Pulmonary disease chest pain

It is important to distinguish GERD symptoms from those of other diseases, especially when chest pain or pulmonary symptoms are present. 

A 67-year-old man with a history of chronic obstructive pulmonary disease presents to the emergency department with high fevers, shaking chills, severe chest pain, and shortness of breath. His family members state that he has been confused all day. He started having a severe cough 2 days ago, with excessive sputum production. He received doxycycline 100 mg twice daily for an upper respiratory tract infection 7 days ago. 

Acute chest syndrome An acute respiratory complication of sicklecell disease characterized by chest pain, fever, and pulmonary infiltrates. 

Symptoms Onset of symptoms may be either abrupt or gradual. Inhalational exposure produces fever commonly in excess of 102 degrees F, rigors, sweats, myalgias, headache, pleuritic chest pain, cervical adenopathy, hepatosplenomegaly, and generalized papular/ pustular eruptions. Acute pulmonary disease can progress and result in bacteremia and acute septicemic disease. 

Pulmonary infection This form of the disease can produce a clinical picture of mild bronchitis to severe pneumonia. The onset of pulmonary melioidosis is typically accompanied by a high fever, headache, anorexia, and general muscle soreness. Chest pain is common, but a nonproductive or productive cough with normal sputum is the hallmark of this form of melioidosis. 

CHF congestive heart failure CHI closed head injury CLA cis-linoleic acid CLL chronic lymphocytic leukemia CML chronic myelogenous leukemia CMV cytomegalovirus CNS central nervous system Comps complications COMT catechol-O-methyltransferase Contra contraindicated COPD chronic obstructive pulmonary disease COX cyclooxygenase CP chest pain... 

At age 12, the patient was admitted with acute chest pain from a left spontaneous pneumothorax (air within the pleural cavity).This required hospitalization and chest tube insertion, but he recovered without sequelae. After the resolution of this problem, pulmonary function testing revealed findings of both severe airway obstruction and destruction of alveolar lung tissue, consistent with emphysema. No further pulmonary problems occurred until the patient was age 16 years, when he developed occasional episodes of bronchospasm (spasmodic contraction of the smooth muscles of the bronchus). Pulmonary function studies at that time, though improved from those immediately following his pneumothorax, still revealed combined obstructive and destructive lung disease. 

A 54-year-old man with severe triple vessel coronary artery disease took six modified-release diltiazem tablets 180 mg following an episode of severe angina, and 10 hours later developed bradycardia, hypotension, and severe pulmonary edema, but was free of chest pain (21). After intensive hemodynamic monitoring and noradrenaline treatment, his renal, respiratory, and cardiac problems recovered to baseline over the next 48 hours. Diltiazem overdose was confirmed by a diltiazem serum concentration of 1230 ng/ml (usual target range 40-160 ng/ml). 

After administration of vinorelbine, chest pain occurs in up to 5% of patients. However, subsequent analysis showed that most patients had underlying cardiovascular disease or a tumor in the chest, making interpretation difficult (2,20). Three patients developed acute cardiopulmonary toxicity after vinorelbine therapy (25). The symptoms mimicked acute cardiac ischemia, but with no electrocardiographic changes or raised cardiac enzymes. In two patients, tachypnea, rales, wheezing, and severe dyspnea responded to inhaled salbutamol. One patient developed pulmonary edema and bilateral pleural effusions, which contained no malignant cells when drained. 

Chronic exposure to insoluble beryllium compounds, particularly the oxide, leads to berylliosis (a chronic granulomatous disease), which begins with a cough and chest pains. In most cases, these symptoms soon lead to pulmonary dysfunction. The latency period ranges from months to 25 years. Diagnosis based on clinical, radiographic, and lung function evidence has been found to be difficult. 

Some of the clinical consequences in SS disease include megaloblastic erythropoiesis, aplastic crisis, stroke, bone pain crisis, proneness to infection particularly by Pneumococcus, Salmonella, and Haemophilus due to hypos-plenism and acute chest syndrome. Prophylactic use of penicillin and antipneumococcal and Haemophilus vaccines has aided in the management of life-threatening infectious complications of SS disease. Neonatal screening has been used in the identification of infants with sickle cell disease so that risk of infection can be modulated by appropriate immunizations and penicillin prophylaxis. The acute chest syndrome characterized by chest pain is due to clogged pulmonary capillaries in a small number of studies, patients have been treated with inhaled nitric oxide, which dilates blood vessels with clinical improvement. 

B. Clinical Features. The disease begins 1-6 hours after exposure with a sudden onset of fever, chills, headache, myalgia, and nonproductive cough. In more severe cases, dyspnea and retrosternal chest pain may also be present. Fever, which may reach 103-106°F may last 2-5 days, but cough may persist 1-4 weeks. In many patients nausea, vomiting, and diarrhea will also occur. Physical findings are often unremarkable. Conjunctival injection may be present, and in the most severe cases, signs of pulmonary edema would be expected. In moderately severe laboratory exposures, lost duty time has been < 2 weeks, but, based upon animal data, it is anticipated that severe exposures will result in fatalities. 

ACUTE HEALTH RISKS exposure to very high levels of Silica, Cristobalite can cause a serious lung disease called Silicosis Simple Silicosis may only cause changes in chest x-ray with severe cough, shortness of breath, wheezing, decreased pulmonary function, fever, fatigue, chest pains, and loss of appetite. 

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