Stroke Article Compendium

This exclusive JEMS stroke article compendium presents a concise summary of information presented throughout six articles designed for education and reference about devastating and unusual strokes; their prehospital assessment and declarations; stroke resuscitation and care.

The articles also include first-hand accounts of amazing stroke recovery by JEMS Editor Emeritus A.J. Heightman, and Anne Mullally, Stryker’s Vice President and General Manager for Emergency Care.

Table of Contents

Article 1: Nashville EMS Crew Alertly Activates Stroke System, By Jimmy Closser, BSN, RN, CEN, AEMT

Article 2: Forgotten Stokes: Vertebral Artery Dissections & Occlusions, By A.J. Heightman, MPA, EMT-P

Article 3: Vanderbilt’s Quick Response Key After Chiropractic-Related Stroke, By A.J. Heightman, MPA, EMT-P

Article 4: Out-of-Body Experience: JEMS Editor-Emeritus Survives Ventricular Arterial Occlusion, By A.J. Heightman, MPA, EMT-P

Article 5: EMS Industry Leader’s Story: Surviving Two Vertebral Artery Dissections, By Anne Mullally

Article 6: Technology and Apps Improve the Stroke Treatment Processes: How a Stroke Center Combined Advanced Cerebrovascular Imaging Software and a Secure Mobile Communication Platform to Enhance Processes for Stroke Treatment, By A.J. Heightman, MPA, EMT-P

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Nashville EMS Crew Alertly Activates Stroke System

By Jimmy Closser, BSN, RN, CEN, AEMT

Thirty-year-old Dean Meyers was serving food to the homeless at a Nashville, Tennessee, homeless shelter when he began to complain about not feeling well. A friend then called 911.

Medic 18 responded to what was dispatched as a 30-year-old male “sick person.” 

The ambulance arrived nine minutes after the 911 dispatch center received the initial call. “Fast 2″ (An NFD Fast Response Vehicle that responds to “Hot” calls) arrived on scene with Medic 18. Fast 2 is a call sign for a vehicle that fire department EMT/paramedics use to respond to medical calls to save valuable time instead of a larger engine company.

Medic 18 paramedic James Gupton made first patient contact. Gupton didn’t realize it at the time, but Dean Meyers wasn’t the average “sick person”/medical call so commonly received and managed by Nashville EMS crews. 

Dean was experiencing nausea and vomiting, slurred speech and ataxia that became more apparent on further examination.

First responders had established IV access and paramedic Gupton felt the patient, despite his young age, had possibly suffered a stroke, so he and his partner Casey Barnes rapidly packaged Meyers, called in a stroke alert via 800 mhz radio transmissionand transported him to Vanderbilt University Medical Center. 

During transport, he was noted to be hypertensive, but otherwise stable. A 12-lead ECG was obtained and transmitted electronically while en route.  

Report was given, and a Stroke Alert was called prior to the ambulance’s arrival.

Upon arrival at Vanderbilt’s emergency department, Dean was taken directly to the CT Scanner per Vanderbilt protocol. A scan was immediately performed showing no intracranial hemorrhage. Therefore, Alteplase was administered per American Heart Association guidelines just 61 minutes from the patient’s last known well time.

While TPA was infusing, a CTA of the head and neck with perfusion was performed and a Basilar Artery Occlusion was found at its Apex. (See Figure 1).  

The scan showed Dean was actively having a stroke during this CT scan time window.

Rohan Chitale, MD, a neurosurgeon at Vanderbilt University Medical Center, performed an endovascular intervention called mechanical thrombectomy to restore blood flow through the Basilar Artery shown in Figure 1.

Mechanical thrombectomy is a minimally invasive procedure in which specialized equipment is utilized to remove a clot from a patient’s artery. A stent retriever is then pushed through the clot. After the stent retriever is through, it expands to the size of the artery wall.

Within 13 minutes of the procedure performance, Dr. Chitale and his team restored blood flow to the artery. Dean immediately began feeling better (See Figure 2).

Discussion

Ischemic stroke accounts for 87% of CVAs.¹

Of these, approximately 20% are the result of vertebrobasilar artery occlusion (VBAO).^2—5 The mortality of VBAO can reach 80—95% without successful treatment (See Figure 3).^{3, 6—8}

This stroke diagnosis (Basilar Artery Occlusion) typically has a greater than 90 percent mortality rate. Neurologists normally see severe changes in examination with this diagnosis. 

As one of the most commonly missed strokes, a basilar occlusion is often hard to recognize. Patients usually appear to be seizing and become unresponsive or they have extreme, fluctuating symptoms. It is common for the work-up in emergency departments to be seizure related, and often head and neck CTA’s are not initially performed.

Altered mental status is a common presenting complaint in the emergency department. Cerebrovascular accidents (CVAs) are one of the most serious etiologies for altered mental status.

Medic 18’s on scene assessment and report of a suspected stroke was therefore critical to Meyer’s placement into the stroke protocol and procedures that saved his life.

When a Basilar Artery Occlusion goes unrecognized and the patient doesn’t wakeup, decerebrate posturing often occurs. CT scans are then ordered.

The brainstem and the midbrain are called “high real estate areas.” This territory is very sensitive to lack of blood flow, even for short periods of time and almost immediately infarct or die. This why a quick and accurate diagnosis is critical.

As Stroke Coordinator at VUMC, I expected to see a very sick ICU patient when making morning rounds the morning after Dean’s admission and care. I was shocked to see Dean sitting in a lounge chair playing video games in his room as if nothing had happened to him. I thought I was in the wrong room. One of the most incredible pieces to this story is that there was zero stroke infarct around the midbrain/brainstem where we would expect to see it. 

Dean’s doctors were also amazed at the finding in the field. As Closser researched the patient history and prehospital care, I realized that Meyers was saved due to the in-depth assessment and suspicion of stroke by Medic 18’s crew.

Conclusion

Acute basilar artery occlusion has a very high mortality rate. As few as 3-to-5 percent of people with basilar artery occlusion make a full neurological recovery in the absence of interventions to achieve recanalisation or reperfusion.¹²

Annual stroke rates for patients with symptomatic intracranial vertebral and basilar artery stenosis are 8% and 11%, respectively.¹³

Recognition of stroke is sometimes difficult to differentiate from the various causes of mimics. Determining the “last known well” of a patient and comparing it to the onset of the patient’s symptoms can often be difficult for EMS providers to determine accurately. 

The Medic 18 crew on scene recognized that this change in Dean Meyers’ mental status happened abruptly at 7 p.m., and shortly before they were dispatched. This was crucial information for Vanderbilt Stroke Team physicians to better ascertain a probably differential in care diagnosis.

We sometimes cannot determine the exact known onset of the stroke yet confirming the last witnessed “last known well time” is so vitally important. The care in the hospital is completely dictated on this key bit of information. Sometimes spending that extra 60 seconds obtaining a family contact phone number and onset of symptoms will be the determining factor if treatment is delivered expeditiously.

References

1. American Heart Association Heart Disease and Stroke Statistics Writing Group Heart disease and stroke statistics — 2010 update: A report from the American Heart Association. Circulation. 2010;121:e46—e215. [PubMed] [Google Scholar].

2. Baird TA, Muir KW, Bone I. Basilar artery occlusion. Neurocritical care. 2004;3:319—30. [PubMed] [Google Scholar].

3. Savitz SI, Caplan LR. Vetebrobasilar disease. N Engl J Med. 2005;352:2618—26. [PubMed] [Google Scholar].

4. Bogousslavsky J, Van Melle G, Regli F: The Lausanne stroke registry: analysis of 1,000 consecutive patients with first stroke. Stroke. 1988;19:1083—92. [PubMed] [Google Scholar].

5. Vemmos K, Takis C, Georgilis K, et al. The Athens stroke registry: results of a five-year hospital-based study. Cerebrovasc Dis. 2000;10:133—42. [PubMed] [Google Scholar].

6. Brandt T, von Kummer R, Muller-Kuppers M, et al. Thrombolytic therapy of acute basilar artery occlusion: variables affecting recanalization and outcome. Stroke. 1996;27:875—81. [PubMed] [Google Scholar].

7. Lindsberg PJ, Soinne L, Roine RO, et al. Options for recanalization therapy in basilar artery occlusion. Stroke. 2005;36:203—4. [PubMed] [Google Scholar].

8. Lindsberg PJ, Mattle HP. Therapy of basilar artery occlusion: a systematic analysis comparing intra-arterial and intravenous thrombolysis. Stroke. 2006;37:922—8. [PubMed] [Google Scholar]

9. Pirau L, Lui F; Vertebrobasilar Insufficiency. StatPearls Publishing 2019.

10. Vertebrobasilar Occlusion and Vertebral Artery Syndrome. https://patient.info/doctor/vertebrobasilar-occlusion-and-vertebral-artery-syndrome.

11. Gur AY, Lampl Y, Gross B, et al; A new scale for assessing patients with vertebrobasilar stroke-the Israeli Vertebrobasilar Stroke Scale (IVBSS): Inter-rater reliability and concurrent validity. Clin Neurol Neurosurg. 2007 Jan 23.

12. Park KW. Park JS, Hwang SC, Im SB, Shin WH, Kim BT: Vertebral Artery Dissection: Natural History, Clinical Features and Therapeutic Considerations. J Korean Neurosurg Soc. 2008 Sep; 44(3): 109—115. www.ncbi.nlm.nih.gov/pmc/articles/PMC2588305/.

13. Thanvi B, Munshi SK, Dawson SL, Robinson TG. Carotid and vertebral artery dissection syndromes. Postgrad Med J. 2005;81:383—388. [PMC free article] [PubMed] [Google Scholar].

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Forgotten Stokes: Vertebral Artery Dissections & Occlusions

By A.J. Heightman, MPA, EMT-P

Paramedics are rarely taught about Vertebral Artery Occlusions (VAO) and Vertebral Artery Dissections (VAD), but they occur rather frequently. These include occlusions and dissections of the vertebra arteries that feed into the basilar artery. It is reported that 25% of lesions causing strokes occur in the vertebrobasilar circulation.¹

The vertebral arteries branch off the subclavian arteries, passing toward the head or anterior end of the body through the costotransverse foramina of the sixth to second cervical vertebrae.

They enter the skull through the foramen magnum, merging at the pontomedullary junction to form the basilar artery which divides into two posterior cerebral arteries at the upper pons.

At the base of the brain, the carotid and basilar systems join to form the circle of Willis. This arrangement of collateral circulation may allow adequate brain perfusion even with occlusion of a main vessel.²

Atherosclerosis, the most common vascular disease affecting the vertebrobasilar system, affects large vessels, causing narrowing and occlusion. It can affect just one vertebral artery. It needs to produce stenosis at the origins of both vertebral arteries to cause vertebrobasilar ischaemia. But, even with vertebral artery occlusion, collaterals (the circle of Willis) may prevent ischaemia.¹

Death or major disability is the result of occlusion of large vessels in the vertebrobasilar system. However, many lesions arise in smaller vessels with a wide variety of focal neurological deficits. Stroke scoring systems to evaluate patients have been developed but are of limited use for vertebrobasilar stroke.³

Vertebral Artery Dissections

When a tear occurs in one of the major cervicocerebral arteries and allows blood to enter the wall of the artery and split its layers, the result is either stenosis or aneurysmal dilatation of the vessel. Vertebral artery dissection (VAD) is an infrequent occurrence but is a leading cause of stroke in young and otherwise healthy patients.⁴

The term dissection implies a tear in the wall of a major artery leading to the intrusion of blood within the layers of an arterial wall (intramural hematoma). This causes stenosis of the lumen when blood collects between the intima and media or an aneurysmal dilatation of the artery when the hematoma predominantly involves the media and adventitia.⁵

VAD was long thought to be a rare cause of stroke, particularly in the absence of trauma, and the diagnosis was usually not made until the postmortem examination.^6-7 This changed in the late 1970s when studies led to the recognition of the clinical and radiologic features of dissection syndromes facilitating their antemortem diagnosis.⁶

The overall incidence of VAD is approximately 1-1.5 per 100,000.⁸ Spontaneous dissections of the carotid and vertebral artery account for only about two percent of all ischemic strokes^9-11, but they are an important cause of ischemic stroke in young and middle-aged patients and account for 10 to 25 percent of such cases.

Spontaneous dissections of the vertebral arteries affect all age groups, including children, but there is a distinct peak in the fifth decade of life. ^9,11-12

Although there is no overall sex-based predilection, women are on average about five years younger than men at the time of the dissection.¹¹

A tear in the wall of an artery leads to a collection of blood between the layers of the artery, leading to formation of an intramural hematoma. However, there is no universal agreement as to which wall is the primary site of dissection.

Some authorities consider a rupture within the connective tissue and vasa vasorum of the media as the most probable initial event in dissection. The intramural hematoma may then later penetrate the intima and reconnect with the true arterial lumen. Others think that an intimal tear occurs, which allows blood under arterial pressure to enter the wall of the artery.⁷

Patients with a spontaneous dissection of the vertebral artery are thought to have an underlying structural defect of the arterial wall, although the exact type of arteriopathy remains elusive in most cases.⁷

Environmental Factors

Patients with a spontaneous VAD frequently have a history of a minor precipitating event.^6-7 Some precipitating events associated with hyperextension or rotation of the neck include practicing yoga, painting a ceiling, coughing, vomiting, sneezing, the receipt of anesthesia and the act of resuscitation.¹¹ These neck movements, particularly when they are sudden, may injure the artery as a result of mechanical stretching.

Chiropractic manipulation of the neck has been associated with both VAO and VAD.¹³ It has been estimated that as many as one in 20,000 spinal manipulations causes a stroke.²¹ (See related article: Quick Response Key After Chiropractic-Related Stroke).

A recent history of a respiratory tract infection can also be a risk factor for spontaneous VADs.¹³ The possibility of an infectious triggering VAD is supported by the finding of a seasonal variation in the incidence of spontaneous VADs, with a peak incidence in the fall.¹³

Spontaneous VAD is mainly divided into two types : 1) the ischemic type, which is manifest by ischemic symptoms and/or infarction of the vertebrobasilar circulation due to arterial narrowing and thromboembolism; and 2) the hemorrhagic type, which presents as a subarachnoid hemorrhage (SAH) caused by rupture of an intradural vertebral artery dissecting aneurysm.⁴

Extracranial VADs

Neck trauma may precede an extracranial VAD. The vertebral artery is very mobile and vulnerable to mechanical injury at C1 to C2 as it leaves the transverse foramen of the axis vertebra and suddenly turns to enter the intracranial cavity.⁴

Clinical manifestations include severe neck pain mostly in the occipitocervical area followed after a variable interval by ischemic symptoms.⁴

In some patients there may not be any ischemic symptoms. They may commonly present with dizziness, vertigo, double vision, ataxia and dysarthria.  

Occasionally, spinal cord infarctions occur because branches of the extracranial vertebral artery that supply the cervical spinal cord are involved.⁴

Intracranial VADs

More than 50% of intracranial VADs are associated with subarachnoid hemorrhage (SAH).⁵ Since Yonas et al.) described the pathological and radiographic features of intracranial dissecting aneurysm as a cause for SAH, it has been increasingly recognized as a cause of SAH with an unfavorable prognosis and a high rate of rebleeding.¹⁴

One-to-10% of all intracranial non-traumatic SAH are caused by ruptured intracranial dissection, and in children, the rate may be even higher.

The majority of hemorrhagic intracranial arterial dissection is located in the posterior circulation most likely reflecting its structure since histological studies have shown that the intradural vertebral artery has a thin media and adventitia with fewer elastic fibers, so dissections of the intradural vertebral artery are prone to result in SAH, in contrast to dissections of other vessels.^15-16

Brain stem infarctions and aneurysmal arteries presenting as space occupying lesions are other manifestations.

In the past, intracranial dissections were considered neurologically devastating or fatal, but modern technology has led to increased recognition that patients with intracranial dissections also may have only minor symptoms.¹⁷

Extracranial VADs generally carry a good prognosis. A literature review reports 50% of cases having no neurological deficit; 21% mild deficits only; and 25% moderate to severe deficits; the remaining 4% having died.⁵

Intracranial dissections are usually associated with severe neurological deficits or SAH and carry a poor prognosis.

The risk of a recurrent dissection in an initially unaffected artery is about two percent during the first month but then decreases to a rate of only about 1 percent per year.¹¹

However, the increased risk persists for at least a decade and possibly longer.³⁸ The risk of a recurrence is higher in young patients with a heritable arteriopathy.³⁶ Only rarely do dissections recur in the same artery.^9-11

Most VADs heal spontaneously.⁷ However, an urgent surgical intervention may be required in patients presenting with SAH.

Once again, good prehospital assessment and recognition of stroke systems and moving the patient rapidly through the stoke protocol can be lifesaving for VAD patients.

Vertebral Artery Occlusions

Ischemic stroke accounts for 87% of CVAs.^22-23 Of these, approximately 20% are the result of vertebrobasilar artery occlusion (VAO).^24-27 The mortality of VAO can reach 80 to 95% without successful treatment.^34,27-29

The clinical presentation of VAO varies with the area of ischemia and cause of occlusion. Vertebral Artery Occlusion results in proximal VBA territory ischemia.^33,35 Occlusion near the origin of the vertebral artery (extracranial) causes ischemia in the medulla and/or cerebellum and commonly presents as brief transient ischemic attacks (TIAs).^26,35

The most common initial symptoms reported include vertigo, dizziness, nausea, vomiting and head or neck pain are.^26—34

Other common signs and symptoms include weakness, hemiparesis, ataxia, diplopia, pupillary abnormalities, speech difficulties and altered mental status.^{25—26, 32, 34}

Approximately 20% of all strokes are the result of vertebrobasilar artery occlusion (VAO) which have a mortality rate of 80-95% without treatment.^22-30

Occlusion of an intracranial vertebral artery can cause ischemia in the lateral medulla resulting in Wallenburg Syndrome (decreased pain/temperature of the ipsilateral face and contralateral body, Horner’s syndrome, limb ataxia, hoarse voice, dysphagia).²⁶ Dizziness, diplopia and signs of lateral medullary or cerebellar ischemia may result from extension of or embolism from an extracranial vertebral artery dissection (VAD) into the intracranial vertebral artery.^26,36

Ischemia in the middle VBA territory is usually caused by occlusion of the basilar artery. This can cause pontine damage resulting in “Locked-In Syndrome” (quadriplegia, anarthria, preserved consciousness).^35,37

Distal basilar artery occlusion is most commonly embolic, usually from cardiac or vertebral artery sources, and results in ischemia of the rostral midbrain and thalamus.^33-35 This presents with the characteristic “top-of-the-basilar syndrome” (coma, midbrain ocular-motor signs — small poorly reactive pupils and defective vertical gaze, hemiparesis, hemiataxia).^26-27,31

Symptoms associated with vertebral artery occlusive disease include dizziness; vertigo; diplopia; perioral numbness; blurred vision; tinnitus (a condition in which a consistent noise is heard in the ear in the absence of an external source of sound); ataxia; bilateral sensory deficits and syncope.³⁸

It is important to note that each of these can be caused by other disease entities, including cardiac arrhythmias, orthostatic hypotension, and vestibular disorders.³⁹

• Prevent aspiration pneumonitis.
• Control of body temperature.
• Control of blood glucose.
• Treatment to maintain cerebral blood flow (Managing blood pressure)
• Over-enthusiastic treatment of hypertension should be avoided.
• Treat hypertension, if a hypertensive emergency exists, with one or more of these concomitant medical issues:

1. Hypertensive encephalopathy.
2. Hypertensive nephropathy.
3. Hypertensive cardiac failure/myocardial infarction.
4. Aortic dissection.
5. Pre-eclampsia/eclampsia.⁴⁰

Treatment for hypotension:

1. Intravenous fluids to maintain intravascular volume with isotonic fluids.
2. Inotropes or vasopressors may be required.

Treatment for respiratory complications:

1. Assess respiratory drive, gag reflex, cough reflex (to expel secretions).
2. Consider endotracheal intubation (Glasgow Coma Scale less than eight).
3. Sedation and muscle relaxation may be needed if agitated or resisting mechanical ventilation, but these will have to be reversed before a full neurological assessment can be carried out.

The neurological deficit of a Vertebral Artery Occlusion can be further complicated by:

• Pneumonia (particularly aspiration pneumonia).
• Deep vein thrombosis and pulmonary embolism.
• Myocardial infarction.

Prognosis for VAOs

This depends on the extent of disease; however:

• Acute basilar artery occlusion has a very high mortality rate.
• As few as 2-5% of people with basilar artery occlusion make a full neurological recovery in the absence of interventions to achieve recanalization or reperfusion.⁴⁰
• Annual stroke rates for patients with symptomatic intracranial vertebral and basilar artery stenosis are 8% and 11% respectively.³⁹

Patient History is Important

Patient history is important in the recognition of vertebral occlusions and dissections. The onset and duration of symptoms may vary with aetiology.¹

Basilar artery thrombosis may be preceded by transient ischemic attacks (TIAs) for days or weeks prior to occlusion (seen in half of patients who experience a vertebrobasilar stroke).

Embolic events cause sudden and dramatic symptoms without prodrome.

They may (rarely) be brought on by turning the head (temporarily occluding one vertebral artery, with insufficient collaterals due to advancing atherosclerosis).¹

Some occlusions have been reported after a patient has their neck manipulated at a chiropractor or even in the wash tub at a beauty parlor (AKA “Beauty Parlor Stroke”).^13-21 (See related sidebar article: Quick Response Key After Chiropractic-Related Stroke).

Symptoms reported with vertebrobasilar strokes include:¹

• Vertigo is common and may be the only symptom.
• Nausea, vomiting or non-productive “heaving” may occur.
• Disturbance of consciousness.
• Headache (often describe as sudden and extremely painful).
• Visual disturbance (oculomotor signs such as nystagmus, diplopia and pupillary changes).
• Visual field defects.
• Speech disturbance (for example, dysarthria and dysphonia).
• Sensory changes in the face and scalp.
• Ataxia.
• Contralateral motor weakness (may cause a “drop attack”).
• Sensory disturbance affecting pain and temperature.
• Incontinence.

There may also be a history of associated risk factors.

Things to Look for During Prehospital Examination

• Abnormal level of consciousness.
• Hemiparesis or quadriparesis (usually asymmetrical).
• Bulbar manifestations (facial weakness, dysphagia, dysarthria, dysphonia).
• Pupillary and oculomotor abnormalities.
• Tremor, ataxia and mild hemiparesis.
• Horizontal gaze palsy.
• Ataxia (ipsilateral).
• Tongue, soft palate, vocal cord, sternocleidomastoid paralysis (ipsilateral).
• Tachycardia and dyspnea (cranial nerve X).
• Palatal myoclonus (involuntary jerking of the soft palate, pharyngeal muscles and diaphragm).
• Causes ipsilateral tongue paresis with deviation to the side of the lesion.
• Contralateral hemiplegia with facial sparing.

General Treatments Measures¹

• Prevent aspiration pneumonitis.
• Control of body temperature.
• Treatment to maintain cerebral blood flow (Managing blood pressure) But over-enthusiastic treatment of hypertension should be avoided.
• In patients considered for intravenous thrombolysis, blood pressure reduction to 185/110 mm Hg or lower should be considered.¹⁸
• Treat hypotension (IV fluids to maintain intravascular volume with isotonic fluids; Inotropes or vasopressors may be required).
• Treatment respiratory complications (Assess respiratory drive, gag reflex, cough reflex (to expel secretions).
• Consider endotracheal intubation (Glasgow Coma Scale less than 8).
• Sedation and muscle relaxation may be needed if agitated or resisting mechanical ventilation – but these will have to be reversed before a full neurological assessment can be carried out.

Possible Complications¹

The neurological deficit can be further complicated by:

• Pneumonia (particularly aspiration pneumonia).
• Deep vein thrombosis and pulmonary embolism.
• Myocardial infarction.

Prognosis

• Acute basilar artery occlusion has a very high mortality rate.
• As few as 2-5% of people with basilar artery occlusion make a full neurological recovery in the absence of interventions to achieve recanalization or reperfusion.¹⁹
• Annual stroke rates for patients with symptomatic intracranial vertebral and basilar artery stenosis are 8% and 11%, respectively.²⁰
• Certain syndromes may have a good prognosis in terms of long-term functional outcome but still carry a risk of death in the acute phase from, for example, aspiration pneumonia in the lateral medullary syndrome. One study suggested that basilar artery diameter >4.3 mm could be a marker for high risk of fatal stroke.²¹

Conclusion

Vertebral Artery Occlusions (VAO) and Vertebral Artery Dissections (VAD) of the vertebra arteries that feed into the basilar artery occur frequently with 25% of lesions causing strokes that occur in the vertebrobasilar circulation.

The vertebral arteries branch off the subclavian arteries, passing toward the head or anterior end of the body through the costotransverse foramina of the sixth to second cervical vertebrae.

Death or major disability can result from occlusion of large vessels in the vertebrobasilar system. However, many lesions arise in smaller vessels with a wide variety of focal neurological deficits.

The circle of Willis is at the base of the brain, where the carotid and basilar systems join. It’s important for EMS responders to realize that this arrangement of collateral circulation may allow adequate brain perfusion even with occlusion of a main vessel.²

Atherosclerosis affects large vessels, causing narrowing and occlusion and can affect just one vertebral artery. It needs to produce stenosis at the origins of both vertebral arteries to cause vertebrobasilar ischaemia. But, even with vertebral artery occlusion, collaterals (the circle of Willis) may prevent ischaemia.¹

Approximately 20% of all strokes are the result of vertebrobasilar artery occlusion (VAO) which have a mortality rate of 80-95% without treatment.^22-30

A Vertebral Artery Dissection (VAD) is a tear in the wall of a major artery leading to the intrusion of blood within the layers of an arterial wall (intramural hematoma).

Spontaneous dissections of the vertebral arteries affect all age groups, including children, but there is a distinct peak in the fifth decade of life.

Some precipitating events associated with hyperextension or rotation of the neck include practicing yoga, painting a ceiling, coughing, vomiting, sneezing, the receipt of anesthesia and the act of resuscitation.¹¹ These neck movements, particularly when they are sudden, may injure the artery as a result of mechanical stretching.

Chiropractic manipulation of the neck has been associated with both VAO and VAD.¹³ It has been estimated that as many as 1 in 20,000 spinal manipulations causes a stroke.²¹

EMS personnel must be aware of these conditions and assess, treat and transport patients in these categories as they would with other strokes.

References

1. Pirau L, Lui F; Vertebrobasilar Insufficiency. StatPearls Publishing 2019.

2. Vertebrobasilar Occlusion and Vertebral Artery Syndrome. https://patient.info/doctor/vertebrobasilar-occlusion-and-vertebral-artery-syndrome.

3. Gur AY, Lampl Y, Gross B, et al; A new scale for assessing patients with vertebrobasilar stroke-the Israeli Vertebrobasilar Stroke Scale (IVBSS): Inter-rater reliability and concurrent validity. Clin Neurol Neurosurg. 2007 Jan 23.

4. Park KW. Park JS, Hwang SC, Im SB, Shin WH, Kim BT: Vertebral Artery Dissection: Natural History, Clinical Features and Therapeutic Considerations. J Korean Neurosurg Soc. 2008 Sep; 44(3): 109—115. www.ncbi.nlm.nih.gov/pmc/articles/PMC2588305/.

5. Thanvi B, Munshi SK, Dawson SL, Robinson TG. Carotid and vertebral artery dissection syndromes. Postgrad Med J. 2005;81:383—388.

6. Fisher CM, Ojemann RG, Roberson GH. Spontaneous dissection of cervico-cerebral arteries. Can J Neurol Sci. 1978;5:9—19.

7. Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med. 2001;344:898—906.

8. Bogousslavsky J, Regli F. Ischemic stroke in adults younger than 30 years of age. Cause and prognosis. Arch Neurol. 1987;44:479—482.

9. Bassetti C, Carruzzo A, Sturzenegger M, Tuncdogan E. Recurrence of cervical artery dissection. A prospective study of 81 patients. Stroke. 1996;27:1804—1807.

10. Giroud M, Fayolle H, Andre N, Dumas R, Becker F, Martin D, et al. Incidence of internal carotid artery dissection in the community of Dijon. J Neurol Neurosurg Psychiatry. 1994;57:1443.

11. Schievink WI, Mokri B, O’Fallon WM. Recurrent spontaneous cervical-artery dissection. N Engl J Med. 1994;330:393—397.

12. Schievink WI, Mokri B, Piepgras DG. Spontaneous dissections of cervicocephalic arteries in childhood and adolescence. Neurology. 1994;44:1607—1612.

13. Hufnagel A, Hammers A, Schonle PW, Bohm KD, Leonhardt G. Stroke following chiropractic manipulation of the cervical spine. J Neurol. 1999;246:683—688.

14. Yonas H, Agamanolis D, Takaoka Y, White RJ. Dissecting intracranial aneurysms. Surg Neurol. 1977;8:407—415.

15. Sasaki O, Ogawa H, Koike T, Koizumi T, Tanaka R. A clinicopathological study of dissecting aneurysms of the intracranial vertebral artery. J Neurosurg. 1991;75:874—882.

16. Anxionnat R, de Melo Neto JF, Bracard S, Lacour JC, Pinelli C, Civit T, et al. Treatment of hemorrhagic intracranial dissections. Neurosurgery. 2003;53:289—300. discussion 300-301.

17. Caplan LR, Biousse V. Cervicocranial arterial dissections. J Neuroophthalmol. 2004;24:299—305.

18. Stroke and transient ischaemic attack in over 16s: diagnosis and initial management; NICE Guidance (May 2019).

19. Brott TG, Halperin JL, Abbara S, et al; 2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease.

20. Pico F, Labreuche J, Gourfinkel-An I, et al; Basilar artery diameter and 5-year mortality in patients with stroke. Stroke. 2006 Sep37(9):2342-7. Epub 2006 Aug 3.

21. https://news.vumc.org/2016/12/01/quick-response-key-after-chiropractic-related-stroke/:Quick Response Key After Chiropractic-Related Stroke

22. American Heart Association Heart Disease and Stroke Statistics Writing Group Heart disease and stroke statistics — 2010 update: A report from the American Heart Association. Circulation. 2010;121:e46—e215.

23. www.ncbi.nlm.nih.gov/pmc/articles/PMC3099615/.

24. Baird TA, Muir KW, Bone I. Basilar artery occlusion. Neurocritical care. 2004;3:319—30.

25. Savitz SI, Caplan LR. Vetebrobasilar disease. N Engl J Med. 2005;352:2618—26.

26. Bogousslavsky J, Van Melle G, Regli F. The Lausanne stroke registry: analysis of 1,000 consecutive patients with first stroke. Stroke. 1988;19:1083—92.

27. Vemmos K, Takis C, Georgilis K, et al. The Athens stroke registry: results of a five-year hospital-based study. Cerebrovasc Dis. 2000;10:133—42.

28. Brandt T, von Kummer R, Muller-Kuppers M, et al. Thrombolytic therapy of acute basilar artery occlusion: variables affecting recanalization and outcome. Stroke. 1996;27:875—81.

29. Lindsberg PJ, Soinne L, Roine RO, et al. Options for recanalization therapy in basilar artery occlusion. Stroke. 2005;36:203—4.

30. Lindsberg PJ, Mattle HP. Therapy of basilar artery occlusion: a systematic analysis comparing intra-arterial and intravenous thrombolysis. Stroke. 2006;37:922—8. [PubMed] [Google Scholar]7. Lindsberg PJ, Soinne L, Roine RO, et al. Options for recanalization therapy in basilar artery occlusion. Stroke. 2005;36:203—4. [PubMed] [Google Scholar]8. Lindsberg PJ, Mattle HP. Therapy of basilar artery occlusion: a systematic analysis comparing intra-arterial and intravenous thrombolysis. Stroke. 2006;37:922—8.

31. Brandt T. Diagnosis and thrombolytic therapy of acute basilar artery occlusion: a review. Clinical and Experimental Hypertension. 2002;24:611—22.

32. Ferbert A, Bruckmann H, Drummen R. Clinical features of proven basilar artery occlusion. Stroke. 1990;21:1135—42.

33. Voetsch B, DeWitt LD, Pessin MS, et al. Basilar artery occlusive disease in the new England medical center posterior circulation registry. Arch Neurol. 2004;61:496—504.

34. von Campe G, Regli F, Bogousslavsky J. Heralding manifestations of basilar artery occlusion with lethal or severe stroke. J Neruol Neurosurge Psychiatry. 2003;74:1621—6.

35. Caplan LR, Chung C-S, Wityk RJ, et al. New England medical center posterior circulation stroke registry: I. Methods, data base, distribution of brain lesions, stroke mechanisms, and outcomes. J Clin Neruol. 2005;1:14—30.

36. 3614. Wityk R, Chang H, Rosengart A, et al. Proximal extracranial vertebral artery disease in the New England medical center posterior circulation registry. Arch Neruol. 1998;55:470—8

37. Virgile RS. Locked-in syndrome: case and literature review. Clin Neurol Neurosurg. 1984;86:275—9.

38. https://patient.info/doctor/vertebrobasilar-occlusion-and-vertebral-artery-syndrome.

39. Brott TG, Halperin JL, Abbara S, et al; 2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease.

40. Stroke and transient ischaemic attack in over 16s: diagnosis and initial management; NICE Guidance (May 2019).

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Vanderbilt’s Quick Response Key After Chiropractic-Related Stroke

By A.J. Heightman, MPA, EMT-P

In December of 2016, Ashley Johnson suffered the same type of stroke that killed model and social media star Katie May earlier in the year after a chiropractic neck manipulation. The 29-year-old Johnson survived, however, because of quick recognition and rapid Stroke Team response.¹

The chiropractor’s office, where Johnson had been going for pain management treatments, dialed 911 when she reported being dizzy and having double vision. Spring Hill EMS responded and had her airlifted to Vanderbilt University Medical Center (VUMC) where a team, including neurosurgeons, was on standby awaiting the helicopter’s arrival. The stroke team administered tPA to dissolve her blood clot before it could do permanent brain damage.

Lisa Hermann, MD, the Vanderbilt neurologist who treated her, reported that the stroke had resulted from a vertebral artery dissection after a neck manipulation. The exact incidence of the potentially deadly complication from the chiropractic procedure is unknown and estimates vary.

Ashley, a Columbia, Tennessee, resident sought chiropractic treatments to avoid having to take pain medications and said she never considered the possibility of a stroke from neck manipulation. The symptoms from a vertebral artery dissection started immediately after the neck manipulation.

She suffered her stroke Oct. 26, a week after news broke that the Los Angeles County Medical Examiner’s office had ruled that social media star Katie May’s Feb. 4 death was due to a stroke caused by a chiropractic neck manipulation. May was just 34.

Kiersten Espaillat, DNP, then stroke coordinator for the Vanderbilt Stroke Center, said vertebral arterial dissection strokes like Johnson and May suffered can be missed in younger people, delaying medical interventions that can save lives and prevent permanent brain damage.

“I guess the difference between me and the social media celebrity, is that she went home,” Johnson said. She didn’t seek medical help. There is no way that I could have gotten to the car to drive home.”

Ashley was back at home in a couple of days with her 3-year-old son. Before leaving Vanderbilt, she said, “Everybody from A to Z helped save my life,” and specifically thanked the EMS responders for making the decision to have her airlifted to VUMC.

Reference

1. news.vumc.org/2016/12/01/quick-response-key-after-chiropractic-related-stroke/:Quick Response Key After Chiropractic-Related Stroke

About the VUMC Stroke System

Treating over two thousand patients with stroke annually, Vanderbilt University Medical Center is a Joint Commission Comprehensive Stroke Center, the highest certification level given.

The Vanderbilt Stroke Center rapid response for treating stroke patients has received the American Stroke Association’s Honor Roll-Elite Plus recognition. This designation is given in recognition for performance beyond the requirements for the American Stroke Association’s Gold Plus Quality Achievement Award.

Mechanical thrombectomy is just one of the many acute neuro interventional procedures offered at VUMC. Awarded top honors by the American Heart Association for quality and timeliness, VUMC is a proud participant in Get with the Guidelines winning Elite Plus and Gold Plus recognition.

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Out-of-Body Experience: JEMS Editor Emeritus Survives Ventricular Arterial Occlusion

By A.J. Heightman, MPA, EMT-P

It was May 16th. I flew home on a long, late flight from Pennsylvania to San Diego after a busy week of lectures and article interviews. I was tired; but felt fine except for a stiff neck that nagged me for weeks. I had gone to my chiropractor for neck adjustment and electrical stimulation to relax my tight muscles before I travelled.

A week before flying to Pennsylvania, while waiting in my car for my wife as she shopped in a nearby store, I turned my head to the right, and it felt like it locked in place. Simultaneously, I felt a sharp pain like I had never felt before in the back of my neck.

Then, in an instant, the pain went away, and I could again move my neck freely. It was so startling to me that I told my wife about it when she got back in the care. Her response was, ” You better go to the doctor to have that checked.”

My response was, “I will after I get back from Pennsylvania.”

Back to May 16th

My son Steve, daughter-in-law Jessica, and our granddaughters Harper, 4, and Zoey, 6 months, were in town for a funeral in Jess’ family.

I was anxious to see them. Our granddaughters were in bed when I got home so I enjoyed a few drinks with the gang.

It was almost midnight. My son and daughter-in-law had just gone upstairs when I suddenly felt the worst headache I had ever experienced.

I told my wife, “I feel like someone just shot me in the head!”

I started to feel strange and began to become very diaphoretic. I knew something bad was happening and didn’t want my wife to see if happening, so I told her to go up to bed and I would be right up.

After she went upstairs, I tried to get out of my chair but had no feeling or control on my left side and fell to the floor.

I tried to get up, but just flopped further to my left on the floor. My wife heard me fall and came downstairs.

The rest of the evening was an out-of-body experience for me.

I couldn’t believe it; I was suffering a stroke.

“No, this can’t be happening to me. I know all about strokes and this is not the way I wanted to end up.”

I had lectured on strokes and thought I knew all the causes and treatment options.

• I knew stroke is the fifth-leading cause of death for Americans, killing 140,000 Americans each year – 1 out of every 20 deaths.
• Someone has a stroke every 40 seconds and, every 4 minutes, someone dies of stroke.
• Nearly 1 of 4 strokes happen to people who have had a previous stroke.
• About 87% of all strokes are ischemic strokes, in which blood flow to the brain is blocked by a clot. The other 13% can be puzzling occlusions and dissections.
• Stroke is a leading cause of serious long-term disability and reduces mobility in more than half of stroke survivors age 65 and over.
• Amazingly, in 2009, 34% of those hospitalized for stroke were under the age of 65.

It turns out, I luckily fell into that 13% of patients suffering puzzling vertebral artery occlusions and dissections.

My Vertebral Artery Occlusion

Mine turned out to be a Vertebral Artery Occlusion (VAO) with no clot found or removed. It was like a sudden clamp was placed on my vertebral artery. It was puzzling to me and my physicians and the hospital nursing staff.

I honestly had never heard or studied about the vertebral artery in paramedic training, let alone occlusions or dissections of them; but they occur rather frequently. I also didn’t know the two vertebral arteries traverse the vertebra into the basilar artery.  

Worse yet, I didn’t know that Basilar Artery Occlusions typically have a greater than 90 percent mortality rate.

Emergency Response Offers Teaching Moments

My son, trained as an EMT, called 911 and performed a stroke assessment on me. He was certain that I had suffered a stroke. It was frightening to him and terrifying to me, not only that it appeared I was suffering a stroke, but also I was having one in front of my family.

The fire department sent an ALS Engine and ALS ambulance to my house. As foggy as I was, I remember looking up as six firefighter paramedics entered the room — in turnout gear but no helmets.

I actually chuckled to myself because during my February lecture on professionalism at the JEMS‘ EMS Today Conference in Maryland, I told the audience that my father, a lifetime EMS provider in Scranton, Pennsylvania, remarked he thought it was inappropriate that firefighters responded to assist on medical calls, entered residences in bunker gear that had been soiled in fires, and were possibly coated with carcinogens.

Here I was, just three month later and I had six firefighters in my living room in soiled bunker gear. Go figure. It was a great teaching moment I did not know if I would ever be able to share with others. 

Another great teaching moment occurred when a young paramedic looked at me down on the floor and said: “Sir, do you think you could get up and sit on our stretcher?”

I remember thinking: “Dude, I’m having a stroke and can’t move my left arm or leg. If I could do that, I would have done it when you brought the stretcher into the living room!”

Much of their assessment and care is a blur to me, but I remember looking around for a suction unit as I started to violently “heave.”

It’s always a pet peeve of mine that crews always bring in their monitor/defibrillator with them, but rarely carry in a portable suction unit, the reason A proceeds B and C in the ABCs.

As sick as I was, I also remembered a lecture comment by a trauma surgeon when I was a new paramedic attending a continuing education class at our trauma center. He was discussing critical head injuries and noted what he termed violent “heaving” that often results from them.

I immediately knew I was in trouble — with a serious brain injury that was causing the “heaving.”

The teaching moments continued when I realized that they were running “Code 3″ to the hospital and had called in a “Stroke Alert.”

I thought — great job guys. Now I have a chance.

But when I started to again violently heave, I looked around and saw that there was only one medic in the back of the rig with me. The engine company peeled off and went back to quarters and left just one paramedic to manage my care.

That solo medic was busy tapping info into his tablet computer and radioing in his report. So, he handed me a little vomit bag to hold with my “good” arm.

There was no airway medic to have suction ready, no one to put an oxygen mask on my face, and no one to set up the IV that finally got inserted as the back-up alarm on the ambulance sounded at the ED entrance.

The message: If you go “Code 3″ — bring more than one crew member for me!

As they rushed me through the emergency department — directly to the CT scanner, it was frightening to hear them say to my wife “He’s had a stroke!” I thought: “Me, a stroke? No, this can’t be how my life ends.”

It was even more frightening when I laid in the CT Scan and realized that — if they did find a clot — they would not be able to inject a clot buster because I was on Eliquis and would suffer a cranial bleed.

Fortunately, I had suffered a Ventricular Arterial Occlusion that temporarily shut down blood supply to the right side of my brain and affected my ability to move the left side of my body.

I could hear and talk but was confused. They performed multiple stroke assessments on me and had me take the pointing finger of my right hand and attempt to touch my nose. I failed it every time, being way left of target — my nose.

The vision in my left eye was also affected. When I looked to my left, out into the hallway of the Nero ICU, I saw burry, double-vision objects. Again, a scary time as I laid in bed contemplating my future.

I always wanted to die quickly and, hopefully, peacefully and never wanted to end up being a burden on my wife and family or, worse yet, confined to a bed in a nursing home. I have great respect for the staff of nursing care facilities having been to many of them throughout my EMS career and seeing the patients and medical problems and obstacles they had to deal with on a daily basis.

I had lifted frail patients soaked in urine onto my stretcher countless times and never mined it one bit because they could not care for themselves and were always grateful for my care and compassion. But I never wanted to be on the receiving end of that care and compassion.

Amazing Self Recovery

After two days in the Nero ICU unit, with nurses seated in the doorway to make sure I did not get out of bed on my own, I began to self-heal and regain all motor and visual functions back.

My recovery amazed me and the staff, because, as the statistics show, it doesn’t happen all that often. I really did not know that or how lucky I was at the time. All I knew is that I was getting better!

The result? I was one of the lucky 13% who did not have a clot that caused permanent brain damage.

My doctors could not find a clot either because there was none, or it did not show up on the CT scans. They first thought I had a Transient Ischemic Attack (TIA), a condition I saw in patients frequently. They then thought I might have had a vertebral artery dissection (VAD). But, again, nothing showed up on the CT scan.

My symptoms and self-recovery process led the physicians to believe that I had suffered a temporary vertebral artery occlusion (VAO) possibly brought on by some rough chiropractic treatments by a new chiropractor unfamiliar with me or my stiff neck history.

They felt I might have had swelling that was increased after manipulation of my neck and that a turn of my neck at home somehow occluded my vertebral artery.

I began physical therapy (PT) right away and was humbled to have to use a wheeled walker that I had always seen older folks using to slowly navigate the halls of the Nero ICU.

I wondered if I was going to end up having to use one the rest of my life. Again, a very scary out-of-body experience.

The morning of my third day in the hospital, my physical therapist told me that, if I could walk the ICU floor and climb up and down two flights of stairs by just holding onto the handrail, I could be discharged to home. Oh boy, what an offer!

What she didn’t know was that I had a great incentive to get it accomplished. My son, daughter-in-law, and two beautiful granddaughters were leaving the next day and I would get a chance to see the little ones before they left — if I passed my “PT test.” 

Strangely, I remembered John Wayne in classic scene in one of my favorite corny war movies “The Wings of Eagles” — filmed in 1957. 

It’s the true story of Frank “Spig” Wead, a U.S. Navy aviator who helped promote United States Naval aviation from its inception through World War II. Commander Wead was a recognized authority on early aviation. Following a crippling spinal injury at his home in 1926, Wead was placed on the retired list.

John Wayne played the role of “Spig” Wead. The inspirational (true) scenes occurred while he was in rehab with his Navy pal and military rehab trainer “Jughead” (played exceptionally well by Dan Dailey) at a Naval Hospital in San Diego.

Jughead shows up with some alcohol and a mirror and tells John Wayne (“Spig”), flat on his stomach that they were going to start to get the correct brain signals to his feet.

Jughead makes Spig start saying “I’m gonna move that toe.”

Spig does a half-hearted job of saying it initially, but Jughead soon gets him going with coaching and some alcohol sipped through a straw and before you know it, they are both yelling “I’m gonna move that toe!” They are unsuccessful for days, but do not give up.

The next day, Jughead returns with a ukulele and a big mirror that he absconded from a brothel It is signed by a “Lady of the Evening” and positions it so Spig can watch his toes while in his flat, face-down position— more mental encouragement that was now linked to their joint chanting of “I’m gonna move that toe!”

Jughead, chomping on a cigar, puts down the cigar, takes a chug of whiskey, then starts playing the ukulele and singing loudly, getting Spig into it.

His doctor arrives and tells Spig not to overdo it. Spig, frustrated with his condition, tells the doctor, “One of us is going to give; either me or that big toe!”

As the doctor is leaving the room, he slyly hands a bottle of whiskey to Jughead and tells him that, although it’s strictly against regulations, he might want to give Spig “just a few drops” – which Jughead agrees to do.

During a surprising moment, after weeks of encouragement and exercises to move his toe, Jughead looks down and suddenly sees Spig moving his toe. Jughead runs out of the room screaming about Spig’s great accomplishment, kisses Spig’s grouchy nurse and then faints and slides to the floor.

Spig goes on to a near full recovery and back to active duty, commanding an aircraft carrier.

In the 1930s, now able to walk with the assistance of canes, became a screenwriter, becoming involved in more than 30 movies. He also published several books, short stories and magazine articles.

Amazingly, he returned to active duty during World War II, initially working in a planning role. But he later undertook sea duty in the Pacific, where he did an amazing job of attacking Japanese forces in 1943—44. He was placed on the retired list in mid-1945.

“˜I’m Gonna Climb Those Stairs’

As I walked down the hallway that morning, with my rehab nurse at my side, I silently chanted (over and over), “I’m gonna climb those stairs.”

Thinking of seeing my beautiful granddaughters, I made it up and down the two flights of stairs like a champ. I was released that afternoon, saw my family, hugged my granddaughters and had a beer in honor of Spig.

I’ve made a full recovery, returned to work with JEMS and returned to shopping at hardware stores.

I now just live with the fear of another arterial occlusion. It’s a common fear among all survivors so I just live my life with what I jokingly call “reckless abandon” and continue to educate the EMS community about these rare occlusions and other maladies we were never taught about in our EMS training programs.

Clip that shows the inspirational “I’m gonna move that toe!” sequence in “The Wings of Eagles” can be found here.

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EMS Industry Leader’s Story: Surviving Two Vertebral Artery Dissections

By Anne Mullally

I don’t consider myself one to play the odds. I don’t gamble in Vegas and don’t buy PowerBall tickets. This is probably in part because I have already run the table having survived two vertebral artery dissections.

The story was as unbelievable as it was mundane. It was January 2004, and I suddenly started suffering from constant nausea, severe headaches and episodic vertigo. The obvious choices were considered and crossed off the list. Head cold, inner ear infection, high blood pressure. Nothing.

Every day I would go to work and deal with the nausea, vertigo, hot/cold flashes, but continued to travel for work as necessary. One day, I distinctly remember driving down the road and feeling like I was spinning in circles in my car on a sheet of ice, which in January in Michigan is entirely possible. It turned out to be just another vertigo spell; but it was very scary.

Another day, I was flying to a big corporate meeting and felt so sick that I was afraid I was going to throw up on the plane, the same plane our CEO was on. That is called a near career-limiting moment.

Finally, I couldn’t take it anymore and went back to my general practitioner (GP) and begged for an MRI. I just had a bad feeling. You can imagine his surprise when the MRI revealed a right Vertebral Artery Dissection (VAD). Of course, my GP asked me all the logical questions: was I involved in an auto accident (no); suffered trauma (no); visited a chiropractor (no, I don’t see one); fall off my horse (yes I owned one and no I didn’t fall off recently).

With no clear answer on “why” a VAD occurred, I was immediately put on Warfarin and lived on Warfarin for five years.

A follow up MRI scan showed that the artery did regain some limited blood flow. Obviously after a VAD with no clear cause and being pregnant at 34, I had my OB physician appropriately paranoid. I lived on Lovenox injections while trying to conceive and, throughout my entire pregnancy, I received one shot per day in my ever-growing abdomen.

Then, at the time of my scheduled C-section, I was carefully weaned me off blood thinners entirely for 24 hours and then put back on 24 hours later. My body responded by creating large hematomas in my c-section incision, which earned me a wound vac for six weeks to aid in healing. It was all worth it, as a beautiful new baby girl joined our family.

After years on the blood thinner, I scheduled a visit for a second opinion with the Cleveland Clinic in 2008, to see if remaining on the blood thinner was necessary considering the long term effects of Warfarin.

I was “cleared” to discontinue the blood thinner and to stay on baby aspirin indefinitely. Victory!

Flash forward to July 2012. It was a stressful period at work, and I suffered a very severe headache that lasted for a week. I chalked it up to stress, but then, began to experience recurrent vertigo.

Then, one day, while I was sitting at work, I started suffering tingling on my face and my left arm began to go numb. While I tried to rationalize in my head why it would be completely ridiculous for me to even think stroke symptoms, I decided that, since I was now responsible for another human life, I should drive myself to the emergency department (so maybe a call to 911 would have been more appropriate, but I was not about to make a scene at the office — typical of those of us involved in EMS).

Not surprisingly, as soon as I told the ER staff my present and past medical history, including the VAD, I was immediately rushed back for an MRI. This time I quickly learned that my left vertebral artery dissected spontaneously and was distally occluded. Additionally, a left internal carotid pseudoaneurysm was found. I was admitted to quickly get blood thinner on board. Imagine trying to explain to your five-year-old not to worry about mommy as she laid in a hospital bed hooked up to IVs.

The symptoms subsided after a couple days and I was released to go home with injectable warfarin until my levels were at an acceptable risk-reduced state.

At this point, my GP from small-town Michigan was absolutely baffled by my case and recommended a visit to Mayo Clinic Neurology. Arrangements were made and I visited the Mayo Clinic in September 2012 for a complete work up, including ECG, assessment for all forms of connective tissue disorders (Marfan, Loeys-Dietz, Ehlers-Danlos), plus an Ambry genetics panel.

The good news out of this visit was that it was confirmed that they did not identify any genetic abnormalities that could be at risk for me passing VAD on to my children, which was my first and most important concern.

Their best assessment was there was a genetic abnormality of the connective tissue which seems to have manifested in my vertebral arteries. I am now included in Mayo’s genetic database in case any future links are identified.

The best news is that it has been almost eight uneventful years now.

We added another daughter to our family right after my second VAD, which was a great, unexpected blessing. I am fortunate now to be able to enjoy almost everything that I have loved doing, other than scuba diving where pressure changes could affect my vertebral arteries.

I consider myself very lucky that my symptoms never manifested themselves more dramatically and impactful than they did. Clearly, life had more in store for me, so I will continue to live it to the fullest and make the biggest impact possible: for my husband, my girls and for our emergency services industry.

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Technology and Apps Improve the Stroke Treatment Processes: How a Stroke Center Combined Software and a Secure Mobile Communication Platform to Enhance Processes for Stroke Treatment

By A.J. Heightman, MPA, EMT-P

Miami Valley Hospital health system, a 970-bed comprehensive stroke center in Dayton, Ohio, is the first in the world to combine the advanced cerebrovascular imaging software, RapidAI, and Pulsara’s secure mobile communication platform to improve stroke care processes.

In a case study featuring the Miami Valley Hospital system, the success the hospital achieved from integrating the two innovative technologies to improve stroke treatment processes and speed communications for the condition was highlighted.

With up to 60 individuals responding to one stroke case – EMS providers, neurologists, CT technologists, nurses, and consulting and emergency physicians – having the right communication technology in place and used effectively is critical to patient outcomes.

During complex conditions like stroke, there is a tremendous amount of information that needs to be generated and communicated, including the level of blood flow to the patient’s brain, something that can only be seen with advanced imaging.

Miami Valley needed a way to capture and communicate this data and critical details instantly to accelerate the diagnosis and treatment of patients experiencing an acute stroke. So, they added RapidAI to their established Pulsara communication workflow.

The Pulsara platform allows facilities to easily create a dedicated patient channel, build a team around their stroke activation system and communicate using audio, live video, instant messaging, data, images, and key benchmarks. Studies report an average decreased treatment time of nearly 30% when using Pulsara.

The RapidAI software platform uses artificial intelligence to process critical stroke imaging information, shortening to five minutes a data interpretation process that traditionally took a CT technologist at least 20 minutes — a 75% reduction in time; 15 precious minutes saved that can help the team to make decisions that can improve patient outcomes. 

In the last year since the Pulsara and RapidAI integration, the team at Miami Valley has been able to reduce inefficiencies and delays in stroke treatment, activating the appropriate interventions sooner – an achievement that has resulted in better outcomes for stroke patients.

Equally important is the fact that the integrated data and notification system enables the entire stroke team to be notified and provided with the imagery and data in real time, something that had yet to happen at any other stroke center in the world. This allows neurologists to make critical decisions, such as when it’s safe to remove a blood clot, and when and if clot-busting medication can be used.

This instant coordination of care helps the hospital buy more time for a stroke patient. Prior to integrating the technologies, Miami Valley’s stroke team knew a CT scan was underway, but not necessarily when it was completed. Now, all members receive an alert as soon as the images are available, and the neurologists can evaluate the results immediately on their mobile devices. This allows the team to begin the most appropriate interventions faster since physicians no longer have to pull the needed information manually.

By reducing delays in stroke treatment through innovative communication and technology, Miami Valley Hospital is setting new standards of stroke care.

Click here to download the full case study.