*7.3.1.1 Oliguemia stage*

*Advancement and New Understanding in Brain Injury*

*7.2.3 Vasospasm stage*

**7.3 Traumatic brain injury**

deficits.

TCD is able to identify the state of cerebral circulatory hyperdynamia and, consequently, guide the management of the hemodynamic condition of patients in order to avoid brain swelling associated with this condition. At this stage, situations that worsen the condition of brain hyperemia, such as hypercapnia, systemic arterial hypertension, anemia, and hypermetabolic brain conditions (e.g., seizure) should be avoided. In the study of cerebral autoregulation (CAR) the ability of the brain to maintain constant blood flow dynamics regardless of variations in systemic blood pressure is evaluated. SAH is one of the pathologies in which ra is impaired, which requires adequate systemic blood pressure levels to prevent hyperemia or oliguemia. TCD can identify CAR impairment through the relationship between flow velocity oscillations in the face of MAP changes (spontaneous or provoked); and this analysis is performed through modeling used in signals analysis, requiring the use of specific software for this purpose. Thus, TCD can help identify the most appropriate blood pressure range in impaired states.

Vasospasm in SAH is one of the main causes of late cerebral ischemia. Therefore,

There are several reasons that determine late cerebral ischemia in SAH-related vasospasm: 1) vasospasm intensity; 2) occurrence in multiple arteries or sequential vasospasm in "Tanden"; 3) presence or absence of activated collateral circulation; 4) early onset of vasospasm; 5) fast vasospasm progress (elevation of >25 cm/s/day); 6) associated tissue hypermetabolism; 7) mitochondrial tissue dysfunction; 8) presence of intracranial hypertension; 9) associated circulatory oliguemia; 10) impaired brain microcirculatory reserve; 11) preexistence of intracranial stenosis [60].

TCD is capable of detecting vasospasm in the middle and basilar cerebral arteries with high sensitivity and specificity [60]. Classically, vasospasm can occur between 4 and 14 days after the day of bleeding, and in some cases (13% of patients) can be detected early in the first 48 hours or late after 17 days. The possibility of monitoring vasospasm intensity may allow the optimization of clinical management. In severe vasospasm, the conjunction of other hemodynamic factors also observed by TCD determines the indication of, in addition to clinical measures, such as the use of vasoactive drugs and/or endovascular interventional treatment. The opportunity for the evolutionary follow-up of the response obtained to the treatment adopted is also an important benefit of TCD at this stage. **Table 2** shows the diagnostic and classifi-

Intracranial circulatory abnormalities occur frequently in patients with TBI. Ischemic brain lesions can be identified in about 90% of patients who die after severe TBI [61], suggesting that changes in systemic and/or brain blood flow dynamics are frequent causes of ischemia and unfavorable outcomes. Studies of blood flow and brain metabolism suggest that hyperemic brain phenomena are the

As in SAH, there is a definition of 3 hemodynamic stages after severe TBI. The oliguemia stage occurs on the day of TBI (day 0) and is characterized by a reduction

cation criteria of vasospasm severity by TCD using Mv and LI.

most frequently found in comatose patients after severe TBI [62].

*7.3.1 Brain hemodynamic phases after severe TBI*

its early recognition is mandatory in the clinical management of neurocritical patients. Before symptoms arise, vasospasm can be detected by TCD. Thus, clinical treatment of vasospasm can be instituted early, before the installation of neurological

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Cerebral changes in the acute stage of moderate or severe TBI, characterized by reduced blood flow velocity and increased PI in intracranial arteries, can be revealed by TCD, including during the first three hours after TBI occurrence. At this stage, TCD should be used early in order to guide therapeutic approaches. When oliguemia has been demonstrated, the possibilities of systemic blood pressure insufficiency of maintaining CBF dynamics (MAP below the autoregulation range), hyperventilation with reduction of partial arterial CO2 pressure, resulting in cerebral microvasculature vasoconstriction, posttraumatic thrombosis of the carotid arteries, and intracranial hypertension (especially if associated with increased PI) should be considered. The reduction in blood flow velocity in cerebral arteries may also be due to brain hypometabolism that may be associated with severe brain lesions. Presence of oliguemia may be associated with a higher risk of brain ischemia and an unfavorable prognosis [63].
