Intracranial traumatic

The use of acetazolamide in the presence of unrecognized cerebral edema due to fat embolism, with sudden normalization of brain C02, as occurred in this patient when her previous state of hypocapnia was no longer sustained by ventilatory effort, resulted in cerebral acidosis, vasodilatation, and a further increase in intracranial pressure. This proved catastrophic and led to brainstem herniation and brain death. Acetazolamide should be avoided if at all possible in patients with bony and traumatic brain injuries, particularly during weaning from mechanical ventilation, since it can precipitate coning in patients with raised intracranial pressure. 

Kahveci et al. (13) compared the cerebral protective effects of two known protective anesthetics, isoflurane and propofol, in combination with hypothermia (33-34°C) after traumatic brain injury (TBI). In that study, the authors found that propofol anesthesia plus hypothermia following TBI was better than the isoflurane-hypothermia combination because it reduced intracranial pressure and increased cerebral perfusion pressure under those conditions. 

Kahveci F. S., Kahveci N., Alkan T., Goren B., Korfali E., and Ozluk K. (2001) Propofol versus isoflurane anesthesia under hypothermic conditions effects on intracranial pressure and local cerebral blood flow after diffuse traumatic brain injury in the rat. Surg. Neurol. 56, 206-214. 

Deliberate mild hypothermia has been shown to be an extremely effective means of neuroprotection during periods of ischemia in experimental models. Intraoperative mild hypothermia has become a standard of practice for many neurosurgeons performing complex intracranial procedures. Recent findings of neurologic benefit in prospective, randomized, controlled clinical studies of cardiac arrest patients are encouraging, but more research is required to confirm and extend these positive results to other patients with stroke and traumatic insults. Further investigation must be completed to establish the optimal time and duration when treatment should be instituted to offer the optimal protection for patients with acute ischemic and traumatic injuries. 

Hypothermia-induced coagulopathy in patients with severe TBI has important clinical implications. In addition to the intracranial hemorrhages caused by their primary traumatic injury, these patients have a 20-30% incidence of delayed posttraumatic intracranial hemorrhage. However, at least one report found that treatment with moderate hypothermia did not result in increased rates of secondary delayed intracranial hemorrhages as compared to normothermic controls (19). 

A significant reduction of the ICP was seen, which was similar to the results of Marion and Shiozaki, who used hypothermic therapy in traumatic brain injuries (37,38). With an unaffected mean arterial blood pressure (MABP) and increased cerebral perfusion pressure (CPP), hypothermic therapy appeared to benefit stroke patients, as uncontrolled intracranial hypertension is the main cause of death in the first week after stroke. However, rewarming the patients consistently led to a secondary rise of ICP, which required additional ICP therapy with mannitol. In some cases it even exaggerated the initial ICP levels (Fig. 3). 

Related to the post-traumatic microvascular damage is the pathophysiological process of vasogenic brain edema that represents a disruption of blood-brain barrier integrity, resulting in sodium and protein accumulation and osmotic fluid expansion of the brain extracellular space. Clinically, this is reflected by an increase in intracranial pressure which, if unchecked, can cause secondary compressive injury to vital brain structures. 

Differential diagnosis of spontaneous and traumatic intracranial haemorrhage. Journal of Neurology, Neurosurgery and Psychiatry 54 1118... 

Increased ICR and, thus, papilledema have many causes. Any intracranial space-occupying lesion may create increased ICR. Superior sagittal sinus thrombosis, spinal cord tumors with associated elevated CSF protein, spinal cord injuries, and traumatic brain injmy may all cause papilledema. 

Glucocorticoids are recommended for the treatment of CNS disorders as they stabilize microvas-cular permeability, reduce edema formation, reduce intracranial pressure, decrease oxygen-derived free radicals and prevent post-traumatic autodestruction of nervous tissue. Their clinical use in equine medicine includes the treatment of brain and spinal cord trauma, cerebral edema associated with neonatal maladjustment syndrome (NMS), endotoxic shock and EPM. This is despite the fact that the safety and efficacy of glucocorticoids in the treatment of many types of nervous system inflammation has not been established and their use and dosing schedules continue to be debated. 

Increased Permeability. The permeability of the blood-CSF barrier to plasma proteins is increased by high intracranial pressure resulting from a brain tumor, intracerebral hemorrhage, or traumatic injury. In addition, increased permeability to proteins is seen with inflammation associated with bacterial or viral meningitis, encephalitis, or... 

CCS, Glasgow Coma Scale BP, blood pressure HR, heart rate RR, respiratory rate CSF, cerebrospinal fluid TBI, traumatic brain injury ICP, intracranial pressure CPP, cerebral perfusion pressure ABC, arterial blood gas CBC, complete blood count Na, sodium K, potassium Cl, chloride Mg, magnesium Ca, calcium P, phosphorus CT, computed tomography. 

Tokutomi T, Morimoto K, Miyagi T, et al. Optimal temperature for the management of severe traumatic brain injury Effect of hypothermia on intracranial pressure, systemic and intracranial hemodynamics, and metaboUsm. Neurosurgery 2003 52 102-111. 

Slavik RS, Rhoney DH. Indomethacin A review of its cerebral blood flow effects and potential use for controlling intracranial pressure in traumatic brain injury patients. Neurol Res 1999 21 491 99. 

Yamaura A, Ono J, Hirai S (2000) Clinical picture of intracranial non-traumatic dissecting aneurysm. Neuropathology 20 85-90... 

Comparative studies In a randomized controlled trial of thiopental and pentobarbital in the control of refractory intracranial hypertension in 44 patients with severe traumatic brain injuries the former was more efficacious in reducing refractory intracranial pressure (OR = 5.1) [9(T]. There were no differences in adverse effects with respect to infections or the SOFA score before or maximum score attained between the two groups almost all of the patieuts had hypotension on at least one occasion. 

A 14-year-old girl with a severe traumatic brain injury developed a raised intracranial pressure, which was treated with 2900 mg of thiopental over 42 hours. Before the infusion she had hypokalemia (2.5 mmol/1), which was corrected, but it persisted despite potassium replacement of 200 mmol. She suddenly developed tachycardia, anterior ST segment changes, and atrial fibrillation 7 hours after the end of the infusion. Her serum potassium peaked at 7.0 mmol/1 and hyperkalemia persisted for 36 hours. 

Perez-Barcena J, Llompart-Pou JA, Homar J, Abadal JM, Raurich JM, Frontera G, Brell M, Ibdnez J, Ibtihez J. Pentobarbital versus thiopental in the treatment of refractory intracranial hypertension in patients with traumatic brain injury a randomized controlled trial. Crit Care 2008 12(4) R112. 

Wassef SN, Abel TJ, GrossbachA,ViljoenSV, Jackson AW, Howard III MA, et al. Traumatic intracranial hemorrhage in patients taking dabigatran report of 3 cases and review of the literature. Neurosurgery 2013 73(2) E368-74. 

Allard, C.B., Scarpelini, S., Rhind, S.G., et al, 2009. Abnormal coagulation tests are associated with progression of traumatic intracranial hemorrhage. J. Trauma 67, 959-967. 

Chesnut, R.M., Temkin, N., Carney, N., Global Neurotrauma Research Group, 2012. A trial of intracranial-pressure monitoring in traumatic brain injury. 

Jiang, J.-Y., Xu, W., Li, W.-R, et al., 2005. Efficacy of standard trauma craniectomy for refractory intracranial hypertension with severe traumatic brain injury a multicenter, prospective, randomized controlled study. J. Neurotrauma 22, 623-628. 

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