Bilateral hyphemas as a result of air bag deployment

Bilateral hyphemas as a result of air bag deployment

CORRESPONDENCE 2. Jaworski A, Fischer R, Lippmann M: Boerhaave's syndrome: Computed tomographic findings and diagnostic considerations. Arch Intern M...

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2. Jaworski A, Fischer R, Lippmann M: Boerhaave's syndrome: Computed tomographic findings and diagnostic considerations. Arch Intern Med 1988;148:223-224 3. Waits HD: Postemetic hematomas: A variant of the MalloryWeiss syndrome. Am J Surg 1976;132:320-321 4. Atefi D, Homey JT, Eaton SB, et al: Spontaneous intramural hematoma of esophagus. Gastrointest Endosc 1978;24:172-174 5. Mion F, Bernard G, Valette PJ, et ak Spontaneous esophageal hematoma: Diagnostic contribution of echoendoscopy. Gastrointest Endosc 1994;40:503-505 6. Meier JH, Zeitlin JH, Smith MT: Post-sclerotherapy intramural esophageal hematoma: endoscopic and radiologic findings. Gastrointest Endosc 1992;38:102-103 (letter) 7. Furukawa H, Hara T, ['aniguchi T, et al: A case of spontaneous intramural hematoma of the esophagus. Gastroenterol Jpn 1993;28: 81-87 8. Murata N, Kuroda T, Fujino S, et al: Submucosal dissection of the esophagus: A case report. Endoscopy 1991 ;23:95-97 9. Han SY, McEIvein RB, Aldrete JS, et al: Perforation of the esophagus. AJ R Am J Roentgenol 1985; 145:537-540

PASTEURELLAMULTOCIDAAS A CAUSE OF ACUTE ADULT EPIGLOTTITIS To the Editor.'--Acute epiglottitis in the adult can be unpredictable, rapidly progressive, and quickly fatal. The most frequent bacterial agents are Haemophilus influenza type B, Streptocococcus pneumoniae, and Staphylococcus aureus. Viral agents have also been implicated. PasteureIla multocida is found naturally as part of the oral flora of many animals, including domestic dogs and cats. P multocida is commonly known to cause skin, bone, and joint infections due to animal bites, as well as upper respiratory tract, intraabdominal, and central nervous system infections in pet handlers with nonbite exposure. This report presents a nonbite exposure to P multocida resulting in bacteremia and acute adult epiglottitis. Report of a case. A 43-year-old woman arrived in the emergency department (ED) complaining of a mild sore throat for 2 days with an acute increase in pain, dysphagia, and odynophagia over the preceding 2 hours. The patient reported low-grade fevers and some difficulty breathing on the morning of presentation. There had been no known exposure to illness. The patient's medical history included migraine headaches, a tonsillectomy as a child, and a hysterectomy. She did not smoke and denied drug use. She was employed by an animal hospital and had a pet dog and cat. There were no bites reported. Vital signs on admission were: pulse, 127 beats/rain; blood pressure, 142/94 mm Hg; respirations, 32 breaths/rain and shallow; and temperature, 102.6°F (oral). Pulse oximetry was 96% oxygen saturation on ambient air. Physical examination noted an anxious white woman seated upright in the bed. The patient's voice was muffled and communication was difficult because of trismus and drooling. Oral examination found no tongue edema, symmetric tonsillar crypts, and a midline uvula. The pharynx was erythematous with no exudate. There were large, tender anterior cervical lymph nodes present bilaterally. The remainder of the physical examination was normal. A flexible nasopharyngoscope (NP scope) was used in the ED to visualize the epiglottis. A hugely edematous, erythematous epiglottis was discovered. The patient tolerated the NP scope well. An otolaryngologist was consulted and arrived shortly thereafter to evaluate the patient. Additional studies included a normal chest radiograph and normal electrocardiogram. Laboratory data included hemoglobin, 14 g; hematocrit, 42.4%; white blood cell count, 17,600/~JL; sodium, 136 mEq/L; potassium, 3.8 mEq/L; chloride, 101 mEq/L; carbon dioxide, 21 mEq/L; glucose, 128 mg/dL; blood urea nitrogen, 15 mg/dL; and creatinine, 0.9 mg/dL. Blood cultures and a throat culture were also obtained. The patient was given 10 mg


dexamethasone intravenously and 3.0 g ampicillin/sulbactam intravenously. The patient was admitted to the intensive care unit and experienced increasing respiratory distress. The patient was taken to the operating room and a tracheostomy was performed. Postoperatively, the patient did well and continued to receive antibiotics and steroids. On postoperative day 2, blood cultures (four out of four bottles) grew P multocida sensitive to ampicillin, ampicillin/ sulbactam, and cephalothin. The throat culture grew only normal oral flora. The patient did well and had her tracheostomy tube removed on postoperative day 6. The patient was discharged 2 days later. Blood and throat cultures are used to identify the causative organism in adult epiglottitis. The most common bacterial pathogens are H influenza type B, H parainfluenzae, S aureus, and gram-negative organisms. Viral pathogens have also been suggested. Candida albicans has been seen in immunocompromised patients) Throat cultures, although occasionally positive, frequently reveal only normal oral flora. P multocida infections typically follow animal bites or animal exposures. Nonbite exposures typically involve the respiratory tract, intraabdominal sites, or the central nervous system in those people who have frequent animal contact. Patients with nonbite exposure probably have nasopharyngeal colonization with spread from the upper respiratory tract to adjacent anatomic structures. 2 This patient, a 43-year-old animal hospital worker and pet owner, was likely exposed to P multocida both at home and at work. The patient had no bite exposure and describes herself as a "passionate animal lover," frequently allowing her dog and cat to lick her face and "kiss" her. It seems likely that through this repeated exposure, colonization of the upper respiratory tract occurred and subsequently the patient developed acute epiglottitis and an associated bacteremia. Acute epiglottitis in the adult population can rapidly compromise the airway and be quickly fatal or have a more indolent, less severe course. Although classic teaching suggests that H influenza type B is the most common cause, a number of diverse pathogens have been implicated. In this case, P multocida bacteremia from a nonbite exposure was the cause of epiglottitis in a middle-aged woman. WILLIAMA. JENKINS,MD Department of Emergency Medicine Westmoreland Regional Hospital Greensburg, PA

References 1. Walsh TJ, Gray WC: Candida epiglottitis in immunocompromised patients. Chest 1987;91:482 2. Weber DJ, Wolfson JS, Swartz MN, et al. Pasteurella multocida infections. Report of 34 cases and review of the literature. Medicine 1984;63:133-154

BILATERALHYPHEMASAS A RESULT OF AIR BAG DEPLOYMENT To the Editor." Though relatively uncommon, I ocular injuries in automobile collisions as a result of inflation of the "supplemental inflatable restraint," or "air bag," may be expected in greater numbers as the prevalence of vehicles equipped with such restraints increases. We present a case of a 22-year-old man who incurred bilateral gross hyphemas as the result of air bag deployment. Bilateral hyphemas have not been reported previously in this connection. A previously healthy unrestrained passenger in a single-vehicle straight-on impact with a curb at 25 miles per hour arrived in the emergency department by ambulance. He complained of bilateral



eye pain and an inability to see, which began immediately after the air bag deployed. The patient's only apparent injuries were to his face. He did not wear contact lenses or glasses; he believed his visual acuity to have been normal in each eye before the collision; he had consumed 65 ounces of malt liquor and fortified wine in the 3 hours before the collision. He recalled no burns and no powders or liquids having contacted his face or hands, except for the copious irrigation with normal saline he had received during transport. Assessment of vital signs revealed blood pressure of 166/90 mm Hg, pulse of 114 beats/rain, respirations of 24 breaths/rain, and temperature of 98.4°E He was awake and alert, tearful, anxious, and immobilized supine on a backboard with full spinal precautions. Examination of his head found numerous minor facial abrasions and contusions. There were shallow lacerations of the right eyebrow and fight upper eyelid, abrasions at the base of the nose without crepitation, and edema of the upper lip. Examination of the eyes was remarkable for clouding of the superior hemispheres of both corneas, with pink-tinged fluid visible in the anterior chambers. A small subconjunctivalhemorrhage was apparent in the left eye lateral to the cornea. Visual acuity was limited to light perception without the ability to detect hand motion with either eye. Direct and consensual reactivity in 3-ram, equal pupils was present; there was no afferent pupillary defect. Extraocular movements were intact to command. The fundi were difficult to visualize through the diffuse pink staining in the anterior chambers, but appeared normal with sharp optic disks. The ears revealed normal tympanic membranes without otorrhea. The nasal mucosa was without hemorrhage. There was neither rhinorrhea nor septal hematoma. The throat was clear. The remainder of the physical examination was normal; the cervical spine, chest, abdomen, and pelvis were cleared clinically. Irrigation of the eyes with normal saline via Morgan lenses was continued. The diagnosis of bilateral gross hyphemas with decreased visual acuity prompted immediate ophthalmologic consultation. Additional findings by the ophthalmologist included normal tear pH (-7.4) and bilateral linear abrasions on the inferior hemispheres of both corneas. Other causes of acute vision loss excluded by history and ophthalmologic examination were central retinal artery or vein occlusion, functional blindness, temporal arteritis, and retinal detachment. Maxillofacial computed tomography indicated orbits, globes, and extraocular musculature to be intact. Intraocular pressure was 23 mm in the right eye, and 22 mm in the left by applanation tonometry. The patient was admitted to the hospital. The hyphemas layered out to approximately 40% of anterior chamber volume, and resolved over a period of 4 days. Previous reports of eye injuries from air bags mention infrequent comeal-scleral injuries (including corneal abrasion, 2 corneal alkali keratitis, 3,4 corneal endothelial cell loss), hyphema, 5,6 infrequent vitreous hemorrhage and retinal detachment, 7-9 and infrequent orbital fractures.8 Hyphema, or blood extravasated into the anterior chamber of the eye, results from disruption of vessels in the iris or ciliary body. Often the blood layers because of gravity. Symptoms include pain, photophobia, blurring of vision, somnolence, or restlessness. Intraocular pressure increase can produce nausea and vomiting. Emergency department management includes keeping the patient supine with the head of the bed elevated at 30 to 45 degrees, covering the eyes with protective shields, and obtaining urgent ophthalmologic consultation. Aspirin and other platelet inhibitors should be avoided. Total hyphemas may require surgical evacuation. Complications include rebleeding (16% to 25% of cases, usually 2 to 5 days after injury when the initial clot retracts and loosens), blood pigment staining of the cornea which may persist for years, and secondary glaucoma. 1° Mydriasis and cycloplegia with anticholinergic medications help to prevent rebleeding by preventing movement of the injured iris or ciliary body. Intrave-

nous aminocaproic acid can prevent rebleeding by inhibiting fibrinolysis, thus slowing clot retraction and clot loosening. Air bags are round, rubber-lined nylon bags inflated by converting sodium azide to nitrogen gas. The bags are vented by exhaust ports or a porous panel on the back of the air bag module. An air bag inflates in less than 50 msec, and deflates in about 2 seconds) ,4 Air bags are estimated to provide a 28% reduction in driver fatalities compared to three-point restraints alone1°; similar reductions in fatalities may be expected for passengers as well. Suspicion of ocular injury associated with facial impact with an air bag should be high. Urgent ophthalmologic consultation is mandatory in cases of hyphema. JAMESW. ZACOVIC,MD TIMOTHYD. McGUIRK,DO KEVlNJ. KNOOP,MD

Department of Emergency Medicine Naval Medical Center Portsmouth, VA

References 1. Huelke DF, Moore JL, Ostrom MO: Air bag injuries and occupant protection. J Trauma 1992;33:894-898 2. Larkin GL: Airbag-mediated corneal injury. Am J Emerg Med 1991 ;9:444-446 3. Ingraham HJ, Perry HD, Donnenfeld ED: Air-bag keratitis. New Engl J Med 1991 ;324:1599-1600 4. Smally AJ, Binzer A, Dolin S, et al: Alkaline chemical keratitis: Eye injury from airbags. Ann Emerg Med 1992;21:1400-1402 5. Mishler K: Hyphema caused by air bag. Arch Ophth 1991;109: 1535 6. Lesher MP, Durrie DS, Stiles MC: Corneal edema, hyphema, and angle recession after air bag inflation. Arch Ophthalmo11993;111: 1320-1322 7. Rimmer S, Shuler J: Severe ocular trauma from a driver's side air bag. Arch Ophthalmol 1991 ;109:774 8. Scott IU, John GR, Stark W J: Airbag-associated ocular injury and periorbital fractures. Arch Ophthalmol 1993; 111:25 9. Whitacre MM, Pilchard WA: Air bag injury producing retinal dialysis and detachment. Arch Ophthalmol 1993;111:1320 10. Antosia RE, Partridge RA, Virk AS: Air bag safety. Ann Emerg Med 1995;25:794-798

TRANSLARYNGEALGUIDED INTUBATIONIN THE AIRWAY OF A PATIENTWITH ACUTE GASTROINTESTINAL HEMORRHAGE To the Editor:--We report a case of a patient with acute gastrointestinal hemorrhage who was very agitated and needed heavy sedation to facilitate diagnosis and treatment. To prevent aspiration during massive bleeding, the airway was eventually secured by translaryngeal guided intubation (TLI).I A 47-year-old man with acute gastrointestinal hemorrhage was admitted to the medical intensive care unit for resuscitation and treatment. He was pale and frightened, extremely agitated, and having constant hematemesis. His pulse was weak, with a rate of 124 beats/rain and his blood pressure was 78/56 mm Hg. The lungs were clear to auscultation, and heart examination showed no abnormal findings. Anesthesiology services were called to help in securing the airway so that the intensivist would be able to safely sedate/paralyze the patient. Blind nasal intubation failed, and several attempts made the patient more agitated and combative. We eventually employed a somewhat invasive technique--TLI--to solve the problem. After skin preparation with 7.5% providone-iodine (Betadine; Purdue Frederick, Norwalk, CT) and local anesthetic infiltration using 1.0 mL of 0.5% lidocaine (Xylocaine; Astra USA, Inc, Westborough, MA), an 18-gauge thin-wall intravenous needle/ catheter was inserted cephalad into the larynx via the cricothyroid