A more limited role for “stroke rescue”

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Recent randomized controlled studies continue to debunk the perceived benefits of mechanical clot retrieval over FDA approved intravenous thrombolysis with tissue plasminogen activator (tPA) for the treatment of acute stroke.

Intravenous tPA  is much more widely available than the costlier mechanical clot retrieval systems.

We recently posted a study that showed both treatments were equally effective for acute stroke treatment.

Another study showed that outcomes were the same for patients who received intravenous thrombolysis alone compared to those patients who received iv tPA and were then transferred to a “stroke rescue” center for mechanical clot retrieval (so called “drip and ship”).

In other words, most stroke patients can be effectively treated at primary stroke centers.

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If you think you are having a stroke, call 911 and get yourself to the nearest hospital,

Time is brain!

Mechanical clot retrieval may still be an option for stroke patients who have an occluded artery, but cannot receive tPA because they are on blood thinners, have had recent surgeries, or are seen more than 4.5 hours since stroke onset.

Yet more data that supports the importance of stroke prevention over stroke treatment.

Click here to find out more about our innovative TIA rapid evaluation center, which targets high risk patients for intensive stroke prevention strategies.

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Intrathecal baclofen for spasticity in non-ambulatory patients

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We have already made several posts about intrathecal baclofen for reducing spasticity and improving function in ambulatory patients:

However, intrathecal baclofen can also be used in patients with spasticity who are non-ambulatory or bedbound:

Normalizing muscle tone may not improve function, but it alleviates pain, allows for better positioning and hygiene, and improves quality of life.

Click here to find out more about our spasticity center.

Neuromuscular respiratory failure

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Each lung is composed of >300 million tiny membrane bound sacs of air sacs (alveoli) which if spread out would cover a piece of ground roughly the size of a tennis court.  The purpose of this giant membrane is to exchange oxygen from the air for carbon dioxide from the blood stream.

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If the lungs become congested (or filled with fluid) from infection (pneumonia) or heart failure, it becomes harder to extract oxygen from the air:

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Treatment includes adding extra oxygen to the air to make this process more efficient.

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However, gas exchange across the alveoli can only occur if fresh air is brought into the lungs, and stale air is moved out, a process known as ventilation.  The diaphragm and muscles of the chest wall act like a giant bellows to make this happen:

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These muscles can become weak in nerve or muscle diseases such as Guillain-Barré syndrome, polio, amyotrophic lateral sclerosis (ALS), Duchenne Muscular Dystrophy and myasthenia gravis.

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These patients are evaluated by pulmonary function testing, which will usually show a low forced vital capacity, low cough flow, and in advanced cases, elevated end-tidal carbon dioxide level.

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Patients with this type of ventilatory failure do not need extra oxygen, their lungs can extract oxygen from air normally, they need mechanical assistance moving air across their lungs:

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Early neuromuscular respiratory muscle weakness causes nocturnal hypoventilation.  This is because the weakened diaphragm is even more inefficient when laying supine in bed with the stomach contents pressing up on it.

Nocturnal hypoventilation presents with daytime sleepiness, early morning headaches, fatigue, and impaired cognition.

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Click here to take an on-line test, and find out how sleepy you are during the day.  If you score 10 or higher, you might have a problem!

Nocturnal hypoventilation is best treated using a non-invasive respirator at night, either with a face or nose mask:

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Other patients use a negative pressure respirator vest, or cuirass, which requires the patient to wear an upper body shell  attached to a pump which actively controls the respiratory cycle:

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Neuromuscular respiratory failure also leads to an ineffective cough, which in turn predisposes patients to aspiration, retention of secretions, or pneumonia.  Affected patients need to learn to use the cough assist machine when they get a minor respiratory tract infection to help them clear their secretions and prevent pneumonia:

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More severe neuromuscular ventilatory failure leads to rapid shallow breathing, accessory respiratory muscle use, thoracoabdominal paradox (inward motion of the abdomen during inspiration), and ultimately high blood levels of carbon dioxide.

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Thoracoabdominal paradox – Normal (upper) abdomen moves outward with inspiration (diaphragm contraction). NM weakness (lower) abdomen moves in when patient inspires using accessory muscles.

In these cases, respiratory support is needed day and night.

Some patients can continue to use non invasive respiratory support, sleeping with a face or nose mask, and using a mouth piece intermittently during the day:

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Others cannot tolerate noninvasive ventilation or have anatomic abnormalities that preclude fitting of noninvasive ventilators.  Some disease, such as advanced ALS and Duchenne muscular dystrophy, affect the upper airway muscles as well as the diaphragm, impairing swallowing and compromising airway protection from aspiration.  These patients can chose to be managed with invasive respiratory support using a tracheotomy and conventional ventilator.

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Click here and and here to find out more about the management of neuromuscular respiratory failure.

New study compares steroid regimens in boys with Duchenne Muscular Dystrophy

Duchenne muscular dystrophy (DMD) affects 1 in 3,600 boys and is caused by a mutation in the dystrophin gene, resulting in progressive muscle weakness.

Affected male children are normal at birth, but develop signs of muscle weakness before age 6, usually first affecting the legs and pelvis, causing difficulty getting up from the floor or a sitting position, and difficulty climbing stairs. Untreated boys are usually wheelchair dependent by age 12.

Ongoing research is leading towards pre-symptomatic diagnosis of DMD, and there has been some progress in genetic therapy for affected boys identified in these early stages of the disease.

However, so far corticosteroid therapy is the only treatment that has been shown to increase muscle strength in boys already affected with symptoms of DMD.

Steroids can cause side effects, and there is wide variability whether doctors doctors prescribe prednisone or deflazacort, as well as the dosing, duration of steroid use or even whether steroids are prescribed at all.

A new study aims to answer some of these questions.

The study is looking to enroll boys aged 4-7 with genetically confirmed DMD who have not taken steroids before.

They will be included in the study for 3-5 years and receive either:
1. Prednisone 0.75mg/Kg/d, or
2. Prednisone 0.75mg/Kg/d 10days on then 10 days off, or
3. Deflazacort 0.9mg/Kg/d

They will need hospital visits every 3 months for the first 6 months, then every 6 months thereafter.

This study is available locally at Penn Sate Hershey Medical Center – parents or physicians of interested patients should contact Beth Stephens at 717-531 0003 extension 283395 or by email for more information.

Monmouth Stroke Service Success Story: Great outcome after emergent carotid endartercomy

Case presentation prepared by Drs N. Nachimuthu and M Chan, Residents, Dept of Internal Medicine, Monmouth Medical Center

Introduction:

When feasible, administration of tissue plasminogen activator (tPA) is the standard of care for treatment of acute ischemic stroke to improve outcomes. Treated patents may be found on subsequent work up to have significant stenosis of one or both carotid arteries. Carotid endarterectomy (CEA) has been shown to be more effective than medical therapy for preventing subsequent strokes in patients with symptomatic stenosis. However, the timing of CEA after ischemic stroke with or without administration of tPA remains controversial, particularly in patients with critical stenosis or unstable symptoms.

To better illustrate this dilemma, we present the case of a 43 year old male who presented with symptoms of acute stroke, was given tPA within the recommended time frame, but was subsequently found to have high grade carotid stenosis and fluctuating symptoms. We follow with a review and discussion of recent literature showing that in select cases, CEA can be done early with no increase in perioperative complications or adverse events.

Case report:

A 43 year old man presented to our Emergency Room after he was found to be restless in bed by his wife at 12:30am on the day of admission. He was also unable to express himself and was noted to have had a right sided facial droop. He was last observed to be asymptomatic 1 hour and 45 mins earlier when he was getting ready for bed at 10:45pm.

The patient arrived at the ER at 1:15am and a code stroke was immediately called. Initial examination revealed aphasia, disorientation, and right-sided facial droop, with a NIH stroke score of 5. There was no motor weakness and the rest of the neurologic exam was unremarkable. Vital signs were stable and within normal limits. A stat CT scan was done which did not show any hemorrhage or findings of ischemia:
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After the CT scan, the patient initially showed some improvement in speech and orientation with the NIH stroke score dropping to 2. It seemed that treatment with tPA might not be necessary.

However, at 2am the patient’s symptoms again worsened acutely. Repeat NIH stroke score was 6 at 1:50am. tPA was given at 2:10am, 3 hours and 25 mins from last known normal.

Following tPA administration, the patient seemed to be improving again and was admitted to the ICU for close observation. However, a few hours later, at 6am, the patient again worsened. He had new right sided weakness and worsening of his aphasia and right facial droop. Given the fluctuating course of the patient’s symptoms he underwent a repeat stat CT of the head to rule out a bleed. This was negative. A CT angiogram of the head and neck was done at the same time, and this showed severe stenosis (almost total occlusion) of the left internal carotid artery:

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At this point, our multidisciplinary stroke team suggested that he undergo emergent carotid endarterectomy to prevent further deterioration of his neurologic status. This was a controversial decision, but after discussing the risks and benefits of the procedure, the patient consented and a carotid endarterectomy was done urgently and completed at 12:05am on the second hospital day, or 21 hours and 55 mins from administration of tPA.

Intraoperatively, the patient was found to have left internal carotid artery narrowing secondary to hemorrhagic plaque and dissection:

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The patient experienced no intraoperative complications. Post-operatively, he was started on Lovenox at 1mg/kg every 12 hours. He did develop a hematoma on the site of the CEA, and Lovenox and antiplatelets were immediately stopped. Aspirin at 325mg daily was resumed after a day and Plavix 75mg daily was resumed the next day, after the hematoma had shown signs of resolution. The patient experienced no further complications.

He underwent a repeat CT scan after surgery, more than a day from symptom onset, which did show an evolving left hemispheric stroke:

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However, clinically, in the hours following CEA, his right sided weakness improved.

By the time the patient was discharged to a rehabilitation facility, he had only mild aphasia, a residual right facial droop, but no motor deficits.

Discussion:

Many vascular surgeons suggest waiting 6-8 weeks after acute stroke before considering CEA, because of fear or bleeding or extension of cerebral infarction during the surgery. However, this delay can lead to recurrent stroke or complete occlusion of the carotid artery.  Moreover, more recent studies have shown that urgent early CEA can be performed on patients with evolving symptoms without additional risks.

We feel that our patient’s near complete recovery was the direct result of early CEA, done despite the recent stroke and potential hemorrhagic complications associated with the use of tPA.

These types of complicated medical decisions can only be made after discussion between neurologists, intensivists and vascular surgeons in a multidisciplinary stroke center.

Click here to find out more about Monmouth’s Certified Stroke Center.

A less invasive surgical treatment for spinal stenosis?

…..The jury is still out!….

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First, the problem:

Lumbar spinal stenosis is an abnormal narrowing (stenosis) of the spinal canal that can lead to compression of the cauda equina, resulting in pain, numbness, and weakness in the legs.

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Affected patients complain of back pain, leg pain and weakness, worse with prolonged standing and walking, better with sitting or flexing the spin forward (such as pushing a supermarket trolley).

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Next, the solution(s):

This stenosis (or narrowing) is caused by degenerative bone spurs, disc disease and ligamental hypetrophy.  While many patients try conservative measures including physical therapy and epidural injections, spinal stenosis is a mechanical problem, and usually necessitates a mechanical (surgical) solution to alleviate symptoms.  Consider the analogy of a blocked sewer pipe – you can try pouring chemicals down the sink, but ultimately you know you are going to need to call a plumber  (Rota-Rooter)!

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Traditional surgical management calls for a lumbar laminectomy to decompress the spinal canal and alleviate symptoms.

In some cases,  laminectomy can leave the spine unstable necessitating a spinal fusion using bone garft, rods and screws (“hardware”) done at the same time, and this major surgery can lead to an extended recovery period of months to a year.

Implantation of a interspinous spacer has been proposed as a less-invasive alternative surgical option than spinal fusion:

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Which is better?

A recent study compared the outcomes of these techniques in 99,000 Medicare patients who underwent surgery for spinal stenosis from 2006 to 2009.

6,000 patients who underwent implantation of new interspinous spacers were compared with 76,000 who underwent laminectomy, and 17,000 patients who underwent laminectomy with spinal fusion.

The results showed that patients treated with spacers had the lowest rate of major medical complications: 1.2%, compared to 1.8%with laminectomy and 3.3% with spinal fusion. Patients receiving spacers also spent less time in the hospital: average 1.4 days versus 2.7 days in the decompression group.

However, patients receiving spacers had the highest rate of revision surgery – about 17% of patients receiving spacers needed a second operation on the lumbar spine, compared to only 8.5%  in the laminectomy group and about 10% in the fusion group.

Patients receiving spacers tended to be older and to have other medical problems. With adjustment for these and other factors, patients in the spacer group were more than twice as likely to require repeat surgery.

Hospital payments for spacer surgery were greater for decompression alone, but less than for fusion procedures

Other than the need for repeat surgery (presumably because initial surgery was ineffective), the study did not look at pain control or functional outcome between the groups.  More data is needed.

Nevertheless, so far it looks as if the higher cost and higher re-operation rate with spacers may argue in favor of conventional decompression surgery, except in higher risk older patients with medical problems.