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Objective: Chylothorax presenting in a child without a well defined etiology may be a manifestation of child abuse. We recently observed a child with bilateral chylothoraces who demonstrated coexisting nonaccidental injuries. It is our intention to alert physicians to the association of chylothorax with nonaccidental trauma and review the prior medical literature. Design: Case report. Setting: Pediatric emergency department and intensive care unit. Patient: An 18-month-old female child who presented with respiratory distress and failure to thrive. Interventions: Diagnostic and therapeutic thorocentesis. Skeletal survey and radionuclide bone scan. Nutritional support. Outcome measures: Pleural fluid is characterized as chylous if it contains significant numbers of lymphocytes and lipid. Unexplained fractures of the ribs and long bones in varying stages of healing are considered nonaccidental. Failure to thrive may be considered nonorganic when nutritional support alone results in significant weight gain. Results: Our patient presented with respiratory distress of one-week duration and failure to gain weight during the prior five months. The chest radiograph demonstrated bilateral pleural effusions, which were aspirated. The aspirate contained 1733 cells/mm3 (98% lymphocytes), which were lipid laden. The triglyceride concentration was 806 mg/dl. A skeletal survey demonstrated bilateral first rib, clavicle, and ulnar fractures. A radionuclide bone scan additionally revealed multiple vertebral body fractures. Nutritional support alone resulted in significant weight gain. The patient was reported to local authorities as having been abused. Conclusion: Child abuse should be considered as an etiology for cryptogenic chylothorax. Further studies should be undertaken in this circumstance to search for coexisting injuries, which may indicate nonaccidental trauma.

To determine if routine, noninvasive parameters could be measured which predict early (4-6 hour) discharge from the emergency department (ED) in mildly symptomatic and asymptomatic victims of childhood near-drowning, a retrospective cohort study was undertaken. Patients with fresh water near-drowning were studied over a 3-year period who presented with Glascow Come Scale (GCS)or =13 and required no advanced life support prior to oror =4 hours after ED presentation. Three groups of patients were found: 39 patients (81%) had normal pulmonary examination (PEx) and normal room air oxygen saturation (RASaO2) by 4 to 6 hours and did not deteriorate during the hospital admission (24 hours); 5 patients (10%) had normal PEx by 4 to 6 hours and RASaO2 by 8 to 12 hours and did not deteriorate during hospitalization (24 hours). Four patients (8%) were hospitalized for more than 24 hours. No patient with normal RASaO2 at 6 hours deteriorated while in the hospital (CI 92.3-100%). Children who present to the ED with GCSor =13 and have normal PEx/respiratory effort and RA-SaO2 more than 95% at 4 to 6 hours after ED presentation can be safely discharged home.

This is a report of an intentionally administered overdose of dimenhydrinate to a 4 month-old infant who subsequently presented with status epilepticus, coma, and life threatening ventricular dysrhythmias. Initial toxicologic analysis of the serum by fluorescence polarization immunoassay was positive for tricyclic antidepressants. Repeat analysis of the serum at 6 hours post ingestion by gas chromatography mass spectrometry analysis defined diphenhydramine 4.8 micrograms/mL. The infant was managed with IV sodium bicarbonate as utilized in tricyclic antidepressant intoxication. The dysrhythmias resolved and the infant recovered without sequelae.

A 9-month-old infant was inadvertently administered azithromycin 50 mg/kg, taken from floor stock, instead of the prescribed ceftriaxone. Shortly thereafter, she became unresponsive and pulseless. The initial heart rhythm observed when cardiopulmonary resuscitation was started was a wide-complex bradycardia, with a prolonged rate-corrected QT interval and complete heart block. The baby was resuscitated with epinephrine and atropine, but she suffered severe anoxic encephalopathy. Torsade de pointes and QT-interval prolongation have been reported after administration of macrolide antibiotics, including azithromycin, both intravenously and orally. This has occurred especially in the context of coadministered drugs that inhibit the cytochrome P450 (CYP) 3A4 isoenzyme, such as ketoconazole and astemizole. However, bradycardia with complete heart block has not, to our knowledge, been reported specifically with intravenous administration of azithromycin alone, either with therapeutic doses or overdose. Clinicians should be alerted about the potential of azithromycin to cause life-threatening bradycardia, and pharmacy systems should be implemented to ensure special care in the safe administration of this drug, especially when dispensed from a point-of-care source.

Gold salts continue to serve an important role in the therapy of rheumatoid arthritis. Despite their characterisation as highly dangerous, life-threatening reactions are unusual. Parenteral gold preparations are available as sodium aurothiomalate and aurothioglucose. The former, which is prepared in aqueous solution is occasionally associated with hypotensive episodes after administration, whereas the latter, suspended in sesame oil, is not. These, so-called “nitritoid” reactions have been described as frightening but transient and have been attributed to the more rapid absorption of the aqueous preparation. Severe acute reactions, including myocardial infarction and angina, have been reported after sodium aurothiomalate injection. We report cerebral ischaemia and death following a nitritoid reaction. A 71-year-old woman undergoing therapy for rheumatoid arthritis was initiated on gold salts, having had a poor response to non-steroidal agents and sulphasalazine. At the time that gold therapy was initiated, her therapeutic regimen consisted of prednisone, 10 mg orally once daily. Sodium aurothiomalate was administered, 25 mg intramuscularly, once a week, and increased 2 weeks later to 50 mg weekly. Other medical problems included hypertension, which was being treated with the angiotensin-converting enzyme (ACE) inhibitor, captopril, and cerebrovascular disease. She had experienced a cerebrovascular accident, leaving her with a facial palsy and unilateral weakness. Her response to gold was satisfactory, and therapy was continued for a period of 31 weeks. Moments after her routine gold injection, and without apparent change in any clinical condition, she experienced nausea, vomiting, diaphoresis, and a feeling of impending doom. Her blood pressure at the time was 85/50 mm Hg. She was treated with diphenhydramine and epinephrine with prompt clinical response and was discharged. 2 weeks later, gold therapy was resumed in the form of aurothioglucose 50 mg intramuscularly, which was well tolerated, without hypotension or other side-effects. After 14 weeks of further therapy, the patient was admitted to hospital that in addition to the androgen receptor, another factor, ARA70, may be required to enhance the agonistic activity of hydroxyflutamide. These findings may raise some concerns about treatment of prostate cancer with supposedly pure antiandrogens in maximal androgen ablative therapy. Finding molecules that interfere with the interaction between the androgen receptor and ARA70 may be valuable in delaying the emergence of androgen resistance.

To the Editor.— We read with interest the article by Griffin et al 1 that recently appeared in JAMA and concur with the authors that the incidence of encephalopathy with permanent neurological sequelae after diphtheria-tetanus-pertussis (DTP) immunization is low, and is probably lower than that calculated from the often-quoted British National Childhood Encephalopathy Study. 2 These data reinforce the conclusion that DTP vaccination is safe in an overwhelming number of children. We believe, however, that it is hazardous to draw the conclusion, as the authors do, that DTP immunization might never cause permanent neurological disease. The absence in this population of unexplained encephalopathy does not help to reconcile the reports of such events in the case literature and of their continued observation by individual pediatricians. It has been suggested that most of these events are coincidental occurrences, 3 but none were observed in this prospective study: their absence does not

Poisoning is an uncommon manifestation of child abuse. The intentional administration of water to a child as a form of punishment has rarely been reported as the responsible substance among children who have been poisoned. We describe a case of a 5-year-old girl presenting with severe hyponatremia due to acute water intoxication. The patient was brought to the emergency room in status epilepticus. A history was obtained from the child's mother stating that the patient had been playing outside when she collapsed. She had had no known prior illnesses. Laboratory evaluation included a hemoglobin of 10.1 mg%, glucose of 60 mg%, serum sodium of 107 mEq/l, potassium of 3.2 mEq/l and chloride of 71 mEq/l. A CAT scan obtained approximately 1 h after admission revealed generalized cerebral edema. Careful examination of the skin revealed multiple linear ecchymosis of varying ages on the back and thighs and a hand print on the right flank. In addition, the child demonstrated severe failure to thrive with height, weight and bone age compatible with a 2.5-year-old girl. Appropriate therapy for severe hyponatremia was successfully instituted. For the next 12 h she was deeply somnolent, but the following morning was alert and conversant. She stated that she “would be good if she didn't have to drink any more water”. The child's mother subsequently admitted that she frequently used water ingestion as a form of punishment. The child stabilized metabolically and demonstrated rapid in-hospital weight gain. She was placed in foster care at discharge and has had no further hyponatremia or seizures. In our patient, hyponatremic seizures represented a manifestation of chronic and systematic abuse due to intentional water intoxication. Primary caregivers and pathologists should be aware that hyponatremia without underlying disease may be evidence of child abuse.

To increase understanding of childhood sexual abuse, we reviewed the hospital records of 113 girls and 17 boys who were the victims of sexual offenses. They were two to 16 years of age and seen in an 18-month period. Thirty had had medical or social problems. Four had previously been raped. Children under eight years old were more likely to know the assailant, to be victims of recurrent sexual or physical abuse, to report crimes without intercourse, and to present with an abused sibling (P less than 0.05). Incest victims were younger than other victims (P less than 0.05). Forty-three children had physical trauma. No pregnancies occurred, although diethylstilbestrol was not routinely used. Three girls had gonorrhea. Seventy-two patients were referred to hospital social services, and 41 to 17 other agencies. Victims and their siblings are at high risk of repeated abuse. Antibiotics and diethylstilbestrol are not routinely indicated. Follow-up may be best achieved by a central agency.

Low-velocity penetrating craniocerebral trauma may present as an apparently trivial injury. A case is presented which illustrates the need to suspect a penetrating injury whenever a low velocity object strikes the head.

In Reply .—There is merit in some, but not all, of Dr Poulton's criticisms. Our report 1 on bacterial tracheitis did not detail the exact circumstances of every patient whose case we reported, and these circumstances have some bearing on Dr Poulton's comments. In our article, we combined all of the complications encountered by these children, both before and while being treated in our pediatric intensive care unit. The two deaths Dr Poulton mentioned were tragedies that led us to review and revise extensively our intensive care protocols. These deaths represent the only deaths from inflammatory airway disease in our pediatric intensive care unit during the last ten years. It is more than a coincidence that both of these deaths were associated with bacterial tracheitis. It was not until after we appreciated the seriousness of bacterial tracheitis that a protocol was developed to cope adequately with this disease. Dr Poulton