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8 results

  • Chapter 7 - Neonatal Encephalopathy

  • from Part II - Practice of Neuromonitoring: Neonatal Intensive Care Unit
  • Edited by Cecil D. Hahn, Courtney J. Wusthoff
  • Book:
    Neuromonitoring in Neonatal and Pediatric Critical Care
    Published online:
    08 September 2022
    Print publication:
    15 September 2022, pp 103-115

  • Summary

    Neonatal encephalopathy (NE) is the term used to describe persistent neurological dysfunction evident in the first few days after birth. The commonest cause of NE is hypoxia-ischemia, but a similar clinical presentation may occur in other conditions. EEG is essential to grade the severity of neonatal encephalopathy, monitor response to anti-seizure therapy, and to predict outcome early in the neonatal period in infants with NE. Because therapeutic hypothermia is often used in neonatal encephalopathy, the impact of hypothermia on EEG findings is important to consider. EEG evolution and outcome prediction is altered by therapeutic hypothermia. Seizures are common in NE, and seizure burden is also altered by hypothermia. EEG and aEEG can assess severity of NE and predict outcome more accurately than clinical assessment alone. This chapter discusses the various uses of EEG and aEEG in neonatal encephalopathy.

  • Altered biventricular function in neonatal hypoxic-ischaemic encephalopathy: a case–control echocardiographic study

  • Gabriel Altit, Sonia Lomeli Bonifacio, Carolina V. Guimaraes, Ganesh Sivakumar, Beth Yan, Valerie Chock, Krisa Van Meurs, Shazia Bhombal
  • Journal:
    Cardiology in the Young / Volume 33 / Issue 9 / September 2023
    Published online by Cambridge University Press:
    06 September 2022, pp. 1587-1596
    • Article
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  • Background:

    In newborns with hypoxic-ischaemic encephalopathy, more profound altered right and left ventricular function has been associated with mortality or brain injury. Mechanisms underlying cardiac dysfunction in this population are thought to be related to the persistence of increased pulmonary vascular resistance and myocardial ischaemia. We sought to compare cardiac function in newborns with hypoxic-ischaemic encephalopathy to controls using echocardiography.

    Methods:

    We did a retrospective case–control study with moderate or severe hypoxic-ischaemic encephalopathy between 2008 and 2017. Conventional and speckle-tracking echocardiography measures were extracted to quantify right and left ventricular systolic and diastolic function. Fifty-five newborns with hypoxic-ischaemic encephalopathy were compared to 28 controls.

    Results:

    Hypoxic-ischaemic encephalopathy newborns had higher estimated systolic pulmonary pressure (62.5 ± 15.0 versus 43.8 ± 17.3 mmHg, p < 0.0001) and higher systolic pulmonary artery pressure/systolic blood pressure ratio [101 ± 16 (iso-systemic) versus 71 ± 27 (2/3 systemic range) %, p < 0.0001]. Tricuspid annular plane systolic excursion was decreased (7.5 ± 2.2 versus 9.0 ± 1.4 mm, p = 0.002), E/e’ increased (7.9 ± 3.3 versus 5.8 ± 2.0, p = 0.01), and right ventricle-myocardial performance index increased (68.1 ± 21.5 versus 47.8 ± 9.5, p = 0.0001) in hypoxic-ischaemic encephalopathy. Conventional markers of left ventricle systolic function were similar, but e’ velocity (0.059 ± 0.019 versus 0.070 ± 0.01, p = 0.03) and left ventricle-myocardial performance index were statistically different (77.9 ± 26.2 versus 57.9 ± 11.2, p = 0.001). The hypoxic-ischaemic encephalopathy group had significantly altered right and left ventricular deformation parameters by speckle-tracking echocardiography. Those with decreased right ventricle-peak longitudinal strain were more likely to have depressed left ventricle-peak longitudinal strain.

    Conclusion:

    Newborns with hypoxic-ischaemic encephalopathy have signs of increased pulmonary pressures and altered biventricular systolic and diastolic function.

  • Effect of prehospital initiation of therapeutic hypothermia in adults with cardiac arrest on time-to-target temperature

  • Eric M. Schenfeld, Jonathan Studnek, Alan C. Heffner, Marcy Nussbaum, Kathi Kraft, David A. Pearson
  • Journal:
    Canadian Journal of Emergency Medicine / Volume 17 / Issue 3 / May 2015
    Published online by Cambridge University Press:
    02 June 2015, pp. 240-247
    Print publication:
    May 2015
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  • Objective: Despite growing adoption, the impact of prehospital initiation of therapeutic hypothermia on outcomes of cardiac arrest patients is unknown. The objective of this study was to determine if prehospital administration of cold intravenous fluids improved the time-to-target temperature.

    Methods: All patients enrolled in an institutional post– cardiac arrest treatment pathway were prospectively registered into a quality assurance database. Patients undergoing cooling induction on hospital arrival were compared to those receiving a new treatment protocol initiated during the study period involving prehospital cooling with 4°C (39.2°F) normal saline. The primary outcome was the time-to-target temperature. Secondary outcomes included emergency medicine system transport time metrics, mortality, and neurologic status at discharge and 1 year.

    Results: One hundred thirty-two patients were enrolled during the study period. The initial rhythm was ventricular fibrillation/tachycardia in 63% and asystole/pulseless electrical activity in 36%. Eighty patients received prehospital cooling and 52 patients did not and comprised the historical control group. Time-to-target temperatures were not significantly different between prehospital and hospital cooled groups (256 v. 271 minutes, respectively, p=0.64), nor was there any improvement in hospital survival (54% v. 50%, p=0.67), good neurologic outcome (49% v. 44%, p=0.61), or 1- year survival (49% v. 42%, p=0.46) between the two groups. Transport times were longer in the prehospital cooled group.

    Conclusions: Out-of-hospital cardiac arrest patients treated with prehospital cooling before arrival at our urban hospital did not have faster time-to-target temperature or improvement in outcomes compared to patients cooled immediately on emergency department arrival. Further research is needed to determine if any benefits exist from prehospital cooling prior to its widespread adoption.

  • Targeted temperature management: It is not yet time to change your target temperature

  • David Clinkard, Andrew Cameron, Daniel Howes, Ian Ball
  • Journal:
    Canadian Journal of Emergency Medicine / Volume 17 / Issue 6 / November 2015
    Published online by Cambridge University Press:
    05 February 2015, pp. 706-708
    Print publication:
    November 2015
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  • Clinical question

    In unconscious patients of out-of-hospital cardiac arrest, does targeted temperature management to 36°C (96.8°F) improve outcomes compared to the standard target of 32°C–34°C (89.6°F–93.2°F)?

    Article chosen

    Nielson N, Wetterslev J, Cronberg T, et al. Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med 2013;369:2197-2206.

    Objective

    To determine which temperature, 33°C (91.4°F) or 36°C (96.8°F), is associated with lower mortality and better neurologic function after cardiac arrest.

  • Combination of veno-arterial extracorporeal membrane oxygenation and hypothermia for out-of-hospital cardiac arrest due to Taxus intoxication

  • Aurélie Thooft, Ahmed Goubella, David Fagnoul, Fabio S. Taccone, Serge Brimioulle, Jean-Louis Vincent, Daniel De Backer
  • Journal:
    Canadian Journal of Emergency Medicine / Volume 16 / Issue 6 / November 2014
    Published online by Cambridge University Press:
    04 March 2015, pp. 504-507
    Print publication:
    November 2014
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  • A young woman presented with cardiac arrest following ingestion of yew tree leaves of the Taxus baccata species. The toxin in yew tree leaves has negative inotropic and dromotropic effects. The patient had a cardiac rhythm that alternated between pulseless electrical activity with a prolonged QRS interval and ventricular fibrillation. When standard resuscitation therapy including digoxin immune Fab was ineffective, a combination of extracorporeal membrane oxygenation (ECMO) and hypothermia was initiated. The total duration of low flow/no flow was 82 minutes prior to the initiation of ECMO. After 36 hours of ECMO (including 12 hours of electrical asystole), the patient’s electrocardiogram had normalized and the left ventricular ejection fraction was 50%. At this time, dobutamine and the ECMO were stopped. The patient had a full neurologic recovery and was discharged from the intensive care unit after 5 days and from the hospital 1 week later.

  • Case 95 - Myastheniccrisis

  • from Section II - Neurocritical care
  • 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 321-323

  • Summary

    The major factors in predicting neurologic dysfunction secondary to cardiac arrest involve the extent of brain insult as a function of time to return of circulation. The use of induced hypothermia has been studied as a way to combat neurologic injury for nearly five decades. This chapter presents a case study of a 37-year-old female with a history of chronic back pain and depression following a witnessed cardiac arrest 1 week after beginning risperidone therapy. The use of therapeutic hypothermia is widely accepted as the standard of care for preserving neurologic function following cardiac arrest. Cooling should be performed in all postcardiac arrest patients regardless of documented dysrhythmia, but supportive data are strongest for patients who are post ventricular fibrillation. Therapeutic hypothermia has been shown to be relatively safe and effective, and should be considered in the treatment of comatose patients following cardiac arrest.

  • Case 94 - Rhabdomyolysis

  • from Section II - Neurocritical care
  • 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 317-320

  • Summary

    Therapeutic hypothermia has been shown to improve outcome in patients after cardiopulmonary resuscitation and might prove helpful for other circumstances in which a compromise of neurologic function is expected. Cooling a patient to mild or moderate hypothermia is usually performed by conductive, convective surface cooling, cold infusions, gastric lavage, passive cooling by leaving the anesthetized patient uncovered in a cool environment, or through a combination of these methods. Endovascular cooling techniques seem to be superior for rapid induction of hypothermia and for maintenance of stable temperature as compared with surface-cooling techniques. The majority of therapeutic hypothermia trials for brain protection have involved surface-cooling techniques that require mechanical ventilation in intubated and paralyzed patients. Drugs such as meperidine, dexmedetomidine, clonidine, nefopam, and buspirone alone, as well as in various combinations, reduce the shivering threshold and thus complement external and internal cooling.

  • Chapter 32 - Unconventional strategies for respiratory support

  • from Section III: - Organ dysfunction and management
  • Edited by Fang Gao Smith, University of Warwick
  • Edited in association with Joyce Yeung
  • Book:
    Core Topics in Critical Care Medicine
    Published online:
    06 July 2010
    Print publication:
    22 April 2010, pp 251-256

  • Summary

    Current theories on the concept of a post-resuscitation syndrome describe the development of a systemic inflammatory response/sepsis following resuscitation from cardiac arrest. Critical care treatments during the post-resuscitation phase should focus on correcting hypoxia and hypercarbia, optimizing organ perfusion, identifying and treating the underlying cause of the cardiac arrest and optimizing neurological outcomes. Several randomized controlled trials and a meta-analysis have shown that therapeutic hypothermia is associated with improved survival and neurological outcome in initially comatose survivors of cardiac arrest. Observational studies in cardiac arrest survivors have shown that hyperglycaemia after return of spontaneous circulation is associated with an adverse outcome. Myocardial dysfunction is common after cardiac arrest and usually starts to improve within 72 hours after return of spontaneous circulation. Acidosis and control of seizures are explained in this chapter. The ability to predict the likely neurological outcome of a patient following admission to critical care is important.