Category: Emergency Room

Another Emergency Room Visit

Yikes……………. I was at the ER last night for my wife. Just after my son has been complaining of chest pain, my wife woke up yesterday complaining of chest pain in the middle of her chest. So, off to the Providence Everett ER room. I have to say, they were great! She had a couple of EKG tests that did come back with a slight abnormality, as well as a d-dimer test and a few other blood tests plus a chest X-Ray.

We left after about 3 hours there and my wife is going to get stress test done early this week. She is still sleeping and I am hoping that her pain has gone away. However, I am concerned it could be something else like a clogged artery to the heart? Or high cholesterol, but hopefully the stress test and possible echo cardiogram will shed some light.

I have my first of 2 appointments with the doctor at Virginia Mason tomorrow about my value and aortic root issue as well as on 12/3 my appointment with Dr. James Brevig who did my original emergency open heart surgery at Providence Everett.

GOD…. Please help our family to get through this and have the hope to be strong in our faith.

Brian 🙂

Emergency Medicine & Acute Care Series – Aortic Dissection Diagnosis

Granted, it’s a bit old, still worth viewing.
Brian 🙂

Anthem’s new policy will scare away patients who need the emergency room

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by Dr. Aida Cerundolo |  

I once cared for a patient in her 20s who came to the emergency room for a sore throat and a rash. While she was in no acute distress, she explained that her throat hurt and unusual bumps were erupting on her hands.

But then she mentioned starting a new antibiotic. My internal alarms sounded. Her symptoms were signs of a potentially life-threatening condition that required specialty services not available at my small hospital. I arranged for transfer to a tertiary care center. The next week I received a follow-up letter from her care team. No more than 36 hours after I saw her, she was in the intensive care unit, on a ventilator, fighting for her life.

The lesson is that even if not every rash and sore throat is a life-threatening condition, life-threatening conditions don’t always present themselves as obvious emergencies.

Anthem Inc., a for-profit managed healthcare company, appears to disagree. Beginning Jan. 1, 2018, Anthem will not cover the cost of services rendered in a New Hampshire emergency room for conditions deemed, after the fact, to be non-emergent. If Anthem determines that a medical problem could have been handled at a non-emergent clinic, the patient is on the hook for the cost. This rule is also being more diligently enforced in Kentucky, Virginia, Georgia, and Missouri.

Anthem is justifying the move by pointing to significantly higher emergency room costs compared to non-emergent clinics, citing such so called “non-emergency” services as annual sports physicals, pregnancy tests and ingrown toenails. They argue this cost is inevitably passed on to consumers.

However, the list of Anthem’s non-emergent diagnoses does not stop there. Under this enforced policy, more ambiguous complaints like chest pain with breathing and bloody urine can also be deemed unworthy of an ER visit. The American College of Emergency Physicians has uncovered almost 2,000 of these non-emergent diagnoses in Missouri alone.

Hindsight is always 20/20. But patients don’t have the benefit of a medical evaluation and test results, nor the medical training to help them decide on their on whether their condition merits emergency treatment. And for that reason, the Prudent Layperson definition was added to the federal Emergency Medical Treatment and Labor Act (EMTALA) in 1994, defining an emergency condition as one that would lead a prudent layperson, with an average knowledge of medicine, to believe that his or her health is in jeopardy. It is the patient’s presenting symptoms, not the final diagnosis, that legally determines authorization and payment for emergency claims.

But even emergency physicians are not soothsayers. EMTALA mandates that no patients are turned away from the emergency room without a medical screening exam to rule out dangerous conditions. If a patient presents with chest pain, the bucket of possible diagnoses is overflowing, from benign ailments like muscle strain or heart burn, to life-threatening conditions like heart attack, pulmonary embolism or aortic dissection. Testing is often required to tease out the difference.

And, yes, amid these casualties, there may also be some reduction in non-emergent ER visits.

Rather than penalizing patients who believe their condition warrants an emergency visit, incentivizing them when they utilize appropriate services instead will likely also reduce non-emergent ER visits, and not deter patients from seeking appropriate emergency care when they should. By denying payments for certain non-emergent diagnoses determined after the fact, Anthem is merely pushing a healthcare cost hot potato off their lap and into the arms of legally obligated emergency care providers.

How many patients will suffer preventable injury or even death because they now fear a bill for a legitimate emergency department visit? That hindsight will be 20/20.

Dr. Cerundolo is a physician practicing emergency medicine in New Hampshire.

 

 

Emergency Room Doctors…. Low probability of them correctly diagnosing an Aortic Dissection

After just reading this article:

These conclusions are puzzling to say the least. What about checking the BP at all four extremities? Both legs (ankles) and both arms, I thought one of the “clear” signs was the difference in BP is a clear sign of a possible AD and or what about the d-dimer test like I had? As a concerned love one, you had better make sure if you have ANY doubt to stress the need for a CT and not an Echo or sent to the CATH Lab. I just heard a horror story about a person who had this happen to him and had he had an ER doctor like I had, he’d been in a much better place than he is now.

Conclusion

The diagnosis of aortic dissections by emergency physicians is rare and challenging. An emergency physician seeing 3,000 to 4,000 patients a year would diagnose an aortic dissection approximately every three to four years.

CONCLUSION
We found aortic dissections to be rare, diagnosed approximately once for every 12,200 ED patients and once for every 980 atraumatic chest pain patients. Although ordering CTs in low-probability patients may not be the best strategy, missing the diagnosis can have devastating consequences for the few patients that actually have a dissection. These findings may be useful for clinicians as they weigh the risks and benefits of ordering CTs, and also for physicians currently involved in litigation regarding failure or delay in diagnosing aortic dissection.

Fit 55-year-old man who died might have survived if condition correctly diagnosed before released from hospital

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UK manRick Dickinson pictured with his mum Joy. PIC: SUPPLIED
RICK Dickinson was a fit 55-year-old who might not have died if his condition had been correctly diagnosed before he was sent home from hospital, a coroner has found.

The popular entrepreneur, who had worked overseas before coming home to Brisbane to help look after his ageing mother, died alone at his home, as a result of a ruptured aortic dissection.

It is an uncommon, life-threatening condition that occurs when there is a weakening of the inner layer of the aorta, causing a tear.

After feeling acute chest pain and lower back and leg numbness while exercising at a gym on June 26, 2013, Mr Dickinson was taken by ambulance to St Andrew’s War Memorial Hospital.

An inquest into his death has exposed a flawed handover system and a series of mistakes and oversights by an experienced hospital doctor and nurses.

But Mr Dickinson’s family, who worked for 18 months to get an inquest, believes the hospital should have apologized and been held more responsible.

Paramedics told a nurse Mr Dickinson had experienced chest pain, but this was not passed on to other nurses, who also failed to take regular observations.

State Coroner Terry Ryan found the medical care of Dr Paul Cole, a senior emergency doctor, who failed to take a full, comprehensive history from Mr Dickinson, was “well below standard’’.

“Rick’s death was preventable … correct diagnosis and the commencement of treatment before the catastrophic rupture gave him a chance of surviving this life-threatening condition,’’ he said.

But being discharged gave Mr Dickinson little, if any, chance of survival. Experts agreed Dr Cole should have examined Mr Dickinson’s chest, heart and cardiovascular system, and not discharged him before delayed test results were known. The focus had been on his back and leg pain, instead of his chest pain.

While in hospital Mr Dickinson told his brother and sister, by phone, his pain felt like “a ball of air ripping through his chest’’.

Mr Ryan recommended continued education to ensure aortic dissection was highlighted in training of emergency staff.

His sister, Julie Dickinson, said friends’ knowledge of Rick’s death had helped save at least two lives and the hospital had since introduced a deterioration detection tool. But his family still feels Dickinson’s loss.

“He was the funniest man I knew. He was gregarious and free-spirited. The laughter has gone out of our lives,’’ Ms Dickinson said.

Young Woman’s ‘Hysteria’ Turned Out to Be Deadly Heart Condition

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By Cari Nierenberg, Contributing Writer | August 21, 2015 04:10pm ET

A woman in Germany who went to the emergency room because she felt “hysterical” ended up not having a psychiatric disorder as doctors originally suspected. Instead, she had a serious heart condition that could have killed her, according to a new report of her case.

Although the woman’s symptoms seemed to be mainly psychological in nature and she was not in any pain, her doctors noticed some key physical clues that led them to the correct diagnosis, and likely saved her life. The case shows that people who have physical illnesses may have no physical pain but instead have psychiatric symptoms, the doctors who treated her wrote in their report.

The 29-year-old woman was a medical student, and was taken by ambulance to the emergency room in June 2014. She said she thought she was having a “nervous breakdown” as a result of having an emotional argument with her boyfriend earlier that day.

By the time she got to the hospital, she was extremely agitated. The woman seemed very anxious and was constantly tossing and turning on the stretcher, said Dr. Thilo Witsch, a cardiologist at the University of Freiburg Heart Center in Freiburg, Germany, and the lead author of the case report, published online Aug. 10 in The Journal of Emergency Medicine.

Her restlessness made it difficult for the staff to get a detailed medical history or do a thorough physical exam, and she was unable to lie still for routine procedures, like taking her blood pressure, Witsch said. Her heart rate was rapid, and she was breathing fast.

In addition to the young woman’s anxiety, which she attributed to the stress of fighting with her boyfriend, she described feeling mild numbness and tingling in her hands and feet. But she was not experiencing any pain and had no history of mental illness. [16 Oddest Medical Cases]

The doctors requested she be seen by a psychiatrist because they thought she might have a panic disorder with hyperventilation syndrome, a condition in which a person breathes too heavily or deeply because they feel like they are not getting enough air.

But then, the woman’s medical team picked up on some signs that her symptoms were not linked to her emotional distress but instead were a physical health problem.

Witsch said his suspicions were first raised when he noticed a slight bluish tinge to the woman’s lips, and how pale her complexion was. She also had a very subtle, mottled skin discoloration on her arms and legs. These symptoms usually result from poor circulation and blood not getting to these parts of the body.

He then received her blood test results, which did not indicate she had hyperventilation syndrome, he said.

Aortic dissection

A closer physical exam showed that the woman had reduced blood flow in both of her arms as well as her legs, and diagnostic testing finally revealed her condition: The woman had an aortic dissection, which is a tear in the inner wall of the aorta, the large blood vessel that routes blood from the heart to other parts of the body, including the limbs and internalorgans, Witsch told Live Science.

Specifically, this woman had a tear in the section of her aorta that was close to her heart, known as a Stanford type A dissection, which is a medical emergency requiring immediate treatment. A substantial percentage of people with this type of aortic dissection die, even with optimal treatment, Witsch noted.

People with this type of aortic dissection usually have intense chest pain, according to the case report.

Ignoring the woman’s physical signs because they were masked by psychological symptoms could have had fatal consequences in this case.

“In a very busy emergency room, her physical findings may have easily been overlooked because these patients may get labeled as ‘psychogenic,’ meaning they have a psychological origin rather than a physical one,” Witsch said.

He said it’s not unusual for heart conditions to be accompanied by psychiatric symptoms, especially anxiety. This may be due to the activation of the sympathetic branch of the nervous system, which responds to stress and speeds up the heart rate, Witsch said. [11 Tips to Lower Stress]

Aortic dissections are relatively uncommon, and when they do occur, they usually strike much older adults, typically people in their 60s and 70s. When this condition turns up in younger people, there’s often a strong genetic predisposition, as doctors eventually learned was the case for this young woman, whose mother had an aortic dissection when she was 40.

Aortic dissections in younger people can also be caused by genetic diseases that weaken the aortic wall, such as Marfansyndrome, Witsch noted.

The woman needed surgery to remove the damaged area of her aorta and replace it with a synthetic tube, called a graft. She spent 19 days in the hospital.

Witsch said he last saw the woman three months after her surgery, in October 2014. She had not had any similar episodes of anxiety, had no medical complaints and was continuing with her medical studies. Because she had been a smoker, she was advised to quit in order to keep her heart healthy for a long time.

Five Common Causes of Sudden Unexpected Death Every EMS Provider Should Know

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SD covYou’re called to the scene where a 50-year-old male was working in his yard when his wife witnessed him collapse. He’s found pulseless and apneic with no signs of trauma. His wife is performing CPR when you arrive.

What are the five common causes of sudden death that could have led to his demise, and what are some symptoms the patient may have been experiencing in the hours or days leading to his arrest?

Introduction

EMS providers are often faced with patients in cardiac arrest. Many of these patients have complicated medical histories and have been ill for a long period of time. This article will discuss the five major causes of acute sudden death that may occur without warning in previously healthy patients, with a focus on the etiology, recognition and treatment of these conditions. The article is written to better allow prehospital providers to consider these causes and initiate appropriate time-sensitive care whenever possible.

The five causes of sudden death discussed in this article are: fatal arrhythmias, acute myocardial infarction, intracranial hemorrhage/massive stroke (cerebrovascular accident), massive pulmonary embolism and acute aortic catastrophe.

1. Arrhythmia

There are many causes of fatal arrhythmias including cardiomyopathies,1,2 inherited defects in the conduction system (such as prolonged-QT syndrome or Brugada syndrome),3 and the most commonly associated factor: ischemic injury from acute myocardial infarction (AMI) or previous infarct.4 Electrolyte imbalance can lead to arrhythmias and sudden death, such as hyperkalemia seen in patients with end stage renal disease on hemodialysis and hypokalemia in patients taking diuretics. Both of these are usually asymptomatic, but can prolong the QT interval leading to torsades de pointes.5,6 Other potential causes of malignant arrhythmias include illicit drug ingestion, medications that prolong the QT interval, acute changes in pH, worsening heart failure, Wolff-Parkinson-White syndrome and commotio cordis following chest trauma.

A significant number of patients who suffer sudden cardiac death will have no preceding symptoms. Other patients may have a history of chest pain, shortness of breath, palpitations, dizziness or syncope. Thus, even healthy, relatively young patients with “minor complaints,” such as palpations, need to be taken seriously and should be carefully monitored en route to the hospital.

These complaints should always prompt EMS providers to consider arrhythmia as a potential cause of the patient’s symptoms. To that end, patients with these complaints always need what we refer to as the “opening gambit”: oxygen, oxygen saturation monitoring, IV access, continuous cardiac monitoring and a 12-lead ECG.

Sudden death from a cardiac cause accounts for the majority of events, with estimates as high as 80%.4 Less than 8% of patients who have arrested will survive to be discharged from the hospital, and those who do live are likely to present with shockable rhythms.7 (See Figure 1 download below.) Unfortunately, it appears that only about one quarter of out-of-hospital cardiac arrests will have unstable v tach or v fib, and the remaining 75% who present in pulseless electrical activity (PEA) or asystole will have a bleak prognosis.7

Early defibrillation is the reason patients in v fib have a four-fold increase in odds of survival compared to those found in PEA, and nearly 20-fold increase in odds of survival compared to patients found in asystole.8

In the case of v fib patients, it’s estimated that every one minute in delay of defibrillation will decrease the chance of survival by up to 10%.7 For this reason, encouraging automated external defibrillator (AED) placement wherever there are large crowds or sporting events is essential.

Key concepts: Fatal arrhythmias are a common cause of sudden death. Early recognition of patients at the risk for these arrhythmias and appropriate treatment of reversible causes saves lives.

Patients found in v fib or v tach stand a much greater chance of survival when early defibrillation and high-quality chest compressions are delivered.

2. Acute Myocardial Infarction (AMI)

Another cause of sudden death is AMI. Plaques that develop within arteries progress over time and eventually rupture and occlude blood flow. Much like a sprinter will feel a burn in his muscles as he fatigues at the end of a race, the lack of adequate oxygen delivered to the heart (ischemia) results in fatigue that causes the anginal symptoms experienced by most patients during acute coronary syndrome (ACS).9 If ischemia affecting a large enough area of the heart is prolonged, extensive cell death follows and results in an AMI. Damage to the conduction pathways within the heart can degenerate into bradycardia, heart block, unstable v tach, v fib or PEA with the common endpoint of asystole. In the hundreds of thousands of cardiac arrests in out-of-hospital settings each year, approximately 80% are thought to be related directly to ischemic heart disease.4

When a patient presents with symptoms suggestive of AMI, it’s critically important to obtain a 12-lead ECG, which can help confirm the diagnosis of ST elevation myocardial infarction (STEMI). However, only 20–60% of patients having an AMI will initially have an ECG showing a true STEMI on presentation.10 (See Figure 2 download below.)

It’s important to realize there are many mimics of AMI that require different management.11 Furthermore, there are many atypical presentations of AMI that won’t be immediately recognized if a provider isn’t aware of them. For example, it’s been estimated that as many as one in four patients with AMI won’t have chest pain.9 Missed cardiac ischemia is more common in patients with atypical symptoms, younger patients, the elderly, women and minorities.12

The five most common atypical symptoms of an AMI are:

1. Dyspnea;
2. Diaphoresis;
3. Central nervous system (CNS) symptoms including syncope, presyncope, dizziness, and stroke-like symptoms;
4. Gastrointestinal symptoms including nausea and non-localizing mild abdominal discomfort; and
5. Weakness.

The classic presentation of AMI is chest pain. The pain is sometimes difficult to delineate from indigestion, but several factors are known to increase the likelihood that a patient’s chest pain is related to ischemia. Pain that’s similar to a previous heart attack, pain that radiates to either or both arms, and pain that’s precipitated by exertion increase the likelihood that a patient’s chest pain is associated with an AMI or ischemia preceding an AMI.10

Factors associated with chest pain that decrease the likelihood of an AMI or an ischemic etiology are pain that is sharp, stabbing, worse with respiration, positional or worse with pressure applied to the affected area.10 Pain relieved by nitroglycerin isn’t predictive of ischemic chest pain.10 It’s best to have a high index of suspicion for possible signs and symptoms of ACS and to remember: Atypical is typical! Doing more 12-lead ECGs rather than less should be the practice pattern for all providers working in EMS and EDs.

In the presence of an AMI, expedient transport to the nearest medical center that can offer specialized cardiovascular intervention is paramount. Minimizing the time to percutaneous intervention will improve the patient’s outcome and chance of survival.7 While en route to a specialized medical facility, remember that administration of aspirin has been shown to significantly improve mortality.7

Key concepts: Time is muscle, and early recognition of patients suffering an AMI, even in the absence of chest pain or ECG changes, will ensure the opportunity to intervene appropriately isn’t missed. EMS providers must maintain a high index of suspicion for AMI as patients will often not present with a “classic history.”

3. Intracranial Emergencies

Intracranial catastrophe is an often overlooked cause of sudden death. Unlike other tissues in the body, the brain has a uniquely limited capacity to tolerate low oxygen delivery. This is the same reason ensuring appropriate blood flow through maintaining adequate blood pressure and oxygenation in head trauma patients is emphasized in Prehospital Trauma Life Support (PHTLS) training. In the case of a cerebralvascular accident (CVA), the blood flow to a part of the brain has stopped due to either obstruction from an embolism or from the rupture of a vessel carrying blood to the affected area of the brain. (See Figure 3 download below.)

In nonhemorrhagic strokes, where thrombolytic therapy is thought to benefit certain subpopulations of patients when delivered within the first several hours, timely transport is imperative. These patients can present with syncope, vertigo, facial droop, dysarthria, unilateral weakness, unilateral loss of sensation or hemiparesis. Initial assessment should include a blood glucose measurement as hypoglycemia can mimic stroke-like symptoms. Cardiac monitoring is also important as strokes have been associated with ensuing fatal arrhythmias leading to sudden unexpected death.13

In the case of a massive hemorrhagic CVA, which is associated with markedly elevated blood pressures and obtundation, patients frequently die before the initiation of medical therapy.14 Declining mental status in particular is one of the early signs of increased intracranial pressure, a harbinger of impending fatal herniation of the brain. However, there are many patients who can potentially benefit from emergent therapy and thus transport shouldn’t be delayed so that timely diagnosis and management can be initiated at a medical center capable of providing advanced care. Either type of a CVA (hemorrhagic or nonhemorrhagic) can be devastating and can lead to lifelong disability or death even when treated early and aggressively.

The adage “time is brain,” copied from “time is muscle,” is meant to emphasize that in the cases where intervention is possible, the sooner it’s initiated, the more hopeful the patient’s prognosis will be.

Subarachnoid hemorrhage (SAH) is another CNS cause of stroke and sudden death. Most commonly a result of a ruptured intracranial aneurysm, SAH often presents with the rapid onset of a severe headache often referred to as a “thunderclap headache.” Other signs and symptoms may include nausea, vomiting, neck stiffness or focal neurologic deficits. Beware of patients who experience syncope during exertion, sexual intercourse, or after developing “the worst headache of their life,” as these are classic presentations of a subarachnoid hemorrhage due to a rupture of an arteriovenous malformation or cerebral aneurysm.

Key concepts: As with other causes of sudden death, patients with intracranial emergencies may have no preceding symptoms. However, signs and symptoms such as new or worsening headaches, focal neurologic complaints and declining mental status can be seen. A glucose value should always be obtained to avoid missing hypoglycemia and profound hyperglycemia. When transporting patients with suspected intracranial hemorrhage/CVA, it’s critical to avoid hypotension or hypoxia as both will significantly increase morbidity and mortality. To that end, paramedics should rarely use antihypertensives in patients suspected of a CVA and should carefully monitor oxygenation.

4. Pulmonary Embolism (PE)

PE classically occurs more frequently in the elderly, cancer patients, patients who recently underwent surgery, patients on estrogen-containing medications, the bedbound and those who’ve previously had a deep venous thrombosis (DVT) or PE. Virchow’s Triad describes the three factors that are ultimately found to cause almost every PE:

1. Stasis of blood flow (e.g., immobilization);
2. A hypercoagulable state (e.g., estrogen therapy, smoking and inherited causes); and
3. Vascular injury (e.g., trauma—even relatively minor).

However, a PE can occur in patients with none of these risk factors known prior to presentation. Alarmingly, in one study it was estimated that sudden death was the first manifestation of PE in as many as 25% of patients. Of these, dyspnea and chest pain were the predominantly associated symptoms.15 Unexplained dyspnea should always raise the suspicion of a pulmonary embolism.

A PE occurs when a thrombus, commonly from a lower extremity DVT, becomes dislodged and embolizes via the inferior vena cava to the right side of the heart. Once ejected from the right ventricle, it enters the pulmonary circulation where it wedges into the branches of the pulmonary arteries, inhibiting blood flow through the lung. This also reduces oxygenation of venous blood prior to its return to the rest of the body. If the blood clot is large enough, cardiovascular collapse will occur as a result of obstructive shock. The left ventricle will be unable to deliver enough blood to the brain and body, resulting in the patient becoming hypotensive and obtunded.

Many patients who have a PE will often present with sinus tachycardia early on without any other findings. The combination of tachycardia, decreased oxygen saturation and pleuritic chest pain should prompt the provider to consider PE. Although associated with PE, hemoptysis is rarely, if ever, present. In the presence of a large PE, an initial ECG may show signs of right heart strain16 (see Table 1 and Figure 4 downloads below), although further testing will be required to confirm the diagnosis.

In patients suspected of having a PE, it’s important to secure the ABCs (airway, breathing, circulation) with oxygen, pulse oximetry, IV access, cardiac monitoring and obtaining a 12-lead ECG while expediting transport. In cases of cardiovascular collapse or submassive PE with imminent collapse, interventions such as thrombolytic therapy or endovascular clot removal can not only be lifesaving, but also prevent progression to right heart failure. Thus, early recognition and timely transport is essential to the patient’s outcome.

Key concepts: While acute pulmonary embolism often presents with pleuritic chest pain, signs and symptoms such as unexplained tachycardia, syncope, hypoxia, hypotension, anxiety and/or right heart strain should immediately prompt a provider to consider the diagnosis of PE. In such cases, supportive care and timely transport can be not only lifesaving, but also prevent long-term consequences from right heart failure and pulmonary hypertension.

5. Aortic Catastrophe

Lastly, acute aortic catastrophe, namely dissection or aneurysmal rupture, can cause sudden death. In patients with vascular disease (often the result of long-term comorbidities such as hypertension, high cholesterol or smoking), turbulent blood flow in the aorta can lead to outpouchings (aneurysms) of the arterial wall at points of stress due to weakening of the vessel from atherosclerosis.

While initially benign, as these aneurysms grow in diameter over the years, they become increasingly at risk for rupture.17

An aortic aneurysm, although generally painless, can cause pain that radiates to the back or flank when acutely expanding or upon rupturing. Aortic rupture results in extensive internal bleeding. After exsanguination from the rupture, but prior to death, PEA is likely to be encountered due to extensive volume loss.18 Whenever a patient over the age of 60 has a chief complaint of back, flank or abdominal pain, it’s essential aortic aneurysm always be high on the differential diagnosis.18 A large pulsatile mass palpated in the mid-abdomen makes the diagnosis much more likely, though is often not appreciated. These patients will require management in an intensive care unit and, very likely, surgery if the aneurysm is rapidly expanding or has already ruptured.

If the aorta’s wall is weakened by chronic changes from vascular disease, it becomes more susceptible to shearing stress that can tear the normal layers of the aorta apart. There are three layers of the healthy aorta that keep blood within the artery. Hypertension can cause blood to “dissect” through the innermost layer into the middle layer and then proceed to tear the wall of the aorta apart internally in a phenomenon called aortic dissection.17 This distinguishes a dissection from an aneurysm because in aneurysms the three layers of the aorta remain intact and instead bulge out together from their normal position. (See Figure 5 download below.)

Aortic dissection often presents with chest pain, described as “ripping” or “tearing” radiating to the back. Pain from aortic dissection is sudden and maximal in intensity at onset for the majority of patients.10

This is unlike angina, which builds in intensity and is rarely felt as ripping or tearing. In approximately one third of patients with aortic dissection, there will be a greater than 15 mmHg difference in systolic blood pressure between the upper extremities and approximately one quarter will have a diastolic murmur.19 However, neither of these findings are likely to be appreciated in the field. Patients are usually elderly (on average 65 years old), hypertensive (approximately 50% of patients), and sometimes have neurological deficits (less than 1 in 5 patients with dissection).20

It’s important to realize aortic dissection can often mimic ACS.11 As the treatment for ACS requires anticoagulation, appropriate recognition of a dissection saves lives as incorrectly diagnosing a dissection as ACS and treating with anticoagulation can lead to aortic rupture. Thus, any interventions beyond aspirin for chest pain should be pursued only after the diagnosis of dissection has been considered and thoughtfully ruled out.
Key concepts: Aortic rupture from aneurysm or dissection requires the thoughtful practitioner to first consider the diagnosis in any patient with chest pain, flank pain, abdominal pain or sudden collapse.

This is particularly true in elderly patients with hypertension who present with either ripping or tearing chest pain in the case of dissection, or in the case of ruptured aortic aneurysm patients presenting with severe back, flank or abdominal pain. Reducing hypertension and tachycardia while expediting transfer to a specialized medical center is critical.

Conclusion

Through improved awareness, the skilled provider will be able to more efficiently initiate appropriate therapy and avoid the pitfalls of misdiagnosis and resultant unintended harm to the patient. It’s held true for centuries that history and physical examination are an essential guide to the medical management of our patients, and these shouldn’t be undervalued. It’s also important to remember the basics: securing ABCs, opening the gambit and expediting transport to a qualified medical center.

References
1. Tabib A, Loire R, Chalabreysse L, et al. Circumstances of death and gross and microscopic observations in a series of 200 cases of sudden death associated with arrhythmogenic right ventricular cardiomyopathy and/or dysplasia. Circulation. 2003;108(24):3000–3005.
2. O’Mahony C, Elliott P, McKenna W. Sudden cardiac death in hypertrophic cardiomyopathy. Circ Arrhythm Electrophysiol. 2013;6(2):443–451.
3. Bastiaenen R, Behr ER. Sudden death and ion channel disease: Pathophysiology and implications for management. Heart. 2011;97(17):1365–1372.
4. Myerburg RJ, Junttila MJ. Sudden cardiac death caused by coronary heart disease. Circulation. 2012;125(8):1043–1052.
5. Krahn LE, Lee J, Richardson JW, et al. Hypokalemia leading to torsades de pointes. Munchausen’s disorder or bulimia nervosa? Gen Hosp Psychiatry. 1997;19(5):370–377.
6. Alpert MA. Sudden cardiac arrest and sudden cardiac death on dialysis: Epidemiology, evaluation, treatment, and prevention. Hemodial Int. 2011;15(Suppl 1):S22–S29.
7. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;61(4):e78–e140.
8. Teodorescu C, Reinier K, Uy-Evanado A, et al. Survival advantage from ventricular fibrillation and pulseless electrical activity in women compared to men: The Oregon Sudden Unexpected Death Study. J Interv Card Electrophysiol. 2012;34(3):219–225.
9. Panju AA, Hemmelgarn BR, Guyatt GH, et al. The rational clinical examination. Is this patient having a myocardial infarction? JAMA. 1998;280(14):1256–1263.
10. Swap CJ, Nagurney JT. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA. 2005;294(20):2623–2629.
11. Brywczynski J, Mckinney J, Brown A, et al. STEMI mimics: Five cases that look & sound like a STEMI, but may not be. JEMS. 2013;38(12):38–43.
12. Jones ID, Slovis CM. Pitfalls in evaluation the low-risk chest pain patient. Emerg Med Clin North Am. 2010;28(1):183–201.
13. Sörös P, Hachinski V. Cardiovascular and neurological causes of sudden death after ischaemic stroke. Lancet Neurol. 2012;11(2):179–188.
14. Huang J, van Gelder JM. The probability of sudden death from rupture of intracranial aneurysms: a meta-analysis. Neurosurgery. 2002;51(5):1101–1107.
15. Lucena J, Rico A, Vázquez R, et al. Pulmonary embolism and sudden-unexpected death: Prospective study on 2477 forensic autopsies performed at the Institute of Legal Medicine in Seville. J Forensic Leg Med. 2009;16(4):196–201.
16. Hunt JM, Bull TM. Clinical review of pulmonary embolism: Diagnosis, prognosis, and treatment. Med Clin North Am. 2011;95(6):1203–1222.
17. Ashley EA, Niebauer J. (2004.) Cardiology explained: Chapter 12: Aneurysm and dissection of the aorta. NCBI Bookshelf. Retrieved Feb. 2, 2014, from www.ncbi.nlm.nih.gov/books/NBK2210/.
18. Pierce LC, Courtney DM. Clinical characteristics of aortic aneurysm and dissection as a cause of sudden death in outpatients. Am J Emerg Med. 2008;26(9):1042–1046.
19. Klompas M. Does this patient have an acute thoracic aortic dissection? JAMA. 2002;287(17):2262–2272.
20. Siegal EM. Acute aortic dissection. J Hosp Med. 2006;1(2):94–105.

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Painful Leg? Think Aortic Dissection

Letter to the Editor: Painful Leg? Think Aortic Dissection
article source:

Editor:

I read Dr. Jennifer Wiler’s December article, and one thing that was conspicuously absent on the differential list for acute arterial occlusion was aortic dissection. (“Painful Lower Leg and Foot,” EMN 2012;34[12]:24; http://bit.ly/ZdsdAm.)

I had a very interesting case of dissection that presented as a pulseless right lower extremity. Had I followed standard treatment per this article, this patient would have had a heparin bolus and no imaging. (He had sudden onset leg pain and obviously pulseless leg.) His vitals were totally normal (mild hypertension), and he was in severe pain from leg ischemia.

The only reason I even considered dissection in my differential was because I just happened to be in the room with EMS, and they described that he was initially hypotensive and pale on their arrival, but their fluid bolus of 50 ml corrected all that! He had no chest pain, back pain, shortness of breath, or other complaints except leg pain.

I am planning on writing this as a case report, but just wanted to let you know there could be some danger involved in not considering dissection in the differential here (or talking with your EMS crew)!

Mark Collins, MD

Indianapolis

Dr. Wiler responds: You are correct, Dr. Collins. Aortic dissection is a rare but serious cause of acute limb ischemia. Excellent save on your case!

A 47-year-old man comes to your ED with complaints of chest pain

A 47-year-old man comes to your ED with complaints of chest pain that radiates to his neck, nausea, shortness of breath (SOB), and weakness on one side of his body. The triage nurse notes that he’s diaphoretic, pale, and appears apprehensive. His heart rate is 116 and his BP is 188/104. The patient states that the chest pain occurred suddenly without any precipitating factors. A 12-lead ECG reveals sinus tachycardia. This patient may be experiencing acute aortic syndrome—a term that encompasses aortic dissection, penetrating atherosclerotic ulcer, intramural hematoma, aortic aneurysmal leakage, and ruptured abdominal aortic aneurysm. Can you recognize this life-threatening emergency?
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How does it happen?
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To understand how an aortic dissection occurs, let’s first look at the anatomy of the aorta. The aorta is the largest artery in the body, composed of three layers: inner, middle, and outer. The inner layer—the tunica intima—is a thin, delicate layer in which blood flows through. The middle layer—the tunica media—gives the aorta its strength and elasticity. When this middle layer weakens, the outer layer—the tunica adventitia—swells and forms an aneurysm (see Picturing a dissecting aneurysm).

The pulsing pressure of arterial blood flowing through the aorta continues to weaken the vessel walls, and the aneurysm continues to enlarge further than its normal 2 to 5 cm (0.8 to 2 in) diameter. If the extension continues, the weakened inner layer may tear. This tear will allow the blood to flow freely between the arterial walls, causing a separation or dissection.
Figure. Picturing a …
Figure. Picturing a …
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Who’s at risk?

There are several risk factors for aortic dissection. The majority (over 70%) of patients who experience an aortic dissection have a history of hypertension. The increase pulse pressure of continuous hypertension damages the muscle layers of the aorta, leaving it vulnerable to dissection.

Other risk factors include:

* gender—aortic dissection is three times more common in men than women

* race—Black patients are at increased risk

* age—roughly 75% of aortic dissections occur in people between the ages of 40 and 70, but risk peaks in the 60s and 70s

* genetic connective tissue disorders—Marfan syndrome, Ehlers-Danlos syndrome, and Turner syndrome

* genetic cardiac anomalies—coarctation of the aorta (a narrowing in the descending aorta) or bicuspid aortic valve (causes blood to regurgitate and increases aortic dilation)

* blunt trauma—a blow to the aorta can cause a tear and subsequent acute dissection; the patient’s chest hitting the steering wheel during a motor vehicle accident is the most common trauma cause

* surgical complications—aortic dissection can be a complication of surgical procedures, including coronary artery bypass grafting, aortic and mitral valve repairs, and cardiac catheterization

* cocaine or methamphetamine use—may produce a sudden and profound hypertensive and tachycardic episode

* pregnancy—approximately one half of women under age 40 who experience an aortic aneurysm are in their third trimester of pregnancy

* atherosclerosis— the buildup of plaque in the lining of the arteries, which may cause a weakening of the arterial walls.

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Know the signs and symptoms

No one sign or symptom can positively identify acute aortic dissection. To remember the signs and symptoms, use the acronym

HELP I’M DYING.

* Hypertension/hypotension and hoarseness

* Erase of vision

* Loss of consciousness (syncope)

* Pain (sudden onset of chest pain that often has a tearing or ripping quality; patients may also have neck, jaw, throat, or teeth pain, but there may be no pain in up to 10% of patients)

* Increasing temperature (fever)

* Mental status altered

* Diaphoresis

* Yes, I have trouble swallowing (dysphagia)

* Impending doom (anxiety)

* Nausea and vomiting

* Gasping for breath (SOB)

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Diagnosis STAT!

The patient’s history is one of the important first steps in trying to establish a diagnosis. It’s imperative to consider not only the symptoms, but also the risk factors of high BP, genetic or family history, and the presence of other medical conditions that may predispose the patient to aortic dissection.

Diagnostic tests include:

* 12-lead ECG to rule out acute myocardial infarction (MI)

* chest X-ray, which exposes a widened aorta in up to 90% of patients with an aortic dissection; the chest X-ray reveals no abnormalities in 10% of patients

* computerized tomography (CT) scan of the chest and abdomen is the test of choice for aortic dissection and provides a quick, clear picture of the type and location of the dissection

* magnetic resonance imaging (MRI) reveals the type and extent of the dissection; the MRI takes much longer to perform than a CT scan, diminishing its usefulness

* transesophageal echocardiography (TEE) for unstable patients unable to be transported to radiology

* blood work for elevated cardiac markers (creatine kinase isoenzymes, myoglobin, and troponin 1 and T levels) when the dissection extends to the coronary arteries; increased blood urea nitrogen and creatinine levels indicate renal artery involvement and a low hemoglobin/hematocrit level may indicate leakage.

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Classify it

The Stanford classification system is the most widely used system to classify aortic dissections. The classification of the dissection will determine the course of treatment. There are two types of dissections:

* type A dissection: a dissection to the ascending aorta that requires surgical intervention

* type B dissection: a dissection of the descending aorta, most often treated medically with routine monitoring and prescribed medications.

In comparison, the DeBakey classification system is based on the site of origin, with type I originating in the ascending aorta and propagating to at least the aortic arch, type II originating in and confined to the ascending aorta, and type III originating in the descending aorta and extending distally or proximally.
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Treat it

If the patient is experiencing a type A dissection, emergency surgical intervention is frequently required. The surgery is typically performed as an open procedure, with an incision in the chest or abdomen to provide direct access to the aorta. The area of the aorta with the intimal tear is resected and replaced with a graft to restore blood flow through the aorta. In some cases, the aortic valve may need replacement.

Some patients may be candidates for the minimally invasive approach called endovascular stent graft repair instead of open surgery. In this procedure, a small incision is created in the groin and a stent graft is inserted into the femoral artery. Using fluoroscopy and TEE, the stent graft is guided through the aorta to the aneurysm. After the stent graft is in place, the blood will flow through it instead of through the aneurysm, eliminating the risk of rupture. In order to be a candidate for this procedure, the patient must be in stable condition and the dissection must be located in the descending aorta.

Patients with uncomplicated type B dissections are best treated with drug therapy. The primary goals of drug therapy are the reduction of BP and heart rate, and the control of pain and anxiety. The systolic BP goal is 100 to 120 and the heart rate goal is less than 60. Therapies include beta-blockers for BP and heart rate control, and vasodilators if additional BP control is needed. Titratable beta-blockers, such as esmolol or labetalol, are best, followed by a vasodilator, such as nitroprusside, for optimal BP. If vasodilators are contraindicated, calcium channel blockers, such as verapamil, diltiazem, or nifedipine, may be administered. Opioids, such as morphine sulfate, are given to reduce pain.
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Watch out for complications

To remember the possible complications of aortic dissection that can occur pre- and postoperatively, use the acronym DOSED.

* Damage to the aortic valve

* Organ damage, most likely kidney failure or life-threatening damage to the intestines

* Stroke due to involvement of one or more arteries supplying portions of the central nervous system

* Excess leakage from the aortic valve (aortic regurgitation)

* Death, most likely caused by severe internal bleeding into the lining around the heart

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What happens next?

Typically, the patient will remain in the hospital for 2 to 10 days, depending on the type of treatment received. Patients who recover from aortic dissection have a 5-year survival rate of up to 80% and a 10-year survival rate of about 50%. After discharge, the patient must be monitored closely for signs and symptoms of late complications, such as another dissection, development of aneurysms in the weakened aorta, and an increase in aortic insufficiency. Long-term management includes aggressive, vigorous BP control. The BP goal is below 120/80 to decrease the force of left ventricular contractions and lower systemic pressure. Beta-blockers are preferred, but calcium channel blockers may be prescribed for patients who can’t tolerate them.

To remember what to teach your patient after aortic dissection, use the acronym NOT GOING TO DIE.

* No driving for 1 to 2 weeks

* Only ingest a diet low in sodium and cholesterol

* The importance of maintaining a healthy weight

* Get emergency help if you’re experiencing chest pain or other signs and symptoms of dissection

* Only lift things under 10 lb (4.5 kg) for 4 to 6 weeks

* Incision must be kept clean and dry

* Need for repeat CT scan at 1, 6, and 12 months

* Go to your healthcare provider for scheduled appointments

* The importance of aneurysm screening for at-risk family members (particularly those who have hypertension, who smoke, or who are older)

* Observe for any signs and symptoms of dissection

* Don’t smoke

* Include daily exercise when cleared by your healthcare provider

* Emphasize the importance of taking medications as prescribed

It’s so important to consider the psychological effects that aortic dissection may have on many patients. The fear of another incidence weighs heavily on the mind of the recently diagnosed patient. This devastating feeling is sometimes described like a human time bomb waiting to go off again without warning. The patients who experience this overwhelming feeling of impending doom need to be referred to counseling and support groups.
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Wrapping it up

Cardiovascular disease is the leading cause of death in most Western societies. Aortic diseases constitute an emerging share of the burden. An acute aortic dissection is the most common life-threatening disorder of the aorta, affecting nearly 10,000 people per year in the United States. It requires immediate recognition and treatment. If left untreated, about 33% of patients die within the first 24 hours, 50% die within 48 hours, and 75% will die within 2 weeks. You must act quickly to increase the patient’s chance of survival; however, the symptoms of aortic dissection are frequently misconstrued for other medical diagnoses. These may include acute MI, pulmonary embolism, stroke, and pericarditis. In fact, 65% of aortic dissections are misdiagnosed, leading to its high mortality.

All patients who’ve been diagnosed with this condition must be treated with extremely aggressive medical therapy, follow-up visits, and serial imaging. It has been estimated that nearly one third of the patients who survived initial treatment for acute dissection will experience dissection extension or aortic rupture, or will require surgery for aortic aneurysm within 5 years of initial diagnosis. The risk is especially greater in the first few months after initial therapy.

As a nurse, you can play a crucial role in improving the outcome for patients with aortic dissection. Providing lifesaving interventions is possible only when knowledgeable healthcare providers can immediately detect the signs and symptoms of this potentially deadly condition. With aortic dissection, it’s crucial to remember that every second counts!
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memory jogger

To remember the signs and symptoms of aortic dissection, use the acronym
Figure. No caption a…
Image Tools

HELP I’M DYING.

* Hypertension/hypotension and hoarseness

* Erase of vision

* Loss of consciousness (syncope)

* Pain (sudden onset of chest pain that often has a tearing or ripping quality; patients may also have neck, jaw, throat, or teeth pain, but there may be no pain in up to 10% of patients)

* Increasing temperature (fever)

* Mental status altered

* Diaphoresis

* Yes, I have trouble swallowing (dysphagia)

* Impending doom (anxiety)

* Nausea and vomiting

* Gasping for breath (SOB)

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memory jogger

To remember the possible complications of aortic dissection, use the acronym DOSED.
Figure. No caption a…
Image Tools

* Damage to the aortic valve

* Organ damage (kidney failure or life-threatening damage to the intestines)

* Stroke

* Excess leakage from the aortic valve (aortic regurgitation)

* Death (usually caused by severe internal bleeding into the lining around the heart)

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memory jogger

To remember what to teach your patient after aortic dissection, use the acronym NOT GOING TO DIE.
Figure. No caption a…
Image Tools

* No driving for 1 to 2 weeks

* Only ingest a diet low in sodium and cholesterol

* The importance of maintaining a healthy weight

* Get emergency help if you’re experiencing chest pain or other signs and symptoms of dissection

* Only lift things under 10 lb (4.5 kg) for 4 to 6 weeks

* Incision must be kept clean and dry

* Need for repeat CT scan at 1, 6, and 12 months

* Go to your healthcare provider for scheduled appointments

* The importance of aneurysm screening for at-risk family members (particularly those who have hypertension, who smoke, or who are older)

* Observe for any signs and symptoms of dissection

* Don’t smoke

* Include daily exercise when cleared by your healthcare provider

* Emphasize the importance of taking medications as prescribed

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Learn more about it
Braverman AC. Acute aortic dissection: clinician update. http://circ.ahajournals.org/content/122/2/184.long.
Coughlin RM. Recognizing aortic dissection: a race against time. Am Nurse Today. 2008;3(4):1–3.
Della Croce H. Aortic dissection. RN. 2007;70(3):26–31.
Ham S. Emergency repair of aortic dissection in a 37-week parturient: a case report. AANA J. 2010;78(1):63–68.
Ignatavicius D, Workman D. Medical-Surgical Nursing. 7th ed. St. Louis, MO: Elsevier; 2012:796–797.
Lee CA. Aortic dissection: the tear that kills. Nurs Manage. 2007;35(2):25–32.
Mancini MC. Aortic dissection. http://emedicine.medscape.com/article/2062452-overview.
Mayo Clinic. Aortic dissection. http://www.mayoclinic.com/health/aortic-dissection/DS00605/DSECTION=causes.

LifeInTheFastLane.com-Die like a king article

Great read!

Atypical Presentation of Ascending Aortic Dissection

Introduction: Ascending aortic dissection is a rare cause of acute chest pain. Hypertension is the most common risk factor. Other contributing factors include smoking, dyslipidemia and connective tissue diseases. The classic presentation in patients with an aortic dissection is acute severe tearing chest pain radiating to the back. Chest x-rays are commonly abnormal and aid in the diagnosis of aortic dissection. According to the article “Does this Patient have an Acute Thoracic Dissection?” published in JAMA in 2002, the sensitivity of the chest x-ray for acute thoracic dissection is 90%.
Case: In our case, the patient was a 44 y/o male with a history of hypertension and tobacco use that presented to a community emergency department shortly after the onset of pain.

Patient vital signs on arrival were blood pressure 128/73, heart rate of 74, respiratory rate of 20, temperature 36.1 degrees Celsius, and SpO2 of 96% on 2 liters. At first, his presentation was concerning for acute coronary syndrome, but the differential diagnosis was broadened after the patient’s pain did not resolve with NTG and multiple doses of morphine. Physical exam showed the patient to be in mild distress and holding his chest. A III/VI diastolic murmur at the 2nd intercostal space on the right sternal border consistent with aortic insufficiency was noted. Despite a normal chest x-ray and a repeat EKG which showed ST elevation in the anterior leads, the patient was sent for STAT CT scan of his chest to rule out a dissection. During the work-up, the patient became hypotensive and fluid resuscitation was required. The CT scan showed an intramural thrombus, which is consistent with a dissection at the aortic root. The patient was then transferred to a tertiary care center for emergent cardiothoracic surgery. He underwent a successful aortic root replacement, had an uneventful 2 weeks hospital stay and was discharged home.
Discussion: We encountered a case of ascending aortic dissection in which the patient had a normal chest radiograph. According to Harwood-Nuss’, patients with aortic dissection commonly have an abnormal chest radiograph with a widened mediastinum being found 65% to 85% of the time. Patients with aortic dissection also classically present with hypertension, but in our case, the patient was normotensive and progressed to a significantly low diastolic pressure of 28 mmHg. We hypothesize that this was secondary to the patient having a significant diastolic murmur on physical exam, a finding that is consistent with aortic insufficiency. As a result, it appeared as if the patient’s systemic blood pressure was low, but at the dissection’s origin, the blood pressure was likely elevated. According to Harwood-Nuss’, aortic insufficiency occurs only 16% to 20% of the time in patients with aortic dissection. In conclusion if an aortic insufficiency murmur is heard then you should definitely look for an aortic dissection.

Remember that relying on a chest x-ray to determine if aortic dissection is not 100%.

Article Source

Emergency Room Questions and what should be done for possible Aortic Dissections

I emailed a few of my good buddies for their opinions. I asked them if they were ER doctors, what would be the 3 or 4 things that they would look for or do:

Careful history, exam ( murmur, differential pulses), ECG CXR and blood test D-dimer (positive)/ cardiac enzymes (negative) then CTA. From one surgeon:
____________________________________________________________
Mostly history and physical

…Solicit complaints of chest pain or upper back pain.

EKG

If EKG nml – CT scan
____________________________________________________________

Here a good article as well: Emergency Department Care
http://emedicine.medscape.com/article/756835-overview#aw2aab6b4

Emergency Department Care

The mortality rate of patients with aortic dissection is 1-2% per hour for the first 24-48 hours. Initial therapy should begin when the diagnosis is suspected. This includes 2 large-bore intravenous lines (IVs), oxygen, respiratory monitoring, and monitoring of cardiac rhythm, blood pressure, and urine output.

Clinically, the patient must be assessed frequently for hemodynamic compromise, mental status changes, neurologic or peripheral vascular changes, and development or progression of carotid, brachial, and femoral bruits.

Aggressive management of heart rate and blood pressure should be initiated.

Beta blockers should be given initially to reduce the rate of change of blood pressure (dP/dt) and the shear forces on the aortic wall.

The target heart rate should be 60-80 beats per minute.

The target systolic blood pressure should be 100-120 mm Hg.

End organ perfusion should be evaluated. Balancing the risks of dP/dt on the aortic wall versus the benefits of acceptable end organ perfusion may be a difficult clinical decision.

Retrograde cerebral perfusion may increase the protection of the central nervous system during the arrest period.

The mortality rate from aortic arch dissections is about 10-15%, with significant neurologic complications occurring in another 10% of patients. The mortality rate is influenced by the patient’s clinical condition.

The American College of Radiology has established ACR Appropriateness Criteria for the diagnosis and treatment of suspected aortic dissection.[1]
Type A dissections

Urgent surgical intervention is required in type A dissections.

The area of the aorta with the intimal tear usually is resected and replaced with a Dacron graft.

The operative mortality rate is usually less than 10%, and serious complications are rare with ascending aortic dissections.

The development of more impermeable grafts, such as woven Dacron, collagen-impregnated Hemashield (Meadox Medicals, Oakland, NJ), aortic grafts, and gel-coated Carbo-Seal Ascending Aortic Prothesis (Sulzer CarboMedics, Austin, Tex), has greatly enhanced the surgical repair of thoracic aortic dissections.

With the introduction of profound hypothermic circulatory arrest and retrograde cerebral perfusion, the morbidity and mortality rates associated with this highly invasive surgery have decreased.

Dissections involving the arch are more complicated that those involving only the ascending aorta, because the innominate, carotid, and subclavian vessels branch from the arch. Deep hypothermic arrest usually is required. If the arrest time is less than 45 minutes, the incidence of central nervous system complications is less than 10%.

Aortic stent grafting is a challenging technique. It may prove feasible and has offered good results in a small series of patients. It may be a reasonable alternative in high-risk patients in the near future.
Type B dissections

The definitive treatment for type B dissections is less clear.

Uncomplicated distal dissections may be treated medically to control blood pressure. Distal dissections treated medically have a mortality rate that is the same as or lower than the mortality rate in patients who are treated surgically.

Surgery is reserved for distal dissections that are leaking, ruptured, or compromising blood flow to a vital organ.

Acute distal dissections in patients with Marfan syndrome usually are treated surgically.

Inability to control hypertension with medication is also an indication for surgery in patients with a distal thoracic aortic dissection.

Patients with a distal dissection are usually hypertensive, emphysematous, or older.

Long-term medical therapy involves a beta-adrenergic blocker combined with other antihypertensive medications. Avoid antihypertensives (eg, hydralazine, minoxidil) that produce a hyperdynamic response that would increase dP/dt (ie, alter the duration of P or T waves).

Survivors of surgical therapy also should receive beta-adrenergic blockers.

A series of patients with type B dissections demonstrated that aggressive use of distal perfusion, CSF drainage, and hypothermia with circulatory arrest improves early mortality and long-term survival rates.

Endovascular stenting remains an option for treatment of some type B dissections. Some studies recommend that patients with complicated acute type B dissections undergo endovascular stenting with the goal of covering the primary intimal tear.[2]
Definitive treatment

Definitive treatment involves segmental resection of the dissection, with interposition of a synthetic graft.

When thoracic dissections are associated with aortic valvular disease, replace the defective valve.

With combined reconstruction–valve replacement, the operative mortality rate is approximately 5%, with a late mortality rate of less than 10%.

Operative repair of the transverse aortic arch is technically difficult, with an operative mortality rate of 10% despite induction of hypothermic cardiocirculatory arrest.

Repair of the descending aorta is associated with a higher incidence of paraplegia than repair of other types of dissections because of interruption of segmental blood supply to the spinal cord.

The operative mortality rate is approximately 5%.

In a study by Mimoun et al of patients with Marfan syndrome who had acute aortic dissection, the patients were found to have a better event-free survival when there were no dissected portions of the aorta remaining after surgery

Emergency Room Error Leads to Undiagnosed Aortic Dissection

Emergency Room Error Leads to Undiagnosed Aortic Dissection – Cook County Jury Awards $3.7 Million in Estate of Michael Hamilton v. Excell Emergency Care, LLC

A Cook County circuit court returned a $3.76 million verdict in the case of Estate of Michael Hamilton v. Excell Emergency Care, LLC, et al., No. 07 L 6654. The Cook County medical malpractice alleged that the decedent, Michael Hamilton, would still be alive if not for the preventable emergency room errors committed at St. James Hospital.

Hamilton presented to the emergency room at St. James Hospital in Chicago Heights complaining of abdominal pain. Hamilton had been at work in a local paint factory when he began feeling dizzy, sweaty, nauseous, and having severe chest pains. Co-workers reported that he was pounding his chest with his fist and laying down in extreme pain. They called an ambulance and he was rushed to the emergency room.

However, by the time that Hamilton presented to the emergency room his severe pains had diminished substantially. Jose Almeida, M.D., the emergency room physician treating Hamilton, failed to document the details of Hamilton’s symptoms and pain at work. Therefore, rather than investigating the cause of Hamilton’s severe pain, he was simply diagnosed with abdominal pain and sent home with no further instructions.

Less than a week later, the 35 year-old was found dead at his home. A medical examiner determined that Hamilton had died of an aortic dissection, which occurs when the bleeding occurs into the aorta. Because the aorta is the major artery carrying blood out of the heart, when there is bleeding in this area it affects the blood flow throughout the whole body. An aortic dissection is considered a medical emergency.

At the time of his death, Hamilton lived with his mother, Evelyn Hart, who brought the Chicago wrongful death lawsuit against St. James Hospital and the emergency room doctor who misdiagnosed Hamilton’s symptoms. The Illinois lawsuit alleged that Dr. Almeida had chosen not to take the necessary steps to diagnose Hamilton’s aortic dissection and contended that had Dr. Almeida taken those steps that Hamilton could have been saved.

At trial, the decedent’s medical experts claimed that the emergency room doctor should have been more thorough when documenting the events that occurred at Hamilton’s work. The medical experts contended that it was the medical standard of care for a physician to document the events leading up to chest and abdominal pain when taking the patient’s medical history and that to not do so was a substantial emergency room error. Dr. Almeida and his experts retorted that he had satisfied the standard of care and not done anything wrong.

Decedent’s attorneys also were critical of Dr. Almedia for not ordering a CT scan given Hamilton’s complaints of chest pain and that this mistake led to the eventual misdiagnosis. If a CT had been ordered it would have likely shown Hamilton’s aortic dissection and would have at least ruled out any other potentially life-threatening conditions. The defense responded by pointing out how rare aortic dissections are, especially in someone in their 30s. The defense maintained the emergency room doctor had acted appropriately in response to someone who presented with abdominal pain that then resolved while he was in the emergency room.

However, the standard practice for physicians is to rule out the most serious cause of abdominal pain first, gradually moving from most life-threatening problems to more common causes. This was obviously not done in Mr. Hamilton’s case, which was likely why the Cook County jury found in favor of the decedent’s estate. The $3.76 million verdict will go to Hamilton’s 12 year-old daughter, who was his only surviving heir.

It’s your GUT feeling that might save your life or a loved one

 I received a call today from a lady who’s husband recently suffered a Type B aortic dissection.  I was so thrilled to have her call me and reach out for help. What I learned from speaking with her is that she’s one driven woman. Apparently, her husband had been working on remodeling the up stairs bathroom. He had come down the stairs and sat on the couch complaining of back pain and that his legs were going numb. She said that she immediately decided to take him to the local ER room. She made another “key” decision – to call a friend to have him meet her at the ER. This was a long time friend of her husband. Apparently, they got to the ER and did a few tests, only to have the ER department want to send him home.  It was then that the wife and her friend of the husband decided that their “gut” feeling and intuition was required and kicked in! They refused to let their friend/husband just be sent home to die. They demanded that they get a CT done and sure enough, it was obvious that he’d had a descending dissection (type B). The next intuition move that was also another “key” to the successful outcome was to request a Life Line helicopter ride versus staying in traffic. She knew that time is NOT on your side during a dissection. The surgeon was waiting at the U of Penn and there they had the surgery.

My point in all this and as I mention right on my home page, you MUST demand a complete explanation and proof that if they are going to send home your loved one, they better have PROOF that they can justify it. Otherwise, stay in their and fight for more tests and a CT to rule out any type of Ascending or Descending aortic dissection.

I hope this helps!

Brian

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