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Pediatric Neurologic Emergencies – Maria Antonia Valencia-Moral, MD February 12, 2010 Italicized words - audio Lecture Outline - Definition and Pathophysiology, Identification, Work up, Initial management of: o Impairment of consciousness and coma o Status epilepticus o Acute paralysis (not discussed) I. - Consciousness Definitions 2 components: awareness as a function of the higher cortical areas and awake/wakefulness as a function of the ARAS (Ascending Reticular Activating System) Consciousness: spontaneously occurring state of AWARENESS of self and the environment Unconsciousness: is the opposite and may be physiologic (sleep) or pathologic (coma) which is really the emergency situation Categories of Impaired Consciousness - Impairment of consciousness with activated mental status – they are awake but they are confused o Hallucinations o Delusions o Delirium - Impairment of consciousness with reduced mental state o Obtundation – responsive to other stimuli other than pain; lethargy - drowsy o Stupor – responsive to pain o Coma – is really the emergency situation, unresponsive to pain - Impairment along the continuum of coma-vegetative state-minimally conscious state and related conditions – persistent vegetative state/PVS Pathophysiology - Consciousness is the result of the interplay between the: o Cerebral cortex o Ascending reticular activating system - Coma is produced by conditions causing a pathology either in: o Bilateral cerebral cortical dysfunction – cannot be one-sided only; or there may be onesided lesion but in the presence of mass edema, the other side can also be affected o ARAS dysfunction – brainstem tumor that can damage the ARAS even if the cerebral cortex is intact o Both Figure 1. Regulation of consciousness. Evaluation - Clinical evaluation – ABC’s of life support – first line of support o Airway o Breathing o Circulation - Identification of cause - History - General physical examination - Neurological examination Historical Cues Symptoms/Historical Cues Sudden onset Kerosene stove use or heaters Probable Etiology Convulsions or if post-ictal state, the patient can recover; intracranial hemorrhage Ingestion of a drug or toxin Suggests elevated cranial pressure: neoplasm, hydrocephalus, migraine syndromes Traumatic Brain Injury: epidural, subdural, subarachnoid Infectious causes: meningitis, encephalitis, abscess Inborn errors of metabolism, drug overdose, munchausen’s syndrome by proxy Carbon monoxide poisoning General Physical Examination PE findings Probably Etiology Preceded by sleepiness or unsteadiness Headache History of Trauma Fever Intermittent coma Fever Hypothermia Tachycardia Bradycardia Tachypnea Slow, irregular, periodic breathing Hypotension Hypertension Infection, heat stroke Drug intoxication Hypovolemic shock, Tachyarrythmias Myocardial injury, late effects of hypoxemia or increased ICP; in Cushing reflex there is increased ICP and to compensate, the mean arteriolar pressure (MAP) will increase to increase cerebral perfusion bradypnea and bradycardia along with hypotension Abnormality of oxygenation, acidosis, brainstem lesions causing central neurogenic hyperventilation Toxic ingestion or increased ICP Shock, adrenal insufficiency Hypertensive encephalopathy or as a reaction to increased ICP 3 Goals for the Initial Assessment - To confirm the diagnostic impression from the History and PE - To localize the level of neurologic dysfunction - To serve as a basis for comparison of future examinations so you will know if the patient is improving or deteriorating 5 Pathophysiologic variables: - Mental status - Respiratory patterns - Pupillary sizes and reactivity - Oculo-cephalic and oculo-vestibular responses (Doll’s eyes) – reflects the brainstem integrity - Motor responses Mental status - The use of lethargy, obtundation, stupor and coma does not give much clinical significance. - Best to describe the patient’s response to various stimuli – where Glasgow Coma Scale is needed - Attempts to test for higher cortical function should be made when they begin to rouse from their coma state. Respiratory Patterns Respiratory pattern Cheyne-Stokes Respiration Central Neurogenic Respiration Apneustic breathing Ataxic breathing Pattern Crescendo-decrescendo hyperventilation alternating with Apneusis Continuous rapid respiration causing acidosis Periodic apnea after prolonged inspiration and expiration Chaotic breathing – no pattern Localization Bilateral cerebral dysfunction or upper diencephalic dysfunction Midbrain dysfunction Pontine damage Medullary dysfunction Ineffectual breathing Very shallow Depression of respiratory centers; can be secondary to drug overdose like Phenobarbital or phenytoin Pupillary Sizes and Reactivity Pupillary Reaction and Size Normal reaction Pathology Hemispheric lesions since papillary reaction is a brainstem function, not the cerebral cortex; in cortical blindness, there is a lesion in the occipital lobe, the papillary response is normal but the patient cannot see Small reactive pupils Barbiturate/narcotic intoxications Anisocoric – very serious condition wherein the Uncal herniation oculomotor nerve on one side is being compressed Mid position, fixed Midbrain lesions Pinpoint Pontine lesions, opiates and derivatives intoxication Bilaterally dilated and non-reactive – most serious Medullary pathology condition, can be fatal since the medulla is where the cardiac and respiratory centers are located Oculo-cephalic (Doll’s eyes) and Oculo-vestibular (Ice-water Calorics) Responses - To test for the patients in altered conscious state - Brainstem tests - Do Doll’s eye first – if no response, proceed with calorics testing - Think of “COWS” when doing calorics: “cold means the movement of the eye is toward the opposite side; and if it’s warm it is toward the same side” (C –old O – pposite W – warm S – Same) - Absence of response indicates poor prognosis – the response should be symmetric and bilateral. - Both of these tests will determine the integrity of the brainstem Motor Responses - Note the symmetry of movement in patients who cannot follow commands. Ex. Patient thrashing about all limbs – no paralysis; asymmetric movements suggest a hemiparesis. - Note appropriate responses to stimulus in “socially” acceptable sites like the supraorbital ridge, sternum, and the nails. - Note abnormal postures if present: decorticate and decerebrate posturing - Check for DTRs and plantar responses to be able to localize the lesion. Figure 2. Decerebrate and decorticate postures. Glasgow Coma Scale – the most important scale to be used Function Eye Opening Verbalization Adults Spontaneous To Command To Pain None Oriented Disoriented Inappropriate Incomprehensible Motor None Obeys commands Localizes Withdraws Reflex flexion Reflex extension None Children Spontaneous To sound To pain None Appropriate for age, flexes and follows, social smile Inconsolable cry Persistently irritable Restless, lethargic None Spontaneous Localizes Withdraws Reflex flexion Reflex extension None Total score The lowest score is 3 not zero. Score 4 3 2 1 5 4 3 2 1 6 5 4 3 2 1 15 Causes of Alteration in Sensorium - Metabolic, toxic, infectious - Supratentorial mass lesions that compress or displace the diencephalon or brainstem - Subtentorial mass or destructive lesions that compress or damage the ARAS - Traumatic axonal injury that affects both cerebral hemispheres, the ARAS or their interconnections. Management - Question informants thoroughly. - ABC’s first - Draw blood for: depending on your working diagnosis o Culture – for infectious causes o CBC – also for infectious cause o Electrolytes – since these are rapidly reversible causes for coma o Sugar - hypoglycemia o BUN, creatinine o Serum osmolality o ABG o Ammonia o Toxic drug screen o Liver function tests o Coagulation profile o Antiepileptic drug levels - Ancillary procedures (when appropriate) o Neuroimaging (CT scan or MRI) – usually do it for all coma patients o Lumbar puncture - if you’re thinking of infection o EEG – if you’re thinking if seizure Treatment Goals - Ensure oxygenation - Maintain circulation - Give glucose - Correct acid-base and electrolyte imbalance - Consider specific antidotes like drug overdose or dose exposure - Reduce increased intracranial pressure: you may elevate the head up to 45° to increase jugular venous pressure, regulate the respiration to avoid bradypnea or decrease perfusion in the brain. Bradypnic environment tends to retain CO2 causing vasodilatation and further increase ICP. We ventilate the patient and monitor PCO2 which should not be over 35mm; and we can also give osmotic diuretics like mannitol. - Stop seizures - Treat infection - Adjust body temperature – keep them normothermic or slightly hypothermic which is neuroprotective - Manage agitation II. Status Epilepticus Definitions: - Seizure: an abnormal excessive neuronal discharge arising from the brain capable of causing alteration in function and/or behavior; it depends on what part of the brain has the condition Convulsion: a type of seizure with a motor component Epilepsy: recurrent unprovoked seizures (operational definition is more than two unprovoked seizures) Status epilepticus: a single seizure lasting at least 30 minutes or recurrent seizures lasting > 30 minutes without fully regaining consciousness between seizures Epidemiology (Hauser 1990) - Incidence of 41 patients per year per 100,000 population - 50 episodes of status epilepticus per year per 100,000 - Projected that between 102,000 and 152,000 events occur in the US annually There is a higher incidence among less than 1 year with bimodal contribution with increased incidence in adults over 40 years. 4 Major Etiologies - Febrile – the most common etiology for children - Acute symptomatic encephalopathies ex. meningitis - Remote symptomatic encephalopathies ex. HIV - Idiopathic - 4% are secondary to progressive CNS disease Pathogenesis: can lead to significant morbidity and mortality - Cellular ischemic changes begin to occur in 15-30 minutes - Irreversible damage begins at 90-120 minutes of continuous seizures - Damage is due to the combined effects of: hypotension, hyperthermia, hypoglycemia and acidosis - The immature brain is more susceptible to seizures (higher incidence among less than 1 year old) because the synapses are still not well-developed. But is relatively more resistant to sequelae (higher in adults). Therefore, there is higher recovery rate and lower mortality among children having status epilepticus. Treatment goals - Ensure adequate oxygenation and circulation - Terminate clinical and electrical seizure activity as soon as possible - Prevent seizure recurrence - Identify and treat precipitating factors: hypoglycemia, electrolyte imbalance, low drug levels, fever - Prevent systemic complications - Evaluate and treat the cause Figure 3. Protocol for Treatment of Status Epilepticus. Every 5-10 days, you are assessing the child or the adult. Usually the first line of treatment is benzodiazepam because they are fast-acting. But if they don’t respond to the initial doses, long-acting convulsants are already used. There is a need to load since the goal of treatment is to achieve therapeutic dose in lesser duration (within 24 hours); as compared to giving a maintenance dose that will take four half-lives of the drug to maintain the therapeutic level which will account for 20 days. Management - Supportive care - Lab testing: blood glucose, blood gas, electrolytes, CBC, AED levels, cultures, toxic screens, urine drug and metabolic screen - Neuroimaging - Lumbar puncture - EEG monitoring Morbidity and Mortality - Common sequelae: o Intellectual dysfunction o Permanent neurologic deficits – usually weakness depending on what part of the brain is affected o Continuing recurrent seizures - Mortality rates are higher in adults than in children - About 5% in children – but still serious because the children have the higher probability to live so they will also spend that whole lifetime with their seizure.