Hypoxic ischemic encephalopathy

HYPOXIC ISCHEMIC ENCEPHALOPATHY

PRECEPTORDR MAMTA BHUSHAN SINGH

PRESENTER:DR SUCHARITA RAY

Case vignetteA 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.

Clinical ExaminationGeneral 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)

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 ?

The First Big Question…


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

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

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 necrosisIschemia alone caused necrosis in 4 of 12 rats, despite PaO2 > 100 mm Hg.

Miyamoto et al. Neurology; 2000 Jan 25;54(2):362-71

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

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 EEGAnd 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

PATHOPHYSIOLOGY

SEVERE INJURY

LESS SEVERE INJURY

Lai M, Yang S. Perinatal Hypoxic-Ischemic Encephalopathy J Biomed Biotechnology; 2011

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

Post–Cardiac Arrest Syndrome: Pathophysiology, Neurologic Manifestations, and Potential Treatments

Syndrome Pathophysiology Clinical Manifestation Potential Rx

Post cardiac Impaired cerebrovasc Coma Therapeutic hypothermiaArrest brain autoregulation Seizures Early hemodynamicInjury 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.

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

Background and methods:

4.5-year prospective observational studyStudy period: January 2009 till August 2013An 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

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

Caronna and Finklestein. Neurological syndromes after cardiac arrest. Stroke. 1978; 9:517-520

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 hours3> Purposive movement of limbs at any timeEEG does not have a role in the diagnosis/prognosis or therapy during any phase of HIE

PARADIGM SHIFT

THE MOST ISCHEMIA SUSCEPTIBLE AREAS OF THE BRAIN:

1.The cortical projection neurons2.The posterior cingulate cortex/precuneus3.Medial prefrontal cortex4.Bilateral temporoparietal junctions [collectively termed Default Mode Network 5.Cerebellar Purkinje cells6.CA-1 area of the hippocampus

J J Caronna and S Finklestein. Neurological syndromes after cardiac arrest. Stroke. 1978; 9:517-520

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


•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



•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 cortexGutierrez LG: CT and MR in non-neonatal hypoxic-ischemic encephalopathy: radiological findings with pathophysiological correlations. Neuroradiology 2010, 52:949–976

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


• 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


NCCT Head:

Bilateral hyperdense caudate and putamina and subtle increased cortical density

1.Severe grey matter necrosis.

2.Reversal of normal white/grey matter density.

NCCT Head performed 40 minute down time following cardiac arrest.

Severe hypoxic ischemic encephalopathy with multifocal

infarctions

(including midbrain, bilateral thalamic, multifocal supratentorial cortical)

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

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.

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

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 trauma2.birth asphyxia3.Drowning4.status epilepticus5.bacterial meningitis6.Encephalitis7.post-cardiac arrest hypoxia

Chavhan GB. Twenty classic signs in neuroradiology: A pictorial essay. Indian J Radiol Imaging. 19 (2): 135-45.

Cranial CT after cardiac arrest demonstrating watershed infarction between the anterior and middle and between the middle and posterior cerebral arteries

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

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

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

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

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

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

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

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.

ILCOR Levels of evidence for prognostic studies.LOE P1: Inception (prospective) cohort studies (or meta-analyses ofinception 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-sampleLOE P3 Retrospective cohort studiesLOE P4 Case seriesLOE P5 Studies not directly related to the specific patient/population (e.g.different patient/population, animal and mechanical models)

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

SUMMARY OF EVIDENCE FOR MRI BRAIN


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


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 transaminase3.Lactate dehydrogenase4.Pyruvate (Serum/CSF)

THE THREE PROMISING BIOMARKERS STUDIED:

Neuron-specific enolase (NSE)Protein soluble in 100% ammonium sulfate (S-100)Interleukin-8 (IL-8)

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

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

The Big Question…What is the likely diagnosis ?


Salazar-Reyes H, Varon J: Hypoxic tissue damage and the protective effects of therapeutic hypothermia. Crit Care & Shock 2005;8:28-31.

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

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

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

CirculationVolume 127(14):1538-1563

April 9, 2013

Copyright © American Heart Association, Inc. All rights reserved.

Strategies for Improving Survival After In-Hospital Cardiac Arrest in the United States: 2013 Consensus Recommendations

Copyright © American Heart Association, Inc.

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


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.

Therapeutic Hypothermia

• 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.


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


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


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 arrivalABG 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

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

OTHER PROMISING STRATEGIES !!!

The Big Questions…



Based on the diagnosis does the neurologic examination exclude the possibility of a good Outcome ?

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.

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.

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.

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

Decision Algorithm for Use in Outcome Prediction for Comatose Survivors of Cardiac Arrest

Wijdicks EFM et al Practice parameters. Neurology 2006; 67:203-10

NEUROPROGNOSTICATION IN PATIENTS OF HYPOXIC ISCHEMIC ENCEPHALOPATHY:

Use of therapeutic hypothermia as a treatment modalityUse of sedatives and analgesicsOrgan failure and shockPhenomenon of self fulfilling prophecyPrognostication 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.



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 reflexesMotor responses Myoclonus


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


Methods:Systematic Review of a total of 73 studies

Predictors were based on the following: 1.Clinical examination2.Electrophysiology3.Biomarkers and4.Imaging


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.


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.


Recent parameters incorporated in prognostication of HIE:

Somatosensory evoked potentials [SSEP]

Neuron specific enolase (NSE)

Neuroimaging

• 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

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 stemand the spinal cord

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Hypoxic ischemic encephalopathy

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