Neurologic emergencies: Neurologic emergencies Thomas P. Bleck MD FCCM The Louise Nerancy Eminent Scholar in Neurology and Professor of Neurology, Neurological Surgery, and Internal Medicine Director, Neuroscience Intensive Care Unit The University of Virginia


Slide2: the old bible


Slide3: the new bible


Consciousness : Consciousness Consciousness can be divided into two constructs: Arousal Content Arousal without content defines the vegetative state


Consciousness: Consciousness Content does not appear to exist without arousal Sleep is a special state in which the brain does not permit most of the motor output used to determine consciousness


Unconsciousness: Unconsciousness Consciousness depends on the interaction of the midbrain/thalamic reticular system (reticular activating system) and the cerebral cortex Thus, only a limited number of anatomic problems can cause unconsciousness: Dysfunction of the midbrain/thalamic reticular system Dysfunction of both cerebral hemispheres A combination of the above two problems


The RAS mediates arousal: The RAS mediates arousal The RAS receives input from all major afferent tracts, and projects widely to the thalamus, basal forebrain, and the cerebral hemispheres. The crucial segment of the RAS for arousal is between the rostral midbrain and the midpons.


The RAS mediates arousal: The RAS mediates arousal Isolated lesions to this portion of the RAS produce coma, whereas lower lesions do not. Damage to the thalamus or hypothalamus can also alter consciousness, reflecting connections of these structures and the RAS; bilateral involvement is usually required


Slide9: reticular activating system (a.k.a. ascending arousal system)


The cerebral cortex mediates content: The cerebral cortex mediates content If both cerebral hemispheres are dysfunctional, as in a severe metabolic encephalopathy, there is no detectable content Less severe diffuse disorders impair consciousness Focal hemispheral disorders do not by themselves affect consciousness Herniation or elevated ICP may alter consciousness


Focal lesions may be confused with disorders of consciousness: Focal lesions may be confused with disorders of consciousness Receptive (Wernicke’s) aphasia may be interpreted as confusion Right parietal lesions may cause apraxia of eye opening Thalamic or hippocampal lesions may impair memory Pontine infarction may interrupt most efferent pathways, producing the ‘locked-in’ syndrome


Definitions: delirium: Definitions: delirium Plum and Posner: “a floridly abnormal mental state characterized by disorien-tation, fear, irritability, misperception of sensory stimuli, and, often, visual hallucinations.”


Definitions: acute confusional state: Definitions: acute confusional state “an acute organic mental syndrome featuring global cognitive impairment, attentional abnormalities, a reduced level of consciousness, increased or decreased psychomotor activity, and a disordered sleep-wake cycle” Always consider thiamine deficiency! Lipowski ZJ 1990


Definitions: Definitions Obtundation: the patient appears to sleep more hours than expected, but has some spontaneous awakening Stupor: only awakens when stimulated Coma: does not awaken Vegetative state: after a period of coma, sleep-wake cycles return but there is no awareness


Prognosis in the vegetative state: Prognosis in the vegetative state


Herniation: Herniation Everything you know is wrong.


Standard model: Standard model diencephalon midbrain pons temporal lobe uncus midline inferred force vector causing transtentorial herniation


Standard model: Standard model midbrain temporal lobe uncus third cranial nerves cavernous sinuses third nerve palsy from compression cistern obliterated


Current model: Current model diencephalon midbrain pons temporal lobe uncus midline force vector displacing diencephalon laterally cistern widened


Current model: Current model temporal lobe uncus third cranial nerves cavernous sinuses third nerve palsy from stretch cistern widened midline


Slide21: Ropper, 1998


Slide22: hemorrhagic contusion enlarged ispilateral cistern compressed cerebral peduncle (Kernohan’s notch phenomenon producing ipsilateral hemiplegia Young et al, 1998


Slide23: brain abscess enlarged cistern Bleck et al, 2000


Resuscitation in coma: Resuscitation in coma Airway protection Blood pressure and pulse Unexplained bradycardia: remember spinal cord injury Sedative drugs and positive pressure ventilation will reliably reduce preload


Urgent corrective measures: Urgent corrective measures Hypotension Hypoxia Hypoglycemia Thiamine deficiency Narcotic overdose naloxone Benzodiazepine overdose Limited role for flumazenil, especially if mixed ingestion suspected


Evaluation of the comatose patient: Evaluation of the comatose patient What’s the point? The examination is tailored to allow a rapid distinction between Processes primarily affecting the brainstem, which need emergent imaging and Processes causing bilateral hemispheral dysfunction, in which imaging is a secondary concern


Evaluation of the comatose patient: Evaluation of the comatose patient Historical information Rate of unconsciousness Immediate vs. slowly progressive Head injury Focal complaints before loss of consciousness Seizure activity Potential ingestions and exposures Potential for cervical spine injury


Evaluation of the comatose patient: Evaluation of the comatose patient Physical examination focused on Pupillary responses Extraocular movements Spontaneous roving eye movements Cervico-ocular reflexes (if cervical spine is intact!) Vestibulo-ocular reflexes Vertical eye movements


Slide29: parasympathetic control of pupil size


Slide30: sympathetic control of pupil size


Slide32: III III VI VI VIII VIII MLF Neck stretch receptors - +


Slide33: COR in neutral position


Slide34: COR with head turned to right


Slide35: COR with head tipped back


Evaluation of the comatose patient: Evaluation of the comatose patient Respiratory pattern Posthyperventilation apnea Cheyne-Stokes respiration Hyperventilation Central neurogenic hyperventilation Central reflex hyperpnea


Evaluation of the comatose patient: Evaluation of the comatose patient Apneustic respiration Cluster (Biot) breathing Ataxic respiration Apnea


Evaluation of the comatose patient: Evaluation of the comatose patient Motor responses Defensive or localizing Withdrawal Flexor (decorticate) posturing Extensor (decerebrate) posturing Leg flexion


Ancillary evaluations in coma: Ancillary evaluations in coma Blood and urine studies interpret ABGs in light of respiratory pattern CT scanning Best for acute blood and bony lesions MRI Not usually used emergently for coma evaluation LP


Levy et al: prediction of return to independent function outcome in anoxic coma: Levy et al: prediction of return to independent function outcome in anoxic coma


Edgren et al: prediction of return to independent function outcome in anoxic coma: Edgren et al: prediction of return to independent function outcome in anoxic coma


Resuscitation: Resuscitation Airway protection Blood pressure and pulse Unexplained bradycardia: remember spinal cord injury Sedative drugs and positive pressure ventilation will reliably reduce preload


Urgent corrective measures: Urgent corrective measures Hypoxia Hypoglycemia Thiamine deficiency Narcotic overdose naloxone Benzodiazepine overdose Limited role for flumazenil, especially if mixed ingestion suspected


Increased ICP: Increased ICP There is rarely a reason to treat ICP without knowing what it is. In addition to controlling ICP, one must consider cerebral perfusion: CPP = MAP – ICP Be careful regarding interventions that lower ICP but may also lower MAP even more


Increased ICP: Increased ICP Hyperventilation will lower ICP quickly but at the potential cost of cerebral ischemia Mannitol (0.25 gms/kg) works over minutes to hours Steroids work over many hours for vasogenic edema associated with tumors and abscesses but not strokes


Increased ICP: Increased ICP The best treatment for elevated ICP is craniectomy But you have to decide whether it is best for the patient High-dose barbiturates lower ICP by decreasing oxygen demand But also lower MAP


Stroke: Stroke If you suspect that an inpatient is having a stroke, call for the acute stroke intervention team (instead of paging the neurology resident on call) Check ABCs Check glucose Call the page operator and ask that the team be paged emergently


Stroke: Stroke If possible, stroke patients should receive thrombolytic therapy Three hour time window Potential for intra-arterial thrombolysis up to six hours Many contraindications Don’t use up the time trying to decide what to do; call the acute stroke intervention team Don’t treat hypertension unless thrombolysis is imminent


Seizures: Seizures Most seizures end spontaneously within 5 -7 minutes Average duration about 90 sec Protect the patient from injury Don’t put anything inside the patient’s mouth The vast majority of seizures should not be treated emergently But consider the patient’s other problems, which may suggest earlier therapy (e.g., acute MI)


Seizures: Seizures After about five minutes, the chance that the seizure will end spontaneously becomes small Treatment then indicated in most adult patients to prevent status epilepticus Always think about hypoglycemia as a possible cause Can cause focal or generalized seizures


Seizures: Seizures Terminating seizures lasting longer than five minutes Lorazepam 0.1 mg/kg No value to higher doses We may occasionally use smaller doses or other drugs for diagnostic reasons, but this is rarely useful without an EEG running


Preventing seizure recurrence: Preventing seizure recurrence Depends on etiology and precipitants Lorazepam usually adequate for several hours Consider loading with phenytoin or fosphenytoin 20 mg/kg Fosphenytoin is safer for peripheral veins but has the same risk of hypotension and arrhythmias (and is many times as expensive) Consider valproate 20 – 30 mg/kg if liver OK and concerned about respiratory depression


Anticonvulsant ‘levels’: Anticonvulsant ‘levels’ The ‘therapeutic range’ is only a rough guide Check levels in the morning before the first dose for efficacy Check levels for toxicity when symptoms occur Patients with renal or hepatic dysfunction may need ‘free’ (unbound) levels checked


Status epilepticus: Status epilepticus Prolonged seizure activity causes neuronal and systemic damage ABCs Effective choices to terminate SE: Lorazepam 0.1 mg/kg Phenobarbital 20 mg/kg Diazepam 0.15 mg/kg plus phenytoin 20 mg/kg


Status epilepticus: Status epilepticus About 20% of patients will appear to stop seizing but will actually enter non-convulsive status epilepticus Call us if the patient does not start improving quickly


Status epilepticus: Status epilepticus If the primary choice fails, don’t waste time on another conventional anticonvulsant Midazolam or propofol Need EEG monitoring and intubation by this point Prevent recurrence Manage complications


Neurogenic respiratory failure: Neurogenic respiratory failure Oxygenation abnormalities Neurogenic pulmonary edema Ventilatory abnormalities Sensor failure (brainstem doesn’t know PaCO2 is rising) Brainstem lesion Intoxication Effector failure Spinal cord or neuromuscular failure


General points on effector failure: General points on effector failure Patients are awake and may be dyspneic until PaCO2 is very high Since they can’t maintain tidal volume, they increase rate Initially may overcompensate and lower PaCO2 below 40 torr Atelectasis may impair oxygenation When vital capacity below 20 mL/kg need to be in ICU May require intubation for airway protection or hypoventilation


Effector failure: Effector failure Spinal cord lesions above C4 affect diaphragm Lesions between C5 and T7 affect parasternal intercostals Can’t generate effective negative intrapleural pressure Use accessory muscles to move rib cage Very likely to fail


Effector failure: Effector failure Lower motor neuron Poliomyelitis syndrome associated with West Nile Need not have encephalitic symptoms Appears to be permanent Treatment trial should open soon Other viral infections Progressive disease like ALS sometimes go undiagnosed until pneumonia causes respiratory failure to supervene


Effector failure: Effector failure Peripheral nerve (e.g., Guillain-Barré, critical illness polyneuropathy) Motor finding with sensory complaints Become areflexic (but may not be at first) CSF protein goes up (by second week) but few or no cells Pleocytosis: consider acute HIV Treatment: Support Plasma exchange or IVIg for GBS


Effector failure: Effector failure Neuromuscular junction disorders Purely motor, but some diseases may have additional symptoms and findings Myasthenia gravis Botulism Organophosphate intoxication Insecticide Nerve agents


Effector failure: Effector failure Diagnosis best made by EMG Limited value of edrophonium testing Determine whether defect is pre- or post-synaptic and proceed accordingly MG: IVIg or plasma exchange; cholinesterase inhibition Botulism: antitoxin Organophosphates: atropine and PAM


Effector failure: Effector failure Muscle disorders May occur acutely (viral, drug induced) or have worsened slowly History of proximal weakness Treatment depends on etiology


Meningitis: Meningitis Most patients can be tapped safely Pneumococcal and meningococcal meningitis can kill the patient before the scan is completed If LP is delayed, get blood cultures and start ceftriaxone 2 gms q12h and vancomycin 1 gm q12h on way to CT If Listeria suspected, add ampicillin 2 gms q4h or sulfa-trimethoprim (as 5 mg/kg trimethoprim) q6h Consider dexamethasone 0.15 mg/kg q6h


Encephalitis: Encephalitis Usually subacute change in mental status with fever HSE: diagnosis by MRI and PCR Acyclovir 15 mg/kg q8h x 21 days Entering the arboviral season West Nile likely to be prominent this year Eastern equine also likely