3 phases after severe head injury:
1. hypoperfusion and cerebral ischemia (24h)
2. rebound hyperemia (24-72h)
3. post-traumatic vasospasm (4-14d)
Methods to detect Post-trauma Vasospasm
1. Cerebral angio
3. AVDO2 – cerebral arteriovenous difference of oxygen – lower value suggests hyperaemia
4. xenon clearance method / cerebral perfusion studies
5. shape of TCD waveform – no dicrotic notch in hyperaemia
Lindegaard ratio: ratio between mean velocity in MCA and mean velocity in cervical ICA, if 3 or more then the high intracranial velocity likely to be due to vasospasm
Incidence of post-traumatic vasospasm: (see tables below)
10-39% in anigio studies (done once post-trauma)
higher in TCD studies (multiple evaluations because noninvasive, so incidence is bloated)
*Presence of SAH did not correlate with inc incidence of post-trauma vasospasm (37.9% vs 31.3% p=0.34)
*Thick layers of subarachnoid blood on CT had a tendency to develop post-trauma vasospasm (44.4% vs 31.3%) but not significant. (low sample size)
*Statistically significant increase in incidence of post-traumatic vasospasm with EDH and SDH. Patients with ICH tend to develop post-trauma vasospasm more often but not statistically significant.
Onset and Duration:
Onset mean of 5days (2-8d)
Peak at 5-7 days
Tend to be short lasting; prolonged vasospasm correlated closer with SAH on initial CT
*Note that >10% of patients with post-trauma vasospasm have no blood in CSF – there must be a separate pathophysiology for vasospasm in this group.
GCS also correlated with incidence of vasospasm.
Pathophysiology of Vasospasm
1. strongest correlation is between volume of subarachnoid blood on early CT – blood components (RBC, platelet-rich plasma, oxyHb, thrombin) directly cause vasospasm or induce release of vasoconstrictors from endoth cells (TXA2, endothelin) or hypothalamus
*TXA2 and endothelin are potent, long-lasting vasoconstrictors
2. mechanical stretching and pulling – but based on experiments, spasm only lasts for <1h
3. release of vasoactive substances from parenchyma (endoth cells, blood cells, neurons, glia)
But not all vasospasm leads to cerebral injury – vasospasm detected in >2/3 of aSAH, but only about half develop ischemic symptoms
1. increased flow
2. extraction of more osygen from blood when flow is reduced
3. ability of collateral vasculature to compensate
Treatments used in aSAH may be deleterious in TBI. Where aneursyms can be secured in aSAH, source of bleeding in tSAH is oftentimes not correctible by surgery. Induced hypertension may increase cerebral edema in TBI. Probably best method is to maintain euvolemia and prevent hypotension.
Nimodipine in preventing post-trauma vasospasm has mixed results, but most studies show a trend towards improvement in vasospasm as well as clinical parameters.
Surg Neurol. 2000 Feb;53(2):126-30. Risk factors for the development of post-traumatic cerebral vasospasm. Zubkov AY1, et al.
J Clin Neurosci. 1998 Apr;5(2):146-54. A review of cerebral vasospasm. Part IV. Post-traumatic vasospasm. Zurynski YA1, Dorsch NW.
Neurol Res Int. 2013;2013:415813. doi: 10.1155/2013/415813. Epub 2013 Jun 19. Cerebral vasospasm in traumatic brain injury. Kramer DR1, et al.