Neurological Prognostication After Cardiac Arrest Murad Talahma, M.D. Neurocritical Care Ochsner Medical Center

Transcription

1 Neurological Prognostication After Cardiac Arrest Murad Talahma, M.D. Neurocritical Care Ochsner Medical Center Financial Disclosure None 1

2 Introduction Each year, 356,000 Americans are treated by EMS for OHCA, and 209, 000 are treated for an IHCA. Between 50 and 90% of OHCA patients with (ROSC) die in the hospital. Two-thirds dies from neurological injury, most of the times due to withdrawal of life support (WLST). 26% of the patients who had early WLST might have survived had lifesustaining therapy not been withdrawn, 64% of these might have had functionally favorable survival(based on two prognostic models). Nationally, eliminating WLST < 72 and its attributable mortality might save as many as 2300 lives after OHCA, of which a majority might have functionally favorable recovery. WLST because of assumed poor prognosis is the most common proximate cause of death after OHCA. (self-fulfilling prophecy). Neurological prognostication prior to therapeutic hypothermia(th) ERA 2

3 Neurological prognostication post therapeutic hypothermia(th) ERA TH can significantly impact normal body function and recovery. Significant sedation might be used during TH. TH cause reduction in drug clearance. 3

4 4

5 HACA (Europe) Bernard (Australia) Initial rhythm VF or VT VF Target T C 33 C # hypothermia patients # standard treatment patients Hypothermia duration Morbidity reduction Mortality reduction hrs 12 hrs ARR 16%, NNT 6 ARR 16%, NNT 4 ARR 14%, NNT 6 ARR 17%, NNT 6 Current AHA guidelines 5

6 33 C or 36 C Justin Smith 6

7 Justin smith When to prognosticate? No TH Delay final prognostication until at least 72h post arrest. With TH Delay prognostication until at least 72 hours of normothermia has passed. 7

8 General Concepts Compared to poor outcome, good neurological recovery is more difficult to predict because the absence of unfavorable markers does not guarantee good outcomes. Use a multimodal approach, combining clinical examination with additional methods, consisting of electrophysiology, blood biomarkers, and brain imaging. Tough balance: Providing inappropriate treatment in patients with no chance of recovery, Vs. withhold treatments prematurely in those that have a chance for good neurologic outcome. Prognostication tools 1. Clinical Neurological Exam 2. EEG 3. SSEP 4. Biomarkers 5. Brain Images 8

9 Neurological Exam A. Myoclonic Status Epilepticus B. Pupillary Reaction C. Corneal Reflexes D. Motor Response Neurological Exam A. Myoclonic Status Epilepticus Myoclonus is a brief, sudden and involuntary muscular twitching. Status myoclonus as continuous multifocal twitches lasting for more than 30 min and involving several parts of the body. Lance Adams syndrome: a chronic form of postanoxicmyoclonus which occurs in conscious patients, it is triggered by voluntary movements and it is often limited to the limb being moved (action myoclonus). Status myoclonus of early onset (<24 h after cardiac arrest) was previously considered a reliable sign of poor prognosis, but good outcomes have been reported in patients treated with TTM. Post-hypoxic myoclonic SE was reported in 20% of patients (similar with or without TH); 9% of them showed a good neurological recovery outcome. 9

10 Neurological Exam B. Pupillary Reaction ** Pupillary reflex is not influenced by the effect of muscle relaxants. ** Quantitative detection using a pupillometer may increase accuracy of this sign. Bilateral absence of pupillary light reflexes at 72 h after cardiac arrest is a robust indicator of poor prognosis with or without TH. absence of pupillary reflexes during the first 24 h after arrest is not incompatible with good recovery, particularly in TH. The presence Pupillary reflexes at 72 h is nota strong indicator of good prognosis. Neurological Exam C. Corneal Reflexes ** Can be affected by sedation and NM blocking. Bilateral absence of corneal reflexes at 72 h from CA has a slightly less specificity than pupillary reflexes to predict poor outcome (FPR 0.5% vs 0-5%) 10

11 Neurological Exam D. Motor Response ** Highly affected by sedatives and NM blockers. An absent or extension motor response to pain at 72 h from ROSC (or >72 of euthermia) is a sensitive, but non-specific sign of poor outcome (FPR 10 40%) Neurological Exam Pupillary Reaction > Corneal Reflexes > Motor Response > Myoclonic Status Epilepticus 11

12 Prognostication Tools 1. Clinical Neurological Exam 2. EEG 3. SSEP 4. Biomarkers 5. Brain images EEG High FPR A. Highly malignant: burst suppression, GPDs on a suppressed background B. Benign: continuous, normal voltage. C. Intermediate malignancy: low-voltage, discontinuous background and presence of periodic, rhythmic and epileptiformdischarges on a normal voltage background. 12

13 Prognostication Tools 1. Clinical Neurological Exam 2. EEG 3. SSEP 4. Biomarkers 5. Brain images SSEP Obtained using an electrical stimulus to the median nerves; cortical responses (N20, expected to appear 20 ms after nerve stimulation). Reliable only when peripheral (N9) and spinal (N13) responses are clearly identified. Less affected by sedative drugs or hypothermia. Bilateral absence of the N20 response is strongly correlated with a poor outcome, both during (FPR 0%)and after (0 5%) TH. The presence of N20 has a poor sensitivity to predict good outcome. 13

14 Prognostication Tools 1. Clinical Neurological Exam 2. EEG 3. SSEP 4. Biomarkers 5. Brain images Biomarkers 1. NSE: Before TH, a serum NSE concentration > 33 µg/l between 24 h and 72 h after cardiac arrest was strongly associated with poor outcome. TH can cause false elevation of NSE, if the same cut off is used FPR to predict poor outcome would range from 7 to 30%. Other causes of elevated NSE, hemolysis, the presence of small cell lung carcinoma and neuroendocrine tumor. No clear cut-off correlates with poor prognosis in TH patients but chances of meaningful recovery are very low with levels>80 2. S-100b: Less commonly available Very short half life Rarely used for prognostication purposes 14

15 Prognostication Tools 1. Clinical Neurological Exam 2. EEG 3. SSEP 4. Biomarkers 5. Brain images Brain images Imaging studies are not affected by sedation and paralysis. Only small studies reviewed the role of brain images in prognostication. The use of signs of anoxic brain injury in MRI brain for prognostication is associated with FPR of 9%. MRI findings should always be integrated with other tools to predict poor outcome in these patients. 15

16 Summary Use a multimodal approach using a combination of at least three different prognostic tools to increase the predictability of the outcome. Referral to experienced centers would be necessary in case of patients with uncertain prognosis and/or absence of multimodal approach. If the results of prognostic tests produce conflicting results or prognostication remains uncertain, further clinical observation and reevaluation is recommended Avoid the trap of a self-fulfilling prophecy. 16