Intensive Care Unit, Northampton General Hospital, Cliftonville, Northampton NN1 5BD, UK
*Corresponding author. E-mail: gwgfrench@doctors.org.uk
Accepted for publication: January 12, 2004
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Abstract |
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Br J Anaesth 2004; 92: 7604
Keywords: brain, braindeath; brain, electroencephalography; brain, evoked potentials; complications, brainstem death
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Introduction |
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She was intubated on arrival while performing manual in-line stabilization. At the same time, a left-sided chest drain was inserted because of the clinical suspicion of rib and sternal fractures and a left-sided pneumothorax. She had bruising of her chest consistent with a seat belt injury. Her systolic arterial pressure was noted to be 60 mm Hg with cool peripheries and she was hypothermic with a rectal temperature of 34°C. Abdominal examination was unremarkable. Central nervous system examination revealed bilateral fixed and dilated pupils and generalized hypotonia with no elicitable reflexes or anal tone.
A cervical spine X-ray showed a Hangmans fracture of C2 (fracture of the pedicle) with displacement and a likely traction injury to the spinal cord (Fig. 1). A chest X-ray confirmed the position of the chest drain in situ with left-sided shadowing, and the pelvic X-ray was unremarkable. Unfortunately, on that day the CT scanner was not available, so she underwent a chest and abdominal ultrasound scan which showed a 3 mm pericardial effusion but no obvious abdominal trauma. All blood tests were normal apart from a white cell count of 26.5 x 109 litre1. Following initial fluid resuscitation, she was started on dopamine and norepinephrine and transferred to the ITU.
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On day 3, a CT scan of the brain showed loss of grey-white differentiation, widespread oedema, and reduced attenuation consistent with coning. Her case was discussed between the ICU consultants who decided to proceed with an EEG and brainstem auditory evoked potentials monitoring in the hope of offering non-heart beating donation. The EEG showed a grossly abnormal trace with no evidence of cerebral activity. The evoked potentials showed an A-line ARX Index (AAITM) of not greater than 12 at any time (mostly 46), and frontalis activity was completely absent (Fig. 2). The AEP line did not show any improvement at any time.
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The patients husband and family were kept informed throughout, and when the results of the CT scan were confirmed, they requested that cardiopulmonary resuscitation should not be performed in the event of a cardiac arrest. When all the test results were available, the family requested that treatment be withdrawn. The lead consultant discussed the case with the Coroner and was advised to obtain legal advice.
The Medical Defence Union were consulted in conjunction with the hospital legal team. They advised that in the absence of the ability to complete the brainstem death tests, and that providing we were confident that brainstem death had taken place, it would be advisable to obtain an expert opinion from a neurologist or neurosurgeon. If they were in agreement, it would then be appropriate to withdraw all support. They added that even if we could not reach a confident diagnosis of brainstem death, but concluded that there was no prospect of recovery in any form, then it might still be appropriate to withdraw support, but only after further legal advice, and with the active and documented agreement of all the patients family. A second opinion was therefore requested from a consultant neurologist who agreed that the patient was brainstem dead. The possibility of organ donation was raised with the family but it was explained that this would require further legal advice and would therefore incur further delays. They agreed that this was undesirable. On day 4 following admission, the family visited to bid farewell before all support was withdrawn. The patient died later that evening and subsequently underwent a Coroners post mortem.
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Discussion |
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All international brain codes follow the same step-by-step procedure of establishing aetiology, exclusion of potentially reversible syndromes, and demonstrating the clinical signs of brain deathcoma, brainstem areflexia, and apnoea. However, there are important differences between countries (Table 1).
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EEG
The EEG records the spontaneous bioelectrical activity of the cerebral cortex to a depth of about 5 mm but does not register the electrical activity of the lower brain stem. Following more than 8 min of complete anoxia as a result of circulatory arrest, the EEG becomes irreversibly isoelectric and is a reliable test of brain death.4 A number of problems with the technique are recognized. Electromagnetic fields in the ICU can pose difficulties in obtaining artifact-free traces,3 5 and the EEG is very sensitive to drug effects.3 6 7 It is uniform practice throughout the world only to consider the diagnosis of brain death after the exclusion of confounding factors, including the presence of sedative drugs. Blood levels of sedative drugs must therefore be tested before the EEG examination, which can only be interpreted with certainty in the absence of any sedatives.8 In this case, the patient was not sedated from admission with the intention of performing brainstem testing when it was appropriate to do so. The EEG should be recorded continuously for 30 min to demonstrate irreversible bioelectrical silence.8 All international brain codes that allow the use of confirmatory tests allow the use of the EEG, with the exception of Denmark, where angiography is required3 (refer to Table 1). In one series of patients fulfilling the clinical diagnosis of brain death, 20% of patients had residual EEG activity that lasted up to 168 h.9
Evoked potentials
Evoked potentials are elicited by adequate stimulation of peripheral receptors and are recorded from the scalp. The diagnosis of brain death often uses median nerve evoked somatosensory potentials (SEP) or brainstem auditory evoked potentials (BAEP). Numerous reports have shown both the SEP and BAEP to be abolished in the presence of the clinical signs of brain death.10 11 Both tests are unsuitable for patients with primary infratentorial lesions,3 6 such as space-occupying lesions of the posterior fossa and vertebrobasilar thrombosis. The successive loss of all intracranial BAEP responses (waves IIV) in repeated tests confirms the loss of function of the acoustic pathways of the brainstem and also the clinical signs of brain death.12 Evoked potential testing is non-invasive and can be performed at the bedside. It is also virtually independent of the effects of sedative medication. In primary infratentorial lesions, an EEG is also mandatory, as the activity of the cerebral cortex can survive the loss of brainstem function by a number of hours or days. Evoked potentials are allowed as a technical test in half of all European countries (Table 1).3
Arteriography
Digital subtraction angiography is widely regarded as the gold standard test. It is performed with the catheter tip in the aortic arch and injection of contrast into each of the four arteries supplying the brain At least two injections, 20 min apart, must show no filling of the intracranial arteries.8 While this method has the advantage of directly confirming the cessation of cranial blood flow, there are several reservations about the method. These include the hazards of transporting and positioning the patient outside the intensive care unit,3 the possibility of allergic reactions to the contrast media,6 the increased risk of nephrotoxicity from contrast media and increased rejection rate in organ recipients following such studies.5 The incidence of anaphylaxis with the newer anionic contrast media is unknown but is thought to be very small however, and the risk of nephrotoxicity does not affect acceptability for organ donation. Digital subtraction angiography is accepted by all countries that allow technical tests for confirmation of the clinical signs of brainstem death (Table 1).3
Transcranial Doppler
This is a useful bedside technique. A reduction in the middle cerebral artery flow velocity to under 10 cm s1 and the observation of a counterbalancing short forward flow during early systole with a short retrograde flow in early diastole should indicate brain death.12 As a technique, it has been found to have a sensitivity of 91.3% and a specificity of 100%.5 Transcranial Doppler (TCD) occasionally demonstrates brain death patterns in patients who are clinically brain dead and who have EEG activity.13 The signals may also be normal in patients with primary infratentorial lesions and in patients with anoxic brain damage after cardiac arrest.14 The velocities may be affected by marked changes in PaCO2, haematocrit, and cardiac output.14 The technique requires considerable practice and skill. Only in Germany is TCD accepted as a confirmatory test; in Austria, angiography must be used in addition (Table 1).3
Scintigraphy
Cerebral perfusion can be examined by sequential cerebral scintigraphy using 99mTc-labelled DPTA or more reliably, with 99mTc-labelled hexamethylpropyleneamine oxime. Following an i.v. bolus of the tracer, the absent uptake of the tracer into the intracranial cavity confirms the loss of cerebral perfusion.15 This method can be performed at the bedside, taking approximately 15 min, and is accepted in both Germany and Switzerland.3
In our patient, an EEG and evoked potentials were chosen as these were the most readily available tests within our district general hospital. Had the EEG not been isoelectric at the time of testing, we would probably have proceeded to digital subtraction angiography or repeated the EEG. Neither scintigraphy nor transcranial Doppler were available. More recently, the assessment of brain death using instant spectral analysis of heart rate variability has been described.16 However, the technique has yet to be validated on a large number of patients and any patients on treatment known to interfere with the heart rate, such as inotropes, are unsuitable for testing. To our knowledge, this is the first case report of brainstem death testing in the presence of high spinal cord injury.
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