MUSCULOSKELETAL COMPLAINTS are commonly seen in the quick care (QC) and emergency care setting. Having a keen awareness of not only the patient's complaint but also the vital signs and other presenting signs and symptoms are of extreme importance. In the case presented in this article, the provider's recognition of abnormal vital signs led to a completely different diagnosis than one would expect with back and shoulder pain.
CASE FOR REVIEW
A 39-year-old man presented to the emergency department (ED) with a complaint of pain in the upper back between the shoulder blades for 1 week. He had been seen by his primary care provider 10 days before coming to the ED and was given an intramuscular injection, hydrocodone and acetaminophen (Vicodin) and cyclobenzaprine (Flexeril). The patient reported that a chest radiograph was negative for infiltrates. The patient reported increased severity of symptoms prior to the ED visit. The pain radiated to the left shoulder. This patient was assigned an Emergency Severity Index score of four and was triaged to the QC area of the ED.
The patient's past medical history was significant for gastroesophageal reflux disease, and current medications include lansoprazole (Prevacid) 30 mg daily, hydrocodone and acetaminophen (Vicodin), and cyclobenzaprine (Flexeril).
The patient denied any food or medication allergies, unsure of last tetanus immunization, smokes a half a pack of cigarettes daily, drinks alcohol three to four times a week, and denied illicit drug use. Significant family medical history included a father who had received a coronary artery bypass graft at 78 years of age.
HISTORY OF PRESENTING ILLNESS
The patient presented in no apparent distress but is complaining of increasing thoracic back pain radiating to the left shoulder. The pain was described as sharp and increased with left arm movement. There was no numbness to the left arm and fingers. The patient has experienced shortness of breath the day before arriving to the ED.
PATIENT ASSESSMENT
The patient presented awake, alert, and oriented. Vital signs are as follows: heart rate, 124 beats/min; blood pressure, 128/82 mmHg; respiratory rate, 20 per min; temperature, 36.9 [degrees]C (98.4 [degrees]F) orally; and pulse oximetry, 97% room air.
Skin. Warm, dry, and pink.
Head, eyes, ears, nose, and throat. head normocephalic, pupils equal, round, reactive to light and accommodation, extraocular movements intact, free of icterus and pale conjunctiva.
Ears, nose, and throat/mouth unremarkable.
Neck. Supple no masses, lesions, or lymphadenopathy. Full range of motion.
Chest/respiratory lungs were clear to auscultation in all fields. No rhonchi, wheeze, or rub.
Heart. S1-S2 with no murmurs, gallops, or rub were auscultated.
Gastrointestinal. No masses. Bowel sounds in all four quadrants. Nontender, nondistended abdomen.
Genitourinary. Unremarkable.
Pelvis. Unremarkable.
Extremities. Unremarkable.
Musculoskeletal/Extremities. Bilateral paraspinal tenderness-thoracic region. No spasm, costovertebral angle tenderness, or limited range of motion. Strength 5/5 bilaterally.
Neurologic. Motor and sensory normal. Deep tendon reflexes were 2+ bilateral ankles and biceps. Glascow Coma Scale score = 15. Cranial nerves II-XII grossly intact.
Psychiatric. Unremarkable.
Emergency department course
The provider ordered the following:
Cervical and thoracic spine plain radiographs-three views
Computed tomography (CT) chest (to rule out aortic dissection)
12-lead electrocardiogram (ECG)
Heart monitor
Laboratory testing
Basic metabolic panel
Complete blood count
Sedimentation rate
Troponin
PT/INR/PTT
Medications
Ketoralac (Toradol) 30 mg intravenous
Normal saline (0.9%) 500 ml/hr followed by 100 ml/hr
The results of the diagnostic testing are as follows:
ECG. Sinus tachycardia with nonspecific T wave abnormality in the anterior leads (Figure 1).
Cervical and thoracic spine. Normal examination.
CT chest. No aortic dissection or dilatation. Cardiomegaly with pericardial effusion up to 1.2 cm linear atelectasis or infiltrate at lung bases. Trace pleural effusions (Figure 3).
CT abdomen. Prior cholecystectomy and appendectomy. Abdominal aorta normal. Mild splenomegaly.
Complete blood count. White blood cell 16.7, hemoglobin 14.5, hematocrit 43.2, and platelets 548.
Basic metabolic panel. Within normal limits.
Sedimentation rate. 19
PT/INR/PTT. 11.4/1.1/29.6
Consultation. A cardiology consult was initiated and stat bedside noninvasive echocardiogram was ordered. The result of the echocardiogram was circumferential pericardial effusion measuring 1.2 cm considered to be small to moderate; mild concentric left ventricular hypertrophy. The aorta, bilateral atria, and ventrical were normal size. Left ventricular systolic and diastolic functions were normal. Ejection fraction was 65% and all valves were normal.
ED Patient Management
This patient was administered levofloxacin (Levaquin) 500 mg intravenously and ibuprofen 600 mg orally. The patient was admitted to the hospital for repeat echocardiograms and further treatment.
Initial chest radiography was repeated twice during admission showing bilateral pleural effusions and cardiomegaly (Figure 3). Workup for autoimmune disease and human immunodeficiency virus was negative. Lyme titer was negative. Blood cultures were negative. Repeat echocardiogram 3 days after admission showed improvement. Medications included nonsteroidal anti-inflammatory pain medication, a proton pump inhibitor for history of gastroesophageal reflux disease and a [beta]-blocker for tachycardia. The patient was discharged 5 days after admission with the discharge diagnoses of (1) pericarditis with pericardial effusion, resolved; (2) left shoulder pain possibly secondary to pericarditis, resolved; (3) tachycardia; and (4) gastroesophageal reflux disease.
ANATOMY AND PHYSIOLOGY OF THE PERICARDIUM
The pericardium consists of two layers that envelop the heart. The visceral layer, or epicardium, is single layer membrane composed of mesothelial cells that adhere to the myocardium. The parietal layer is composed mainly of collagen and elastin fibers. The two layers are separated by a potential space that can contain up to approximately 50 ml of serous fluid. The parietal pericardium attaches to the diaphragm, sternum, and other structures by ligaments that ensure a relatively fixed position of the heart. The structures are innervated by the mammary artery and phrenic nerve (Braunwald, Zipes, Libby, & Bonow, 2004; Marx, Hockenberger, & Walls, 2010).
The pericardium has numerous functions. These functions include lubrication of the heart, heart position, prevention of infection and overdilatation, atrial filling, and maintenance of a normal pressure-volume relationship of the cardiac chambers. Abnormal accumulation of fluid can occur with obstruction of drainage from the venous and lymphatic system (Braunwald et al., 2004; Marx, et al., 2010)
BACKGROUND
A pericardial effusion is defined as the presence of an abnormal amount and/or character of fluid in the pericardial space. It is usually caused by an inflammatory process, in response to disease or injury. Some specific causes of pericardial effusion can be viewed in Table 1 (Strimel, Sovari, Assadi, & Kocheril, 2009; Sugiura, Kataoka, Matsymura, Takeuchi, & Doi, 2009).
In addition, pericardial effusion may also occur when the flow of pericardial fluids is blocked or when blood accumulates within the pericardium, as with cardiac surgery or trauma (Table 1). In many cases, the cause of pericardial effusion can be determined, but in others it is not apparent even with a thorough diagnostic evaluation.
Most small effusions are asymptomatic, being found only on autopsy. Malignant neoplasms have a high prevalence rate, up to 21%, with human immunodeficiency virus showing 5%-43% prevalence. The development of pericardial effusion is not specific to race, gender, or age, though it is most common to occur between 40 and 50 years of age.
CLINICAL MANIFESTATIONS
Clinical manifestations of a pericardial effusion are dependent on the rate of fluid accumulation in the pericardial sac. Symptoms of slow progressing effusions (even up to 2 L of fluid) may be nonexistent, with rapid accumulation of up to 80 ml causing severe symptoms. Manifestations of pericardial effusion include dyspnea, orthopnea, chest pain, cough, painful breathing, especially when lying down, and dizziness and syncope, all very nonspecific to the disease process occurring (Braunwald et al., 2004; Marx et al., 2010; Strimel et al., 2009).
The advanced practice nurse (APN) should specifically question the patient about subjective cardiopulmonary symptoms. Should a patient report any of the above symptoms, the APN should also look for the following signs on examination.
* Pericardial friction rub
* Tachycardia
* Tachypnea
* Tubular breath sounds over left lung base or axilla
* Poor peripheral pulses, edema
* Signs of impending or fulminate cardiac tamponade include the following:
* Hypotension, jugular vein distention, muffled heart sounds (Beck's triad)
* Decrease in systolic blood pressure more than 10 mmHg with inspiration (pulsus paradoxus). (Braunwald et al., 2004; Marx et al., 2010; Strimel et al., 2009)
Advanced practice nurses need to recognize that patient presentation will be affected by the degree of cardiac output and therefore the severity of effusion. Besides pleural effusion, other differential diagnoses should be considered. Some examples of these diagnoses include but are not limited to cardiomyopathy, acute pericarditis, pulmonary edema, and pulmonary embolism.
Pericarditis is considered to be the most common associated diagnosis with pericardial effusion. It is associated with severe pleuritic sharp chest pain, which may radiate to the trapezius region. The pain is relieved by sitting forward and is worsened when the patient lies down. A recent history of fever, cough, dyspnea, and sometimes hiccoughs may be associated symptoms of a patient presenting with pericarditis. Physical examination may reveal patient with low-grade fever that is anxious, with tachycardia and a friction rub that can be heard. The friction rub consists of the three components of ventricular systole, early diastolic filling, and atrial contraction and is heard loudest at the left sterna border with the patient leaning forward (Braunwald et al., 2004).
DIAGNOSTIC EVALUATION
In order to determine the cause of the patient's clinical manifestations, a complete workup should be obtained (Table 2). A baseline chest radiograph should be obtained, which shows an enlarged cardiac silhouette (water bottle or flask-shaped). Cardiomegaly is apparent with a minimum of 200-250 ml of pericardial fluid but will usually have normal pulmonary vasculature. Another reliable sign that can be viewed on chest radiography is a pericardial fat pad sign. The pericardial fat pad sign represents separation of the parietal pericardial fat from the epicardium and is visualized as a linear lucency between the anterior surface of the heart and chest wall (Braunwald et al., 2004). However, radiography is not the most reliable method of establishing a diagnosis.
Imaging
Echocardiography is the noninvasive modality of choice for confirming the diagnosis of pericardial effusion. This modality differentiates pericardial fluid from increased heart chamber size and evaluating wall motion abnormalities. Small effusions may begin over the left ventricle and progress anteriorly, laterally, and behind the left atrium becoming circumferential. The increase in fluid circumferentially can lead to cardiac tamponade (Braunwald et al., 2004). Cardiac tamponade is distinguished on echocardiogram as diastolic collapse usually beginning at the right ventricular wall. Overall sensitivity in identifying pericardial effusion may be as high as 96% (Wills, Young, & White, 2010).
Computed tomography and magnetic resonance imaging can also be used for technically difficult echocardiogram but are not first-line diagnostic studies. Both modalities are useful adjuncts to echocardiography giving more detailed information on the nature of the pericardial fluid. However, neither CT nor resonance imaging is recommended in patients requiring prompt management and treatment decisions. (Braunwald et al., 2004; Goldman et al., 2007; Marx et al., 2010).
Electrocardiography
The ECG typically exhibits reduced voltage and in severe cases electrical alternans. Electrical alternans is reflective of the heart swinging anterior and posterior with each heartbeat. When pericarditis is associated with pericardial effusion, ECG findings may be consistent with pericarditis with widespread ST elevation, T-wave abnormalities, and PR depression (Braunwald et al., 2004; Strimel et al., 2009).
Pericardiocentesis can be performed diagnostically or therapeutically but can have complications of cardiac dysrhythmias, pneumothorax or perforation of the myocardium, or coronary vasculature. Gross appearance of the pericardial fluid can help differentiate the cause (Marx et al., 2010).
CLINICAL MANAGEMENT
Initial management of the patient with pericardial effusion includes volume augmentation with intravenous fluids, which increases the filling pressure with hopes of overcoming the pericardial constriction. Pericardiocentesis is the treatment of choice when imminent or actual pericardial tamponade is present.
Serial echocardiograms are recommended to assess the effects of treatment modalities and to evaluate extension of effusion and development of tamponade (Saito et al., 2008). The incidence of pericardial effusion resulting in tamponade has been estimated to be 3 per 100,000 patients per year (Wills et al., 2010). Other treatment modalities are geared toward the actual cause of the pericardial effusion (i.e., pericarditis, autoimmunity, neoplasm, or trauma; see Table 3).
IMPLICATIONS FOR PRACTICE
The patient discussed in this article presented with upper back and shoulder pain and shortness of breath the day before presenting to the ED. One sign that alerted the provider to conduct an extensive workup was a heart rate of 124 beats/min. It is a basic measurement taken by the triage nurse and can have a great impact on the course of evaluation, diagnosis, and treatment by the provider.
Tachycardia is easy to overlook. Anxiety and pain are common upon entrance to the ED and can induce a mild tachycardia. Abnormal vital signs can also be caused by fever, pulmonary embolism, pericardial effusion, pneumothorax, and numerous other diagnoses. Vital signs should always be the first objective sign providers review. They can be the difference between a simple and more complex workup.
It is important for APNs to always review and consider reasons for abnormal vital signs. Commonly, patients are sent to the QC area of the ED with "minor" complaints. However, we must all be astute to the zebra among the horses.
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