Download RPC Case 23

Objectives:
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Describe and be able to clinically evaluate the differential diagnosis
of acute neurologic deficits
Describe risk factors for TIA’s and strokes
Describe the neuroanatomy and resulting neurological deficits that
result from a stroke involving the MCA and Broca’s Area.
Discuss the evaluation (including imaging: CT vs. MRI) and
treatment options for TIA’s and CVA’s
Define Amaurosis Fugax and describe its etiology
Describe the indications for Carotid Endarterectomy
Describe the different kinds of aphasia
Discuss the varied presentations of TIA’s
List the symptoms and signs of Bell’s Palsy
Describe Inclusion criteria for tPA therapy in a stroke patient
Describe the treatment of elevated BP in the first three days
following a stroke
Describe 3 aspects of post CVS care that are important to the wellbeing of the patient:
a. Evaluate for Depression
b. PT/OT/ST
c. Maximize medical management of co-morbid conditions
USC Case # 7: TIA/CVA
You are a working in Stuart with Dr. Cole in an office down the street from Patrick
County Community Hospital. It’s Monday morning and you and your attending just
finished rounding on all your patients in the hospital. You are sitting down to catch up on
your online clinical cases when your nurse walks into your office and says Ned
Throckmorton needs to be seen. Ned, despite being a difficult patient, is a terrifically fun
guy and everyone is quite fond of him. You always look forward to seeing him on the
rare occasions when he not only makes, but also keeps, an appointment. You went into an
exam room to see why Ned is here.
Ned, a 72 year old Right-handed man was brought in by his girlfriend who reported that
"All of a sudden he dropped his spoon of Count Chocula cereal, his face sagged and now
he can’t talk."
What is the differential diagnosis at this point?
The top 3 on the differential for an acute neurological deficit are:
1. Stroke
2. Stroke
3. Stroke
Other diseases that can present with acute neurologic deficits of this type are: post-ictal
(seizure) paralysis (Todd’s paralysis), Migraines (of the complicated type),
hypoglycemia, hyperglycemia, and multiple sclerosis, intracranial cancer.
Before going onto the history, what must you assess to ensure the safety of Ned? In
any patient with an acute life threatening injury, what do you want to do?
Check the ABC’s--Airway! Breathing! Circulation! Before getting a detailed history, we
must first assess the severity and acuity of Ned’s condition. Stroke patients face the
greatest mortality risk within hours of their strokes, then within a few days (when
cerebral edema becomes maximal - usually within 3 days after the acute event), so if
stroke is on your differential, make sure your patient is stable and your facility is
adequately equipped to care for the patient.
In general, up to 20% of all stroke patients die during hospitalization! Negative predictive
factors include: advanced age, coma on admission, hemorrhagic strokes, large ischemic
strokes (hemispheric or brainstem/cerebellar involvement), and other comorbid medical
conditions, especially heart disorders.
Ned seems stable. What further information do you want to include in the history?
Our goals from the history should be to get information that allows us to focus the
differential, define a possible lesion, which will influence our treatment plans. For
example, a small lacunar stroke indicates small vessel disease, usually the result of
diabetes and hypertension. This is best treated with anti-platelet agents like aspirin and
Plavix to prevent future strokes. On the other hand, large strokes for the most part
indicate large vessel and heart disease (such as embolic events) and are often treated with
coumadin to prevent strokes in the future. The time of onset is important since if it is less
than 3 hours (4.5 hrs for select patients) and there are no contraindications, then the
patient is a potential candidate for intravenous tPA (tissue plasminogen activator).
To do this, we need information about the course of the present illness, are symptoms
getting better or worse? Was the onset sudden? Was the onset associated with anything
out of the ordinary, like shaking, or a headache? We need to define the symptoms better:
which side of the face and arm, any other body involvement? We need to define the
aphasia better. In any neurologic patient, handedness is a key historical point to indicate
speech dominance.
The symptoms began 5 hours ago when Ned and his girlfriend were having breakfast. He
suddenly dropped a spoon from his right hand and his girlfriend noticed a right facial
droop. More strikingly, Ned, normally quite a BS’er, completely ceased speaking. He
could grunt and say "hello," but that was all. His girlfriend Franny was understandably
alarmed by Ned’s state and said "we need to go see the doctor". Ned not only could
follow the commands given by Franny, but unlike his usual self, he walked to the car
without further coercion.
Since the onset of the problem, Ned’s condition neither worsened nor remitted. There
were no other symptoms around this time such as repetitive movements, or complaints of
headache, chest pain, or palpitations before the onset of symptoms.
Given the information we have, where in the brain is the lesion? What vascular
territory is involved, Anterior Cerebral Artery (ACA), Middle Cerebral Artery
(MCA), Posterior Cerebral Artery (PCA), or the Basilar Artery?
There is a rather large lesion of the left frontal cortex in the left MCA territory. Like all
neurologic lesions, we can arrive at this conclusion by taking the short road or the long
road. The short road involves recognizing this as a classic Broca’s aphasia coupled with
right sided weakness involving the face and arm more than leg. This is referable to
Broca’s area and abutting regions of the face and arm representations of the motor
homunculus.
The long road arrives at the same conclusion by tracing the structures involved back to
find an anatomical relationship. Let’s look at the three symptoms, facial weakness, arm
weakens, and speech; and work from distal to proximal to find an area of convergence:
1. Right facial weakness: referable to a lesion (distal to proximal) of the right facial
muscles, right peripheral facial nerve, right facial nerve nuclei, left corticobulbar tracts
through internal capsule, left cortical motor strip.
2. Right arm weakness: referable to a lesion (distal to proximal) of the right peripheral
nerves/brachial plexus, right motor neuron cell bodies in the spinal cord, right descending
corticospinal tract, pyramidal decussation in the medulla, contralateral crus cerebri,
internal capsule and cortical motor strip.
3. Aphasia: One gets a fairly obvious impression of the patient’s difficulty expressing
himself with preserved receptive language (he is able to understand language as he
follows commands, but cannot get words out). This puts the lesion in the cortex of the left
frontal lobe with preservation of temporal (Wernike’s) cortical areas.
Conclusion: the area of convergence of these tracts/areas is the left frontal cortex. The
lesion is secondary to the MCA because the arm and hand representations of the motor
homunculus are supplied by this vessel and are involved in this case. The leg regions of
the motor homunculus is supplied by the ACA and is spared, unless there is internal
capsule involvement (lenticulostriate branches from MCA).
Past Medical History:
Significant for Hypertension, hypercholesteremia and type II DM. Ned is noncompliance
on medication. Ned stated in the past, much to your disapproval, "I don’t like drugs and I
don’t like doctors, you can give ‘em to me, but I don’t have to take ‘em." Franny recalls
an episodic "mini-stroke" one year ago. Upon further questioning, we learn the patient
presented with loss of vision in one eye lasting 15 minutes. Subsequently he was
convinced to undergo a carotid endarterectomy for symptomatic carotid stenosis of 98%.
Since that time, he has been lost to F/U.
Allergies: NKDA
What are the risk factors of stroke?
Older person who smoke, with poorly control HTN, DM, heart disease (Atrial fibrillation
especially), and increased cholesterol, run a high risk for stroke. Women who smoke and
take Oral Contraceptives put themselves in a hypercoaguable state. Smoking is always
contraindicated! The risk of Oral Contraceptives is even greater in women over age 35
who smoke and have a migraine headache history.
In young people, strokes are more likely to be secondary to a long list of really unusual
neurologic diseases or to another long list of things that makes them hypercoaguable.
Although beyond the scope of this case, one should be aware that young patients with
strokes get careful workups to determine the cause so treatment can be directed
appropriately.
What do you think non-compliance rates are for anti- hypertensive medications?
There is a 50% noncompliance rate within 1 year. As the silent killer, hypertension rarely
causes symptoms. Remember that symptoms are the things a patient notices, signs are
things you notice or elicit. On top of the inherent problem of getting patients to take a pill
for no apparent reason, the pills have real and unpleasant effects. Beta-blockers can cause
fatigue, orthostatic hypotension, and (most importantly) sexual dysfunction. Diuretics
make the poor patient urinate frequently. Even the latest wonder drugs, the ACE
inhibitors, make some people cough, make food taste bad (dysgusia), and angioedema in
a few unlucky patients. Many a patient’s first problem with hypertension is when they
have a stroke. Screening and patient education are crucial in preventing poor outcomes
due to hypertension.
What is a TIA?
A Transient Ischemic Attack, or in common parlance, a "mini-stroke," can be thought of
as a quickly resolving stroke causing no permanent damage. Basically, neurologists
believe that something bad, like a blood clot, cholesterol, etc., embolizes into the cerebral
circulation, lodges and prevents blood from reaching brain tissue. Unlike a stroke, the
material quickly dissolves and blood flow is restored. Although completely wrong in
terms of pathophysiology, one can think that in terms of severity:
TIA is to stroke as Angina is to MI.
By the consensus reached by some committee 30 years ago, TIAs must last no longer
than 24 hours. Most last 2-15 minutes and resolve completely, as the use of "transient"
implies.
One study showed that TIAs predict future strokes within 5 years in about 25% of
patients. The incidence of stroke after presenting with a TIA is approximately 5-10%
within the first month after the TIA. The rate of MIs in this group’s 5-year time period
was about 20%. Needless to say, the popular neurologic designation of TIAs as
"Harbingers of doom" is apt.
How often do TIAs present with syncope?
Never (well, never say never) despite commonly seeing TIA on the differential of
syncope.
What do we call painless loss of vision lasting 10 or 15 minutes? What structures is
it referable to? What is the vessel and what vascular lesion is it most commonly
associated with?
Amaurosis fugax classically presents when a cholesterol plaque in the internal carotid
breaks off and slips into the first vessel leaving the intracranial portion of the internal
carotid, the ophthalmic artery. It blocks flow to the retina, thus producing ischemia and
loss of retinal function. As the embolic plaque dissolves, retinal function returns to the
patient’s great relief. Pts. need to be worked up for carotid stenosis and if no stenosis is
found, then a full stroke workup is in order.
Ned underwent carotid endarterectomy (CEA) at that time indicated by significant
symptomatic carotid artery stenosis. Was this proper management?
Yes. Currently, risk benefit analysis indicates that symptomatic patients with more than
70% stenosis benefit from a CEA, but only if the surgeon can give less than 3%
morbidity and mortality. If not, (to the consternation of vascular surgeons of the 1960’s,
who performed these procedures on everyone with a bruit) the risk benefit ratio would
suggest close observation.
The effectiveness of carotid endarterectomy (CEA) for moderate to severe asymptomatic or
symptomatic carotid artery stenosis has been established in large randomized trials.
Prophylactic carotid endarterectomy in patients with asymptomatic carotid stenosis prior to
cardiac or general surgery has no demonstrated benefit. For patients with indications for
bilateral carotid endarterectomy, a staged rather than combined procedure is performed.
Uptodate.com
Medical History:
Meds: HCTZ 25 mg PO qd, Captopril 50 mg PO bid, Glyburide 6 mg PO qAM, Zocor
20 mg qd and baby aspirin qd, but patient admits to taking it only when he feels his blood
pressure or blood sugar is high.
FH: Parents died of old age, has 2 sons and 1 daughter, all three in good health.
SH: Lives with girlfriend of 10 years who encourages patient to take meds and not to
smoke. Unfortunately, the patient remains quite compliant on his pack per day habit of 50
years. He drinks 2 beers per day and does not take illicit drugs. He is a retired machinist
from Calesco.
Physical Exam:
Vital signs: Temp: 98.6, BP: 170/100, Pulse: 88, Resp: 20.
What risk factors does Ned have for stroke?
HTN, DM II, lipid disorder, smoking, carotid artery stenosis, and a history of a TIA. He
doesn’t have a known heart condition, but given this history of coronary risk factors, one
may wonder if this is a subclinical problem at the moment.
What do you make of the BP? What stage is it? Will you treat it with IV antihypertensives?
First of all, it is high. High blood pressure is present in up to 85% of acute stroke patients
and should NOT be treated aggressively (unless there is reason to believe there is an
intracranial bleed) during the first several days of an acute ischemic stroke.
There are two reasons not to treat hypertension in this setting. First of all, autoregulation
happens to be absent within the ischemic area. Second of all, stroke patients are very
sensitive to small doses to antihypertensives. Thus, any drug can cause severe drop in
blood to an already ischemic brain tissue. A mean arterial pressure (MAP) <130-140 or
SBP<220 is generally acceptable, unless thrombolytic therapy is given (BP goal should
be <185/110 before/after treatment). This patient’s blood pressure doesn’t require
treatment at present.
General appearance: Obese patient, appears stated age, no acute distress.
HEENT: PERRL, EOMI, Left fundi with cholesterol (Hollenhorst) plaques, mucus
membranes moist.
Neck: No bruit bilaterally. No Jugular Venous Distension.
Heart: RRR without murmur, rub, or gallop.
Lungs: Clear to Auscultation bilaterally
Ab: Obese, Non-tender, non-distended, + bowel sounds in all 4 quadrants
Ext: No Cyanosis, clubbing, or edema.
Neuro:
Mental status: Alert. Pt. cannot repeat, cannot name, speech is restricted to word "hello."
Follows commands appropriately. Pt. cannot write sentence, writes "Hello." Can copy
figures.
Cranial Nerves:
II right homonymous inferior quadrantanopia.
III, IV, VI: EOMI
V: facial sensation intact.
VII: Right lower facial droop, flattened nasolabial fold. Wrinkles brow symmetrically.
VIII: Hearing grossly intact.
IX, X: gag intact, palate rises symmetrically.
XI: shrugs symmetrically.
XII: tongue midline.
Motor: RUE 0/5 proximally and distally. RLE 4/5 proximally, 5/5 distally.
All left extremities are 5/5 proximally and distally.
Reflexes: No reflexes, RUE in all muscle groups. Otherwise 2/4 and symmetric with
downgoing toes.
Sensory: Pin, vibration, position tested. All slightly decreased in RUE. Otherwise
preserved.
Cerebellar function: nl. Finger to nose on L. Nl. Heel shin B.
Gait: nl. Romberg: nl.
Osteopathic exam: compensatory changes at the Lumbar, Thoracic and Cervical region.
Should the lack of a bruit reassure you that the carotids are clear and not a source
of stroke?
NO. A 99% stenosis or100% occlusion will obviously result in a minimal/no flow state
and thus no bruit. A bruit is formed when blood, normally flowing in a smooth, "laminar"
manner, becomes turbulent as it passes through a stenotic blood vessel. One can hear the
turbulence as a bruit. But the obvious tautology emerges: turbulent blood flow requires
blood flow. So a bruit entails flow and no bruit means either laminar flow or no flow. In
this case, with Ned’s history, one should assume a stenosis and check it with a carotid
duplex.
What sort of Aphasia is this?
Broca’s, or expressive.
What if the patient had the same defects, but could repeat?
Transcortical motor/expressive aphasia.
What if the patient made quite a bit of speech, but most of it was gibberish, and
could not follow commands?
Wernike’s or receptive.
What do the findings on CN VII indicate?
Sparing of the forehead occurs with upper motor neuron (UMN) lesions of CNVII. This
is due to bilateral projections from cortex to the portion of CNVII innervating the
forehead. Basically, the forehead receives innervation from both cortical hemispheres,
making it difficult to knock out with a process occurring above the 7th cranial nerve. A
peripheral VII lesion would involve the forehead, as in Bell’s Palsy.
What tests would you like to order right now before we do anything therapeutic?
How about later, when the patient is stable and treated appropriately? Remember,
don’t shotgun or do the ‘neuro SMAC’. Think about why you would order things.
Not all patients will be able to afford testing even though you want to get it.
ALWAYS get the patient’s refusal on the testing. Do not ASSUME that the patient
cannot afford the test…lawsuits have come from this.
If the patient is more than 4.5 hours past the time of onset of his symptoms, he
would therefore not be eligble for tPA thereapy. The following table describes
inclusion and exclusion criteria for tPA therapy:
Eligibility criteria for the treatment of acute ischemic stroke
with recombinant tissue plasminogen activator (alteplase)
Inclusion criteria
Clinical diagnosis of ischemic stroke causing measurable neurologic deficit
Onset of symptoms <4.5 hours before beginning treatment; if the exact time of stroke onset is not known, it
is defined as the last time the patient was known to be normal
Age ≥18 years
Exclusion criteria
Historical
Significant stroke or head trauma in the previous three months
Previous intracranial hemorrhage
Intracranial neoplasm, arteriovenous malformation, or aneurysm
Recent intracranial or intraspinal surgery
Arterial puncture at a noncompressible site in the previous seven days
Clinical
Symptoms suggestive of subarachnoid hemorrhage
Persistent blood pressure elevation (systolic ≥185 mmHg or diastolic ≥110 mmHg)
Serum glucose <50 mg/dL (<2.8 mmol/L)
Active internal bleeding
Acute bleeding diathesis, including but not limited to conditions defined in 'Hematologic'
Hematologic
Platelet count <100,000/mm3*
Current anticoagulant use with an INR >1.7 or PT >15 seconds*
Heparin use within 48 hours and an abnormally elevated aPTT*
Current use of a direct thrombin inhibitor or direct factor Xa inhibitor with evidence of anticoagulant
effect by laboratory tests such as aPTT, INR, ECT, TT, or appropriate factor Xa activity assays
Head CT scan
Evidence of hemorrhage
Evidence of a multilobar infarction with hypodensity involving >33 percent of the cerebral hemisphere
Relative exclusion criteria•
Only minor and isolated neurologic signs
Spontaneously clearing stroke symptoms
Major surgery or serious trauma in the previous 14 days
Gastrointestinal or urinary tract bleeding in the previous 21 days
Myocardial infarction in the previous three months
Seizure at the onset of stroke with postictal neurologic impairments
Pregnancy
Additional relative exclusion criteria for treatment from 3 to 4.5 hours from
symptom onset
Age >80 years
Oral anticoagulant use regardless of INR
Severe stroke (NIHSS score >25)
Combination of both previous ischemic stroke and diabetes mellitus
Having ruled out tPA, We must evaluate this patient to arrive at the most effective
treatment plan
To start with, get the basics:
1. CT(brain) to R/O subarachnoid or intracerebral hemorrhage. Even with no
history/exam findings suggestive of a bleed on our exam, it’s important to verify it before
thrombolysis. Large strokes very often bleed within the ischemic area. This is called
hemorrhagic transformation in which thrombolysis is contraindicated. Rarely, a subdural
hemorrhage or a tumor can produce acute neurologic symptoms by pressing on brain
structures. A CT will eliminate this as a possibility. We basically need the CT as soon as
the patient is stable before we begin thrombolytic therapy.*CT without contrast. Contrast
material is irritating to the brain and can cause seizures.
2. BMP (Basic Metabolic Panel) (sodium, potassium, glucose, BUN, creatinine): to pick
up hypoglycemia and hyperglycemia, which can cause neurologic defects.
3. CBC (Complete Blood Count): we’re really just looking for risk factors, like platelet
dysfunction and infection that can precipitate a stroke.
4. PT, PTT: Looking for a coagulopathy and more important, as mentioned above, in
young patients. Also, patients presenting with a stroke already on anticoagulant therapy
(Heparin, Coumadin), will require these results prior to consideration of thrombolytic
therapy.
5. Sed Rate: Infection and autoimmune diseases like vasculitis.
After that, when the issue of therapy has been settled, we should look for the source of
the stroke:
1. CXR (PA and Lateral): looking for an enlarged heart or widened mediastinum (? aortic
dissection) that served as an embolic source.
2. EKG: looking for arrhythmia(especially atrial fibrillation) or an acute MI, that served
as an embolic source.
3. Carotid duplex: Provides fast, noninvasive information about the degree of stenosis of
the internal carotid.
4. Echocardiogram: looking for mural thrombus formation, valvular defects, and poor
heart function that could make for sluggish blood more likely to clot.
Ned is pretty stable, he was transferred urgently by car to the emergency
department (right across the street) at the hospital for further evaluation and
treatment.
Labs: CT: normal. Some evidence of cortical atrophy which is expected on a patient of
his age.
CBC:
Patient Values
White Blood Cells
10,000
Hematocrit:
51%
Platelets:
254,000
BMP:
Sodium:
143
Potassium:
3.8
Chloride:
98
HCO3:
25
Blood Urea Nitrogen (BUN): 19*
Creatinine:
1.3*
Glucose:
265*
Normal values
4500-11,000
41-53%
150,000-400,000
136-143
3.5-5.0
95-105
22-28
7-18
0.6-1.2
70-110
Calcium:
Coags:
PT:
PTT:
Rheum:
ESR:
9.9
8.4-10.2
11
27
11-15
25-40
13
0-15
What do you think of the normal CT (brain)? Does it change your working
diagnosis?
No, well, perhaps it did change the reader’s diagnosis, but it should NOT. It takes from
24 to 48 hours for a stroke to show up on CT. One would not expect the CT to show
changes within the 2 hours since Ned. had the stroke onset. The CT findings support a
stroke that has not "declared itself" on CT by effacing the gray white junction and
creating a hypodense area.
So was doing a CT (brain) a waste of time and money?
No. We now know, as indicated above, the patient doesn’t have evidence of an
intracerebral hemorrhage. Had he been bleeding, then giving thrombolytics would have
made consequences of a bleed worse.
How will you treat the patient after a normal CT (brain)?
Treating stroke with tPA is like doing an injection-once it is in, it is in and you can’t take
it back.
After making sure the A, B, Cs are intact, getting a CT and eliminating a bleed, one
should proceed with immediate thrombolysis with tPA in a patient who is only 2 hours
post stroke. This is done according to a hospital protocol (check your hospitals protocol).
One should have access to skilled nursing and immediate neurosurgery in case the patient
would develop an intracranial hemorrhage.
The rate of a bleed within 3 days after has been found in studies to be between 2 and
7.4%
Although patients are more likely to have bleeds with tPA, patients are also more likely
to recover more function. Again, the risk benefit analysis indicates we should treat with
tPA in the absence of contraindications.
If thrombolytic therapy (intravenous tPA) is not given, one should be given an
antiplatelet agent (aspirin, clopidogrel, aggrenox) or possibly placed on anticoagulant
therapy (heparin) and admitted to a hospital with highly skilled nursing care - usually
either an ICU or monitoring setting. If intravenous tPA is given, the patient should not
receive antiplatelet or anticoagulant therapy for 24 hours after tPA infusion.
Of note, heparin was found to be of no benefit, and some detriment in the treatment of
acute stroke. Most doctors do not anticoagulate in the acute setting.
After the patient received intravenous tPA and 24 hours later aspirin, a CXR, echo, and
EKG failed to demonstrate any abnormalities. He was admitted to a telemetry monitoring
section of the hospital and immediate consults to physical and speech therapy. A carotid
duplex showed 90-99% proximal internal carotid artery stenosis on the left and 20% on
the right.
What happened to the left side after the last CEA?
Restenosis.
When does the maximal brain edema occur after infarction?
Three days after the acute event, edema becomes maximal. Changes in mental status in a
post CVA patient should be aggressively worked up including a CT scan as the problems
may be due to an intracranial bleed.
Ned’s hospital stay is without event. He was transferred to a general medical floor from
the step down unit. When he was stable (1-2 months later), he underwent another left
CEA without problems. His frustration with lack of expressive language is obvious and
the therapists report a lack of motivation.
What do you think is at the root of Ned’s lack of motivation?
Depression classically follows a Broca’s aphasia in particular and strokes in general. It is
estimated that post-stroke depression occurs in 40% of survivors! Post-stroke depression
is correlated with both loss of function and proximity of the stroke’s damage to the
frontal lobes. One should treat these psychiatric manifestations aggressively. In the
absence of heart disease, the tricyclic antidepressant nortriptyline (Aventyl or Pamelor)
has been shown to be more effective than fluoxetine (Prozac). Weird but true.
You put Ned on Nortriptyline with good results in affect and motivation towards therapy.
He also begins to take his old medications and became diligent in the treatment for his
lipid disorder, HTN and DM, plus quit smoking (aggressive risk factor management)!!!!.
He also remains on aspirin 325mg per day with regard to future stroke prevention. Within
one month Ned has a speech vocabulary of 20 words. He continues making steady
improvements and is discharged to home with Franny as caretaker. He also had a cardiac
stress test along the way, to assess for significant comorbid/ subclinical coronary artery
disease (more likely to die from an MI than a stroke over the long-term; higher incidence
of comorbid CAD in individuals with documented proximal carotid artery disease), and
this study was negative. Within a year Ned has only residual right arm and face
weakness, and talks slowly with barely a hint of the neurologically devastated picture he
presented with. Franny brought you cookies for helping Ned out.
Readings: Rakel’s Textbook of Family Medicine pp 1004 - 1009