Isoflurane-Associated Mydriasis Mimicking Blown Pupils in a Patient Treated in a Neurointensive Care Unit

2016 ◽  
Vol 78 (04) ◽  
pp. 403-406 ◽  
Author(s):  
Eva Korf ◽  
Volker Tronnier ◽  
Jan Gliemroth ◽  
Jan Küchler
Keyword(s):  
Computed Tomography ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Cranial Computed Tomography ◽  
Elevated Intracranial Pressure ◽  
Neurointensive Care Unit ◽  
Intravenous Treatment ◽  
Cerebral Herniation ◽  
Diagnostic Investigations

AbstractWe report a misinterpretation of bilateral mydriasis as blown pupils related to elevated intracranial pressure (ICP) under volatile sedation with isoflurane (Anesthetic Conserving Device [AnaConDa], Hudson RCI, Uppland Vasby, Sweden) in a 59-year-old patient with a severe traumatic brain injury with frontal contusion. The patient showed bilateral mydriasis and a missing light reflex 8 hours after changing sedation from intravenous treatment with midazolam and esketamine to volatile administration of isoflurane. Because cranial computed tomography ruled out signs of cerebral herniation, we assumed the bilateral mydriasis was caused by isoflurane and reduced the isoflurane supply. Upon this reduction the mydriasis regressed, suggesting the observed mydriasis was related to an overdose of isoflurane. Intensivists should be aware of the reported phenomenon to avoid unnecessary diagnostic investigations that might harm the patient. We recommend careful control of the isoflurane dose when fixed and dilated pupils appear in patients without other signs of elevated ICP.

Cerebral Metabolism and Blood Flow Following Traumatic Brain Injury

2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Marike Zwienenberg ◽  
Kee D Kim ◽  
Kiarash Shahlaie
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Cerebral Autoregulation ◽  
Cerebral Metabolism ◽  
Elevated Intracranial Pressure ◽  
Metabolic Demand ◽  
Cerebral Metabolic Rate

The management of traumatic brain injury focuses on the prevention of second insults, which most often occur because of a supply/demand mismatch of the cerebral metabolism. The healthy brain has mechanisms of autoregulation to match the cerebral blood flow to the cerebral metabolic demand. After trauma, these mechanisms are disrupted, leaving the patient susceptible to episodes of hypotension, hypoxemia, and elevated intracranial pressure. Understanding the normal and pathologic states of the cerebral blood flow is critical for understanding the treatment choices for a patient with traumatic brain injury. In this chapter, we discuss the underlying physiologic principles that govern our approach to the treatment of traumatic brain injury. This review contains 3 figures, 1 table and 12 references Key Words: cerebral autoregulation, cerebral blood flow, cerebral metabolic rate, intracranial pressure, ischemia, reactivity, vasoconstriction, vasodilation, viscosity

Trauma: Traumatic Brain Injury

2018 ◽  
pp. 95-100
Author(s):  
Ruchir Gupta
Keyword(s):  
Traumatic Brain Injury ◽  
Substance Abuse ◽  
Acute Respiratory Distress Syndrome ◽  
Cervical Spine ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Glasgow Coma Scale ◽  
Elevated Intracranial Pressure ◽  
Intraoperative Management ◽  
History Of

In this chapter the essential aspects of anesthesia for traumatic brain injury are discussed. Subtopics include manifestations and treatment of elevated intracranial pressure (ICP), Glasgow Coma Scale (GCS), drugs used to lower ICP, and patient monitoring. The case presented is an emergent craniotomy. The chapter is divided into preoperative, intraoperative, and postoperative sections with important subtopics related to the main topic in each section. Preoperative topics discussed are evaluation of trauma, use of the GCS in this case, assessing intracranial hypertension, history of substance abuse, and clearing the cervical spine. Issues related to intraoperative management in this case include induction and use of blood products. Postoperative concerns addressed include polyuria and acute respiratory distress syndrome.

scholarly journals Prehospital management of traumatic brain injury

2008 ◽  
Vol 25 (4) ◽  
pp. E5 ◽  
Author(s):  
Shirley I. Stiver ◽  
Geoffrey T. Manley
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Prehospital Care ◽  
Major Determinant ◽  
Neurological Injury ◽  
Raised Intracranial Pressure ◽  
Long Term Outcome ◽  
Cerebral Herniation ◽  
Prehospital Management

The aim of this study was to review the current protocols of prehospital practice and their impact on outcome in the management of traumatic brain injury. A literature review of the National Library of Medicine encompassing the years 1980 to May 2008 was performed. The primary impact of a head injury sets in motion a cascade of secondary events that can worsen neurological injury and outcome. The goals of care during prehospital triage, stabilization, and transport are to recognize life-threatening raised intracranial pressure and to circumvent cerebral herniation. In that process, prevention of secondary injury and secondary insults is a major determinant of both short- and longterm outcome. Management of brain oxygenation, blood pressure, cerebral perfusion pressure, and raised intracranial pressure in the prehospital setting are discussed. Patient outcomes are dependent upon an organized trauma response system. Dispatch and transport timing, field stabilization, modes of transport, and destination levels of care are addressed. In addition, special considerations for mass casualty and disaster planning are outlined and recommendations are made regarding early response efforts and the ethical impact of aggressive prehospital resuscitation. The most sophisticated of emergency, operative, or intensive care units cannot reverse damage that has been set in motion by suboptimal protocols of triage and resuscitation, either at the injury scene or en route to the hospital. The quality of prehospital care is a major determinant of long-term outcome for patients with traumatic brain injury.

Computed Tomographic Brain Density Measurement as a Predictor of Elevated Intracranial Pressure in Blunt Head Trauma

2007 ◽  
Vol 73 (10) ◽  
pp. 1023-1026 ◽  
Author(s):  
Kenji Inaba ◽  
Pedro G.R. Teixeira ◽  
Jean-Stephane David ◽  
Carlos Brown ◽  
Ali Salim ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Injury Severity ◽  
Density Measurement ◽  
Elevated Intracranial Pressure ◽  
Icp Monitoring ◽  
Brain Ct ◽  
Blunt Head Trauma ◽  
Brain Density

There are no independent computed tomography (CT) findings predictive of elevated intracranial pressure (ICP). The purpose of this study was to evaluate brain density measurement on CT as a predictor of elevated ICP or decreased cerebral perfusion pressure (CPP). A prospectively collected database of patients with acute traumatic brain injury was used to identify patients who had a brain CT followed within 2 hours by ICP measurement. Blinded reviewers measured mean density in Hounsfield Units (HU) within a 100-mm2 elliptical region at four standardized positions. Brain density measurement was compared for patients with an ICP of 20 or greater versus less than 20 mm Hg and CPP of 70 or greater versus less than 70 mm Hg. During a 2-year period, 47 patients had ICP monitoring after brain CT. Average age was 40 ± 18 years old; 93.6 per cent were male; mean Injury Severity Score was 25 ± 10; and Glasgow Coma Scale was 6 ± 4. There was no difference in brain density measurement for observer 1, ICP less than 20 (26.3 HU) versus ICP 20 or greater (27.4 HU, P = 0.545) or for CPP less than 70 (27.1 HU) versus CPP 70 or greater (26.2, P = 0.624). Similarly, there was no difference for observer 2, ICP less than 20 (26.8 HU) versus ICP 20 or greater (27.4, P = 0.753) and CPP less than 70 (27.6 HU) versus CPP 70 or greater (26.2, P = 0.436). CT-measured brain density does not correlate with elevated ICP or depressed CPP and cannot predict patients with traumatic brain injury who would benefit from invasive ICP monitoring.

Long-term outcomes and prognostic factors in pediatric patients with severe traumatic brain injury and elevated intracranial pressure

2008 ◽  
Vol 2 (4) ◽  
pp. 240-249 ◽  
Author(s):  
Jay Jagannathan ◽  
David O. Okonkwo ◽  
Hian Kwang Yeoh ◽  
Aaron S. Dumont ◽  
Dwight Saulle ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Pediatric Patients ◽  
Elevated Intracranial Pressure ◽  
The Mean

Object The management strategies and outcomes in pediatric patients with elevated intracranial pressure (ICP) following severe traumatic brain injury (TBI) are examined in this study. Methods This study was a retrospective review of a prospectively acquired pediatric trauma database. More than 750 pediatric patients with brain injury were seen over a 10-year period. Records were retrospectively reviewed to determine interventions for correcting ICP, and surviving patients were contacted prospectively to determine functional status and quality of life. Only patients with 2 years of follow-up were included in the study. Results Ninety-six pediatric patients (age range 3–18 years) were identified with a Glasgow Coma Scale score < 8 and elevated ICP > 20 mm Hg on presentation. The mean injury severity score was 65 (range 30–100). All patients were treated using a standardized head injury protocol. The mean time course until peak ICP was 69 hours postinjury (range 2–196 hours). Intracranial pressure control was achieved in 82 patients (85%). Methods employed to achieve ICP control included maximal medical therapy (sedation, hyperosmolar therapy, and paralysis) in 34 patients (35%), ventriculostomy in 23 patients (24%), and surgery in 39 patients (41%). Fourteen patients (15%) had refractory ICP despite all interventions, and all of these patients died. Seventy-two patients (75%) were discharged from the hospital, whereas 24 (25%) died during hospitalization. Univariate and multivariate analysis revealed that the presence of vascular injury, refractory ICP, and cisternal effacement at presentation had the highest correlation with subsequent death (p < 0.05). Mean follow-up was 53 months (range 11–126 months). Three patients died during the follow-up period (2 due to infections and 1 committed suicide). The mean 2-year Glasgow Outcome Scale score was 4 (median 4, range 1–5). The mean patient competency rating at follow-up was 4.13 out of 5 (median 4.5, range 1–4.8). Univariate analysis revealed that the extent of intracranial and systemic injuries had the highest correlation with long-term quality of life (p < 0.05). Conclusions Controlling elevated ICP is an important factor in patient survival following severe pediatric TBI. The modality used for ICP control appears to be less important. Long-term follow-up is essential to determine neurocognitive sequelae associated with TBI.

Sign in / Sign up

Export Citation Format

Share Document