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Roy C. Watkins, MD, Edith L. Hambrick, MD, Miriam Martin, MD, and Michael Washington, MD Washington, DC

This case study describes a patient with multiple trauma associated with acute visual impairment. Funduscopic examination revealed scattered and confluent cotton wool exudates bilaterally. This retinopathy was first described by Othmar Purtscher, an Austrian ophthalmologist, in 1910, which he later referred to as "angiopathia retinae traumatica." (J NatI Med Assoc. 1993;85:557-559.)
Key words * trauma * retinopathy Purtscher's retinopathy * traumatic retinopathy * visual impairment

Patients with multiple blunt and penetrating trauma associated with internal organ injuries and fractures frequently present to the emergency department. However, trauma associated with visual impairment without severe, direct trauma to the maxillofacial or orbital areas is an unusual clinical finding. Studies by Holt et all have shown that 75% of ophthalmic injuries are associated with midfacial fractures and that 12% of these patients had severe visual impairment with 3% experiencing blindness in one eye.

A 27-year-old white male was brought to the emergency department by paramedics after he was knocked from his bicycle and hit by a van. After
From the Departments of Emergency Medicine and Ophthalmology, Howard University College of Medicine, Washington, DC. Requests for reprints should be addressed to Dr Roy C. Watkins, Medical Director, Providence Hospital of Cook County, 500 E 51st St, Chicago, IL 60615.

receiving the telemetry call, the trauma team was mobilized immediately. On admission, the patient was alert and oriented, and denied any loss of consciousness or retrograde amnesia. His Glasgow coma score was 15. His blood pressure was 130/70 mm Hg, his pulse was 84 beats/minute, his respiration was 18 breaths/minute, and his temperature was 99F The primary assessment revealed an alert patient without respiratory difficulty and a stable cardiovascular system. A large bore intravenous catheter was placed, blood was collected for laboratory tests, and an infusion of crystalloid was initiated. The secondary assessment revealed several minor contusions over the facial area. The pupils were equal, approximately 3 mm, and the patient was clinically blind in both eyes with a visual acuity <20/200 and was only able to detect light. A neurological examination revealed no focal findings. The quadriceps DTRs were 3 + equal, and the plantar reflexes were flexor. The examination of ears and mouth was unremarkable. There was a large 15 cm x 15 cm ecchymotic area over the midanterior aspect of the chest. Respirations were 18 breaths/minute and regular with normal breath sounds; no wheezing or rales were detected. The cardiac evaluation revealed S1 and S2 to be within limits. There was no cardiomegaly, gallops, rubs, or muffled heart tones. The patient's abdomen was flat, soft, and nontender. Bowel sounds were normal with no palpable masses. The genitalia appeared normal without evidence of trauma. The rectal examination revealed a 1 + prostate, and the stool guaiac was negative. An examination of the extremities revealed abrasions over the knees, with abrasions and deformity of the left shoulder area.


A funduscopic examination was performed by dilating the pupils with 1% tropicamide and 2.5% phenylephrine hydrochloride. The funduscopic examination revealed cotton-wool like exudates bilaterally without hemorrhages or papilledema. Because of the mechanism of injury, a cross-table lateral cervical spine radiograph was performed. No subluxation or fractures were rrevealed, and this was followed by a complete cervical spine series. After these radiographs were reviewed and found to be negative, radiographs of the skull, left shoulder, left scapula, and left clavicle were taken, as well as both knees and the right wrist. These studies revealed fractures of the left scapula and left clavicle. A computed tomography (CT) scan of the skull was negative. A CT scan of the abdomen and pelvis, using intravenous and oral contrast enhancement, also were negative. Because of the large contusion and ecchymotic area over the anterior aspect of the chest, arterial blood gases and additional radiography of the chest and sternum were taken. In addition, an ECG and echocardiogram were performed of the heart and aorta. Blood gases were within normal limits, the radiographs were negative, and the echocardiogram did not reveal any abnormal aortic dilatation, pericardial effusion, or abnormal cardiac wall motion. The creatinine kinase, MB fraction, was within normal limits. The patient's complete blood cell count, SMA-6, PT, and PTT profile were within normal limits, and the blood alcohol was 40 mg/dL. The patient was admitted to the medical intensive care unit. His hospital course was unremarkable. His visual acuity improved daily, and he was discharged on the third hospital day to be followed up in the orthopedic and ophthalmology clinics. The clinical diagnosis of multiple trauma included: minor facial trauma with facial abrasions; trauma to the chest, sternum, knees, right wrist, left scapula, and left clavicle; fractures of the left clavicle and left scapula; and Purtscher's retinopathy.

delayed4 and that visual impairment may be unilateral or bilateral. The prognosis is good, and sight gradually improves, returning to the pretraumatic visual acuity level in many cases. Purtscher2'3 theorized that this retinopathy was a result of an increase in the cerebrospinal pressure that was transmitted from the subarachnoid space to the optic nerve producing lymphatic stasis in the perivascular spaces of the retinal vessels. Fritz and Hogan5 described a patient with multiple fractures who also developed oval and round subretinal exudates but no hemorrhages. They attributed these findings to fat embolization. Similar funduscopic findings have been described in some patients with acute pancreatitis. Metastatic fat embolization to the fundus has been proposed as one of several mechanisms for this retinopathy.6 While most attribute these changes to fat emboli,7'8 others have attributed this retinopathy to increases in arterial hydrostatic or venous intravascular pressures.9'10 Purtscher's retinopathy may be the result of several pathophysiological processes. This pathologic process may occur immediately or may be delayed and is accompanied by a degree of visual impairment. Other studiesI 1'12 using fluorescein angiography have revealed early findings of capillary vessel leakage, blocked choroidal fluorescence, occluded retinal arterioles, and areas of capillary nonperfusion. Recent studies have demonstrated Purtscher's-like funduscopic changes after retinobulbar anesthesia.13 The work of Jacob et al'4 suggested this retinopathy also may be the result of complement-induced leukoembolization.

Patients brought to the emergency department with multiple trauma associated with acute visual impairment should have a complete eye examination. Patients with a mild degree of visual impairment may not be detected. To date, this retinopathy has not been linked to any significant pathophysiological process or complication such as metastatic pulmonary or cerebral fat embolization, and the prognosis is good. There are varying degrees of this retinopathy. In some cases, there are exudates while in other cases, there are exudates and hemorrhages accompanied by moderate to severe visual acuity losses. This retinopathy may represent an ophthalmologic syndrome induced by a variety of mechanisms, such as trauma, metastatic fat embolization, and complement-induced leukoembolization.

Purtscher initially described this retinopathy in a patient who had sustained head trauma accompanied by loss of vision.2 He later referred to this entity as "angiopathia retinae traumatica."3 In the case reported here, multiple oval white spots and intraretinal hemorrhages were observed in the posterior polar-region. Since the original description of this retinopathy, other studies have indicated that these funduscopic changes may occur early at the onset of the trauma or be


Literature Cited 1. Holt JE, Holt GR, Blodgett JM. Ocular injuries sustained during blunt facial trauma. Ophthalmology. 1983;90:14-18. 2. Purtscher 0. Noch Unbekannte befund, Nach Schadeltrahmer. Ber Deutch Ophth Ges. 191 0;36:294-301. 3. Purtscher 0. Angiopathia retinae traumatica Lymphorrhagien des augengrundes albrecht von Graefes. Arch fur Ophth. 1912;82:347-371. 4. Marr WG, Marr EG. Some observations on Purtscher's disease: traumatic retinal angiopathy. Am J Ophthalmol. 1 962;54:693-705. 5. Fitz MH, Hogan MJ. Fat immobilization involving the human eye. Am J Ophthalmol. 1948;31 :527-534. 6. Inkeles DM, Walsh JB. Retinal fat emboli as a sequela to acute pancreatitis. Am J Ophthalmol. 1976;80:935-938. 7. DeVoe AG. Ocular fat embolism; clinical and pathological report. Arch Ophthalmol. 1950;43:857-863. 8. Kearns TP. Fat embolism of retina. Am J Ophthalmol. 1956;41 :1-2. 9. Bedell AJ. Traumatic retinal angiopathy. Arch Ophthalmol. 1939;22:351-358. 10. Lyle DJ, Stapp JP, Bulton RP. Ophthalmologic hydrostatic pressure syndrome. Am J Ophthalmol. 1957;44:652-657. 11. Kelley JS. Purtscher's retinopathy related to chest compression by safety belts; fluorescein angiographic findings. Am J Ophthalmol. 1972;74:278-283. 12. Burton TC. Unilateral Purtscher's retinopathy. Ophthalmology. 1980;87:1096-1105. 13. Lemagne JM, Michiels X, Causenbroeck SV, Snyers B. Purtscher's-like retinopathy after retinobulbar anesthesia. Ophthalmology. 1990;97:859-861. 14. Jacob HS, Goldstein IM, Shapiro L, Craddock PR, Hammerschmidt DE, Weissman G. Sudden blindness in acute pancreatitis. Possible role of complement-induced retinal leukoembolization. Arch Intern Med. 1981;141:134-136.

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oin us In San Antonio this summer.

August 7-12, 1993
Attend the 98th Annual Convention of the National Medical Association and participate in our scientific sessions, special workshops and symposia, exhibits, and much more.

And while you're in San Antonio, visit the Alamo, stroll the River Walk, and visit the Mission San Jose.
For more information on how to register, contact:
National Medical Association 1012 Tenth St, NW Washington, DC 20001 (202) 347-1895