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Blindness Due to Anterior Ischemic Optic Neuropathy in a Burn Patient
Anterior ischemic optic neuropathy (AION) is a process limited to the anterior neural pathways of the visual sense, as opposed to injuries affecting the posterior pathways (the occipital lobe). Arteritic AION is usually due to giant cell arteritis. Nonarteritic AION is generally diagnosed in elderly patients with diabetes, hypertension, coronary artery disease, or chronic renal failure.
There are numerous reports on the association between visual loss and surgical procedures involving the orbital floor or the zygomatic bone.4–6 The loss of vision in these cases is due to optic nerve injury or increased intraocular pressure resulting in ischemia of the optic nerve.
Other surgical procedures not directly damaging the optic nerve may also cause AION, such as coronary bypass surgery,1,3 bilateral radical neck dissections,7 hemodialysis,2 hip surgery,8 and lumbar spine surgery.9 The cause of postoperative AION in these instances has been thought to be related to hypotension, hemorrhage, and positioning.9–13 AION is a previously unrecognized cause of blindness in the trauma victim.
A recent study reported 9 patients with AION among 350 trauma patients requiring massive fluid resuscitation.14 These patients had evidence of global hypoperfusion, systemic inflammatory response syndrome, massive resuscitation, and high ventilatory support requirements.
We here report the case of a 27-year-old burn patient suffering a burn injury involving 85% of his body surface area (BSA) (60% full-thickness), who developed bilateral blindness due to AION. To our knowledge, this is the first report of AION in a burn patient.
CASE REPORT
A 27-year-old male was admitted to our intensive care burn unit (ICBU) after having suffered massive burns in an industrial fire. The patient was intubated on the scene and fluid resuscitation was started. On admission, blood pressure was 99/59 mm Hg, heart rate 117 bpm, and temperature 35.1°C. BSA burned was 85% (60% BSA full-thickness).
Mechanical ventilation, sedation, analgesia, and early enteral nutritional support were administered. A fiberoptic bronchoscopy revealed inflammatory signs in the lower airway. The patient continued to receive fluid therapy titrated to the urine output. During the first 48 hours after admission, 42 liters of crystalloid were administered to maintain hemodynamic stability.
Despite the administration of large amounts of fluids, the patient required noradrenaline to maintain blood pressure.
Because of a concern of fluid overload, a pulmonary artery catheter was inserted. Forty-eight hours after admission systemic arterial pressure was 132/80 mm Hg, pulmonary arterial pressure 28/17 mm Hg, right atrial pressure 4 mm Hg, pulmonary artery occlusion pressure 6 mm Hg, and cardiac output 7 liters/min.
During his prolonged ICBU stay, he developed a number of complications, including hypothermia, several episodes of sepsis and shock, renal failure, and thrombocytopenia.
He remained hypothermic on admission (temperature _35.5°C) for 5 hours, and on 26 more days, during a total of 135 hours until postburn day (PBD) 92. He required noradrenaline to maintain blood pressure during 40 days (from PBD 46 to PBD 86).
Invasive monitoring reasonably ruled out hypovolemia as the cause of shock and cardiovascular parameters were consistent with a normal blood volume. He developed pneumonia and bacteremia due to methicillin-resistant Staphylococcus aureus, and burn wound infection due to Pseudomonas aeruginosa. He also presented nonoliguric renal failure (creatinine _ 2.0 mg/dL, due to sepsis and nephrotoxic agents, for 11 days), thrombocytopenia, and ileus, requiring parenteral nutrition for 62 days despite the insertion of a nasojejunal tube.
He never had significant gas exchange impairment (PaO2/FIO2 _ 200 at all times). He did not present signs of abdominal compartment syndrome, such as high airway pressures, abdominal distension, or oliguria.
He was operated on 12 times. Due to grafting procedures on the back, repeated several times due to wound infection and graft failure, he was in prone position during 26 days (from PBD 25 to PBD 28, from PBD 37 to PBD 45, and from PBD 72 to PBD 89).
Serial ophthalmologic examinations were performed during the postburn period. Palpebral edema and corneal exposure were diagnosed on PBD 16, and corneal ulcers due to corneal exposure on PBD 47.
CASE REPORT
With appropriate treatment and supportive measures, the patient overcame all trauma-related complications, and sedation and analgesia were finally discontinued on PBD 114 to wean the patient off the ventilator.
He was extubated on PBD 137. When the patient was able to communicate, it was noted that he was unable to look at close objects. Bilateral nonreactive mydriasis was first noted on PBD 141. A funduscopic examination revealed signs of bilateral optic atrophy, with spared vasculature and arterial narrowing in the right eye, and white vascular cords in the left eye.
A CT scan of the head showed no evidence of cerebral infarction. He was discharged to the ward, where he continued the recovering phase. He was discharged from the hospital with complete visual loss.
DISCUSSION
There have been very few reports on the association between trauma and blindness.15,16 One case of trauma-induced AION was reported in the German literature at the beginning of the last century,15 and another case was reported in the British literature in 1949.16
A recent study reported 9 patients with AION among 350 trauma patients requiring massive resuscitation (_20 liters over the first 24 hours), having excluded patients with head trauma, facial fractures, or direct orbital injuries.14 In five cases, blindness was unilateral. All nine patients had evidence of global hypoperfusion, systemic inflammatory response syndrome, massive resuscitation, and high ventilatory support requirements. Six patients developed severe abdominal compartment syndrome.
The mechanism or mechanisms involved in the development of AION in trauma patients are unknown. The common denominator of AION after trauma seems to be a severe inflammatory response syndrome after profound hemorrhagic shock and massive volume resuscitation,14 accompanied is some cases by abdominal compartment syndrome.
The increase in intraabdominal pressure is known to be associated with intracranial hypertension.17 Although the impact of venous hypertension on optic nerve perfusion is speculative, increased intracranial pressure may compromise the optic compartment and contribute to the pathogenesis of AION.
Hypothermia, in addition to its impact on the coagulation cascade, alters red blood cell rheology and increases serum viscosity, and may also contribute to optic nerve ischemia.
Anatomic variations could predispose to optic nerve ischemia under certain circumstances. In a series of patients with AION it was reported that the cup-disc ratio was lower in the affected aye as compared with the healthy eye or with other causes of blindness.18 It was postulated that crowding of the optical nerve fibers within the optic canal, caused by resuscitation-induced edema, or a small scleral canal at the lamina cribrosa, produces venous outflow obstruction and increases pressure within the optical nerve.
The low incidence of AION among trauma patients as well as the high incidence of monocular presentation suggests that anatomic variations may be a major contributor to the development of AION.
It has been reported that prone positioning was common among patients developing AION in trauma victims.14 Prone positioning increases intraocular pressure, as seen in patients who develop AION after spinal surgery.9 Increased intraocular pressure reduces perfusion of the pial arteries resulting in local ischemia of the optic nerve head.
There are very few reports of visual loss in burn victims. Jie et al. reported the case of a 2-year-old girl (BSA burned 22%) who had a sudden visual loss on PBD 15.19 Pupillary responses, corneal reflexes, and the optic fundi were normal.
The definitive ophthalmologic diagnosis of this case was not reported and the visual loss improved over time. The authors speculated that blood supply to the cerebral cortex could have been inadequate during the shock phase after burn trauma.
The same report19 describes the additional case of a 2-year-old girl with burns over 20% of her BSA, who was first noted to be deaf and unseeing 3 weeks after trauma. Eye examination revealed that pupils reacted to light and the fundi were normal, as well as the cerebral pathways.
Sight commenced to return 4 months after injury, and recovery was complete shortly thereafter.
The clinical findings of those cases19 is not consistent with the diagnosis of AION, as pupillary response and corneal reflexes were normal, no abnormality was seen on funduscopic examination, and visual loss was transient. Thus, the case we report here is to our knowledge the first description of AION in a burn victim. Our case met a large number of the proposed risk factors for the development of AION in trauma patients, including massive fluid resuscitation, prone positioning, and hypothermia. He did not have abdominal compartment syndrome, suggesting that factors related to systemic hypoperfusion, shock, and probably prone position may be more relevant than intraabdominal hypertension for the development of AION in this case.
This case suggests that certain burn victims may be at risk of developing AION and irreversible visual loss.
Whether massive fluid resuscitation, abdominal compartment syndrome, hypothermia, and prone positioning are factors associated with AION requires further studies.
From the Servicio de Cirugía Plástica (A.V.), Servicio de Cuidados
Intensivos y Unidad de Grandes Quemados (J.A.L.), and Servicio de Oftalmología
(M.-L.B., Y.G.), Hospital Universitario de Getafe, Madrid, Spain.
Address for reprints: Alfonso Vallejo, MD, Servicio de Cirugía Plástica,
Hospital Universitario de Getafe, 28905 Madrid, Spain;
REFERENCES
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Source: The Journal of TRAUMA Injury, Infection, and Critical Care
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