Case Study Of Pericarditis

A 68 year old male presented to the emergency department at 0800 hours via ambulance after experiencing chest discomfort and intermittent palpitations since 0500 hours. Prior to presentation, the patient stated he

presented with chest pain and an exacerbation of chronic iron deficiency anemia. The patient was examined and given a chest x-ray along with and ECG to assess heart function. The patient complained of shortness of breath and a tight feeling in his chest when he was breathing. The patient has history is sick sinus syndrome, therefore the patient was aware of the symptoms and has felt them before. The patient’s medical history also includes obesity, hypertensive heart disease, A-Fib, CAD, venous stasis ulcers, and a history of EtOH abuse. The patient presented with +1 pitting edema in the lower extremities, with a cool temperature symmetrically. The patient’s capillary refill was less than 3 seconds with Dorsalis pedis pulses +1 and Posterior tibialis pulses +1 symmetrically. The patient’s vital signs were BP-112/69, RR-20, P-70, T-36.2 degrees C and SpO2 94% on room air. The patient’s white blood cell count was within normal limits, therefore an infection is not suspected. The patient’s BMI was 35, therefore considering him obese. Since the patient presented with chest pain, the patient was given a medication to control his heart rhythm and

Physical Examination: General: The patient is an alert, oriented male appearing his stated age. He appears to be in moderate distress. Vital signs: blood pressure 132/78 and pulse 68 and regular. Temperature is 38.56 oC (101.4 oF). HEENT:Normocephalic, atraumatic. Pupils were equal, round, and reactive to light. Ears are clear. Throat is normal. Neck: The neck is supple with no carotid bruits. Lungs: The lungs are clear to auscultation and percussion. Heart: Regular rate and rhythm. Abdomen:Bowel sounds are normal. There is rebound tenderness with maximal discomfort on palpation in the right lower quadrant. Extremities: No clubbing, cyanosis, or edema.

Patient complained she was short of breath and experiencing severe pain between her shoulder blades. She stated that she has been feeling nasuseated for the past 3 hours. She states she has a history of stable angina and is currently taking medication as needed. She states she did not take the nitroglycerin because she was not experiencing chest pain, just back pain. She states that her last check-up with the Pulmonologist showed that her EKG did not show any changes since her last visit. She denies episodes of syncope. The patient does report that she tripped over something on the floor, which resulted in her falling and hitting her back on a large table. In addition, she states that her heart rate has been ranging from 130/ 90 to 140/92. Patient states her Primary care physician placed her on blood pressure medication 2 months ago due to the increase.

With acute aortic insufficiency, pulse pressure widens as the valve deteriorates. Signs and symptoms may include a bounding pulse, atrial and ventricular gallops, chest pain, palpitations, pallor, crackles, dyspnea, and jugular vein distention, may also be present.

Few days back, the patient had a CABG surgery and was send home under stable conditions. Family member noticed SOB and weakness from the patient and was directed to attend the ED. As they got to the ED, the emergency department nursing staff noticed SOB with pericardial hematoma and immediate drainage was necessary. A chest tube was placed as a treatment option.

At today's visit she is found in her room sitting in her recliner. She reports chronic, intermittent, dull, achy, lower back pain. Her current pain regimen is effective for her pain according to the facility staff. The staff reports that the patient is sleeping more hours during the day. She has increased generalized weakness. No acute distress noted this visit.

Mr. Heart, a 72-year-old male admitted for an elective open heart procedure has the following medical and surgical history: coronary heart disease; arthritis; hypothyroidism; diet controlled diabetes; underwent appendectomy; arthroscopic right knee surgery; and two cardiac stents. No history of smoking and weights 160 lbs. at 5’ 11”.

Since it has been determined by researchers that causative agents of infective endocarditis play a major role in treatment, it is important to know what exact causes those are. In a study by Zauner et al. (2013), “IE-causing pathogens were Staphylococcus aureus, viridans streptococci, enterococci, streptococci, coagulase-negative staphylococci, and miscellaneous pathogens” (637). Depending upon the organism that infects the heart, there are different outcomes. For example, those infected by staphylococcus aureus suffered noticeably higher sepsis rates, or severe blood infections. S. aureus also tended to cause more cases of emboli activity, or blockages in the bloodstream. In contrast, other organisms affected the body differntly.

An additional study investigated the usefulness of histopathological findings in the diagnosis of infective endocarditis. Histopathology is the study of tissues viewed under a microscope to determine manifestations of disease. In countries outside of the United States, histopathological findings are the gold standard in confirming infective endocarditis in humans. Researchers intended to challenge this idea and see if histopathological findings really are the best form of diagnosing infective endocarditis, and if those findings can stand by

This patient is a 73-year-old female who required inpatient hospitalization due to end stage renal disease secondary to persistent bacteremia and other underlying conditions. She was admitted to Truman Medical Hospital for further treatment and evaluation due to complaints of severe bilateral flank pain for three days that worsened with movement. She also reported shortness of breath and had been constipated for 3-4 days.

prescribed methylpredisone 4mg for 6 days and ibuprofen 600 mg PRN for pain. Her last

Pericarditis is a broad term for a condition in which the thin, sac-like membrane surrounding the heart, called the pericardium, becomes irritated and inflamed. It could arise from a previous illness or it could develop as a surgical disorder. Acute pericarditis develops suddenly and could last for several months. Constrictive pericarditis occurs when the two layers of the pericardium fuse together and become fibrous, compressing the heart. This limits the diastolic filling of the ventricles. The pericardium is composed of an inner and outer layer. Normally, a small amount of fluid exists between these two layers. When the pericardium is inflamed, extra fluid collects between these layers and results in the compression of the heart, making it more difficult for the heart to pump. When symptoms persist for longer than usual, it is considered to be chronic pericarditis, which often results in constrictive pericarditis (National Heart, Lung, and Blood Institute , 2012). Viral infections are most often the cause, resulting in viral pericarditis.

Patient is a 45 yo male; 5’7”, 221 lbs who entered the emergency room at 6:30 am on 9/7/14 with severe chest pain (onset at 6:00 am) radiating to his arm, L arm numbness and nausea and vomiting. Past medical history reported by wife includes peptic ulcer, tobacco use (1-2ppd for 27 years), elevated blood pressure (controlled by lopressor). Wife did not know of any family history but reports patient’s father is deceased, died at 42 in his sleep. Mother alive and with high blood pressure.

5. KoparalS ,Vurol M, Sayen B, PasaogluL, Elverici E, DedeD. Isolated pericardial hydatidcyst in an asymptomatic patient, a remark on its radiologic diagnosis. Clin Imaging 2007 Jan-Feb;31(1):37-9.