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Cardiorespiratory - The Management of Pericarditis - Essay Example

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From the paper "Cardiorespiratory - The Management of Pericarditis", cancer represents one of the most frightening diagnoses in medicine, despite cardiovascular diseases’ prominence in worldwide mortality rates. The reason for such an attitude on this diagnosis is based on several beliefs…
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Cardiorespiratory - The Management of Pericarditis
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First and of the teacher of the 24 November, 2008 Cardiopulmonary symptoms Cancer represents one of the most frighteningdiagnosis in medicine, despite cardiovascular diseases' prominence in worldwide mortality rates. The reason for such an attitude toward this diagnosis is based in several, widely accepted, in both patients and physicians, beliefs; cancers have a higher ratio of incidence to mortality than cardiovascular diseases, despite the latter's higher incidence and mortality rates. Also, treatment of cancers is far more difficult, unpleasant and extended than treatments of cardiovascular diseases, with sometimes mixed results. There has been a significant improvement in treatment of some cancers, while others still elude the important discoveries necessary to successfully manage, and in time, defeat such cancers. According to World Health Organization, in 2007 7,9 million people died from cancer, which is 13% of all deaths in the world. It is estimated that 9 million people would perish till 2015, and 11,4 million till 2030. Even though the WHO stresses that most of the cancers are found in low and middle income countries, cancers are quite prevalent in Western countries. For example, according to the American Cancer Association (ACA), in 2005 559 312 people died from cancer, or 22,8% of all deaths, which is only 4% less than heart diseases. The cancer which we are going to focus on is the most prevalent cancer amongst cancer patients- lung cancer. The WHO states that 1,4 million people have died of lung cancer in 2007 and it is still the most prevalent cancer in both men and women, with 31% of cancer deaths amongst men and 26% of cancer deaths amongst women in the US, according to the ACA. A male, non-smoking, 48 year-old patient presents with chest pain and shortness of breath, and a detailed anamnesis morbi is taken. Indeed, these are symptoms that can be attributed to many illnesses such as pneumonia, pulmonary embolism, pleuritis, lung cancer, and rib fractures. Also, there are several examples of cardiac induced chest pain, which is usually a sigh of a problem that requires and urgent reaction, mainly myocardial infarction. The patient also presented with fever, sweating, general weakness and loss of weight. More information is necessary, so the patient is asked if there are any other symptoms (cough, headaches and similar ailments) and how long have tehy lasted. A cough less than 3 week is usually referred to as a acute cough and it would be a sigh of upper respiratory infection, especially the common cold. It can also be a result of pneumonia, and the presence of a postnasal drip can also point to rhinitis or sinusitis that can be allergic, viral, or bacterial in origin. Cough may rarely be the only presenting symptom of pulmonary embolus. In the elderly, acute cough may signify aspiration or heart failure, as conditions that are more serious. A cough lasting more than 3 months to up to 2 years represents a chronic cough and can be usually found in smokers, caused by chronic bronchitis. There is a possibility of an upper airway tumor's presence, which is less common, but should be considered. The most common causes regardless of smoking history include postnasal drip syndrome, gastroesophageal reflux disease (GERD), asthma (cough-variant asthma), and use of ACE inhibitors. Less common causes include eosinophilic bronchitis (characterized by sputum eosinophilia without airway hyperresponsiveness) and bronchiectasis. The causes of chronic cough in children are similar to those of adults, but aspiration and pertussis must also be considered. Tracheobronchitis after a upper respiratory infection is a common cause of cough but rarely lasts more then 3 after the infection. The patient stated that he had a cough that lasted more than three months, and it had no hemotyzis, which is typical, but not necessary, sign of cancer or tuberculosis. Symptoms in other organ systems, such as the urinary, nervous and locomotory, were not reported. The patient is then asked when did the symptoms first appeared, to which he stated that they appeared around 3 months ago. A detailed anamnesis vitae is taken, where past diseases are analyzed. The patient stated that he had generally good health, and had no previous surgeries performed on him. In case of his family anamnesis, the patient presented that he was married and having two children, none of which had genetic diseases. Also, he stated that his parents were deceased, and that his mother suffered from hypertension while his father was healthy, and that his maternal grandfather had cardiovasculary problems, which would point to predisposition to cardiovasculary. His other grandparents were generally healthy. As previously mentioned, this non-smoking, male patient stated that he was working as a construction worker, having a body mass index within the normal boundaries, but clearly towards the lower end because of the weight loss experienced recently. Drinking moderately, the patient has also stated that he has taken few medications during his lifetime, generally aspirin and occasionally antibiotics. He also stated that he had no allergies to any foods and medications. We then proceed to a physical examination of the patient. An examination on the eyes and lymph nodules showed nothing unusual, while we can detect swollen fingers, indicating several diseases, such as bronchial carcinoma, chronic pulmonary diseases such as emphysema, lung apses, bronchoectasies, then asbestos poisoning and fibrosing alveolitis. It can also point to congenital heart anomalies and bacterial endocarditis, as well as ulcerating colitis, celiac disease, Crohn's disease and cirrhosis. However, from our analysis of the anamnesis, we can concluded that there are few diseases that might be responsible for such a symptom, mainly bronchial carcinoma, asbestos poisoning as a result of his working environment and other chronic pulmonary diseases. Lymph nodes are normal during palpation. The abdomen is soft to the touch and it does not produce pain, the liver and spleen are not palpable. We then move on to a physical examination of the chest. It is symmetrical, with the lateral diameter larger than the anteroposterior diameter and its movement during respiration is normal on both sides, which is a normal find. We palpate the chest firstly by placing the index finger in the fossa suprasternalis. If there were pathological processes such as atelectasis, pneumothorax or hyperthireoidism, the index finger would slide on the opposite side of the pathological condition. However, no such sign was found. Then a palpation of the ribs was performed, which showed neither broken ribs or signs of highly developed tumor. Placing the tips thumbs together on the spinal cord and the fingers on both hands into the intercostal regions we can determine the mobility of the chest through the distance between the fingers during inspirium and exspirium. It is an important palpating technique, as it can determine the existence of conditions that effect one side of the chest such as fibrothorax, pleural effusion and pneumothorax. We can also establish normal paramaters through the detection of fremitus pectoralis, which is the detection of vibrations on the walls of the chest during speech. A percussion of the chest follows palpation. It is performed by using the middle finger of the left hand, placed parallel of the ribs in the intercostal regions. We strongly tap the left finger with the middle finger of the right hand while moving only the wrist of the right hand. We perform percussion on both sides of the chest. Percussion sound can vary from sonar in healthy patients, hypersonar with increased amount of air such as in emphysema, relative bluntness, found in consolidations of the lungs and absolute bluntness, found in pleural effusion. A relative blunt sound was detected in the specific patient, indicating some consolidation in the lungs. We also use percussion do determine respiratory mobility and it is usually the preferred method. Mobility was present in the patient, just as it was determined with the palpation. Auscultation of the patient is performed with a stethoscope, where the patient was asked to take deep breaths and to exhale through the mouth. While normal bronchovesicular breathing is found in the apex of right lung, in projection with the main bronchi, the patient showed a pathological breathing, indicating an early or incomplete consolidation of parenchyma. The intensity of breathing was vesicular (normal), as well as the ratio of inspirium and expirium. The existence of accessory murmurs was also detected, and they were nonconsonant bronchiogenic in nature. Its existence confirmed the presence of consolidated masses that affect the bronchial airways. Because of the consolidation, we can detect bronchophonia, which is sound transferred to the surface of the chest and audible when the patient is saying words such as "ninety-nine). This leads us to the conclusion of the existence of chronic pneumonia, tuberculosis, plural apses or other chronic pulmonary diseases, including lung cancer. Auscultation of chest revealed, however, more symptoms, that may cast a shadow on exclusively pulmonary diagnosis. Between the lower left sternal edge and the cardiac apex, during a suspended respiration, a distinctive friction rub can be detected its superficial, creaky, or scratchy character, it can be likened to the sound of walking on dry snow or the squeak of a leather saddle. This distinctive friction rub is a specific sign of pericarditis, and appropriate test to confirm should be considered. However, while pericarditis would also explain the general chest pain, as well as the other pulmonary symptoms, pericarditis can also represent a complication of several pulmonary diseases, such as tuberculosis, lung cancer and other chronic pulmonary diseases. Furthermore, the patient did not report severe retrosternal and left precordial pain, which is quite common in pericarditis, only a general chest pain, located in the lower part of the chest, as well as sternally. It is also important to mention that a severe retrosternal pain alleviated by sitting up and leaning forward may not appear in the development of tuberculosis, as well as lung cancers. Therefore, the patient would be subjected to a PPD test for the presence of tuberculosis, as well as an electrocardiogram (ECG), echocardiogram, chest X-ray to as well as standard blood tests such as sedimentation and white cell count to eliminate any infections A skin test (PPD) is used to prove tuberculosis infection: 0.1 mL of PPD is placed intradermally on the volar surface of the forearm by means of a 26-gauge needle. At 48-72 h after injection, the diameter of induration, not erythema, is measured. A positive skin test reaction is caused by a delayed-type hypersensitivity response, which is directed at the tuberculosis protein antigens. The criteria vary for interpreting a PPD test as positive. An indurationmore than 5 mm is considered positive in patients who are at high risk of infection and developing disease; these include patients with known or suspected HIV infection, which includes all injection drug users. This group also includes close contacts of patients with active disease and patients with a chest x-ray suggestive of previously inactive tuberculosis. An induration of more than 10 mm is considered positive in patients who are at intermediate risk of infection and developing TB. This group includes known HIV-negative injection drug users, immigrants from high-prevalence countries (such as Asia and Mexico), residents of long-term care or correctional facilities, locally identified high-prevalence groups (migrant workers, the homeless, and high-risk racial or ethnic groups), and children smaller than 4 years old. Patients also at intermediate risk of TB include those with an immunosuppressive illness other than HIV or those receiving immunosuppressive therapy. These include patients with diabetes, renal failure, or hematologic malignancies or those receiving steroids on a long-term basis (more than 15 mg of prednisone). Finally, an induration of 15 mm is considered positive in patients with no known risk of developing TB or being infected with TB. Our patient however, has not shown a positive PPD, eliminating tuberculosis as a positive diagnosis. When the ECG is concerned, the ECG may either confirm the clinical suspicion of pericardial disease or first alert the clinician to the presence of pericarditis. Serial tracings may be needed to distinguish the ST-segment elevations caused by acute pericarditis from those caused by acute myocardial infarction or normal early repolarization. The ST-T-wave changes in acute pericarditis are diffuse and have characteristic evolutionary changes. In the first stage, ST-segment elevations (which differ from ischemic ST-segment elevations by their upward concavity and seldom exceed 5 mm in height) typically occur within a few hours of the onset of chest pain and persist for hours or days. Depression of the PR segment (except in lead aVR) occurs in this stage and differentiates acute pericarditis from early repolarization variants. In the second stage, the ST segments return to baseline; at this point, the T waves may appear normal or exhibit a loss of amplitude. In the third stage, tracings show inversion of T waves. T-wave inversions may persist indefinitely. The ECG normalizes in the variably present fourth stage. In a typical case of acute pericarditis, the approximate time frame for these ECG changes is 2 weeks. However, only about 50 percent of patients with acute pericarditis display all four ECG stages, and variations are very common. Atrial arrhythmias complicate 5 to 10 percent of cases of acute pericarditis. The ST-segment elevation seen in acute pericarditis can usually be distinguished from that of acute myocardial infarction by the absence of Q waves, the upwardly concave ST segments, and the absence of associated T-wave inversions. The acute ST-segment elevation of the Prinzmetal variant of angina is more transitory and is associated with ischemic pain. Although the ST-segment elevation in the early repolarization variant (common in young individuals, especially blacks, athletes, and psychiatric patients) may simulate the ECG of acute pericarditis, the former is distinguished by the absence of PR-segment depression and evolutionary ST-T-wave changes. The patient showed one specific stage of the ECG of pericarditis, specifically, inversion of T waves located mostly in pericarditis that results from a complication of tuberculosis or lung cancer. The standard chest x-ray is taken from back to front (posteroanterior view) to minimize x-ray scatter that could artificially enlarge the cardiac silhouette and from the side of the chest (lateral view). In uncomplicated acute pericarditis, the chest radiograph is generally normal. However, an enlarged cardiac silhouette may be evident because of a moderate or large pericardial effusion. The chest radiograph may provide evidence of tuberculosis, fungal disease, pneumonia, or lung cancer. The chest radiographs show both an enlarged cardiac silhouette as well as a round opacity, located in the right middle lobe, near the lung hilus and projecting towards the heart. This would almost certainly confirms pericarditis caused by the metastasis of lung cancer. However, echocardiography and a biopsy are necessary to confirm the working diagnosis. Echocardiography can be used to identify pericardial loculations, fibrous strands, and pericardial tumors and specifically for this patient, the size of effusions. Pericardial effusions may be concentric or loculated. In general, small effusions are seen posteriorly rather than anteriorly on supine imaging. Moderate-sized (100-500 mL) nonloculated effusions are present both anterior and posterior to the heart, and this was the size of the effusion detected in the patient. Large nonloculated effusions (more than 500 mL) are circumferential and frequently allow free motion of the heart within the fluid-filled space. With the pericarditis confirmed, we now move to confirm the existence of lung cancer. An excision or a needle punch sample of lung tissue is taken under sterile technique and examined microscopically for cell morphology and tissue anomalies. The test procedure and the purpose of the test are explained to the patient. Pre-procedure sedation and analgesia are provided and the patient is transported to operating or procedure room. The patient is informed of the importance of lying still during the biopsy to prevent injury, and the patient is usually without food for 8 hours prior to the procedure. The patient is placed in a semi-Fowler's position and his vital signs should be closely observed, until the patient is stable. The patient is closely observed for symptoms of a hemothorax or pneumothorax. Histologic findings showed the presence of a lung cancer, specifically adenocarcinoma of the bronchoalveolar carcinoma subtype. There are four types of lung cancers: squamous cell carcinoma, adenocarcinoma, small cell carcinoma, large cell carcinoma, of which adenocarcinoma is the most common type of lung cancer in women and nonsmokers, as our patient. As compared to squamous cell cancers, the lesions are usually more peripherally located, and tend to be smaller. They vary histologically from well-differentiated tumors with obvious glandular elements to papillary lesions resembling other papillary carcinomas to solid masses with only occasional mucin-producing glands and cells. About 80% contain mucin. At the periphery of the tumor, there is often a bronchioloalveolar pattern of spread. Adenocarcinomas grow more slowly than squamous cell carcinomas but tend to metastasize widely and earlier. Peripheral adenocarcinomas are sometimes associated with areas of scarring. Adenocarcinomas, including bronchioloalveolar carcinomas, are less frequently associated with a history of smoking (still, greater than 75% are found in smokers) than are squamous or small cell carcinomas ( more than 98%). K-RAS mutations are seen primarily in adenocarcinoma, with a much lower frequency in nonsmokers (5%) than in smokers (30%). p53, RB, and p16 mutations and inactivation have the same frequency in adenocarcinoma as in squamous cell carcinoma. Bronchioloalveolar carcinoma occurs in the pulmonary parenchyma in the terminal bronchioloalveolar regions. It represents, in various series, 1% to 9% of all lung cancers. Macroscopically, the tumor almost always occurs in the peripheral portions of the lung either as a single nodule or, more often, as multiple diffuse nodules that sometimes coalesce to produce a pneumonia-like consolidation. The parenchymal nodules have a mucinous, gray translucence when secretion is present but otherwise appear as solid, gray-white areas that can be confused with pneumonia on casual inspection. Because the tumor does not involve major bronchi, atelectasis and emphysema are infrequent. Histologically, the tumor is characterized by a pure bronchioloalveolar growth pattern with no evidence of stromal, vascular, or pleural invasion. The key feature of bronchioloalveolar carcinomas is their growth along preexisting structures without destruction of alveolar architecture. This growth pattern has been termed "lepidic," an allusion to the neoplastic cells resembling butterflies sitting on a fence. It has two subtypes: nonmucinous and mucinous. The former has columnar, peg-shaped, or cuboidal cells, while the latter has distinctive, tall, columnar cells with cytoplasmic and intra-alveolar mucin, growing along the alveolar septa. Ultra structurally, bronchioloalveolar carcinomas are a heterogeneous group, consisting of mucin-secreting bronchiolar cells, Clara cells, or, rarely, type II pneumocytes. Nonmucinous bronchioloalveolar carcinomas often consist of a peripheral lung nodule with only rare aerogenous spread and therefore are amenable to surgical resection. Mucinous bronchioloalveolar carcinomas, on the other hand, tend to spread aerogenously, forming satellite tumors. These may present as a solitary nodule or as multiple nodules, or an entire lobe may be consolidated by tumor, resembling lobar pneumonia. Such lesions are less likely to be cured by surgery. Analogous to the adenoma-carcinoma sequence in the colon, it is proposed that adenocarcinoma of the lung arises from atypical adenomatous hyperplasia progressing to bronchioloalveolar carcinoma, which then transforms into invasive adenocarcinoma. This is supported by the fact that lesions of atypical adenomatous hyperplasia are monoclonal and they share many molecular aberrations with invasive adenocarcinomas. Microscopically, atypical adenomatous hyperplasia is recognized as a well-demarcated focus of epithelial proliferation composed of cuboidal to low columnar epithelium. These cells demonstrate some cytologic atypia but not to the extent seen in frank adenocarcinoma. It should be pointed out, however, that not all adenocarcinomas arise in this manner, nor do all bronchioloalveolar carcinomas become invasive if left untreated. Major treatment decisions are made on the basis of whether a tumor is classified as a small cell lung carcinoma (SCLC) or as one of the non-small cell lung cancer (NSCLC) varieties (squamous, adenocarcinoma, large cell carcinoma, bronchioloalveolar carcinoma). We proceed to stage the adenocarcinoma. Staging consists of two parts: first, a determination of the location of tumor (anatomic staging) which was previously determined and, second, an assessment of a patient's ability to withstand various antitumor treatments (physiologic staging). In a patient with NSCLC, resectability (whether the tumor can be entirely removed by a standard surgical procedure such as a lobectomy or pneumonectomy), which depends on the anatomic stage of the tumor, and operability (whether the patient can tolerate such a surgical procedure), which depends on the cardiopulmonary function of the patient, are determined. The various T (tumor size), N (regional node involvement), and M (presence or absence of distant metastasis) factors are combined to form different stage groups. We determined that there was a presence of distant metastatic disease (stage IV disease), which is usually incurable. We proceed to palliative care and treatment of pericarditis, which could be immediately life threatening. The management of pericarditis associated with a specific cause is addressed primarily to that underlying cause. However, since the inability to effectively treat the adenocarcinoma, a single course of nonsteroidal antiinflammatory therapy will effectively control the illness, and the pericarditis will resolve without sequelae. In rare cases, frequent and severe recurrences despite aggressive medical therapy have prompted pericardiectomy, which is a possible treatment for our patient. Unfortunately, this procedure is usually ineffective, probably because of residual pericardial tissue or a shift of the inflammatory process to the pleura. References: 1. Abeloff, Martin D et al. Abeloff's Clinical Oncology. London: Churchill Livingstone, 2008. 2. American Cancer Society: Cancer facts and figures 2007. July 2008. American Cancer Society. 25th November, 2008 [http://www.cancer.org/docroot/STT/content/STT_1x_Cancer_Facts_and_Figures_2008.aspfrom=fast] 3. Beers, Mark H. and Robert Berkow. The Merck Manual of Diagnosis and Therapy. New York: John Wiley & Sons, 1999. 4. Cagle, Philip T. et al. Color Atlas and Text of Pulmonary Pathology. New York: Lippincott Williams & Wilkins, 2007. 5. --- et al. Transbronchial and Endobronchial Biopsies. New York: Lippincott Williams & Wilkins, 2008 6. DeVita, Vincent T. at al. DeVita, Hellman, and Rosenberg's Cancer: Principles & Practice of Oncology. New York: Lippincott Williams & Wilkins, 2008. 7. Dubin, Dale. Rapid Interpretation of EKG's. New York: Cover Publishing Company, 2000. 8. Fauci, Antony S. et al. Harrison's Principles of Internal Medicine. Philadelphia: McGraw-Hill, 2008 9. Feigenbaum, Harvey et al. Echocardiography. New York: Lippincott Williams & Wilkins, 2004 10. Fuster, Valentin et al. Hurst's the Heart. Philadelphia: McGraw-Hill Professional, 2007. 11. Holler, Teresa. Cardiology Essentials. New York: Jones and Bartlett, 2007. 12. Jarvis, Carolyn. Physical Examination & Health Assessment. New York: Saunders, 2007. 13. Kumar, Vinay et al. Robbins Basic Pathology. New York: Saunders, 2007. 14. McPhee, Stephen J. and Maxine A. Papadakis. Current Medical Diagnosis and Treatment 2009. Philadelphia: McGraw-Hill Professional, 2008. 15. Polverosi. R et al. Diffuse Lung Diseases: Clinical Features, Pathology, HRCT. New York: Springer, 2006. 16. Porth, Carol Mattson. Essentials of Pathophysiology: Concepts of Altered Health States. New York: Lippincott Williams & Wilkins, 2006. 17. Roth, Jack A. et al. Lung Cancer. New York: Wiley-Blackwell, 2008. 18. Schlossberg, David. Tuberculosis and Nontuberculosis Mycobacterial Infections. Philadelphia: McGraw-Hill Professional, 2005. 19. Spodick, David H. The Pericardium: A Comprehensive Textbook. Informa HealthCare, 1997. 20. World Health Organization: Cancer. July, 2008. The World Health Organization. 25th November, 2008 [http://www.who.int/mediacentre/factsheets/fs297/en/index.html]. Read More
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