Heart rate < 120/min
No relevant calvarial defects
Criteria for brain death: evidence of phasic flow and/or small systolic peaks twice at an interval of at least 30 minutes, on each occasion bilaterally at the middle cerebral artery or intracranial internal carotid artery, or with duplex ultrasound in the internal carotid artery extracranially and in the basilar or vertebral artery intracranially, or with duplex ultrasound in the vertebral artery extracranially.
Doppler ultrasound can be used independently of the type of cerebral damage—i.e., even in cases of toxic injury. When an appropriate acoustic window is used, a false-positive finding cannot occur when an experienced examiner uses the above criteria. False-negative findings are possible:
With cerebral arteriovenous malformations with shunt flow
In the absence of raised intracranial pressure
When perfusion re-starts (with intracranial pressure declining
again)
In infants with open fontanelles and sutures
In the case of the proximal vertebral artery, due to branches not supplying the brain
In a purely extracranial examination, due to residual perfusion of the internal carotid artery via the ophthalmic artery
Vasospasm monitoring in subarachnoid bleeding
The vasospasm that mainly occurs from days 4 to 10 can be recorded and monitored using transcranial Doppler (TCD) follow-up observations and by measuring velocities particularly in the middle cerebral artery main trunk:
Borderline: Vmean ≥ 120 cm/s
Pathological: Vmean ≥ 160 cm/s
Critically raised: Vmean ≥ 200 cm/s, Vmax ≥ 300 cm/s
Suspicious: increases in flow velocities ≥ 50% or ≥ 40 cm/s/d during the first 6–7 days (Grosset 1993)
Pulsatility index (PI) > 1, resistance index (RI) > 0.6 (Klingelhöfer et al. 1991)
Ratio of the maximum velocities in the middle cerebral artery and internal carotid artery (the middle cerebral artery/internal carotid artery index) ≥ 3
Caution:
False-negative findings may occur when nonspastic vascular segments are examined.
False-negative findings may occur with simultaneous raised intracranial pressure and consequently reduced flow velocities (pulsatility parameters should therefore also be used).
Prior arteriosclerotic stenoses.
Hyperperfusion (middle cerebral artery/internal carotid artery index < 2).
1.2.5 Treatment
1.2.5.1 Conservative treatment
The treatment strategy depends in principle on multiple factors and should be decided on an individual basis. Risk factors such as nicotine consumption, lipid disorders, hypertension, and diabetes should be eliminated or treated.
In patients with asymptomatic stenoses that are not hemodynamically relevant, invasive treatment is not currently recommended, but drug therapy with platelet inhibitors is recommended, possibly in combination with lipid-lowering agents.
Patients with symptomatic stenoses that are hemodynamically relevant initially receive drug treatment, and invasive therapy is only considered if symptoms recur. The WASID study found no benefit with warfarin administration in comparison with aspirin in patients with symptomatic intracranial stenoses. In comparison, the risk of stroke during the first year was 12% in the aspirin group and almost as high in the warfarin group at 11%; in the second year, the figures were 15% and 13%, respectively. However, as major hemorrhage only occurred in 3% of the patients in the aspirin group in comparison with 8% in the warfarin group, treatment with vitamin K antagonists is now obsolete. Treatment with dual platelet inhibition (e.g., aspirin and clopidogrel) should therefore be considered, particularly when an ischemic event has occurred during single antiplatelet treatment. Individual testing of drug efficacy is advisable in any case, as there is a high percentage (up to 30%) of low responders and nonresponders, although no data in this population that correlates responder rates and clinical events.
When ischemic symptoms recur during medication, the indication for PTA and, if appropriate, stent placement should be considered. A recently published study (the SAMMPRIS study) did not observe any clear benefits with an invasive approach using stenting—a finding that requires further research after optimization of patient selection and concomitant drug therapy.
As mentioned above, it is therefore absolutely imperative to differentiate between embolic and hemodynamically relevant stenoses. In stenoses that have hemodynamic effects, with clinical symptoms, conservative therapy is only appropriate in combination with endovascular therapy (PTA, possibly with stent assistance) in order to improve perfusion. If this is not technically possible, attention should be given to ensure that blood pressure is not reduced too much, to avoid negative effects on the collateral supply.
The treatment of intracranial vascular occlusions also depends on clinical symptoms. Conservative treatment for acute stroke includes normalization of general parameters (cardiovascular and pulmonary function, as well as fluid balance and metabolic parameters) and oxygenation. If a patient reaches hospital within the “thrombolysis window” (usually < 6 hours after the start of symptoms), systemic intravenous thrombolysis therapy (up to 4.5 hours after the initial symptoms) or local intra-arterial embolectomy or thrombolytic therapy can be carried out. The 4.5-hour time interval currently applies to systemic intravenous thrombolytic therapy (with recombinant tissue plasminogen activator, rt-PA). In all cases, the earlier the patient is treated, the better the clinical outcome is. In what is known as the “bridging approach,” intravenous treatment (two-thirds of the total dosage, with 10% of that as a bolus) is combined with intra-arterial therapy. The initial intravenous thrombolysis allows rapid initiation of treatment and may optimize the efficacy of the endovascular intra-arterial therapy.
1.2.5.2 Endovascular intra-arterial therapy
Endovascular