1128
BRIEF REPORTS
no role for sophisticated enhanced elimination techniques except for multiple doses of oral activated charcoal. Cholestyramine resin directly binds lipid soluble substances and the bile salts, and therefore reduces the formation of emulsions. This minimizes the GI uptake and reabsorption of lipid soluble substances. Its administration may therefore be useful by enhancing drug fecal elimination by interrupting the enteroenteric and biliary-enterohepatic recirculation.6 Lindane resistance occurs throughout the world (i.e., Central and South America, Egypt, Haiti, and New Zealand), but remains uncommon or underreported in the United States (an outbreak was reported in Texas in 1991). In those Lindane-resistant infestations, permethrin has been shown to be effective. Permethrin, a synthetic pyrethraid that is sold over-the-counter, is a neurotoxin producing paralysis and death of a wide variety of ectoparasites by disrupting the sodium channel currents in the nerve cell r n e m b r a n e ~ . ~Generally, J~ permethrin efficacy has been reported to exceed 89%. In comparative clinical trials, the cure rate for permethrin was higher (i.e., 90%) than that of Lindane (i.e., 60%).7J2 Permethrin is indicated for use in patients of any age, and its Food and Drug Administration (FDA) pregnancy classification is category B. I t has a very low mammalian toxicity profile and its overall incidence of reported adverse events has been reported to be -2.5 per 1,000 applications, which is low for any topical medication.l0JZSince April 1996, the FDA reclassified Lindane as a second-line treatment for lice and scabies for patients who are intolerant of other treatments or who have not responded to other treatments.2
CONCLUSIONS The use of Lindane for scabies is not without potential complication. Although Lindane remains effective as an insecticide, its implied neurotoxicity has led many to advocate for the use of much safer products such as permethrin, which is 40 to 400 times less likely to cause toxic effects. Only if medically indicated, limited quantity of Lindane should be prescribed cautiously and under
BRIEF REPORTS
close monitoring. In addition, proper patient education must be given about its use and potential toxic effects. Patients should be made aware that the drug must not be shared with others and that a qualified medical evaluation is warranted before use to prove diagnosis and assess possible medical contraindications of therapy.l By following these preventive measurements, misuse, overuse, and even unintentional ingestion will be minimized, which will ultimately reduce the potential of morbidity and mortality.Jose ERICDiAZ, MD, Director. Medical lbxicology, Department of Emergency Medicine, Cooper Hospital1 University Medical Center. Camden, NJ
Keu words. Lindane (hexachlorocyclohexane); neurotoxicity; seizure; adverse drug reactions and interactions (side effects); insecticide; treatment.
References 1. Rasmussen JE. The problem of Lindane. Am Acad Dermatol. 1981; 5:50716. 2. Lindane. Clinical Pharmacology on Physicians' Online. Gold Standard Multimedia Inc. Copyright 1994- 1997 (http: Nwww.gsm.com). 3. Ginsburg CM, Lowry W, Reisch JS.
I
Absorption of Lindane (gamma benzene hexachloride) in infants and children. J Pediatr. 1977; 91:998- 1000. 4. Ellenhorn MJ. Pesticides: Organochlorines. Ellenhorn's Medical Toxicology-Diagnosis and Treatment of Human Poisoning, 2nd Ed. 1997, pp 155, 1625-6. 5. Davies JE,Dedhia HV, Morgade C, et al. Lindane poisonings. Arch Dermatol. 1983; 119142-4. 6. Solomon BA, Hault SR, Carr EM, et al. Neurotoxic reaction to Lindane in an HIV-seropositive patient-an old medication's new problem. J Fam Pract. 1995; 40:291-6. 7. Brown S, Becher J, Brady W. Treatment of ectoparasitic infections: review of the English-language literature, 19821992. Clin Infect Dis. 1995; 2O(suppl 1): S104-S109. 8. Fischer TF. Lindane toxicity in a 24year old woman. Ann Emerg Med. 1994; 24~972-4. 9. Carlton FB, Simpson WM, Haddad LM. Pesticides-Organochlorine Insecticides. In: Haddad LM, Shannon M W , Winchester JF (eds). Clinical Management of Poisoning and Drug Overdose, 3rd Ed. Philadelphia: W. B. Saunders, 1998, pp 841-2. 10. Rasmussen JE. Scabies. Pediatr Rev. 1994; 15:llO-4. 11. Zakhari S. Cardiovascular toxicology of halogenated hydrocarbon and other solvents. In: Acosta D (ed). Cardiovascular Toxicology. New York: Raven Press, 1992, pp 409-54. 12. Meinking TL, Taplin D. Safety of permethrin vs Lindane for the treatment of scabies. Arch Dermatol. 1996; 132: 959-62.
Testicular Infarction in a Patient with Epididymitis
Epididymitis is a n inflammation limited to the epididymis, occurring in approximately 1in 1,000 men per year.' I t is a common cause of acute scrota1 pain and edema.' Although this condition is often easily treated with antibiotics and analgesics, it may lead to more serious sequelae, including orchitis and abscesses. Testicular infarction, although rare, has been reported as a potential serious complication of epididymitk2 We discuss a case of testicular infarction due to unremitting epididymitis. CASE
REPORT
A 43-year-old white male presented to the ED complaining of a 2-day history of the gradual onset of left
I
groin and testicular pain radiating to his lower abdomen. The patient denied flank pain, hematuria, dysuria, penile discharge, trauma, fevers, chills, nausea, or vomiting. There was no prior history of testicular torsion. The patient stated that he had had unprotected sexual intercourse 3 weeks prior. He had a past history of hepatitis C. He denied IV drug use or prior sexually transmitted diseases. On presentation the patient was a well-developed male who appeared to be in mild discomfort particularly with movement below the torso. Vitals signs revealed a temperature of 98.2"F, pulse 94 beatdmin, respiratory rate 20 breathdmin, and blood pressure 142/88 mm Hg. Examination of the head, ears, eyes, nose, and throat was normal. Lungs were
ACADEMIC EMERGENCY MEDICINE
November 1998. Volume 5 . Number 11
clear and there were no audible cardiac murmurs. The abdomen was soft and nontender with normal bowel sounds. There was no costovertebral angle tenderness to percussion. Testicular examination revealed an edematous left testicle with severe tenderness to palpation. The epididymidscrotal sulcus was not palpable. The patient had a n equivocal Prehn's test with minimal cremaster reflex. There was no scrotal ecchymosis, penile lesions, adenopathy, or evidence of hernias. The patient underwent a color Doppler ultrasonography of the testes, which demonstrated severe epididymitis (Figs. 1 and 2). There was evidence of testicular venous outflow obstruction, with venous obstruction near the head of the epididymis and subsequent diminished flow through the left testicle. There was no evidence of testicular torsion. These findings were believed to be consistent with epididymo-orchitis. The patient was prescribed antibiotics (quinolone) and nonsteroidal anti-inflammatory drugs, and was instructed to elevate the scrotum, use cool compresses, and wear a scrotal support. The case was discussed with the urologist on-call, and follow-up was arranged. The patient returned 2 days later complaining of increased testicular swelling. The patient was admitted to the urology service and received IV antibiotics. The patient continued taking ceftriaxone and gentamicin for 48 hours, which was then changed to oral quinolone and doxycycline. Urine culture revealed no growth. On hospital day 4, the patient had improved, with less scrotal swelling and a nontender prostate. He was discharged to home. The patient returned 2 weeks later with persistent scrotal pain. A repeat color Doppler ultrasonography demonstrated an enlarged epididymis and absent flow to the left testicle and epididymis consistent with infarction (Figs. 3 and 4). The patient underwent left scrotal exploration, which revealed necrotic epididymis and testes; orchiectomy was performed. There was no testicular torsion. Pathologic examination demonstrated hemorrhagic infarction of the testes and epididymis, believed to be secondary to a smoldering chronic epididymitis with resultant vascular disturbance in the spermatic cord.
1129
Figure 1. Ultrasonogram showing infarcted epididymis (El.
Flaure 2. Color flow Doppler ultrasonogram showing mildly decreased testicular (TI flow ( U F F O W ) .
DISCUSSION
farction after epididymitis have been reported in t h e urologic literat~re.~+ The ~ true incidence of Epididymitis is a disease primarily this disease process is unknown and of adults and seldom occurs in pre- may be underestimated. pubertal boys. Chlamydia and gonTesticular infarction in this case orrhea are the most common epidid- was due to testicular venous outflow ymal pathogens in men younger obstruction from the significant epithan 35 years, whereas Escherichia didymal swelling. Four factors have coli, enterococci, Pseudomonas, and been postulated in contributing to Proteus are typically found in older this condition: 1) edema of the epimen.' Although most infections are didymis may compress adjacent limited to the epididymis, progres- veins draining the testes2; 2) inflamsion may occur, resulting in testicu- mation of t h e spermatic cord (fular or epididymal abscesses o r epi- niculitis) causes edema, which may didymo-orchitis. result in irreversible lymphatic, veTesticular ischemia secondary to nous, and eventually arterial obepididymitis is infrequently recog- struction of the spermatic vasculanized and rarely diagnosed in time turez; 3) vascular compression by to salvage the involved testes2 Mit- edema at the external inguinal ring temeyer et al. reported no cases of may occurs; and 4 ) bacterial toxins testicular infarction in a large series may contribute to the vascular (n = 610) of acute e p i d i d y m i t i ~ . ~thrombus by causing endothelial Nonetheless, cases of testicular in- damage.6
1130
BRIEF REPORTS
BRIEF REPORTS
matic cord that develops or persists during treatment of the epididymitis7; and 5)repeated febrile episodes while patients are taking suitable medications.6 When these findings are present, color flow Doppler should be considered to rule out testicular infarction. SUMMARY
To the authors' knowledge, this case
Ftgure 3. Ultrasonogram showing inhomogeneous testicular (T) echogenicity consistent with ischemia.
is unique to the emergency medicine literature. Although testicular infarction from epididymitis is rare, i t should be considered as a complication of severe or unresolving epididymitis. These patients should be daced on broad spectrum antibiotcs, i.e., quinolones; color flow Dopper of the testes should be obtained; Ind urologic consultation should be onsidered for possible admission Ind surgical exploration. -SEAN R. WE, MD, MARIA PELUCIO, MD, and ~ I C H A E L GIBBS, MD, Department f Emergency Medicine, Carolinas ledical Center, Charlotte, NC words. testicular; infarction; pididymitis; Doppler; ischemia; crotum.
ley
Zeferences 1. Drotman DP. Epidemiology and treat-
Figure 4. Color flow Doppler ultrasonogram showing absent testicular (T) ment of epididymitis. Rev Infect Dis. flow (arrow). 1984; 4(suppl):S788.
Color Doppler sonography has a n important role in evaluating cases of acute testicular ischemia by demonstrating decreased blood flow. Color Doppler sonography has replaced nuclear isotope scintigraphy in many institutions. Furthermore, it may allow differentiation between torsion and epididymitis, and can delineate a n epididymal abscess or malignancy. Testicular torsion is characterized by a global decrease in testicular flow.7 The hypoperfused testicle resulting from epididymitis has decreased flow to the testicle, whereas peripheral flow in the scrotum is i n c r e a ~ e d This . ~ has important implications since many patients who are eventually explored for persistent epididymitis and are found to have a necrotic testicle may be mistakenly given the diagnosis of missed torsion.' The onset of vascular compro-
mise, which typically occurs within 6 hours in testicular torsion, is difficult to recognize clinically in epididymitis. Several clinical findings may alert the clinician to the possibility of testicular infarction in the patient with epididymitis. These include: 1) severe unresolving epididymitis despite appropriate conservative treatment?; 2) testicular pain of sudden onset developing in patients who initially improved with antiobiticsl; 3) history of recurrent epididymitis in patients who have acute epididymiti~~; 4) tenderness and palpable thickening of the sper-
I I
2. Vordermark JS, Favila M. Testicular necrosis: a preventable complication of epididymitis. J Urol. 1982; 128:1322-4. 3. Mittemeyer BT, Lennox KW, Borski AA. Epididymitis: a review of 610 cases. J Urol. 1966; 95:390-5. 4. Kirk D, Binge11 JC, Feneley RCL. Infarction of the testis: a complication of epididymitis. Br J Urol. 1982; 54:311-2. 1. Costas S,Van Blerk PJP. Incision of the external inguinal ring in acute epididymitis. Br J Urol. 1973; 45555-8. 6. Renckien RK, Du Plesis DJ, De Haas LS: Venous infarction of the testis-a cause of non-response to conservative therapy in epididymolorchitis. S Afr Med J. 1990; 78:337-8. 7. Eisner DJ, Goldman SM, Petronis J, Millmond SH. Bilateral testicular infarction caused by epididymitis. AJR. 1991; 157~517-9.
The Effect of Heliox on Croup: A Pilot Study
In laryngotracheobronchitis (croup), the inflammation of the narrow subglottis may cause significant air-
I
I
way obstruction. Until the airway inflammation resolves, a fixed upperairway obstruction exists. Heliox
