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49 Cards in this Set
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- Back
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Meningitis
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Defined as inflammation of the protective membrane surrounding the brain and spinal cord.
Multiple categories of meningitis: Aseptic (chemical, carcinomatous) Viral Bacterial Fungal Can present with a variety of symptoms, most commonly: HA and fever HA, N/V HA, fever, N/V HA, fever, N/v, photophobia HA, fever, N/V, photophobia, stiff neck |
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Meningitis signs
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Meningeal irritation:
Nuchal rigidity, kernig’s sign, brudinski’s sign Other signs: AMS-lethargy or coma Signs of increase ICP: papilledema, abducens (CN VI) Palsy, bulging fontanelle in infants, cushings reflex (HTN, bradycardia, irregular respirations) |
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Kernig’s sign
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is positive when the leg is fully bent in the hip and knee, and subsequent extension in the knee is painful
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Brudinski’s sign
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is the appearance of involuntary lifting of the legs in meningeal irritation when lifting a patient's head
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Meningitis clinical exam
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General Exam- pay close attention to signs of URI
Neurologic Exam- Check mental status, cranial nerves, assess for ICP with fundoscopic exam and by palpating the fontanelle, and check for signs of meningeal irritation. - Meningeal signs (Nuchal rigidity, Kenig’s and Brudinski’s |
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Meningitis Laboratory assessment
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CBC, Complete Chemistry, PT/PTT, bHCG (if applicable), blood and urine cultures
Determine necessity for LP (lumbar punctures is the most important procedure in diagnosing CNS infections) |
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Meningitis Radiological Assessment
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Determine need for CT-noncontrasted if no localizing signs, contrasted if mass suspected or focal deficits.
CT is rarely indicated, but often performed in the acute setting. |
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CSF studies
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obtained from the LP is sent for a variety of studies that help us further determine the etiology for a patient’s signs and symptoms.
Tube #1 – glucose and protein Tube #2 – cell count and differential Tube #3 – gram stain and routine culture, cyrptococcal antigen, AFB stain and culture, possibly bacterial antigens. Tube #4 – VDRL, or viral studies (PCR and culture) Total CSF is approximately 140mL in a normal adult. It is replenished at a rate of 0.2-0.5 mL per minute CSF glucose is normally 2/3 of serum glucose CSF protein will change based on number of cells. Important in traumatic tap. Protein increases by 1 for every 1000 rbc’s. High protein may make the CSF appear yellow, this does not always indicate blood. CSF usually contains between 0-5 mononuclear WBC’s. |
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Viral meningitis
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CSF studies often are nonrevealing. Frequently seen in children, clusters of cases have been reported.
Frequently caused by enterovirus, arbovirus or adenovirus Look for exanthem, conjunctival hemorrhage, herpangina, pleurodynia, and pericardial rub on exam. Typically occurs during the summer months Treatment is supportive care. Signs and symptoms often abate within a week. |
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Bacterial meningitis
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Variety of Etiologies based on age at time of infection
CSF Studies Reveal Low glucose (<40% serum) Elevated Protein >200 PMN’s Occasional small amount of blood. |
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Complications of meningitis in children
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Variety of Etiologies based on age at time of infection
CSF Studies Reveal - Low glucose (<40% serum) - Elevated Protein - >200 PMN’s Occasional small amount of blood. |
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encephalitis
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Defined as diffuse inflammation of the brain parenchyma, often associated with meningitis
Fairly rare diagnosis (<20K cases annually) with an approximate 10% mortality rate. |
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Clinical features of encephalitis
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Headache, malaise, myalgia as a prodrome
Progression in hour to one to two days to include - H/A, fever, nuchal rigidity, photophobia - May also have AMS (delerium, disorientation, confusion) Focal Neurologic Deficits- hemiparesis, aphasia, cranial nerve deficits, and possibly seizure. |
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Encephalitis etiologies
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Usually viral in origin (most commonly)
- HSV1 - Arboviruses (Eastern Equine, West Nile) - Enterovirus (Polio) - Less Common (CJD, measles, mumps, rubella, EBV, CMV, VZV, rabies) - Nonviral Infectious Causes (immunicompromised) - Toxoplasmosis - Asperigillosis Special Note: When bacterial infections involve the brain it is called “cerebritis” or “abscess” depending on the presence or absence of a capsule. |
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Encephalitis risk factors
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Infectious Encephalitis is rare
Risk Factors include: - AIDS (CD4 <200) - Other forms of immunosuppression (chemotherapy) - Travel to third world countries Bats and mosquito exposure in endemic areas |
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Encephalitis diagnosis
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Encephalitis diagnosis In diagnosing encephalitis you use the same approach as diagnosing meningitis with some notable exceptions.
- First stabilize the patient- treat the seizures if they are occurring - Labs: CBC, CMP, PT/PTT U/A, blood and urine cultures. - LP: CSF for cell count, protein, glucose, culture (viral, bacterial, fungal, bacterial antigens, VDRL, Viral PCR (HSV I and II), fluid for cytology (evaluates for cancer cells). - Radiology –MRI is very sensitive for diagnosing viral encephalitis on T2 sequencing. Also rules out abscess or other mass lesion. |
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Treatment of viral encephalitis
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Supportive Care
Seizure treatment if necessary - Use prophylaxis in severe cases of encephalitis Use of antiviral agents when appropriate - IV Acyclovir- used with HSV, VZV, EBV - Ganciclovir and foscarnet have been shown to be effective in treating CMV encephalitis - Ribavarin-used in LaCrosse (California Encephalitis) |
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Encephalitis outcomes
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Highly variable outcomes which are dependent on both the specific etiology and severity of the infection
Eastern Equine Encephalitis- 80% have significant neurological sequelae EBV and LaCrosse Encephalitis- only 5-15% have neurologic sequelae HSV-a small NIAID-CASG trial showed of 32 people treated with acyclovir: 26 (81%) survived 12 (46%) had no or only minor sequelae 11(42%) required continuous care |
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Brain abscess
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brain abscess is a focal, suppurative infection within the brain parenchyma which is typically surrounded by a vascular capsule
Uncommon; incidence is ~1/100K persons per year |
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Brain abscess risk factors
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Otitis Media and Mastoiditis
Paranasal Sinusitis Pyogenic infections in the chest or other body sites Penetrating Head Trauma Neurosurgical Procedures Dental Infections |
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Brain abscess etiologies
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Otitis and Mastoiditis
- Cause up to 33% of abscesses - Predilection for temporal lobe and cerebellum. - Common Organisms are Streptococci, Bacteroides, and Pseudomonas. Paranasal Sinusitis - Causes frontal lobe abscesses - Same organisms as otitis but also Staph auereus and Haemophillus Hematogenous Spread Account for 25% of all brain abscesses |
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Clinical presentation of a brain abscess
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Clinical symptoms are highly variable depending on location and size of the lesion.
Less than 50% of cases have the classic triad headache, fever, and focal neurologic deficits. Most common symptom is headache (75%) Focal deficits (ie. aphasia, hemiparesis, or visual field cuts) are noted in ~60% Seizure occurs in 15-35% of patients Most patients don’t present to the hospital until 11-12 days after initial symptom onset. |
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Treatment of brain abscess
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Treatment is two pronged approach coupling high dose empiric antibiotics and neurosurgical drainage.
Antibiotics for “community acquired” abscess in immunocompetent host begins with a third generation cephalosporin and metronidazole - For post neurosurgical procedure abscess, use ceftazidime and vancomycin (covers Staph and Pseudomonas) Drainage is achieved via a sterotaxic guidance. Therapy is modified based on gram stain and culture results. Glucorticoids should NOT be given unless there is significant periabscess edema |
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Subdural empyema
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Subdural abscesses are quite rare.
They are related to extension of a sinus infection or rarely meningitis. These cases are a neurosurgical emergency and requires burr hole or craniotomy for drainage. Treat with cefotaxime and metronidazole until the culture returns. |
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Epidural emypema
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Suppurative infection which occurs in the potential space between the inner skull and the dura.
Also very rare (<2% of all intracranial infections) Usually develop as complication of craniotomy or compound skull fracture. Can be related to spread of infection from mastoiditis, sinusitis, or otitis media. Clinical presentation is often fever, H/A, nuchal rigidity. Wound will likely look infected. Treat with emergent drainage and IV vancomycin and metronidazole. |
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Opportunistic CNS infections
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variety of opportunistic infections that have been described in AID’s patients. Below are the most common:
Cryptococcus Toxoplasmosis CMV Progressive Multifocal Leukoencephalopathy (PML) |
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Cryptococcus
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Cryptococcus neoformans is the leading cause of infectious meningitis in patients with AIDS
- Occurs in 20% of AIDS cases in Africa C. neoformans is a fungus found in soil contaminated with pigeon feces. Infection is acquired through inhalation and is hematogenously spread to the meninges and brain. H/A and fever are the hallmark. Meningeal signs are mild Other signs are AMS, CN dysfunction, papilledema. Diagnosis is made by CSF analysis with india ink and testing for the capsular antigen. Treat with Amphotericin B followed by fluconazole. |
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toxoplasmosis
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Toxoplasmosis is often a late complication of HIV with CD4 counts <200/uL
Thought to be a “reactivation syndrome” Presents as fever, headache, and focal neurologic deficit or seizure. Diagnosis is made based on MRI. Treat with sulfadiazine and pyrimethamine with leucovorin for 4-6 weeks. If you have a positive IgG for toxoplama at the time of diagnosis of HIV you should be given prophylaxis when CD4 counts are less than 100/uL. - Prophylaxis is TMP/SMX daily until CD4 is greater than 200/uL Has a predilection for affecting the basal ganglia |
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cytomegalovirus
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Cytomegalovirus cause retinitis, encephalitis, myelitis, and polyradiculopathy in patients with AIDS.
Tends to only affect individuals when CD4 counts are <50/uL Causes gait disturbance, parastehsias, areflexia, ascending sensory loss, and urinary retintion when it affects the lumbar and sacral spinal cord. Clinical course is rapidly progressive. Treatment is with gancivlovir which can lead to quick recovery. |
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neurocysticercosis
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Most common parasitic CNS disease
Aquired through ingestion of T. solium eggs in undercooked pork. Often presents as seizure or focal deficit. Diagnosed using MRI or CT. Treatment - Seizure treatment. No prophylaxis until after first spell Abendazole (anti-helminthic treatment) is controversial |
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Assist control Ventilatory support
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Rate: set
Tidal Volume: set PIP: variable PEEP: set FiO2: set Simplified: the machine gives the patient a breath every (x) seconds,the rate at which you set, regardless of the pressure it takes to force the breath in. Concern: patient fights vent and barotrauma from high pressures. |
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Pressure support ventilation
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Rate: variable
Tidal Volume: variable PIP: set PEEP: set FiO2: set Simplified: the machine gives the patient a breath every time he/she initiates one and will push that breath in with the amount of pressure you have set regardless of what volume of air that results in. Concerns: lack of spontaneous breathing and lack of appropriate volume given to patient with resistant airways. |
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Increased intracranial Pressure
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The brain is a “closed box.”
Anything that causes a mass lesion can cause - stroke, bleed, tumor, trauma, hydrocephalus Symptoms: Headache, AMS, Nausea/vomititing (often projectile) Signs: Papilledema -disruption of axonal transport and venous return ( may not be present until several days after increased ICP develops Diplopia: downward traction on CN VI Cushing’s triad |
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Cushing’s Triad
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Hypertension: possibly to overcome ICP to provide CPP
Irregular Respiration: Cheyne-Stokes but can be any form Bradycardia: possibly in reaction to HTN |
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Herniation syndromes
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Subfalcine herniation
B: Uncal transtenstorial herniation C: Central herniation D: External herniation E: Tonsillar herniation |
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Transtentorial herniation
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Herniation of medial temporal lobe
Often called “uncal herniation” when uncus involved Uncus slips inferiorly through tentorial notch Recognized clinical triad of: – Blown pupil – Hemiplegia Coma |
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Uncal Herniation triad
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“Blown pupil”: CN III is leaves the midbrain directly under the tentorium. The parasympathetic fibers travel superficial in this nerve and are susceptible to compression.
- (85% of time it is the ipsilateral pupil that is involved) Hemiplegia: compression of cerebral peduncles - Most times is contralateral to herniation ( why is this?) - Hint: where does the cotical spinal tract decusate? Coma: Damage to reticular activating system |
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Central herniation
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Often with hydrocephalus or diffuse edema
Causes traction on abducens nerve against clivus causing lateral rectus palsy |
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Tonsillar Herniation
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The cerebellar tonsils slip through the foramen magnum
Compression of medulla results Causes respiratory arrest, BP instability, and death |
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Stroke patient in the ICU
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Blood pressure management
– Hypertension vs. Hypotension Hyperglycemia Hyperthermia Respiratory support DVT prophylaxis Anti-platelet therapy |
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Ischemic stroke blood pressure management
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the brain plays a role in setting the BP normally. If the BP goes up after a stroke then it must need that blood pressure to maintain perfusion past the stenosis. Dropping it acutely might causes the stroke to enlarge.
many stroke patient’s are hypertensive at a baseline and their curve may be shifted to the right! Hypotension can take place as well but is less common. Remember the cerebral perfusion curve is still in play and now the brain is trying to drive perfusion past a stenosis. You must consider an MI if this occurs as ischemic heart disease is extremely common with stroke. Fluid resuscitation needs to occur; however, do not use more dilute fluid than normal saline as you want to avoid cerebral edema. - Remember that the peak swelling after a stroke is between 48-72 hours. Pressors may be used if necessary. |
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Intervention of BP control in ischemic stroke
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mixed data on this but current recommendations are:
- Intervene if two consecutive BP’s 5 minutes apart are SBP >220 or MAP >130 - If tPA was given then maintain BP <185/110 - Agents ( some conflicting reports) 1st choice: Labetalol IV (NINDS trial) & American Stroke Association 2nd choice: Nitroprusside IV (NINDS trial) 2nd choice: Nicardipine IV (American Stroke Association) 3rd choice: Nitroglycerin: only if tPA not used The truth is, Nicardipine and Nitroclycerin can cause increased ICP 2/2 vasodilatation. Beta blockers avoid this and are therefore a good choice. Plus they can be titrated easily. Cardene (Nicardipine) can as well but the IV site has to be changed often. |
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Hyperthermia in stroke pt
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Hyperthermia can be detrimental to acute ischemic stroke patients.
Mechanism: increase in neurotransmitters, damaging ischemic depolarization, and impaired energy metabolism Patients with fevers need immediate anti-pyretics and cooling blankets. Hypothermia may be an acute treatment in the future just as it has proved itself in MI patients. |
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Nutrition in post stroke patients
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Dysphagia is common in post-stroke patients. It is common to place an “NPO” order when they are admitted
However!!! - in the first week after a stroke the patient enters a hyper-metabolic state with increased catabolism of protein and fat. Many studies have showed that we malnourish stroke patients by doing this. Feed or Ordinary Food trial (large multi-centered study): showed initiation of tube feeds within the first 7 days after stroke showed a 5.8% absolute reduction in case fatality compared with those where it was started after 7 days. |
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Blood pressure control in Hemorrhagic strokes
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BP naturally elevates after ICH and will decline over 7 days with most drastic decline in 1st 24 hours
Keep SBP <180 and MAP 1130. Some say 160/90 might be a reasonable goal Agent Labetalol, Nicardipine, Esmolol, Enalapril, Hydralazine, Sodium nitroprusside ( consider infusion vs. intermittant administration) |
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Hemorrhagic strokes and coagulation
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Anti-coagulants
- Often these are being taken by the patient - Immediate reversal of INR is necessary - Vitamin K: takes 6 hours to work and has to be infused slowly - Fresh Frozen plasma: has to be crossed and thawed but corrects INR quickly. - Drawback: patient receives a lot of volume - Prothrombin complex concentrate (PCC) - Low volume, no thawing, no compatibility issues and contains factors II, VII, IX, and X Not proven in studies to have improvement in clinical outcome |
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Hemorrhagic stroke in an antiepileptic
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30 day seizure incidence: 8.1% Rate varies by location: cortical more likely than deep ICH Over 1/2 of seizures in studies were sub-clinical Often Keppra, Dilantin, or BDZ used (ggt) |
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Hemorrhagic stroke DVT prophylaxis
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Increased risk due to immobilization
Risk is somewhere between 1.9 -16% in 10 days Intermittant compression devices are the standard Heparin 5000U TID started on day 2 after ICH has been shown to be safe For patients that do develop a DVT or PE with an ICH -consider an IVC filter (although not great literature to support that these are efficacious) |
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Acute medical management of increased ICP
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Step 1: Determine the cause
- Ex: SAH: you should suspect hydrocephalus from impaired CSF absorption and a ventricular drain is the treatment - Ex: Stroke: cytotoxic edema is to blame and a drain is useless - Ex: Tumor: steroids may decrease the inflammation and therefore the mass effect Step 2: Raise head of bed >30 degrees - Non-invasive and little to no side effects Step 3: Consider ventriculostomy: goal is to maintain ICP <20 and CPP >70 Step 4: Osmotherapy - Mannitol Q4 hours to maintain sOSM <320 - Hypertonic saline - Problems: temporary 24-48 hours and then fluid shifts begin reversing Step 5: Steroids? - Indicated in vasogenic edema from tumors or abscess - No indication in head trauma, ischemic, nor hemorrhagic stroke Step 6: Sedation and possibly paralytic - Morphine, Propafol, Versed Step 7: Hyperventilation: goal of PCO2 of 25-30 - Mech: decreased PaCO2 causes cerebral vasoconstriction decreasing amount of blood volume lowering ICP Problem: not dramatic results, temporizing as cerebral interstitium buffers after several hours, often get a rebound increased ICP when stop hyperventilation Other: other modalities are out there but have less evidence Pentobarbital coma Hypothermia: not great evidence but theoretically may limit damage by decreasing toxic metabolites Hemi-craniectomy |
