|
Chronic Abdominal Pain in Childhood: Diagnosis and Management
TABLE 1
Five Components of the Evaluation of Children with Abdominal Pain
History
• Location, intensity, character and duration of pain, time of day or night that pain occurs
• Appetite, diet, satiety, nausea, reflux, emesis
• Stool pattern, consistency, completeness of evacuation
• Review of systems: weight loss, growth or pubertal delay, fever, rash
• Medications and nutritional interventions
• Family history, travel
• Interference with school, play, peer relations and family dynamics
Physical examination
• Weight, height, growth velocity, pubertal stage, blood pressure
• Complete physical examination
• Objective abdominal findings: location, rebound, mass, psoas sign
• Liver, spleen and renal size, ascites, flank pain
• Perianal findings: rectal and pelvic examinations, stool testing for occult blood
Laboratory tests
• Complete blood count with differential, erythrocyte sedimentation rate
• Urinalysis and urine culture
• Laboratory tests individualized according to indication
--Stool testing and culture for polymorphonuclear leukocytes, parasites, Giardia antigen
--Serum chemistry profile, amylase level
--Pregnancy test, cultures for sexually transmitted diseases
--Breath hydrogen test: lactose, fructose
--Serologic testing for amebae, Helicobacter pylori
Imaging studies individualized according to indication
• Abdominal and pelvic sonography
• Upper gastrointestinal contrast study with small bowel testing, abdominal computed tomography
• Upper endoscopy, colonoscopy, laparoscopy
Empiric interventions
• Patient and parent education
• Symptom diary of pain, bowel pattern, diet and associated features, response to intervention
• Constipation investigated as a factor
• Dietary interventions, including adjusted fiber intake, reduced lactose intake, reduced juice intake
• Trial of peptic management
 |
Evaluating for Peptic Disease
|
 |
Specific Disease States
Recurrent Abdominal Pain Syndrome
Recurrent abdominal pain syndrome is a prepubertal functional pain with two distinct peaks of frequency. The first peak occurs between five and seven years of age, with equal frequency in boys and girls and in 5 to 8 percent of children. It is often attributed to the adjustment to parental separation when starting school. The second peak, with a prevalence approaching 25 percent, occurs between eight and 12 years of age and is far more prevalent in girls.6 The pain is vague (identified by the patient's whole hand at the umbilicus) and is unrelated to meals, activity or stool pattern. Patients are not awakened by the pain. An epigastric location is reported by 10 percent of patients. It is accompanied by autonomic features such as pallor, nausea, dizziness, headache and fatigue. The family history is often positive for functional bowel disease such as irritable bowel syndrome.7 The physical examination is striking for its normality, and the screening laboratory investigations are by definition normal.
The management of recurrent abdominal pain begins with the acknowledgement that the pain is real, that extensive investigations are not warranted and that the child must emphasize normality by remaining in school, continuing activities and resuming a normal diet. Psychologic evaluation and management will be necessary if the degree of incapacity persists. In older children and adolescents, a component of recurrent abdominal pain syndrome is seen in cases of depression or panic disorder with a learned symptomatic conversion reaction and associated weight loss. The performance of laboratory tests with negative results may increase the level of anxiety in older children.
True irritable bowel syndrome occurs infrequently before late adolescence.7 It is best characterized as an intestinal dysmotility with intervals of nuisance diarrhea or constipation. The pain is dull, crampy and located in the left lower quadrant or periumbilical region. As in cases of recurrent abdominal pain syndrome, autonomic features are common. Stress is implicated in the flare-up of symptoms, and a positive family history is common. Management includes dietary factors such as exclusion of contributory lactose intolerance and the addition of fiber to the diet, instruction in stress management techniques and, rarely, the use of antispasmotic medications.
Constipation
Constipation is a major cause of chronic abdominal pain in children from toddler age to the preteen years. Constipation is best defined as the failure to achieve complete evacuation of the lower colon rather than in terms of infrequency or firmness of stool. The etiology of constipation in most children is an interval of being "too busy" to evacuate completely, producing a dilated lower colon, erratic stool patterns and frequent encopresis. The parents usually do not understand what is causing the child's discomfort. The child avoids passing the hard stool. The diet is usually high in constipating foods (i.e., cheese, pasta, starches) and low in fiber. The process is usually quite advanced before the family physician is made aware of the problem. Aside from complicating encopresis and bleeding from rectal fissures, symptoms include crampy pain that occurs during large meals and varies greatly in intensity, reduction in appetite and distention of the abdomen (from stool and gas) that occurs in the evening.
The management goal is complete evacuation of the lower colon on a nearly daily basis. This is achieved by whatever means is necessary until muscle tone can be restored over two to six months.8 Initially, a high fiber intake may aggravate the process as a result of increasing bulk in the absence of contractile tone. Therefore, stool softeners such as lactulose (Duphalac) or mineral oil are used first. These are combined with "motivation to go," which can be achieved in some children with behavior-modification sticker charts but usually requires a stimulant medication such as magnesium hydroxide (Milk of Magnesia) or senna (Senokot). The child is encouraged to establish the "habit" of toilet use with the use of a daily calendar, rewards for attempting defecation and rewards for absence of encopresis. Dietary efforts begin with reducing intake of constipating foods and eventually including increased fiber. Initial management may require use of an enema or suppository, which is repeated only if failure to evacuate exceeds three days. Both softening and stimulant medications are initiated at dosages of one to three teaspoons daily and adjusted to the response of averaging two soft stools a day for six to eight weeks. At that point, most children can tolerate a transition to increased dietary fiber and habitual toilet use.
Peptic Disorders
The peptic disorders include reflux esophagitis, antral gastritis, gastric and duodenal ulcer, and H. pylori infection. Gastroesophageal reflux in children has recently been reviewed in another article.9
As we mentioned in the section on history, the signs and symptoms of peptic disease include early morning pain, early satiety, night arousal and a positive family history. The pain may be epigastric or periumbilical and is remarkably consistent in character. Occult bleeding is frequent with ulceration and less common in gastritis.10
The major risk factor for peptic ulcer disease in childhood is genetic predisposition: 50 percent of children with duodenal ulcer have a first-degree relative with peptic ulcer disease. The prevalence of duodenal ulcer is two to three times higher in boys than in girls. Gastric ulcer occurs substantially less often than duodenal ulcer, but the prevalence is equal in boys and girls. The approach to peptic management is summarized in Figure 1.
Stress ulcers account for more than 75 percent of peptic disease in infants and young children. Stress ulcers usually present with acute, relatively painless, dramatic upper gastrointestinal bleeding, features shared with gastric ulceration resulting from use of nonsteroidal anti-inflammatory drugs (NSAIDs).10 Zollinger-Ellison syndrome with a gastrin-producing tumor is very rare in children; the diagnosis is pursued only in children with multiple ulcers. Acute bleeding is common in children with chronic renal failure, sickle cell disease, cystic fibrosis and cirrhosis.
Antral gastritis is a common peptic presentation in children. Children present with chronic epigastric pain, early satiety with nausea, modest weight loss and a low frequency of family history of peptic disease. Gastric emptying is impaired, and reflux symptoms may be prominent. Results of the stool test for occult blood are usually negative. Radiographic studies are either normal or demonstrate pylorospasm. Many children with antral gastritis have an acute onset of gastritis, often in the context of a viral-like illness.
Endoscopic investigation is generally indicated in the context of active, persistent or recurrent bleeding, with significant morbidity from weight loss, anorexia or chest pain, or for clarification of abnormal findings on radiographic studies. Children with suspected but uncomplicated peptic disease are usually treated with H2 blockers, with endoscopy deferred for pain that persists for more than four weeks, recurrent disease, suspected H. pylori or exclusion of eosinophilic gastritis or enteropathy.4
The medical management of peptic disease is summarized in Table 2. Sucralfate (Carafate), an aluminum sucrose gel, is particularly effective in the treatment of medication-induced gastritis.
TABLE 2
Management of Childhood Peptic Disease
--------------------------------------------------------------------------------
Drug
--------------------------------------------------------------------------------
Availability
--------------------------------------------------------------------------------
Dosage
--------------------------------------------------------------------------------
H2-receptor blockers
Cimetidine (Tagamet) 300 mg per 5 mL, 200-, 300-, 400-, 800-mg tablets 20 to 40 mg per kg per day, in divided doses every 6 hours
Ranitidine (Zantac) 75 mg per 5 mL, 150-, 300-mg tablets 4 to 8 mg per kg per day, in divided doses every 8 to 12 hours
Nizatidine (Axid) 150-, 300-mg capsules* 4 to 8 mg per kg per day, in divided doses, every 12 hours
Famotidine (Pepcid) 40 mg per 5 mL, 20-, 40-mg tablets 1 to 2 mg per kg per day, once or twice daily, maximum dosage: 40 mg per day
Proton pump inhibitors
Omeprazole (Prilosec) 10-, 20-mg capsules* 0.5 to 3 mg per kg per day, in divided doses every 12 hours
Lansoprazole (Prevacid) 15-, 30-mg capsules* 0.3 to 1.5 mg per kg per day, in divided doses every 12 hours
--------------------------------------------------------------------------------
*--Since no liquid formulations are available at this time, the capsules are opened, and the contents are mixed in an acidic vehicle such as apple juice, applesauce or yogurt.
NOTE: Medication is taken on the schedules given for six to eight weeks, then once daily for four weeks. Diet--Patients should be instructed to eat multiple modest meals and avoid overeating, to minimize caffeine intake and to avoid eating foods that appear to cause pain. Heartburn--To reduce heartburn, patients can be instructed to take an antacid such as Mylanta, Maalox or Milk of Magnesia, in a dosage of 0.5 mL per kg per dose 1 hour after meals and at bedtime, or a low-dose, over-the-counter histamine H2-blocker such as Tagamet, Pepcid, Zantac or Axid, at one half the usual prescription dosage. Mucosal protection--To enhance mucosal protection, patients can take sucralfate (Carafate) and/or bismuth subsalicylate (Pepto-Bismol) or ranitidine bismuth citrate (Tritec).
Periodic Syndrome or Cyclic Vomiting/Abdominal Migraine
Gee's original description of a syndrome with "fits of vomiting ... with disease-free intervals" in 1882 has held up well in the clinical definition of periodic syndrome, which is now called cyclic vomiting syndrome or abdominal migraine of childhood.17 Children present with episodic nausea, abdominal pain and usually significant emesis, typically beginning during the night or early morning hours and lasting from six to 48 hours, with intervening intervals of weeks to months with no symptoms or findings at all. The majority of children have a family history of migraine and may have other autonomic features such as pallor, explosive diarrhea, lethargy and tachycardia. Of note, headache is rare in children with cyclic vomiting syndrome, although it may evolve into more classic migraine in adolescence. Treatment is usually early intervention with antiemetics or migraine medications.
Inflammatory Bowel Disease
Abdominal pain is frequently reported in children with ulcerative colitis and Crohn's disease. The pain, which typically occurs in the lower abdomen, is cramping in nature and increases after meals or activity. The pain is reduced by eating smaller meals, which contributes to the anorexia and growth impairment that occur in children with inflammatory bowel disease. The diagnosis is relatively easy when the child has bloody diarrhea, the need to defecate during the night, perianal disease or an ileal mass on abdominal examination. More subtle features include delayed puberty, anemia that is unresponsive to iron therapy, recurring oral aphthous ulcers, chronic liver disease, or large joint synovitis or arthritis.18 The diagnosis is established by small bowel barium contrast x-ray and colonoscopy with biopsies. The management of inflammatory bowel disease in childhood is summarized in Table 3.
TABLE 3
Management of Inflammatory Bowel Disease in Children
--------------------------------------------------------------------------------
Supportive care for child and family
• Provide educational materials for child, parents, teachers
• Give information about support groups for children and parents
• Offer psychologic counseling for depression, denial and noncompliance
• Expect reactive self-manipulation of medication dosages and diet
Nutritional support
• Correct deficits of macronutrients and micronutrients
• Deliver 125 percent of calories for height age
• Recommend routine multivitamin and mineral supplements
• Discourage "quick cure" diets and fads
• Administer intravenous nutrition to patients with intractable Crohn's disease or fistula and before surgery
• Consider consumption of an elemental diet as primary therapy in patients with small bowel Crohn's disease
Anti-inflammatory/immunomodulatory medication
• Prednisone (oral, intravenous, topical enema)
--Valuable in all forms, but use must be balanced against side effects
--Useful as chronic alternate-day therapy in adolescent patients with Crohn's disease
• Salicylates: sulfasalazine (Azulfidine), mesalamine (Asacol, Pentasa, Rowasa), aminosalycylic acid (Paser Granules)
--Valuable in treating mild to moderate colitis
• Metronidazole (Flagyl; possibly ciprofloxacin [Cipro] as well in older children)
--Useful in treating Crohn's perianal or fistula disease
--Also useful in treatment of complicating Clostridium dificile infection
• Azathioprine (Imuran)/6-mercaptopurine (Purinethol)
--Valuable in treating moderate to severe Crohn's colitis, ulcerative colitis
• Fish oil (EPA, Sea Omega, Promega)
--Valuable in treating mild ulcerative colitis
Surgical resection
• Total colectomy is curative in cases of ulcerative colitis
• Useful in cases of toxic megacolon, and dysplasia in patients with ulcerative colitis
• Useful in treating Crohn's obstruction, fistula, abscess
• Useful when medical therapy fails or side effects of medication are intolerable
--------------------------------------------------------------------------------
Information from O'Gorman M, Lake AM. Chronic inflammatory bowel disease in childhood. Pediatr Rev 1993;14:475-80.
Differential Diagnosis by Source
Four major sources can potentially contribute to the presentation of abdominal pain. These are: intra-abdominal, extra-abdominal, metabolic, and neurogenic.
Intra-abdominal Pain
In this area, because the most likely sources will be either infection or obstruction of a hollow viscous, the pain will characteristically be visceral or somatic, but can also be referred. Peritoneal irritation or inflammation (peritonitis), obstruction of a hollow viscous, and vascular disorders are the more frequent causes for acute abdominal pain intra-abdominally [5,9].
Peritoneal inflammation (peritonitis) can be either primary or secondary, the latter being the more common of the two. Primary peritonitis is most likely to be caused by bacteria such as E.Coli, Streptococcus, Pneumococcus, or Mycobacterium Tuberculi. Primary peritonitis is also called "spontaneous" peritonitis. Secondary peritonitis is most often caused by pelvic or abdominal trauma, and by such diseased organs as gallbladder, appendix, and pancreas. The bacteria found closely parallel those of the intestine [10]. The patient will complain of relatively sharp, constant pain (sometimes crampy) which may be well localized, with location dependant on the source of the infection or parietal irritation. In the instance of appendicitis, the pain may start in the mid-epigastric area then localize to the RLQ. With peritonitis the pain generally stays where it starts.
Obstruction of a hollow viscus will usually include either the ureter, biliary tree, or intestine, and is one of the most common sources of acute abdominal pain [11,7]. Source of the obstruction can include calculi, adhesions, neoplasm, volvulus, or intussusception [12]. In any patient presenting with abdominal pain with a history of abdominal surgery, intestinal obstruction secondary to adhesions must be considered and ruled out. In the obstructed patient who is heme positive rectally, neoplasm must be ruled out!
Because of the increase in laparoscopic procedures, for both diagnostic and therapeutic reasons, be sure to check the umbilicus or abdominal wall for easily missed, small, well-healed elliptical or annular scars (as a clue to past abdominal surgery). This relatively well-tolerated procedure can be done as a "mini" laparoscopy in outpatient surgical centers and well-equipped emergency departments, so might have been forgotten by the patient. Laparoscopy can significantly assist in diagnosing the patient with equivocal abdominal pain, and can change the diagnosis in greater than 20% of cases, depending on the population involved. The treatment may change in greater than 10% of the patients so examined [1315].
Vascular disorders usually will involve either a ruptured or rapidly dissecting abdominal aortic aneurysm (AAA), an infarcted bowel, or pelvic deep vein thrombosis (DVT). Pelvic DVT may be diagnosed only after the clot moves (usually to the lung). A history of immobilization, injury, recent fracture (long bones), or coagulopathy (cancer, oral contraceptive use, pregnancy, some types of bacteremia) should raise a red flag regarding DVT [9].
If the patient presents with abdominal pain then progresses to toxic symptoms (fever, leukocytosis, possibly mentation changes) consider bowel infarction or infection. Bowel infarction differs from an AAA presentation in that it presents as an increasingly toxic appearance versus the shock symptoms of a rapidly dissecting or ruptured AAA (severe pain, severe hypotension, tachycardia, decreasing level of consciousness). Dissecting AAA pain is often described as "tearing" in nature, accompanied by mid to lower back pain, whereas the pain of bowel infarction is "severe" and often uncontrollable with medication and may be in conjunction with hematemesis and/or melena [10]. The pain of infection compared to these other two entities is more constant and not so severe, although it can escalate as time goes by.
Extra-abdominal Pain
Three main sources of extra-abdominal pain include the thorax, the abdominal wall, and the pelvis. The thorax can present a sometimes confusing picture as symptoms may also be referred from either the pelvis or the abdomen. Keep an eye toward cardiac origin when thoracic symptoms are present. In the thoracic area, the major entities are pulmonary embolism (PE), pneumonia, pneumothorax, esophageal disease, and cardiac [10]. A chest radiograph will help with diagnosis of the first three entities mentioned. Both viral and bacterial pneumonia, as well as PE, can refer pain to the abdomen as well as to the shoulder (also seen with some diaphragmatic or pelvic pathology).
Abdominal wall pain will most commonly be related to either infection of the soft tissue, or to trauma. Light palpation is the most valuable technique to help with differentiating abdominal wall lesions from deeper abdominal structure involvement. Infection can sometimes present obscurely, as in the case of a urachal tract/canal infection. This entity, an infection of the canal which in the fetus extends from the bladder to the umbilicus (normally obliterated after birth), can present with the appearance of an omphalitis (an infection or inflammation of the umbilicus). A urachal tract/canal infection is potentially quite serious. An omphalitis appearance, abdominal pain, and concomitant urinary tract infection should focus the diagnosis. Overt infection, as in the case of an obvious abscess, is more easily identified. The depth of the abscess should always be of concern, especially when close to the umbilicus, where the abdominal wall is thinner.
Trauma can include mild strains, contusions, hematomas, and penetrating wounds. The penetrating wound may be small in nature and not easily seen, particularly if not bleeding at the abdomen's surface. While abdominal wall injury may give a "mild" appearance, it can be associated with underlying organ tears, rupture, or contusions. In abdominal trauma, the spleen is the most commonly injured organ, especially in blunt abdominal trauma; the onset of symptoms can be immediate or delayed. Include possible splenic rupture in the differential diagnosis in the patient with LUQ abdominal pain and anemia of recent onset [6].
Any person with a possible blow to the abdomen should have orthostatic blood pressures taken, careful palpation of the abdomen, and consider imaging the abdomen; serial hemoglobin and hematocrits should be done if necessary. Nontraumatic splenic rupture is often associated with acute infectious mononucleosis. Therefore, if nontraumatic splenic injury is being considered, the history should include any recent sore throat and fatigue, and the exam should check for cervical lymphadenopathy.
In the female pelvis, high acuity sources of abdominal pain include ectopic pregnancy, ovarian torsion, spontaneous or threatened abortion, and ovarian cyst rupture [9]. Lower acuity entities include salpingitis (PID), tubo-ovarian abscess (TOA), and hydrosalpinx. TOA and PID can smolder and be more insidious in onset and can present with low-level pain and intermittent low-grade fever over days to weeks (related to the slow buildup of "irritating" products produced by the infection) [7]. In TOA and PID, the erythrocyte sedimentation rate (ESR) is often elevated (above 15) while the CBC may or may not show an increased white blood cell count with a neutrophilic shift.
In women with a recent history of PID, even though treated, there can be up to a 15% or greater incidence of subsequent TOA, and up to 20% or so recurrence of PID; these initial incidence and recurrence rates vary according to the population involved. A woman with a history of PID has an up to 8% increased risk for ectopic pregnancy. The risk of ectopic pregnancy and fertility problems increases with subsequent pelvic infections [9]. Unfortunately, women who have had pelvic infections also have a greater chance for adhesions and bowel obstruction. Adhesion-related pain may be mistaken for endometriosis and mild pain is sometimes attributed to Mittleschmerz.
Ectopic pregnancy can cause unilateral or generalized abdominal pain with or without vaginal bleeding; a pelvic hematoma may be present [2]. Ectopic pregnancy can present with syncope alone, however abdominal pain (usually unilateral) usually will become noticeable relatively quickly (see Table 2) [9]. Syncope can of course be due to many other things, including pulmonary hypertension, cardiac arrhythmias, drugs (variety), transient ischemic attacks (TIA), carotid sinus syndrome, psychogenic causes, and postural hypotension [16]. However, the simple question "have you ever had these symptoms before," may bring out a history of a prior ectopic pregnancy or PID, or other pelvic or abdominal pathology.
In any woman of childbearing age presenting with referred or lower abdominal pain, do a pregnancy test (urine HCG) and consider a serum HCG. If either test is positive do a quantitative HCG and consider doing serial quantitative HCGs. Also, draw a hemoglobin and hematocrit for baseline. The patient should be assessed for vaginal bleeding (obtain a "pad" count if possible), checked for orthostatic hypotension, and receive an intravenous line (for volume support, if necessary).
Sometimes a palpable adnexal mass (the tubal pregnancy) may be noted on examination [2], and cervical motion tenderness (CMT) will be noted. This is opposed to the non-tender cervix observed with an intrauterine pregnancy; remember however that the woman with an intrauterine pregnancy may have a concurrent PID. A menstrual history should be taken, including at least the last two normal menses. Be sure to obtain the "first day" of the last normal menses. Inquire as to a history of ectopic pregnancy, pelvic infection, and abortion (threatened, spontaneous, or therapeutic). If the patient is knowingly gravid, obtain the estimated date of delivery; if this is not known, use the first day of the last normal menses as the reference point. Do not use the patient's estimation of the number of weeks or months pregnant (potentially less accurate).
Metabolic
Metabolic disorders include diabetic ketoacidosis (DKA), porphyria, insect trauma, systemic lupus erythematosus (SLE), and sickle cell disease [7,10]. Alcoholic ketoacidosis and coma secondary to hypoglycemia should be considered in the differential. DKA is an emergent condition caused by decreased insulin and a soaring blood glucose, with the patient ketotic and metabolically unstable. This entity can be brought on by a variety of problems including infection, poor diabetic control (may be either noncompliance in a new diabetic, or a "brittle" diabetic), myocardial infarction (MI), or of no easily elicitable cause. Steroid use can also trigger acute changes. Presentation can range from weakness, to abdominal pain with nausea and vomiting, to coma. There may be the telltale "fruity breath," signs of dehydration (patient feels dry, or thirsty and is orthostatically unstable), and tachycardia.
The laboratory studies in the patient with DKA may show an elevated potassium due to acidosis, otherwise there is electrolyte depletion ( i.e. serum ketones, urine ketosis, and glycosuria). Unless the patient has preexisting cardiac disease with ECG changes the rhythm will most likely be sinus tachycardia. Because acute MI or congestive heart failure may be involved, these entities must be taken into account before starting the IV fluid bolusing that helps clear the sugar and rehydrate the patient (i.e. typically 1L/Hr, unless CHF or acute MI is present) [17].
Porphyria can present with abdominal pain, muscle spasm, nausea, vomiting, and peripheral neuritis. The spleen may be enlarged and the urine may contain various porphyrins; a history of photosensitivity may also be elicited. Patients with porphyria should not take alcohol, barbiturates, chloroquine, or sulfonamides as these can precipitate an attack. Because of the many types of porphyrins, and their ubiquitous relationship to bodily functions, multiple organs can potentially be involved in an acute attack. However, the three main areas of involvement in porphyria are usually neurologic, gastrointestinal, and psychologic [9].
Of the insect trauma most associated with abdominal pain, the black-widow spider, the brown recluse spider, and the scorpion are most often discussed. However, bees, wasps, ants, and ticks, among others, may also trigger the same symptoms. There may be major reactions such as cyanosis, stridor, dyspnea, and shock (necessitating admission for airway management), or milder but worrisome symptoms such as wheezing, pruritis, flushing, and nausea [9]. The only indication of insect trauma may be a small puncture site with localized erythema. If a patient wakes up with an itching, erythematous tiny puncture site, with abdominal pain subsequent to that, suspect a spider bite as the source. Mild symptoms must still be treated with an eye toward possible progression to a more serious reaction. There may be initial erythema at the sting/bite site, which can progress to blisters and ulceration, depending on the insect.
Treatment depends on level of involvement and airway compromise, plus whether or not infection or skin compromise is present. Insect bite treatment may include epinephrine and/or antihistamines, incision and drainage of the abscess site (I & D), antibiotics, and admission for airway control. In the case of necrotizing reactions, later skin grafting may be needed. The tetanus immunization status of the patient should be determined, and a Diphtheria/Tetanus (Td) booster given if necessary. Outpatient management may range from antihistamines (intra-muscular [IM] or intravenous [IV], or PO); steroids (IM or IV, or PO); the PO steroid dose can be either a "pulse" (same amount each day for short period, usually 5 days) or a "taper" ( decreasing dose every 2 to 3 days for variable number of days); and antibiotic(s) (if there is any concern regarding infection). If infection is present then give a full course of antibiotics, typically 10 days; if providing prophylaxis with an antibiotic, then a shorter course may be appropriate, typically 3 to 5 days (assuming close follow-up). Secondary infection must be considered if infected 48 to 72 hours after the initial skin trauma.
Systemic lupus erythematosus (SLE) may be insidious in onset. When presenting in an acute fashion, SLE may appear somewhat like porphyria (i.e splenomegaly, with concomitant abdominal pain, peripheral neuropathies, and photosensitivity may be present). SLE may be confusing and not the first diagnosis to come to mind when a patient presents. The diagnosis is often one of elimination [9]. Because the patient may present only with fever, arthralgias, or perhaps a rash (not as common as the first two signs/symptoms), arthritis, dermatitis, and fever of unknown origin may be considered. Among the blood tests used to help with the diagnosis are the ESR, anti-nuclear antibody (ANA), and anti-DNA [18]. A urinalysis may show hematuria, and the patient may have renal involvement.
Sickle cell disease, when the patient is in crisis, may present with abdominal and/or leg pain, fever, headache, or epistaxis. Typically the patient or family member will quickly identify the patient as having the disease. Although the practitioner may feel the need to quickly help the patient with pain relief and correction of dehydration, infection must be ruled out with appropriate cultures and blood tests, as well as performing a thorough physical examination [17]. If it appears the patient is possibly infected or in more than mild crisis, then admission to the hospital for definitive treatment and close observation is usually advised. Any African American presenting with leg or abdominal pain should be considerately questioned regarding sickle cell disease (to determine whether they have the trait or disease).
Neurogenic
This category consists primarily of abdominal pain of either spinal disc disease or viral disease (Varicella Zoster) etiology [12]. Degenerative disc disease from osteoarthritis (with osteophyte formation and disc-space narrowing, depending on the dermatome), may cause pain around the abdomen. The postherpetic neuritis and acute pain associated with the active infection of Varicella Zoster can also cause pain around the abdomen. The Zoster lesions are usually midline to midline, unilaterally, with the pain following the same pattern as the lesions (if present); if no lesions are present (e.g. the prodrome, or postherpetic neuritis) then the patient may view the pain as more diffuse and less well defined even though it follows certain dermatomes.
Life-Threatening Causes of Abdominal Pain
Abdominal aortic aneurysm
The AAA lesion can be static or mobile, in that it may arrest at a certain size, or insidiously enlarge until decompensating at a certain point. A chest radiograph will often detect such a lesion especially if there is any calcification of the lesion. However, computed tomography or an abdominal ultrasound examination are more accurate ways to determine the lesion size.
AAA's are usually asymptomatic up to about 4 cm in diameter; however, if they continue to enlarge they can then cause a rapid decompensation of the affected area by either rupture or dissection. The pain is described as tearing, and severe back pain (mid to lower) may be the only symptom; the pain can be confused with severe back muscle spasm. Pain of this origin may also radiate to the genitals, sacrum, or flank, so can also be confused with severe ureteral colic. However, the patient, at some point, will rapidly decompensate, showing fluctuating blood pressures. The patient will be significantly hypertensive at first with the pressures later dropping out to perhaps only a palpable and quite low systolic pressure. The pain will be uncontrollable and the patient very agitated and anxious at first, then will become "shocky" quickly. A pulsatile abdominal mass between the epigastric notch and the umbilicus will often be felt. The "classic" sign of lower extremity ischemia with "purple toes" may be noted. This sign is usually only present when the patient is at the end-stage of decompensation. The primary concern is volume (IV) and blood pressure support plus supplemental oxygen (during rapid transport to imaging and the operating theater). If possible, blood type, crossmatch, and screen should be done during referral/transport to surgical care [1].
Ruptured ectopic pregnancy
Ectopic pregnancy is seen in up to 1% of all pregnancies (increased in women with PID, previous ectopics, TAB, or abdominal surgery). Look for late or missed menses, breast tenderness, unexplained weight gain, nausea, and, of course, rapid onset of usually unilateral lower quadrant abdominal pain [9]. Syncope might be the only presenting complaint; vaginal spotting or an overt vaginal bleed may be noted. The practitioner should do a pregnancy test and obtain timely surgical/OB GYN consultation. If ectopic pregnancy is suspected (i.e. a pregnant woman with abdominal pain, vaginal bleeding, with an "acute" appearance), volume support (IV) and transport to the appropriate hospital is most prudent. Do not waste time obtaining studies other than drawing a H & H and quantitative HCG for baseline, and transport under close observation [1].
Splenic rupture
The spleen is the most commonly injured organ in (blunt) abdominal trauma; splenic rupture may be associated with other injuries also. As with an AAA, the patient may be initially hypertensive and tachycardic, but will relatively quickly become shocky, hypotensive, and develop syncope. There may be (left) "shoulder strap" pain, plus left upper quadrant abdominal pain. In a teenager without trauma, be sure to think of possible mononucleosis. In splenic rupture, intravenous volume and blood pressure support, oxygen as needed, and rapid transport for definitive imaging and/or surgery are indicated. Consult with a surgeon as soon as possible and transport under close observation.
Myocardial infarction
Men over age 40 and women over age 50 are suspect when presenting with epigastric pain. Consider obtaining an electrocardiogram (ECG) in this age-group (although this may not show diagnostic changes). When cardiac origin is suspected, don't let the patient minimize the symptoms or refuse the ECG (remember "denial"). While myocardial infarctions "classically" present with anterior chest pressure or pain, the patient may also have a gastritis/heartburn sensation, coupled with nausea, and diaphoresis. Other, more vague symptoms ("I just don't feel right"), may be the only indication that further investigation is needed.
Take the time to get a good history, review the chart, and discuss with a cardiology specialist if there are any concerns regarding the patient's symptoms, status, or electrocardiogram. If the patient's abdominal pain is the main finding and the rest of the physical exam is not alarming you may wish to try a "GI cocktail" (a combination of liquid antacid, viscous Xylocaine and [optional] liquid Donnatal) to see if it changes the epigastric symptoms. If the pain is relieved, the patient is stable, and the ECG is normal, myocardial infarction may be less suspected. However, if there are concerns regarding patient risk factors (smoking, overweight, elevated cholesterol, hypertension, angina) then the need for further evaluation (stress test) can be discussed with a cardiology specialist. If the patient presents acutely (i.e. with pain, with ECG changes, with an elevated creatine kinase (CK), with positive CK-MB (heart isoenzyme) fraction [18], or with unstable vital signs) or, if the pain is relieved with nitroglycerin (Ntg), then she or he should be monitored, with IV access, supplemental oxygen, and transported quickly via critical care transport; utilizing protocols for thrombolytic therapy if warranted. Use Ntg to relieve the pain only if the patient is not hypotensive. Remember that Ntg can relieve esophageal spasm, so if it is given for epigastric pain before the GI cocktail and the patient experiences pain relief, the results may be misleading.
Bowel obstruction
Bowel obstruction can present differently depending whether the patient is early or late in the process (i.e. partial vs. complete obstruction). Vomiting may occur upon obstruction, when there is a decreased ability to pass gas, increased cramping, and subsequent distention of the abdomen. Upon digital rectal examination, the rectal vault may be full or empty. The bowel sounds may be diminished or with peristaltic "rushes" or high-pitched tinkling. On the radiograph, there are usually large dilated loops of bowel (usually small bowel), with or without air-fluid levels [11]. Adhesions are the most frequent cause, so always check the surgical history! Neoplasm is another common reason for obstruction.
Treatment, after diagnosis, is to keep the patient NPO, obtain IV access and correct any volume and electrolyte depletion. Obtain primary care/surgical consultation before giving any pain medication and transport the patient under observation.
Summary
Because proper evaluation of the abdomen can be labor and time-intensive, with significant patient discomfort involved, it is prudent that the provider have a well-organized and systematic approach. The use of recording devices (a chart to record the H&P and any studies done, plus disposition) for inclusion in the patient record, and a standardized approach will help minimize diagnostic digression and increase accuracy of diagnosis [1] Utilize available resources in a timely manner, with appropriate referral for definitive care to ensure an optimal outcome. Be sure to include consideration of physical and other factors which might affect the patient's presentation
Many abdominal pain presentations will require physician/specialist consultation. It should go without saying that before making the consultation call, the primary care provider must know the patient's history, progression of symptoms, and result of studies already performed. When discussing studies, if possible compare data with last tests (as with H&H, radiographs etc.) and have a working diagnosis. Suggestions for further work-up (studies, admission, surgery etc.) also can help move the patient's care forward.
details are in my surgical lectures gi
some part of these chart are not just for pediatric disease but also adult
Table 6. Consulting Tips
Know the chronology of the pain
Know the pain rating (1-10/10) and the progression characteristics of the pain
Know the pertinent patient history (always obtain patient's chart or pertinent faxed information if possible); include ETOH and NSAID use if applicable
Know and be able to accurately describe your physical findings and current patient status; include studies already done as well as those you are asking about performing
Be clear as to (a) where and when further patient work-up will be done, (b) how patient will be transported, and (c) who will be seeing or admitting the patient, and what instructions are there for the patient "at this time"
Keep the patient NPO from entry into the system to time of disposition, unless instructed otherwise by the attending or sub-specialist
Table 8. Complicating Factors in Assessment of Acute Abdominal Pain
Young age--inaccurate body perception, inaccurate historian, must rely on caretaker and the examination for data, and must consider psychosocial aspects re: child care/abuse
Immunosuppression--HIV infection/AIDS, corticosteroid use, immunosuppressive drugs
Pregnancy--abdomen distorted from the normal, organ location may change, must factor in symptoms of pregnancy
Pain medication--changes perception of pain, may cause constipation
Obesity--distorts from a flat abdomen, makes organ palpation or pelvic exam difficult
Old age--atypical presentation of pain [location, severity, may not mount fever]
A
Diffuse Pain
Peritonitis
Acute Pancreatitis
Sickle Cell Crisis
Early Appendicitis
Mesenteric Thrombosis
Gastroenteritis
Dissecting or Rupturing Aneurysm
Intestinal Obstruction
Diabetes Mellitus
|
B
Right Upper Quadrant Pain
Acute Cholecystitis and Biliary Colic
Acute Hepatitis
Hepatic Abscess
Hepatomegaly Due to Congestive Failure
Perforated Duodenal Ulcer
Acute Pancreatitis (bilateral pain)
Retrocecal Appendicitis
Herpes Zoster
Myocardial Ischemia
Right Lower Lobe Pneumonia
|
C
Right Lower Quadrant Pain
Appendicitis
Regional Enteritis
Meckel's Diverticulitis
Cecal Diverticulitis
Leaking Aneurysm
Abdominal Wall Hematoma
Ruptured Ectopic Pregnancy
Twisted Ovarian Cyst
PID
Mittelschmerz
Endometriosis
Ureteral Calculi
Seminal Vesiculitis
Psoas Abscess
Mesenteric Adenitis
Incarcerated, Strangulated Groin Hernia
D
Left Upper Quadrant Pain
Gastritis
Acute Pancreatitis
Splenic Enlargement, Rupture, Infarction,
Aneurysm
Myocardial Ischemia
Left Lower Lobe Pneumonia
E
Left Lower Quadrant Pain
Sigmoid Diverticulitis
Leaking Aneurysm
Ruptured Ectopic Pregnancy
Mittelschmerz
Twisted Ovarian Cyst
PID
Endometriosis
Ureteral Calculi
Seminal Vesiculitis
Psoas Abscess
Incarcerated, Strangulated Groin Hernia
Regional Enteritis
Types of Abdominal Pain
Visceral:
|
Crampy, colicky
May be ill-defined Can be associated with:
Appendicitis
Cholecystitis
Bowel obstruction
Renal colic
|
Somatic::
|
Chemical or bacterial source Sharp and more constant than visceral pain Usually more localized to the area of pathology Can be associated with:
Varicella Zoster (Viral)
Peritonitis
Late appendicitis
|
Referred:
|
Distant to the affected organ(s) Can be associated with:
Cardiac: may be high or low, from arm or neck, down to ant. chest or the epigastric region
Renal colic: may refer to the thigh, genitalia, LQ's of the abdomen, or to the costo-vertebral angles
Inguinal hernia: may refer pain to the genitalia or to the LQ's of the abdomen (affected side)
Abdominal Aortic Aneurysm: refers to the mid to lower back
|
 Topographical Areas of the Abdomen
 Oval and flattened both anteriorly and posteriorly
 Contains both fixed and relatively mobile organs
 Comprising the abdomen proper and the pelvis
 Can be divided into either regions (9) or quadrants (4)
 Contains organs which may overlap both regions or quadrants
 The area just above the symphsis pubis is referred to as the supra-pubic area
 The lateral portions are referred to as flanks
 The inguinal or groin area lies just above the inguinal ligament in a groove between the anterior abdomen and the thigh
 The costo-vertebral angle (CVA) is the area formed (posteriorly) by the twelfth rib and the Psoas muscle
 The umbilicus lies approximately in the center of the abdomen, at the level of the 3rd to 4th lumbar vertebrae
 McBurney's point lies between the umbilicus and the anterior superior iliac crest (ASIC) at approximately 4 to 5 cm above and medial to the ASIC
|
Acute Abdominal Pain by Rapidity of Onset
Gastrointestinal
|
 |
Extra-gastrointestinal
|
Perforated ulcer
Ruptured abscess or hematoma
Intestinal infarct
|
Abrupt onset
(instantaneous)
|
Ruptured or dissecting aneurysm
Ruptured ectopic pregnancy
Pneumothorax
Myocardial infarction
Pulmonary infarct
|
Perforated viscus
Strangulated viscus
Volvulus
Pancreatitis
Biliary colic
Mesenteric infarct
Diverticulitis
Penetrating peptic ulcer
High intestinal obstruction
Appendicitis (gradual onset more common)
|
Rapid onset
(minutes)
|
Ureteral colic
Renal colic
Ectopic pregnancy
|
Appendicitis
Strangulated hernia
Low small intestinal obstruction
Cholecystitis
Pancreatitis
Gastritis
Peptic ulcer
Colonic diverticulitis
Meckel's diverticulitis
Crohn's disease
Ulcerative colitis
Mesenteric lymphadenitis
Abscess
Intestinal infarct
Mesenteric cyst
|
Gradual onset
(hours)
|
Cystitis
Pyelitis
Salpingitis
Prostatitis
Threatened abortion
Urinary retention
Pneumonitis
|
Characteristics and Management of the Life-threatening
Causes of Acute Abdominal Pain
Known Source
|
Type of Pain
|
Physical Changes
|
Initial Action
|
Known Source
|
Type of Pain
|
Physical Changes
|
Initial Action
|
Abdominal aortic aneurysm
|
Referred
Mid to lower back or mid to upper abdominal pain
|
Pulsatile mid to upper abd. mass. with A-P & lateral movement
Hyper then hypotensive, then shocky
Lower extremity ischemia ("blue toes")
|
O2, high flow
Rapid intravenous volume & blood pressure support
NPO
Rapid transport to imaging with close surgical support
Admit
Type & Xmatch
|
Bowel obstruction
|
Visceral
Crampy w/partial obstruction and constant with complete
Diffuse, ill-defined
|
Inability to pass gas
Belly distended and tympanic
Abdominal X-ray shows large dilated loops of small or large bowel, w/ or w/o air-fluid levels
|
I.V. access/NPO
Rapid surgical consult regarding definitive care
Pain relief (discuss with surgeon)
Transport/Admit
Type & Xmatch
|
Ruptured spleen
|
Somatic
Instantaneous to rapid onset
LUQ or "shoulder strap" areas
Hx of abdominal trauma
|
Hyper then hypotensive, then shocky
May be snycopal
|
Rapid intravenous volume support
NPO
Rapid surgical consult
Transport/Admit
Type & Xmatch
|
Ruptured ectopic pregnancy
|
Somatic or referred
Uni or bilateral LQ in woman of child-
bearing age (do a pregnancy test)
|
May be syncopal Localized RLQ or LLQ abdominal pain
Hypotensive/shock
Possible vaginal bleeding
Check first day of last menses
|
I.V. access/NPO
Quantitative BHCG
Check w/ OB-GYN re: pain relief
Transport/Admit
Rh/Type & Xmatch
|
|