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EM II Neuro Emerg.
EM II Neuro Emergencies
| Question | Answer |
|---|---|
| What is a neurological emergency? | Any structural or functional abnormality of the CNS which has an acute onset: stroke, seizure, trauma, altered mental status, HA |
| Initial evaluation | ABCs, finger stick glucose, eight elements: mental status, cerebral fxn, cranial nerves, sensory examination, motor examination, reflexes, cerebellar, gait |
| mental status testing | nl conversation, count forward or backward, Folstein mini mental status exam, ask about short term/long term events |
| Expressie Aphasia | Broca's aphasia (more ventral) |
| Receptive Aphasia | Wernicke's Aphasia (more dorsal) |
| Cerebral fxn | language, aphasia, identify objects |
| Motor/Sensory | Sensory, Motor, Reflexes |
| Cerebellar/Gait | Cerebellar: rapid alternating hand movements. Finger to nose. Gait: Romberg test, heel to toe walking, walking backwards |
| Hypocapnia increases cerebral | vasoconstriction |
| Medications used Emergently | Thiamine (prevents wernickes encephalopathy), Narcan (nalaxone) opioid antagonist, Dextrose (D50) correct hypoglycemia. Romazicon (flumazenil) benzodiazepine antagonist. (for test: dextrose, thiamine, narcan) |
| AVPU | alert verbal pain unresponsiveness |
| Glasgow coma scale components | eye opening (4), verbal (5), motor (6) |
| Levels of altered mental status | obtundation, stupor, coma |
| Obtundation | lethargic, blunted cognition, awake but somnolent or slowed, arousable |
| Stupor | asleep/semi comatose. Only arouses when stimulated (sternal rub, pinch skin), reverts back to sleep when stimulus withdrawn |
| coma | eyes closed, unresponsive |
| Evaluation of Coma | ABCs, GCS, localizing signs (systemic vs focal source), Uncal herniation (3rd cranial nerve dysfunction, ispilateral pupil dilated/non-reactive) drowsy to unresponsive. Central herniation (decorticate posturing, biots (irregular respiration) |
| Metabolic Causes of Coma | Metabolic: Encephalopathy (hypoxia, metabolic: uremic, hepatic, electrolytes), toxins, drugs, environmental, sepsis |
| Structural Causes of Coma | Trauma, Stroke (ischemic, hemorrhagic), tumors, seizures, Infections (cysticercosis: pork tapeworm) |
| Hypoxic Encephalopathy | increases in cell water, edema, death. Brain cells die within 5 minutes, hyperbaric oxygen therapy |
| Metabolic Encephalopathy | hypoglycemia, hyperglycemia, hepatic, ureic, hypertensive |
| Hypoglycemia | starts with confusion/delirium, cerebral metabolic rate for glucose, reduced synthesis of neurotransmitters, neuronal death ensues, tx with dextrose (give thiamine before; not b/c DM) |
| HHNC | hyperosmolotic hypergylcemic non-ketotic coma |
| Hyperglycemia | most commonly associated with HHNC, severe dehydration (osmotic shift of fluid), Fluid deficit (may be more than 10 liters), not ketotic |
| grossly dehydrated but non-ketotic | give fluids. 2-3 liters in first few hours |
| Hepatic Encephalopathy | associated with cirrhosis, portal blood diverted to systemic circulation through portosystemic collateral vessels. Neurotoxic substances: Ammonia, GABA (BBB more permeablet to GABA in cirrhosis, worse with meds that affect GABA (benzos) |
| Tx of Hepatic Encephalopathy | Lactulose: inhibits intestinal ammonia production, patient needs to have 2-4 loose stools daily. ABX: metronidazole, neomycine, PO vanco. Decreases colonic concentration of ammonia producing bacteria |
| Uremic Encephalopathy | return to |
| Hypertensive Encephalopathy | pressure is so high that you lose the BBB integrity and fluid floods brain. Tx: lower bp slowly. No more than 25% initially. Sodium Nitroprusside, labetalol, trimethaphan, nicardipene |
| Top poisons in toxic encephalopathy | lead, cyanide, carbon monoxide. Drugs: opiates, benzos, paralytics, ecstasy, neuroleptics (toxic levels of seizure meds) |
| Aniscoria | unequal pupils may be caused by an optic nerve lesion, or pressure on the optic nerve, or baseline for that patient |
| Pupil exams | Symmetry, Size: Blow pupils, Pin point (opiates, cholinergics), Dilated (anticholinergics, sedatives) |
| Neuroleptic malignant syndrome | Muscular rigidity, hyperthermia, altered mental status. Can occur with any antipsychotic agent (haldol, compazine, reglan, phenergan, any dopamine antagonist). Tx: benzos, rapid cooling, muscle relaxants, dopamine agnoists |
| concern in chronic alcoholics | wernicke's encephalopathy. |
| Wernicke's Encephalopathy | acute onset: confusion, visual changes, ataxia. Cause: Thiamine (vit b-1) deficiency. Associated with Korsakoff Psychosis. Tx: Thiamine - IV "banana bag", IM |
| Korsakoff Psychosis results from | Thiamine deficiency (usually seen in alcoholics) |
| Meningitis | Infxn of the meninges, CSF bathes the brain and spinal cord, Sources: viral, bacterial, fungal, other sources in immunocompromised. To Dx: CT first to r/u increased ICP, then LP if permissible |
| Location for LP | L3-L4 interspace. Tubes 1 and 4: cell count and diff. Tube 2: gram stain, culture, AFB, india ink. Tube 3: Protein and glucose |
| Syncope Definition | it is a sx. Transient, self-limited LOC, onset is relatively rapid, reocvery is spontaneous, complete and usually prompt. |
| The underlying mechanism of Syncope is | a transient global cerebral hypoperfusion |
| Syncope: neurally-mediated reflex syncopal syndromes, orthostatic, cardiac arrhythmia as primary cause (must always be ruled out) and | structural cardiac (valvular) or cardiac dz (tumors), cerebrovascular |
| Non-syncopal attacks | with impairment of LOC, without LOC |
| Causes of Syncope: neurally-mediated reflex syncopal syndrome | vasovagal faint (common faint), carotid sinus syncope, situational faint: acute hemorrhaging, coughin, sneezing, GI stimulation, Micturation, post-exercise |
| Orthostatic Causes of Syncope | Autonomic failure (primary, secondary, drugs and alcohol), volume depletion (hemorrhaging, diarrhea, addison's dz) |
| Cardiac arrhythmias as primary cause of Syncope | sinus node dysfunction, atrioventricular conduction system dz, paroxysmal supraventricular and ventricular tachycardias, inherited syndromes, implanted devices |
| Structural causes of syncope | valvular dz, acute MI, Obstructive cardiomyopathy, atrial myxoma, acute aortic dissection, pericardial dz, PE, Cerebrovascular (vascular steal syndromes) |
| Causes of non-syncopal attacks | Metabollic disorders, epilepsy, intoxications, TIA |
| Disorders resembling syncope wtihout LOC | cataplexy, drop attacks, psychogenic, TIA of carotid origin |
| Vasovagal syncope | standing or sitting, lasts 10sec to few min, no postictal period. Decrease in arterial pressure and HR produce CNS hypoperfusion, Precipitated by: emotional upset, sight of blood, prolonged motionless standing |
| Evaluation of Syncope | H & P, ECG, Orthostatics, EKG, Imaging (when indicated): CT chest or abdomen/pelvis, pelvic US, Labs, Re-appraisal, Tx |
| Evaluation for blood loss in syncope | GI, pelvic (ruptured ectopic pregnancy) or trauma |
| Pseudo Seizure | Physical movement without EEG evidence of seizure. Non-epileptic seizure, psychogenic, associated with conversion and panic disorder. Check CK, lactate (should be elevtted in true seizure), may respond to saline placebo |
| Primary Seizure | no cause can be found. Secondary=due to mass lesion |
| Sudden LOC without loss of postural tone | Absence |
| Petit mal | Absence, no postictal state, may occur>100x/day, typically found in school age children |
| Focal Seizures | more localized in the brain. Simple (no LOC) or complex (consciousness affects, usually temporal) |
| CK levels and lactate in seizures | elevated! |
| Seizure mimics | hyperventilation (carpal pedal spasm due to hypocapnia), movement disorders, narcolepsy, cataplexy |
| Status Epilepcticus | 5 or more minutes of seizure activity. Stop the seizure! Morbidity due to hypoxemia, hyperthermia, circ collapse and neuronal death. Intubate for airway control. Tx: benzos, Phenytoin, Phenobarbital |
| If you give ativan and patient continues to seize, then... | general anesthesia (knock em out), phenobarb coma, Propofol, up to 30 % of status epilepticus pt may go on to refractory status |
| Stroke/TIA | any disruption of blood flow to a local region of the brain. May be ischemic or hemorrhagic (determines your tx) |
| Hx in a pt with stroke/TIA | HTN, CAD, DM, Previous TIA's, Timing (very important) |
| PE of Stroke pt | LOC, Visual fields, Motor, Cerebellar, Sensation/Neglect, Language, Cranial nerves |
| Ischemic stroke causes | Embolic (20%) cardiac source most common (atrial fib). Thrombotic (80%), similar mechanism to MI |
| TIA | Neuro deficits: resolve within 24 hours, often within 30 minutes. Extra-cranial carotid artery strokes may occur. 10% of pts with TIA will return with CVA within 90 days |
| Hemmorrhagic strokes | sub arachnoid, intracerebral, amyloidosis, coagulopathies, head trauma in pts with anticoagulants |
| Anterior Cerebral Artery | Contra lateral leg > arm weaknessMild cortical sensory defects |
| Middle Cerebral Artery | Contra lateral weakness/numbnessFace/arm > legMay gaze toward affected sideIf dominant hemisphere, aphasia may occur |
| Posterior Cerebral Artery | May be dramatic or subtleDizziness, vertigo, diplopia, dysphagia, CN palsies |
| Basilar Artery | brainstem, cerebellum, visual cortex. Hallmark findings: crossed neuro deficits; ipsilateral cranial nerve wtih contra lateral motor weakness. Locked in sydrome (complete and severe paralysis.. except eye movement.. completely aware) |
| ____ is Due to injury, tumor, or stroke to a portion of the pons | Locked in Syndrome |
| hemorrhagic syndromes | return |
| subarachnoid hemorrhage | "worst HA of my life", occurs more commonly in women, usually occipital or nuchal in location, vomiting, sudden onset |
| Subarachnoid Hemorrhage DX | CT brain within 24 hours (most sensitive during this time frame), Lumbar puncture (xanthocromia present 12 hours post-bleed; nl CSF is crytstal clear) |
| Tx of Subarachnoid Hemorrhage | Nimodipine (CCB, Reduces Cerebral vasospasm), Phenytoin. HHH therapy: hypertensive, hypervolemic, hemodilutional |
| Caused by tearing of the bridging veinsAcceleration/deceleration injuryAtrophied brains more susceptible.Slow bleeding.Can be acute, sub acute, or chronic | Subdural Hematoma |
| Tearing of middle meningeal arteryDoes not cross suture linesLucid interval following initial LOC | Epidural Hematoma |
| If a CT is negative, you may need an ___ to r/o SAH | Lumbar puncture |
| When a pt presents with CVA sx | practitioner assesses pt within 10min, CT done within 25 min, CT read within 20 min |
| Tx of Stroke | Airway! Supplemental O2, do not lower BP unless>180/100 (labetalol, NTG) |
| Inclusion Criteria for Thrombolysis | Age>18 yo, Time of WITNESSED event<3 hours. Post tx: no ASA or Heparin in the first 24 hours |
| Antiplatelet agents in post-stroke pt | important for secondary stroke prevention. These are not thrombolytics, they are for prevention. For when your pt is stabilized and going home. ASA, Dipyridamole, Clopidogrel |
| Stroke Mimics | Transverse Myelitis, Bells Palsy, Guillain-Barre, Myesthenia Gravis |
| Transverse Myelitis | Rapid onset of motor and sensory loss. Sphincter disturbances, usually idiopathic. Motor weakness, sensory loss or paresthesia, back and radicular pain. Supportive tx only |
| Bell's Palsy | CN VII paralysis, abrupt, isolated, unilateral peripheral facial paralysis, diagnosis of exclusion. Be careful in dx without CT in elderly and high risk pts. Tx: supportive |
| Guillain-Barre Syndrome | return |
| Myasthenia Gravis | rare, autoimmune disorder. Bulbar (eye) muscles most commonly affected. Acetylcholine receptor antibodies. Caused by dysfunction of the thymus gland (75%). May be precipitated by infxn or surgery. Tx: ABCs, intubate if necessary. Neostigmine is the DOC. |
| Fevers and HA is _____ until proven otherwise | meningitis |
| Studies for HA workup if not cluster or migraine | CT scan, Lumbar Puncture, MRI |
| Life threatening HA | SAH, Meningitis, Tumor, other bleeding |
| Thiamine is used to prevent | Wernicke's encephalopathy |
| decorticate posturing is suggestive of | central herniation |
Created by:
ltm12