Alkinoos Athanasiou, Ioannis Balogiannis, Ioannis Magras
  1. Department of Neurosurgery, AHEPA, University General Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece
  2. Lab of Medical Physics, Faculty of Medicine, School of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece

Correspondence Address:
Alkinoos Athanasiou
Department of Neurosurgery, AHEPA, University General Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece


Copyright: © 2017 Surgical Neurology International This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article: Alkinoos Athanasiou, Ioannis Balogiannis, Ioannis Magras. Lasting bilateral mydriasis after traumatic brain injury may not always be a lost case. 26-Sep-2017;8:229

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Background:Lasting bilateral mydriasis and absence of pupillary light reflex following severe traumatic brain injury (TBI) are considered signs of irreversible brainstem damage and have been strongly associated with poor outcome.

Case Description:A young female patient presented with severe TBI, contusions, and diffuse brain edema. She was initially treated medically, but developed delayed secondary refractory intracranial hypertension and bilaterally dilated, non-reactive pupils for 12 h. Wide decompressive craniectomy and dural incisions were performed. The patient presented gradual improvement in her clinical condition [Glasgow Coma Scale (GCS) 13/15]. Delayed recurring infections lead to the patient's death due to sepsis after 3 months.

Conclusion:In light of recent studies, lasting bilateral mydriasis may not always be considered a decisive factor for non-escalation of treatment, as variability among TBI patients and outcomes has been demonstrated. Wide decompressive craniectomy is viable for controlling refractory intracranial hypertension in hemodynamically stable patients.

Keywords: Brain edema, decompressive craniectomy, dilated pupils, intracranial hypertension, traumatic brain injury


Lasting bilaterally dilated and unreactive pupils after a severe traumatic brain injury (TBI) are usually considered a sign of irreversible brainstem damage and have been strongly associated with a very poor outcome (death, vegetative state, or severe disability) in the majority of patients.[ 2 4 5 10 ]

A mark of 6 h of lasting bilateral mydriasis has been considered an almost definite prognostic factor for mortality of those patients;[ 15 ] although, in general, some degree of variability of TBI outcomes has been also demonstrated, especially with regards to children and younger patients.[ 1 ]

Hereby, we present a case of short-term recovery by a young patient that presented secondary intracranial hypertension following TBI and was treated with decompressive craniectomy after 12 h of fixated dilated pupils. We discuss on the possible significance of this previously unreported, to our best knowledge, outcome.


A 19-year-old woman was admitted comatose at the Emergency Department after a fall from a motorbike (reported low speed but no helmet) with severe TBI. She presented with a GCS of 5/15 (by component: Eyes 1, verbal 2, and motor 2) and 3 mm non-reactive pupils bilaterally. The computed tomography (CT) brain scan at admission showed few left frontal and temporal contusions, a small left frontal epidural hematoma and diffuse brain edema [ Figure 1 ] and the decision was for nonsurgical management.

Figure 1

Brain CT scan at admission, showing contusions at left frontal and temporal lobes and diffuse brain edema area


The patient was intubated and admitted to the intensive care unit (ICU) after placement of an intraparenchymal catheter for measuring and managing of intracranial pressure (ICP) [ Figure 2 ]. The patient was treated conservatively and her condition remained stable with ICP readings of 7–17 mmHg for the following 6 days.

Figure 2

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


On the afternoon of the 7th 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). Initial decision was for conservative treatment using mannitol, hyperventilation, and barbiturate coma that controlled the ICP in a range of 17–27 mmHg, but[ 4 ] despite that, mydriasis was resistant for >12 h. A reassessment of the patient's condition led to a decision for a final attempt at salvaging the patient by performing decompressive craniectomy.

The pupils were checked immediately before the operation, but no recovery was observed. 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. 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. Furthermore, due to excessive swelling of the underlying brain, we decided to perform dural incisions instead of flap durotomy [Figures 3 and 4 ].

Figure 3

Intraoperative photo of the patient's brain (swollen) immediately after the craniectomy, before dural incision. Despite the wide craniectomy and decompression our impression was that dural opening would cause bilateral encephalocele, so the decision was to perform multiple dural incisions instead


Figure 4

The craniectomy parts resynthesized: six burr holes were used in total and the bone was cut parallel to the sagittal venus to avoid injury. Care was taken in adequately decompressing the temporal and parietal lobes


While immediately postoperatively the patient pupils did not change, the patient's condition presented gradual improvement over the period of the next 3 weeks. She was able to be decommitted from mechanical ventilation, be transported back to the neurosurgical ward and commence physiotherapy, and active kinesiotherapy. The patient's tracheostomy was removed and the patient's outcome at 1 month post-injury was at Glasgow Outcome Scale (GOS) 4 (moderate disability), reaching a GCS of 13/15 (by component: eyes 4, verbal 3, and motor 6). A 1-month post-injury magnetic resonance imaging (MRI) scan also showed significant improvement of the intracranial lesions [ Figure 5 ].

Figure 5

T1-weighted axial MRI scan + gd enhancement, one month post-injury, showing significant improvement of brain edema and haemorrhagic lesions


The patient's significant improvement was halted by complications in the form of delayed recurring refractory infections (pulmonary and systematic sepsis) and her clinical status gradually deteriorated, leading to her death due to sepsis after 3 months (ultimately GOS 1) despite combined management with the hospital's infections team.


Lasting bilaterally fixated pupils has been proposed as a decisive factor for non-escalation of treatment.[ 2 ] 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. 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.

A known study has evaluated the effect of mydriasis duration on the outcoume of TBI patients treated with craniotomy.[ 15 ] 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.[ 15 ] 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.

The aggressive surgical management (wide decompressive craniectomy) has been shown to benefit patients with delayed or refractory intracranial hypertension after severe TBI,[ 6 7 8 9 14 17 ] but mydriasis with absence of light reflex is still associated to poor results.[ 13 ] Early intervention has shown promising results and should be preferred.[ 12 15 ] Younger patients still seem to benefit the most from decompressive craniectomy.[ 11 16 18 ]


The presence of lasting bilateral mydriasis should not always be considered a decisive factor for non-escalation of treatment.[ 3 ] Variability among TBI patients and outcomes has been demonstrated and should be taken into account, especially for younger patients.[ 1 ] Wide bi-fronto-parieto-temporal decompressive craniectomy is a viable option for controlling refractory intracranial hypertension and its secondary effects in hemodynamically stable patients.[ 9 ]

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