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Neurological Disorders expert questions Altered mental state - Coma DIS Ex Coma is a state of reduced alertness and responsiveness from which the patient cannot be aroused. The Glasgow Coma Scale is a widely used clinical scoring system for alterations in consciousness. Advantages are a simple scoring system and assessment of separate verbal, motor, and eye-opening functions. Disadvantages include lack of acknowledgement of hemiparesis or other focal motor signs and lack of testing of higher cognitive functions. Differential Diagnosis of Coma Coma from Causes Affecting the Brain Diffusely Encephalopathies Hypoxic encephalopathy Metabolic encephalopathy Hypoglycemia Hyperosmolar state (e.g., hyperglycemia) Electrolyte abnormalities (e.g., hyper- or hyponatremia, hypercalcemia) Organ system failure Hepatic encephalopathy Uremia/renal failure Endocrine (e.g., Addison, hypothyroid, etc) Hypoxia CO2 narcosis Hypertensive encephalopathy Toxins Drug reactions (e.g., neuroleptic malignant syndrome) Environmental causes—hypothermia, hyperthermia Deficiency state—Wernicke encephalopathy Sepsis Coma from Primary CNS Disease or Trauma Direct CNS trauma Vascular disease Intraparenchymal hemorrhage (hemispheric, basal ganglia, brainstem, cerebellar) Subarachnoid hemorrhage Infarction Hemispheric, brainstem CNS infections Neoplasms Seizures Nonconvulsive status epilepticus Postictal state History Certain points in history may be especially useful The circumstances and rapidity with which neurologic symptoms developed; The antecedent symptoms (confusion, weakness, headache, fever, seizures, dizziness, double vision, or vomiting); The use of medications, illicit drugs, or alcohol; and Chronic liver, kidney, lung, heart, or other medical disease. Direct interrogation of family and observers on the scene is an important part of initial evaluation. Ambulance officers often provide the most important clues. General physical examination Vitals including temperature should be measured quickly o Fever s/o sepsis, systemic infection or hypothalamic failure o Very high temperatures with neurological signs and seizures s/o heat related illness o Hypothermia – alcoholic, barbiturate, sedative intoxication, peripheral circulatory failure or hypothyroidism o Tachypnea – systemic acidosis or pneumonia o Abnormal respiratory patterns – brainstem disorders o Marked hypertension – hypertensive encephalopathy or Cushing’s response to raised ICP o Hypotension – alcohol or barbiturate intoxication, hemorrhage, MI, sepsis, profound hypothyroidism or Addisonian crisis Funduscopic examination – o Subhyaloid hemorrhages – SAH o Exudates, hemorrhages, vessel changes, papilledema – hypertensive encephalopathy o Papilledema – increased ICH Skin petechiae – TTP, meningococcemia, bleeding disorder causing ICH Neurologic examination Position in bed – o presence or absence of movements o Focal weakness or flaccidity Abnormal movements – o Twitching movements – seizures o Multifocal myoclonus – metabolic disorder e.g. uremia, anoxia or drug intoxication (SS) – asterixis Abnormal posturing o Decorticate – flexion of the elbows and wrists and supination of the arm – bilateral damage beyond the midbrain o Decerebrate – extension of elbows and wrists with pronation of arms – damage to motor tracts in midbrain or caudal diencephalon Level of arousal Brainstem reflexes o Pupillary responses to light o Spontaneous and elicited eye movements o Corneal responses and o Respiratory patterns Presence of these responses usually means a lesion above the brainstem most probably the hemispheres. Pupillary signs – to suggest cranial nerve damage and response to naloxone in case of pinpoint pupils Ocular movements o The eyes look toward a hemispheral lesion and away from a brainstem lesion o Oculocephalic reflexes – integrity of brainstem Laboratory studies and Imaging Bedside BSL – hypo- or hyper-glycemic Arterial blood gases – helpful in patients with lung disease and acid-base disorders Laboratory EUC- electrolyte abnormalities, serum osmolarity, renal function Ammonia – hepatic encephalopathy Toxicologic analysis o Ethanol level - > 43mmol/L (0.2g/dl) impaired activity, >65mmol/L (0.3g/dl) stupor in nonhabituated patients, >0.4g/dl in chronic alcoholics o Drug levels where applicable e.g. lithium, carbamazepine, valproate etc. Radiologic studies CXR – pneumonia or aspiration CT brain – structural lesions of brain. Lesions in coma that may be missed on a CT include o Bilateral hemisphere infarction o Acute brainstem infarction o Encephalitis/ meningitis o Mechanical shearing of axons in head trauma o Sagittal sinus thrombosis o Subdural hematomas isodense with adjacent brain tissue Other investigations EEG – rarely diagnostic but useful in metabolic and drug induced states; also in clinically unrecognised seizures in HSV encephalitis or Prion disease Lumbar puncture – in diagnosis of meningitis/ encephalitis and sometime SAH. Cerebrovascular disease patterns in coma Basal ganglia and thalamic hemmorhage – acute onset of vomiting, headache, hemiplegia and characteristic eye signs Pontine hemorrhage – sudden onset, pinpoint pupils, loss of reflex eye movements, ocular bobbing, posturing, hyperventilation and excessive sweating Cerebellar hemorrhage – occipital headache, vomiting, gaze paresis and inability to stand Basilar artery thrombosis – neurologi prodrome or warning spells, diplopia, dysarthria, vomiting, eye movement and corneal response abnormalities and asymmetric limb paresis Subarachnoid hemmorhage – precipitous coma after headache and vomiting Common hemispheric strokes – do not directly cause coma, except when edema surrounding large infarct act as a mass Coma – general management The immediate goal in a comatose patient is prevention of further nervous system damage. Correct 6Hs rapidly o Hypotension o Hypoglycaemia o Hypercalcemia o Hypoxia o Hypercapnia o Hyperthermia Airway protection – if there is apnea, upper airway obstruction, hypoventilation or emesis, or risk of aspiration IV access – naloxone or dextrose as indicated, thiamine with glucose in c/o malnourished patients Thrombolytic therapy – for basilar thrombosis with brainstem ischemia once hemmorhage excluded Antibiotic therapy in case of meningitis or sepsis early Status epilepticus DIS Ex In the past, status epilepticus was defined as either continuous seizure activity for 30 min or more, or two or more seizures that occur without full recovery of consciousness between the attacks. It remains unclear how long a seizure can continue before permanent neurologic sequelae ensue. Although this question has never been satisfactorily answered, it does appear that the longer seizures are allowed to continue, the more likely that permanent CNS injury will result. Thus treatment should be initiated as soon as possible in all patients with continuous seizure activity lasting more than 10 min. The longer the seizure is allowed to continue, the more difficult it will be to control. Causes of Secondary Seizures Trauma (recent or remote) Intracranial hemorrhage (subdural, epidural, subarachnoid, intraparenchymal) Structural abnormalities Vascular lesion (aneurysm, arteriovenous malformation) Mass lesions (primary or metastatic neoplasms) Degenerative diseases Congenital abnormalities Infection (meningitis, encephalitis, abscess) Metabolic disturbances Hypo- or hyperglycemia Hypo- or hypernatremia Hyperosmolar states Uremia Hepatic failure Hypocalcemia, hypomagnesemia (rare) Toxins and drugs (many) Cocaine, lidocaine Antidepressants Theophylline Alcohol withdrawal Drug withdrawal Eclampsia of pregnancy (may occur up to 8 weeks postpartum) Hypertensive encephalopathy Anoxic-ischemic injury (cardiac arrest, severe hypoxemia) Treatment The goal of treatment of status epilepticus is seizure control within 30 minutes of presentation. Morbidity is due to hypoxemia, hyperthermia, circulatory collapse and eventual neuronal injury. Headache and facial pain Headache represents up to 4% of all ED visits. Most ED patients have benign primary headache syndromes, but approximately 3 – 4% may have serious or secondary pathology. Etiology and Classification History Headache pattern – important features include first severe headache, worst ever headache, steady worsening headache over several days or significant differences from prior headaches. Onset - sudden onset headache especially when occurring with exertion is an independent predictor of IC pathology – especially 25% of these patients will have SAH. Headache location – nonspecific and diagnosis should not be based on this. Occipitonuchal headache location in ED patients is an independent predictor if IC pathology (PPV 16%). It is also the most common location of headache for SAH. Associated symptoms – h/o syncope, altered LOC, confusion, neck pain or stiffness, persistent visual disturbance, fever or seizure. Other history – medications (nitrates, MAOIs, anticoagulants), h/o trauma, toxic exposure. Past history – past headaches and investigations, Comorbid conditions such as malignancy, HIV, coagulopathy or hypertension. Family history – migraine headaches may have positive family history. h/o SAH in first and second degree relatives. Physical examination Fever – infection e.g. meningitis, sinusitis Marked hypertension – hypertensive urgency or emergency Sinus palpation for tenderness Temporal artery palpation for tenderness or reduced pulsation Dental and TMJ examination Eye examination to rule out acute glaucoma, visual field defects or iritis Fundoscopy – s/o papilledema or subhyaloid hemmorhages in SAH Focused neurological examination mandatory Look for signs of meningeal irritation Special aspects Women – migraine more common, ask for menstrual history, OCP use, pregnancy and menopause Pregnancy – always consider preeclampsia, migraine improves in 60-70% patients in pregnancy Older age – new onset in patient >50years usually have secondary cause HIV/AIDS – high risk for IC SOL and pathologic infections Historical Features Suggesting Secondary Headache Acute onset Worst ever Posttraumatic Awakens from sleep With fever Aggravated by: sneezing, coughing, Valsalva, lying down Morning vomiting Altered mental status Change in behavior Change in pattern Toxic exposure Positive family history for migraines or subarachnoid hemorrhage Investigation Data collected from history and physical examination allows for risk stratification of patients presenting with headache in to groups needing emergent, urgent or outpatient care. Once the information is collated they may be divided into categories. Indications for emergent neuroimaging Presence of new focal neurologic deficits Acute sudden onset of headache HIV positive patients with a new headache Patients >50 years with a new headache ACEP Headache Categories Headache Category I. Examples Critical secondary causes requiring emergent identification Subarachnoid hemorrhage, meningitis, brain and treatment tumor with raised ICP II. Critical secondary causes not necessarily requiring emergent identification or treatment Brain tumor without raised ICP III. Generally benign and reversible secondary causes Sinusitis, hypertension, post–lumbar puncture headache IV. Primary headache syndromes Migraine, tension type, or cluster Diagnostic adjuncts CT brain o Usually non-contrast CT brain conducted. o Use of contrast associated with 10% risk of minor reactions and 0.1% risk for severe reactions. o If IC SOL highly suspected, contrast study may be conducted o Negative CT scan does not exclude SAH Lumbar puncture o Indicated when meningitis suspected or when CT negative in highly suspected SAH o Contraindications – suspicion of raised ICP o Raised ICP can be excluded by the combination of (all three present) Absence of papilledema Normal LOC and Normal neurologic examination o If these conditions are met, then a CT scan is not required prior to LP, especially if the CT scan is likely to be delayed. MRI brain o Cost and restricted availability limits utility in emergency situations o More sensitive in evaluating brain injuries, difuse axonal injuries, parenchymal contusions, isodense SDH and most tumors Subarachnoid Hemorrhage Of all sudden, severe headaches presenting to ED with a normal neurologic examination, 12 % have SAH. SAH occurs in young people, with a median age of 50 years. Mortality rates from SAH are high, 50% die within 6 months. Clinical features Almost half patients with SAH have no clinical findings at presentation – no neurodeficit, normal vitals, normal LOC and no neck stiffness Headaches most commonly severe and of sudden onset, but may be subtle. Location of headache usually occipitonuchal with many atypical presentations e.g. neck pain Resolution of pain even without treatment does not exclude the diagnosis Radiation of pain down the cervical spine suggests tracking of SAH down the spinal canal Hunt and Hess Classification of Subarachnoid Hemorrhage Classification Symptoms Grade I Asymptomatic or minimal headache and mild nuchal rigidity Grade II Moderate to severe headache, nuchal rigidity, no neurologic deficit other than cranial-nerve palsy Grade III Drowsiness, confusion, or mild focal deficit Grade IV Stupor, moderate to severe hemiparesis, possible early decerebrate rigidity, vegetative disturbance Grade V Deep coma, decerebrate rigidity, moribund appearance Diagnosis CT scan brain Sensitivity of newer generation CT scans is about 93% within 24hrs of onset of symptoms and higher if within 12hrs No study to date has shown CT conclusively ruling out SAH at even 12hrs. Sensitivity of CTB falls to just over 80% at 24hrs and then rapidly declines. Latest guidelines still mandate LP after negative CTB Lumbar puncture LP performed 12hrs or longer after onset of headache and spectrophotometry conducted to look for xanthochromia is nearly 100% sensitive for u to 2 weeks following a bleed. Xanthochromia checked visually may result in 50% false negative rates. LP may be delayed for 12hrs after onset of symptoms while awaiting development of xanthochromia Traumatic taps and xanthochromia on LP, all warrant CNS vascular imaging Treatment Rebleeding and vasospasm are major complications in SAH Risk of rebleeding is highest in first 24hrs In patients with raised BP, lowering systolic BP to 160mmhg and/or maintaining a MAP of 110mmhg is associated with lower risk of rebleeding and a decreased mortality rate Maintain BP at prehemorrhage levels if known Cerebral ischemia caused by vasospasm occurs from 2 days to 3 weeks after aneurysm rupture. Nimodipine PO 60mg q6h, reduces the incidence and severity of vasospasm and should be given to all patients with SAH In patients unable to tolerate orally, nimodipine infusion should be instituted Seizures and persistent vomiting can cause elevations in systemic and ICP. Prophylactic phenytoin loading is recommended. Nausea and vomiting treated promptly with antiemetics Analgesia appropriately managed For candidates with good neurologic condition (Hunt and Hess grades 1 to 3) Early angiography and surgical intervention recommended Alternative approaches for appropriate aneurysms include endovascular obliteration through use of intraluminal platinum coils or detachable balloon embolisation. Bacterial Meningitis In cases of bacterial meningitis, the two most critical actions in the emergency department are to suspect it and to begin empirical treatment promptly. Epidemiology Attack rates are age-specific ranging from 400/100000 in neonates to 1-2/100000 in adults 2/3rd cases are in children Long term complications such as cognitive defects, epilepsy, hydrocephalus and hearing loss affect 25% of survivors Prior to 1985 – H.influenzae (45%), S. pneumoniae (18%) and N. meningitidis (14%) But now after universal Hib vaccination programs, S.pneumoniae and N. meningitidis predominate Pathophysiology Encapsulated organisms from host airway → invade, survive and disseminate through bloodstream → gain access to subarachnoid space → subcapsular constituents trigger inflammatory cascades in host → clinical picture of fever, meningismus and eventually altered mental status. Clinical features Signs and symptoms 25% cases s/s are classical with little diagnostic challenge Rapidly developing fever, headache, stiff neck, photophobia and altered mental status Seizures occur in 25% of patients Features may be non-specific in the very young and the very old. History regarding living conditions, trauma, immunocompetence, immunization and antibiotic use should be sought Brudzinski sign – flexion of hips and knees in response to passive neck flexion Kernig sign – contraction of hamstrings in response to knee extension while hip is flexed Examination of skin to seek for purpuric rash Cutaneous stigmata e.g. petechiae, splinter hemorrhages and pustular lesions should be aspirated and gram stained and cultured Paranasal sinues percussed and ENT examined for evidence of primary infection Funduscopy to assess for papilledema Neurologic examination – seek evidence of focal neurologic deficit e.g. disordered eye movements, visual field defects, facial asymmetry and hemiparesis Diagnosis Lumbar puncture is the only confirmatory investigation which can diagnose or rule out meningitis LP should be carried out as soon as it is deemed safely possible; its timing should not impede the early administration of empirical antibiotics Blood cultures yield responsible organisms in only 50% of cases LP should be considered before neuroimaging in these cases o Age <60 yrs o Immunocompetent o No h/o CNS disease o No recent seizure <1 week o Normal sensorium and cognition o No papilledema o No focal neurologic deficit Coagulopathy is considered as a relative contraindication. Infusion of clotting factors may be considered in haemophiliac patient. Infusion of platelets may be considered in case of severe thrombocytopenia, but no safe level for platelets has been ever investigatively proven. CSF analysis should be done for cell counts, gram stain, culture, CSF glucose and protein levels at the least. Additional tests which may be required in suspected cases include: o Viral cultures in viral meningitis o Tests for Borrelia antibodies in c/o Lyme disease o India ink or serum cryptococcal antigen in immunocompromised patients o AFB stain for mycobacteria in c/o suspected tuberculous meningitis o Agglutination tests for bacterial antigens in c/o partially treated cases – e.g. S. Pneumoniae, H. Influenza, group B streptococci and N.meningitidis. LP may be negative in early bacterial meningitis and repeated LP may be conducted if there is strong clinical suspicion despite initial negative LP results LP is contraindicated if there is infection in overlying skin Lumbar puncture findings Parameter Normal Opening < 170mm pressure WBC <5 mononuclear % PMN 0 Glucose >2.2mmol/dL Protein <50mg/dL Gram stain Cytology - Bacterial >300mm Viral 200mm Neoplastic 200mm Fungal 300mm >1000/µL >80% <2.2mmol/dL >200mg/dL + - <1000/µL 1-50% >2.2mmol/dL <200mg/dL - <500/µL 1-50% <2.2mmol/dL >200mg/dL - <500/µL 1-50% <2.2mmol/dL >200mg/dL + Treatment Ideal management has several goals. These include: Rapid administration of a bactericidal antibiotic that gains rapid entry into the subarachnoid space In some cases, use of anti-inflammatory agent to suppress the normal inflammatory processes, which are amplified by antibiotic-induced bacteriolysis Counter the adverse effects of increased ICP and vasculopathy, which may lead to brain ischemia Empirical antibiotic therapy Patient category Potential pathogens Empirical therapy Age 18 – 50 years S. Pneumoniae, N. Meningitides Ceftriaxone 2g IV q12h + Vancomycin or Rifampicin >50 years S. pneumoniae, N. Meninigitidis, L. Ceftriaxone 2g IV q12h + Monocytogenes, aerobic GN bacilli ampicillin 2g IV q4h + vancomycin or Rifampicin Special circumstances CSF leak with h/o closed head S. pneumoniae, H. Influenzae, GBS Ceftriaxone 2g IV q12h trauma Recent penetrating head injury, S. aureus, S. Epidermidis, Vancomycin 25mg/kg IV load then neurosurgery or VP shunt diphtheroids, aerobic GN bacilli 19mg/kg by nomogram plus ceftazidime 2g IV q8h Immunocompromised host S. Pneumoniae, N. Meningitides, L. Vancomycin as above + ampicillin Monocytogenes, aerobic GN bacilli 2g IV q4h + ceftazidime 2g IV q8h Any patient Herpes simplex virus suspected Add Acyclovir 10mg/kg IV q8h Steroids in meningitis Number of anti-inflammatory drug have been shown to improve outcomes in experimental meningitis, but only glucocorticoids and specifically dexamethasone have been tested in clinical trials Dexamathasone given to adults with bacterial meningitis (10mg IV 15min before antibiotic therapy, then 6hrly for 4 days) appears to decrease morbidity and mortality due to S. Pneumoniae but not N. Meningitides Supportive management Surveillance and correction of complications o Seizures – phenytoin loading o Hyponatremia o Hydrocephalus and o CVA General treatment measures – maintain normal blood volume Avoid hypotonic fluids Monitor sodium levels closely to detect SIADH or cerebral salt wasting Correct hyperpyrexia Correct coagulopathies with specific replacement therapy For marked cerebral edema, as noted by CT findings o Head elevation o Hyperventilation to PaCO2 of 25-30 mmhg o Mannitol o Measure ICP and MAP to monitor CPP Chemoprophylaxis Chemoprophylaxis for meningitis or other infections caused by N. Meningitides and H. Influenzae type b is offered to close contacts of the index case. Among close contacts there will be a person or persons asymptomatically carrying the organism which caused the index infection. Chemoprophylaxis aims to eradicate asymptomatic carriage in the network of contacts to prevent further spread to susceptible members in the group. N. meningitides 1. Ceftriaxone 250mg IM as single dose (preferred option during pregnancy) OR 2. Ciprofloxacin (adult >12yrs of age) 500mg orally as a single dose (preferred in women on OCP) OR 3. Rifampicin 600mg (neonate 5mg/kg, child 10mg/kg) orally BD for 2 days (preferred in children) H.influenzae type b 1. Rifampicin 600mg (neonate 10mg/kg, child 20mg/kg up to 600mg) orally daily for 4 days OR 2. Ceftriaxone 1g (child 25mg/kg up to 1g) IM daily for 2 days (limited data) 3. Where index case is <2yrs of age, commence full course of Hib vaccination ASAP after recovery, regardless of previous immunization. 4. Unvaccinated contacts <5yrs should be immunized ASAP. Cerebrovascular Accidents Cerebrovascular disease comprises disorders in which there is disturbance of blood supply to the brain. Stroke is the most important manifestation of cerebrovascular disease. A stroke occurs when an artery supplying blood to a part of the brain suddenly becomes blocked (ischemic stroke – 85%) or bleeds (hemorrhagic stroke – 15%). Stroke poses a significant burden on patients and their families as well as on the health system and aged care services. Each year about 40000-48000 stroke events occur in Australia and was the cause of nearly 7% of all deaths. Etiologic Classification Ischemic stroke o Thrombosis Atherosclerotic disease Vasculitis Dissection Polycythemia Hypercoagulable states Infectious diseases – HIV, syphilis, TB, aspergillosis and trichinosis o Embolism Cardiac sources Valvular vegetations Mural thrombi (AF,AMI or dysrhythmias) Paradoxical emboli (ASD, VSD) Cardiac tumors Artery-to-artery emboli Fat emboli Particulate emboli from IV drug injection Air emboli Septic emboli o Systemic hypoperfusion Cardiac failure – diffuse injury in watershed areas at periphery of cerebral vascular supply territories Hemorrhagic stroke o Intracerebral hemorrhage o Subarachnoid hemorrhage Berry aneurysm rupture Rupture of AVM o Bleeding diatheses Anticoagulant use Thrombolytic use o Vascular malformations o Cocaine use Anatomy of brain blood supply Vascular supply of brain divided into anterior and posterior circulations Anterior circulation – o Common carotid arteries divide into right and left internal and external carotid arteries at the level of the mandible o ICA course intracranilly in cavernous sinus along sella turcica giving ut first branch the ophthalmic artery – supplying optic nerve and retina o ICA terminates by branching into anterior and middle cerebral arteries at the circle of Willis. o Anterior circulation supplies blood to optic nerve, retina and frontopareital and anterotemporal lobes of the brain Posterior circulation – o Derived from two vertebral arteries that ascend through the transverse processes of the cervical vertebrae o Vertebral arteries enter cranium through foramen magnum, supplying cerebellum vis the posteroinferior cerebellar arteries. o Vertebral arteries join to form the basilar artery, which branches to form the posterior cerebral arteries o Posterior circulation supplies the brainstem, cerebellum, thalamus, auditory and vestibular functions of the ear, medial temporal lobes and the visual occipital cortex The anterior and posterior circulations join at the circle of Willis, potentially allowing collateral flow. The amount of collateral flow determines the extent of neurological deficit a complete carotid occlusion on one side can cause. Pathophysiology of stroke Ischemic stroke Neurons are very sensitive to changes in cerebral blood flow and die within minutes of complete cessation of blood flow Despite complete occlusion, some collateral supply usually persists In the region of the stroke, cells vary from irreversibly injured neurons in the centre to reversibly injured neurons in the periphery (the penumbra) Degree and duration of occlusion determines the viability of the cells in the penumbra The earlier reperfusion occurs, the greater the chance of survival – basis for IV and intra-arterial thrombolytic therapy and use of neuroprotective agents Hemorrhagic stroke ICP rises following vascular rupture with a corresponding short-term decrease in global perfusion ICP and CPP gradually improve, but do not return to baseline Marked reduction in perfusion occurs around the area of hemorrhage probably due to local compression Blood breakdown products from ICH also mediate vasoconstriction into wider area of brain, remote from the location of bleed. Clinical features History H/o HT, CAD and DM all suggestive of underlying atherosclerotic disease and suggest thrombosis H/o AF, valvular replacement or recent MI all suggest embolism Question regarding recent TIAs, similar transient neurological symptoms prior to the stroke s/o thrombosis whereas multiple TIAs in different distributions s/o embolism Sudden onset of symptoms usually s/o embolic or hemorrhagic stroke Associated symptoms of headache, vomiting or recent trauma should be sought and recorded Recent h/o neck injury, MVA, chiropractic manipulation or sports related injury s/o carotid or vertebral artery dissection h/o straining or coughing s/o ruptured aneurysm Physical examination General examination temperature – s/o infection or secondary to aspiration skin examined for signs of o emboli – Janeway lesions and Osler nodes o bleeding disorder – ecchymosis or petechiae funduscopic examination – o papilledema to r/o mass lesion, cerebral vein thrombosis or hypertensive crisis o pre-retinal hemorrhage – SAH o evidence of hypertensive retinopathy cardiovascular examination to look for AF, CCF or valvular disease Neurologic examination Basic neurologic assessment can be broken down into six major areas: 1. level of consciousness – simple questions TSP, simple commands 2. visual assessment – visual fields and extraocular movements 3. motor function – upper limb check for pronator drift, lower limb: lift legs of bed for 5s, gait assessment 4. sensation and neglect – pinprick testing, identifying numbers on plams, double simultaneous extinction; neglect also checked by asking patient to draw a box or house 5. cerebellar function – giat, finger-to-nose and/or heel-to-shin testing 6. cranial nerves – each nerve individually assessed Stroke syndromes Transient ischemic attack TIA is a neurologic deficit that resolves within 24h (although most resolve within 30m) and is most commonly associated with thrombotic strokes Many clinical TIAs may be associated with CT findings of infarction 10% of patients with TIA may return to ED with a stroke within 90 days, with half of these in just 2 days. Ischemic stroke syndromes Artery involved Clinical features (syndrome) Anterior cerebral artery Contralateral leg weakness > arm weakness infarction Mild cortical sensory deficits May preserve speech or motor actions and respond slowly Middle cerebral artery Contralateral weakness and numbness infarction Affecting face and arm > leg Aphasia (receptive, expressive or both) if dominant hemisphere involved In right handed patients and 80% of left handed patients, left hemisphere is dominant Inattention, neglect or extinction on double-simultaneous stimulation – non-dominant hemisphere involvement Constructional apraxia – inability to draw objects May be dysarthric but not aphasic Homonymous hemianopia and gaze preference to side of infarct may be present Posterior cerebral artery May be unaware of deficit until tested infarction Motor involvement minimal and visual cortex abnormalities may go unrecognized Light-touch and pinprick sensations may be significantly reduced Vertebrobasilar Dizziness, vertigo, diplopia, dysphagia, cranial nerve palsies syndrome Bilateral limb weakness singly or in combination Hallmark is crossed neurologic deficit i.e. ipsilateral CN deficits with contralateral motor weakness Lateral medullary Specific posterior circulation stroke involving vertebrobasilar arteries (Wallenburg) syndrome and/or posterior inferior cerebellar artery Ipsilateral loss of facial pain and temperature Contralateral loss of same senses over the body Gait and limb ataxia Partial ipsilateral CN lesions of V, IX, X, and XI in varying combinations Ipsilateral Horner syndrome may be present Basilar artery occlusion Severe quadriplegia, coma and the locked-in syndrome Lesions in pontine tectum – complete motor paralysis except for upward gaze Cerebellar infarction Present following ‘drop attack’ with sudden onset of inability to walk or stand Often accompanied by vertigo, headache, nausea, vomiting and neck pain CN abnormalities often present Lacunar infarction Pure motor or sensory deficits caused by infarction of small penetrating arteries Commonly associated with HT Lesions primarily in the pons and basal ganglia Management of adult stroke – Australian guidelines Pre-hospital care Ambulance services, health care professionals and general public should receive education concerning the importance of early recognition of stroke, emphasising stroke is a medical emergency Stroke patients should be given a high priority grouping by ambulance services Ambulance services should be trained in the use of validated pre-hospital stroke screening tools Ambulance services should preferentially transfer suspected stroke patients to a hospital with stroke unit care, where feasible. Early assessment and diagnosis Assessment of TIA All patients with suspected TIA should have a full assessment of stroke risk at initial point of health care contact Following investigations should be undertaken routinely for all patients with suspected TIA: o FBC, EUC o Cholesterol level o Glucose level and o ECG Patients classified as high risk should have an urgent CTB (<24hrs) Carotid duplex ultrasound undertaken urgently in patients with carotid territory symptoms Patients classified as low risk should have a CTB and carotid ultrasound as soon as possible (48-72hrs) Triage in ED Diagnosis should be reviewed by a clinician experienced in the evaluation of stroke Emergency department staff should use validated stroke screen tool to assist in rapid accurate assessment Local protocols should be developed jointly by staff from prehospital services, ED and stroke unit to expedite early transport, referral and access to imaging. Imaging All patients with suspected stroke should have an urgent CTB or MRB (<24hrs) A repeat CT or MRI should be considered if clinical condition deteriorates All patients with carotid territory symptoms should have urgent carotid duplex study to consider carotid revascularization Investigations Following investigations to be conducted routinely in all patients with stroke o FBC, EUC o ECG o ESR and/or CRP o Fasting lipids and o Glucose Selected patients may require further additional investigations o Angiography o CXR o Syphilis serology o Vasculitis screen and o Prothrombotic screen Acute medical and surgical management Ischemic stroke and TIA Thrombolysis o IV rt-PA in acute ischemic stroke should be undertaken in patients satisfying inclusion and exclusion criteria o IV rt-PA should only be given under authority of specialist physician with expert knowledge of stroke management, experience in use of IV thrombolytic therapy. o Thrombolysis should only be undertaken in a hospital setting with appropriate infrastructure o De-identified data from all patients treated with thrombolysis should be recorded in a central register to allow monitoring, review, comparison and benchmarking of key outcome measures over time Antithrombotic therapy o Aspirin (150-300mg) should be given ASAP after onset of stroke symptoms (<48hrs) if CT/MRI excludes hemorrhage o Routine use of anticoagulation (IV heparin) in unselected patients with TIA/ ischemic stroke is not recommended Blood pressure lowering therapy o If BP is extremely high, institute or increase anti-HT therapy with close monitoring only by 10-20% o Pre-existing anti-HT therapy should be continued (PO or NG) provided there is no significant hypotension or contraindication Surgery for ischemic stroke o Selected patients (18-60 yrs of age) with significant MCA infarction should be urgently referred to neurosurgical team for consideration of hemi-craniectomy o Insufficient evidence at this stage to recommend intracranial endovascular surgery Intracerebral hemorrage Hemostatic drug rFVIIa is experimental and only used in clinical trial settings Routine surgery for supratentorial ICH is not recommended except o Stereotactic surgery for deep ICH o Craniotomy ofr superficial hematoma Surgical evacuation for cerebellar hemisphere hematomas >3cm may be undertaken In ICH patients with hypertension the MAP should be maintained below 130mmhg. General stroke care Physiological monitoring - regular Regular vital signs (P, BP, T, O2 sat) GCS and focal neurological deficits BSL Oxygen therapy For hypoxic patients Glycemic control Diabetic patients should have BSL closely monitored Intensive, early maintenance of euglycemia is currently not recommended Hypoglycaemia is to be avoided Neuroprotective agents Only used in clinical trial settings ABCD tool for risk stratification of TIA patients A → age > 60 years (1point) B → blood pressure > 140/90mmhg (1point) C → clinical features: unilateral weakness (2points), speech impairment without weakness (1point) D → duration: >60mins (2points), 10-59mins (1point) and D → diabetes (1point) ABCD >4 → high risk – admitted to stroke unit to facilitate rapid assessment and treatment ABCD <4 → low risk – managed in community by GP, private specialist or TIA clinic where available Thrombolysis criteria Patient selection criteria Indications 1. Onset of ischemic stroke within the preceding 3 hours 2. Measurable and clinically significant deficit on NIHS scale examination 3. Patient’s CT does not show hemorrhage or non-vascular cause for symptoms 4. Patient’s age >18 years Absolute contraindications 1. Uncertainty about time of onset e.g. waking up from sleep 2. Coma or sever obtundation with fixed eye deviation and complete hemiplegia 3. Only minor stroke deficit which is rapidly improving 4. Seizure at onset of stroke 5. Hypertension: systolic BP ≥185mmhg or diastolic BP ≥110mmhg on repeated measures 6. Clinical presentation s/o SAH despite normal CT 7. Presumed septic embolus 8. Patient receiving heparin within the last 48hrs and has elevated APTT or known h/o bleeding disorder 9. INR >1.5 10. Platelet count < 100000/µL 11. Serum glucose < 2.8 mmol/L or >22.0 mmol/L Relative contraindications – use with caution, weight benefit risk ratio 1. Severe neurological impairment, NIHSS score >22 2. Age > 80years 3. CT evidence of extensive MCA territory infarction 4. Stroke or serious head trauma in past 3 months 5. Major surgery within past 14 days 6. Known h/o ICH, SAH, AM or intracranial neoplasm 7. Suspected recent MI <30 days 8. Recent biopsy or surgery of parenchymal organ with risk of unmanageable bleeding e.g. liver 9. Recent trauma with internal injuries or ulcerated wounds 10. GIT or urinary tract hemorrhage within last 30 days 11. Arterial puncture at noncompressible site within last 7 days 12. Concomitant serious, advance or terminal illness