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Hypoxic ischemic encephalopathy

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Hypoxic ischemic encephalopathy, neurocritical care, prognostic factors regarding brain death

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Hypoxic ischemic encephalopathy

  1. 1. HYPOXIC ISCHEMIC ENCEPHALOPATHY PRECEPTOR DR MAMTA BHUSHAN SINGH PRESENTER: DR SUCHARITA RAY
  2. 2. Case vignette A 62yr old man hypertensive while arguing with his son suddenly complained of dizziness and collapsed. He was taken to the hospital within 20 minutes and on the way became unresponsive to his sons frantic attempts at communication. Emergency Evaluation: Cyanosed and pulseless. CPR started immediately. ECG: V Fib requiring a 200-joule biphasic shock followed by CPR and then finally a 360 joule biphasic shock with conversion to a wide-complex rhythm at 120 bpm. The BP was 120/70 mm Hg. Estimated time from collapse to return of spontaneous circulation (ROSC) was 15 minutes. He was intubated and then transported to the emergency department (ED) of a local hospital.
  3. 3. Clinical Examination General Examination: Unremarkable Neurologic examination: No response to verbal stimulation and no eye opening to noxious stimulation. He had reactive pupils, trace corneal reflexes, weakly present horizontal oculocephalic reflexes, no gag reflex, and a weak cough reflex. Upon noxious stimulation, he had extensor posturing of the arms and triple flexion in legs. The Glasgow Coma Scale (GCS) score was 4. (E1V1M2)
  4. 4. The Big Questions… What is the likely diagnosis ? How to best treat this condition? Based on the diagnosis does the neurologic examination exclude the possibility of a good Outcome ?
  5. 5. The First Big Question… What is the likely diagnosis ?
  6. 6. WHAT IS HYPOXIC ISCHEMIC ENCEPHALOPATHY • Hypoxic-ischemic encephalopathy (HIE) is a syndrome of acute global brain injury resulting from critical reduction or loss of blood flow and/or supply of oxygen and nutrients. • Some of the terms used to describe this clinical syndrome include: • Anoxic encephalopathy • Post-cardiac arrest syndrome* • Term is used to indicate that the phase of resuscitation has ended with resumption of spontaneous circulation and the complex changes that occur secondary to it
  7. 7. Mechanism of hypoxia/ischemia Causes Cardiac arrest followed by respiratory depression Massive blood loss, septic/traumatic shock, and heart disease, such as AMI or ventricular arrhythmia Respiratory failure followed by cardiac arrest with poor inspired oxygen Tracheal compression/obstruction, drowning, strangulation, aspiration of gastric content, or during GA if the inspired gas is oxygen poor Respiratory muscles weakness Guillain-barré syndrome, amyotrophic lateral sclerosis, myasthenia gravis) or central nervous system injury (mainly spinal cord injury) Reduced oxygen carriage by the blood Carbon monoxide poisoning Histotoxicity Cyanide poisoning. Ropper AH, Brown RH. 2014. Adams and Victor’s principles of neurology, Mc Graw Hill CAUSES OF HYPOXIC ISCHEMIC ENCEPHALOPATHY
  8. 8. Q: IS HYPOXIA ALONE SUFFICIENT FOR CAUSING BRAIN NECROSIS? ANSWER: FALSE Unlike ischemia and hypoglycemia, hypoxia alone is rarely responsible for brain necrosis Study subjects: Physiologically monitored Wistar rats subjected to hypoxia alone (PaO2 = 25 mm Hg) at maintained blood pressure (30 mm Hg) versus Ischemia alone (unilateral carotid ligation) via unilateral carotid ligation and each of the parameters graded with the other kept constant. Hypoxia alone, with normal BP for 15 minutes: No necrosis Ischemia alone caused necrosis in 4 of 12 rats, despite PaO2 > 100 mm Hg. Miyamoto et al. Neurology; 2000 Jan 25;54(2):362-71
  9. 9. WHAT FACTORS TO KEEP IN MIND IN A CASE OF HYPOXIA/ISCHEMIA: •The event causing the cut off of oxygen/blood supply •The rate at which the disruption of blood/oxygen supply takes place •Previous comorbid factors •Compensatory mechanisms if any THE INHERENT PROPERTY OF THE OXYGEN CARRYING MECHANISM
  10. 10. Situation Amount Clinical consequence Normal brain blood supply 55 ml/min/ 100 g None Normal brain oxygen supply 4 mg/min/100 g Acute drop in blood flow 25 ml/min/ 100 g Slowing of the EEG And syncope or impaired consciousnessDrop in oxygen saturation <2mg/min/100gm Refractory shock, post cardiac arrest, cyanide poisoning 12 to 15 ml/min / 100 g Electrocerebral silence, coma, and cessation of most neuronal metabolic and synaptic functions 8 to 10 ml/min/ 100 g. Neuronal death Oxygen supply< 1 mg/min/100 g Ropper AH, Brown RH. 2014. Adams and Victor’s principles of neurology, Mc Graw Hill THRESHOLDS FOR BRAIN TISSUE FOR ISCHEMIA/HYPOXIA
  11. 11. PATHOPHYSIOLOGY
  12. 12. SEVERE INJURY LESS SEVERE INJURY Lai M, Yang S. Perinatal Hypoxic-Ischemic Encephalopathy J Biomed Biotechnology; 2011
  13. 13. The Molecular Pathway: Interweaving apoptosis and necroptosis pathways after HI insult. Thornton C. Role of mitochondria in apoptotic and necroptotic cell death in the developing brain, Clin Chim Acta (2015); Still in press
  14. 14. Post–Cardiac Arrest Syndrome: Pathophysiology, Neurologic Manifestations, and Potential Treatments Syndrome Pathophysiology Clinical Manifestation Potential Rx Post cardiac Impaired cerebrovasc Coma Therapeutic hypothermia Arrest brain autoregulation Seizures Early hemodynamic Injury Cerebral edema Myoclonus optimization Postischemic Cog. Dysfunction Airway protection and neurodegeneration Persistent veg state mechanical ventilation Sec. Parkinsonism Seizure control Cortical stroke Controlled reoxygenation Spinal stroke (SaO2 94% to 96%) Brain death Supportive care Neumar et al Post–Cardiac Arrest Syndrome. ILCOR Consensus statement. 2453. Circulation. 2008;118:2452–2483.
  15. 15. Atypical Posthypoxic neurologic sequelae •Progressive Extrapyramidal syndrome •Korsakoff syndrome •Parkinsonian syndrome with cognitive impairment (mc due to CO poisoning), •Choreoathetosis •Cerebellar ataxia •Intention (action) myoclonus, •Seizures. •With prominent ischemia is prominent, two main syndromes are seen, visual agnosia (Balint syndrome and cortical blindness) and “man in the barrel” syndrome (severe bilateral arm weakness) Commichau C. (2006). Hypoxic-Ischemic encephalopathy, in Neurological therapeutics principles and practice, Noseworthy JH. 528-537
  16. 16. Background and methods: 4.5-year prospective observational study Study period: January 2009 till August 2013 An aetiology study group examined 302 episodes of IHCA. The purpose was to investigate the causes and cause-related survival in patients who had inhospital cardiac arrest (IHCA). To evaluate whether these causes were recognised by the ETs. D. Bergum et al. Causes of in-hospital cardiac arrest – Incidences and rate of recognition. Resuscitation 87 (2015) 63–68
  17. 17. RESULTS OF THE STUDY: •Cause of IHCA reliably determined in 258 (85%) episodes •The cause was correctly recognised by the ET in 198 of 302 episodes (66%). •Cardiac causes were (156, 60%) and hypoxic causes (51, 20%) were present. •The cause-related survival was 30% for cardiac aetiology and 37% for hypoxic aetiology. D. Bergum et al. Causes of in-hospital cardiac arrest – Incidences and rate of recognition. Resuscitation 87 (2015) 63–68
  18. 18. Caronna and Finklestein. Neurological syndromes after cardiac arrest. Stroke. 1978; 9:517-520
  19. 19. J J Caronna and S Finklestein. Neurological syndromes after cardiac arrest. Stroke. 1978;9:517-520 Signs indicating a favorable prognosis: 1> Spontaneous roving horizontal eye movements at 12 to 24 hours 2> Speech and comprehension within the first 48 hours 3> Purposive movement of limbs at any time EEG does not have a role in the diagnosis/prognosis or therapy during any phase of HIE
  20. 20. PARADIGM SHIFT
  21. 21. THE MOST ISCHEMIA SUSCEPTIBLE AREAS OF THE BRAIN: 1.The cortical projection neurons 2.The posterior cingulate cortex/precuneus 3.Medial prefrontal cortex 4.Bilateral temporoparietal junctions [collectively termed Default Mode Network 5.Cerebellar Purkinje cells 6.CA-1 area of the hippocampus J J Caronna and S Finklestein. Neurological syndromes after cardiac arrest. Stroke. 1978; 9:517-520
  22. 22. NEUROIMAGING OF HYPOXIC ISCHEMIC ENCEPHALOPATHY 1.The white matter of the brain is susceptible to hypoxic-ischemic events and may be involved, even when the insult is systemic and generalized. 2.Thus a leukoencephalopathy can be the end result of long-standing hypertension or a single hypotensive episode, e.g. perinatal hypoxia. 3.The changes can occur in the setting of global hypoxia in the presence of focal or global ischemia. 4.The changes vary according to age and severity and are not specific Gutierrez LG: CT and MR in non-neonatal hypoxic-ischemic encephalopathy: radiological findings with pathophysiological correlations. Neuroradiology 2010, 52:949–976
  23. 23. NEUROIMAGING OF HYPOXIC ISCHEMIC ENCEPHALOPATHY •What structures does a HIE involve in neuroimaging ? Severe global hypoxic-ischemic injury in this population primarily affects the gray matter structures: • Basal ganglia • Thalami • Cerebral cortex (in particular the sensorimotor and visual cortices, although involvement is often diffuse) • Cerebellum • Hippocampi Gutierrez LG: CT and MR in non-neonatal hypoxic-ischemic encephalopathy: radiological findings with pathophysiological correlations. Neuroradiology 2010, 52:949–976
  24. 24. NEUROIMAGING OF HYPOXIC ISCHEMIC ENCEPHALOPATHY •Why the grey matter is preferentially involved in hypoxic damage ? The gray matter contains most of the dendrites where postsynaptic glutamate receptors are located. Hence early to be involved in the excitotoxicity. It is also more metabolically active than white matter •Why is cerebellum more affected in older but spared in children? The relative immaturity of Purkinje cells (which are normally exquisitely sensitive to ischaemic damage) in neonates somehow protects the cerebellar cortex Gutierrez LG: CT and MR in non-neonatal hypoxic-ischemic encephalopathy: radiological findings with pathophysiological correlations. Neuroradiology 2010, 52:949–976
  25. 25. NEUROIMAGING FEATURES OF HYPOXIC-ISCHEMIC ENCEPHALOPATHY• Diffuse oedema with effacement of the CSF-containing spaces • Decreased cortical gray matter attenuation with loss of normal gray-white differentiation • Decreased bilateral basal ganglia attenuation • Reversal Sign: Reversal of the normal CT attenuation of grey and white matter, demonstrated within the first 24 hours. •White Cerebellum Sign: Diffuse oedema and hypoattenuation of the cerebral hemispheres with sparing of the cerebellum and brainstem, resulting in apparent high attenuation of the cerebellum and brainstem relative to the cerebral hemispheres Gutierrez LG: CT and MR in non-neonatal hypoxic-ischemic encephalopathy: radiological findings with pathophysiological correlations. Neuroradiology 2010, 52:949–976
  26. 26. • Linear hyperdensity outlining the cortex as well as linear cortical enhancement (later and less evident signs), corresponding to Cortical Laminar Necrosis • Falx cerebri and tentorium cerebelli can appear hyperdense to ischaemic brain parenchyma and is one of the causes of pseudo-subarachnoid hemorrhage * Both the reversal sign and the white cerebellum sign indicate severe injury and a poor neurologic outcome Radiographic features Gutierrez LG: CT and MR in non-neonatal hypoxic-ischemic encephalopathy: radiological findings with pathophysiological correlations. Neuroradiology 2010, 52:949–976
  27. 27. NCCT Head: Bilateral hyperdense caudate and putamina and subtle increased cortical density
  28. 28. 1.Severe grey matter necrosis. 2.Reversal of normal white/grey matter density. NCCT Head performed 40 minute down time following cardiac arrest.
  29. 29. Severe hypoxic ischemic encephalopathy with multifocal infarctions (including midbrain, bilateral thalamic, multifocal supratentorial cortical)
  30. 30. Recent resuscitation from CPR: Cerebral Oedema leading to decreased parenchyma attenuation and engorgement and dilatation of the superficial venous structures due an increased intracranial pressure Huang BY, Castillo M. Hypoxic-ischemic brain injury: imaging findings from birth to adulthood. Radiographics. 28 (2): 417-39,2009
  31. 31. Cortical layers 3, 4, and 5 have higher metabolic demands and hence lead to cortical laminar necrosis. The gyriform high attenuation (likely caused by local hemorrhage) is believed to be caused by the accumulation of denatured proteins in dying cells It does not represent presence of hemorrhage.
  32. 32. Low density of caudate head and lentiform nucleus. This vagrant was found unconscious on the street, bottle of alcohol in hand. Huang BY, Castillo M. Hypoxic-ischemic brain injury: imaging findings from birth to adulthood. Radiographics. 28 (2): 417-39,2009
  33. 33. White cerebellum sign (Reversal sign or dense cerebellum sign) Diffuse decrease in density of the supratentorial brain parenchyma, with relatively increased attenuation of the thalami, brainstem and cerebellum. This sign indicates irreversible brain damage and has a very poor prognosis Theories proposed for this sign : 1.Raised intracranial pressure causes partial venous obstruction resulting in distension of deep medullary veins. 2.Preferential flow to posterior circulation. 3.Transtentorial herniation partially relieving the increased intracranial pressure, and thus increase perfusion of central structures. It is associated with : 1.severe head trauma 2.birth asphyxia 3.Drowning 4.status epilepticus 5.bacterial meningitis 6.Encephalitis 7.post-cardiac arrest hypoxia Chavhan GB. Twenty classic signs in neuroradiology: A pictorial essay. Indian J Radiol Imaging. 19 (2): 135-45.
  34. 34. Cranial CT after cardiac arrest demonstrating watershed infarction between the anterior and middle and between the middle and posterior cerebral arteries
  35. 35. NEUROPATHOLOGY OF VEGETATIVE STATE AFTER AN ACUTE BRAIN INSULT Adams JH. The neuropathology of the vegetative state after an acute brain insult. Brain 123, 1327–1338, 2000. (A) Gross specimen demonstrating watershed infarcts (B) Low magnification view of the cerebral cortex
  36. 36. NEUROPATHOLOGY OF VEGETATIVE STATE AFTER AN ACUTE BRAIN INSULT Adams JH. The neuropathology of the vegetative state after an acute brain insult. Brain 123, 1327–1338, 2000. (B) Area of necrosis involves layers II to V of cortex (C) Pyknotic and eosinophilic cerebral cortex
  37. 37. SEQUENCE EARLY LATE T1WI Subtle swelling of grey matter structures Laminar cortical necrosis after 2 weeks Cortical necrosis,Passive ventricular enlargement (Ventriculomegaly,) PVWM volume loss, PV cavitation, thin callosum T2WI T2 signal in PVWM (edema, ischemia, or infarction), focal T2 signal (hemorrhagic necrosis) Residual Basal Ganglia hyperintensity, Gliosis, thalamic scarring, PV cysts Demyelination DWI Normal before 24 h of life. 1st 24 hours, cerebellar hemispheres, basal ganglia, or cerebral cortex , perirolandic and occipital cortices). ADC normalizes within 10-12 days. Pseudonormalization of DWI MRI CHANGES IN HIE
  38. 38. 35-year-old patient who had experienced an ischemic event several weeks earlier. Axial T1-weightedMR image: Bilateral serpiginous high signal intensity in the cortex of the occipital lobes (greater on the left side), A finding that is compatible with cortical necrosis Huang BY, Castillo M. Hypoxic-ischemic brain injury: imaging findings from birth to adulthood. Radiographics.28 (2): 417-39, 2009
  39. 39. MRI findings. FLAIR images (a) High signal intensity areas in bilateral periventricular white matter and pallidal nuclei. DWI imaging (b) show similar high signal intensity in the PWM, with diffuse low signal intensity in the ADC map (c). Follow up one month later shows resolution
  40. 40. Delayed White Matter Injury (Postanoxic Leukoencephalopathy) •Uncommon syndrome of delayed white matter injury, 2-3% patients of HIE. •Usually occurs weeks after a hypoxic-ischemic event e.g CO poisoning. •Period of relative clinical stability/improvement, followed by an acute neurologic decline with delirium, personality changes, intellectual impairment, movement disorders, or, rarely, seizures •May even show steady decline without a lucid interval •Approximately 75% of patients have complete or near-complete recovery over the next 6–12 months. •In the remaining patients, there may be residual dementia. •Rarely, the condition may progress to paresis, a vegetative state, or death
  41. 41. Immediate period after causative insult: No WM Abnormalities on conventional imaging Period of delayed neurologic decline: DWI: Diffuse confluent areas of restricted diffusion throughout the cerebral white matter T2WI: Corresponding hyperintensity on T2-weighted images is also seen. Postanoxic Leukoencephalopathy Neuroimaging Roychowdhury S. Postanoxic encephalopathy: Review of MR findings. J Comput Assist Tomogr 1998;22:992–94
  42. 42. Postanoxic Leukoencephalopathy Neuroimaging Postanoxic leukoencephalopathy in an adult patient who had experienced respiratory arrest 2 weeks earlier. (a, b) Axial T2-weighted (a) and diffusion-weighted (b) MR images show diffuse white matter hyperintensity.(c) On the corresponding ADC map, the white matter is hypointense, a finding that indicates restricted diffusion.
  43. 43. ILCOR Levels of evidence for prognostic studies. LOE P1: Inception (prospective) cohort studies (or meta-analyses of inception cohort studies), or validation studies of a clinical decision rule (CDR) LOE P2: Follow-up of untreated control groups in randomized controlled trials (or meta-analyses of follow-up studies), or derivation studies of a CDR, or validation studies of a CDR using a split-sample LOE P3 Retrospective cohort studies LOE P4 Case series LOE P5 Studies not directly related to the specific patient/population (e.g. different patient/population, animal and mechanical models)
  44. 44. SUMMARY OF EVIDENCE FOR NCCT HEAD D.K. Hahn et al. Quality of evidence in studies evaluating neuroimaging for neurologic prognostication in adult patients resuscitated from cardiac arrest.Resuscitation 85 (2014) 165– 172; 167
  45. 45. SUMMARY OF EVIDENCE FOR MRI BRAIN D.K. Hahn et al. Quality of evidence in studies evaluating neuroimaging for neurologic prognostication in adult patients resuscitated from cardiac arrest.Resuscitation 85 (2014) 165– 172; 167
  46. 46. CONCLUSIONS FROM THE STUDY • There is insufficient scientific evidence to support or refute the use of neuroimaging • There is an abundance of data in the current literature, • The majority of these studies are limited by their design. • These limitations include: • Retrospective design, • Small cohort size, • Lack of control for confounders • Early withdrawal of care, • Lack of blinding • Lack of comparison with standard clinical methods of prognostication D.K. Hahn et al. Quality of evidence in studies evaluating neuroimaging for neurologic prognostication in adult patients resuscitated from cardiac arrest.Resuscitation 85 (2014) 165– 172; 167
  47. 47. Biochemical markers (NSE, S-100, IL-8) as predictors of neurological outcome in patients after cardiac arrest and return of spontaneous circulation BIOMARKERS THAT HAVE BEEN STUDIED SO FAR: 1.Brain creatine phosphokinase (CPK BB) 2.Glutamate transaminase 3.Lactate dehydrogenase 4.Pyruvate (Serum/CSF) THE THREE PROMISING BIOMARKERS STUDIED: Neuron-specific enolase (NSE) Protein soluble in 100% ammonium sulfate (S-100) Interleukin-8 (IL-8)
  48. 48. Konstantinos A. Biochemical markers (NSE, S-100, IL-8) as predictors of neurological outcome in patients after CA AND ROSC. Resuscitation (2007) 75, 219—228
  49. 49. Konstantinos A. Biochemical markers (NSE, S-100, IL-8) as predictors of neurological outcome in patients after CA AND ROSC. Resuscitation (2007) 75, 219—228
  50. 50. The Big Question… What is the likely diagnosis ? How to best treat this condition?
  51. 51. Salazar-Reyes H, Varon J: Hypoxic tissue damage and the protective effects of therapeutic hypothermia. Crit Care & Shock 2005;8:28-31.
  52. 52. TREATMENT OF A CASE OF HYPOXIC ISCHEMIC ENCEPHALOPATHY Emergent Medical Stabilization Therapeutic Hypothermia Seizure and Myoclonus Management ICP Management General Intensive Care Management PROGNOSTICATION © 2013 Neurocritical Care Society Review Course
  53. 53. EMERGENT MEDICAL STABILIZATION  Securing Airway IV Access-preferably Central Venous Access NPO, orogastric tube with low intermittent suction Urinary Catherter with Strict I/O Monitoring Monitoring of vitals, administration of vasopressors if required Ruling out concomitant other pathologies like SAH, CVA etc © 2013 Neurocritical Care Society Review Course
  54. 54. Strategies for Improving Survival After In-Hospital Cardiac Arrest in the United States: 2013 Consensus Recommendations by Laurie J. Morrison, Robert W. Neumar, Janice L. Zimmerman, Mark S. Link, L. Kristin Newby, Paul W. McMullan, Terry Vanden Hoek, Colleen C. Halverson, Lynn Doering, Mary Ann Peberdy, and Dana P. Edelson Circulation Volume 127(14):1538-1563 April 9, 2013 Copyright © American Heart Association, Inc. All rights reserved.
  55. 55. Strategies for Improving Survival After In-Hospital Cardiac Arrest in the United States: 2013 Consensus Recommendations Copyright © American Heart Association, Inc.
  56. 56. Seizure and Myoclonus Management  Incidence of non-convulsive status epilepticus can be as high as 24% which signifies a worse prognosis  Continuous VEEG monitoring for the same is standard of care  Insufficient evidence to recommend prophylactic use of antiepileptics  Less sedating agents and/or those with short half lives (midazolam, levetiracetam, phosphenytoin or valproic acid) to avoid clouding the neurologic evaluation and neuroprognostication  Acute post hypoxic myoclonus (PHM) occurs in about 30%:  Status myoclonus  Multifocal myoclonus.  Subcortical myoclonus: Rx with clonazepam. Propofol, may also be useful though longer term control after weaning is problematic Copyright © American Heart Association, Inc.
  57. 57. Patel R, Jha S. Intravenous valproate in post-anoxic myoclonic status epilepticus: A report of ten patients. Neurol India 2004;52:394-6 Intravenous valproate in post-anoxic myoclonic status epilepticus: A report of ten patients • Study of the efficacy of intravenous VP in 10 patients who developed MSE following anoxic cerebral injury in the peri- and postoperative (within 24-48 hours) period. • MSE was terminated with iv VP alone in 6 patients and the time duration for the termination of MSE was between 2-10 hours. • An additional infusion of a second AED, I/V diazepam/lorazepam, one each was required in 2 patients to terminate MSE. • The time taken for the termination of MSE was 26 and 38 hours. Limitation: Continuous EEG monitoring was not done and serum valproate levels were not measured.
  58. 58. Therapeutic Hypothermia
  59. 59. • Therapeutic hypothermia has demonstrated a robust benefit with a number needed to treat (NNT) of six. • Survival benefit for out of hospital cardiac arrest with VT/VF as initial rhythms or asystole or PEA • Many methods to induce hypothermia, ranging from physical surface cooling on the (ice packs, cold baths, special pads, helmets, etc), intravenous infusions of chilled fluids, endovascular devices, intraperitoneal, and endonasal cooling systems. • The duration of the method in the original 2002 European study maintained hypothermia for 24 hours and Australian study was for 12 hours. Copyright © American Heart Association, Inc.
  60. 60. ICP Management •Cerebral edema apparent on the initial cranial CT in approximately 30% of patients following cardiac arrest •In case of cerebral herniation, the use of hypertonic saline and osmotherapy in an attempt to reverse herniation is indicated Copyright © American Heart Association, Inc.
  61. 61. General Intensive Care Management Hemodynamic Management: MAP of 60 or SBP of 90 mmHg to maintain organ perfusion; however a MAP of 70-100 mmHg may be considered to augment cerebral perfusion pressure (CPP) in cases of cerebral edema and elevated intracranial hypertension. Mechanical Ventilation: Discontinue 100% FiO2 once ROSC is achieved Arterial oxygen saturation of 94-98% soon as possible post resuscitation * Hyperoxia seems to have detrimental effects Normocapnea with PCO2 between 40-45 mmHg and ETCO2 35-40 mmHg Copyright © American Heart Association, Inc.
  62. 62. Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. Objective: Postresuscitation hyperoxia is associated with increased mortality. Design, Setting, and Patients Multicenter cohort study: Project IMPACT database of intensive care units (ICUs) at 120 US hospitals (2001 - 2005) Main Outcome Measure In-hospital mortality. Inclusion criteria: Age > 17 years, nontraumatic cardiac arrest, CPR within 24 hours prior to ICU arrival ABG within 24 hours following ICU arrival. Patients were divided into 3 groups hypoxia, hyperoxia and normoxia based on predefined parameters J H Kilgannon et al. (Reprinted) JAMA, June 2, 2010—Vol 303, No. 21 2165
  63. 63. Results Of 6326 patients, 1156 had hyperoxia (18%), 3999 had hypoxia (63%), and 1171 had normoxia (19%). The hyperoxia group had significantly higher inhospital mortality (732/1156 [63%; 95% confidence interval {CI}, 60%-66%]) Normoxia group (532/1171 [45%; 95% CI, 43%-48%]; Hypoxia group (2297/3999 [57%; 95% CI, 56%-59%] Controlling for confounders (age, preadmission functional status, comorbid conditions, vital signs, and other physiological indices), hyperoxia exposure had an odds ratio for death of 1.8 (95% CI, 1.5-2.2). Conclusion Among patients admitted to the ICU following resuscitation from cardiac arrest, arterial hyperoxia was independently associated with increased in-hospital mortality compared with either hypoxia or normoxia. J H Kilgannon et al. (Reprinted) JAMA, June 2, 2010—Vol 303, No. 21 2165
  64. 64. OTHER PROMISING STRATEGIES !!!
  65. 65. The Big Questions… What is the likely diagnosis ? How to best treat this condition? Based on the diagnosis does the neurologic examination exclude the possibility of a good Outcome ?
  66. 66. Outcome of coma by etiology Death Persistent vegetative state Good recovery Hypoxic-Ischemic 58 20 8 Toxic-Metabolic 47 6 25 Cerebrovascular 74 7 3 Total 61 12 10 Adapted from Bates D.The prognosis of medical coma. J Neurol Neurosurg Psychiatry. 2001;71(Suppl 1): i20–3.
  67. 67. Cardiac arrest survivors treated with or without mild therapeutic hypothermia: performance status and quality of life assessment •To determine long-term neurological and psychological status in cardiac arrest survivors •To compare neuropsychological outcomes between patients treated with mild therapeutic hypothermia (MTH) vs patients who did not undergo hypothermia treatment •Single-center, retrospective, observational study on 28 post-cardiac arrest adult vs 37 control group patients, hospitalized at the same center following cardiac arrest in the preceding years and fulfilling criteria for induced hypothermia but not given it.
  68. 68. Results: No statistically significant differences in physical functioning found between groups either at the end of hospital treatment or at long-term follow-up (DRS: p = 0.11; Barthel Index: p = 0.83). In long-term follow-up, MTH patients showed higher vitality (p = 0.02) and reported fewer complaints on role limitations due to emotional problems (p = 0.04) compared to the control group. No significant differences were shown between study groups in terms of physical capacity and independent functioning. Conclusion: To conclude, in long-term follow-up, MTH patients showed higher vitality and reported fewer complaints on role limitations due to emotional problems compared to the control group. This suggest that MTH helps to preserve global brain function in cardiac arrest survivors. However, the results can be biased by a small sample size and variable observation periods.
  69. 69. Majority of studies done have so far predicted an outcome no better than a vegetative state or severe disability with total dependency at 3 to 6 months after arrest (a Glasgow Outcome Scale score of 3 or less) Vegetative state= wakefulness but no evidence of conscious awareness. Wijdicks EFM et al Practice parameters: prediction of outcome in comatose survivors after CPR. Neurology 2006; 67:203-10
  70. 70. Decision Algorithm for Use in Outcome Prediction for Comatose Survivors of Cardiac Arrest Wijdicks EFM et al Practice parameters. Neurology 2006; 67:203-10
  71. 71. NEUROPROGNOSTICATION IN PATIENTS OF HYPOXIC ISCHEMIC ENCEPHALOPATHY: Use of therapeutic hypothermia as a treatment modality Use of sedatives and analgesics Organ failure and shock Phenomenon of self fulfilling prophecy Prognostication not the same for different causative etiologies. No good evidence from well-designed studies to support early prognostication (< 72 hours) in cardiac arrest survivors treated with TH. Wijdicks EFM et al Practice parameters: prediction of outcome in comatose survivors after CPR. Neurology 2006; 67:203-10
  72. 72. NEUROPROGNOSTICATION IN PATIENTS OF HYPOXIC ISCHEMIC ENCEPHALOPATHY: Neuroprognostication is vital and yet one of the most controversial topics in post resuscitation care. To date there is no adequate paradigm to prognosticate HIE treated with TH Prognostication parameters exist for HIE without TH as a intervention as far back as 2006 by AAN. Traditional prognostication parameters: Brainstem reflexes Motor responses Myoclonus Wijdicks EFM et al Practice parameters: prediction of outcome in comatose survivors after CPR. Neurology 2006; 67:203-10
  73. 73. Objectives: •Review and update of the evidence on predictors of poor outcome in adult comatose survivors of cardiac arrest •Patients may be either treated or not treated with controlled temperature •Identification of gaps in knowledge and suggestion of a reliable prognostication strategy. C. Sandroni et al. Prognostication in comatose survivors of cardiac arrest. Resuscitation 85 (2014) 1779– 89
  74. 74. C. Sandroni et al. Prognostication in comatose survivors of cardiac arrest. Resuscitation 85 (2014) 1779– Methods: Systematic Review of a total of 73 studies Predictors were based on the following: 1.Clinical examination 2.Electrophysiology 3.Biomarkers and 4.Imaging
  75. 75. C. Sandroni et al. Prognostication in comatose survivors of cardiac arrest. Resuscitation 85 (2014) 1779–89 Results and conclusions: •The quality of evidence was low or very low for almost all studies •In patients who are comatose with absent or extensor responses at ≥72 h from arrest, either treated or not treated with controlled temperature •Bilateral absence of either pupillary and corneal reflexes or N20 wave of short- latency somatosensory evoked potentials were identified as the most robust predictors.
  76. 76. C. Sandroni et al. Prognostication in comatose survivors of cardiac arrest. Resuscitation 85 (2014) 1779–89 USEFUL BUT LESS ROBUST PREDICTORS: •Early status myoclonus •Elevated values of neuron specific enolase at 48–72 h from arrest •Unreactive malignant EEG patterns after rewarming •Presence of diffuse signs of postanoxic injury on either CT or MRI. * Prolonged observation and repeated assessments should be considered when results of initial assessment are inconclusive.
  77. 77. NEUROPROGNOSTICATION IN PATIENTS OF HYPOXIC ISCHEMIC ENCEPHALOPATHY: Recent parameters incorporated in prognostication of HIE: Somatosensory evoked potentials [SSEP] Neuron specific enolase (NSE) Neuroimaging
  78. 78. • Large unmet gap in knowledge, attitude and practice in patients with in hospital or out of hospital cardiac arrest • At our level accurate diagnosis should be achieved at the earliest and aggressive management should be pursued in triaged patients • Efforts must be placed on creating new hospital protocols that emphasize the importance of achieving mild hypothermia within the first hours after cardiopulmonary arrest, as well as detecting and promptly treating any kind of seizure • Neuroprognostication should take into account not only clinical signs but also laboratory parameters TAKE HOME MESSAGE
  79. 79. DURATION OF HYPOXIA CLINICAL SIGNS •Up to 1 minute Unconsciousness, convulsions, Miosis, abolished pupillary reflex •After 2 minutes Mydriasis, the abolition of corneal reflex •After 5 minutes Cerebral cortex suffering irreversible damage •After 15 minutes Irreversible damage at brain stem and the spinal cord

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