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Background: Elevated intracranial pressure (ICP) is a common manifestation of severe brain injury, that requires rapid diagnosis and therapeutic intervention. The use of an intracranial catheter remains the gold-standard method for diagnosing intracranial hypertension, however this modality is not always feasible and/or available. As a result, non-invasive techniques for the evaluation of the ICP have been developed and are frequently used in the clinical practice. The optic nerve sheath diameter (ONSD) has been reported to be increased in patients with intracranial hypertension. Direct measurement of the ONSD is possible by means of optic nerve sonography.
Brain death (BD) is defined as the irreversible cessation of all hemispheric, cerebellar and brain stem functions. Since cerebral circulatory arrest (CCA) is an imperative feature of BD, cerebral blood flow tests are widely advocated to confirm the findings of the clinical examination. Angiography has been considered the gold stand ...
Background: Elevated intracranial pressure (ICP) is a common manifestation of severe brain injury, that requires rapid diagnosis and therapeutic intervention. The use of an intracranial catheter remains the gold-standard method for diagnosing intracranial hypertension, however this modality is not always feasible and/or available. As a result, non-invasive techniques for the evaluation of the ICP have been developed and are frequently used in the clinical practice. The optic nerve sheath diameter (ONSD) has been reported to be increased in patients with intracranial hypertension. Direct measurement of the ONSD is possible by means of optic nerve sonography.
Brain death (BD) is defined as the irreversible cessation of all hemispheric, cerebellar and brain stem functions. Since cerebral circulatory arrest (CCA) is an imperative feature of BD, cerebral blood flow tests are widely advocated to confirm the findings of the clinical examination. Angiography has been considered the gold standard in the diagnosis of BD, but is invasive. Transcranial Doppler sonography (TCD) offers a non-invasive means to assess cerebral hemodynamics, however its application may limited by a bilateral absence of bone windows, which precludes the evaluation of the anterior cerebral circulation, thereby rendering confirmation of CCA unfeasible. In such cases, CCA could be confirmed by means of transorbital Doppler sonography (TOD) of the internal carotid arteries (ICAs).
Providing the family with a realistic understanding of the patient’s condition is considered a demanding and important part of intensive care unit (ICU) practice. A satisfactory explanation of BD may help relatives accept the death of their relative, promote the grieving process, and possibly ease the decision for organ donation. Reporting the results of ancillary tests could improve the relatives’ comprehension and satisfaction with the medical information.
Objective: The purposes of this study were to evaluate whether a) optic nerve sonography can provide accurate detection of intracranial hypertension and/or ICP monitoring in brain-injured patients b) TCD offers accurate confirmation of CCA in patients with clinical diagnosis of BD c) the addition of TOD of the ICAs improves the efficacy of the TCD protocol in confirming CCA d) reporting the angiographic and sonographic confirmation of CCA to relatives of brain-dead patients improves their comprehension and satisfaction with the medical information.
Materials and methods: From the 197 ICU patients who were included in the study, 106 suffered from brain injury, whereas 67 had no intracranial pathology and served as control individuals. Initially, brain-injured patients were evaluated clinically (Glasgow Coma Scale) and using a semiquantitative (I to VI) neuroimaging scale (Marshall Scale). Thereafter, the patients were divided into those with moderate (Marshall Scale = I and Glasgow Coma Scale > 8 [n = 35]) and severe (Marshall Scale = II to VI and Glasgow Coma Scale ≤ 8 [n = 71]) brain injury. Upon admission, all patients underwent non-invasive measurement of the ICP (estimated ICP, eICP) by TCD, and synchronous ONSD measurements by optic nerve sonography, whereas invasive ICP measurement using an intraparenchymal catheter was performed in 32 patients with severe brain injury. In patients with severe brain injury, the above measurement were repeated twice during their hospitalization.
Forty-six clinically brain-dead patients underwent four-vessel angiography, TCD of the basilar and middle cerebral arteries, and TOD of the ICAs. Relatives were randomly allocated to 23 in whom BD was presented as a clinical diagnosis (group I) and to 23 in whom BD was presented as a clinical diagnosis confirmed by TCD and angiography (group II). Comprehension and satisfaction of the relatives were assessed using an interview and a questionnaire.
Results: ONSD and eICP were both significantly increased (6.2 ± 0.7 mm and 27.5 ± 6.9 mmHg, respectively; P < 0.0001) in patients with severe brain injury as compared with patients with moderate brain injury (4.2 ± 0.9 mm and 12.2 ± 3.7 mmHg) and compared with control individuals (3.5 ± 0.8 mm and 9.9 ± 3.7 mmHg). In patients with severe brain injury, the correlation between the ONSD measurements and the neuroimaging scale results was strong upon admission (r = 0.82), and in the second (r = 0.76) and third (r = 0.77) evaluation (P < 0.001). In the same subjects, the correlation between the ONSD measurements and the eICP was strong upon admission (r = 0.80), weak in the second (r = 0.53) and relatively strong in the third (r = 0.65) evaluation (P < 0.001). In the patients with severe brain injury who underwent invasive measurement of the ICP, the latter correlated with the ONSD measurements (r = 0.68, P = 0.002). The best cut-off value of ONSD for predicting elevated ICP was 5.7 mm (sensitivity = 74.1% and specificity = 100%).
Both angiography and TCD verified CCA in all cases (k = 1). In 7 patients with failure of the transtemporal approach, CCA was confirmed by the transorbital recordings. The addition of TOD enabled 15.5% more cases of CCA to be diagnosed by TCD. Group II exhibited improved comprehension and satisfaction rates (P < 0.05).
Conclusions: ONSD measurements correlate with non-invasive and invasive measurements of the ICP, and with head computed tomography scan findings in brain-injured adults. Hence, optic nerve sonography may serve as an additional diagnostic tool
that could alert clinicians to the presence of elevated ICP, whenever invasive ICP evaluation is contraindicated and/or is not available. Alterations in ONSD strongly correlated with neuroimaging results among patients with severe brain injury. The addition of TOD increases the efficacy of TCD in confirming CCA in BD. Reporting confirmation of CCA to families of brain-dead patients may improve their comprehension and satisfaction with the provided medical information.
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