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retrospectivelydesire a different course of action. How many will remember their choice as their decision, and how many will feel they were misled or misinformed and subsequently sue for malpractice? Of the parents who acknowledge some responsibility, how many will be burdened with guilt over decisions they made that affected their children (especially when cost is a significant factor in many such decisions, according to the authors)? In summary, I agree that it is important to talk to parents, educate them about the risks and benefits of various diagnostic and treatment plans, and obtain informed consent (and documentall of this). However, parents usually expect and trust the physician to suggest a course of action that he or she feels is best on the basis of knowledge and clinical experience.Parentsshouldn't be expectedto make the medical decisions physicians have been trained to make. "Option packages"and statistics (especiallythose subject to debate or of limited applicability to a particular patient, as above)are not what most patients really want from their EDvisits. A well-trained physician acting in good faith who communicates with patients his or her assessmentand recommendationsis the true preferenceof most patients.
Daniel F Brennan, MD, FACEP EmergencyMedicine Residency Program OrlandoRegionalMedical Center Orlando, Florida 1.Cheng TL, Partridge JC: Effect of bundling and high environmental temperature on neonatal body temperature. Pediatrics 1993;92:238240. 2. Baraff LJ, Oslund SA, Schriger DL, et al: Probability of bacterial infections in febrile infants less than three months of age: A meta-analysis. Pediatr Infect Dis J 1992;11:257-264. 3. McCarthy CA, Powell KR, Jaskiewics JA, et al: Outpatient management of selected infants younger than two months of age evaluated for possible sepsis. Pediatr Infect Dis J 1990;9:385389. 4. Dagan R, Powell KR, Hall CB, et of: Identification of infants unlikely to have serious bacterial infection although hospitalized for suspected sepsis. J Pediatr 1985; 107:855-860. 5. Anbar RD, Richardson-de Corral V, O'Malley PJ: Difficulties in universal
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application of criteria identifying infants at low risk for serious bacterial infection. J Pediatr 1986;109:483-485. 6. Avne.rJR, Crain EF, Baker MD: Failure to validate the Rochester criteria for evaluation off&rile infants (abstract). AmJ Dis Child 1993; 147:441. 7. Baskin MN, O'Rourke EJ, Fleisher GR: Outpatient management offebrile infants 28 to 89 days of age with intramuscular administration of ceftriaxone. J Pediatr 1992;120:22-27. 8. Marshall R, Teele DW, Klein JO. Unsuspected bacteremia due to Haemophilus influenza: Outcome in children not initially admitted to the hospital. J Pediatr 1979;95:690-695. 9. Dashefshy B, Teele DW, Ktein JO: Unsuspected meningococcemia. J Pediatr 1983;102:69-72. 10. Bratton L, Teete DW, Klein JO: Outcome of unsuspected pneumococcemia in children not initially admitted to the hospital. J Pediatr 1977;90:703-707.
In reply: In general we agree with the comments of Dr Brennan.We specifically mentionedthe issues of study bias, framing bias, and implications of outcome in the discussion. We believe the rate of 1.4% is a correct approx]mationof the true risk and is supported by the referencesin the manuscriptand in more recent work by Jascowitz et aP, but we recognizethat this numberis disputed. This is the reasonan expert panel could not come to a consensus about outpatient managementof febrile infants, specifically evaluation without lumbar puncture or parenteral antibiotic therapy.2 Readersmust recognizethat in pediatricians' offices, children such as those we describedare frequently managedwith careful parental observationonly. The Rochester criteria are a compromisebetween this practice and the residencytraining procedureof admitting all febrile infants less than 2 months old. The use of temperature and WBC count as continuous rather than dichotomous variables is preferable,as Dr Brennan suggests. I presumeDr Brennanis being facetious in suggestingtreatment without testing. This is inappropriate because it would encouragethe widespread use of ceftriaxone, which could result in increasedbacterial resistanceto this class of agents. Furthermore,should the
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patient fail to improve,interpretation of subsequenttests such as blood cultures and lumbar puncturewould be difficult. Most infants with cerebrospinalfluid pleocytosishave aseptic meningitis,and this would result in such infants being unnecessarily treated for bacterial meningitis. Ultimately the question is, When is it appropriatefor us as physicians to inform our patients of the reasons for therapy and involve them in medical decisionmaking?It is common practice to inform patients whenever there are alternative treatment options or there is a real risk of serious morbidity Dr mortality. If one is culturing and treating all febrile infants, then this discussion may not be necessary.However,if one performs no testing and administers no antibiotics, then perhaps parents should be informed of the risk associated with such managementstrategy. It certainly is greater than the risk of a lumbar puncture, a procedure for which one routinely obtains consent. The purpose of our researchwas to determinewhether parents could understandthe risks and benefits associatedwith two alternative treatment options and to determine their preferencebetween them. The fact that parents could understand the risks and benefits is important in itself. We now feel more comfortable using the Rochestercriteria knowing that most patients can understandthe risks associated with this strategy and prefer it to more extensive testing and treatment. Most of our patients do not just ask us to do what we think is best. They frequently want information on why we propose specific therapies and whether alternatives are available. This challenges us to be familiar with the specific risks underlyingthe treatments that we recommend.As an educator, I trust that Dr Brennanrecognizesthe need to inform physicians-in-trainingof these risks (ie, the rationale for medical tenets).
Larry J Baraff, MD UCLAEmergencyMedicine Center LosAngeles, California 1. JaskiewiczJA, McCarthy CA, Richardson AC, et al: Febrile infants at low risk for serious bacterial infection: An appraisal of the Rochester criteria
and implications for management: Febrile Infant Collaborative Study Group. Pediatrics 1994;94:390- 396. 2. Baraff LJ, Bass JW, Fleisher GR, et al: Practice guidelines for the management of infants and children with fever without source 0-36 months of age. Pediatrics 1993;92:1-12.
Corticosteroids Precipitating Hypocalcemic Encephalopathy In Hypoparathyroidism To the Editor. A 35-year-oldwoman, known to have rheumatoid arthritis, was administered 80 mg of methylprednisolone intramuscularlybecauseof acute exacerbationof her joint symptoms. She presentedto the emergencydepartment 10 hours later with altered sensoriumand generalizedconvulsions. Examinationrevealedan unconscious woman 130 cm tall and weighing 45 kg with a round face, short neck, and missingteeth. The physiognomywas reminiscent of Albright's osteodystrophy. The patient's convulsions were frequent and of short duration. Findingson examinationof the heart, chest, and abdomenwere normal.No signs of meningealirritation or any obviousfocal neurologicdefect were noted. Chvostek'sand Trousseau's signs were present. ECG revealed prolongation of the QT interval (QTo, .658 seconds). The hemogramwas normal,and blood sugar, urea,serum bilirubin, aminotransferases,alkaline phosphatase,sodium,and potassiumwere Within normal limits. Serumcalcium and phosphoruswere 1.89mmol/L and 2.38 mmol/L, respectively.Serum magnesiumwas normal.Arterial blood gas analysisshowed mild metabolicalkalosis.A blood sample for parathyroidhormoneestimation was obtained.Resultsof chest radiographywere normal. Radiographyof the hands showed no shortenedmetacarpals.Computed tomographyof the head revealedcalcification of the basal ganglia. A clinica[ diagnosis of hypoparathyroidismwith Albright's esteodystrophywith hypocalcemic
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metabolic encephalopathywas made, and the patient was treated with IV calcium gluconate.The seizures stopped promptly, and the patient regainedconsciousness.No anticonvulsantswere administered. The parathyroidhormonelevel in the sample obtained earlier was 5.3 pg/mL (normal, 12 to 72 pg/mL). The patient was started on oral calcium and calcitriol. She madesteady progressthereafter.Her serumcalcium and phosphoruslevelsafter 4 weeks of therapywere 2.5 mmol/L and 1.1 mmol/L,respectively. We believe that in this patient with hypoparathyroidism,administration of corticosteroids precipitated severehypocalcemia,which led to metabolic encephalopathy. Corticosteroidsare known to lower serum calcium by reducing intestinal calcium absorption, impairing conversion of cholecalciferol to 25hydroxycholecalciferoland increasing protein binding of calcium by way of corticosteroid-inducedalkaloSiS.1'2 That prednisolonecausesa prompt decreaseof serum calcium in patients with hypoparathyroidismis borne out by a recent case report, in which significant hypocalcemia developedin a child with hypoparathyroidism on administration of prednisolone for an unrelated condition, despite 1-o~-D3 treatment and serum 1,25-(0H)2 D3 levels in the high normal range. Becausecorticosteroids are widely used for a variety of conditions, it is essential to recognize that administration may worsen hypocalcemiain disordersassociated with low serum calcium level. Furthermore,failure to recognize hypocalcemiaas the cause of seizures may lead to inappropriate use of anticonvulsantssuch as phenytoinwith consequentworsening of the convulsionsdue to aggravation of hypocalcemia.Prolongation of QTc on the ECG in the absenceof history of drug intake should arouse suspicion of hypocalcemia.
Rohini Hand& MD, DNB &off Prakash Wall, MD, MNAMS RaghuInderSing& MD Departmentof Medicine PraveenAggarwal, MD, DNB Departmentof EmergencyMedicine Aft India Institute of Medical Sciences New Delhi, India
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1. Avioli LV, Birge SJ, Lee SW: Effects of prednisolone on vitamin D metabolism in man. J Clin Endoerir~ol Metab I968;29:1347-1352. 2. Chesney RW, Mazess RB, Hamstra AJ, et al: Reduction of serum 1,25 dihydroxyvitamin D3 in children receiving glucocorticoids. Lancet 1978;2:1123-1125. 3. Vardi P, Benderly A, Etzioni A, et al: Hypocalcemia induced by glucocorticoids in a child with hypoparathyroidism treated with 1alpha-hydroxy vitamin D3. Eur J Paediatr 1985;144:280-282.
Teaching Procedures on the Newly Dead To the Editor. In a recent issue of Annals three papers--one by Goldblatt, one by Iserson, and one by Knopp--discussed the important question of whether it is ethical and justifiable to teach emergencyprocedureson newly dead patients [January 1995;24:86-90,91-94, 99-100]. As anesthesiologistsinvolved in the teaching of such skills to medical students and other medical personnel, we would like to comment. There is no doubt that we have an obligation to ensuringthat emergency medical team membersin the future achievethe best competence possible in the treatment of acutely ill and injured patients. Few skills are more vital than the ability to secure the airways, specifically, performing endotrachealintubation. Nor is there any question that junior doctors today seldom get enough training to perform this demanding psychomotorskill and that newly dead patients representa valuable teaching source.1 We agree with Dr Iserson that no substitute model can mimic the anatomy or tissue resilience of a living or newly dead patient. The ethical concerns about the use of newly dead patients in teaching and training are justified and real. It remains a puzzleto us, however, why medical and "ethical" alliances seem to be far less concernedabout the ethical implications of the use of living and dying patients for teaching purposes (eg, in conjunctionwith anesthesia,surgery, and resuscita-
tion) in Europeand in the United States. In some countries, as in our own, there is assumedconsentfor teaching of intubation techniqueson living patients in relation to anesthesiafor surgery but not for use of a newly dead bodyfor the same purpose.2,3 This practice, in which teaching and training take place in an ill-defined ethical context, conveysdubious moral and ethical values to trainees. This moral and ethical lack of perspective is even more surprising becausethe actual opinion of the general public seems largely unknown. In a randomsurvey(N=971), we found that most (58%; 95% confidence interval, 55 to 61) of the general public said they would permit a close relative to be used to teach intubation technique.4 We sharethe viewpoint of Iserson and Orlowski et al5 that in the real world of emergencymedicine the concept of proxyconsent for the teaching of intubation skills is impractical. Insteadwe must adopt an open strategy with a presumed consent becausethrough open disclosure that the practice of teaching advanced airway management on newly deceased patients is both necessary and important, the potential patients (eg, the individual) will have the opportunity to refuse the procedure by advance directive. However,with regardto the issue of more mutilating emergencyprocedures (eg, clampingof the thoracic aorta), we agreethat these procedures should be performed after informed consent has been obtained 6,7 because they can also be accomplished with cadavers in rigor mortis.~
GuttormBrattebd, 11/10 Departmentof Anaesthesia and Intensive Care HaukelandHospital Haukeland, Norway Torben Wisborg,MD, DEAA NorwegianAir Ambulance Bergen, Norway 1. BrattebĀ¢ G, Seim 5H: Teaching and training of invasive procedures on cadavers. Lartcet 1988;2:1078-1079. 2. Reintubering i opplceringsoyemed citer at doden hat inntrcldt. Tidsskr Nor Laegeforen 1991;111:2181.
3. Tonks A: Intubation practice on cadavers should stop. BMJ 1992; 305:332. 4. Brattebo G, Wisborg T, Solheim K, et al: Public opinion on different approaches to teaching intubation techniques. BMJ 1993;307:1256-1257. 5. Orlowski JP, Kanoti GA, Mehlman MJ: The ethics of using newly dead patients for teaching and practicing intubation techniques. N EnglJ Med 1989;319:439-441. 6. Burns JP, Reardon FE, Truogh RE): Using newly deceased patients to teach resuscitation procedures. N EngI J Med 1994;331:1652- 1655. 7. McNamara RM, Monti S, Kelly JJ: Requesting consent for an invasive procedure in newly deceased adults. JAMA 1995;273:310- 312.
Identification and Triage of Nonemergency Patients From the ED To the Editor. I read with great interest the article by Derlet et al on the triage of nonemergency patients from the emergency department [February 1995;25:215-225]. lain interested in research addressing the use and misuse of the ED and know the extensive work involved, and I applaud the interest and dedication shown by the authors in attempting to study this difficult issue in a scientific manner. As much as I find that the method used was carefully designedand implemented, I object to the conclusions drawn from the analysis of the results. (1) An 18% rate of triage out of the ED was reported. This number reflects a rate for only a subgroup of emergencypatients (ie, the adults who presented to the ambulatory triage area). However,when the total population (patients who arrive by ambulanceand the pediatric clientele)is included,the rate falls from 18% to 10%. Eventhen, I believe that the percentagedoes not accurately reflect the effect or the absolute numberof patients. The study showed that 16 patients per 24 hours were triaged out, representing slightly more than 5 patients per 8-hour shift. Giventhe criteria
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AUGUST 1995