Hypoxic ischaemic encephalopathy ppt.pptx

Hypoxic-Ischemic Encephalopathy (HIE) is a type of brain injury caused by lack of oxygen and blood flow to the brain, usually around the time of birth.
It can lead to developmental delays, seizures, or cerebral palsy.
Severity ranges from mild to severe depending on how long the brain lacked oxygen.
Early treatment like cooling therapy (therapeutic hypothermia) may reduce brain damage.

1. Brain Injury after Cardiac Arrest Presenter : Dr sushrutha Moderator : Dr sanjay

2. References Emergent Management of Hypoxic-Ischemic Brain Injury.Alexis Steinberg, MD, MS.Neurocritical Care p. 588-610June 2024, Vol.30, No.3 Brain Injury after Cardiac Arrest  Eelco F.M. Wijdicks  MD, PhD Neurologic Clinics, 2025-02-01, Volume 43, Issue 1, Pages 79-90. Improving Outcomes After Post–Cardiac Arrest Brain Injury: A Scientific Statement From the International Liaison Committee on Resuscitation, Circulation . 2024;150:e158–e180. DOI: 10.1161/CIR.0000000000001219 Sandroni, C., Cronberg , T. & Sekhon , M. Brain injury after cardiac arrest: pathophysiology, treatment, and prognosis.  Intensive Care Med   47 , 1393–1414 (2021). Bradley’s textbook of Neurology, 8 th edition .

3. One of the most common consult for a neurologist for a patient post CPR ??? NEURO PROGNOSTICATIONNNN…..

4. Introduction Anoxia - complete lack of oxygen delivery (e.g., complete cessation of blood flow during cardiac arrest) Hypoxia- with some degree of continued blood flow Hypoxic-ischemic brain injury — Less well defined and less clearly understood than anoxic-ischemic injury Can occur in patients with respiratory arrest or severe hypoxemia ( e.g.,asphyxia ) neuronal oxygen stores are depleted within 20 seconds of cardiac arrest, and cerebral necrosis occurs as a result of ischemia * * Bradley textbook of neurology

5. Etiopathogenesis Primary( ischaemic ) and secondary (reperfusion) injury Primary injury : Cardiac Arrest and Cessation of Blood Flow - no flow phase Energy Depletion - depletion of ATP  Na+/K+ ATPase pumpfailure cytotoxic edema Depolarization and Calcium Influx - k+ efflux from the cells and membrane depolarization occurs, opening voltage-gated Ca²⁺ channels

6. Secondary injury Initiation of CPR and ROSC - CBF is partially restored (low-flow)-suboptimal to sustain neuronal integrity Glutamate and excitotoxicity –intracellular ca+2  cytoplasmic calcium accumulation from the endoplasmic reticulum  activates Ca²⁺-dependent enzymes proteases and phospholipases neuronal damage Immune Activation and Inflammation-leucocytes  amplifies the inflammatory response  Leukocyte adhesion to the endothelial cells of the cerebral microvasculature cytokines release  vasogenic edema and further injury to neuronal tissue

7. Other causes – increased ICP and dysfunction ofcerebral autoregulation

8. Examination Early awakening after CPR, clinical signs of localizing pain stimuli, and following commands – good outcome Examination of brainstem reflexes- because resilient to anoxic-ischemia Motor response to pain Attention to myoclonus spontaneous or elicited eye movements Fixed, dilated pupils presenting 6 hours after resuscitation are a sign of poor prognosis Sustained upward gaze indicative of global bi hemispheric injury ,including thalamus mechanism -is a complete disinhibition of the vestibulo -ocular reflexes from the cerebellar flocculus

9. Myoclonus status epilepticus -defined as continuous and vigorous jerking movements involving facial muscles, limbs, and abdominal muscles elicited or aggravated by touch or hand clap and may also involve the diaphragm – complicate ventilation Classically considered agonal phenomenon indicating poor prognosis Poor motor response to pain ≠ poor outcome

10. MANAGEMENT of Primary brain injury prevention Shortening the time to chest compressions and ROSC Key actions by the AHA chain of survival : 1.Immediate recognition of cardiac arrest with activation of emergency response systems, early CPR , and rapid defibrillation of shockable rhythms 2.Laypeople can effectively deliver CPR without extensive training and apply automated external defibrillators 3.Interventions to improve time to CPR and defibrillation- Protocols to enhance early recognition by laypeople and dispatchers Dispatch-assisted CPR Smart technologies for activation of lay responders Increased public access to defibrillators public education and training on CPR and defibrillation.

11. Secondary brain injury approach Degree of initial brain and systemic injury can be categorized by using risk stratification scores Pittsburgh Cardiac Arrest Category Revised post-Cardiac Arrest Syndrome for Therapeutic hypothermia [ rCAST ] Full Outline of UnResponsiveness [FOUR] A neurologist’s views on the patient’s severity of injury may help clinical teams decide about performing aggressive interventions

12. Wijdicks EF, Bamlet WR, Maramattom BV, Manno EM, McClelland RL (2005). "Validation of a new coma scale: The FOUR score". Annals of Neurology

13. Low severity: rCAST ≤ 5.5 Moderate severity: rCAST 6.0–14.0 High severity: rCAST ≥ 14.5 Revised Post-Cardiac Arrest Syndrome for Therapeutic hypothermia – rCAST score

14. emergencymedicine.pitt.edu/patient-care/post-cardiac-arrest-service/ pittsburgh -cardiac-arrest-category

15. Prevention of secondary brain injury

16. Aim to prevent secondary brain injury by correcting pathophysiologic processes Prevention of Rearrests Optimization of mean arterial pressure Cerebral perfusion Oxygenation and ventilation Intracranial pressure and edema Temperature control Cortical hyper excitability - seizures

17. Prevention of rearrests Main aim is to prevent rearrests , identify etiologies and treat them Ex :spontaneous pneumothorax needle insertion and AMI  PCI

18. Optimization of mean arterial pressure After hypoxic-ischemic brain injury, lower limit of autoregulation ( ie , the MAP below which oligemic flow occurs)is often right-shifted or sometimes absent Adequate cerebral perfusion is necessary to prevent secondary brain injury Cerebral hypoperfusion may occur hours to days after arrest Goal 65 to 80mm Hg Individualized target

19. Intracranial Pressure and Edema Cerebral edema  ICP  herniation  brain death Early cerebral edema seen on CT of the brain predicts a worse outcome ICP can be measured with invasive and noninvasive monitors, allowing for goal-directed treatment Rewarming after hypothermic temperature control may worsen cerebral edema Cardiac arrest impairs the ability of the brain to buffer rapid shifts in serum osmolarity .Ex- hyperglycemia and hyperuremia So goal is to prevent rapid shift in temperature and osmolarity

20. Ventilator management Current recommendations are to maintain normoxia after cardiac arrest An RCT compared PaO2 of 68 to 75 mm Hg Vs 98 to 105 mm Hg  no difference in the primary outcome of death and severe neurologic injury * Target pa02 75 to 100 mm Hg Hypoxia and severe hyperoxia should be avoided *Schmidt H, et al.Oxygen targets in comatose survivors of cardiac arrest. N Engl J Med 2022;387(16):1467-1476. doi:10.1056/NEJMoa2208686

21. Hyperventilation  hypocapnia  cerebral vasoconstriction  cerebral ischemia Mild therapeutic hypercapnia can improve cerebral blood flow and may reduce biomarkers of brain injury Target pac02 : 35 to 45 mm Hg and avoid hypocapnia Eastwood G, et al. Mild hypercapnia or normocapnia after out- ofhospital cardiac arrest. N Engl J Med 2023;389(1):45-57. doi:10.1056/NEJMoa2214552

22. 33°C (91°F) for 24 hours Vs 37°C (99°F) No difference in functional neurologic outcome or mortality

23. Temperature management

24. Reduction in core temperature with ice packs, rapid infusion of cold IV fluids, and the use of external cooling devices or endovascular cooling systems Temperature management initiated in 2–3 hours to reduce core temperatures to 32°C–36°C and is maintained for 24 hours, followed by gradual rewarming Sedation and neuromuscular blockade are needed to control shivering Systemic complications - pneumonia, cardiac arrhythmias, pancreatitis, and hyperglycemia Benefit not established in inhospital CPR and cardiac rythmn other than ventricular fibrillation

25. Seizure Comatose after arrest develop hyperexcitable EEG changes Seizures may contribute to secondary brain injury Unclear - aggressive suppression of rhythmic or periodic EEG patterns improves neurologic outcomes Neurologic outcomes of comatose patients were similar when rhythmic or periodic discharges (greater than 0.5 Hz) on EEG were treated with an aggressive Vs standard management * Few patients had true electrographic seizures (10%) or a continuous background ASM – GTCS ,myoclonus, NCSE , or ictal interictal continuum when a continuous or reactive background is observed * Ruijter BJ, et al. Treatment of electroencephalographic status epilepticus after cardiopulmonary resuscitation(TELSTAR): study protocol for a randomized controlled trial. Trials 2014;15:433. doi:10.1186/ 1745-6215-15-433

26. Myoclonus Most Common after cardiac arrest Historically thought to indicate a universally poor prognosis Development of a continuous cortical background on EEG despite postanoxic myoclonus is associated with delayed awakening (days to weeks)

27. Video of lance adams syndrome

28. Assessment of the Validity of the 2HELPS2B Score for Inpatient Seizure Risk Prediction. JAMA Neurol. 2020 Apr 1;77(4):500-507

29. NEUROPROGNOSTICATION Incorrectly predicting good outcome  early withdrawal of support of those who may recover Incorrectly predicting the potential for awakening  prolonged and costly care  s urvival with poor quality of life No gold standard approach to prognostication in hypoxic-ischemic brain injury

30. Pre hypothermia era CPR circumstances not predictive of outcome Eye movement abnormalities insufficiently predictive Invariably poor neurological outcome Myoclonus status epilepticus within the first 24 Absence of pupillary responses within day 1–3 after arrest Absence of corneal reflexes within day 1–3 Absent or extensor motor responses after day 3

31. Neurologic examination Full Outline of UnResponsiveness (FOUR) score Motor response localizing – good prognosis Absent pupillary and corneal reflexes bilaterally for ≥72 hours, Status myoclonus <48 hours with associated highly malignant EEG pattern- poor prognosis Done – Daily , 72 hours after arrest , off sedation Brainstem reflexes are crucial because brainstem is relatively resistant to anoxic-ischemic injury Absence of pupil or corneal reflexes indicates severe and widespread injury that also involves much of the cortex

32. EEG Good prognosis- Early return of continuous, reactive,normal voltage background Poor prognosis - Highly malignant pattern (suppressed or burst suppressed, with or without epileptiform discharges Frequency – Continuous monitoring until awakening; or routine EEG at 12-24 hours and repeated after sedation weaning (48-72 hours) for patients still comatose Reactivity should be assessed because its presence predicts better outcome “Highly malignant” patterns defined by the American Neurophysiological Society - suppressed background, suppressed background with continuous periodic discharges, and burst suppression These predict a poor outcome with 50% sensitivity and 100% specificity A continuous background with preserved background reactivity is considered “benign” and has a positive predictive value of about 80% for good outcomes * *Rossetti et al., 2017

33. cEEG monitoring - increases the detection of epileptiform activity But has not shown better prognosis , though treated

34. 1.DWI MRI in anoxic-ischemic injury shows diffuse cortical hyperintensities indicative of cortical injury, likely laminar necrosis 2.T2 hyperintensity involving the cortex 3.T1 contrast enhancement in the basal ganglia 4.NCCT shows diffuse cerebral edema , loss of gray -white differentiation

35. SSEP - Amplitude of N20 potentials ≥2.5 mV – good prognosis and absent after >48hrs poor prognosis Serum Neuron-specific enolase ≤17 mg/L – good prognosis and higher levels poor prognosis CT brain - Diffuse anoxic brain injury (reduced gray-white matter differentiation/ratio and sulcal effacement)- poor prognosis CT on admission helps exclude a central nervous system cause of cardiac arrest ( eg , intracranial hemorrhage) MRI BRAIN - Necessary only if initial CT doesn’t show severe anoxic brain injury Advanced techniques DTI and fMRI might be considered in specialized centers

36. S = sedatives, A = analgesics, B = neuromuscular junction blockers, H = hypothermia ,BSR brain stem relexes

37. Longterm outcome Ranges from functional independence to death Commonly reporting scales include 1.modified Rankin Scale ( mRS ) 2.Cerebral Performance Category, dichotomized as either a good or poor outcome Poor outcomes include patients who have died,are comatose, or are awake and functionally dependent - mRS 4 to 6 or Cerebral Performance Category 3 to 5

38. Majority of patients regain consciousness in 4 to 6 days Awakening can be delayed up to 2weeks – TTM and usage of sedatives MCC of death -withdrawal of life sustaining therapies based on perceived poor neurologic prognosis

39. Conclusion Anoxic-ischemic injury to the brain is damaging at ictus and often leads to prolonged coma, and in many patients a persistent unconsciousness can be anticipated if care is not withdrawn Continuous care of comatose patients after cardiopulmonary arrest results in a major burden to the healthcare system, and family members should be adequately informed about the chances of recovery There is some indication that treatments are on the horizon, but for now, early resumption of circulation is the best guarantee for awakening

40. Thank you