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Visualizing Impending Cerebral Circulatory Arrest Caused by Intracranial Hypertension Following Aneurysmal Subarachnoid Hemorrhage.

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Visualizing Impending

Cerebral Circulatory

Arrest Caused by

Intracranial

Hypertension Following

Aneurysmal

Subarachnoid

Hemorrhage

To JNA Readers:

Intracranial hypertension may represent an important complication during the early phase following aneurysmal subarachnoid hemor-rhage.1 Timely diagnosis of intra-cranial hypertension is essential to avoid secondary brain ischemia; however, intracranial pressure (ICP) monitoring requires the insertion of catheters either within the brain ven-tricles or parenchyma, and hence, in-vasive ICP monitoring is not frequently utilized.2 Transcranial Doppler can be used for noninvasive ICP estimation through calculation of the pulsatility index (PI).3 We de-scribe a case where noninvasive ICP monitoring with transcranial color-coded Doppler (TCCD) rapidly identified a condition of severe intra-cranial hypertension, which led to a life-saving treatment.

A 38-year-old man was admitted to the emergency department with a World Federation of Neurological Surgeons (WFNS) score of II (Glas-gow Coma Score = 14, no motor def-icit) following a brief loss of consciousness. An initial brain com-puted tomographic (CT) scan showed a subarachnoid hemorrage (Fisher grade 3) with mild hydrocephalus of the ventricular temporal horns (Fig. 1). A brain CT angiogram showed a 5-mm saccular aneurysm at the right A1-A2 anterior cerebral artery junction. Shortly after the admission to the neurosurgical ward, he became restless

and agitated with further deterioration of his neurological condition

(WFNS = IV, Glasgow Coma

Score = 12, mild left upper limb hem-iparesis, slight right > left anisocoria with preserved pupillary reactivity to light) and no evidence of seizures. A second brain CT was unchanged, but urgent TCCD of the right middle cer-ebral artery demonstrated a critically low diastolic blood flow velocity of 18.2 cm/s, yet normal systolic flow ve-locity of 130 cm/s, indicating prevailing cerebral blood flow during the systolic phase of the cardiac cycle (Fig. 1B). Middle and anterior cerebral arteries were opening during cardiac systole and then rapidly closing during dia-stole, indicating severe intracranial hypertension with impending cerebral circulatory arrest. (Supplemental Digi-tal Content 1, http://links.lww.com/ JNA/A31. Ultrasound Video clearly demonstrating the arteries opening during systole and closing during dia-stole before external ventricular drain [EVD] placement.) The PI was 2.64, corresponding to an estimated ICP of 40 mm Hg. An EVD was immediately placed, which showed an ICP reading of 35 mm Hg measured after rapid loss of 5 mL of cerebrospinal fluid during the procedure. Following further drainage of 20 mL, ICP reduced to a value of 10 mm Hg. The second TCCD examination showed diastolic flow ve-locity (41.9 cm/s) and PI (1.05) had returned to normal (Fig. 1C). After EVD placement, the neurological con-dition rapidly improved with reso-lution of the neurological deficits within 6 hours. After successful em-bolization of the aneurysm, the patient was transferred to the neurosurgical ward and after 1 week was eventually discharged to a rehabilitation center where he fully recovered.

The use of TCCD allowed rapid detection of severe intracranial hy-pertension causing a critical reduction of the cerebral blood flow. Direct visualization of middle and anterior cerebral arteries with use of TCCD showed the vascular lumen closing during the diastolic phase of the car-diac cycle and opening only during

the systolic phase. After exclusion of rebleeding, the hydrocephalus ap-peared to be the likely cause leading to emergent EVD placement. Invasive monitoring confirmed the estimated ICP that was well above established threshold for treatment. Rapid im-provement of the neurological con-dition after cerebrospinal fluid drainage definitely confirmed the di-agnosis of hydrocephalus-associated intracranial hypertension.

Intracranial hypertension due to rebleeding and hydrocephalus occurs in nearly 50% of aneurysmal sub-arachnoid hemorrhage patients, in-cluding those presenting with good clinical grades, and can be associated with secondary cerebral infarction and worsening of outcome.4 How-ever, ventricular volume may not al-ways correlate with increased ICP causing delays in decision making. In fact, as shown in this case, acute hy-drocephalus may lead to a critical reduction of cerebral blood flow dis-pite apparently unchanged cerebral ventricle volumes.

Transcranial Doppler can be used for noninvasive ICP estimation, both through use of PI, indicating intracranial hypertension if above 1, and with estimation of specific ICP values.5Importantly, TCCD provides a unique method for directly visualizing major cerebral arteries of the circle of Willis and their acute modification due to intracranial hypertension.

Frank Rasulo, MD*w Simone Piva, MD* Nazzareno Fagoni, MD* Nicola Latronico, MD*w

*Department of Anesthesia, Critical Care and Emergency, Spedali Civili University Hospital wDepartment of Medical and Surgical Specialties, Radiological Sciences and Public Health, University of Brescia Brescia, Italy

REFERENCES

1. Nornes H. The role of intracranial pressure in the arrest of hemorrhage in patients with ruptured intracranial aneurysm. J Neuro-surg. 1973;39:226–234.

The authors have no funding or conflicts of interest to disclose.

C

ORRESPONDENCE

J Neurosurg AnesthesiolVolume 00, Number 00, ’’ 2015 www.jnsa.com|

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2. Grote E, Hassler W. The critical first minutes after subarachnoid hemorrhage. Neurosurgery. 1988;22:654–661.

3. Bellner J, Romner B, Reinstrup P, et al. Transcranial Doppler sonography pulsatility

index (PI) reflects intracranial pressure (ICP). Surg Neurol. 2004;62:45–51. 4. Van Gijn J, Kerr RS, Rinkel GJE.

Sub-arachnoid haemorrhage. Lancet. 2007;369: 306–318.

5. Schmidt EA, Czosnyka M, Matta BF. Non-invasive cerebral perfusion pressure (nCPP): evaluation of the monitoring methodology in head injured patients. Acta Neurochir Suppl. 2000;76:451–452.

FIGURE 1. A, Bilateral subarachnoid hemorrhage in the cerebral sulci, basal cisterns, perivascular spaces, left posterior ventricular horn and in the third ventricle; initial signs of mild hydrocephalus of the temporal horns. B, Transcranial color-coded Doppler (TCCD) examination showing signs of intracranial hypertension, as demonstrated by the presence of a low diastolic flow velocity of 18.2 cm/s, a pulsatility index (PI) of 2.64, and noninvasive intracranial pressure (ICP) estimation was 40 mm Hg. C, TCCD showing both systolic and diastolic flow velocity returning to normal values after EVD placement, with a net reduction of the PI (1.05) and the noninvasive ICP estimation value (10 mm Hg).

Correspondence J Neurosurg Anesthesiol  Volume 00, Number 00, ’’ 2015

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|www.jnsa.com Copyrightr2015 Wolters Kluwer Health, Inc. All rights reserved.

Figura

FIGURE 1. A, Bilateral subarachnoid hemorrhage in the cerebral sulci, basal cisterns, perivascular spaces, left posterior ventricular horn and in the third ventricle; initial signs of mild hydrocephalus of the temporal horns

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