Abstract

A 6-year-old girl is brought to the emergency department because of acute abdominal pain of 18 hours’ duration. She has had two previous hospital admissions with the same clinical presentation. The pain resolved spontaneously in the past without any intervention.On examination, the child is afebrile, but appears anxious and pale. Her respiratory rate is 22 breaths/min, pulse rate is 94 beats/min, and blood pressure is 115/60 mm Hg. There is tenderness on palpation of the left upper and lower abdominal quadrants and the left flank. On deep palpation of the abdomen, a mass is identified on the left. Remaining physical findings are normal.Complete blood count, blood urea nitrogen, serum creatinine, electrolytes, amylase, and liver function tests yield normal results. Findings on urinalysis include a positive reaction to blood on dipstick and microscopy that reveals 1 to 2 white blood cells and 7 to 8 red blood cells per high-power field. Urine culture is sterile, and a radiograph of the abdomen does not reveal any abnormality. Additional imaging establishes the diagnosis.An 8-year-old boy undergoing maintenance therapy for acute T-cell lymphoblastic leukemia presents with a 2-day history of somnolence, slurred speech, and abnormal head movements. He receives methotrexate, prednisone, mercaptopurine, vincristine, dapsone for Pneumocystis carinii pneumonia prophylaxis, and acyclovir for viral retinitis. He has had no upper respiratory tract symptoms, diarrhea, vomiting, fever, trauma, ingestions, headache, rash, arthralgias, ill contacts, or recent travel.On physical examination, the boy is difficult to arouse but can be prompted to answer questions. He has a normal temperature and blood pressure of 100/52 mm Hg. His neurologic evaluation reveals brisk reflexes, normal tone, flexor plantar responses, and no papilledema or meningismus. Motor evaluation is precluded by his mental status.Laboratory findings include: hemoglobin, 9.8 g/dL (98 g/L), white blood cell count, 1.9×103/mcL (1.9×109/L) with an absolute neutrophil count of 1.3×103/mcL (1.3×109/L), and platelet count 266×103/mcL (266×109/L). Blood chemistry levels are normal (serum glucose of 116 mg/dL [9.5 mmol/L]) except for an aspartate aminotransferase level of 92 U/L and alanine aminotransferase level of 172 U/L. He has a negative urine drug test result and undetectable acetaminophen and salicylate levels. Computed tomography and magnetic resonance imaging of the brain reveal no abnormalities, and an electroencephalogram shows no seizure activity. Results of lumbar puncture are normal, including extensive cultures. No blasts are seen in the cerebrospinal fluid. The patient is monitored in the intensive care unit and treated with broad-spectrum antibiotics pending culture results. Over the next 3 days, while receiving antibiotic therapy, his mental status improves completely. Additional history reveals the cause of his mental status changes.A 14-year-old girl has experienced left lower quadrant abdominal pain, weakness, and a 20-lb (9-kg) weight loss over the past 2 months. The pain is sharp, intermittent, and nonradiating. She denies other abdominal or urinary symptoms but reports the recent onset of a cough productive of yellow, nonbloody sputum and feeling feverish. She has been treated empirically at a clinic with an antispasmodic for irritable bowel syndrome and then with antibiotics for presumed Helicobacter pylori infection. She did not complete either therapy, and her symptoms have progressed. She is an immigrant from Mexico who has lived in North Carolina for the last 2 years and denies recent contact with ill people.On physical examination, the girl appears cachectic and has a temperature of 102.3°F (38.7°C), respiratory rate of 18 breaths/min, and pulse oximetry reading of 100% on room air. Her lungs are clear to auscultation, and her abdomen is mildly distended, with voluntary guarding over the left lower quadrant and suprapubic region.Radiographs of her chest reveal ill-defined opacities in the left upper and right middle lobes. Computed tomography of chest, abdomen, and pelvis reveals the same pattern of infiltrates, as well as hilar lymphadenopathy and many large, low-attenuating lymph nodes throughout the abdomen. A procedure is performed that reveals the diagnosis.A 17-year-old girl who has type 1 diabetes mellitus is admitted to a Midwestern hospital because of an extensive right-sided pneumonia. In the last month, she has experienced intermittent fever, night sweats, pleuritic chest pain, decreased appetite, weight loss, weakness, malaise, and a cough productive of yellow sputum. A chest radiograph has shown dense consolidation of the right upper lobe, extending into the right perihilar area, and patchy infiltrates in the right lower lobe, as well as a small pleural effusion. She has not improved, despite treatment with levofloxacin for 7 days and clarithromycin for 10 days. She smokes cigarettes and has had multiple sexual partners. A classmate was diagnosed recently as having tuberculosis (TB).On physical examination, the girl does not appear toxic. Her oral temperature is 98.6°F (37°C), pulse is 144 beats/min, respirations are 40 breaths/min, and blood pressure is 110/62 mm Hg. Breath sounds are diminished at both bases, with fine crackles in the right upper lung fields.Laboratory findings include a white blood cell count of 24.9×103/mcL (24.9×109/L) with 42% neutrophils, 40% bands, 12% lymphocytes, and 6% monocytes, platelet count of 602×103/mcL (602×109/L), and normal levels of electrolytes, urea nitrogen, creatinine, and glucose. The erythrocyte sedimentation rate is 112 mm/h. A new radiograph documents extensive consolidation of the right lung and a pleural effusion on the right side. In addition, computed tomography shows a large cavity in the right upper lobe, smaller cavities in the remainder of the right lung, and ill-defined tiny nodular densities in the left base. An intradermal tuberculin test is negative.A specific procedure establishes the diagnosis.An 18-month-old boy is hospitalized after vomiting approximately 1 oz of bright red blood. Yesterday he passed two black, tarry stools. He has complained of mild abdominal pain and fatigue for 3 days, but has had no fever, constipation, diarrhea, or weight loss. He was born at term by uncomplicated caesarean section and had no jaundice or bleeding tendencies. There is no family history of liver diseases or bleeding disorders.On physical examination, the child is pale but not jaundiced. He is afebrile and has a blood pressure of 67/41 mm Hg, heart rate of 131 beats/min, respiratory rate of 32 breaths/min, and capillary refill time of 2 seconds. The skin is clear. His abdomen is soft and not tender or distended. Liver and spleen are not palpable. Rectal examination reveals stool that tests positive for blood. There are no fissures or hemorrhoids.Laboratory findings are as follows: hemoglobin, 5.6 g/dL (56 g/L); hematocrit, 17.5% (0.175); mean corpuscular volume, 82.9 fL; white blood cell count, 11.9×103/mcL (11.9×109/L) with 68% neutrophils and 30% lymphocytes; platelet count, 160×103/mcL (160×109/L); total bilirubin, 0.4 mg/dL (6.8 mcmol/L); alkaline phosphatase, 175 U/L; alanine aminotransferase, 38 U/L; aspartate aminotransferase, 22 U/L; blood urea nitrogen, 36 mg/dL (12.9 mmol/L); and creatinine, 0.6 mg/dL (53 mcmol/L). Prothrombin and partial thromboplastin times are normal. Abdominal radiographs reveal a nonspecific bowel gas pattern.A diagnostic procedure and a radiologic study establish the underlying diagnosis.An 18-month-old boy was well until 2 weeks ago, when he was noted to have fever, rash, and conjunctivitis. Unvaccinated, he was diagnosed as having measles by his primary physician. Since then, his fever has persisted and he has developed irritability, diarrhea, pallor, and abdominal distension.Physical examination reveals an ill-appearing, pale child whose axillary temperature is 101.3°F (38.5°C) and pulse is 156 beats/min. His breath sounds are clear bilaterally. A grade 2/6 early systolic murmur is audible over the left sternal border. His abdomen is distended, and his spleen is palpable 5 cm and liver palpable 4 cm below the costal margin. Skin examination reveals a fine, branny desquamation.Laboratory results are as follows: white blood cell count, 8.0×103/mcL (8.0×109/L) with a left shift; hemoglobin, 7.5 g/dL (75 g/L); hematocrit, 23% (0.23); platelet count, 72×103/mcL (72×109/L); direct antiglobulin test, negative; reticulocyte count, 1% (0.01); erythrocyte sedimentation rate (ESR), 60 mm/h; C-reactive protein (CRP), 7.5 mg/dL (normal, <0.5 mg/dL); serum sodium, 128 mEq/L (128 mmol/L); potassium, 3.2 mEq/L (3.2 mmol/L); blood urea nitrogen (BUN), 8 mg/dL (2.9 mmol/L); creatinine, 0.3 mg/dL (26.5 mcmol/L); bicarbonate, 20 mEq/L (20 mmol/L); aspartate aminotransferase (AST), 106 U/L (normal, 20 to 50 U/L); alanine aminotransferase (ALT), 75 U/L (normal, 5 to 40 U/L); prothrombin time, 12 sec (normal, 10 to 15 sec); partial thromboplastin time, 38 sec (normal, 25 to 34 sec); serum triglycerides, 395 mg/dL (4.5 mmol/L) (normal, <200 mg/dL [2.3 mmol/L]); and serum fibrinogen, 120 mg/dL (1.2 g/L) (normal, 200 to 400 mg/dL [2 to 4 g/L]). Peripheral blood smear shows normal cell morphology. Cultures of the blood, stool, and urine are negative. Serology for Epstein-Barr virus, cytomegalovirus, hepatitis B and C viruses, human immunodeficiency virus (HIV), and parvovirus are negative. The immunoglobulin M antibody to measles is positive. Bone marrow examination reveals the diagnosis.Ultrasonography of the girl’s abdomen revealed a normal right kidney and an enlarged left kidney with thin renal parenchyma and dilatation of the renal pelvis. The initial portion of the left ureter proximal to the kidney had an increased diameter (8.6 mm). Intravenous pyelography confirmed the presence of left hydronephrosis (maximum diameter of the left kidney, 13.5 cm) with thin renal parenchyma (Fig. 1). Excretion of the contrast agent was delayed, and the left ureter was not visualized, even after administration of furosemide. Voiding cystourethrography excluded the diagnosis of vesicoureteral reflux. Decreased function of the left kidney (29% of the total renal function) and slow excretion of the isotope were found on radioisotope renography, indicating urinary tract obstruction. These findings were consistent with ureteropelvic junction (UPJ) obstruction. Left renal pyeloplasty relieved the obstruction.An abdominal mass in a child can have many causes, including a variety of benign and malignant tumors originating in different organs, intestinal disorders, and several renal conditions, such as obstructive uropathy. In addition to having an abdominal mass, this patient had microscopic hematuria, which is defined as the presence of a positive test for blood on dipstick and more than 5 red blood cells per high-power field in freshly voided and centrifuged urine. The combination of hematuria and an abdominal mass on physical examination suggests abnormalities of the kidneys or collecting system.Ultrasonography with Doppler enhancement is a good first diagnostic step. If ultrasonography reveals a renal mass that is not due to hydronephrosis and the nature of the mass is not evident on that procedure or if the mass appears to be caused by an extrarenal process, the next step is computed tomography or magnetic resonance imaging.Nonhydronephrotic renal conditions that can cause a mass include autosomal recessive polycystic kidney disease, an infiltrative process (tumor), and renal vein thrombosis.Autosomal recessive polycystic kidney disease usually involves both kidneys. A typical patient presents with bilateral flank masses in infancy as well as hypertension and hematuria. Benign (hamartoma, hemangioma) or malignant renal lesions may present as unilateral abdominal masses. Wilms tumor is the most common renal malignancy occurring in childhood, affecting one or both kidneys and presenting as a painless mass or occasionally making its presence known with hematuria or abdominal pain. Abdominal neuroblastomas can arise in the adrenals and mimic the clinical picture of Wilms tumor. The acute development of unilateral or bilateral flank masses and pain with gross hematuria may occur in children who experience renal vein thrombosis due to cyanotic congenital heart disease or nephrotic syndrome.Hydronephrosis is caused by impedance of the normal urine flow (obstructive uropathy) or abnormal backflow of urine from the bladder into the kidney (vesicoureteral reflux). A palpable mass indicates that the urine within the renal system is under pressure and requires early surgical intervention. Impedance of the urine flow can occur at several different anatomic levels of the urinary tract (infundibulum, renal pelvis, UPJ, ureter, bladder outlet, urethra) and may be associated with enlargement of the kidney, abdominal pain, and hematuria. The abdominal masses palpated most commonly in infants are polycystic kidneys and hydronephrotic kidneys.A number of disorders can cause obstruction, including tumors, retroperitoneal fibrosis, neurogenic bladder, congenital abnormalities, or calculi. Urolithiasis in childhood may be idiopathic or due to disorders such as hypercalcemic or normocalcemic hypercalciuria, distal renal tubular acidosis, cystinuria, hyperoxaluria, or hyperuricosuria.UPJ obstruction is the most common congenital condition causing urinary tract obstruction. Hydrocalycosis, mid-ureteral obstruction, megaureter, ureterocele, ureteral ectopia, bladder neck obstruction, and urethral valves are other congenital lesions that can cause obstruction. UPJ obstruction presents as fetal hydronephrosis or produces abdominal pain, hematuria, and a palpable mass in infancy or childhood. The obstruction may be accompanied by urinary tract infection. In 20% of cases, the obstruction involves both kidneys.If ultrasonographic findings are consistent with hydronephrosis, the next diagnostic procedure is radioisotope renography with mercaptoacetyltriglycine (MAG3TC 99) and furosemide. Intravenous pyelography can be helpful preoperatively to define the level of obstruction in the urinary tract. An increased concentration of the radiopaque medium with dilatation of the urinary tract usually is found above the point of obstruction, with delayed appearance of the contrast below it. After intravenous administration of furosemide, no radiopaque medium remains in the normal collecting system, but a progressive increase in the concentration of the contrast above the point of obstruction is noted. This finding on imaging correlates with some patients who have UPJ obstruction reporting pain when they receive diuretics.In all cases of hydronephrosis, especially when there is ureteral dilatation, voiding cystourethrography is useful to rule out severe vesicoureteral reflux as the primary abnormality. Rhabdomyosarcoma of the bladder also can present with an abdominal mass.Although it is relatively simple to establish the diagnosis of UPJ obstruction by using appropriate imaging studies, a high degree of suspicion is required to include this entity in the differential diagnosis of recurrent abdominal pain. (Athanasios G. Kaditis, MD, Eleni Papadimitriou, MD, Emmanuel Alexopoulos, MD, Nikolaos Skenteris, MD, University of Thessaly Medical School, Larissa, Greece)Fortunately, this child’s mental status returned to baseline, although his initial evaluation did not reveal a cause for his obtundation. On closer review of his therapy and identifiers on the tablets he had taken, a medication error was discovered. The patient had been given prochlorperazine (Compazine®) erroneously instead of prednisone and had taken up to 40 mg/d on the 3 days preceding admission. This finding explained his self-resolving symptoms, and he improved when the offending medication was discontinued.Mental status changes can range from agitation, restlessness, and delirium to somnolence, lethargy, and coma. The broad differential diagnosis includes infection, intracranial processes (bleeding, seizures, increased intracranial pressure, tumors), metabolic disturbances, poisoning/ingestions, and systemic illnesses. The urgency in determining the true cause stems from the potential for reversing the changes and preventing long-term damage. In this patient, the differential diagnosis is broadened by a history of leukemia and previous exposure to intracranial radiation and intrathecal chemotherapy.The initial steps of caring for a patient who has altered mental status include addressing cardiac and respiratory functions and treating reversible metabolic disturbances such as hypoglycemia rapidly. If the patient is febrile or appears septic, broad-spectrum antibiotics should be initiated, even if the results of an evaluation for infection are incomplete.The central nervous system (CNS) can be imaged efficiently with computed tomography of the brain, which aids in diagnosing acute bleeding, increased intracranial pressure, and the presence of masses. More detailed structural information can be obtained with magnetic resonance imaging. This degree of accuracy was particularly important in this patient because of the history of prior irradiation to the brain and intrathecal chemotherapy, both of which have been associated with long-term damage, including cortical atrophy and leukoencephalopathy.Performing a lumbar puncture is an important diagnostic procedure in evaluating patients who have altered mental status to rule out CNS infection. This study is especially pertinent in immunocompromised hosts, who may develop opportunistic CNS infections with organisms such as Cryptococcus neoformans. For a patient who has a history of leukemia and develops new CNS symptoms, relapse is high on the list of differential diagnoses.Laboratory evaluation of the child who has altered mental status, including a metabolic panel and tests of liver function, can add valuable clues. In this case, the mild elevation of transaminases was believed to be an effect of methotrexate therapy. Serum chemistries should be obtained to rule out metabolic derangements such as hypoglycemia or hypercalcemia. The basic metabolic panel should be used to calculate serum osmolality and identify acidosis or alkalosis, both of which guide the clinician toward a differential diagnosis that includes ingestions as well as diseases such as diabetic ketoacidosis and uremia. Toxic ingestions should be high on the list of causes when a disease is not clear. Urine and serum drug screens often can identify culprits not suggested by results of the history. In this case, prochlorperazine was not included in the panel of drugs screened for in the urine. The specific substances included in drug screening vary among laboratories.Prochlorperazine is a phenothiazine derivative used to control severe nausea and vomiting. Adverse reactions include drowsiness, dizziness, blurred vision, skin reactions, and hypotension, in addition to a severe condition characterized by hyperpyrexia, autonomic instability, rigidity, and altered mental status known as the neuroleptic malignant syndrome. Overdosage symptoms include primarily extrapyramidal dysfunction that produces dystonic reactions as well as CNS depression manifesting as somnolence or coma. Agitation and restlessness also may occur, as might electrocardiographic changes and cardiac arrhythmias. Overdosage can cause fever, convulsions, and autonomic reactions such as dry mouth, hypotension, and ileus. Dystonic reactions can occur in children who are receiving recommended dosages.The causes of altered mental status constitute a broad differential diagnosis. Although it is important to focus initially on the airway, breathing, circulation, and rapidly reversible causes, a carefully performed history and physical examination are vital to diagnosing and managing affected patients successfully.Medication errors occur more commonly than we would like to believe. A careful review of the medication list may provide significant clues. All solid medications have unique identifiers that can be found in reference textbooks as well as online. As in this case, these telltale markings may uncover the cause of the patient’s condition. (Vinod K. Gidvani, MD, Gary Crouch, MD, Walter Reed Army Medical Center, Washington, DC)After performing a careful history and physical examination and reviewing the radiographic findings with the radiologist, the clinicians formulated a differential diagnosis for the patient’s mesenteric adenitis. Potential causes included infection due to Mycobacterium tuberculosis, Yersinia enterocolitica, Y pseudotuberculosis, Salmonella, Escherischia coli, Epstein-Barr virus, Toxoplasma gondii, HIV, Histoplasma capsulatum, and Blastomyces dermatitidis. Malignancies that were considered included Hodgkin and nonHodgkin lymphoma, melanoma, neuroblastoma, and metastatic neoplasms. Among the other possibilities were autoimmune disease (systemic lupus erythematosus), sarcoidosis, rheumatoid arthritis, and chronic granulomatous disease.In evaluating any patient, the clinician creates a rank order hierarchy based on the likelihood of disease, the unique aspects of the history, physical findings, radiographic images, and laboratory data. For example, neuroblastoma is diagnosed more commonly in younger children. Sarcoidosis, although identified more commonly in the southeastern United States (for unknown reasons), usually does not affect Latino patients. Coccidioidomycosis might be high on the list in Arizona, but not in the southeastern United States. Chronic granulomatous disease is inherited by means of X-linked recessive mutation in more than 60% of patients and usually is expressed much earlier in life. The combination of multilobar lung parenchymal disease (Fig. 2) and abdominal lymphadenopathy (Fig. 3) in this patient heightened the concern for TB and lymphoma.The girl was admitted to the general pediatric ward on respiratory isolation. A tuberculin skin test (TST) employing purified protein derivative was placed on her forearm on admission. Samples of sputum for Gram stain, routine culture, and smear and culture for acid-fast bacilli (AFB) were obtained. Two early morning gastric aspirates for AFB smear and culture also were obtained on successive days when the patient no longer could produce sputum. Gram stain of the sputum, AFB smears, a urine pregnancy test, and testing for HIV produced negative results. Stool studies were ordered but never collected because the patient was unable to produce a sample. At 48 hours, the TST was positive at 15×18 mm induration.Due to concerns about multidrug-resistant TB in a foreign-born child, the patient was placed on directly observed therapy (DOT) employing isoniazid (INH), rifampin, pyrazinamide (PZA), and ethambutol. She received 2 weeks of daily DOT, followed by twice weekly DOT. By the second month of therapy, all cultures had become positive for TB that was sensitive to all drugs tested. Ethambutol and PZA were discontinued. More than 2 months into therapy, she continues to receive INH and rifampin and is doing well. The abdominal pain has resolved, and she has regained all lost weight.M tuberculosis is a rod-shaped, aerobic bacterium that is transmitted via respiratory droplets and taken up by pulmonary macrophages and neutrophils in the alveolus. Depending on the virulence of the organism and the microbicidal activity of the host, the organism may cause infection. Once host defenses are overcome, the organism multiplies slowly over a period of weeks to months. When the organism reaches a critical number (1,000 to 10,000 colony-forming units/mL), it is capable of stimulating an immune response and causing a positive response to the TST. Before reaching this point, the organism can spread through the lymphatic system and bloodstream to infect distant sites.Many individuals who have normal host cellular immune responses contain the infection with the help of T lymphocytes and macrophages. A person is at greatest risk of developing the disease within the first 2 years of life and the first 2 years of infection. If the host is immunocompromised for any reason (HIV infection, steroid use, immunosuppressive drug use), he or she is more likely to succumb to disease.Even in children and adolescents who have moderate-to-severe pulmonary TB, the disease usually is clinically silent at the time of diagnosis. It often is discovered because of the history of close contact with another patient who has the disease. Many individuals have latent TB, in which there is infection but no physical or radiologic evidence of active disease. Unfortunately, infants and postpubertal adolescents are more likely to experience progression of latent infection to true disease. Approximately 40% to 50% of infants who have untreated infection develop disease in 1 to 2 years. Other risk factors for progression include immunodeficiency and certain chronic diseases such as malnutrition, chronic renal failure, diabetes mellitus, and lymphoma.The disease may present initially with constitutional symptoms of fever, chills, cough, night sweats, and weight loss. By far, the lungs are the organs associated most commonly with the disease. Findings on chest radiography that support the diagnosis include hilar lymphadenopathy, parenchymal infiltrates, pleural effusion, miliary disease, and cavitary disease. Children who have pulmonary TB are less likely to be infectious than are adults.TB can involve extrapulmonary sites such as the CNS (meningitis, tuberculoma), bones and joints (Pott disease, septic arthritis), blood (miliary TB), ears, mastoids, kidneys, skin, and lymph nodes. Although TB lymphadenitis is one of the more common forms of extrapulmonary disease, it is encountered more frequently in the cervical and supraclavicular nodes. Infections in the abdomen occur far less often. When abdominal involvement does occur, it usually involves the terminal ileum and cecum. Symptomatic TB mesenteric adenitis is very uncommon.Recent data from the Centers for Disease Control and Prevention indicate a declining incidence of TB in the United States. A total of 15,989 cases were reported in 2001, a 2% decrease from 2000 and a 40% decrease from 1992. Children younger than the age of 15 years experienced a reduction in the rate of TB from 3.1 per 100,000 in 1991 to 1.5 per 100,000 in 2001. The decline in TB is overshadowed by a case rate in foreign-born persons that is at least eight times higher than in persons born in the United States. Over the last 5 years, the top five countries of origin of foreign-born persons coming to the United States and having TB are Mexico, the Philippines, Vietnam, India, and China. Unlike the United States, an increasing number of cases of TB are being seen in the eastern Mediterranean, Southeast Asia, and Africa.Acute mesenteric adenitis frequently presents with symptoms of fever, nausea, and abdominal pain. Physical examination may reveal abdominal distension and a palpable mass. The evaluation of abdominal lymphadenopathy depends on the clinical situation. Imaging studies such as computed tomography with contrast of the abdomen and pelvis can help define the location and extent of disease.When TB is suspected, it is important to place a TST, collect a series of three samples of sputum or early morning gastric aspirates, and test for HIV. Species can be identified rapidly with the use of DNA probes in respiratory samples positive for AFB, thereby shortening the time to confirmation. When noninvasive testing fails to secure a diagnosis, open or laparoscopic lymph node resection should be considered.Occasionally, a clinician will be confronted with interpreting a TST in an infant, child, or adolescent who has received the bacillus Calmette-Guérin (BCG) vaccine. This live bacterial vaccine is derived from the strain M bovis and administered to children living outside the United States to prevent life-threatening manifestations of TB in areas where the incidence of TB is much more common. Children who have received this vaccine may experience minor reactions to the TST. Current recommendations are to administer the TST to a patient who has received the BCG vaccine when TB is a consideration. The test should be interpreted as if the child or adolescent has never had the BCG vaccine, and additional investigations should be pursued as warranted based on the results of the test (see Pickering LK, ed. 2003 Red Book: The Report of the Committee on Infectious Diseases. 26th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2003:647).Treatment of TB can be complicated by the number of antituberculous medications and the need to differentiate between latent TB infection and active disease. If the sensitivity of the organism from the source case is known, it is reasonable to tailor therapy accordingly. However, if the source case is unknown and the patient is at risk for infection with multidrug-resistant TB, empiric therapy should include four drugs, usually INH, rifampin, PZA, and ethambutol.When TB is suspected or diagnosed, law requires notification of the public health department. The health department will activate a contact investigation to identify all persons exposed to the source case and screen them for TB. If a clinician waits to inform the health department until after the case is confirmed, an infected person could progress from infection to disease or could spread the infection. The health department also will ensure adequate delivery of the medication, enhancing compliance and monitoring for complications due to illness or treatment.TB is a rare cause of mesenteric adenitis and must be considered in a patient presenting with prolonged symptoms of fever, abdominal distension, and pain. On occasion, this infection has been associated with extrahepati

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