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Chest Pain in a 60-Year-Old Man
HEATHER RYBASACK-SMITH, MD; PAUL PORTER, MD; WILLIAM BINDER, MD
The initial impression was acute coronary syndrome (ACS)
and the patient was given an aspirin and a workup was initiated. The patient’s initial ECG (figure 1) was non- ischemic
and an initial CXR showed no acute abnormalities—there
DR. HEATHER RYBASACK-SMITH: The patient is a 60-yearwas no effusion, widened mediastinum or abnormal aortic
old male who presented to the hospital with the sudden onset
knob, and there was no evidence of congestive heart failure.
of non-radiating anterior chest pain after eating dinner. He
Lab results were significant only for mild hyperglycemia
reported associated nausea and mild shortness of breath. The
(glucose 125 mg/dl), a normal creatinine and a negative tropain was described as moderate in intensity, intermittent,
ponin. Plans were made to admit the patient to the medical
and alleviated by resting and remaining still. He had never
service for a rule out myocardial infarction.
experienced chest pain prior to this episode. His past medical
Several hours into his hospital stay, the patient develhistory was significant for hypertension (treated with lisinoped persistent, sharp chest pain and had a blood pressure of
opril), alcohol abuse, and type II diabetes managed with oral
175/70 mm Hg. A repeat ECG was unchanged. He received
glipizide and metformin. He took a daily aspirin, disulfiram,
sublingual nitroglycerin with minimal affect. Approxia multi vitamin and ibuprofen and smoked ½ pack per day.
mately 3 hours after initial evaluation, the patient became
He was married, employed as a truck driver, and lived with
hypotensive to 75/52 mm Hg with a pulse of 79 beats per
his wife. Initial vital signs included blood pressure of 133/63
minute. He received fluid resuscitation along with blood
with a pulse of 72. Physical exam revealed clear lungs, norproducts and a dopamine infusion, and a surgical consult
mal heart sounds without a murmur or gallop, equal pulses
was requested.
and blood pressures bilaterally and a soft and non-tender
An emergency CTA chest/abdomen/pelvis (figure 2) showed
abdomen. He had no edema. The patient was alert and in
an extensive Type A aortic dissection beginning at the root
no acute distress. On his initial evaluation he was pain-free.
of the aorta and continuing to the
Figure 1. Initial ECG with t wave abnormalities in leads III, avF, and flattened t waves in V5, 6, I, avL
bilateral iliac arteries. It involved the
bilateral subclavian and right brachiocephalic arteries, the celiac axis, and
the left renal artery. There was a large
amount of hemopericardium, and the
left kidney had complete absence of
contrast dye.
From the Case Records of the Alpert Medical School of
Brown University Residency in Emergency Medicine
DR. MARK GREVE: This patient had
none of the classic signs of aortic dissection. What led you to suspect the
diagnosis?
DR. RYBASACK-SMITH: Initially, the
patient’s presentation was concerning
for acute coronary syndrome (ACS).
However, the sudden recurrence of
severe pain with hypotension led
clinicians to quickly reevaluate the
cause of his unremitting pain and
consider other life threatening etiologies, including aortic dissection.
Acute aortic dissection (AAD) is a
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Figures 2a, 2b. Representative cut from initial CT scan showing the dissection flap traversing the aortic arch from the aortic root to the descending aorta.
notoriously difficult diagnosis to make, and is often missed
in the emergency setting. Data from the international registry of aortic dissection (IRAD) revealed that classic findings
such as aortic regurgitation and pulse deficits were only seen
in 31.6% and 15.1% of patients, respectively.1,2 A normal
chest x-ray was noted in about 12.5% of cases and a widened
mediastinum or an abnormal aortic contour can be seen as
infrequently as 20%–60% of cases.2,3,4 While acute onset of
severe chest pain is the most common presenting complaint,
data from IRAD and other sources note painless dissection
in 4.5%–12% of cases, and in one older study up to 27%.1,3,5,6
These patients are likely to be older, chronic steroid users,
patients with Marfans, or those who present with syncope
(9–13% of type A dissections), stroke or congestive heart
failure.1,5 While the majority of patients do report chest
pain, it is usually distinguished as abrupt and sharp, rather
than tearing.1,4,7
The ability of EM physicians (EMPs) to diagnose AAD has
been evaluated in several studies. In 33–57% of cases practitioners do not suspect the diagnosis on initial presentation
and some studies have indicated an overall rate of missed
diagnosis between 40–55%.2,8,9,10 When patients present with
classic findings of chest and back pain, an accurate diagnosis
was made in 86% of cases studied.9
There is a great deal of overlap between the clinical
symptoms and signs of ACS and AAD. ACS is the most
common misdiagnosis and age and anterior chest pain are
confounding factors often leading to premature closure.2
Additionally, evidence of acute ST elevations occur in 1–7%
of patients with proximal aortic dissection. This most commonly occurs in the right coronary circulation as the dissection can extend into the right coronary ostium leading
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to posterior-inferior injury.11 CK-MB and troponin have been
shown to be insensitive in distinguishing between AAD &
ACS, and have been implicated in missed diagnoses.8
Consequences of missed diagnosis are potentially catastrophic. The mortality for Type A dissections without treatment approaches 1–2% per hour in the first 48 hours after
the event.10 Predictors of death and poor outcome include
age >70 years, abrupt onset of chest pain, hypotension/shock
and tamponade, kidney failure, pulse deficit and an abnormal ECG.12 In modern EM, there is a push toward aggressive
treatment for ACS due to worsening outcomes from delayed
reperfusion.13 Yet, the consequences of inappropriate treatment with antithrombotic agents are great and can lead to
delayed diagnosis, major bleeding, greater hemodynamic
instability, increased risk of aortic rupture and an overall
trend toward increased mortality.2 Given the risks of inappropriate antithrombotic treatment in AD and the potential
for misdiagnosis, a low threshold for imaging is appropriate.
DR. ROBERT TUBBS: What type of patient typically presents
with aortic dissection?
DR. WILLIAM BINDER: Numerous primary and acquired
risk factors for AAD have been identified through IRAD
and other studies. These are noted in table 1 and include:
male gender, age >50 years, tobaccos use, DLD, cocaine/
stimulant use, pheochromocytoma, atherosclerosis, connective tissue disorders such as Marfan Syndrome and
vascular Ehlers-Danlos Syndrome, infectious diseases,
inflammatory diseases such as Takayasu and Behcet’s diseases, trauma, chronic corticosteroid use and polycystic
disease.1,14,15 Systemic hypertension is the most common
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DR. PORTER: The patient was initially believed to have
Table 1.
Risk Factor
Comments
Male gender
> 50 years old
Long Standing Arterial
Hypertension
Tobacco use
Dyslipidemia
Cocaine/Crack/stimulants
Pheochromocytoma
Atherosclerosis
Can lead to penetrating ulcer
Connective tissue
disorders/genetically
triggered thoracic aortic
diseases and congenital
disorders
Marfan
Vascular Ehlers-Danlos syndrome (type 4)
Bicuspid aortic valve
Coarctation of the aorta
Hereditary thoracic aortic aneurysm
Loeys-Dietz
Noonan syndrome
Turners syndrome
Infectious Diseases
Syphillis
Salmonella
Tuberculosis
Inflammatory Disorders
Takayasu’s arteritis
Behcet’s disease
Ormond’s disease
Systemic Lupus Erythematosis
Pregnancy
*controversy exists as to whether this is a
risk factor
Iatrogenic causes
Cardiac surgery/Valvular Surgery
Vascular surgery
Catheter/instrumentation
Trauma
Deceleration injury
MVA
Air bag
Fall from height
Other
Weight Lifting
Polycystic Disease
Chronic corticosteroids
risk factor for both Stanford A and B types of dissection.16
However, up to 25% of all patients who present with acute
aortic syndrome, including thoracic aortic dissection, have a
positive family history of aortic disease. Mutations in greater
then a dozen genes are related to syndromic and nonsyndromic
forms of familial thoracic aortic aneurysm and dissection.17
Acute aortic syndromes, whether genetic or acquired,
appear to share a common pathophysiologic pathway: degradation of the medial wall and subsequent stiffening and
fibrosis of the vessel intima. The initial insult can be a result
of genetic or acquired disease such as atherosclerosis, vasculitis, connective tissue or inflammatory diseases, or a bicuspid valve. In hypertension, chronically high pressures lead
to intimal thickening, fibrosis, calcification and fatty acid
deposition; the walls become stiff and weakened. Often a
rupture of a plaque is the nidus for intimal tear, which can
spread anterograde or retrograde to the tear.4,18
DR. MELANIE LIPPMAN: How was the patient managed in
the acute setting?
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ACS and was treated with aspirin, morphine and ondansetron. The patient’s hypotension was treated with fluids and
dopamine. His blood pressure stabilized and the team was
able to obtain a CT demonstrating the dissection and hemopericardium. Norepinephrine was substituted for dopamine to reduce shear stress. The patient was immediately
transferred to the operating room for definitive care.
DR. MEHIR KAMAT: What was the patient’s clinical course?
DR. RYBASACK-SMITH: Upon arrival to the operating room
(OR), the patient’s exam had changed markedly. He was
noted to have a ruddy colored face and chest, a non-palpable
left radial pulse and 1+ trace right radial pulse. He had bilateral edema and mild expiratory wheezes. In the OR he was
noted to have a large pericardial effusion with tamponade
physiology, which was relieved through creation of a pericardial window and extraction of clot. He underwent repair
of the dissection with a tube graft. Post-operatively his ejection fraction was estimated to be 45–50%. The patient was
extubated post- operatively day 0, developed atrial fibrillation requiring amiodarone, and was discharged to home on
hospital day 9 with VNA services. He had minimal blood
flow to his left kidney at time of discharge but had normal
right kidney perfusion. His peak creatinine was slightly elevated at 1.64 mg/dl, but normalized at the time of discharge.
FINAL DIAGNOSIS: Type A Aortic Dissection
References
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3. Hagan PG, Nienaber, CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, Eagle KA. The International Registry of
Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000;283: 897-903.
4. Upadhye S, Schiff K. Acute Aortic Dissection in the Emergency
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11.Hirata K, Wake M, Kyushima M, et al. Electrocardiographic
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AHA Guidelines for the Management of ST-Elevation Myocardial Infarction and Beyond: Review of current STEMI guidelines.
Clinical Cardiology. 2014;37(4):252–259.
14.Sheikh AS, Kamran A, Mazhar S. Acute aortic syndrome. Circulation. 2013;128:1122-1127.
15.Braverman AC. Aortic Dissection: Prompt diagnosis and emergency treatment are critical. Cleveland Clinic Journal of Medicine. 2011;76:685-696.
16.Larson EW, Edwards WS. Risk factors for aortic dissection: a
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Authors
Heather Rybasack-Smith, MD, PGY2 in Emergency Medicine.
Paul Porter, MD, Assistant Professor in Emergency Medicine,
Alpert School of Medicine, Brown University.
William Binder, MD, Assistant Professor in Emergency Medicine,
Alpert School of Medicine, Brown University.
Correspondence
William Binder, MD
[email protected]
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