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13 results

  • 13 - Intracranial Hemorrhage

  • from Section 3 - Neurological Emergencies
  • Edited by Kaushal Shah, Weill Cornell Medical Center, New York, Jarone Lee, Massachusetts General Hospital, Boston
  • Edited in association with Clark G. Owyang, Weill Cornell Medical Center, New York, Benjamin Christian Renne, Massachusetts General Hospital, Boston
  • Book:
    Practical Emergency Resuscitation and Critical Care
    Published online:
    02 November 2023
    Print publication:
    23 November 2023, pp 114-123

  • Summary

    • Intracranial hemorrhage (ICH) occurs when blood occupies space within the calvarium. ICH irritates brain parenchyma and impairs outflow of cerebral spinal fluid (CSF) from the dural sinus venous network, which raises intracranial pressure (ICP) with a resultant decrease in cerebral perfusion.

    • ICH types are defined by the location of the bleeding: intracerebral (within the parenchyma), epidural (between the skull and the dura), subdural (between the dura and arachnoid membrane) and subarachnoid (between arachnoid membrane and pia mater).

    • The skull is inelastic, so blood accumulation increases intracranial pressure.

  • 48 - Severe Traumatic Brain Injury

  • from Section 11 - Trauma
  • Edited by Kaushal Shah, Weill Cornell Medical Center, New York, Jarone Lee, Massachusetts General Hospital, Boston
  • Edited in association with Clark G. Owyang, Weill Cornell Medical Center, New York, Benjamin Christian Renne, Massachusetts General Hospital, Boston
  • Book:
    Practical Emergency Resuscitation and Critical Care
    Published online:
    02 November 2023
    Print publication:
    23 November 2023, pp 516-527

  • Summary

    • Severe traumatic brain injury (TBI) is usually defined as a Glasgow Coma Scale (GCS) score < 9. The goals of early resuscitation should focus on identifying and treating the primary injuries and limiting the negative cascade of secondary injuries such as hypotension and hypoxia. All patients with suspected severe TBI need an emergent computed tomography (CT) scan of the brain to identify hemorrhage immediately following initial stabilization. Ten percent of severe TBI patients have concomitant c-spine injury.

  • Cortical Spreading Depolarization in Chronic Subdural Hematoma: Bridging the Gap

  • Mathieu Levesque, Charles Deacon, Suzie Adam, Christian Iorio-Morin
  • Journal:
    Canadian Journal of Neurological Sciences / Volume 48 / Issue 1 / January 2021
    Published online by Cambridge University Press:
    23 June 2020, pp. 31-37
    • Article
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  • Cortical spreading depolarization (CSD) is recognized as a cause of transient neurological symptoms (TNS) in various clinical entities. Although scientific literature has been flourishing in the field of CSD, it remains an underrecognized pathophysiology in clinical practice. The literature evoking CSD in relation to subdural hematoma (SDH) is particularly scarce. Patients with SDH frequently suffer from TNS, most being attributed to seizures despite an atypical semiology, evolution, and therapeutic response. Recent literature has suggested that a significant proportion of those patients’ TNS represent the clinical manifestations of underlying CSD. Recently, the term Non-Epileptical Stereoytpical Intermittent Symptoms (NESIS) has been proposed to describe a subgroup of patients presenting with TNS in the context of SDH. Indirect evidence and recent research suggest that the pathophysiology of NESIS could represent the clinical manifestation of CSD. This review should provide a concise yet thorough review of the current state of literature behind the pathophysiology of CSD with a particular focus on recent research and knowledge regarding the presence of CSD in the context of subdural hematoma. Although many questions remain in the evolution of knowledge in this field would likely have significant diagnostic, therapeutic, and prognostic implications.

  • Effect of Cerebral Perfusion Pressure on Acute Respiratory Distress Syndrome

  • Sonny Thiara, Donald E. Griesdale, William R. Henderson, Mypinder S. Sekhon
  • Journal:
    Canadian Journal of Neurological Sciences / Volume 45 / Issue 3 / May 2018
    Published online by Cambridge University Press:
    19 February 2018, pp. 313-319
    • Article
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  • Background: Increased cerebral perfusion pressure (CPP)>70 mmHg has been associated with acute respiratory distress syndrome (ARDS) after traumatic brain injury (TBI). Since this reported association, significant changes in ventilation strategies and fluid management have been accepted as routine critical care. Recently, individualized perfusion targets using autoregulation monitoring suggest CPP titration>70 mmHg. Given these clinical advances, the association between ARDS and increased CPP requires further delineation. Objective: To determine the association between ARDS and increased CPP after TBI. Methods: We conducted a single-center historical cohort study investigating the association of increased CPP and ARDS after TBI. We collected demographic data and physiologic data for CPP, intracranial pressure, mechanical ventilation, cumulative fluid balance and delta/driving pressure (ΔP). We collected outcomes measures pertaining to duration of ventilation, intensive care unit admission length, hospitalization length and 6-month neurological outcome. Results: In total, 113 patients with severe TBI and multimodal neuromonitoring were included. In total, 16 patients (14%) developed ARDS according to the Berlin definition. There was no difference in the mean CPP during the first 7 days of admission between patients who developed ARDS (74 mmHg SD 18 vs. 73 mmHg SD 18, p=0.86) versus those who did not. Patients who developed ARDS had a higher ΔP (15 mmHg [5] vs. 12 mmHg [4], p=0.016) and lower lung compliance (35 ml/cmH2O [10] vs. 49 ml/cmH2O [18], p=0.024) versus those who did not. Conclusion: We did not observe an association between increased CPP and ARDS. Patients with ARDS had higher ΔP and lower lung compliance.

  • 18 - Status epilepticus

  • from Section 3 - Neurological emergencies
  • Edited by Kaushal Shah, Jarone Lee, Kamal Medlej, American University of Beirut, Scott D. Weingart
  • Book:
    Practical Emergency Resuscitation and Critical Care
    Published online:
    05 November 2013
    Print publication:
    24 October 2013, pp 130-133

  • Summary

    This chapter discusses the diagnosis, evaluation and management of severe traumatic brain injury (TBI). Early intubation is indicated in all severe TBI patients, and pretreatment may help minimize increase in intracranial pressure (ICP) during intubation. All severe TBI patients should have a neurosurgical evaluation early in their ED course. If the patient has a seizure, treatment and loading with 1g of phenytoin or fosphenytoin is indicated. The decision to place invasive ICP monitoring should generally be made in conjunction with neurosurgery. The indications for invasive ICP monitoring (external ventricular drain or intraparenchymal monitor) include severe TBI and a computed tomography (CT) showing hematomas, contusions, swelling, herniation, or compressed basal cisterns. Propofol or pentobarbital coma may be induced for severe, but nonsurgical TBI. The goal is to reduce cerebral activity and oxygen demand. These agents cause hypotension and decreased cerebral perfusion pressure (CPP) and should only be initiated with neurosurgical input.

  • Section 5 - Respiratory emergencies

  • Edited by Kaushal Shah, Jarone Lee, Kamal Medlej, American University of Beirut, Scott D. Weingart
  • Book:
    Practical Emergency Resuscitation and Critical Care
    Published online:
    05 November 2013
    Print publication:
    24 October 2013, pp 197-228

  • Summary

    This chapter discusses the diagnosis, evaluation and management of intracranial hemorrhage. It describes types of intracranial hemorrhage, including subarachnoid hemorrhage (SAH), subdural hemorrhage (SDH), epidural hemorrhage (EDH) and intracerebral hemorrhage (ICH). Emergent non-contrast head CT is the cornerstone for detection of ICH. MRI is equally effective in identifying ICH and better at detecting predisposing underlying parenchymal or vascular anomalies. Emergency department management focuses on protecting cerebral perfusion by balancing the forces of mean arterial pressure (MAP) and intracranial pressure (ICP). Patients should be positioned with the head of the bed elevated to 30 degrees to support cerebral venous drainage to reduce ICP. The main goal of emergency management is to temporize ICP changes, avoid secondary insults (e.g., hypoxia and hypotension) and protect cerebral perfusion pressure (CPP) while expediting neurosurgical evaluation for possible life-saving surgical intervention.

  • Chapter 50 - Cervical artery dissections

  • from Section 2 - Vascular topographic syndromes
  • Edited by Louis R. Caplan, Jan van Gijn
  • Book:
    Stroke Syndromes, 3ed
    Published online:
    05 August 2012
    Print publication:
    12 July 2012, pp 560-565

  • Summary

    Low-flow infarctions, also called borderzone infarctions, are considered the result of critically reduced cerebral perfusion pressure (CPP) in far-downstream brain arteries that causes critically compromised cerebral blood flow and insufficient oxygen supply in certain vulnerable brain areas. Transhemispheric and interterritorial collateral blood flow via the anterior and posterior communicating arteries and their individual distributions must be considered with respect to the site and size of borderzone infarctions. Cardiac arrest and hypotension can also cause low-flow infarcts that are usually bilateral. Although hypoxic-ischemic cerebellar damage is often found at necropsy, clinical signs of cerebellar dysfunction are rare and are usually overshadowed by cerebral abnormalities. The general medical prognosis of patients with low-flow infarcts is poor. Deaths as a result of cardiovascular complications are frequent and account for about 10% of deaths per year. An important diagnostic improvement in identifying low-flow infarcts was the use of rCBF techniques.

  • 13 - Anaesthesia for intracranial vascular surgery and carotid disease

  • from Section 3 - Neuroanaesthesia
  • Edited by Basil F. Matta, David K. Menon, Martin Smith
  • Book:
    Core Topics in Neuroanaesthesia and Neurointensive Care
    Published online:
    05 December 2011
    Print publication:
    13 October 2011, pp 178-204

  • Summary

    The intracranial pressure (ICP) has three components: an arterial vascular component; a cerebrospinal fluid (CSF) circulatory component; and a venous outflow component. More generally, multiple variables such as the arterial pulsatile pressure, autoregulation and cerebral venous outflow all contribute to the vascular component. Intracranial compliance is a concept often associated with CSF storage. Measurement of brain compliance is classically performed using a CSF bolus injection. In sedated patients with TBI, continuous ICP monitoring is recommended, and can only be achieved by direct invasive measurement. The gold standard for ICP monitoring is a catheter inserted into the lateral ventricle and connected to an external pressure transducer. Cerebral perfusion pressure (CPP)-oriented therapy has been introduced to decrease the risk of ischaemia in post-injury care. Intracranial pressure waveforms include distinct periodic components: heart pulse waves, respiratory waves and quasi-periodic slow vasogenic waves.

  • 19 - Systemic complications of neurological disease

  • from Section 4 - Neurointensive care
  • Edited by Basil F. Matta, David K. Menon, Martin Smith
  • Book:
    Core Topics in Neuroanaesthesia and Neurointensive Care
    Published online:
    05 December 2011
    Print publication:
    13 October 2011, pp 281-300

  • Summary

    The purposes of multimodality monitoring mimic the aims of monitoring: to continuously measure relevant biological variables, to verify the effects of treatment, to identify trends in the clinical evolution of disease, and to contribute to the assessment of prognosis. Multimodality monitoring may indicate associations between parameters and may contribute to clinical research. This chapter shows that good data concerning adequate oxygen delivery to the organs and maintenance of homeostasis are already part of routine intensive care unit (ICU) monitoring. Cerebral perfusion pressure (CPP) is calculated as the difference between mean arterial pressure (MAP) and intracranial pressure (ICP), and represents the driving force for cerebral blood flow (CBF). Multimodality monitoring integrates multiple sources of information in a number of possible combinations. It is around for over two decades, and it is tempting to try to undertake cost-benefit analysis of this approach to patient management.

  • Section 3 - Neuroanaesthesia

  • Edited by Basil F. Matta, David K. Menon, Martin Smith
  • Book:
    Core Topics in Neuroanaesthesia and Neurointensive Care
    Published online:
    05 December 2011
    Print publication:
    13 October 2011, pp 147-270

  • Summary

    The cerebral circulation is protected from systemic blood pressure surges by a complex branching system and two resistance elements: the first of these lies in the large cerebral arteries, and the second in vessels of diameter <100 μm. Endothelial cells in cerebral capillaries contain few pinocytic vesicles and are sealed with tight junctions, without any anatomical gap. Several endogenous substances including catecholamines and vascular growth enhancing factor can dynamically modulate blood-brain barrier (BBB) permeability. Classical cerebral autoregulation assessment does not consider the latency of autoregulatory mechanisms, focusing instead on the maintenance of cerebral blood flow (CBF) at different steady state levels of cerebral perfusion pressure (CPP). Methods of measuring CBF may be regional or global, and may be applicable either to humans or primarily to experimental animals. Severe head injury is accompanied by both direct and indirect effects on CBF and metabolism, which show both temporal and spatial variations.

  • 31 - Ventilation/perfusion abnormalities and capnography

  • from 1 - Ventilation
  • Edited by J. S. Gravenstein, University of Florida, Michael B. Jaffe, Nikolaus Gravenstein, University of Florida, David A. Paulus, University of Florida
  • Book:
    Capnography
    Published online:
    05 August 2011
    Print publication:
    17 March 2011, pp 313-328

  • Summary

    This chapter discusses two roles for capnography in the assessment and treatment of patients in cardiac arrest. It evaluates the efficacy of cardiopulmonary resuscitation (CPR), and cessation of resuscitation. A number of animal studies have shown an excellent correlation between end-tidal carbon dioxide (PETCO2) and cardiac output during states of low flow and during CPR. An animal model with ultrasound flow probes and radioactive microspheres was used to examine the relationships between PETCO2 and cardiac output, cerebral perfusion, and renal perfusion. A number of studies have found that PETCO2 values may change transiently after the administration of intravenous epinephrine or sodium bicarbonate. One of several studies that examined the active compression/decompression CPR (active compression/decompression (ACD)/CPR) technique used PETCO2 as a marker for cardiac output to compare the hemodynamics generated by the ACD/CPR method to standard CPR in the out-of-hospital setting.

  • Case 23 - Postoperativeretroperitoneal bleed

  • from Section I - Neuroanesthesia
  • Edited by George A. Mashour, Ehab Farag
  • Book:
    Case Studies in Neuroanesthesia and Neurocritical Care
    Published online:
    03 May 2011
    Print publication:
    03 February 2011, pp 77-79

  • Summary

    Intraoperative management of subarachnoid hemorrhage (SAH) is high-risk anesthesia with the potential for severe consequences. This chapter presents a case study of a 56-year-old African-American female smoker who presented with sudden onset of frontal headache, vomiting, and neck stiffness. Anesthesia for patients with SAH is challenging. The maintenance of an adequate mean arterial blood pressure, and hence cerebral perfusion pressure (CPP), during the induction of anesthesia is key to prevent ischemic secondary injury. CPP and transmural pressure are essentially influenced by the same variables and are equal to the mean arterial pressure minus intracranial pressure (ICP). Aneurysm rupture during laryngoscopy is an uncommon but life-threatening complication, which should be suspected if severe hypertension and bradycardia develop. Constant vigilance regarding hemodynamic control and preparedness for the possibility of intraoperative aneurysmal rupture are essential for good outcomes.