NRNP Finals 6560 |235 questions and answers

coup-contrecoup injury Dual impacting of the brain into the skull; coup injury occurs at the point of impact; contrecoup injury occurs on the opposite side of impact, as the brain rebounds. Scalp laceration: what, effect, management Primary head injury profuse bleeding - signs of hypovolemia Apply direct pressure Suture/ staple laceration Lidocaine 1% with epi to control bleeding, not close to nose/ ears Skull fracture: types, effect, management Primary head injury Simple: no displacement of bone. Observe and protect spine Depressed: bone fragment depressing thickness of scull Surgery for debridement. Give tetanus and seizure precautions Basilar: fracture at floor of skull Raccoon eye - periorbital bruising battle's sign: mastoid bruising otorrhea/ rhinorrhea - halo sign: do not obstruct flow Give Ab's Oral intubation and oral gastric instead of nasal Brain injury: types, effect, management Primary head injury Concussion: reversible change in brain functioning loss of consciousness, amnesia Do not give opioids, admit for unconsciousness greater than 2min Contusion: bruising to surface of brain with edema Frontal and temporal region Brainstem contusion: posturing, variable temp, variable vital signs N/V, dizziness, visual changes seizure precautions Hematoma - neuro: types, effect, management Epidural hematoma: commonly temporal/ parietal region with skull fracture, causing bleeding into epidural space Loss of consciousness Rapid deterioration: obtunded, contralateral hemiparesis, ipsilateral pupil dilation CT scan (non contrast) Treatment based on Brain trauma foundation. Surgical if greater than 30cm Subdural hematoma most common type of intracranial bleed Acute (hours): drowsy, agitated, confused, headache, pupil dilation, CT scan (noncontrast) surgery for 10mm thickness or 5mm midline shift or for worsening GCS Chronic (days): headache, memory loss, incontinence CT scan (noncontrast) Surgery: burr holes/ crani Cerebral edema/ ICP elevated/ herniation: symptoms, management decreased level of consciousness Blown pupil Cushing triad: HTN (widening pulse pressure), decreased resp rate, bradycardia (means increased intracranial pressure) Neuro exam components AVPU: awake, response to verbal stimuli, painful stimuli, unresponsive GCS: 8 or below is comatose Posturing: decorticate = arms, legs in decerebrate = arms, legs out Electrolyte imbalances in brain injury Hyponatremia: SIADH and cerebral salt wasting Hypernatremia: DI (give mannitol) Management of traumatic brain injury - Consult neurosurgery - Limit secondary injury - Prevent hypotension (syst 90) and hypoxemia (PaO2 60). May give blood to improve tissue perfusion. - Treat cerebral edema: elevate bed, sedate, paralyse, mannitol, hyperventilation (PaCO2 25-30), during first 24hrs. - sedation and analgesia: opioids to reduce ICP (Fentanyl) with propofol. Could give Nimbex or Vec. to help oxygenate/ ventilate - steroids: avoid - Give mannitol or hypertonic saline for herniation: bolus then gtt. monitor serum osmolality, sodium, and bp. - Seizure precautions: give phenytoin or keppra - DVT prophylaxis: stockings, LMWH - head injury means spine injury until proven otherwise - hypothermia: can control ICP (89 - 91F) - decompressive crani: ICP refractory to tx - brain O2 monitoring (jugular vein O2 sats) ICP monitoring For: GCS 3-8 with abnormal CT and comatose pt's with normal CT and older than 40, posturing, hypotension. Normal value: 5-10 mmHg Recommend initiating treatment if ICP > 20 mmHG. Can calculate CPP (CPP = MAP - ICP). Should be 60 Brain death criteria Must have all: No spontaneous movement Absence brain stem reflexes (fixed/ dilated pupils, no corneal reflexes, absent doll's eyes, absent gag, absent vestibular response) Absence breathing drive/ apnea can't be declared brain dead when: hypothermia, drug intoxication, severe electrolyte/ acid-base imbalance EEG, CTA of brain, Cerebral angiography, transcranial doppler Spinal cord trauma: cause and who - MVA, falls, acts of violence, sports, wounds - Rapid acceleration/ deceleration causes hyperextension (fall, rear-end collision)(central cord syndrome), hyperflexion (bilateral facet dislocation), vertical column loading (compression and then shattering from falls/ dive lands on butt, at C1 from diving), whiplash - Distraction injury: from hanging - penetrating trauma: from wound - pathologic fractures (osteoporosis/ cancer) mainly cervical spine. High mortality. More common in men more common in young than old Fractures and vertebrae Cervical: C1-C7. Flexible and small diameter so many fractures Thoracic (T1-T12): connected to ribs. Not common in fractures Lumbar: L1-L5: Very mobile, requires great force to fracture Sacral Spinal cord trauma assessment - History: mechanism of injury, pt's complaints, pre-hospital tx - Physical assessment: treat airway, breathing, circulation (ABC) first. Pulm complication common in quadriplegia. Assess respiratory status: injury above C3 is resp arrest. C5 - C6 spares diaphragm so breathing exists. - grade strengthening (0= no muscle contraction, 5 = full strength) - complete lesion: pt lacks all function below level of spinal cord damage. Poor prognosis. - incomplete lesion: parts of spinal cord intact - sensory function: start at no feeling then go to feeling - evaluate back (log-roll) Motor assessment in spinal cord trauma If unable to do, # above: Deltoids (C4): shrug shoulder Biceps (C5): flex arm and push arms away Wrist (C6): try to straighten wrist while pt tries to flex Triceps (C7): extend arm and try to bend while pt prevents that Intrinsic (C8): fan fingers and push together Hip flexion (L2 - L4): bend knee and apply pressure Knee extension (L2-L4): extend knee with hip/ knee flexed key signs of spinal cord injury - various levels C2-C3: resp paralysis, flaccid paralysis, deep tendon reflexes loss C5-C6: diaphragmatic brething, paralysis of intercostal muscles, quadriplegia, anaesthesie below clavicle, areflexia, fecal/ urinary retention, priaprism T12-L1: paraplegia, anesthesia legs, areflexia legs, fecal/ urinary retention, priaprism L1-L5: flaccid paralysis, ankle/ plantar areflexia Multisystem impact of spinal cord injury Cardiovascular: - hypotension/ spinal shock. Fluid resuscitation (LR) - bradycardia; oxygenate well, normothermia, atropine - vasovagal reflex: limit suctioning length - Poikilothermy - venous thrombosis: dvt prophylaxis - orthostatic hypotension GI: - abdominal injuries: assess for abd distention - curling's ulcer: stress ulcer. Give ranitidine - gastric atony and ileus: NG to LIS - loss of bowel function: initiate bowel program GU: - autonomic dysreflexia: HTN crisis from distended bladder or other noxious stimulu. Decompress bladder. - UTI Musculoskeletal: - paralysis - wounds Psychological: - ineffective coping, powerlessness, denial/ anger/ depression. Be honest with positivity, include pt, interdisciplinary approach Spinal cord lesions/ syndrome Anterior cord syndrome: weakness/ paralysis with loss of sense of pain and temp Posterior cord syndrome: can't feel touch and vibration Central cord syndrome: greater loss in upper extremities than lower Brown sequard syndrome: one side of spinal cord is damaghed by stab/ gun wound. Ipsilateral motor loss and contralateral loss of pain and temp sense. Extremities that can move have no feeling and that have feeling can not move. Spinal cord injury: diagnostics Cervical vertrebrea: lateral xr, then AP (swimmer view) Thoracic vertebrae: lateral and AP xr, view all 12 Lumbar: lateral and AP, view all 5 CT to check for bony fragments Films in flexion. extension to check for fractures Myelogram: detects compression of cord by herniated disks, bone or foreign matter MRI: cord impingement, hematoma, infarct, contusion, hemorrhage. Spinal cord management - Consult neuro - Airway maintenance (do not hyperextend neck when intubating) - immobilization (cervical collar/ spine board) - intravascular fluid (neurogenic shock: warm, dry, brady) - monitor bp (avoid hypotension: keep MAP 85) - Foley - NG - AB for penetrating injury - room temp - good skin care - fixation of spine - fusion: attaching injured vertebrae Key features of dementia - General decrease in level of cognition - thinking, memory, reasoning - Behavioral disturbance - Interference with daily function and independence Not a disease, but group of symptoms by various diseases Alzheimer's disease most common form of dementia Neuritic plaques, neurofibrillary tangles, degeneration of cholinergic neurons causing irreversible neuronal damage. B-amyloid present in high levels. Effect: cerebral atrophy. Causes of brain degeneration Alzheimer's Parkinson's Huntington's Vascular: stroke, arteritis Infectious: HIV, Syphilis, Meningitis, Encephalitis CNS/ toxic: drug overdose Nutritional deficiency: Vit B12, folate deficiency Chronic seizures Lewy body dementia symptoms of dementia - Slow onset - memory loss and confusion - problems with language - impaired abstract reasoning - aphasia, apraxia, agnosia - disorientation - poor judgement - emotional problems - sleeplessness Dementia labs/ diagnostics - History: family/ spouse report - Physical: neuro, cognitive examz: Mini mental State exam (score 23 or less is cognitive impairment), document in 3-6mo intervals - Labs: glucose, electrolytes, magnesium, calcium, liver tests, BUN/ creat, thyroid, Vit B12, HIV, CBC, ABG, cultures, drug screen - CT head/ MRI: for tumor/ infarction - PET scan: differentiate dementia type - EEG - Lumbar: rule out meningitis, neurosyphilis - XR chest: rule out CHF, COPD - ECG - Identify treatable cause DSM-V criteria for dementia 1. Memory impaired 2. At least two of these: aphasia, apraxia, agnosia, disturbance in executive functioning 3. Disturbance of one or two of these disrupts functioning 4. Disturbance not only during delirium Dementia management - supportive: living situation - treat underlying illness - stop nonessential meds - maintain nutrition - avoid restraints, except for safety - address safety issues - cholinesterase inhibitors can improve symptoms mildly (because of cholinergic deficiency) - Alzheimer's related: meds very mild and temporary effect Medication for dementia Mild to moderate Alzheimer's: - Donezepil 5mg, then 10mg after 4-6 wks. Can cause syncope, brady, AV-block, N/V, weightloss - Rivastigmine. With food, can cause hypotension, syncope - Galantimine, 4mg for 4 wks, then 8mg 4 wks, then 12mg. Avoid in renal and liver failure Moderate to severe dementia: - Memantine (N-methyl-d-aspartate rec anatgonist), prevents progression. May be paired with donezepil. May cause Stevens-Johnson's For aggression: - Olanzapine (Zyprexa), Quetiapine (Seroquel), Risperidone, Ziprasidone. Short term. May cause tardive dyskinesia - Haldol may help too for unmanageable aggression. - Benzo's: Clonazepam. May cause paradoxical aggression. Lorazepam For emotional lability: - Imipramine - Setraline - Zoloft - Citalopram multiple sclerosis Disease with myelin sheath destruction causing disruptions in nerve impulse conduction. Acquired, immune-mediated. Relapses/ attacks/ exacerbations and remissions Etiology of MS More women than men Caucasians, more northern European Early onset, 20-40ies Measles, Herpes, Chlamydia, Epstein-Barr Classification of MS Relapsing - Remitting: Clear/ defined episodes of relapse and recovery. No progression between episodes and return to baseline. Most often initial presentation. Secondary progressive: As Relapsing- Remitting, but then progression between episodes. No return to baseline. Primary progressive: Continued disease progression. Minor improvements. Usually after 40yrs. Progressive relapsing. Progressive disease with relapses, and progression in between. Malignant MS: rapid onset, rapid deterioration Benign MS: No deterioration after 10 yrs MS symptoms Subjective: - Motor weakness, stiffness - Numbness, tingling, burning, pain - double vision, dysarthria, dysphasia, vertigo (brain stem) - visual deficits - gait ataxia, tremor, uncoordinated movements (cerebellum) - cognitive dysfunction: memory, processing - fatigue (common!) - sleep disorder - bladder, bowel dysfunction - seizures Objective: - decreased sensation of pinprick, vibratory, temp - Reflex changes: abnormal deep tendon, pos babinski, pos hoffman's - brain stem changes: nystagmus, hearing loss, tinnitus - Cerebellar: ataxia, tremor, poor coordination - visual field changes - frontal lobe: cognitive dysfunction, emotional changes MS diagnostics - neuro exam - MRI (white matter lesions, lesions spinal cord, T1 and T2 lesions) (diagnostic!) - CSF analysis: elevated igG and oligoclonal bands in CSF but not serum MS management - consult neuro - no intervention for mild attack - Acute intervention for relapse with Glucocorticoid (po or iv) - symptom management meds - disease modifying meds: to reduce relapse, delay disability, and decrease MRI lesions: - Fingolimod. For relapsing. May cause brady, AV-block, HTN, diarrhea - Betaseron. For relapsing. May cause depression/ suicidality - Avonex. For relapsing. May cause flu-like symptoms - Rebof. For relapsing. May cause flu like symptoms - Glatiramer acetate. For Relapsing/ remitting. - Mitoxantrone. For sec progressive, progressive, or worsening relapsing/ remitting. Parkinson's disease: what, etiology Neurodegenerative disorder caused by depletion of dopamine-producing cells causing resting tremor, rigidity, slowness of movement. Age onset: 60 more men than women caucasians Environmental (metals such as copper) and genetic factors. Gene: PARK1 Symptoms and diagnostics of Parkinson's - Classic triad: resting tremors, rigidity, bradykinesia - Motor symptoms: postural instability can cause falls - Classic gait: diminshed arm swing, shuffling steps, bent forward, frozen gait - neuropsychiatric: depression, dementia, anxiety, psychosis, sleep disruption - autonomic dysfunction: urinary incontinence, sexual dysfunction, constipation, impaired thermoregulation - Craniofacial: masked face/ expressionless, dysphagia, impaired sense of smell, drooling - H&P - CT and MRI to assess for differential Parkinson's treatment - consult neuro - Pharm to relieve symptoms and improve functioning: Carbidopa-levodopa standard treatment. - Can on/off phenomona with working/ not working of meds. Add catechol-O-methyltransferase - Adequate nutrition - Exercise Dopaminergic agents and Parkinson's Carbidopa-levodopa. Most effective drug. Use with rasagiline. May cause on/ off phenomena, dyskinesia, confusion, headache, hallucinatinos. Dopamine agonists and Parkinson's Pramipexole and Ropinirole May reduce risk for complications and alleviate symptoms. Mono or dual theraoy with levodopa. May cause N/V, dyskinesia, confusion. MAO-B inhibitors and Parkinson's Rasagiline Adjunct therapy May cause serotonin syndrome, dyskniesia, arthralgia, ataxia Amyotrophic lateral sclerosis (ALS): what and etiology Disease of motor neurons causing asymmetric weakness, in upper or lower extremity. Less likely to present with resp weakness, dysarthria or dysphagia Onset age: 50 Men more likely Familial is 10% of cases unknown Average survival: 2-5 yrs Symptoms and diagnostics ALS Classified by number of upper and lower motor neurons in regions of brain Progressive weakness over weeks/ months Sensation intact Muscle atrophy Small muscle fasciculations Hyperreflexia Spasticity Serum CK elevated EMG: denervation Muscle biopsy: atrophic muscle fibers MRI: no abnormality Management of ALS Supportive and palliative: - Immobilty - Altered resp function: ventilation/ suction - Dysphagia/ poor nutrition - pain: pain management - Anxiety - Meds: riluzole. Can extend life by months but not cure. Low back pain - major syndromes 1. Back strain 2. Disk herniation 3. Osteoarthritis/ disk degenration; osteophyte (bone spur) 4. Spinal stenosis: narrowing spinal foramen leading to spinal nerve entrapment Specific findings for back pain - numbness - saddle anesthesia (CA, mass) - bowel, bladder dysfunction (emergency surgery)- pain worse at rest (CA, tumor, infection) - Discitis, epidural abcess (IV drug use) - Decreased rom - Radiculopathy (pain down leg), not with OA - Crossover straight leg test: herniated disk - back, buttock, leg pain when ambulating (neurogenic claudication with spinal stenosis). Also positive straight leg raise test with spinal stenosis xr anteroposterior, to rule out scoliosis, bone spur MRI for soft tissue structure, bulging disk CT for bony imaging Transient Ischemic Attack (TIA): what, etiology Rapid onset of neurological deficit caused by focal brain, spinal cord, or retinal ischemia, resolves in 24hours. - atherosclerotic disease - cardiac emboli, from afib, mi, valvular disease - vasculitis, from lupus - hematologic causes (sickle cell, oral contraceptive) - high risk: older than 45, hx of thrombolytic event, history of spontaneous abortion, autoimmune, family hx - intracranial causes (brain tumor, seizures) - cocaine abuse - migraines TIA risk factors Important risk factor for stroke, especially in first week after Risk factors for TIA: - HTN - Cardiac disease (afib) - smoking - obesity - hyperlipidemia - elderly - DM - alcohol, recr drugs TIA symptoms Carotid artery syndrome: - hemianopia, ipsilateral blindness - visual field cut - parasteshia/ weakness of contralateral arm/ leg/ face - dysarthria, aphasia - confusion - carotid bruit Vertebrobasilar artery syndrome: - bilateral visual disturbances - vertigo and ataxia - N/V - drop attacks TIA diagnostics - Lab: CBC, incl PT, PTT/INR, electrolyres, lipid profile - CT: may reveal ischemia or infarct - MRI: more sensitive than CT. Preferred for vertebrobasilar TIA - duplex US: to identify carotid stenosis - CT angio: to evaluate neck/ brain vessels (normal renal function required) - MR angio: can assess vessels. Good replacement for CTA. - echo or holter for cardiac concern/ assessment - TEE to assess aortic arch, left atrium, patent foramen ovale - cerebral angio if candidate for carotid endarterectomy TIA management - Address underlying risk factors (HTN, DM, hyperlipid, smoking, obesity) - Carotid TIA: surgery if more than 80% occluded. No surgery if less than 50% (cand do stent then). - anticoagulation: heparin - warfarin. Though newer agents (Eloquis). PTT 1.5 - 2.5 x patient's baseline. - Antiplatelet therapy: aspirin or plavix Stroke: what, etiology Rapid onset of neurological deficit lasting longer than 24hours. Leading cause of disability. Ischemic or hemorrhagic. 80% ischemic. - HTN - Cardiac disease (afib) - smoking - obesity - hyperlipidemia (ischemic, low cholesterol hemorrhagic) - elderly - DM - alcohol, recr drugs - female on contraception and smoking Education on stroke - five "suddens" Sudden: weakness speech difficulty visual loss dizziness severe headache ischemic stroke: what, etiology Thrombus in blood vessel in head or neck Predisposing: - atherosclerosis/ hyperlipidemia - HTN - DM - hypotension - smoking - trauma - afib, endocarditis, mitral stenosis (embolism) Ischemic stroke symptoms, based on location Middle cerebral artery: - Hemiplegia (upper and face mostly), hemianesthesia, heminopia - aphasia - neglect Anterior cerebral artery: - hemiplegia (lower mostly), primitive reflexes, confusion, behavioral changes if bilateral anterior Vertebral and basilar arteries: - LOC - vertigo - dyshpagia, diplopia - ipsilateral CN findings - Contralateral sensory deficiency Deep penetrating branches of major cerebral infarction (lacunar infarction): - associated with poorly controlled HTN and DM - contralateral pure motor and sensory deficits - ipsilateral ataxia - dysarthria ischemic stroke diagnostics - CT head without contrast initially, preferable to MRI to rule out hemorrhage. Appears as area of density. - xr chest: possible cardiomegaly, neoplasm (metastasis brain suspicion) - Labs: CBC, Pt, PTT? INR, lipid profile, drug screen, alcohol level - ECG/ holter - MRI/ MRA (diffusion weighted more sensitive to detect cerebral ischemia) - CTA: vascular anatomy. Combine with CT perfusion which can show old infarct and salvageable areas. Ischemic stroke treatment - appropriate time goals - BP control: Only treat if higher than 220 syst and 120 diast., aortic dissection, or receiving t-PA. For t-PA goal goal is less than 185 syst/ 110 diast, before t-PA and less than 180 syst/ 105 diast. after. Use repeat labetolol or nicardipine drip. - Anticoagulation: IV Heparin, bridge to Warfarin (PTT 1.5-2.5 baseline). But newer meds better: Dabigatran, Apixaban (Eliquis - for stroke prevention in afib), Rivaroxaban (stroke prevention afib). No routine labs necessary for those. Not for hemorrhage, cautino after GI bleed - Antiplatelet: Aspirin or Clopidogrel - Mannitol and hypertonic saline for cerebral edema, on second on third day. Monitor serum osmolality. - Corticosteroids to reduce cerebral edema from tumor burden. - surgery for high grade extracranial carotid artery disease (greater than 70%) Time goals of stroke - ED eval within 10min - notify stroke team within 15min - CT scan within 25min - CT scan interpretation within 45min - Thrombolytic (if appropriate) within 60min - Transfer to bed within 3 hrs t-PA - Pt needs to be in 3 - 4.5 hr window - Prior CT to assess for hemorrhage - need to have "last well known" - older than 18 - ischemic stroke - neurochecks q15min for 2hrs, q30min for 6 hrs, q1h till 24hrs Contraindications: - age greater than 80 - previous hemorrhage - previous stroke within 3mo - major surgery last 14 days - Urinary/ GI hemorrhage within 24 days - seizure - PTT and PT elevated - oral anticoag/ heparin with elevated PTT/ PT - glucose less than 50/ greater than 400 - SBP greater than 185 or DBP greater than 110 - active internal bleeding last 22 days Hemorrhagic stroke; what, etiology Resulting from bleeding into subarachnoid space or brain parenchyma SAH: ruptured saccular aneurysm arteriovenous malformation ICH: HTN Predisposing: HTN anticoag/ thrombolytic cocaine alcohol hematologic disorders Symptoms SAH Sudden severe headache "thunderclap headche" or "worst headache of my life". Graded Hunt and Hess): 1: asymptomatic 2: moderate/ severe ha, stiff neck, no focal signs other than CN palsy 3: drowsy, mild focal deficit 4: stupor, hemiparesis 5: deep coma, decerebration Graded (Fisher): 1: no blood detected 2: diffuse/ vertical layers less than 1mm 3: localized clot/ vertical layer 1mm or more 4: intracerebral/ intraventricular clot with diffuse or nob SAH Symptoms ICH - HTN - ha - vomiting (especially cerebral) Basal ganglia: - eyes look to injury - decreased consciousness - contralateral hemiplegia Thalamic: - looking at nose - pinpoint pupils - coma - flaccid quadriplegia Cerebellar: - ipsilateral gaze paralysis - PERRLA - inability to stand/ walk - facial weakness - gait ataxia - vertigo - dysarthria SAH diagnostics - CT head: ischemia or hemorrhage. Sensitive in first 3 days, after that consider LP. hard to see if smaller than 3mm. - LP is strong suspicion bit negative CT. - CSF: bloody ( 103 - 106 RBC), xantochromia (yellow, breakdown of blood) - CTA, prior to clot removal ICH diagnostics - CT without contrast, to confirm bleed and determine size/ site. May reveal structural abnormalities. - Cerebral angio: determine source as aneurysm or an AVM. - MRI/ MRA: structural abnormalities - CBC, PT/ PTT, electrolytes, liver enzymes, kidney function SAH management - ABC's - may place external ventricular drain if hydrocephelus - bedrest strict - cardiac monitoring - treat ha, no NSAIDS (bleeding risk) - no straining/ exertion - stool softener - seizure prophylaxis (Phenytoine or Levetiracetam) - maintain SBP less than 160, may use nicardipine drip, labetolol push, hydralazine of brady - cerebral edema: mannitol or hypertonic saline. - surgical cliiping or coil asap - treat cerebral vasospasm - rebleeding: between day 2 - 19. Repeat CT. - cerebral salt wasting: hyponatremia. Crystalloid fluid replacement when euvolemia: 3% saline for hyponatremia - manage fever ICH management - ABC, intubate/ give O2 - Control HTN. SBP: 140 - 150. Nicardipine, labetolol - CPP: keep at 50 - 70 - pressors if SBP less than 90: Dopamine, epi, levo - maintain ICP less than 20 - mannitol for cerebral edema. For 5 days or less. check serum osmolality. Or 3% saline. - ventricular drain for hydrocephalus - keep euvolemia - seizure precautions (phenytoine, levetiracetam) - control fever - surgery if hemorrhage greater than 3cm cerebral vasospasm - cerebral vasospasms: between day 7 - 10 after aneurysm lasting till day 21 - symptoms: confusion, ams, neuro deficits, ha, increased icp. May cause infarction. - treat: calcium channel blocker: nimodipine. Symptomatic: tripe H. Hypervolemia, hypertension, hemodilution. Meningitis, what and etiology inflammation of arachnoid, dura mater, pia mater or spinal cord due to viral, bacterial, or fungal infection - predisposing: sinusitis, otitis, pneumonia, trauma, congenital malformation Bacterial meningitis Bacterial: - may be fatal in hours - exudate in subarachnoid space, thus thickened CSF and decreased flow Most commonly caused by: - streptococcus pneumoniae (infants) - neisseria meningitidis (school, college, spread of drainage/ blood) - haemophilus influenzae (daycare children - vaccine) - Escherichia coli/ emterobacter/ klebsiella (infants, elderly, immunocompromised) - Atypical: mycobacterium, listeria viral meningitis, what and etiology Pia and arachnoid space filled with lymphocytes but not with exudate. benign and self-limited. In late summer/ early fall. Transmission via cough, saliva, fecal matter Caused by: enterovirus, mumps, varicella, herpes, rubella, cmv, epstein barr, HIV Fungal meningitis, what and etiology Most common in immunocompromised Causes: candida cryptococcus histoplasma aspergillus Meningitis findings and diagnostics - severe ha - stiff neck/ nuchal rigidity - phtophobia - fever - ams - cranial nerve palsy - seizures - kernig's sign: flex at knee, then hip, and extend knee. Causes pain and spasm of hamstring muscles - brudzinski's sign: flex head and neck to chest. Causes legs to flex at hips - n/v - purpura/ petechiae on trunk and le - exaggerated deep tendon reflexes - LP - CT before LP, for ams or focal neuro signs or for CSF bacterial meningitis signs but no organism - bld culture, sputum cult, cbc, bmp - antigen tests and HIV testing LP in bacterial versus viral meningitis Bacterial: - Appearance: cloudy - Opening pressure: elevated (more than 180) - Cells: increased WBC's (100-5000, polynuclear) - Protein: increased (100-500) - Glucose: decreased (5-40) - Culture: bacteria present Viral: - Appearance: clear - Opening pressure: normal (less than 180) - Cells: increased WBC's (100-5000, mononuclear) - Protein: normal or slightly increased (less than 200) - Glucose: normal (greater than 45) - Culture: no bacteria Meningitis management AB's: - 2 -50 yrs: vancomycin plus ceftriaxone - older than 50 yrs: vancomycin, plus ampicillin, plus ceftriaxone - Meningococcal meningitis (college): penicillin or ceftriaxone if pcn allergy - H.influenzae: ampicillin or ceftriaxone - tuberculosis: isoniazid plus pyridoxine, rifampin - s. pneumoniae (infants): add dexamethasone - no hypotonic fluids - amphotericin B for fungal meningitis Cerebral abscess, what and etiology Infected space occupying lesion, from bacterial or fungal source (sinusitis, lung infection, skin infection, trauma) Cerebral abscess findings, diagnostics - ill appearing/ lethargic - signs of increased ICP (n/v, confusion/ ams) - stage 1: ha, chills, fever, confusion, speech disorder - stage 2 (expanding cerebral mass): signs and symptoms of brain tumor: ha, confusion, drowsy, stupor - Lab: increased WBC and ESR - LP (CT prior to LP): elevated opening pressure, mildly elevated protein - CT - MRI: reveals necrosis vs edema Cerebral abscess treatment - AB based on microbiology - surgery and debridement when abscess is greater than 2.5cm Encephalitis, what and etiology Acute inflammation of the brain - most commonly caused by herpes simplex virus - tick infestation - west nile virus - toxoplasmosis (AIDS pt's) - CMV - rabies