T. Geeraerts

Ultrasonography of the optic nerve sheath may be useful for detecting raised intracranial pressure after severe brain injury

ObjectiveTo assess at admission to the ICU the relationship between optic nerve sheath diameter (ONSD) and intracranial pressure (ICP) and to investigate whether increased ONSD at patient admission is associated with raised ICP in the first 48u202fh after trauma.Design and settingProspective, blind, observational study in axa0surgical critical care unit, level 1 trauma center.Patients and participants31 adult patients with severe traumatic brain injury (TBI; Glasgow coma scaleu202f≤u202f8) requiring sedation and ICP monitoring, and 31 control patients without brain injury requiring sedation.Measurements and resultsONSD was measured with axa07.5-MHz linear ultrasound probe. Two TBI groups were defined on the basis of ICP profile. If ICP exceeded 20u202fmmHg for more than 30u202fmin in the first 48u202fh (before any specific treatment), patients were considered to have high ICP; if not, they had normal ICP. The largest ONSD value (the highest value for the right and left eye) was significantly higher in high ICP patients (6.3u202f±u202f0.6 vs. 5.1u202f±u202f0.7u202fmm in normal ICP patients and 4.9u202f±u202f0.3u202fmm in control patients). There was axa0significant relationship between the largest ONSD and ICP at admission (ru202f=u202f0.68). The largest ONSD was axa0suitable predictor of high ICP (area under ROC curve 0.96). When ONSD was under 5.7u202fmm, the sensitivity and negative predictive values for high ICP were 100%.ConclusionsIn the early posttraumatic period, ocular ultrasound scans may be useful for detecting high ICP after severe TBI.

Coma avec mydriase bilatérale au décours de l'utilisation d'un patch de scopolamine en réanimation

We report the case of an ICU patient with previous medical history of head trauma with hydrocephalus requiring ventricular derivation, presenting a coma (Glasgow Coma Score=8) with bilateral mydriasis after the use of transdermal scopolamine (1 mg) for profuse bronchial secretions. Neurological explorations (CT-scan and electroencephalogram) confirmed the absence of organic cause to the neurological deterioration. Neurological status rapidly and completely improved after removal of transdermal scopolamine suggesting a central anticholinergic syndrome.

Coagulation disorders after traumatic brain injury: Pathophysiology and therapeutic implications

Early activation of coagulation is common after traumatic brain injury. Its origin is probably mainly intracerebral, due to tissue factor release from the injured brain. Abnormalities in blood coagulation tests are associated with poor neurological prognosis. Coagulation activation may induce disseminated intravascular coagulation and fibrinolysis. Disseminated intravascular coagulation is linked to brain ischemia caused by intravascular microthrombosis. This review will focus on pathophysiology of coagulation disorders after traumatic brain injury, and on their implications for therapeutic approaches.

Cas cliniqueComa avec mydriase bilatérale au décours de l'utilisation d'un patch de scopolamine en réanimationComa with bilateral mydriasis after use of transdermal scopolamine in ICU

We report the case of an ICU patient with previous medical history of head trauma with hydrocephalus requiring ventricular derivation, presenting a coma (Glasgow Coma Score=8) with bilateral mydriasis after the use of transdermal scopolamine (1 mg) for profuse bronchial secretions. Neurological explorations (CT-scan and electroencephalogram) confirmed the absence of organic cause to the neurological deterioration. Neurological status rapidly and completely improved after removal of transdermal scopolamine suggesting a central anticholinergic syndrome.

Monitorage intracérébral d'un patient ayant un vasospasme

Delayed neurological deficit occurs among 30% of patients after aneurysmal subarachnoid haemorrhage, mainly related to cerebral vasospasm. The early detection of cerebral ischemia remains problematic. Conventional cerebral monitoring (as intracranial pressure and cerebral perfusion pressure) appears to be insufficient, because cerebral ischemia may occur without elevated intracranial pressure. Global cerebral monitoring as venous jugular oxygen saturation are useful for regional monitoring. Local monitoring as oxygen tissue partial pressure (PtiO2) and microdialysis are sensible for brain ischemia detection, but may also ignore episodes occurring in non-monitored brain area. For the detection of most episodes of brain ischemia, several monitoring system should be use performing a multimodal intracerebral monitoring. Brain microdialysis and oxygen tissue partial pressure are promising monitoring system.

Ocular sonography for the detection of raised intracranial pressure

Expert Rev. Ophthalmol. 3(5), 497–500 (2008) “Early diagnosis of raised intracranial pressure is critical for adequate triage and therapeutic intervention. The gold standard for intracranial pressure monitoring is the use of an invasive device, such as intraparenchymal probe or intraventricular drain” Raised intracranial pressure (ICP) is a frequent condition in neurosurgical care and is associated with poor neurological outcome. Invasive devices are the gold standard for continuous and reliable assessment of ICP. Invasive devices for monitoring ICP, however, require expertise and normal coagulation blood tests in order to be placed safely. The optic nerve is surrounded by a dura mater sheath that is distensible when cerebrospinal fluid pressure rises. Measurement of the optic nerve sheath diameter (ONSD) using ocular sonography is a simple and noninvasive tool that can be performed at the patient’s bedside. This method predicts raised ICP in various settings, including

Réunion de neuroanesthésie–réanimationMonitorage intracérébral d'un patient ayant un vasospasmeIntracerebral monitoring of a patient with vasopasm☆

Delayed neurological deficit occurs among 30% of patients after aneurysmal subarachnoid haemorrhage, mainly related to cerebral vasospasm. The early detection of cerebral ischemia remains problematic. Conventional cerebral monitoring (as intracranial pressure and cerebral perfusion pressure) appears to be insufficient, because cerebral ischemia may occur without elevated intracranial pressure. Global cerebral monitoring as venous jugular oxygen saturation are useful for regional monitoring. Local monitoring as oxygen tissue partial pressure (PtiO2) and microdialysis are sensible for brain ischemia detection, but may also ignore episodes occurring in non-monitored brain area. For the detection of most episodes of brain ischemia, several monitoring system should be use performing a multimodal intracerebral monitoring. Brain microdialysis and oxygen tissue partial pressure are promising monitoring system.