Acute abdominal pain is usually a self-limiting, benign condition that is commonly caused by gastroenteritis, constipation, or a viral illness. The challenge is to identify children who require immediate evaluation for potentially life-threatening conditions. Chronic abdominal pain is also a common complaint in pediatric practices, as it comprises 2-4% of pediatric visits. At least 20% of children seek attention for chronic abdominal pain by the age of 15 years. Up to 28% of children complain of abdominal pain at least once per week and only 2% seek medical attention. The primary care physician, pediatrician, emergency physician, and surgeon must be able to distinguish serious and potentially life-threatening diseases from more benign problems ( Table 10.1 ). Abdominal pain may be a single acute event ( Tables 10.2 and 10.3 ), a recurring acute problem (as in abdominal migraine), or a chronic problem ( Table 10.4 ). The differential diagnosis is lengthy, differs from that in adults, and varies by age group. Although some disorders occur throughout childhood (constipation, gastroenteritis, lower lobe pneumonia, urinary tract infections), others are more common in a specific age group (see Table 10.2 ).
| Disease | Onset | Location | Referral | Quality | Comments |
|---|---|---|---|---|---|
| Functional: irritable bowel syndrome | Recurrent | Periumbilical | None | Dull, crampy, intermittent, duration 2 hr | Caused by unknown physiologic factors; diarrhea/constipation are symptoms |
| Gastroenteritis | Acute or gradual | Periumbilical, rectal-tenesmus | None | Crampy, dull, intermittent | Emesis, fever, watery diarrhea or dysentery (mucus and blood) |
| Esophageal reflux | Recurrent, after meals, bedtime | Substernal | Chest | Burning | Sour taste in mouth, Sandifer syndrome |
| Duodenal ulcer | Recurrent, before meals, at night | Epigastric | Back | Severe burning, gnawing | Relieved by food, milk, antacids; family history |
| Pancreatitis | Acute | Epigastric/hypogastric | Back | Constant, sharp, boring | Nausea, emesis, marked tenderness |
| Intestinal obstruction | Acute or gradual | Periumbilical–lower abdomen | Back | Alternating cramping (colic) and painless periods | Distention, obstipation, bilious emesis, increased bowel sounds |
| Appendicitis | Acute or gradual (1-2 days) | Initially periumbilical or epigastric; later localized to the right lower quadrant | Back or pelvis if retrocecal | Sharp, steady | Nausea, emesis, local tenderness with/without fever; patient is motionless |
| Meckel diverticulitis (mimics appendicitis) | Recurrent or constant | Generalized diffuse with perforation: periumbilical–lower abdomen | None | Sharp | Hematochezia: painless unless intussusception, diverticulitis, or perforation |
| Inflammatory bowel disease | Recurrent | Depends on site of involvement | Dull cramping, tenesmus | Fever, weight loss, with/without hematochezia | |
| Intussusception | Acute | Periumbilical–lower abdomen | None | Cramping, with painless periods | Guarded position with knees pulled up, “currant jelly” stools |
| Lactose intolerance | Recurrent with milk products | Lower abdomen | None | Cramping | Distention, gaseousness, diarrhea |
| Urolithiasis | Acute, sudden | Back | Groin | Severe colicky pain | Hematuria; calcification on KUB x-ray study, CT scan |
| Pyelonephritis | Acute, sudden | Back | None | Dull to sharp | Fever, costochondral tenderness, dysuria, pyuria, urinary frequency |
| Cholecystitis/cholelithiasis | Acute | Right upper quadrant | Right shoulder, scapula | Severe colicky pain | Hemolysis with/without jaundice |
| Neonate |
| Necrotizing enterocolitis * |
| Obstruction * |
| Malrotation with volvulus * |
| Idiopathic or drug (indomethacin, steroid)–induced intestinal perforation |
| Infant (<2 yr) |
| Intussusception * |
| Incarcerated hernia * |
| Urinary tract infection * |
| Gastroenteritis * † |
| Intestinal obstruction |
| Malrotation with volvulus |
| Trauma (e.g., abuse) |
| Pneumonitis (lower lobe) |
| Hirschsprung disease |
| Aerophagia |
| Spontaneous bacterial peritonitis |
| Gastroesophageal reflux |
| Child (2-11 yr) |
| Appendicitis * |
| Gastroenteritis * † |
| Trauma * |
| Henoch-Schönlein purpura |
| Hemolytic uremic syndrome |
| Hepatitis |
| Peptic ulcer disease |
| Sickle cell anemia: vasoocclusive crisis |
| Pancreatitis |
| Pneumonia (lower lobe) |
| Abdominal tumors |
| Pyelonephritis/cystitis |
| Testicular torsion |
| Torsed cryptorchid testis |
| Incarcerated hernia |
| Typhlitis |
| Pharyngitis/tonsillitis |
| Meckel diverticulitis |
| Superior mesenteric artery syndrome |
| Mesenteric adenitis |
| Spontaneous bacterial peritonitis |
| DKA |
| Streptococcal pharyngitis |
| Idiopathic * |
| Adolescent (12-19 yr) |
| Appendicitis * |
| Pelvic inflammatory disease * |
| Trauma * |
| Tubo-ovarian abscess |
| Fitz-Hugh–Curtis syndrome |
| Labor (pregnancy) |
| Hepatitis |
| Pancreatitis (any cause) |
| Ectopic pregnancy |
| Crohn disease |
| Ovarian cyst/mittelschmerz * |
| Sickle cell crisis |
| Peptic ulcer disease |
| Omental torsion |
| Psoas abscess or hemorrhage |
| Mesenteric adenitis |
| Urinary tract infection |
| Muscle strain (exercise, coughing) |
| DKA |
| Testicular torsion |
| Idiopathic * |
† Gastroenteritis indicates intestinal infection with viral, bacterial, protozoal, or parasitic agents. Giardiasis and cryptosporidiosis are particularly common and may produce acute or chronic pain.
| Intestinal Perforation | Luminal Occlusion |
|
|
| Vascular Occlusion | Intraabdominal Hemorrhage |
|
|
| Infant (<2 yr) | Child (2-11 yr) | Adolescent (12-19 yr) |
|---|---|---|
|
* See also Table 10.6 .
‡ Includes lactose and sorbitol (and other fruit-juice polyalcohols) intolerance.
§ Hepatic, pancreatic, subphrenic, psoas, perinephric, renal, pelvic.
Pathophysiology of Abdominal Pain
(See Nelson Textbook of Pediatrics, p. 1764.)
Abdominal pain results from stimulation of nociceptive receptors and afferent sympathetic stretch receptors. The pain is classified as visceral or parietal (somatic).
Visceral Pain
Visceral pain receptors are located on the serosa surface, in the mesentery, within intestinal muscle, and mucosa of hollow organs. Pain is initiated when receptors are stimulated by excessive contraction, stretching, tension or ischemia of the walls of hollow viscera, the capsule of a solid organ (liver, spleen, kidney), or of the mesentery. Increased contraction of the smooth muscle of hollow viscera may be caused by infection, toxins (bacterial or chemical agents), ulceration, inflammation, or ischemia. Increased hepatic capsule tension may be secondary to passive congestion (heart failure, pericarditis) or inflammation (hepatitis).
Afferent fibers involved in processing visceral pain are unmyelinated C-fibers that enter the spinal cord bilaterally, resulting in dull, poorly localized pain. Visceral pain is often of gradual onset, and although localization may be imprecise, some general rules may be helpful ( Fig. 10.1 ).
Parietal Pain
Parietal pain arises from direct noxious (usually inflammation) stimulation of the contiguous parietal peritoneum (e.g., right lower quadrant at the McBurney point, appendicitis) or the diaphragm (splenic rupture, subdiaphragmatic abscess). Parietal pain is transmitted through A-delta fibers to specific dorsal root ganglia and thus is usually sharp, and more intense. It can usually be exacerbated by movement or cough, is accompanied by tenderness over the site of irritation, and lateralizes to one of four quadrants. Because of the relative localization of the noxious stimulation to the underlying peritoneum and the more anatomically specific and unilateral innervation (peripheral-nonautonomic nerves) of the peritoneum, it is usually easier to identify the precise anatomic location that is producing parietal pain ( Fig. 10.2 ).
Acute Abdominal Pain
The clinician evaluating the child with abdominal pain of acute onset must decide quickly whether the child has a “surgical abdomen” (a serious medical problem necessitating treatment and admission to the hospital) or a process that can be managed on an outpatient basis. Even though surgical diagnoses are fewer than 10% of all causes of abdominal pain in children, they can be life-threatening if untreated. Approximately 55% of children evaluated for acute abdominal pain have a specific medical diagnosis; in another 45%, the cause is never defined.
History
Obtaining an accurate history is critical for making an accurate diagnosis but is dependent both on the ability and willingness of the child to communicate and on the skill of the parent or guardian as an observer. The person providing an infant’s care is the best source of information about the current illness; the examining physician should try to elicit as much information from the child as possible. Some children give a good account of their illness when they are simply asked to describe it; most children must be asked open-ended, non-leading questions. To determine the presence of anorexia, the physician must ask questions about food intake, the time the food was eaten, and how that behavior compares to the child’s normal intake. The answers are often quite different from the responses to the more general questions “Are you hungry?” and “Have you eaten today?”
During the history taking, the child should remain in the parent’s arms, at play, or comfortably seated beside the parent, as appropriate for the child’s age. While the history is obtained, there is no particular reason that the child should be undressed. The clinician must resist the urge to speed things up by examining the child while taking the history. On occasion, when seeing a seriously ill child, the physician may need to abbreviate the diagnostic process, but taking short cuts may lead to inaccurate conclusions.
Essential Components of the History
Time of onset of pain.
Pain of fewer than 6 hours’ duration is accompanied by nonspecific findings, and observation is often needed to determine the nature of the illness. Pain lasting from 6-48 hours is more apt to have a cause that warrants medical intervention, although delays in presentation and diagnosis in children are not unusual. Timing of the progression of symptoms must be detailed.
Location of pain.
The location of the pain at its onset and any change in location are very important ( Table 10.5 ; see also Table 10.1 ). Most intraperitoneal visceral pain is a response to the stimulation of stretch fibers in the bowel wall and is mediated through the spinal nerves. This pain is sensed as a deep, aching periumbilical pain. Pain caused by inflammation of the parietal peritoneum (acute appendicitis) is localized to the area of the inflamed organ or is diffuse if the inflammation is extensive and involves more of the peritoneal cavity. Pain resulting from obstruction of an organ is localized to the area of that organ and radiates to the commonly innervated region (e.g., stones in the ureter cause intense flank pain with radiation into the groin). Pain that is migratory or fleeting in location is rarely suggestive of a problem requiring operative intervention.
| REFERRED | |
|---|---|
| Extraabdominal Lesion Pain Referred to Abdomen | Intraabdominal Extraperitoneal Origin |
|
|
| RADIATED | |
| Origin Is Primary Site with Simultaneously Perceived Pain in a Secondary Site | |
| |
Character of pain.
The character of the pain is often difficult for the child to describe. Some older children may be able to differentiate cramping, aching, and burning sensations, but most children do not do this well. Children can relate whether the pain comes and goes or is continuous and unrelenting. The character of the pain is usually unknown in the toddler and infant, although the parent can determine whether the discomfort is constant, cramping, or intermittent. If the child intermittently draws the legs up in a flexed position and cries, the clinician can assume that intermittent pain is present.
Child’s activity level.
The effect of the pain on the child’s activities is an important indicator of the severity of the underlying disease. If the pain is sufficiently severe to awaken the child from a sound sleep, it is of much more significance than pain that occurs only at school and never on weekends. If a child has had to avoid a favorite activity, the pain is more apt to have a defined organic cause. This applies only to children with acute abdominal pain because children with chronic functional abdominal pain may wake up from sleep and may miss favorite activities due to pain and disability. Asking whether motion worsens the pain helps differentiate peritoneal irritation or musculoskeletal diseases from more nonspecific problems. The child with acute appendicitis lies motionless, whereas the child with a renal stone, gallstone, gastroenteritis, or pancreatitis may toss and turn and writhe in discomfort. Localized, superficial, tender trigger points in the abdominal wall may suggest abdominal wall (muscle, cutaneous) pain. The localized pain results from entrapment of cutaneous terminal branches of intercostal nerves (7th-12th) penetrating the rectus abdominis muscle and can easily be missed without the proper history or exam.
Gastrointestinal symptoms.
The presence or absence of gastrointestinal symptoms may differentiate intestinal problems (acute appendicitis, gastroenteritis, acute cholecystitis) from those arising from other intraabdominal organs (urinary tract infection, ovarian disease, abdominal wall pain).
Anorexia and nausea are difficult symptoms for a small child to describe. Often, if simply asked whether he or she is hungry, a child will respond in the affirmative. Questions about recent food intake, normal eating habits, the last normal meal, and the current desirability of a favorite food often provide more accurate information about the presence or absence of anorexia and nausea than do direct questions about appetite or nausea.
Vomiting associated with acute pain is usually related to intestinal disease, such as ileus, gastroenteritis, or acute problems of the gastrointestinal tract that warrant surgery. However, vomiting may occur as a response to severe non-intestinal pain such as in testicular torsion; this vomiting is usually not recurring and is not a prominent feature. Vomiting may be a sign of increased intracranial pressure, which may or may not be accompanied by associated headache or vital sign changes (bradycardia, hypertension, irregular respirations), a bulging fontanel, an altered level of consciousness, or neurologic findings (3rd or 6th cranial nerve palsies). Care should be taken to determine whether the pain occurs before or after the onset of the vomiting. With acute surgical lesions (those caused by intestinal obstruction, acute appendicitis, acute cholecystitis), the pain usually occurs before or during the vomiting. If the vomiting occurred before the onset of pain, the clinician should suspect gastroenteritis or another nonspecific problem. The appearance of the vomited material is also important. Feculent or dark-green material suggests intestinal obstruction. Dark brown or frankly bloody material indicates gastritis, prolapse gastropathy, or peptic ulcer disease as the source of pain.
Diarrhea occurs commonly in intestinal diseases of viral, parasitic, or bacterial origin. The stool volume is large, and defecation is usually preceded by cramping pain that is alleviated by the passage of the diarrheal stool. Diarrhea may also occur in the presence of acute appendicitis or other pelvic infections (such as those resulting from pelvic inflammatory disease, tubo-ovarian abscess); in these cases, diarrhea is caused by inflammation and irritation of an area of colon adjacent to an inflammatory mass. The diarrhea in this instance is of small volume and is frequent. It is important to obtain an estimate of the volume and consistency of stool. Diarrhea may also occur in lesions that cause partial obstruction of the bowel, such as strictures, adhesions, and Hirschsprung disease. In this situation, the patient also has some degree of abdominal distention. Constipation alone can cause acute abdominal pain and may also indicate other gastrointestinal dysfunction. Some constipated children present with a picture very similar to that seen in acute appendicitis but have a large amount of stool filling the entire colon. It is therefore important to obtain a good history of not only bowel movement frequency but also consistency as well (see Chapter 16 ). The history and exam is sufficient to make the diagnosis of constipation, and imaging is usually not necessary. Once the diagnosis is made, appropriate treatment should start with a proper clean-out followed by maintenance therapy. The clinician should not be fooled by the symptom of tenesmus, where the patient has a feeling of constantly needing to pass stools despite having an empty colon. Tenesmus can be seen in the setting of proctocolitis or inflammatory bowel disease and is often misinterpreted by the patient as constipation.
Associated symptoms.
The presence of headache, sore throat, and other generalized aches and pains moves the examiner away from a diagnosis of an acute problem warranting surgery and strongly suggests a viral flu-like illness. Asking the child to point to the area of worst pain sometimes results in the child pointing to the head or throat. The examiner must be careful to remember the whole child and not to focus on the abdomen just because that is the area of the presenting complaint. Many systemic diseases directly or indirectly produce abdominal pain and must be considered in the differential diagnosis ( Table 10.6 ).
| Metabolic, Hematologic |
| Acute porphyria |
| Familial Mediterranean fever |
| Hereditary angioedema |
| Sickle cell crisis |
| Leukemia |
| Acute hemolytic states |
| Diabetic ketoacidosis |
| Hemolytic uremic syndrome |
| Addison disease |
| Uremia |
| Electrolyte disturbances |
| Hyperparathyroidism-hypercalcemia (urolithiasis, pancreatitis) |
| Hypertriglyceridemia (pancreatitis) |
| Fabry disease |
| Musculoskeletal |
| Arthritis/diskitis |
| Osteomyelitis |
| Thoracic nerve root dysfunction |
| Trauma/child abuse |
| Hernia |
| Psoas abscess or hemorrhage |
| Neurologic |
| Abdominal epilepsy |
| Abdominal migraine |
| Brain tumor |
| Multiple sclerosis |
| Radiculopathy |
| Neuropathy |
| Herpes zoster |
| Dysautonomia (Riley-Day syndrome) |
| Drugs, Toxins |
| Heavy metal poisoning |
| Lead |
| Arsenic |
| Mercury |
| Mushroom ingestion |
| Narcotic withdrawal |
| Black widow spider bite |
| Infectious, Inflammatory |
| Acute rheumatic fever |
| Infectious mononucleosis |
| Rocky Mountain spotted fever |
| Measles |
| Mumps |
| Pneumonia (lower lobe) |
| Pericarditis |
| Pharyngitis |
| Epididymitis/orchitis |
| Henoch-Schönlein purpura |
| Hemolytic uremic syndrome |
| Systemic lupus erythematosus |
| Endocarditis |
| Anaphylaxis |
| Other |
| Pneumothorax |
| Pulmonary embolism |
| Functional |
| Aerophagia |
Family history and personal medical history.
Viral gastroenteritis, other viral syndromes, and food poisoning may affect the patient’s family or schoolmates; it is important to ask about other family members, classmates, or playmates who have recently had similar symptoms. Certain systemic and inherited diseases, such as sickle cell anemia, diabetes mellitus, celiac disease, spherocytosis, familial Mediterranean fever, and porphyria, are associated with episodes of abdominal pain. A strong family history of migraine headaches in a child with several previous episodes of intense abdominal pain that have resolved, who presents with a new “attack,” suggests the possibility of abdominal migraine. The family must be asked about familial diseases and any previous episodes of pain in the child. Previous intraabdominal operations may result in adhesions that can cause pain, intestinal obstruction, or both. A history of previous intraabdominal surgeries suggests the possibility of bowel obstruction. Some specific medical illnesses result in identifiable or predictable causes of abdominal pain ( Table 10.7 ).
| Historical Factor | Cause of Pain |
|---|---|
| Cystic fibrosis | Pancreatitis, diabetes mellitus, meconium ileus equivalent, appendicitis, intussusception, biliary or urinary stones |
| Sickle cell anemia | Vasoocclusive crisis, cholelithiasis, hepatitis, hemolytic crisis, renal infarction, splenic sequestration |
| Diabetes mellitus | Pancreatitis, gastric neuropathy |
| Cirrhosis, nephrotic syndrome | Primary bacterial peritonitis |
| SLE, other autoimmune disorders | Vasculitis, pancreatitis, serositis, infarction |
| Corticosteroids | Gastric ulceration, pancreatitis |
| NSAID | Ileal perforation, gastric ulceration, renal-papillary necrosis |
| HIV | Gastroenteritis, hepatitis, pancreatitis, esophagitis, lymphoma |
| Mononucleosis | Hepatitis, splenic rupture |
| Henoch-Schönlein purpura | Mucosal hemorrhage, intussusception |
| Hemolytic uremic syndrome | Colitis |
| Upper respiratory tract infection | Pneumonia, mesenteric adenitis |
| Pneumonia | Mesenteric adenitis |
| Prior surgery | Abscess, adhesions, obstruction, stricture, pancreatitis, ectopic pregnancy |
| Inborn errors of metabolism, hypertriglyceridemia, hypercalcemia | Pancreatitis |
| Drugs (valproic acid) | Pancreatitis |
Physical Examination
The physical examination begins when the clinician enters the room and observes the child’s activity and demeanor while obtaining the history. Does the child appear ill? Is the patient lethargic, rolling about in discomfort, alert but lying very still, or bouncing all over the room? Each of these activities conveys a message. The listless, lethargic child may be in shock, dehydrated, and very ill. The child who is crying out loudly and generally dominating the scene probably does not have a problem that warrants surgery and may have mild pain that is self-resolving. The child who seems only mildly ill but moves with great care, if at all, is assumed to have an inflammatory process until it is proven otherwise.
Physical examination techniques and findings are age dependent. Younger children may have difficulty cooperating because of fear or discomfort. Younger children may be more cooperative if kept on their parent’s lap. Older children should be asked to get onto the examination table with as little assistance as possible. If the child does this easily, the probability of an acute intraabdominal inflammatory process is quite low. Outer bulky clothing should be removed to allow good exposure of the abdomen without the child having to feel vulnerable.
The examination must be performed in a relaxed, friendly manner with attention fully focused on the child. An accurate examination depends on the child’s trust and cooperation. A conversation with the child about family, friends, pets, school, sports, music, or other specific interests of that child diverts attention (distraction) from the examination and increases cooperation. The examiner should never surprise the child and should never lie. The first surprise or untruth, such as the statement “This won’t hurt,” destroys any trust that has developed.
Low-grade fever (<38.3°C) is seen in early appendicitis but is also common in many other diseases. The absence of fever does not exclude the diagnosis of acute appendicitis or other problems necessitating surgical intervention. Tachycardia may reflect anxiety or may be caused by dehydration, shock, fever, or pain. Tachypnea suggests a metabolic acidosis (shock, diabetes mellitus, or toxic ingestion), an intrapulmonary process, sepsis, or fever. The vital signs must be viewed in context but may be the first clue to a serious illness.
Examination of the head, neck, chest, and extremities may precede the abdominal examination. In children too young to describe the location of the pain, a careful examination of the ears is important, but can be performed at the end of the examination. Streptococcal pharyngitis or mononucleosis is sometimes accompanied by severe abdominal pain. Affected children will present with fever, appear ill, and have tender cervical adenopathy and an obvious tonsillitis, pharyngitis, or both.
Decreased breath sounds and/or rales in a lower-lung lobe, especially on the right side, may indicate pneumonia. Children with lower lobe bacterial pneumonia present with severe abdominal pain, high fever, tachypnea, and, on occasion, vomiting. This presentation could mimic that of a child with peritonitis; however, the abdominal findings are not consistent with the diagnosis of an acute intraabdominal process, and examination of the lungs should demonstrate the pneumonia.
The abdominal examination should be performed systematically and with the child as comfortable as possible. Before the examiner actually touches the child’s abdomen, he or she should observe it, looking for distention, inguinal masses, peristaltic waves, and scars from old injuries or surgical incisions. Inguinal and femoral hernias are often overlooked but a common cause of abdominal pain. Next, the child should be asked to indicate with one finger the point of greatest pain. The point may be a vague circle in the area of the umbilicus, but if the child specifies a defined spot, the examiner should avoid that area until the remainder of the abdomen has been palpated.
Gentleness is essential to successful palpation of the abdomen. The examiner must warm both hands and the stethoscope before touching the patient. The stethoscope is an excellent tool for palpation of the abdomen. Auscultation of the chest can simply be extended to the abdomen, with the examiner assuring the child that the stethoscope did not hurt on the chest. The initial examination of the abdomen with the stethoscope should be just for listening, with no pressure exerted, so that no discomfort results.
Bowel sounds are usually nonspecific in most children with abdominal pain; however, in certain processes, they are helpful. High-pitched tinkling sounds or rushes are usually associated with an obstructive process. Bowel sounds in gastroenteritis are ordinarily very active and loud but may be normal. Acute appendicitis is accompanied by normal sounds in the early stages, but bowel sounds disappear with diffuse peritonitis.
Watching the child’s reaction to the auscultation may be a valuable clue to areas of true tenderness. As the examiner continues to listen over the entire anterior abdomen, the pressure on the head of the stethoscope increases until the examiner is, in fact, palpating with the stethoscope. This often is a much more reliable method of eliciting true tenderness and guarding than is the palpating hand.
Palpation is begun as far away from the area of pain identified by the child as possible. The examiner’s hand should be softly placed flat (in parallel) on the child’s abdomen. Directing fingers into the abdomen (perpendicular) as a method of palpation is unnecessary and often frightening. The clinician should watch the child’s face, not the abdomen, during the palpation. Some children are extremely stoic, and only the slightest grimace betrays the discomfort they are experiencing. Attention is paid during palpation to the presence of masses. The examiner should focus on finding the location of pain and the presence or absence of guarding or rebound tenderness. Guarding refers to the voluntary or involuntary (often referred to as rigidity) contraction of the abdominal musculature. Fear of pain, rather than actual pain elicited by palpation, is the most common cause for voluntary guarding while involuntary guarding results from reflexive spasms of the abdominal musculature in the setting of peritoneal irritation. A rigid or board-like abdomen is the result of involuntary guarding and cannot be overcome by distraction. Voluntary guarding usually starts before the palpation starts and can be overcome by asking the child to take deep breaths, flexing the knees and hips, or by using other distractions appropriate to the child’s age and temperament. When encountering tenderness, the examiner should palpate only deeply enough to elicit the complaint of pain and some guarding. There is no need to bring on unnecessary pain by deep palpation.
Rebound pain is an indicator of peritoneal irritation and is elicited during examination of the anterior abdominal wall. It occurs when an inflamed focus within the abdomen is compressed and the pressure is then quickly released, resulting in sudden and sometimes severe pain. The standard method to elicit rebound is to palpate deeply, then suddenly remove the palpating hand. Although this sign aids in the determination of the presence of an intraperitoneal inflammatory process, it is not necessary to cause extra discomfort or stress, particularly in younger children; it is not recommended. Peritoneal irritation can also be detected by maneuvers such as asking the child to jump, cough, or tapping the feet while observing for facial signs of discomfort.
Other areas of inflammation can be detected by maneuvers that move muscles adjacent to the inflammation. A positive Carnett test occurs when pain is unchanged or increased when the supine patient tenses the abdominal wall by lifting the head and shoulders off the examining table. Carnett sign is a sensitive tool to discriminate abdominal wall pain from visceral pain. The psoas sign occurs when elevation and extension of the leg against the pressure of the examiner’s hand causes pain. An inflammatory mass, such as an inflamed appendix, a psoas abscess, or a perinephric abscess, in contact with the psoas muscle is the cause of this pain. Likewise, the obturator sign is pain with flexion of the thigh at right angles to the trunk and external rotation of the same leg while the patient is in the supine position. This sign results from contact of an inflammatory mass with the obturator muscle ( Fig. 10.3 ).
