Postoperative vision loss (POVL) is devastating not only for the patient but also
for the anesthesiologist. Posterior reversible encephalopathy syndrome (PRES) is an
infrequent and treatable cause of POVL, which is reported predominantly in rapid hemodynamic
perturbations, endothelial dysfunction, and massive volume resuscitation.[1]
[2] To our knowledge, there are no reported cases of PRES following acute hypertension
for a brief duration of 3 minutes and massive transfusion.
A 55-year-old female with a body mass index (BMI) of 21.82 kg/m2, belonging to the American Society of Anesthesiologists (ASA) physical status class
I, underwent posterior spine instrumentation (T8-L4) for correction of kyphoscoliosis.
She was positioned prone for 9 hours under general anesthesia on a conventional orthopedic
operating table, with soft chest and pelvic supports. Her head was positioned neutrally
on a doughnut, and eye compression was circumvented by periodic confirmation of adequate
periorbital space. Motor and somatosensory-evoked potential recorded no abnormal signals.
Anesthesia was maintained with propofol infusion (75–100 mcg/kg/min), fentanyl (0.5–1
mcg/kg/h), and isoflurane (end-tidal < 0.5%) to allow optimal neurophysiological and
entropy (target 40–60) monitoring. Normothermia was maintained. Ventilation was targeted
to an end-tidal carbon-dioxide of 30 to 40 mm Hg and oxygen saturation > 94%. Intraoperatively,
there was a drop in hematocrit to 25% from a baseline of 30%. Active resuscitation
with crystalloids and blood products was initiated immediately. During resuscitation,
there was a transient fall in arterial blood pressure (BP) to 70/40 mm Hg for 5 minutes.
Noradrenaline infusion was initiated at 0.02 to 0.04 mcg/kg/min. Subsequently, there
was an episode of acute rise of systolic BP to 190 mm Hg, presumably due to an inadvertent
bolus delivery of noradrenaline from the infusion pump. Noradrenaline was stopped
immediately and propofol bolus was administered. BP normalized to 120/80 mm Hg in
3 minutes, and remained within normal range thereafter. Five packs of red blood cells
(1250 mL), plasma (1000 mL), and 4000 mL of crystalloids were administered to cope
with the total blood loss of 2000 mL and urine output of 2000 mL. The hematocrit was
raised to 33% in the next hour. Due to prolonged prone positioning, postoperative
mechanical ventilation was planned, anticipating airway edema. Two hours after shifting
the patient to the postoperative unit, two episodes of generalized seizures occurred
and were treated with phenytoin (1 g intravenous [IV] followed by 100 mg IV tid) and
levetiracetam (500 mg IV bd). She had a persistent staring look. Blood sugar and electrolytes
were normal. CT brain ruled out cerebral hemorrhage and edema, which were suspected
due to the acute intraoperative hypertension and prolonged prone position.[3] On the first postoperative day, there were no seizures, and extubation of trachea
was done. Postextubation, she complained of painless vision loss bilaterally. Ophthalmic
examination revealed bilateral loss of light perception and impaired optokinetic nystagmus,
denoting a cortical pathology.[4] Fundus and light reflex were normal, indicating an intact pathway till midbrain.[5] Other causes of POVL like ischemic optic neuropathy (ION) and central retinal artery
occlusion (CRAO) were ruled out by the absence of relative afferent pupillary defect
and normal findings in fundus. The constellation of symptoms of seizures, altered
sensorium, blindness and the association with acute intraoperative hypertension, and
volume resuscitation directed toward the suspicion of PRES.[1]
[2] MRI of the brain ([Fig. 1A]
[B]) depicted typical bilateral symmetrical T2 hyperintensities in the watershed zones
of occipital and parietal lobes, confirming PRES. Mannitol (20 g IV tid), head-end
elevation, and antiepileptics were continued. On the third postoperative day, the
vision recovered completely, and she was discharged a week later.
Fig. 1 (A, B) MRI brain—fluid attenuation inversion recovery (FLAIR) sequence in axial plane,
showing hyperintensities in bilateral parietal and occipital lobes suggestive of posterior
reversible encephalopathy syndrome (PRES).
PRES is a vasogenic edema reported in cases of hypertensive emergencies, eclampsia,
renal failure, cytotoxic chemotherapy, immunosuppressants, transplant recipients,
and massive transfusion.[1]
[2] Gopalakrishnan et al have reported PRES following sustained elevation in blood pressure.[6] Singh et al reported PRES due to a sudden increase in blood viscosity following
rapid blood transfusion in cases of uterine fibroid with menorrhagia.[2] The endotheliopathy precipitated by acute hemorrhagic shock could lead to a disruption
in the blood-brain barrier (BBB). Although the exact pathophysiology remains unclear,
disruption of the BBB and fluid extravasation due to acute hypertension exceeding
the cerebral autoregulation threshold or endothelial dysfunction remains the most
accepted mechanism.[1]
[2]
[7] In our case, although the episode of hypertension was transient, the association
with endotheliopathy from rapid volume resuscitation could have been the precipitating
cause of PRES. The typical neuroradiological findings in MRI with bilateral and symmetrical
parieto-occipital involvement were consistent with the diagnosis of PRES. POVL following
spine surgery may result from CRAO, central retinal vein occlusion (CRVO), ION, cortical
blindness, PRES, acute glaucoma, or corneal abrasion. Most of the causes except ION
are potentially reversible if diagnosed and treated early. Having a low threshold
of suspicion is cardinal for expeditious treatment of the reversible causes and prevention
of permanent or secondary neurological injury.
