What Hospitalists Need to Know about ICU Neurology

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Felicity Sparks
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1 What Hospitalists Need to Know about ICU Neurology S. Andrew Josephson, MD Department of Neurology, Neurovascular Service University of California San Francisco September 25, 2009 The speaker has no disclosures Case 1 A 45 year-old man collapses at dinner after a Vfib arrest. Within 10 minutes he is intubated by paramedics and normal cardiac rhythm is restored. On exam in the ICU 20 minutes after arrival, he is unresponsive and has fixed and dilated pupils. 1

2 What treatment/diagnostics should you initiate? A. Brain death examination B. Urgent head imaging C. Therapeutic hypothermia D. IV t-pa for presumed stroke E. Corticosteroids to reduce cerebral edema Therapeutic Hypothermia Post Cardiac Arrest 300,000 persons each year in U.S. experience out of hospital cardiac arrest Only 5-30% will recover to function independently Until 2002, most neurologic involvement was limited to prognostication Two landmark studies in 2002 changed this landscape for neurologists (like it or not) N Engl J Med 2002 Feb 21;346(8): N Engl J Med 2002 Feb 21;346(8):

3 The Code s Not Over Until You Cool the Brain Australian and European trials Both randomized between normothermia and hours of mild induced hypothermia with goal degrees Celcius Vfib or (in one) pulseless Vtach 6 month outcomes: Neurologic independence NNT=6 No difference in adverse events N Engl J Med 2002 Feb 21;346(8): N Engl J Med 2002 Feb 21;346(8): Accepted Practice Vfib and pulseless Vtach arrest with known time down Persistent coma (not following commands) 24 hours of induced hypothermia to degrees followed by passive rewarming Sedation maintained to prevent shivering 3

4 Controversies that remain Other rhythms? How fast to cool? Contraindications? How to cool the patient? Ice packs? Invasive cooling? External cooling precisely? What we do: UCSF Cooling Protocol Rapid initiation, then 24 hours Age greater than 18 BP>90 systolic (fluids or pressors o.k.) Known time of arrest Exclusions Terminal illness Severe coagulopathy Pregnancy Paralysis, fentanyl, midazolam 4

5 Shouldn t this work for all Neurologic Injury? No Traumatic Brain Injury Stroke ICH Yes Infants with Hypoxic-Ischemic Injury Maybe Spinal Cord Injury (Kevin Everett) Case 1 (con t) Right before initiating hypothermia, you perform a detailed neurologic examination The patient does not open his eyes and follows no commands Pupils are 6mm and fixed, no corneals, +doll s eyes, no gag, overbreathing the ventilator Extensor posturing in all four limbs Head CT shows some possible early edema 5

6 Which feature of the case portends a poor outcome? A. Fixed and dilated pupils B. No gag reflex C. Extensor posturing in all four limbs D. Edema on head CT E. Nothing here portends a poor prognosis Neurologic Prognosis Following Cardiac Arrest Any clinician can perform One of the most common neurologic consultations in the ICU Important for family communication Fraught with multiple misconceptions Role of imaging Role of early testing (e.g. pupils) Distinction from Brain Death 6

7 Neurologic Prognosis Following Cardiac Arrest Goals Define characteristics that predict a poor outcome accurately without false positives Does not distinguish between excellent and good outcomes All are time based after the initial arrest Must always exclude confounders Medications, ilicits, sedatives Reliable Markers of Poor Outcome: Examination Day 3: Absence of pupillary responses Day 3: absence of motor movements or motor responses other than extension to painful stimulation This is why the 72 hour exam is so key Little we can say at 24 hours or initially 7

Asynchronous, stimulus induced EEG definitively can tell Reliable Markers of Poor Outcome: Evoked Potentials Not

8 Reliable Markers of Poor Outcome: Myoclonic Seizures Myoclonic status epilepticus Bilateral rhythmic synchronous twitches of limbs, trunk or face Distinguish from Generalized tonic-clonic seizures Multifocal myoclonus (difficult) Asynchronous, stimulus induced EEG definitively can tell Reliable Markers of Poor Outcome: Evoked Potentials Not terribly useful at most centers Single most proven predictor Absence of median N20 responses after 72h N Engl J Med 361:

Reliable Markers of Poor Outcome: Biochemical Markers Serum test of neuron-specific enolase (NSE) elevated in days 1-3 A marker of neuronal death Problems Cut-off debated (>33 μg/l) Turnaround time

9 Reliable Markers of Poor Outcome: Biochemical Markers Serum test of neuron-specific enolase (NSE) elevated in days 1-3 A marker of neuronal death Problems Cut-off debated (>33 μg/l) Turnaround time not practical at many centers What about the MRI? Absolutely zero utility in predicting outcome or even evidence of injury in these patients: false negatives and positives Don t even get the study Future and recent research: ADC values Ann Neurol :

10 Hypothermia: A big caveat Zero data on these patients Certainly given success of hypothermia, it could change timing and/or accuracy of these prediction rules/algorithms Case reports of rule violations When does the clock start? Case 2 A 50M recovering from a 2 week course of sepsis and ARDS is found to have symmetric, flaccid weakness in all four limbs On examination, he appears to have normal facial strength but cannot move his limbs despite apparently normal mental status. All reflexes are absent. CK is normal 10

11 Which of the following illnesses is not on the differential diagnosis? A. Guillain-Barre syndrome B. Cervical spine contusion C. Myasthenia gravis D. Critical illness polyneuropathy E. Acute necrotizing myopathy from propofol Critical Illness Polyneuropathy and Myopathy First described in 1980s Patients exhibit muscle wasting and flaccid, symmetric weakness which can be accompanied by inability to wean from the ventilator Polyneuropathy and/or myopathy Often both Difficult to distinguish: normal CK regardless Distinction not clinically important 11

12 Critical Illness Polyneuropathy and Myopathy Common 70% with sepsis 60% with ARDS 50-75% in ICU for > 7 days Estimates depend on definition and sensitivity of testing Why do we care? Prolonged weaning, increased LOS, worse long-term functional recovery, probably increased mortality Critical Illness Polyneuropathy and Myopathy Risk Factors Sepsis, SIRS, Multiorgan Failure Increasing severity of illness Long duration of ICU stay Medications Steroids NMJ blockers Diagnosis: clinical, confirmed if needed by EMG Remember differential including C-spine disease 12

Critical Illness Polyneuropathy and Myopathy Treatment www.neuro.wustl.

for this) Case 3 A 65 year old man with a history of HTN presents 2 hours after the sudden onset of

13 Critical Illness Polyneuropathy and Myopathy Treatment Supportive Reduce steroids and NMJ blockers Intensive insulin therapy (still works for this) Case 3 A 65 year old man with a history of HTN presents 2 hours after the sudden onset of right hemiparesis Exam shows normal vitals except bp 185/95 Neurologic examination Somnolent, Dysarthric Plegic right face, arm and leg 13

14 Which of the following treatments is indicated for this disease? A. Hypothermia B. Surgical evacuation C. Steroids D. Activated Factor VII E. None of the Above Differential Diagnosis for ICH Hypertensive* Trauma* Drugs Amyloid Angiopathy Tumor Vascular Malformation Septic emboli Venous thrombosis Coagulopathy Ischemic Stroke with transformation and many others 14

Hypertensive ICH: Common Locations Management of ICH Blood Pressure Control Decrease aggressively in the acute setting IV nicardipine or IV labetolol Theoretical risk

15 Hypertensive ICH: Common Locations Management of ICH Blood Pressure Control Decrease aggressively in the acute setting IV nicardipine or IV labetolol Theoretical risk of worsening ischemia if drop too much too quickly MAP <110 is a reasonable goal More aggressive than current guidelines Trials underway to determine best strategy 15

16 Management of ICH Correct Coagulopathy If Coumadin-related ICH FFP, Vitamin K Factor IX complex concentrate (Bebulin) Stop all anticoagulants?platelet transfusions if on ASA or Clopidogrel Management of ICH: Myths What not to do. Steroids Prophylactic anticonvulsants Surgery 16

17 Proven Treatments for ICH Surgical treatment for ICH Removing clot would seem intuitive Multicenter randomized trial (STITCH) Absolutely no benefit over medical therapy Perhaps with the exception of hematomas just under the surface (<1cm) Cerebellar ICH excluded Not a neurosurgical disease!!! Lancet. 2005;365(9457):

What about ICH expansion? One-third of hemorrhage undergo expansion in the first few hours Associated with poor outcome Can we stop this? bp control? afviia?

18 What about ICH expansion? One-third of hemorrhage undergo expansion in the first few hours Associated with poor outcome Can we stop this? bp control? afviia? Two large randomized trials in NEJM ( 05, 08) Major focus of current research N Engl J Med May 15;358(20): Case 4 A 56M with a history of lung cancer presents to the ER with increasing lethargy over the last 24 hours. He is admitted to the ICU for observation and while you are taking his history, he quickly becomes obtunded while you are speaking with him and only groans to sternal rub. 18

19 Case 4 (con t) Exam: 37.3, 200/95, 64, 18, 100% RA General examination normal Neurologic coma examination Pupils: 5 to 3 on right, 3 to 2 on left Normal corneals, oculocephalic, gag Motor with withdrawal to deep pain on the right and no response on the left How would you treat his bp of 200/95? A. IV hydralazine B. PO clonidine C. IV nicardipine D. PO nifedipine E. No treatment 19

20 Emergent ICP Management Step 1: Head of bed to 30 degrees Step 2: Hyperventilation Cerebral vasoconstriction with decreased P a CO 2 Onset rapid Lasts only 1-2 hours as buffering occurs Step 3: Mannitol 1 gram/kg IV (50-100g) Removes brain water Tolerance develops, must follow serum osms Step 4: Barbituates (bolus then infusion) Consider ventriculostomy if indicated! Emergent CPP Management Cerebral Perfusion Pressure (CPP) CPP = MAP - ICP 20

21 Delirium Quality Measures in Neurology ICU Patients Incidence nearly 80% in patients without neurologic illness Higher in those with primary neurologic illness Assess for it in the ICU or you won t find it Use the same simple interventions for treatment we utilize in the floor Choose your sedatives wisely: Propofol, Dex Why think about ICU delirium? Important example of organ dysfunction Easy to standardize assessment and care Thought to be underrecognized Mandated by Critical Care Society CMS really wants us to Important association with increased morbidity and mortality in the ICU 21

22 Dexmedetomidine 2007, 09 JAMA Randomized data Dex vs. lorazepam Similar w/ midaz. Decreased delirium and coma Used for 120 hour infusions FDA only approves <24hrs JAMA 2007 Dec 12;298(22): VAP in Neuro Patients Incidence much higher than in other patients (most studies around 15-20%) Higher infectious rate in some conditions such as stroke Definitional? 22

23 VAP in Neuro Patients Examined all UCSF intubated patients for a 2 year period ( ) Yearly VAP rate in patients with neurologic disease higher than MICU patients VAP patients more likely to have longer length of stay and longer time ventilated No difference in mortality Final Thoughts: Quality and Safety Some quality measures may have different rates among neurologic patients and therefore need different approaches to definitions to surveillance to use as quality measures 23

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

Neurological Prognostication After Cardiac Arrest Murad Talahma, M.D. Neurocritical Care Ochsner Medical Center Financial Disclosure None 1 Introduction Each year, 356,000 Americans are treated by EMS