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Clinical Medicine 4 > Lecture 8 (neuro)- Exam 3 > Flashcards

Lecture 8 (neuro)- Exam 3 Flashcards

1
Q

Syncope
* What is Syncope?

A
  • Syncope is a clinical syndrome in which transient loss of consciousness is caused by a period of inadequate cerebral blood flow, most often the result of an abrupt drop of systemic blood pressure.
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2
Q

Syncope:
* Typically, the inadequate cerebral blow flow is what?
* High-risk features includew what? (3)
* What is the most important component of the evaluation to identify the cause of syncope?

A
  • Typically, the inadequate cerebral blow flow is of relatively brief duration (8 to 10 seconds).
  • High-risk features include history of structural heart disease, abnormal ECG, and age older than 60.
  • History is the most important
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3
Q

What are the clinical features of syncope? (6) What do you need rule out? (2)

A
  • Dizziness or lightheadedness
  • Sweating
  • Palpitations
  • Nausea
  • Visual blurring or diminished vision (blackout)
  • At times patient may have no warning symptoms
  • Always rule out acute myocardial infarction if patient is supine or sitting when developing syncope
  • Rule-out hypoglycemia in diabetics
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4
Q

Syncope – Diagnostics
* Why an EKG and labs?

A
  • ECG: rule out cardiogenic causes (specifically arrhythmias), although they may be transient
  • Laboratory: volume loss, renal insufficiency, BNP, troponins
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5
Q

Syncope – Diagnostics
* What are the neurologic studies? (3)

A
  • CT or MR if suspicious for TIA or stroke, or with new onset seizure
  • EEG for seizure as well
  • Carotid Ultrasound with CAD risk factors
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6
Q

Syncope
* If all the diagnostic tests are negative, could it be somatoform disorder?

A

Somatic symptom disorder is characterized by extreme focus on physical symptoms, such as pain or fatigue, that causes major emotional distress and problems functioning.
* pain, fatigue, emotional distress that are the cause of the symptoms

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7
Q

Syncope – Orthostatic Hypotension
* What is orthostatic hypotension? What are the two types?

A

Orthostatic (postural) hypotension, defined as a decrease in systolic blood pressure of at least 20 mmHg, upon assuming upright posture, most often occurring following movement from lying or sitting to a standing position.
* Classic – within 3 minutes of standing
* Delayed – 3 minutes after standing

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8
Q

Syncope – Orthostatic Hypotension
* MCC is due to what? What drink can affect?

A

Most common cause is due to decreased intravascular volume, as may occur with inadequate fluid intake or the result of diuretics
* Alcohol consumption which impairs vasoconstriction is also a cause

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9
Q

Syncope – Orthostatic Hypotension
* What may increase but not a dx factor?
* Delayed type may take a minute to cause what?

A
  • HR may increase 10-25 beats but is not a diagnostic factor.
  • Delayed type may take a minute to cause syncope after standing (higher risk of injury due to inability to protect self), prevalent in elderly.
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10
Q

Cardiogenic Syncope
* Cardiac arrhythmias may cause what? What are examples?

A

Cardiac arrhythmias may cause syncope or near-syncope if the heart rate is either too slow or too fast to permit maintenance of an adequate cardiac output and systemic arterial pressure
* AV blocks, cardiac pauses

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11
Q

Cardiogenic Syncope
* What are the stuctural issues?

A

Structural cardiopulmonary disease
* Valvular disease or Hypertrophic cardiomyopathy

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12
Q

What are the different arrhythmias that can cause syncope? (4)

A
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13
Q

Syncope-Reflex syncope ⭐️
* what is the cause?
* Other names?
* Occurs in patients without what?
* What is emotional vasovagal syncope?

A

Reflex Syncope (neural reflexes affecting HR and BP inappropriately)
* Vasovagal syncope (also known as the “common” or “innocent” faint)
* occurs in patients without apparent cardiac or neurologic disease.
* emotional vasovagal syncope: secondary to fear, pain, hyperventilation, medical procedure, or even yawning.

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14
Q

Syncope – Other Etiologies
* Situational syncope triggered by what?

A

by series of contractions of the urinary bladder, defecation, swallowing, or coughing (vagal stimulation is frequently responsible)

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15
Q

Syncope – Other Associations
* What is POTS?
* What is postprandial hypotension? What can reproduce sxs?

A

POTS – postural orthostatic tachycardia syndrome – excessive increase in heart rate when transitioning from lying to standing, without significant change in blood pressure. Can also occurred during extending periods of standing.

Postprandial hypotension – usually in patients >65yo within 75 mins of having a meal – digestive processes require a large amount of blood to stomach – diverts blood
* Tilt table test can reproduce symptoms

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16
Q

Syncope
* What is the txt for POTS and postprandial hypotension?

A
  • IV fluids if dehydrated
  • Corticosteroids for POTS, helps by increasing blood volume and enhancing vascular tone by increasing volume of blood
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17
Q

General Characteristics - Stroke
* Neurological deficit of sudden onset attributable to what?
* Ischemic stroke caused by what?
* Hemorrhagic stroke associated with what?

A
  • Neurological deficit of sudden onset attributable to the loss of perfusion to a portion of the brain from vascular occlusion or hemorrhage.
  • Ischemic stroke – caused by vascular insufficiency
  • Hemorrhagic stroke – associated with a mass effect from the blood clot impinging on the brain tissue
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18
Q

General Characteristics - Stroke
* What are the major risk factors? (5)
* What is the most significant and treatable risk factors?

A
  • Major risk factors include hypertension, elevated cholesterol levels, diabetes, oral contraceptives, cigarette smoking as well.
  • Hypertension is the most significant and treatable risk factor.
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19
Q

Clinical Features - Stroke
* Sxs begin how?
* What is usually revealed on history and physical exam?
* One can localize the lesion how?

A
  • Signs and symptoms of stroke begin abruptly, and they correlate with the area of the brain that is supplied by the affected vessel.
  • Hemiparesis or hemisensory deficit is usually revealed on history and physical exam.
  • One can localize the lesion to one side, contralateral to these deficits.
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20
Q

Clinical Features - Stroke ⭐️
* Strokes involving the middle cerebral artery will demonstrate what?
* May demonstrate what?

A
  • Strokes involving the middle cerebral artery will demonstrate either aphasia or neglect, depending on whether the infarction affects the dominant or non-dominant hemisphere.
  • May demonstrate contralateral paresis and sensory loss in the face or upper extremity, gaze preference toward the ipsilateral side, and homonymous hemianopsia.
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21
Q

Clinical Features - Stroke ⭐️
* Strokes involving the anterior cerebral artery will present with what? (3)

A
  • Strokes involving the anterior cerebral artery will present with contralateral paresis and sensory loss within the lower extremity.
  • Also, may be weakness or paresthesia’s of the contralateral upper extremity and face.
  • Changes in cognition and/or personality can occur.
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22
Q

Clinical Features - Stroke ⭐️
* Strokes involving the basilar artery infarction may present quite dramatically with what? (2)

A
  • Strokes involving the basilar artery infarction may present quite dramatically with clinical entities like coma, “locked-in” syndrome, cranial nerve palsies, apnea, visual symptoms, dysphagia and dysarthria.
  • Crossed weakness/sensory loss affecting the ipsilateral face and contralateral body.
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23
Q

Thrombotic strokes
* Often preceded by what?
* Where do the blood clots form?
* Accounts for how many strokes?

A

Thrombotic strokes are often preceded by transient ischemic attacks (TIAs)
* blood clot that forms in the arteries supplying blood to the brain
* account for 87% of all strokes

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24
Q

Embolic strokes
* Can occur how?
* What happens with the blood clot?

A

Embolic strokes occur abruptly and without warning
* blood clot from elsewhere in the body travels to the brain and blocks blood flow

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25
Q

Hemorrhagic strokes
* What is the presentation due to?

A

Hemorrhagic strokes are less predictable – presentation is variable due to complications of blood dispersion, cerebral edema, and increased ICP.
* account for 23% of all strokes

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26
Q
A
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27
Q

Stroke Management Timeline ⭐️
* What do you need to do before 45 mins has passed?

A
  • 10 minutes from arrival or sooner: Evaluation by physician
  • ≤ 20 minutes: Stroke or neurologic expertise contacted with pre-notification from EMS or upon arrival POV
  • ≤ 20 minutes: Non contrast CT
  • ≤ 45 minutes or sooner: Interpretation of the non contrast CT scan
  • ≤ 45 minutes - Initiation of thrombolytic therapy
    * up to 24hrs is allowed for intra-arterial fibrinolysis by IR from last known well, symptom onset unknown, or wake up stroke based on advanced imaging
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28
Q

Stroke Management Timeline ⭐️
* When can thrombolytic therapy be given up to 24 hours

A

up to 24hrs is allowed for intra-arterial fibrinolysis by IR from last known well, symptom onset unknown, or wake up stroke based on advanced imaging

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29
Q

Stroke Management Timeline⭐️
* What needs to happen from 90 minutes to 3 hours?
* All can be achieved with the use of what?

A
  • ≤ 90 minutes – door to puncture time for endovascular intervention
  • 120 minutes – Door to revascularization procedure
  • 3 hours – Admission to stroke unit or ICU
  • All can be achieved with use of Telemedicine
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30
Q

sorry it is a lot but no way to break it up

Acute Ischemic Stroke Checklist for 1st Hour ⭐️
* What needs to be done within an hour?(9)

A
  • Vital signs
  • Supplemental oxygen to maintain saturation ≥ 94%
  • Determine time of onset/last known well (LKW)
  • Determine NIHSS score
  • CT, CTA with perfusion (0-24 hours of LKW) or MRI (4.5 – 9 hours of LKW and ineligible for thrombectomy)
  • Medication list – ask specifically about anticoagulants and when medication was last taken/administered
  • IV access – 18g peripheral IV
  • Labs: Fingerstick glucose, CBC with platelets, PT/INR, PTT, and beta-HCG for women of childbearing age.
  • EKG
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31
Q

Stroke: Diagnosis
* Immediately on arrival to an ED, patients should be screened for what? Needs to be taken directly to what?
* If the non-contrast head CT is negative for hemorrhage, what needs to be considered?

A
  • Immediately on arrival to an ED, patients should be screened for stability, undergo rapid clinical stroke assessment, then taken directly for rapid imaging with a non contrast CT scan of the head.
  • If the non-contrast head CT is negative for hemorrhage, an acute ischemic stroke or TIA must be considered for acute onset of neurological symptoms.
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32
Q

Stroke: Diagnosis
* There are several stroke mimics including what?
* Goal is to rule out stroke mimics when?

A
  • There are several stroke mimics including seizures, hypoglycemia, sepsis, fever, migraine and Bell’s palsy.
  • Goal is to rule out stroke mimics as soon as possible but given that acute ischemic stroke treatment is time sensitive, it is not uncommon for them to be treated with thrombolysis.
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33
Q

Time of Symptom Onset: stroke
* Most important information that guides therapy is what?
* All patients with LKW time less than 24 hours should be what?
* What must be established from either the patient or a bystander?

A
  • Most important information that guides therapy is the last known well (LKW) time or time of symptom onset.
  • All patients with LKW time less than 24 hours should be emergently evaluated for an acute ischemic stroke.
  • Last time they were known to be normal without neurological deficits must be established from either the patient or a bystander.
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34
Q

Time of Symptom Onset: Stroke
* If the patient went to bed and awoke with the stroke symptoms, the last known normal time is what? ⭐️
* Thrombolytics should be administered to all patients with LKW time less than what?

A
  • If the patient went to bed and awoke with the stroke symptoms, the last known normal time is when they went to bed.
  • Thrombolytics should be administered to all patients with LKW time less than 4.5 hours that meet the inclusion and exclusion criteria and should be considered for all patients who present between 4.5 to 9 hours, of which they could be wake up strokes.
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35
Q

Vital Signs: Stroke
* Pulse oximetry should guide what?
* What is vital and must be obtained frequently?
* What is uncommon? Why?

A
  • Pulse oximetry should guide whether the patient needs supplemental oxygen to achieve oxygen saturation of 94%
  • Blood pressure measurements are vital and must be obtained frequently.
  • Hypotension is uncommon – may be due to symptoms of previous stroke due to poor perfusion of previously injured tissue.
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36
Q

Vital signs: Stroke
* When does BP need to be lowered?
* What is permissive hypertension?

A

Blood pressure in excess of 220/120 mmHg should be lowered, regardless of the ultimate diagnosis.

Permissive hypertension
* allowing the blood pressure to rise naturally to 220/120 mmHg for those not a candidate for thrombolysis
* this has been suggested as a method to maintain cerebral perfusion

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37
Q

Vital Signs: Stroke
* Target blood pressure for patients eligible for IV alteplase is what?
* Once it is given, BP must be maintained below what?

A
  • Target blood pressure for patients eligible for IV alteplase is less than 185/110 mmHg.
  • Once it is given, BP must be maintained below 180/105 mmHg for 24 hours after administration to limit risk of ICH.
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38
Q

Vital Signs: Stroke
* What are options for BP management? (3)
*

A

Short acting agents such as labetalol, nicardipine or hydralazine are preferred to achieve and MAINTAIN BP less than 180/105 mmHg and are OPTIONS to be considered.
* There is variability in the specific agent used for BP lowering.

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39
Q

BP management in strokes ⭐️
* What has no benefit?
* What is reasonable if BP is over 220/120?

A
  • If BP is < 220/120 mm Hg, treatment of HTN within the first 48 to 72 hours after acute ischemic stroke (AIS) is of no benefit.
  • If BP is 220/120 mm Hg or higher, the benefit of lowering BP is unknown, but lowering by 15% in the first 48 to 72 hours after AIS is reasonable. (hypotension= worsen strokes)
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40
Q

Blood Pressure Management in Strokes⭐️
* If mechanical thrombectomy: It is reasonable to maintain BP how?

A

If mechanical thrombectomy: It is reasonable to maintain BP below 185/110 mm Hg during and for 24 hours after the procedure.

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41
Q

Labs: Stroke
* What do you need to get for acute ischemic stroke?
* What can be done to quickly r/o hypoglycemia?

A
  • Complete CBC for acute ischemic stroke includes capillary blood glucose, CBC with platelets, chemistries, PT/PTT, INR as well as beta-HCG for women of childbearing age.
  • A fingerstick glucose check is a requirement as it can quickly rule out hypoglycemia as a stroke mimic.
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42
Q

Labs: Stroke
* What about tests for anticoagulants?
* What is important?

A
  • What about tests for anticoagulants like direct thrombin inhibitors or direct factor Xa inhibitors – many hospitals do not have these laboratory tests/results available quickly within the thrombolysis window.
  • History is important – compliant with medications, last time dose taken.
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43
Q

Diagnostic Imaging: Stroke
* Non contrast CT of the brain should always be obtained before what? Why?
* Non-invasive CT angiogram of the head and neck should be obtained as well to expedite what?

A
  • Non contrast CT of the brain should always be obtained before thrombolytic therapy administration – if ruptured aneurysm is the cause, then bleeding will be worse.
  • Non-invasive CT angiogram of the head and neck should be obtained as well to expedite the identification of a large vessel occlusion.
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44
Q

Diagnostic Imaging: Stroke
* CTA?
* What is not routinely done?

A
  • CT angiogram will also identify any perfusion deficits that may be caused by the LVO.
  • A chest x-ray is not routinely done in the acute workup phase.
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45
Q

Activate the Stroke Team
* Acute stroke team should evaluate the patient when?
* Consist of what?
* They can help to expedite what?

A
  • Acute stroke team should evaluate the patient within minutes of the patient entering the hospital.
  • Consist of members specifically trained in recognition and acute management of acute ischemic stroke.
  • They can help to expedite patient assessment on arrival and in CT, thereby decreasing time to determine thrombolytic therapy.
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46
Q

NIHSS
* What is it
* What are the ranges?
* NIHSS score may also be used as a guideline to predict what?

A
  • The National Institutes of Health Stroke Scale (NIHSS) is the preferred stroke severity rating scale recommended as a standardized method for examiners to evaluate severity of strokes.
  • Scores range from 0 (no deficit) to 42, severe stroke.
  • NIHSS score may also be used as a guideline to predict a relative risk of ICH after thrombolytics are given.
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47
Q

Fill this in and when do you give TPA?

A

Over 5, you can give TPA

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48
Q

Management of strokes: IV fluids
* What needs to to be corrected and why?

A
  • Hypovolemia should be corrected as in acute ischemic stroke can worsen ischemic injury because of impaired perfusion to the brain tissue.
  • Hypovolemia may exacerbate ischemic brain edema and increase stress on the heart.
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49
Q

Management of strokes: IV fluids
* What is desired? What are the fluids?
* What should be avoided?

A
  • Euvolemia is desired and IV fluids should be normal saline.
  • Hypotonic and dextrose containing fluids should be avoided.
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50
Q

Management of strokes: LKW is less than 3 hours
* What is the medication?
* What needs ot be assessed?
* If still significant stroke-like symptoms without contraindications, what needs to be given?

A
  • Alteplase is a thrombolytic medication and is only approved for treatment of acute stroke in the US.
  • When patients presents less than 4.5 hours since their LKW time, then eligibility for IV thrombolytic therapy should be assessed.
  • If still significant stroke-like symptoms without contraindications, treatment with thrombolytics should proceed.
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51
Q

Management of strokes: LKW is less than 4.5 hours
* What is the issue with IV thrombolysis?
* Additional inclusions to consider if you give thrombolytics in this time frame include what?

A
  • In the US, FDA has not approved thrombolytic use between 3-4.5 hours.
  • However, its use in this timeframe has been endorsed by the AHA and is widely used in the US.
  • Additional inclusions to consider if you give thrombolytics in this time frame include meeting all the criteria if under 3 hours since onset and if they are taking Warfarin, INR is less than 7.
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52
Q

Stroke Management - Thrombolytic Therapy
* What is the eligibility criteria?(3)
* When is it avoided?

A

Eligibility
* Ischemic stroke symptoms causing measurable neurological deficits. These range from mild to disabling to serve stroke symptoms.
* Onset less than 3-4.5 hours from start of symptoms.
* Patient is greater than 18 years of age.

Generally, is avoided with NIHSS of ≤5

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53
Q

Stroke Management - Thrombolytic Therapy exclusion criteria ⭐️
* LKW time greater than what?
* Hx of what?
* Sxs of what?
* What type of malignancy or bleeds within when?

A
  • Time from last known well is greater than 4.5.
  • History of intracerebral hemorrhage or intracranial neoplasm.
  • Signs and symptoms suggestive of subarachnoid hemorrhage, ineffective endocarditis or aortic arch dissection.
  • GI malignancy or recent bleeding within 21 days.
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54
Q

Stroke Management - Thrombolytic Therapy exclusion criteria ⭐️
* Taking what types of meds?
* Platelets than than what?
* Currently taking full treatment dose of what?

A
  • Taking direct thrombin inhibitors or direct factor Xa inhibitors unless a PTT, INR, platelet count are normal or unless they have not taken the dose within last 48 hours.
  • Platelets less than 100K
  • Currently taking full treatment dose of low molecular weight heparin within previous 24 hours.
55
Q

Stroke Management - Thrombolytic Therapy exclusion criteria ⭐️
* if the CT should what?

A

CT shows severe hypoattenuation, hypodensity or intracerebral hemorrhage
* Platelets less than 100
* Internal hemorrhage within the past three weeks.

56
Q

Patient is an IV Thrombolysis Candidate
* Once deemed a candidate for treatment, what needs to be placed?
* Accurate what?
* Initial 10% of total alteplase dose is given by what?

A
  • Once deemed a candidate for treatment, minimum of two IVs must be placed.
  • Accurate weight dosing since Alteplase is a weight-based drug.
  • Initial 10% of total alteplase dose is given by bolus over 1 minute, rest is infused over an hour.
57
Q

Patient is an IV Thrombolysis Candidate
* Continued observation for complications of thrombolytics including what?
* Blood pressure checked when?

A
  • Continued observation for complications of thrombolytics including airway obstruction due to angioedema, hemorrhage, and sudden change in GCS.
  • Blood pressure check should occur every 15 minutes for the first 2 hours, then every 30 minutes for the next 6 hours, then hourly over 16 hours.
58
Q

Management of Hemorrhage Following Alteplase
* Hemorrhagic conversion often occurs following reperfusion therapy, why?
* What may indicate ICH?
* 50% mortality rate if what?
* Treatment consists of what?

A
  • Hemorrhagic conversion often occurs following reperfusion therapy, believed to occur because of the disruption of blood-brain barrier integrity.
  • Acute onset of headache, nausea, vomiting, worsening neurological examination during or following administration of thrombolytics may indicate ICH.
  • 50% mortality rate if bleed occurs after administration.
  • Treatment consists of stopping infusion if still ongoing.
59
Q

Management of Hemorrhage Following Alteplase
* Obtain what labs?
* What dx imaging needs to be done?
* Vital signs when?
* Consider what based on fibrinogen levels?

A
  • Obtain CBC, PT, PTT, INR, fibrinogen levels, type and cross-match.
  • Obtain non contrast CT scan of the head.
  • Vital signs every 15 minutes.
  • Consider Cryoprecipitate and fresh frozen plasma based on fibrinogen levels- - also transaxemic acid administr
60
Q

LKW between 0-6 hours: Endovascular Treatment
* What is mechanical thrombectomy?
* Intraarterial thrombolysis can occur when?

A
  • Mechanical thrombectomy by way of an Interventional Radiologist to retrieve a clot that has created a large vessel occlusion.
  • Intraarterial thrombolysis can occur up to 24 hours from last know well, symptom onset, or wake up stroke based on advanced imaging.
61
Q

LKW between 0-6 hours: Endovascular Treatment
* Endovascular therapy with stent retrievers is recommended over what?
* What is more effective?

A

Endovascular therapy with stent retrievers is recommended over intraarterial fibrinolysis as first-line therapy
* to be able to remove the clot all together instead of waiting for the chemical to break down the clot causing the large vessel occlusion is more effective.

62
Q

Stroke Management - General
* When should asipirin be given?
* Strokes associated with intracranial atherosclerosis, use what?
* An MRI is usually obtained when?

A
  • Aspirin to be administered within 24hrs for those that did NOT qualify for thrombolytic therapy medications, or 24hrs after they received it.
  • Strokes associated with intracranial atherosclerosis, use of high-intensity statin such as atorvastatin therapy for secondary stroke prevention is associated with a reduced long-term risk of ischemic stroke.
  • An MRI is usually obtained after admission and the initial stroke is treated to evaluate extent of damage from perfusion deficits.
63
Q

Stroke Management - Surgical Decompression from Cerebral Edema
* What is the selection criteria?
* When is decompressive craniectomy reasonable?

A
  • Although the optimal trigger for decompressive craniectomy is unknown, it is reasonable to use a decrease in level of consciousness attributed to brain swelling as selection criteria.
  • In patients ≤60 years of age who deteriorate neurologically (decrease GCS) within 48 hours from brain swelling, decompressive craniectomy is reasonable

Can give them a lot of Na to decrease edema

64
Q

Transient ischemic attack
* Transient episode of neurological dysfunction caused by what? What can that lead to?

A

Transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischemia without acute infarction, can lead to:
* transient monocular blindness (Amaurosis Fugax)
* Amaurosis fugax is typically caused by a transient ischemic event in the retina or optic nerve, often due to emboli from carotid artery disease or cardiac sources.
* vertebral basilar syndromes (Dizziness/Vertigo)

65
Q

Transient Ischemic Attack
* Frequently referred to as ?
* Lasts how long?
* What are the additional testing?
* Treat with what if due to a fib?

A
  • Frequently referred to by patients as a mini-stroke.
  • Lasts from minutes up to 24hrs
  • Additional diagnostic testing includes carotid ultrasound for high grade stenosis, EKG for arrythmias, TEE for possible clot present.
  • Treat with ASA/Plavix or Warfarin or Eliquis if due to atrial fibrillation.
66
Q

Carotid Stenosis - Management ⭐️
* Initial testing as part of TIA or ischemic stroke workup could have identified what?
* What are the Occlusive carotid stenosis treatment options? (2)

A

Initial testing as part of TIA or ischemic stroke workup could have identified various levels of carotid stenosis.

Occlusive carotid stenosis treatment options
* carotid endarterectomy vs carotid angioplasty and stent
* carotid stenting is as effective in preventing recurrent stroke as endarterectomy.

67
Q

Carotid Stenosis - Management ⭐️
* Symptomatic carotid stenosis 50-69% if onset of symptoms <2 weeks can be treated with what?
* Asymptomatic carotid stenosis between 60-80% can also be treated with what?
* Carotid stent placement can be conducted for who?

A
  • Symptomatic carotid stenosis 50-69% if onset of symptoms <2 weeks can be treated with stent placement or endarterectomy.
  • Asymptomatic carotid stenosis between 60-80% can also be treated with a high intensity statin, aspirin.
  • Carotid stent placement can be conducted for asymptomatic carotid stenosis >70%
68
Q

Improving Stroke Risk Factor Management – Secondary Stroke prevention ⭐️
* What should happen to the BP?
* What should happen to the lipid levels?

A

Hypertension – secondary stroke prevention guidelines endorse maintaining a blood pressure of < 130/80 mmHg as a target for patients with a stroke or transient ischemic attack.

Hyperlipidemia – benefit of targeting LDL with a goal of < 70 mg/dL in patients with atherosclerosis with a high intensity statin.
* Fasting lipid profile

69
Q

Improving Stroke Risk Factor Management – Secondary Stroke prevention⭐️
* What needs to happen with the Diabetes?
* What needs to happen with the CV disease?
* what needs to happen for stroke prevention?

A
  • Diabetes – guidelines recommend a goal of hemoglobin A1c less than or equal to 7% for most patients.
  • Cardiovascular disease - address atrial fibrillation with an anticoagulant
  • Lifestyle and behavior changes for stroke prevention.
70
Q

Hemorrhagic Stroke - Types
* What is an intracerebral hemorrhage?

A

Intracerebral hemorrhage (ICH) – A focal collection of blood within the brain parenchyma or ventricular system. Includes parenchymal hemorrhage after cerebral infarction from a stroke.
* does not include subdural or epidural hemorrhage

71
Q

Hemorrhagic Stroke - Types
* What is a silent cerebral hemorrhage?

A

Silent Cerebral Hemorrhage – A focal collection of chronic blood products within the brain parenchyma, subarachnoid space, or ventricular system on neuroimaging without a history of acute neurological dysfunction attributable to the lesion.
* blood present but does not cause any symptoms of brain compression

72
Q

Hemorrhagic Stroke - Facts
* ICH increases with what?
* ICH has a higher what than ichemic stroke?
* ICH mortality rate is approximately what?

A
  • ICH increases with age, doubling every 10 years after age 35.
  • ICH has a higher morbidity and mortality than ischemic stroke
  • ICH mortality rate is approximately at 44%.
73
Q

Hemorrhagic Stroke - Facts
* What is the leading cause of ICH? What are other causes?

A

Hypertension resulting in damage and rupture of vessels is the leading cause of ICH (60%)
* other causes include malignancies, AVMs, drug abuse or previous thrombolysis to name a few

74
Q

Hemorrhagic Stroke – Clinical Presentation
* What are all the sxs?(6)

A
  • Sudden Focal Neurologic Deficit
  • HTN (~90%)
  • Headache (~40%)
  • Nausea and Vomiting (~50%) esp. with posterior fossa strokes
  • AMS (~50%) – not common with ischemic strokes-> They cause neurological deficits seen on one side of the body
  • Seizures (~7%)
75
Q

Hemorrhagic Stroke - Management ⭐️
* What do you need to do in the first hour? (4)

A
  • Airway/Ventilation Management
  • Non contrast CT of the head and evaluate for change in GCS.
  • CBC/PT/PTT/INR
  • Coagulopathy reversal
76
Q

Hemorrhagic Stroke - Management:⭐️
* What do you give for reversal of warfarin, factor Xa, diabigatran and plavix/ASA

A
  • Warfarin: (INR goal less than 1.5) Vitamin K IV based on INR, combined with KCENTRA
  • Factor Xa inhibitors like Eliquis/Xarelto – KCENTRA
  • Pradaxa (Diabigatran) – Use of Praxbind, (Idaricizumab) as a reversal
  • Plavix, ASA – DDAVP (Desmopressin) – reduces hematoma growth, improves platelet activity
77
Q

Hemorrhagic Stroke - Management
* What also needs to be done within in the first hour besides ABCs, CT, labs and coagulopathy reversal

A

Goal to maintain systolic blood pressure (SBP goal of 140)

Intracranial pressure management (ICP) monitoring and management
* Mannitol or CSF drainage through an external ventricular drain

Neurosurgical management (if indicated) for hematoma evacuation

78
Q

Subarachnoid Hemorrhage – General Characteristics
* Where is the bleeding? What are the causes (most ⭐️ and least common)

A

Subarachnoid hemorrhage - bleeding into the subarachnoid space (the space between the arachnoid membrane and the pia matter of the brain or spinal cord).
* Trauma is the MOST common cause of all SAH
* 85% are spontaneous, related to aneurysm rupture, such as rupture of a saccular aneurysm
* less commonly caused by an arteriovenous malformation (AVM)

79
Q

Subarachnoid Hemorrhage – General Characteristics
* What are the risk factors? (4)
* Most are found incidentally – how?
* What can also be associated with triggering SAH?

A
  • Risk factors for developing aneurysms include smoking, hypertension, high cholesterol levels and heavy alcohol use.
  • Most are found incidentally – patient gets a CT scan of the head w/o contrast for a headache, vascular malformation found – leads to identification of cerebral aneurysms.
  • Vigorous physical activity and cocaine use are associated with triggering SAH, presumably causing elevation of blood pressure.
80
Q

What is an aneurysem?

A

Aneurysm – a bulging or ballooning area in a weakened area. It is 50% or more of the vessel’s normal diameter.

81
Q

What is gold standard for SAH?

A

Digital retractable angiogram

81
Q

What is this?

A

Subarachnoid hemorrhage aka funky chicken

82
Q

SAH – Clinical Features
* What is the classic presentation?
* Some develop sxs when?
* Those with altered mental status may not be able to provide what?

A
  • Classic presentation of SAH includes the onset of a thunderclap headache with exertion or Valsalva maneuver, this only occurs in a minority of patients.
  • Some develop symptoms during sleep.
  • Those with altered mental status may not be able to provide a history of the headache onset, others may present in a coma.
83
Q

SAH – Clinical Features
* In 10-40% of patients, the acute presenting headache is precented what? What does that lead to?
* May develop what? What are they signs of?

A

In 10-40% of patients, the acute presenting headache is precented by a warning aneurysmal leak leading to a “sentinel headache” which occurs about 2-8 weeks prior to the overt SAH.

May develop a fever, frequently display confusion, coma – nuchal rigidity or other signs of meningeal irritation
* blood travels in CSF down to tailbone along spinal cord, irritant, thus neck and back pain may be a complaint as well

84
Q

SAH – Clinical Features
* What are Some presenting signs and symptoms of SAH that may mimic an alternate diagnosis:?(4)

A
  • Isolated neck pain (cervical muscle strain or degenerative arthritis)
  • Fever and headache
  • Nausea and vomiting
  • Elevated blood pressure or EKG abnormalities
85
Q

SAH – Clinical Features
* What specific finding is suggestive of SAH? What is the work up?
* What can it be the cause? ⭐️

A

Aspecific finding such as a third nerve palsy may also suggest the diagnosis of SAH.
* Isolated third nerve palsy should always be further imaged with a non-contrast CT as well as CTA
* Can be caused by ischemia but also caused by a compressive aneurysm – most likely it is due to a Posterior Communicating Artery Aneurysm.

86
Q

What is this?

A

You can have an aneursym so big that is it pushing up against the nerve

87
Q

SAH – Checklist for the First Hour
* What do you need to do within the first hour?

A
  • Airway, breathing and circulation
  • Head computed tomography (non contrast CT scan as well as a CT angiogram of the head and neck with perfusion)
  • Labs: PT/INR, PTT, CBC, chemistries, troponin, toxicology screen
  • 12 Lead EKG
  • Target SBP goal <140 mmHg
  • Consult neurosurgery team
  • Address hydrocephalus if present
88
Q

SAH – Initial Clinical Evaluation
* Focused clinical evaluation includes what?
* What is a Grading system that use radiological studies to determine severity of the SAH?

A

Focused clinical evaluation includes determining level of consciousness, assessment of potential neurological deficits

Grading systems that use radiological studies to determine severity of the SAH
* Fisher Grading Scale helps predict development of vasospasm as well as delayed cerebral ischemia

89
Q

SAH – Initial Clinical Evaluation
* What is the hunt-hess classification?
* What are the levels?

A

Hunt-Hess classification helps to correlate presenting clinical status with long term neurological outcome

90
Q

SAH – CT Negative for SAH
* What will lumbar puncture show?
* What is MRI highly sensitive for?
* What is CTA for?

A
  • Lumbar puncture with evaluation of cerebrospinal fluid reveals markedly elevated opening pressures and grossly bloody fluid.
  • MRI – highly sensitive for intracranial hemorrhage, including SAH.
  • CT angiogram – designed to diagnose the presence of an aneurysm, not to detect SAH
91
Q

Cerebral angiography (Digital Subtraction Angiogram)
* Should be done when?
* Gold standard for what?
* What does it identify
* Also used to treat what?

A

Cerebral angiography (Digital Subtraction Angiogram) should be done to evaluate the entire vasculature if additional evaluation and identification is needed:
* Gold standard for identification of cerebral aneurysms
* Accurate identification of size of aneurysm
* Also used to treat through stent and/or coiling

92
Q

SAH – Initial Management of SAH
* What is the risk of re-rupture?
* What is the critical during this time?

A
  • Risk of re-rupture is 4-14% in the first 24 hours after a SAH and remains elevated for 30 days.
  • Treating severe hypertension is critical during this time.
93
Q

SAH – Initial Management of SAH
* What is the txt?
* Treatment of hydrocephalus by what?

A
  • Treatment such as securing the aneurysm within the first 24 hours by Interventional Radiologist.
  • Treatment of hydrocephalus by placement of an external ventricular drain.
94
Q

SAH – Seizure Prophylaxis
* Seizure prophylaxis – for new onset seizures after aSAH, treatment with what?
* may increase the risk of what?
* short term treatment is recommended out of concern for what?
* What is the medication?

A

Seizure prophylaxis – for new onset seizures after aSAH, treatment with antiseizure medication for 7 days is recommended.
* may increase the risk of aneurysm re-rupture and elevated ICP if they have another seizure
* short term treatment is recommended out of concern for seizure-related precipitation of aneurysm re-rupture
* generally given Keppra twice daily for 7(seven) days

95
Q

SAH – Coagulopathy
* Like a hemorrhagic stroke, those taking anticoagulant medications should get what?
* Patients taking Warfarin with an INR greater than or equal to 1.4 should be treated with what?

A
  • Like a hemorrhagic stroke, those taking anticoagulant medications should have reversal agents administered.
  • Patients taking Warfarin with an INR greater than or equal to 1.4 should be treated with IV vitamin K and fresh frozen plasma.
96
Q

SAH – Coagulopathy
* When should a patient be treated with transfusion?
* If taking aspirin then platelet transfusion can be given IF what?

A
  • Thrombocytopenia, those with a platelet count less than 100,000 should be treated with platelet transfusion.
  • If taking aspirin then platelet transfusion can be given IF going to surgery, if not then can consider administering desmopressin (DDAVP).
97
Q

SAH – Pain and Anxiety
* Primary goal to assist with achieving patient comfort, treatment of what?
* What is generally given for pain medications?
* Titration of sedative and analgesic medications is what?

A
  • Primary goal to assist with achieving patient comfort, treatment of pain, vomiting and anxiety.
  • Tylenol is generally given for pain medication to include headaches.
  • Titration of sedative and analgesic medications is paramount – avoid over sedation which can mask subtle mental status changes.
98
Q

SAH – Pain and Anxiety
* In some cases, what can help with anxiety?
* Objective is help control what?

A
  • In some cases, short acting benzodiazepines can help with anxiety.
  • Objective is help control a BP elevation due to pain and anxiety
99
Q

SAH – Blood Pressure Management
* Not a lot of data on blood pressure control parameters – goal is what?
* Titratable BP control - SBP between what?
* If aneurysm is secured through placement of coiling and/or a stent, then can allow SBP to be what?

A
  • Not a lot of data on blood pressure control parameters – goal is to “balance risk of stroke, hypertension-associated rebleeding, and maintenance of the cerebral perfusion pressure.”
  • Titratable BP control - SBP between 110-140 if an unsecured aneurysm.
  • If aneurysm is secured through placement of coiling and/or a stent, then can allow SBP to be higher, 110-180.
100
Q

SAH – Delayed Cerebral Ischemia
* A clinical syndrome that occurs in who?
* Develops because of what?

A
  • A clinical syndrome that occurs in SAH resulting in a decline in neurological status.
  • Develops because of narrowing of cerebral arterial vessels, or vasospasm.
101
Q

SAH – Delayed Cerebral Ischemia
* what should be administered?
* delayed cerebral ischemia caused by what? ⭐️
* blood in the subarachnoid is an irritant and causes what?
* What can help?

A

Oral Nimodipine administered
* delayed cerebral ischemia caused by intracranial vasospasm occurs in 70% of patients and starts around day 3 after rupture, peaks 7-10 days and resolves by day 10-14
* blood in the subarachnoid is an irritant, breaks down and factors cause vasospasm
* administering a calcium channel blocker can help reduce the vasospasm and ICP

102
Q

SAH- Additional Management
* What should you be getting daily? What are the goals?

A

Daily CMP – important are the sodium, hemoglobin and electrolytes
* Sodium: maintain between 135-145
* Hemoglobin: keep greater than 8.0
* Magnesium: keep greater than 2.0
* Potassium: keep greater than 3.5

Daily Transcranial Doppler Ultrasound testing – watch for development of arterial vasospasms

103
Q

SAH- Pertinent Clinical Notes
* Presentation is often what?
* Noncontrast CT scan of the head is highly sensitive if done when?
* What should be done if should be done if CT is negative?

A
  • Presentation is often “worst headache of their life”.
  • Noncontrast CT scan of the head is highly sensitive if done within the first hours of the symptom onset.
  • Lumbar puncture should be done if CT is negative, and history is suggestive of a subarachnoid hemorrhage.
104
Q

SAH- Pertinent Clinical Notes
* CT angiogram is helpful for the detection of what? What is the gold standard still?
* Monitor for what?

A
  • CT angiogram is helpful for the detection of bleeding sources. Remember that a digital subtraction angiogram is the gold standard for identification of and treatment of cerebral aneurysms.
  • Monitor for and decrease risk of rebleeding prior to securing the aneurysm, through blood pressure control, minimize overstimulation.
105
Q

SAH- Pertinent Clinical Notes
* Treat what?
* What do you need to give for the prevention of delayed cerebral ischemia (vasospasms)?

A
  • Treat hydrocephalus
  • Initiate nimodipine for the prevention of delayed cerebral ischemia (vasospasms)
106
Q

Arteriovenous Malformations (AVMs)
* What are they?
* What type of defect?
* Complex what?

A
  • Abnormal and tangled connection between arteries and veins, bypassing the normally capillary system.
  • Congenital defect, usually present at birth, not symptomatic until later in life.
  • Complex, tangled web of arteries and veins.
107
Q

Arteriovenous Malformations (AVMs)
* Can present with what? (4)
* What can lead to stroke like sxs?
* Discovered how?

A
  • Can present with headaches, seizures, weakness or numbness in part of the body.
  • Intracranial hemorrhage which can lead to stroke-like symptoms.
  • Discovered incidentally in some cases but if ruptures, may not be identified as source until additional diagnostic testing is done.
108
Q

Arteriovenous Malformations (AVMs)
* What is dx testing?
* What does treatment consist of?

A
  • Diagnostic testing can include MRI as well as cerebral angiography.
  • Treatment can consist of monitoring if they are small, surgical removal as well as endovascular embolization and radiosurgery.
109
Q

Neoplasms Epidemiology
* Approximately half of all primary intracranial neoplasms are what? What is the remainder?
* Most common sources of intracranial metastasis are what? ⭐️⭐️(4)

A
  • Approximately half of all primary intracranial neoplasms are gliomas – remainder are meningiomas, pituitary adenomas, neurofibromas.
  • Most common sources of intracranial metastasis are carcinoma of the lung, breast, kidney, and GI tract.
110
Q

Neoplasm – Clinical Features
* Spinal tumors may lead to what?

A

Spinal tumors may lead to spinal cord dysfunction by direct compression or ischemia secondary to arterial/venous obstruction.

111
Q

Intracranial tumors may produce focal deficits depending on location:
* Frontal
* temportal
* parietal

A
  • Frontal lobe – progressive intellectual decline, personality changes
  • Temporal lobe – seizures, emotional and behavioral changes
  • Parietal lobe – contralateral disturbances of sensation
112
Q

Intracranial tumors may produce focal deficits depending on location:
* occipital lobe?
* Brain stem and cerebellar lesions?

A
  • Occipital lobe – visual field defects, inability to recognize objects
  • Brain stem and cerebellar lesions– cranial nerve palsies, ataxia, incoord
113
Q

Clinical Presentation of Tumors⭐️
* What are the clinical sxs ?(7)

A
  • Headache
  • Seizures
  • Weakness, upper or lower extremities, combination of the two
  • Sensory loss
  • Aphasia
  • Cognitive impairment, memory loss, confusion
  • Visual spatial dysfunction
114
Q

Clinical Presentation of Tumors ⭐️
* What is the ICP classic triad?

A
  • morning HA
  • vomiting
  • lethargy
115
Q

Clinical Presentation of Tumors ⭐️
* What is the crushing triad?

A
  • HTN
  • bradycardia
  • HYPOventilation
116
Q

Benign Brain Tumors- Meningioma
* What is it?
* Peak incidence when?

A
  • Meningiomas are the most common primary central nervous system (CNS) noncancerous tumors and account for approximately one-third of all primary brain and spinal tumors
  • Peak incidence in middle age, very uncommon in children and occur more frequently in women than men.

Think the brain as a large balloon, and the meningioma as a tennis ball that you push into the balloon. It is not inside the brain, but rather outside pushing in.

117
Q

Benign Brain Tumors - Meningioma
* Arises from what?
* What is the clinical presentations?

A

Arise from the arachnoid layer of the meninges – most common spot is the parasagittal region.

Clinical presentation consists of raised ICP, focal neurological signs and epilepsy
* location determines presentation
* slow growing, many years of symptoms before diagnosis

118
Q

Benign Brain Tumors - Meningioma
* What is treatment?

A

Treatment usually observation/surgical removal followed by radiation is reoccurrence.

119
Q

Benign Brain Tumors - Acoustic Neuroma
* What is this? What is found in 98% of patients?

A

Acoustic schwannomas arise from the 8th cranial nerve and first neurologic abnormality is auditory – hearing loss is found in 98% of these patients.

120
Q

Benign Brain Tumors - Acoustic Neuroma
* What is the clinical presentation?

A

Clinical presentation depends on the size with early symptoms are associated with 8th nerve involvement
* tinnitus and unilateral partial or complete sensorineural hearing loss
* vertigo present – maybe confused with Menieres’ disease
* numbness over the face may appear later

121
Q

Benign Brain Tumors - Acoustic Neuroma
* Essential to check what? Why?

A

Essential to check the corneal reflex because loss or depression of this reflex is the most consistent early sign – fifth nerve is lifted by the tumor and fibers for corneal reflex are sensitive.

122
Q

Malignant Brain Tumors - Glioblastoma Multiforme (GBM)
* Glioblastoma is the most common malignant primary brain tumor in who?
* What is the survival rate?
* MRI characteristically shows what?

A
  • Glioblastoma is the most common malignant primary brain tumor in adults, with a median age of onset of approximately 55 to 60 years.
  • Even with adjuvant chemo and radiation therapy following surgical resection, GBM has a high rate of recurrence and rate of survival of about 10-12 months
  • MRI characteristically shows heterogeneous-ring enhanced pattern associated with significant edema
123
Q

Malignant Brain Tumors - GBM
* WHO grade of a GBM is done after what?
* Four grades of what?

A
  • WHO grade of a GBM is done after surgical resection is completed or a biopsy has been obtained.
  • Four grades of astrocytoma – which is the most common type of glioma that arise from the astrocyte cells.
124
Q

Malignant Brain Tumors - GBM
* What are the four grades?

A

WHO Grades I through IV
* Grade 1 generally associated with pediatrics
* Grade 3- 4, aggressive biological characteristics and poor prognosis – require multiple resections, radiation and chemotherapy treatment.
* surgical procedures are to reduce the symptoms, extends life for a period, not curative.

125
Q

Malignant Brain Tumors - GBM
* Following presumptive diagnoses of a glioma, management consist of what?

A
  • surgery
  • radiotherapy
  • other adjuvant treatments – like chemotherapy, radiation therapy
126
Q

Malignant Brain Tumors - GBM
* Surgery is performed with what three principles aims?

A
  • make a definitive diagnosis
  • tumor reduction to alleviate the symptoms of raised intracranial pressure
  • reduction of tumor mass as a precursor to adjuvant treatments
127
Q

All Tumor Work-up
* What is the imaging?

A

CT of the head without contrast, MRI of the head with/without contrast as well to detect the lesion, define its location and size, evaluate extent to which the normal anatomy is distorted, and identify cerebral edema.

128
Q

All Tumor Work-up
* If no previous history known, a CT of what? Why?

A

If no previous history known, a CT of the chest, abdomen and pelvis to look for any other suspected masses – is the mass in the head primary or a result of metastasis.
* 60% of those without any known primary tumor that present with brain metastasis have a primary lung cancer.

129
Q

All Tumor Work-up
* Treatment generally consists of what? Why?

A

Treatment generally consists of dexamethasone for reduction of cerebral edema – helps reduce the symptoms.
* generally, start with 10 mg every 4-6 hours initially

130
Q

All Tumor Work-up
* What is the seizure prophylaxis?

A

Seizure prophylaxis by administration of Keppra daily – if new onset seizure
* generally, continued for another seven days after surgery is conducted

131
Q

All Tumor Work-up
* What is dx only? What does it give?

A

A biopsy if obtained, is diagnostic only. Gives a preliminary and final pathology is completed in two weeks.

132
Q

All Tumor Work-up
* Shunting by way of an external ventricular drain to reduce obstructive hydrocephalus may do what? ⭐️

A

hunting by way of an external ventricular drain to reduce obstructive hydrocephalus may dramatically reduce clinical deficits that the patient experiences because of the compression of the MASS.

Clinical Medicine 4 (13 decks)

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