1Neuro Intensive Care Unit, 2 Department of Ophthalmology and 3Nuffield Department of Anaesthetics, Radcliffe Infirmary, Oxford OX2 6HE, UK*Corresponding author
Accepted for publication: January 4, 2001
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Abstract |
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Br J Anaesth 2001; 86: 71720
Keywords: brain, brainstem death; eye, pupillary reflex
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Introduction |
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Case report |
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On admission, she was unresponsive to command with a Glasgow Coma Score of 4/15, and required immediate tracheal intubation and mechanical ventilation of the lungs. The left pupil was fixed and dilated and the right pupil mid-dilated and reacting sluggishly to light. A computed tomography (CT)-scan showed a large left subdural haematoma with significant midline shift (Fig. 1). Mannitol and vitamin K were administered and she was referred to a regional neurosurgical centre.
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After excluding potentially reversible causes for coma, the first set of brainstem death tests were performed approximately 6 h after admission. All the brainstem reflexes as laid down in the UK guidelines14 were absent apart from the pupillary responses: the pupils were recorded as reacting to light with a consensual response. It was decided to re-test the patient after a 12 h interval. On re-testing, the pupils were found to be active, but not in response to light. They were continuously observed for a period of 10 min and recorded on video. The pupils were mid-dilated and unequal, with the left pupil being larger. They displayed continuous and independent cyclical constriction and dilatation. The constriction phase lasted 2.5 s, and the dilatation phase 10 s, giving a periodicity of 5 min1, which was unrelated to ambient light. At the time when one pupil was constricted, the other pupil was almost maximally dilated and vice versa (Fig. 2). No mydriatics had been used at any point. An EEG showed no cerebral activity, even during stimulation. Subsequently, two further sets of brainstem tests were performed and the patient was declared brainstem dead more than 24 h after the first set of brainstem death tests. Throughout this period, the pupils remained active, but unresponsive to light. The patients organs were used for transplantation. Post-mortem examination revealed a 200 ml subdural haematoma over a swollen left cerebral hemisphere with cerebellar tonsillar herniation and necrosis.
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Discussion |
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To make the diagnosis of brainstem death, a three-stage procedure must be applied. First, certain preconditions must be met showing the patient suffers from a condition that has led to irremediable brain damage. Second, reversible causes of coma such as drug intoxication, hypothermia, metabolic, and endocrine disturbances must be excluded. Third, the absence of brainstem reflexes including the pupillary response to light must be demonstrated.
The bulk of the cranial nerve nuclei lie in close proximity to each other in the brainstem allowing for testing of this structure level-by-level (Fig. 3).5 The ultimate test of brainstem function is the test for apnoea. If no respiratory effort is seen with a PaCO2 >6.65 kPa (50 mm Hg), it can be assumed the patient is brainstem dead. It is recommended that the tests are carried out twice, usually a few hours apart. Such tests, by virtue of their simplicity, objectivity, and reproducibility have served to remove ambiguity from a situation fraught with emotion and potential controversy.
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In alcoholics, a coagulopathy is a well-recognized phenomenon.6 Traumatic head injuries also are often associated with clotting abnormalities. Clotting studies in the context of head injuries are a useful predictor of outcome, with prolongation or shortening of the APTT correlating strongly with death but prothrombin time proving to be of little prognostic value.7 8 This was borne out by this case where the APTT was 87 s (control 40 s) and INR 3.3 but with a platelet count within normal limits. In this patients previous admissions, in spite of significant liver dysfunction, her APTT and INR were within the normal range. The coagulopathy was corrected with the administration of fresh frozen plasma.
This patient presented a dilemma. She fulfilled the preconditions and exclusions for brainstem death. There was an absence of cranial nerve and respiratory function but in spite of this, spontaneous pupillary activity was still evident. The pupillary signs raised two important questions. What was the mechanism of the phenomenon, and what were the implications for the diagnosis of brainstem death? The pupillary response to light requires the presence of an intact reflex arc that passes through the brainstem (Fig. 4). The afferent component is the anterior visual pathway from which fibres pass to synapse in the pretectal nucleus in the mid-brain. The efferent fibres pass to the Edinger-Westphal subnucleii of the oculomotor nerve nucleus, explaining why a bilateral direct and consensual light response is seen when light is shone into one eye. The efferent parasympathetic fibres are a component of the oculomotor nerve, which synapse in the ciliary ganglion in the orbit with the post-ganglionic fibres supplying the pupillary sphincter. A lesion of the efferent pathway results in loss of all ipsilateral pupillary responses, and the pupil is mid-dilated and fixed. Total absence of response to light can occur with total disruption of either afferent or efferent pathways, and with brainstem damage.
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We cannot, therefore, fully explain this phenomenon, nor have we found any similar case report in the literature. This case, in which the spontaneous pupillary activity was initially misinterpreted as a response to light and hence indicative of an intact reflex arc, highlights the importance of thorough technique when testing the pupils. A period of uninterrupted observation is important. This case also shows that pupillary activity in the absence of elicited reactivity does not preclude the diagnosis of brainstem death.
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References |
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