Case Presentation by Dr. Daniel Hutchens
History of Present Illness:
A 52 year old man with a past medical history of hypertension presents to the ED with complaints of acute onset chest pain for 8 hours. The patient was sitting at home when it started and denies any exertional component. The pain is sharp, located retrosternally, and radiates to the left neck and shoulder. The pain is worse during inspiration and when lying flat, and is relieved by sitting upright and leaning forward. Patient took his blood pressure medication at home and did not feel relief so he came to the ED. He does not take aspirin. He feels SOB and states that he had a URI 1 week ago. There has been no recent travel. He states toward the end of the exam that he is worried about the cost of his care as he just lost his job.
Review of Systems:
Admits to a mild cough and occasional dizziness, otherwise negative except as per HPI.
Past Medical History: Hypertension
Past Surgical History: No surgical history
Social History: Denies tobacco, occasional alcohol, occasional marijuana
Family History: HTN, father with an acute MI (AMI) at 65
VS: BP 142/92 mmHg, HR 110, RR 20, O2 Sat 97% on room air, Temp 38.0°C
ENT: PERRLA, EOMI, throat is non-erythematous
Neck: Supple, no carotid bruits
Heart: RRR, there is a high pitched scratching sound heard that remains with suspension of respiration
Lungs: CTAB, no wheezing, no rales, ronchi are heard that remain with suspension of respiration
Abdomen: Soft, nontender, nondistended, positive bowel sounds
Skin: No rash
Neurologic: Gait is normal.
IV access was established; patient was put on oxygen, cardiac monitoring, and given an aspirin. 12 lead EKG was obtained.
A line was placed and labs were sent including a BMP, CBC, coagulation panel, and troponin. CXR was obtained.
Cardiac ultrasound (US) was performed at the bedside.
Labs came back and Troponin I was <0.017. Serum electrolytes as well as BUN and Cr were wnl. CBC and coagulation studies were wnl.
1.) What is the best treatment in this patient’s case?
2.) What is a distinguishing factor for acute pericarditis vs. AMI on EKG?
a. PR interval elevation
b. Inverted T waves in the anterior and inferior leads
c. ST-segment depressions in the precordial leads with reciprocal changes
d. Diffuse ST-segment elevations with no reciprocal changes
3.) How can you use serum biomarkers with EKG to help diagnose acute pericarditis over AMI?
a. Biomarker elevation will be moderate compared to what would be expected in AMI given the EKG findings
b. Biomarker elevation will be higher compared to what would be expected in AMI given the EKG findings
c. Biomarker elevation is never seen in acute pericarditis
d. There is no relation between biomarker elevation and EKG findings in acute pericarditis
Answers to the questions:
1.) b. Ibuprofen
2.) d. Diffuse ST elevations with no reciprocal changes
3.) a. Biomarker elevation will be moderate compared to what would be expected given the EKG findings
The characteristics of this patient’s pain, the physical exam finding of a friction rub, and the EKG findings make the most likely diagnosis acute pericarditis. Acute pericarditis is classified as chest pain for <6 weeks and can resemble cardiac ischemia. It is often severe, retrosternal and left precordial, and referred to the neck, arms, or left shoulder. Pain is often pleuritic but sometimes it is a steady, constricting pain that radiates into either arm. Characteristically, pericardial pain is relieved by sitting up and leaning forward, something you would not see classically with AMI. EKG changes in acute pericarditis will show diffuse, concave ST elevation across multiple leads, usually with PR depression early, then isometric T-waves progressing to ST depression. This is in contrast to EKG changes in AMI, where you would expect more convex ST elevations present in anatomically contiguous leads with reciprocal changes. Acute pericarditis is often accompanied by some degree of myocarditis causing serum biomarkers (troponin) to rise, termed myopericarditis. These elevations, if they occur, are often quite modest compared to the elevations in AMI given the extensive EKG findings of ST-segment elevation.
A pericardial friction rub will be audible in anywhere from 50-85% of patients with acute pericarditis and is pathognomonic. It will have a rasping, scratching, or grating quality. The best way to hear it is to have the patient sit up and lean forward while placing your stethoscope over the lower sternal edge or apex. It is heard best at end-expiration and won’t disappear with cessation of respirations as would a pleural rub. More than 50% of rubs are triphasic and will include an atrial systolic rub preceding S1, a ventricular systolic rub occurring between S1 and S2, and an early diastolic rub occurring after S2. It is not uncommon for patients with acute pericarditis to have a pericardial effusion and a pericardial friction rub can be heard at the start. After enough effusion has accumulated the rub will disappear. US is the best initial test which will show free fluid in the pericardial space. The US from the case shows a small pericardial effusion near the right atrium.
Within the diagnosis of acute pericarditis it is necessary to determine an underlying cause. Different etiologies of are grouped into infectious, noninfectious, or autoimmune. Infectious etiologies include: viral (1-10% of cases, peaks in spring and fall); pyogenic (bacterial from direct pulmonary extension, hematogenous spread, myocardial abscess/endocarditis, post-surgery); tuberculous (suspect in high risk groups and developing countries). Noninfectious etiologies include: post-MI (Dressler’s syndrome); uremia (usually secondary to ESRD or dialysis, will often have normal EKG because little epicardial inflammation occurs); neoplastic (both primary and metastatic); myxedema; traumatic; aortic dissection; sarcoidosis. Autoimmune etiologies include: rheumatic fever; SLE; RA; scleroderma; Wegener’s granulomatosis; drug-induced (procainamide, hydralazine, phenytoin, isoniazide, minoxidil, anticoagulants). An idiopathic cause is responsible for 26-28% of acute pericarditis diagnoses and is the most common etiology given. Many idiopathic cases are likely due to undiagnosed viral infections.
Pericardiocentesis is indicated in patients with effusions larger than 250 mL, effusions where the size increases despite intensive dialysis for 10-14 days, or effusions with evidence of tamponade. The procedure can be performed with or without US guidance, although if it is available US should be used. Before you perform the procedure you should ensure the patient has IV access, is receiving supplemental oxygen, is connected to a cardiac monitor, and continuous pulse oximetry. If time permits you can place an NG tube to decompress the stomach and reduce the risk of a gastric perforation. Either subxyphoid or left sternocostal margin approaches are most often used. The procedure should be performed in a sterile fashion using a spinal needle connected to a syringe with the patient supine if there’s no US guidance, and at 30-45 degrees head elevation if there is. When you’re not using US the needle should be inserted at a 45 degree angle to the abdominal wall and directed toward the left shoulder. With US guidance, insert the needle at a 15-20 degree angle and direct it just under the rib cage toward the left should. The needle is inserted ~5cm while applying negative pressure to the syringe until a return of fluid is noted or a change on the EKG strip is seen. If the EKG pattern shows cardiac injury (ST segment elevation) then you have gone too far, are in direct contact with the myocardium, and should withdraw the needle until the pattern has returned to normal. Withdraw as much fluid as possible. Complications of this procedure are production of pericardial tamponade, laceration of a coronary artery, and induction of cardiac dysrhythmias. Pericardial fluid should be analyzed for red and white blood cells, cytologic studies for cancer, microscopic studies, and cultures. Fluid that returns as an exudate is likely from an inflammatory cause (most commonly viral). Transudative fluid is seen in pressure-related conditions such as congestive heart failure. If red blood cells are seen in the fluid this could represent a complication from acute rheumatic fever, post-cardiac injury, or renal failure (such as in uremic pericarditis). If adenosine-deaminase activity is high, tuberculous pericarditis should be suspected.
Treatment includes empiric anti-inflammatory therapy for acute and recurrent pericarditis secondary to viral or idiopathic cases that are most commonly seen. Currently, aspirin and NSAIDs are the mainstay of therapy. An “attack dose” should be given for 1-2 weeks. For aspirin this is 2-4 g/day, ibuprofen is 600mg TID, indomethacin is 50mg TID. After the attack dose drug tapering may be considered. Colchicine is added in autoimmune conditions and cases of recurrent pericarditis. It interferes with WBC activity and is good for these cases. Attack dose is not necessary with colchicines and 0.5mg BID can be given for 3 months if it’s the first attack or 6-12 months with recurrent attacks. Corticosteroids should be reserved for difficult cases requiring multi-drug therapies and specific medical conditions. This is because while they offer a fast remission, there is a higher risk of recurrences, prolonged course, and side effects with corticosteroids. The corticosteroid of choice is prednisone and is dosed at 0.2-0.5 mg/kg/day. Treatment length for aspirin, NSAIDs, and corticosteroids are usually until symptoms resolve and CRP normalizes. If it is a uremic pericarditis aggressive dialysis is indicated and NSAID therapy will have little effect. Corticosteroids can be used in these cases but typically don’t produce a response for 1-2 weeks.
Disposition depends on etiology. For idiopathic acute pericarditis, high-dose NSAID therapy is the mainstay of treatment and should be continued for 1-4 weeks. At a week’s time, however, if the current NSAID therapy is not working then the NSAID should be switched to another. 60% of patients will recover in 1 week and 80% by 3 weeks. 18% of patients can have recurrent pericarditis which warrants additional therapy with corticosteroids or colchicines. Patients without clinically poor prognostic predictors (fever >38°C, subacute onset, immunosuppression, trauma, oral anticoagulant therapy, myopericarditis, severe pericardial effusion, cardiac tamponade) can be considered “low-risk cases” and assigned to outpatient treatment with high-dose oral NSAID therapy. Otherwise, hospital admission is warranted with a consult to cardiology and any other subspecialties required (ex. In the case of uremic pericarditis you should also consult nephrology).
- Suspect acute pericarditis if chest pain is sudden onset, relieved by sitting up and leaning forward, and is associated with a friction rub.
- EKG in acute pericarditis will show diffuse ST-segment elevations with no reciprocal changes and PR depression early on.
- Cardiac US should be performed in patients with acute pericarditis to rule out a pericardial effusion.
- If a pericardial effusion is present, CXR may show a typical “water bottle” heart, where the heart is enlarged in the shape of a flask or water bottle.
- Aspirin or NSAID therapies remain the mainstay of treatment for the majority of cases of acute pericarditis. However, other etiologies should be investigated with each case and treated appropriately.
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