An injury, illness, or drug can also cause your pupils to dilate.īoth prescription medications and intoxicating, recreational drugs can cause your pupils to dilate. If you have healthy eyes, your pupils will dilate in the dark, pulled open by muscles in the iris of your eye, to allow more light to reach your retina so you can see as clearly as possible. Mydriasis is the medical term for dilated pupils, a condition that can be temporary or long term. Younger patients still seem to benefit the most from decompressive craniectomy.Dilated Pupils: What Drugs Cause Changes in Your Eyes? Early intervention has shown promising results and should be preferred. The aggressive surgical management (wide decompressive craniectomy) has been shown to benefit patients with delayed or refractory intracranial hypertension after severe TBI, but mydriasis with absence of light reflex is still associated to poor results. Nonetheless, the authors report that increasing age predisposing to worse outcome and increased mortality, while more than 50% of patients under 20-year-old (regardless of duration of mydriasis) recovered to be independent. In that series no patient presented dilated pupils for more than 9 h and no patient that was operated after 6 h with fixed dilated pupils survived. Long-term outcome was still negative, but we believe that our intervention was justified by the facts that non-neurological complications were the reason for the patient's death and she presented such an impressive short-term improvement.Ī known study has evaluated the effect of mydriasis duration on the outcoume of TBI patients treated with craniotomy. In our case, the young age of the patient and the relatively controllable range of ICP (17–27 mmHg) counted towards attempting further escalation with surgical treatment. Lasting bilaterally fixated pupils has been proposed as a decisive factor for non-escalation of treatment. Furthermore, due to excessive swelling of the underlying brain, we decided to perform dural incisions instead of flap durotomy. No bony bridge was left above the superior sagittal sinus in the area of the craniectomy undercutting and smoothing was also performed at the edge of the parietal bone. The patient was then operated using a wide decompressive craniectomy that encompassed bilaterally frontal and temporal areas, and extended as far as possible in the parietal bone. The pupils were checked immediately before the operation, but no recovery was observed. A reassessment of the patient's condition led to a decision for a final attempt at salvaging the patient by performing decompressive craniectomy. Initial decision was for conservative treatment using mannitol, hyperventilation, and barbiturate coma that controlled the ICP in a range of 17–27 mmHg, but despite that, mydriasis was resistant for >12 h. On the afternoon of the 7 th post-injury day, while in ICU care, the patient presented an increase in ICP (>25 mmHg with surges of >30) and bilateral non-reactive mydriasis (7 mm). Brain CT scan 24 h post-admission, showing the small left frontal epidural hematoma, slight improvement of brain edema and the tip of the ICP catheter
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