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Brown recluse spider bites to the head: three cases and a review.

Abstract

Consequences of envenomation from the bite of a brown recluse spider (Loxosceles reclusa) range from mild itching to death. The bite of this spider causes the most severe form of arthropod-induced tissue necrosis. These bites pose several challenges to the clinician in that diagnosis can be difficult, systemic manifestations can occur, and healing can be resistant to conventional measures. Bites to the head and neck--particularly the face--are uncommon, and they have not been widely reported in the otolaryngology literature. As experts in facial soft tissue, otolaryngologists and facial plastic surgeons should be able to recognize and treat these lesions. Because no laboratory test is available to identify the cause of symptoms in these cases, the diagnosis is made clinically. Early intervention can make a significant difference in cosmetic outcome, so a high index of suspicion is warranted. Local wound care includes rest, ice, compression, and elevation of the affected part of the body. Drug therapy with dapsone may limit the severity of the bite and prevent complications. Because some bites cause systemic loxoscelism, clinicians should be familiar with its manifestations. When necrosis occurs despite adequate medical treatment, reconstructive procedures should be delayed until healing is complete. We report 3 cases of brown recluse spider bites to the head. These cases illustrate the broad spectrum of the disease course, and they highlight the therapeutic challenges that these lesions pose.

Introduction

Consequences of envenomation from the bite of a brown recluse spider (Loxosceles reclusa) range from mild itching to death. Because no laboratory test is available to identify the spider's venom, the diagnosis is made clinically, based on a combination of signs, symptoms, and history. Most bites are benign, but approximately 10% become significant. (1) Scar formation appears to be more severe in areas that overlie fatty tissue, such as the eyelid. Distinguishing between patients who will develop a severe reaction and those who will not may be difficult, but appropriate intervention within the first few days can make a critical difference in outcome.

The appropriate form of local wound care of brown recluse spider bites has evolved in recent years, and it now includes the application of cool compresses rather than heat. The practice of removing toxin by curettage of the subcutaneous tissue has been discredited, particularly in cosmetically important areas such as the face. Systemic treatment is controversial. The leukocyte inhibitor dapsone probably limits the severity of the bite and prevents complications. Nevertheless, the side effects of dapsone can be severe, and care is warranted in its administration. Prolonged courses of dapsone are indicated under certain conditions. When dapsone therapy is anticipated, the patient's glucose-6-phosphate dehydrogenase (G6PD) level should be measured because patients who have a deficiency of this enzyme are more prone to develop hemolysis while taking dapsone. The ideal course of therapy is to intervene early enough to avoid tissue necrosis.

Despite adequate medical treatment, healing is problematic in some patients--that is, it is slow, often requiring several months. Hyperbaric oxygen therapy may play a role in treating long-standing lesions.

Reconstructive procedures are occasionally necessary. However, it is possible for pyoderma gangrenosum to develop in these wounds, and this can thwart attempts at reconstruction and even lead to a recurrence of lesions months alter the bite.

A significant number of bites are accompanied by a generalized reaction known as systemic loxoscelism. Systemic symptoms are not necessarily directly proportional to the severity of the skin lesion. The otolaryngologist should be aware of the systemic symptoms that might indicate systemic loxoscelism.

In this article, we report the cases of 3 women who experienced a brown recluse spider bite-one on the upper lip, one on the earlobe, and one on the eyelid. Each case illustrates a different presentation and clinical course. The first patient presented acutely and was treated with early, aggressive therapy, which precluded the need for surgical intervention. The second patient presented after several months and experienced the difficulty of a problematic, slowly healing wound. The third patient also presented in a delayed fashion, and she exhibited symptoms of loxoscelism and significant scarring.

Case reports

Patient 1. A 55 -year-old woman was bitten on her upper lip by a brown recluse spider while she was sleeping. Within hours, she developed swelling, redness, burning, itching, and heat in the area. An outside physician prescribed 25 mg/day of dapsone along with a course of cephalexin, and the patient began to improve.

Five days later, however, she was referred to our facility because the swelling, redness, and heat had recurred. She had no fever, hematuria, arthralgia, myalgia, or malaise. Physical examination revealed that the area of swelling, erythema, and heat, in addition to tenderness, extended across her upper lip and down her left cheek (figure 1, A). Her blood count and G6PD level were normal, so we increased the dapsone dosage to 50 mg twice daily. We also started her on a tapering dose of oral methylprednisolone sodium succinate, and we continued her antibiotic. Finally, we prescribed a twice-daily application of topical nitroglycerin, but we discontinued it after 2 days because it caused a headache.

[FIGURE 1 OMITTED]

Improvement was evident 2 days after her referral, although some tingling and numbness persisted. She continued to improve, and the dapsone and other drugs were stopped after 7 days (figure 1, B).

Patient 2. A brown recluse spider bit a 54-year-old woman on her left earlobe while she was sleeping on a piece of furniture that had been in storage until recently. She was treated at an outside facility with a cephalosporin, an antibiotic ointment, an anesthetic ointment, and an oral and a topical steroid.

Despite the intervention, the patient gradually began to lose part of her earlobe. Four months after the bite, she was referred to us for possible earlobe reconstruction. Her open wound site was characterized by persistent redness, severe pain, itching, and drainage (figure 2, A). She had also developed an extensive rash on her face, neck, and left arm, which was diagnosed as a contact dermatitis. Because she reported no other overt symptoms of systemic loxoscelism and because the bite had occurred 4 months earlier, we did not considerusing dapsone. Cultures yielded no growth. A biopsy indicated chronic inflammation of the skin and cartilage.

[FIGURE 2 OMITTED]

We started the patient on an oral cephalosporin and a topical antibiotic ointment, but she continued to complain of itching and pain. She was switched to an antihistamine and a topical steroid cream. Despite these measures, her ear cartilage continued to slowly deteriorate. Four weeks later, we started her on a 3-week course of hyperbaric oxygen therapy. After 2 weeks of oxygen, the wound stabilized. Over the following year, healing was slow and incomplete, and we prescribed another 3-week course of hyperbaric oxygen. By the end of this treatment, the patient's ear had completely healed. One year later, she remained completely healed, but she declined to undergo any reconstruction of her ear (figure 2, B).

Patient 3, A 39-year-old woman was bitten by what we assumed was a brown recluse spider on the left upper eyelid while she was exploring a cave. Coincidentally, she had undergone an uneventful bilateral upper blepharoplasty 3 months earlier. Within hours of the bite, blisters developed on the lid. The patient was evaluated in an emergency room, where the lid was incised and drained. She was given intravenous and oral antibiotics and followed up by an ophthalmologist, who noted persistent swelling. She was placed on a cephalosporin and a steroid.

Three weeks after the bite, the patient was referred to us for evaluation. She complained of pain and itching at the site of the bite, along with fatigue, malaise, arthralgia, nausea, and vomiting. The wound evidenced redness, drainage, and swelling, and there was a small central area of necrosis (figure 3, A). There was no hepatosplenomegaly, but a morbilliform rash developed over her extremities. She was admitted to the hospital for a further work-up. She underwent a G6PD measurement; pending the findings of this test, she was started on low-dose dapsone (25 mg/day). Although her G6PD level was reported as normal, she developed pancytopenia after 1 day of dapsone treatment. The reason for the pancytopenia was not clear, but the dapsone and the cephalosporin were discontinued. She exhibited no hemolysis or hematuria. A biopsy demonstrated chronic inflammation compatible with an arthropod bite.

[FIGURE 3 OMITTED]

The patient was discharged from the hospital, and treatment thereafter was supportive. She continued to complain of symptoms of loxoscelism (pain and itching at the site of the bite, and the fatigue, malaise, arthralgia, nausea, and vomiting), which waxed and waned during the next 3 months. She was started on hyperbaric oxygen therapy, and she began to slowly but progressively improve. After 20 sessions of oxygen therapy (6 months after the bite), the lesion healed, although there were residual scarring and tethering of the lid (figure 3, B). At that point, she was ready to undergo formal reconstruction of the eyelid.

Discussion

The brown recluse spider is also known as the necrotizing spider, fiddleback spider, and violin spider (on its dorsal cephalothorax is a violin-shaped mark). Its color varies from tan to dark brown (figure 4). The adult body is 8 to 9 mm long, and the length of its leg span ranges from 25 to 50 mm.

Brown recluse spiders are found predominantly in the Southern and Midwestern United States. (2) (Because they can travel in luggage, their bites may be seen in other parts of the world, as well.) These spiders are not aggressive, and they tend to avoid humans (noise scares them off), but they will bite when they are threatened or injured. They live in warm, dry places, either outdoors (under the bark of dead trees, under rocks, and in piles of lumber and firewood) or indoors (in dark isolated places such as attics). In fact, bites are more frequent during holidays when people take decorations out of storage. Many other victims are bitten while dressing in clothing that has been undisturbed for some time or when they roll over onto a spider that has crawled into a bed. (2,3)

Controlling infestations is difficult because these spiders can survive for 6 months without food or water and because chemicals strong enough to kill them are also hazardous to humans. (4)

Skin and soft-tissue reactions. The bite of the brown recluse spider causes the most severe form of arthropod-induced tissue necrosis. Its venom is made up of nine different proteins. (5) The primary factor responsible for tissue necrosis is sphingomyelinase. (6) This enzyme interacts with the membranes of erythrocytes, platelets, and endothelial cells. (7) Although sphingomyelinase D is toxic to many types of cell, significant tissue damage requires the participation of the host's own cells, particularly neutrophils and platelets. (8) Following envenomation, the initial injury is endothelial damage to the arterioles and venules, and these vessels become occluded with thrombi made up of neutrophils and platelets. The neutrophils then degranulate and secrete prostaglandin metabolites that contribute to more endothelial damage, which leads to thrombosis, ischemia, and necrosis.

Lysis of red blood cells also occurs to some extent, and it can result in anemia. A spreading circumferential zone of hemorrhage, stasis, and thrombi then moves throughout the fascial layer.

Brown recluse spider bites on the face are uncommon. In one series, only 3% of bites involved the face (only 5% involved the neck). (2) These bites generally go unnoticed at first, although some patients feel a transient stinging sensation. (9) In the 10% of patients who experience a serious reaction, symptoms usually begin in 6 to 12 hours. (1) If tissue changes do not occur by 48 to 96 hours, patients usually will not develop any significant necrosis.

The diagnosis of a brown recluse spider bite is made clinically on the basis of a constellation of signs, symptoms, and history suggestive of exposure to the spider. Diagnostic laboratory tests have been developed, but none is yet commercially available. (10)

There is no relationship between the initial size of the lesion and long-term effects, so all bites must be followed by qualified medical personnel. (11) Within hours, local findings may include itching, pain, swelling, redness, blisters, or pustule formation. (1) Pain is the most common symptom, and it is related either to ischemia secondary to vasospasm or to disruption by the toxin of myelin sheaths on nerve fibers. (12,13) Occasionally, pain becomes so severe that a sympathetic block is necessary. (14)

In cases of necrosis, patients typically develop a blister that becomes a dark-bluish macule; the macule then sinks below the level of the surrounding skin. (1,15) The blister may be surrounded by an ischemic ring that is in turn encircled by an erythematous ring (the "red, white, and blue sign"). (1) Five to 7 days later, the affected area becomes necrotic and eschar forms. The necrosis rarely involves deep fascial structures such as muscles, tendons, or ligaments. (3) The eschar later separates from the surrounding healthy tissue and sloughs, leaving an ulcer. Healing is slow, requiring 2 to 4 months. (15)

Scar formation appears to be more severe in areas overlying fatty tissue, such as the thighs, abdomen, and buttocks. (12) The eyelid, a thin layer of skin overlying a fat compartment, can be considered to be in the same category. (16) After her blepharoplasty, our patient 3 may have experienced a disruption of the fascial planes on a microscopic level, and this might have allowed for freer ingress of toxin into the fat.

Some patients have experienced persistent hypoesthesia or paresthesia, presumably as a result of the effect of sphingomyelinase D on myelin. (13)

The necrotic lesions of the brown recluse spider bite can mimic other diseases, including erythema chronicum migrans, Stevens-Johnson syndrome, Lyell's syndrome (toxic epidermal necrolysis), erythema nodosum, erythema multiforme, herpes simplex infection, purpura fulminans, diabetic ulcer, bedsore, poison oak and poison ivy reactions, gonococcal arthritic dermatitis, urticaria, pyoderma, and cellulitis. (2) If the skin becomes necrotic after 24 to 72 hours, many of these clinical possibilities can be ruled out. If the diagnosis is in doubt, an internal medicine or dermatology consult is indicated.

Management of skin and soft-tissue reactions. Obviously, the ideal scenario is that the practitioner intervene early enough to avoid any loss of skin and soft tissue. Systemic treatment is controversial.

Conservative management. The basic principles of local wound care for brown recluse spiderbites include rest, ice, compression, and elevation (RICE). Applying ice or cold packs to bite sites has been shown to significantly reduce inflammation and slow the evolution of the lesion. (17) On the other hand, applying heat to the site can worsen the situation by inducing the development of blisters, necrosis, or ulcerations. (17) Heat is believed to promote necrosis by potentiating the effects of sphingomyelinase D and lipase. (7)

Prophylactic agents. Prophylactic antibiotics are usually given to prevent secondary infection, although no clinical trials have addressed this specific issue. Antihistamines are administered mainly to relieve pruritus and swelling. Although corticosteroids have been used for their protective effects, they have not been shown to limit the amount of skin necrosis. (18) Aspirin or heparin may be given to counteract platelet aggregation and thrombosis, but their effect is also unproven.

Dapsone. Dapsone (4,4' diaminodiphenylsulfone) inhibits neutrophil migration and endothelial attachment, and it blocks neutrophil secretion of lysosomal enzymes. (19) Dapsone limits the severity of the bite reaction, promotes healing, and prevents complications. (20) There are case reports of patients who were treated with 50 to 200 mg/day of dapsone who experienced a marked decrease in pain, erythema, and induration. (21-23) To date, however, no double-blind, randomized trial has been conducted to compare dapsone and placebo in humans. When dapsone is used, therapy should be continued until the epidermis becomes contiguous and there is no further exudation. Sphingomyelinase D remains in the bite area for more than 3 weeks, so it might be necessary to continue dapsone for at least that long. (3)

Dapsone has many potential side effects, some of them dangerous. They include nausea, dizziness, fatigue, shortness of breath, skin rash, nervousness, toxic hepatitis, cholestatic jaundice, nephrotoxicity, and psychosis, particularly with prolonged therapy. (24-26) Hemolysis and agranulocytosis can occur during the first few days of treatment; as mentioned, hemolysis can also occur in patients with low levels of G6PD. Our patient 3 was forced to discontinue dapsone after 1 day because her hematocrit level fell, even though her G6PD level was normal. Patients on dapsone should undergo serial blood counts to monitor for hemolysis and leukocytopenia.

Hyperbaric oxygen. In an animal study, hyperbaric oxygen therapy was found to be ineffective in reducing lesion size unless the subjects were pretreated. (27) Nevertheless, hyperbaric oxygen was beneficial in 2 of our 3 patients, presumably because it promotes angiogenesis and the formation of granulation tissue in long-standing lesions.

Curettage. In one early series of patients with brown recluse spider bites, Hollabaugh and Fernandes advocated curetting the subcutaneous tissue in the necrotic area of the lesion to prevent the local destructive actions of the toxin. (28) However, curettage is no longer recommended. Rees et al compared early curettage with dapsone therapy and found that the dapsone-treated patients had a lower incidence of delayed wound healing, less need for subsequent surgical excision, a lower rate of hospitalization, and less objectionable scarring than did patients in the curettage group. (20) Another reason that early excision is not warranted is that it is usually difficult to determine exactly how big a lesion is. Therefore, it is now recommended that surgical excision for spider bites be reserved for those patients whose eschars are stable; stability typically occurs in 6 to 10 weeks. It is especially important to eschew curettage on the face, where scarring should be avoided or minimized.

Nitroglycerin. The use of topical nitroglycerin might be supported by the results of studies that have explored the benefits of nitric oxide in tissues, (2) but to date no trial has been conducted on humans with spider bites.

Healing of skin lesions. Healing is problematic in some patients. Until recently, we did not fully understand that venom factors can remain in bite lesions for a relatively long time or that a bite we are treating is actually a recurrence rather than the initial lesion. (29) In patients with more severe bites, eschar may take months to develop and the skin may take several months more to heal. (1) These wounds may progress to significant tissue loss and spreading of ulcerations.

Delayed wound healing can occur despite appropriate medical treatment. (29) Why bites do not promptly heal is not clear, but the persistence of venom in the wound or the generation of secondary inflammatory mediators may play a role. In one study of brown recluse spider bites, Rees et al reported that some patients who had received skin grafts experienced repeated graft rejections for no obvious reason. (29) Eventually, the authors realized that these patients had developed pyoderma gangrenosum. Our patient 2 developed contact dermatitis, which manifested as several satellite lesions on the face, neck, and arm. Although the diagnosis of pyoderma gangrenosum was not made in this patient, the persistent presence of venom or secondary inflammatory mediators may have provoked the dermatitis that she did develop. Pyoderma gangrenosum as a complication of brown recluse spider bites appears to be associated with predisposing factors such as surgery near the time of the bite or a personal or family history of rheumatoid arthritis, ulcerative colitis, or Crohn's disease. (1)

Recurrent lesions may arise months after the bite and in adjacent areas. (29) Hoover et al advocated life-long follow-up at 6-month intervals in such patients to look for the development of squamous cell carcinoma. (30) Because the clinical course of healing is so difficult to predict with any brown recluse spider bite, reconstruction should not be attempted until healing is complete.

Systemic reactions. Systemic loxoscelism is less common than skin necrosis. In one series of bites, the incidence of skin necrosis was 37% and the incidence of systemic illness was 14%. (9)

Systemic symptoms include fever, chills, malaise, nausea, vomiting, arthralgias, myalgias, headache, anorexia, abdominal pain, weakness, and convulsions. (1,12,15,31) Physical findings often include a morbilliform rash. (15) In more severe cases, shock may be present. As the toxin destroys blood cells, hemolytic anemia may ensue. Hemolysis may lead to hemoglobinuria, renal failure, and death. In rare cases, disseminated intravascular coagulation and thrombocytopenia have occurred. (31)

The severity of systemic symptoms is directly proportional to the amount of envenomation but not to the severity of the skin lesion. (32) Patients who are in poor physical condition, the immunocompromised, the very young, and the elderly may experience serious systemic reactions. (2,5) At least 8 presumed deaths have been reported secondary to hemolysis, disseminated intravascular coagulation, renal failure, or pulmonary edema. (3)

When systemic signs occur, they do so in 72 to 96 hours? Our patient 3 began to manifest signs and symptoms of systemic loxoscelism after several days, but they were not formally addressed until 3 weeks after the bite. Sphingomyelinase D is believed to be the primary cause of systemic reactions because it can affect sphingomyelin in many parts of the body, including the nerves, blood cells, and lungs.

Management of systemic reactions. Patients with systemic loxoscelism should have their complete blood count measured to look for evidence of thrombocytopenia, hemolysis, and leukocytosis. A high white blood cell count may indicate systemic involvement. A urinalysis should be performed to look for hemoglobinuria.

Patients suspected of having systemic loxoscelism may require hospitalization. In such cases, volume repletion should be maintained to promote a brisk urine output. (15) Transfusions of packed red cells, platelets, or plasma may be necessary. The use of steroids in these patients is controversial. One study indicated that prednisone, at a dose of 1 to 2 mg/kg/day for 2 to 4 days, may reduce hemolysis and protect the kidneys. (33)

References

(1.) Wilson DC, King LE, Jr. Spiders and spider bites. Darmatol Clin 1990;8:277-86.

(2.) Cacy J, Mold JW. The clinical characteristics of brown recluse spider bites treated by family physicians: An OKPRN Study. Oklahoma Physicians Research Network. J Fam Pract 1999;48:536-42.

(3.) Sams HH, King LE, Jr. Brown recluse spider bites. Dermatol Nurs 1999;11:427-33.

(4.) Hall RD, Anderson PC. Brown recluse spider bites: Can they be prevented? Mo Med 1981;78:243-4.

(5.) Bernstein B, Ehrlich F. Brown recluse spider bites. J Emerg Med 1986;4:457-62.

(6.) Forrester LJ, Barrett JT, Campbell BJ. Red blood cell lysis induced by the venom of the brown recluse spider: The role of spbingomyelinase D. Arch Biochem Biophys 1978;187:355-65.

(7.) Rees RS, Nanney LB, Yates RA, King LE, Jr. Interaction of brown recluse spider venom on cell membranes: The inciting mechanism? J Invest Dermatol 1984;83:270-5.

(8.) Patel KD, Modur V, Zimmerman GA, et al. The necrotic venom of the brown recluse spider induces dysregulated endothelial cell-dependent neutrophil activation. Differential induction of GM-CSF, IL-8, and E-selectin expression. J Clin Invest 1994;94:631-42.

(9.) Wright SW, Wrenn KD, Murray L, Seger D. Clinical presentation and outcome of brown recluse spider bite. Ann Emerg Med 1997;30: 28-32.

(10.) Barrett SM, Romine-Jenkins M, Blick KE. Passive hemagluttination inhibition test for diagnosis of brown recluse spider bite envenomation. Clin Chem 1993;39:2104-7.

(11.) DeLozier JB, Reaves L, King LE, Jr., Rees RS. Brown recluse spider bites of the upper extremity. South Med J 1988;81:181-4.

(12.) Wasserman GS, Siegel C. Loxoscelism (brown recluse spider bites): A review of the literature. Clin Toxicol 1979;14:353-8.

(13.) Gross AS, Wilson DC, King LE, Jr. Persistent segmental cutaneous anesthesia after a brown recluse spider bite. South Med J 1990;83: 1321-3.

(14.) Sams HH, Hearth SB, Long LL, et al. Nineteen documented cases of Loxosceles reclusa envenomation. J Am Acad Dermatol 2001; 44:603-8.

(15.) Hobbs GD, Harrell RE, Jr. Brown recluse spider bites: A common cause of necrotic arachnidism. Am J Emerg Med 1989;7:309-12.

(16.) Edwards JJ, Anderson RL, Wood JR. Loxoscelism of the eyelids. Arch Ophthalmol 1980;98:1997-2000.

(17.) King LE, Jr. Brown recluse spider bites: Stay cool. JAMA 1985;254: 2895-6.

(18.) Anderson PC. Necrotizing spider bites. Am Fam Physician 1982;26: 198-203.

(19.) Bernstein JE, Lorincz AL. Sulfonamides and sulfones in dermatologic therapy. Int J Dermatol 1981;20:81-8.

(20.) Rees RS, Altanbern DP, Lynch JB, King LE, Jr. Brown recluse spider bites. A comparison of early surgical excision versus dapsone and delayed surgical excision. Ann Surg 1985;202:659-63.

(21.) Rees R, Shack RB, Withers E, et al. Management of the brown recluse spider bite. Plast Reconstr Surg 1981;68:768-73.

(22.) King LE, Jr., Rees RS. Dapsone treatment of a brown recluse bite. JAMA 1983;250:648.

(23.) Rees R, Campbell D, Rieger E, King LE. The diagnosis and treatment of brown recluse spider bites. Ann Emerg Med 1987; 16:945-9.

(24.) Wesley RE, Ballinger WH, Close LW, Lay AM. Dapsone in the treatment of presumed brown recluse spider bite of the eyelid. Ophthalmic Surg 1985;16:116-17, 120.

(25.) Wille RC, Morrow JD. Case report: Dapsone hypersensitivity syndrome associated with treatment of the bite of a brown recluse spider. Am J Med Sci 1988;296:270-1.

(26.) Lang PG. Sulfones and sulfonamides in dermatology today. J Am Acad Dermatol 1979; 1:479-92.

(27.) Phillips S, Kohn M, Baker D, et al. Therapy of brown spider envenomation: A controlled trial of hyperbaric oxygen, dapsone, and cyproheptadine. Ann Emerg Med 1995;25:363-8.

(28.) Hollabaugh RS, Fernandes ET. Management of the brown recluse spider bite. J Pediatr Surg 1989;24:126-7.

(29.) Rees RS, Fields JP, King LE, Jr. Do brown recluse spider bites induce pyoderma gangrenosum? South Med J 1985;78:283-7.

(30.) Hoover EL, Williams W, Koger L, et al. Pseudoepitheliomatous hyperplasia and pyoderma gangrenosum after a brown recluse spider bite. South Med J 1990;83:243-6.

(31.) Arnold RE. Brown recluse spider bites: Five cases with a review of the literature. JACEP 1976;5:262-4.

(32.) Taylor EH, Denny WF. Hemolysis, renal failure and death, presumed secondary to bite of brown recluse spider. South Med J 1966;59: 1209-11.

(33.) Wasserman GS, Anderson PC. Loxoscelism and necrotic arachnidism. J Toxicol Clin Toxicol 1983-84;21:451-72.

From the Department of Otolaryngology--Head and Neck Surgery (Dr. Leach and Dr. Bassichis) and the Department of Ophthalmology (Dr. Itani), University of Texas Southwestern Medical Center, Dallas.

Reprint requests: Joseph Leach, MD, Department of Otolaryngology--Head and Neck Surgery, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390. Phone: (214) 648-2430; fax: (214) 648-9122; e-mail:joseph.leach @utsouthwestern.edu
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Author:Itani, Kamel
Publication:Ear, Nose and Throat Journal
Geographic Code:1USA
Date:Jul 1, 2004
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