*7.3.1.3 Vasospasm phase*

Studies with TCD in TBI estimate the occurrence of vasospasm in 50% of patients. There is an important association between vasospasm with severe hemodynamic repercussion and unfavorable neurological prognosis, although this repercussion is lower than in cases of spontaneous SAH. It is important to highlight that posttraumatic vasospasm of the basilar artery doubles the possibility of unfavorable prognosis, compared to patients without spasm of this artery. The duration of vasospasm in patients with TBI tends to be shorter due to the non-inflammatory nature as a cause, unlike subarachnoid hemorrhage. Possibly the origin of traumatic vasospasm is associated with stretching of the arteries during trauma and peak intensity, in many cases, occurs between the fifth and seventh day after trauma, although a duration similar to SAH is observed in some cases [65].

Among other applications of TCD in severe TBI, it is worth mentioning: 1) to detect brain circulatory changes resulting from ICH; 2) to evaluate the degree of autoregulation and cerebrovascular reactivity impairment, enabling the prediction of prognosis; 3) to provide evidence of posttraumatic dissection or thrombosis of the arteries that irrigate the brain, allowing early investigation and adoption of

measures to prevent brain infarctions; 4) to verify relative changes in the dynamics of brain blood flow in response to the treatments instituted.

### **7.4 Intracranial hypertension**

TCD is important for assessing the effects of ICH on brain circulation. It is especially useful in patients where invasive ICP monitoring is absent because it allows the estimation of cerebral perfusion pressure (eCPP) (Section 1.1.2). In addition, changes in intracranial pressure may be associated with alterations in intracranial flow waveform. Thus, the increase in ICP can lead to PI elevation with progressive reduction of mean and diastolic blood flow velocities. In general, PI modifications occur when CPP is less than 70 mmHg2. At the moment when ICP is equal to diastolic systemic blood pressure, the blood velocity of diastolic flow reaches zero, characterizing the momentary absence of cerebral blood perfusion during the diastolic phase of the cardiac cycle [66].

In other situations, even with invasive ICP monitoring, TCD also plays a key role as a real-time evaluator of the efficacy of therapeutic measures used for the treatment of ICH; TCD can also be used as an alternative method to detect erroneous measurements of ICP monitors. Furthermore, TCD may reveal that increased ICP may be associated with hyperdynamic brain circulation due to impaired cerebrovascular autoregulation. In this condition, CPP formula cannot be used as a parameter to improve cerebral perfusion in the presence of ICH.

TCD also allows the evaluation of intracranial compliance by means of simultaneous compression maneuvers of the internal jugular veins and the increase of MAP. Under normal conditions, this maneuver causes a slight increase in brain blood volume and ICP augmentation. In patients with reduced intracranial compliance, venous compression would cause PI elevation and reduction of mean brain blood flow velocities [67] leptomeningeal arteries during acute arterial occlusion. Still in the acute phase, the detection of emboli by TCD in the region of the occluded artery may be indicative of recanalization of this arterial segment.

In the subacute stage of ischemic cerebrovascular disease, TCD assesses the hemodynamic repercussion of extracranial carotid disease through CO2 reactivity tests and the presence and hemodynamic repercussion of intracranial stenosis. Embolic activity in a single intracranial arterial system may suggest an embolic source that originates from the ipsilateral carotid artery (arterial embolism) and this finding is suggestive of an increased risk of recurrence of the ischemic event when embolic activity is detected in multiple intracranial arterial systems such as bilateral carotids and vertebrobasilar, it may be suspected that the emboli have cardiac, aorta and/or paradoxical origin. With the infusion of saline solution with microbubbles (small particles of gas) in peripheral vein, TCD can detect the passage of microbubbles in brain circulation, allowing diagnosis of communication between arterial and venous circulations, such as the oval foramen persistence or pulmonary fistula [68].

In summary, TCD in ischemic cerebrovascular disease allows: 1) to detect intracranial arterial stenosis and occlusions; 2) to study the hemodynamic brain effects resulting from extracranial occlusive carotid diseases; 3) to evaluate the pattern and effectiveness of brain collateral circulation; 4) quantify vascular reserve by means of reactivity tests to carbon dioxide; 5) detect the passage of microemboli, in real time, through intracranial circulation; 6) to monitor the reopening of obstructed intracranial arteries, either spontaneous or consequent to thrombolytic therapy, in the acute stage of the ischemic cerebrovascular event.

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*Management of Patients with Brain Injury Using Noninvasive Methods*

the more changes are observed in cerebral hemodynamics [69].

ics of brain blood flow in patients with ICH and assess CAR [70].

*7.5.2 Sepsis and sepsis-associated encephalopathy*

inflammatory mediators.

volume in septic patients.

**7.6 Brain death**

Several studies show that CBF is compromised in patients with acute or chronic severe liver disease, especially in the presence of hepatic encephalopathy (HE). In this condition, there is impairment of brain autoregulation and, consequently, the variation of MAP may be associated with changes in CBF. Although hyperammonemia is the main cause of HE, recent evidence suggests that abnormalities in CBF may also have some relationship in its pathophysiology. There is a hypothesis that cirrhotic patients with encephalopathy present cerebral vasoconstriction more pronounced and, consequently, progressive PI elevation and BHI reduction as the disease progresses (score CTP ≥ 7 or MELD ≥14). The more severe encephalopathy,

In mild HE, there is also an increase in brain microcirculatory resistance and, consequently, an increase in PI and RI, with a significant correlation with the increase in Child-Pugh score. Therefore, TCD may be an aid in the diagnosis of HE in cirrhotic patients. An important complication of severe HE is intracranial hypertension. This is due to three main mechanisms: 1) brain swelling secondary to the cytotoxic effect of hyperammonemia; 2) breakage of the blood brain barrier and 3) hyperemia secondary to CAR impairment. TCD can provide information regarding the dynam-

Hemodynamic impairment is a fundamental feature of sepsis. Brain microcirculation can be gradually compromised and, consequently, cause significant changes in CBF. These factors play an important role in the etiology of sepsis-associated encephalopathy (SAE) [71]. SAE is a frequent brain dysfunction that occurs in 50% of patients admitted to intensive care units, being one of the most common causes of delirium in

In the early phase of sepsis, there are progressive increases in Mv and PI over

The use of TCD to assess brain hemodynamic patterns has some clinical advantages: 1) TCD can be used to identify cerebral hemodynamic patterns in sepsis that may precede systemic hemodynamic signs; 2) increased PI in confused patients may be an early sign of sepsis and help decrease time to diagnosis [71]; and 3) the identification of real-time CBF changes with TCD, correlating with systemic hemodynamic changes, may improve the management of blood pressure and blood

Brain death is defined as total and definitive cessation of all brain functions. TCD is valued in the medical literature as an examination of choice for this purpose

this population. In addition, SAE is associated with an increase in mortality.

time, which are evident 24 hours after onset; at this stage, CAR may remain unchanged. In contrast, in the posterior stage of sepsis (patients with severe sepsis or septic shock), there are progressive reductions in Mv and PI, as well as impairment of CAR. The increase in PI associated with increased cerebrovascular resistance has been correlated with a higher prevalence of delirium and coma. Many of the factors that lead to changes in CBF (such as changes in CVR and CAR) are often the result of a dysfunction of brain tissue microcirculation due to the release of

*DOI: http://dx.doi.org/10.5772/intechopen.94143*

**7.5 Transcranial Doppler in systemic conditions**

*7.5.1 Liver cirrhosis with encephalopathy and liver failure*
