCHOSOCIAL FACTORS	EXTRA-ABDOMINAL, CO-MORBID, OR OTHER DIAGNOSIS
Inflammatory
Erosive reflux esophagitis	Epigastric or retrosternal, diffuse	Severe: persistent Mild: remits or relapses	Aggravated by the supine position, food	Acid brash Drug history: NSAID, alendronate, calcium channel blockers, α- and β-blockers, anticholinergics, tricyclics	None	Extra-esophageal: asthma, laryngitis, sore throat, recurrent bronchitis or pneumonia, chronic cough, dental erosions, sinusitis Co-morbid or other: scleroderma, diabetes mellitus, Zollinger–Ellison syndrome, obesity, pregnancy
Gastroduodenal ulcer	Epigastric or right upper quadrant, localized	Persistent	Aggravated or relieved by food	Drug history: NSAID, steroids Anemia, often iron deficient	Smoking	Co-morbid: Zollinger–Ellison syndrome, hypercalcemia
Crohn’s disease	Variable, depending on site of disease; diffuse	Remits or relapses	Aggravated by food	Fever, bloody diarrhea, tenesmus, urgency (colonic disease), fistula, intestinal obstruction, anemia, leukocytosis	Smoking	Extra-abdominal: arthritis, pyoderma gangrenosum, erythema nodosum, uveitis, episcleritis, thrombosis Co-morbid: ankylosing spondylitis, primary sclerosing cholangitis
Eosinophilic gastroenteritis	Usually central, may be generalized if eosinophilic ascites	Remits or relapses	Aggravated by food	Mucosal pattern: vomiting, diarrhea Muscular pattern: vomiting, distention Serosal pattern: ascites, eosinophilia	None	Extra-abdominal: pleural effusion
Lupus gut	Variable, depending on site of disease; diffuse	Remits or relapses	Aggravated by food	Diarrhea, fever, anemia, antinuclear antigen or double-stranded DNA positive, decreased C3/C4	Cerebral lupus may mimic psychiatric disease	Extra-abdominal: malar rash, vasculitic rash, arthritis, digital infarcts, cardiopulmonary disease, glomerulonephritis, cerebral lupus
Celiac disease	Central, diffuse	Persistent	Aggravated by fatty food (malabsorption)	Steatorrhea, weight loss (good appetite), anemia (usually iron or folate deficiency), anti–endomysial antibody positive, anti–tissue transglutaminase antibody positive	None	Extra-intestinal: osteopenia, aphthous stomatitis, hyposplenism, fatty liver, infertility, epilepsy, polyneuropathy Co-morbid: dermatitis herpetiformis, type 1 diabetes mellitus, primary biliary cirrhosis, autoimmune hepatitis, Down’s syndrome, autoimmune thyroiditis, immunoglobulin A deficiency
Malabsorption (e.g., tropical sprue, small bowel bacterial overgrowth)	Central, diffuse	Persistent	Aggravated by fatty food	Steatorrhea, travel history (tropical sprue), previous gastrointestinal surgery (bacterial overgrowth)	None	Co-morbid (bacterial overgrowth): small bowel hypomotility (e.g., chronic intestinal pseudo- obstruction)
Ulcerative colitis	Lower abdomen, diffuse	Remits or relapses	Aggravated by food	Pain not prominent unless severe colitis; fever, bloody diarrhea, tenesmus, urgency, anemia, leukocytosis	None	Extra-abdominal: arthritis, pyoderma gangrenosum, erythema nodosum, uveitis, episcleritis, thrombosis Co-morbid: primary sclerosing cholangitis, ankylosing spondylitis
Chronic pancreatitis	Epigastric, localized, radiates to the back and flanks	Remits or relapses	Aggravated by the supine position, food; relieved by sitting forward	Recurrent pancreatitis, weight loss, steatorrhea; amylase may or may not be raised	None	Extra-abdominal: diabetes mellitus Co-morbid: hypertriglyceridemia
Chronic cholecystitis	Epigastric or right upper quadrant, diffuse, radiates to the scapula	Remits or relapses	Aggravated by food	None	None	None
Malignancy
Advanced colorectal carcinoma	Obstructed central, lower abdomen: diffuse Extraluminal invasion: variable, localized	Progressive	Aggravated by food (obstructed)	Family history of cancer, weight loss, change in bowel habit, bloody stools, anemia (often iron deficient)	None	Extra-abdominal: metastases, anemia (particularly iron deficiency), paraneoplastic phenomena
Hepatoma	Right upper quadrant, localized	Progressive	None	Family history of cancer, weight loss, history and signs of chronic liver disease, jaundice, abdominal mass, anemia, abnormal liver function test results, increased α-fetoprotein	None	Extra-abdominal: metastases, anemia, paraneoplastic phenomena
Gallbladder carcinoma	Right upper quadrant, localized	Progressive	None	Weight loss, abdominal mass, anemia	None	Extra-abdominal: metastases, anemia, paraneoplastic phenomena
Pancreatic carcinoma	Epigastric, localized	Progressive	None	Family history of cancer, weight loss, jaundice (if head of the pancreas involved), abdominal mass, abnormal liver function test results with a cholestatic pattern (if head of the pancreas involved)	None	Extra-abdominal: metastases, anemia, paraneoplastic phenomena
Renal carcinoma	Either loin, localized	Progressive	None	Family history of cancer, weight loss, hematuria, abdominal mass, anemia	None	Extra-abdominal: metastases, anemia, paraneoplastic phenomena
Functional
Non-erosive reflux disease	Epigastric or retrosternal, diffuse	Remits or relapses	Aggravated by stress, supine position, fatty food	Acid brash Drug history: NSAID, alendronate, calcium channel blockers, α- and β-blockers, anticholinergics Normal Hb and WCC	Smoking, alcohol, depression, bipolar disorder, schizophrenia, borderline personality	Extra-abdominal: asthma, laryngitis Co-morbid or other: scleroderma, diabetes mellitus, Zollinger–Ellison syndrome, obesity, pregnancy
Nutcracker esophagus	Epigastric or retrosternal, diffuse	Remits or relapses	Aggravated by stress	Dysphagia, normal Hb and WCC	Anxiety, depression, somatization	Co-morbid: gastroesophageal reflux disease
Diffuse esophageal spasm	Epigastric or retrosternal, diffuse	Remits or relapses	Aggravated by food, hot or cold liquids	Dysphagia, normal Hb and WCC	None	None
Functional dyspepsia	Right upper quadrant, epigastric, or left upper quadrant; diffuse or localized, depending on subtype	Remits or relapses	Aggravated by stress, food	Vomiting, bloating, normal Hb and WCC	Anxiety, depression, early life stress	Extra-abdominal: backache, headache Co-morbid: irritable bowel syndrome
Chronic intestinal pseudo- obstruction	Central, diffuse	Mild: remits or relapses Severe: persistent	Aggravated by food	Dysphagia, constipation, abdominal distention, bloating, history of malignancy (paraneoplastic phenomenon), family history of chronic intestinal pseudo-obstruction, drug history (e.g., tricyclics, narcotics, anticholinergics, phenothiazines), orthostatic hypotension, normal Hb and WCC	None	Extra-abdominal: urinary symptoms, neuromuscular symptoms or signs Co-morbid: diabetes mellitus, multiple sclerosis, scleroderma, muscular dystrophy, amyloidosis
Irritable bowel syndrome	Variable, diffuse	Remits or relapses	Aggravated by stress, food	Diarrhea, constipation, or alternating habit; mucus per rectum; bloating; normal Hb and WCC	Anxiety, depression, hypochondriasis, panic, phobia, neuroticism, somatization, post-traumatic stress disorder, early life stress	Extra-abdominal: dyspareunia, impotence, insomnia, fatigue, backache, dysmenorrhea, urinary frequency Co-morbid: functional dyspepsia, fibromyalgia, interstitial cystitis, chronic prostatitis, chronic pelvic pain syndrome, migraine
Functional abdominal pain syndrome	Variable, diffuse	Persistent	Aggravated by stress	No change in bowel habit, onset associated with stressful event or abuse, normal Hb and WCC	Anxiety, depression, somatization	None
Chronic Infection
Esophageal candidiasis	Epigastric or retrosternal, diffuse	Persistent	Aggravated by swallowing	Oral candidiasis	None	Co-morbid: immunosuppression (drug induced, HIV)
Cytomegalovirus infection	Variable, depending on site of disease; diffuse	Persistent	Aggravated by swallowing (esophagus)	Bloody diarrhea (colon)	None	Co-morbid: immunosuppression (drug induced, HIV)
Tuberculous enterocolitis	Variable, depending on site of disease; diffuse	Persistent	Aggravated by food	Weight loss, bloody stools, change in bowel habit, fever, abdominal mass, fistulas, travel to endemic area, exposure to patient with tuberculosis, monocytosis	None	Extra-abdominal: pulmonary tuberculosis, rash (erythema nodosum) Co-morbid: immunosuppression (drugs, HIV), malnutrition
Tuberculous peritonitis	Generalized	Persistent	None	Weight loss, ascites, fever, travel to endemic area, exposure to patient with tuberculosis, monocytosis Peritoneal fluid: increased cell counts, stain positive for acid-fast bacilli	None	Extra-abdominal: pulmonary tuberculosis, rash (erythema nodosum) Co-morbid: immunosuppression (drugs, HIV), malnutrition
Miscellaneous
Chronic mesenteric ischemia	Variable, diffuse	Remits or relapses	Aggravated by food	Bloody stools, anemia	None	Co-morbid: atherosclerotic disease
Adhesions	Variable, diffuse	Remits or relapses	Aggravated by food	Previous abdominal or pelvic surgery	None	None

Hb, hemoglobin; HIV, human immunodeficiency virus; WCC, white cell count.

Box 53-1

Extra-abdominal Causes of Abdominal Pain

Cardiothoracic

Angina
Myocardial infarction
Pneumonia
Pneumothorax
Pulmonary infarction
Pulmonary empyema

Neurological

Radiculopathy
Herpes zoster
Abdominal migraine
Tabes dorsalis

Hematological

Henoch–Schönlein purpura
Sickle cell crises

Metabolic or Endocrinological

Diabetic ketoacidosis
Acute intermittent porphyria
Lead poisoning
Addison’s disease
Hypercalcemia
Uremia

Miscellaneous

Familial Mediterranean fever
Narcotic withdrawal

Acute versus Chronic Abdominal Pain

A key criterion to narrow the differential diagnosis is based on the acute or chronic nature of the pain. However, whereas chronic pain always reflects a chronic disease process, acute pain can result from a one-time acute intra-abdominal event or be the first or recurring manifestation of a chronic condition. For example, a duodenal ulcer may be manifested acutely and for the first time in the patient’s history in the form of a perforation, or it may be a chronic condition with epigastric pain recurring for many years. Cholelithiasis is a chronic disease, yet the first manifestation of cholecystitis may be an acute abdomen. Abdominal pain arising from pancreatic inflammation may be a one-time acute event (e.g., acute gallstone pancreatitis), or it may occur in the form of chronically recurring episodes of severe acute pain in the case of chronic pancreatitis. On the other hand, some patients with chronic pancreatitis may have chronic pain. In the case of chronic FGIDs such as irritable bowel syndrome (IBS), the initial manifestation may be acute and can mimic other causes of acute abdominal pain such as acute appendicitis, Crohn’s disease, diverticulitis, or intestinal obstruction. However, in the majority of cases a history of preceding episodes of abdominal pain or discomfort can be elicited.

In this chapter we refer to acute abdominal pain as any abdominal pain of non-recurrent nature and chronic abdominal pain as any abdominal pain that has repeatedly occurred over a 3-month period, either as a chronic or as an intermittent symptom. It must be emphasized that this definition does not resolve the problems discussed but merely provides a general framework for discussion of the many causes of abdominal pain.

Approach to Patients with Acute Abdominal Pain

From a teleological viewpoint, there is no adaptive advantage for the individual to precisely localize visceral pain. In the case of somatic pain, localization is important for the ability of the organism to protect itself against further injury by withdrawal from and avoidance of a noxious stimulus, whereas in the case of visceral pain, the noxious stimulus is within, and the only protective mechanism that the body can use is to expel the noxious stimulus. This difference is reflected in the different properties of the somatoparietal and visceral components of abdominal pain. An algorithm for the diagnostic work-up of acute, recurring abdominal pain is presented in Figure 53-3 .

Figure 53-3, Algorithm for a diagnostic work-up of acute right upper quadrant abdominal pain.

Location of Pain

Based on the relatively small number of mechanically sensitive spinal afferents innervating healthy viscera, the convergence of visceral and deep somatic afferents onto the same spinal neurons, and the divergence of spinal afferents over several spinal segments, visceral pain is poorly and inconsistently localized and generally has a dull, aching, or cramping quality. For example, human studies have shown that balloon distention of the bile duct of post-cholecystectomy patients leads to epigastric pain in the majority of patients (47%), consistent with the expected localization of visceral pain of foregut origin. However, 18% of patients experienced pain in the right upper quadrant, 16% experienced localized pain in the back, and 19% experienced no pain at all ( ). This variation is seen in clinical practice: patients with choledocholithiasis commonly have epigastric pain, but a significant proportion have right upper quadrant pain. On the other hand, somatoparietal structures are more densely innervated by spinal afferents, which results in better localization of pain.

Visceral pain is commonly experienced about the midline of the abdomen. Pain in the embryological foregut, midgut, and hindgut is experienced in the upper, middle, and lower portions of the abdomen, respectively. This concept is well illustrated by patients with acute appendicitis, in whom the initial pain is poorly localized in the central part of the abdomen even though the appendix is physically located in the right iliac fossa. At this stage the inflammation is limited to the appendix, and nociception is transmitted predominantly via visceral afferents. When the inflammation progresses and involves the parietal peritoneum, the pain then becomes accurately localized to the right iliac fossa.

The visceral afferent mechanisms and pathways responsible for signaling acute tissue injury to the central nervous system are not static and non-linear: acute inflammation and tissue injury will result in the recruitment of previously mechano-insensitive afferents, in addition to sensitization of mechanically responsive afferent fibers. This so-called peripheral sensitization is followed by the development of sensitization at the spinal and supraspinal level (central sensitization), which results in lowering of thresholds for autonomic reflexes and a change in conscious perception of the affected organ. The changes resulting in sensitization of afferent pathways are in part counteracted by endogenous pain inhibitory pathways. Consistent with the concept of central sensitization, spontaneous pain and pain associated with contractions and palpation develop, as well as atypical and enlarged referral areas. Thus, abdominal pain may be associated with pain at sites distant from the afflicted organ.

Sensitization of dorsal horn neurons distal to the site of predominant visceral afferent input, which normally receive only subthreshold input from these visceral afferents, can result in a situation in which visceral pain may be perceived to originate from the area supplied by the corresponding somatic afferents. Examples are acute cholecystitis, where pain may be referred to the shoulder or scapula; acute pancreatitis, where pain may be referred to the back; or nephrolithiasis, where pain may be referred to the groin area. Figure 53-1 illustrates the segmental level of visceral innervation and the corresponding dermatomes.

Chronology

The temporal characteristics of pain are an important aspect of assessment and yield useful information. A sudden onset of severe pain that progresses rapidly is usually indicative of serious pathology and may be due to perforation of viscera or catastrophic vascular events such as embolic mesenteric ischemia or a dissecting aortic aneurysm. The time course of abdominal pain can be constant or colicky. Pain caused by parietal inflammation and capsule distention is usually constant, whereas pain from obstruction of viscera with peristaltic activity tends to be colicky. The frequency of the colic can help distinguish the cause of pain from various intra-abdominal organs. Colicky pain from the tubular GI tract generally occurs repeatedly over minutes, whereas the time course of biliary colic may occur over a period of hours to days. A long duration of pain over weeks suggests a chronic cause, and a short duration can be due to either an acute cause or the initial onset of chronic abdominal pain. The chronology of the different types of abdominal pain is illustrated in Figure 53-2 .

Figure 53-2, Typical chronologies of abdominal pain.

Aggravating and Relieving Factors

Important components of the history are the factors that aggravate or alleviate the pain. Parietal pain is worsened by movement, which includes deep inspiration and coughing. In contrast, patients with intestinal obstruction or renal colic tend to writhe about in an attempt to find relief of their pain, but without success. Posture can exacerbate or relieve certain types of abdominal pain. Pain from retroperitoneal structures, such as the pancreas, is worsened in the supine position and relieved by leaning forward or assuming a fetal position.

Pain from the GI tract may be worsened by food. It is important to distinguish between exacerbation of pain directly related to food intake and nausea or loss of appetite. Many causes of abdominal pain may result in nausea and avoidance of food, but food intake may not necessarily worsen the pain. Examples are abdominal pain secondary to liver congestion and ureteric obstruction. The temporal relationship between food intake and exacerbation of the pain should also be considered in the evaluation. For example, pain from the upper GI tract worsens within minutes after food intake, whereas colonic pain may worsen after hours of food intake. On the other hand, food may relieve or worsen symptoms from upper gastrointestinal lesions such as gastroduodenal ulcers. Relief of pain after vomiting suggests pathology in the stomach or proximal part of the small bowel, whereas relief after defecation suggests colonic disease.

Quality

The quality of the pain is not generally helpful in the clinical setting because patients often describe the quality of pain differently. A useful exception is the tearing pain of a dissecting aortic aneurysm. Description of the severity of the pain by the patient is also subjective and in itself conveys little diagnostic value. However, if associated with signs of autonomic activation, such as sweatiness and nausea, it suggests severe pain. This is particularly useful in situations in which the pain is episodic and the patient is asymptomatic at the time that the history of the pain is elicited. Examples include the pain of renal colic and choledocholithiasis.

Associated Features

Certain features associated with abdominal pain provide vital clues to the cause and, when present, allow physicians to quickly narrow the differential diagnosis. Patients with abdominal pain and jaundice are likely to have hepatobiliary pathology, patients with abdominal pain and hematemesis are likely to have an upper GI lesion, and the association of abdominal pain and bloody stools suggests distal colonic pathology. Fever is often associated with acute abdominal pain, but not with chronic functional abdominal pain. Vomiting is commonly associated with many causes of abdominal pain but is rare in functional pain syndromes (despite the common presence of nausea). With obstruction of the proximal part of the small intestine, vomiting is particularly prominent, with onset immediately following food intake. In the later stages of large bowel obstruction, the vomitus may look feculent. Figure 53-3 illustrates how the key points in the history can be used in the assessment of acute right upper quadrant abdominal pain.

Physical Examination

The physical examination should start with a general inspection of the patient. The initial appearance provides useful information about whether the patient is gravely ill. Drowsiness, diaphoresis, and tachypnea mandate urgent attention. The vital signs must be assessed to exclude shock, which may be due to sepsis or hypovolemia. Patients who are curled tightly in the fetal position are likely to have peritoneal irritation, whereas patients who writhe about are more likely to have visceral pain. Evidence of recent alcohol ingestion suggests a possible relationship of the abdominal pain with chronic alcohol abuse, such as in chronic pancreatitis.

On examination of the abdomen it is also very useful to inspect the patient for jaundice, which would indicate a hepatobiliary source of the pain. Stigmata of chronic liver disease—such as palmar erythema, spider nevi, and Dupuytren’s contracture—should be sought because this would point toward a hepatic cause of the pain and possibly a pancreatic source since chronic liver disease and pancreatitis often co-exist in patients with high alcohol intake. The abdomen may also be grossly distended with intestinal obstruction or with severe ascites. In addition, the abdomen should be inspected carefully for scars, hernia, or bruises.

Palpation of the abdomen should begin at a site distant from the pain. This will allow the patient to get accustomed to the examination and reduce voluntary guarding. Careful palpation will often identify organomegaly and mass lesions and will localize areas of tenderness. Involuntary guarding is due to reflex contraction of the abdominal muscles as a result of increased pressure on inflamed peritoneum. Its presence suggests peritonitis, but in practice it is difficult to distinguish from voluntary guarding by the patient. With severe peritonitis, the abdomen will feel board-like from generalized abdominal wall contraction. Rebound tenderness is another feature of peritonitis and is elicited by gradually applying pressure on the abdomen and suddenly removing the examining hand. In severe cases, rebound tenderness can be elicited by quickly removing the stethoscope or by shaking the bed.

Absent bowel sounds on auscultation suggest ileus, whereas tinkling bowel sounds are heard with intestinal obstruction. Bruits may be heard over a hepatoma or an aortic aneurysm. Rectal examination is an essential component of the physical examination. The presence of bloody stools indicates lower colonic pathology, and melena suggests upper GI pathology. In patients with acute urinary retention, prostatomegaly or fecal impaction may be detected during the rectal examination. A vaginal examination should be done to exclude adnexal masses and pelvic inflammatory disease.

A systemic examination should also be performed because causes of abdominal pain may be associated with pathology in other systems. For example, the presence of atrial fibrillation and left-sided cardiac murmurs predisposes to embolic mesenteric ischemia. In addition, a systemic examination may detect extra-abdominal causes of abdominal pain, such as pneumothorax and pneumonia.

Initial Investigations

A complete blood count is useful in assessing acute abdominal pain. A raised white cell count with neutrophilia is sensitive but not specific for inflammation and infection. Low hemoglobin may reflect an underlying chronic process. Liver function tests should be performed when hepatobiliary pathology is suspected since this can help distinguish between hepatocellular and cholestatic disease. Serum amylase is useful to exclude acute pancreatitis, but raised levels may also be seen in patients with diabetic ketoacidosis and visceral perforation, albeit mildly. In patients with a history suggestive of urinary tract pathology, urinalysis is mandatory. It is important to perform a pregnancy test on women of childbearing age because an ectopic pregnancy can sometimes be hard to diagnose.

In all patients, radiographs of the chest and the abdomen should be performed. An erect chest radiograph is useful when perforation of a viscus is suspected, whereas erect and supine abdominal radiographs are helpful to identify evidence of intestinal obstruction or calcifications. In patients with biliary pain, ultrasound should be done to look for dilated biliary ducts and the presence of gallstones. A computed tomography scan of the abdomen is useful in searching for lesions in the solid intra-abdominal organs. Both computed tomography and ultrasound allow detection of small amounts of intra-abdominal fluid, which is suggestive of perforation and leakage of fluid from intra-abdominal viscera.

Some of the causes of acute abdominal pain and their characteristic features are listed in Table 53-1 .

Intra- versus Extra-abdominal Pain

Acute abdominal pain may not always be due to intra-abdominal pathology. It can sometimes be caused by referred pain from extra-abdominal sites (see Box 53-1 ). The pain of myocardial ischemia may localize to the upper part of the abdomen, and pleuritic chest pain or pain associated with a pulmonary embolism may be perceived to originate from the left or right hypochondrium. Systemic illnesses may cause non-specific abdominal pain, which can be severe. Examples include diabetic ketoacidosis, lead poisoning, and acute intermittent porphyria.

Approach to Patients with Chronic Abdominal Pain

Although mortality from causes of chronic abdominal pain is much lower than that from causes of acute abdominal pain, chronic abdominal pain causes significant morbidity, impairment of health-related quality of life, and a considerable burden of illness, and it is a far more common reason for seeking health care. Within the category of chronic abdominal pain, gastroesophageal reflux disease (GERD) and the so-called functional syndromes are by far the most common group of disorders. Surveys have shown that 35%–41% of symptomatic outpatient visits to gastroenterologists are for FGIDs alone. IBS accounts for 12% of patients seen in primary care practice and for up to 28% of referrals to gastroenterologists ( ). The prevalence of FGIDs and common organic causes of abdominal pain is presented in Table 53-3 . The details of these specific abdominal states are discussed later in this chapter. First, we review some general considerations.

Table 53-3

Prevalence of Common Functional and Organic Causes of Chronic Abdominal Pain

DIAGNOSIS	PREVALENCE
Organic ^∗
Erosive esophagitis	2 per 100
Gastroduodenal ulcer	2 per 100
Celiac disease	3–30 per 10,000
Ulcerative colitis	4–10 per 10,000
Crohn’s disease	1–10 per 10,000
Chronic pancreatitis	3 per 10,000
Functional
Gastroesophageal reflux disease ^†	7–18 per 100
Functional dyspepsia ^‡	15–20 per 100
Irritable bowel syndrome ^§	4–14 per 100
Functional abdominal pain syndrome ^¶	2 per 100

∗ Yamada T 1999 Textbook of gastroenterology, 3rd ed. Lippincott, Williams & Wilkins, Philadelphia.

† Shaheen N, Provenzale D 2003 The epidemiology of gastroesophageal reflux disease. American Journal of the Medical Sciences 326:264–273.

‡ Locke GR III 1998 Prevalence, incidence and natural history of dyspepsia and functional dyspepsia. Baillières Cinical Gastroenterology 12:435–442.

§ Drossman DA, Camilleri M, Mayer EA, et al 2002 AGA technical review on irritable bowel syndrome. Gastroenterology 123:2108–2131.

¶ Drossman DA 1996 Chronic functional abdominal pain. American Journal of Gastroenterology 91:2270–2281.

The approach to patients with chronic abdominal pain is similar to that highlighted for acute abdominal pain. However, psychosocial factors, co-morbid conditions, and extraintestinal manifestations are even more important in making a diagnosis. A crucial aspect of the evaluation of chronic abdominal pain is to distinguish organic from functional causes of pain. Useful (but not totally reliable) indicators of organic disease (so-called red flags) include features of weight loss, bloody or melenic stools, steatorrheic stools, and a strong family history of carcinoma. Anemia, particularly iron deficiency anemia, detected on laboratory investigation argues against the diagnosis of an FGID and requires further evaluation. An algorithm for the approach to patients with chronic abdominal pain is shown in Figure 53-4 .

Figure 53-4, Algorithm for a diagnostic work-up of chronic upper abdominal pain.

Location of Pain

Patients with chronic abdominal pain may have atypical referral areas. The pain of chronic pancreatitis may be manifested as back pain, whereas patients with an FGID tend to report abdominal pain that is diffuse and may involve various atypical regions of the abdomen or even extra-abdominal sites. For example, sigmoid pain may be referred to the left upper quadrant or right lower quadrant and gastric pain to the right upper quadrant. In rare cases, patients report radiation of abdominal pain to the lower extremities, the back, or the entire side of their body. This alteration in viscerosomatic referral has been reproduced experimentally ( Fig. 53-5 ). When balloons were distended at different sites in the colon or stomach, patients with IBS or functional dyspepsia (FD) localized pain to different and larger areas in the abdomen than did healthy control subjects ( ). Because of these altered referral patterns, localization of the pain may be less helpful in assessing the cause of chronic abdominal pain in patients with a possible FGID.

Figure 53-5, Viscerosomatic pain referral patterns in response to colonic balloon distention are larger in patients with irritable bowel syndrome (IBS) than in healthy control subjects because of the altered pain perception in those with functional gastrointestinal disorders.

Pain from carcinoma of solid abdominal organs occurs late in the disease and is due to stretching of the organ capsule from tumor growth or invasion of the capsule. Consequently, this pain is well localized. Pain from carcinoma of the GI tract also occurs late in the disease and not until the tumor has resulted in luminal obstruction or has invaded adjacent tissues.

Quality of Pain

As in the assessment of acute abdominal pain, the quality of chronic abdominal pain is generally unhelpful. However, a burning sensation is typical of GERD. Heartburn is defined as a burning feeling rising from the stomach or lower part of the chest up toward the neck, and when heartburn is a major or sole symptom, GERD is the cause in at least 75% of patients ( ). However, distention (and possibly contractions) of the distal esophagus can also be experienced as a burning sensation. In contrast to the esophagus, where burning quality appears to be the predominant qualitative descriptor of pain, a burning quality of abdominal pain may be an indication of a neuropathic origin of the pain, particularly when constant and unrelated to food intake or defecation. In patients with functional abdominal pain syndrome (FAPS; see the section Functional Abdominal Pain Syndrome ), the pain is frequently described in emotional or symbolic terms such as “like a knife stabbing” or “an emptiness.”

Chronology

Symptoms of functional and inflammatory GI disorders, as well as those of chronic pancreatitis, tend to relapse and remit with time, the exception being FAPS, where the pain may be constant ( ). In contrast, the pain from advanced malignancy of solid visceral organs is constant and, in the absence of intervention, is invariably progressive, usually over a period of weeks to months.

Aggravating and Relieving Factors

Food Intake

In a significant number of patients with chronic pain arising from the GI tract, symptoms worsen after food intake. This aggravation of symptoms may be related to specific food items (fatty foods or milk products); may be related to food intake in general; or may even be triggered solely by the thought, smell, or sight of food before any food enters the GI tract. Food-induced exacerbation of symptoms is more characteristic of FD (see the section Functional Dyspepsia ) than of IBS (see the section Irritable Bowel Syndrome ). With advanced carcinoma, pain is not related to food, the exception being pain as a result of obstruction in GI malignancies. Unlike other FGIDs, the pain from FAPS is characteristically not affected by food intake.

Stress

Patients with chronic GI disorders frequently report a history of stressful life events preceding an exacerbation of symptoms. This association is most characteristic for FGIDs and for severe, sustained stressors such as loss of a family member, difficult divorce proceedings, or financial distress. The role of stress in symptom exacerbation is not limited to functional GI pain but has also been reported with inflammatory bowel disease (IBD) and GERD ( ). For example, a population-based study found that 64% of patients with GERD had exacerbation of symptoms with stress and that GERD patients who are chronically anxious and exposed to long periods of stress are more likely to exhibit stress-induced symptom exacerbation. A history of aversive early life events—or a history of physical or sexual trauma—greatly enhances an individual’s vulnerability for stress-related conditions such as IBS. Thus, the likelihood of functional GI syndromes developing later in life is higher in patients with aversive early life events such as loss of the primary caregiver, divorce of parents, or abuse.

Psychiatric Co-morbidity

Alterations in mood and affect and psychological factors are strongly associated with FGIDs and should be actively sought whenever assessing a patient with chronic abdominal pain. Patients with an FGID frequently have a history of co-existing anxiety and, less often, depression. Hypochondriasis, anxiety, neuroticism, and somatization have also been reported to be important in predicting the likelihood of IBS-like symptoms developing after an enteric infection (i.e., postinfectious IBS [PI-IBS]) ( ).

In what are currently referred to as primary motility disorders of the esophagus (syndromes that are typically manifested as retrosternal or epigastric pain and discomfort), psychological factors may play an important pathophysiological role as well. For example, patients with chest pain and either a hypertensive lower esophageal sphincter, nutcracker esophagus, or hypotensive contractions have a higher incidence of somatization, depression, and anxiety than do control subjects ( ).

Lifestyle Factors

Lifestyle factors can have a major impact on the development of chronic abdominal pain. A history of heavy alcohol intake may lead to chronic pancreatitis. Alcoholic liver cirrhosis is a risk factor for the development of hepatoma. Sexual orientation and intravenous drug abuse may increase the probability of opportunistic infections as a cause of chronic abdominal pain in patients infected with human immunodeficiency virus (HIV). Travel to endemic areas may predispose to chronic infections such as tuberculosis of the abdomen and giardiasis.

Associated Features

When chronic abdominal pain from an advanced malignancy is present, it is almost invariably associated with significant weight loss (a red flag). In practice, this means that all patients with abdominal pain and significant weight loss should be assumed to have an organic cause until proved otherwise. Pain from chronic infections may also be associated with weight loss.

The relationship of pain to sleep is sometimes useful in discriminating FGIDs from organic disorders. Poor sleep tends to increase the severity of functional GI pain, whereas improvement in sleep quality has the opposite effect. It has generally been assumed that the symptoms of an FGID do not typically occur during sleep whereas pain from organic causes such as malignancy and GERD may wake patients from sleep. However, recent reports have challenged this clinical wisdom by showing that a large number of patients with an FGID are awakened by their abdominal pain ( ).

The appearance of stool is useful in the differential diagnosis. Steatorrhea is associated with malabsorption from intestinal causes or chronic pancreatitis. Bloody stools suggest distal inflammatory colonic pathology such as ulcerative colitis or advanced malignancy, and melena or hematemesis may indicate the presence of a bleeding peptic ulcer.

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here