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The author acknowledges substantial use of the work of I. Kaur in the previous editions of this chapter.
To guide the clinical approach, abdominal pain is classified as either acute or chronic/recurrent. Acute abdominal pain demands rapid diagnosis and appropriate intervention so that catastrophic outcomes can be avoided. Chronic or recurrent abdominal pain is most often attributed to functional abdominal pain disorders (FAPDs) stemming from biopsychosocial processes. FAPDs must be differentiated from organic causes of chronic/recurrent abdominal pain associated with either physiologic, structural, or biochemical abnormalities.
Signs and symptoms of medical and surgical conditions that cause acute abdominal pain have considerable overlap. Severe pain lasting <48 hours with vomiting, muscle guarding, and rebound tenderness are classic findings for an acute surgical abdomen, but the absence of these findings does not exclude one entirely. Findings that provide some reassurance against a serious medical problem include (1) normal growth and physical examination; (2) the absence of anemia, elevated inflammatory markers, and blood in stool; and (3) pain limited to the periumbilical area. On the other hand, alarm features that should prompt evaluation for a pathologic organic etiology include persistent right upper or lower quadrant pain, dysphagia, odynophagia, symptoms of urinary tract infection (UTI), persistent vomiting, gastrointestinal (GI) bleeding, anemia, nocturnal diarrhea, arthritis, perirectal disease, involuntary weight loss, faltering of linear growth, delayed puberty, unexplained fever, and a family history of inflammatory bowel disease, celiac disease, or peptic ulcer disease.
Medical history should include risk factors such as abdominal trauma or surgery and a family history of inflammatory bowel disease, as well as medications that could alter the clinical presentation such as anti-inflammatory agents, analgesics, and antibiotics. Age is an important stratifying factor for likelihood of conditions. l Across all ages, gastroenteritis, urinary tract infections, and constipation are common medical causes of abdominal pain, while appendicitis is the most common indication for surgery. Necrotizing enterocolitis targets premature infants; colic is a disorder of infants; and incarcerated inguinal hernia, intussusception, and Hirschsprung disease predominate in infants and toddlers. Volvulus with malrotation usually manifests in infancy but can occur at any age. Considerations for children and adolescents include the multisystem inflammatory syndrome in children (MIS-C) associated with SARS-CoV-2 infection, Henoch Schönlein purpura, mesenteric lymphadenitis, peptic ulcer disease, diabetic ketoacidosis, sickle cell crisis, inflammatory bowel disease, cholecystitis, and pancreatitis. Some genitourinary disorders occur predominantly or exclusively in adolescents, such as dysmenorrhea, pelvic inflammatory disease (PID), ectopic pregnancy, and ovarian/testicular torsion.
Many features of abdominal pain can be understood by appreciating the sensory innervation of the structures of the abdomen. Autonomic nerve fibers located within all layers of the abdominal organs and the mesentery primarily recognize pain induced by mechanical factors (distension, contraction, traction, compression, and torsion), ischemia, and inflammation. Visceral pain typically is perceived as dull, aching, nauseating, and difficult to localize. Somatic afferent nerve receptors in the parietal peritoneum, abdominal muscle, and skin respond to irritation from infectious, chemical, or inflammation producing continuous, sharp, well-localized pain that is exacerbated by movement; these are the underpinnings of rebound tenderness that is present in peritonitis.
Visceral pain typically manifests in areas corresponding to the embryonic origin of the affected structure. As a result, disorders occurring in the lower esophagus, stomach, duodenum, liver, and pancreas cause upper abdominal pain. Disorders of the small bowel, appendix, and proximal colon result in periumbilical pain. Distal colonic and genitourinary tract disorders cause lower abdominal pain.
Visceral pain also can be referred to distant sites that share the cutaneous dermatome at the same spinal cord level as the visceral sensory afferent nerves. Examples of referred pain are scapular pain from biliary colic, groin pain from renal colic, and shoulder pain from irritation of the diaphragm. Pain only localizes to the involved site when the overlying parietal peritoneum or abdominal wall structures become inflamed and stimulate somatic afferent nerves.
In the evolution of acute appendicitis, the migration of pain from the periumbilical pain (visceral pain from appendiceal obstruction) to the lower right quadrant pain (somatic pain from peritoneal irritation) illustrates the principles of pain localization. Similarly, cholecystitis begins with epigastric pain but migrates to the right upper quadrant when the inflamed gallbladder contacts the parietal peritoneum.
Bacterial and protozoal colitis and early intussusception produce crampy pain that is intermittent, while pain from appendicitis, intestinal obstruction, and late-stage intussusception is constant. Vomiting and diarrhea are dominant features of gastroenteritis, while abdominal pain is not expected to be severe or the foremost complaint. On the other hand, abdominal pain is severe and the dominant complaint in acute appendicitis and peritonitis and in some cases of MIS-C, while other symptoms are less significant. Burning stomach pain relieved by food or antacids suggests a peptic ulcer. Pain exacerbated by a fatty meal can be occur with cholecystitis.
The nature of vomiting can provide diagnostic clues. Abdominal pain generally precedes vomiting in a surgical abdomen, while vomiting precedes abdominal pain in medical conditions such as gastroenteritis. Gastric obstruction produces nonbilious vomiting. Vomiting associated with intussusception can be nonbilious initially then become bilious with progressive obstruction. High small-bowel obstruction causes bilious emesis early in the course, whereas distal small-bowel obstruction causes delayed emesis that can progress to feculent emesis. Large-bowel obstruction produces late-onset emesis or no emesis.
The presence and quality of hematochezia narrows the differential diagnosis. So-called currant jelly stools (due to a mixture of blood and mucus) suggest intussusception. Large watery bloody stools suggest Shiga toxin-producing Escherichia coli (STEC) infection, while frequent scant loose stools with cramps and tenesmus suggest dysenteric colitis caused by bacterial or protozoal pathogens, and inflammatory bowel disease.
If possible, younger children should remain in their parent’s arms and be observed first from a distance for breathing patterns and general appearance. Children with peritoneal irritation remain still and resist movement while those with visceral pain are often writhing with discomfort. The patient who holds one hip flexed and externally rotated is likely to have acute appendicitis or an iliopsoas or obturator internus muscle abscess or myositis, or primary pathology in the hip.
Tachypnea, increased work of breathing, grunting, nasal flaring, and/or retractions suggest pneumonia with pain that is referred to the abdomen. Rapid, shallow breathing is seen with abdominal processes that cause splinting of the diaphragm. Acidosis-related vomiting, dehydration, compromised bowel, infection, or diabetes causes deep, rapid breathing (Kussmaul respirations). Fever suggests an inflammatory or infectious process.
The abdomen is observed for distention or scaphoid appearance and auscultated for presence and character of bowel sounds. The abdomen then is palpated gently beginning at the site most distant from that reported as painful to determine the degree and location of abdominal tenderness, rebound tenderness, abdominal rigidity (e.g., peritonitis), edema of the abdominal wall, a mass (e.g., intussusception, tubal pregnancy, ovarian cyst, malignancy, hydronephrosis), or organomegaly. Percussion can reveal a fluid wave indicating ascites or fullness and tenderness of bladder. Tenderness at the costovertebral angle should be ascertained. A rectal examination can reveal sphincter tone, masses, and fecal blood.
Additional important observations include pulmonary auscultation for signs of pneumonia and skin inspection for an exanthem (e.g., Henoch Schönlein purpura). Evidence of pharyngitis (erythema, exudate), scarlatiniform rash, or tender cervical lymphadenopathy should prompt an evaluation for group A streptococcal (GAS) pharyngitis or, if stools are loose, Yersinia gastroenteritis.
Conditions in which acute abdominal pain is a cardinal feature are discussed with a focus on the early clinical approach. Many specific clinical syndromes, diagnostic studies, and management considerations are covered in more depth in other chapters in Part II of the textbook. Abdominal pain as part of a syndrome of fever of unknown origin is discussed in Chapter 15 .
The term acute abdomen generally refers to the sudden onset of severe abdominal pain that demands urgent medical attention, often involving surgical consultation. Underlying causes include infection, inflammation, ischemia, and/or intestinal obstruction, and manifest as abdominal distension, tenderness, and involuntary muscle guarding. Hemodynamic instability and sepsis can be present. The major causes that require urgent evaluation are described below.
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