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Appalachian Student Research Forum

Office of Research and Sponsored Programs

Division VI

Abstracts Submitted:Division VI - Case History


PERIPHERAL EDEMA AND PERSISTENT DYSPNEA IN A PATIENT WITH ASTHMA.

Ahmad Halawa, Guha Krishnaswamy, Dept.of Internal Medicine, East Tennessee State University, Johnson City, TN37614.

Introduction: Obstructive sleep apnea (OSA) is characterized by repeated episodes of apnea in sleep accompanied by hypoxemia. Patients tend to be obese and upper airway collapse with respiration is accepted as one mechanism for apnea. Apnea leads to hypoxemia, which in turn leads to pulmonary vasoconstriction and pulmonary hypertension. OSA can be accompanied by hypertension, cardiac failure and increased incidence of stroke and coronary artery disease. Patients with asthma or COPD who are obese or develop cushingoid states due to frequent use of glucocorticoids may be especially prone to OSA.

Case Presentation: 67year old white gentleman with past medical history of chronic asthma, rhino sinusitis and hypertension was seen in the asthma clinic complaining of persistent dypnea and cough. Patient complained of swelling of his feet, daytime fatigue and early morning headaches. The patient had a 30-pack year history of smoking but denied any alcohol use. He was treated with Salmeterol 2 puffs twice daily, Irpratropium bromide 2 sprays 4 times/day as needed, Triamcinolone acetonide 2 sprays twice/day all to the lungs. He was also taking Montelukast sodium 10 mg/day. In spite of aggressive therapy, he continued to have recurrent coughing, nocturnal wheezing, dypnea and increasing peripheral edema. His weight was 275.0 IB, and BMI 39.5. Blood pressure was: 155/85 and heart rate:72 . Examination was positive for obesity, a short thick neck and peripheral edema. Cardiac and abdominal exam were within normal limits. Chest exam showed expiratory wheezing, and there was no evidence of clubbing or cyanosis. Arterial blood gases showed a pH of 7.43,PCO2: 42.5mm HG, PO2: 65 mmHG and calculated A-a gradient of 34 mm Hg. Pulmonary functions test revealed FVC: 2.92L(66% of normal), FEV1: 2.09L(69% of normal) FEV1/FVC ratio was 71%. Echocardiogram showed right ventricular hypertrophy. Pulse Doppler showed shortened pulmonary artery acceleration time, suggestive of mild pulmonary hypertension. On Polysomnography, the patient had 69 obstructive events, an apnea index of 89.1 an O2 saturation of 83.3% and a mean saturation of 91.7%. These findings were consistent with moderate obstructive sleep apnea.

Conclusion: This patient had asthma with OSA and resultant right ventricular disease. Untreated OSA can be associated with hypoxic pulmonary vasoconstriction leading to pulmonary hypertension The combination of airway obstruction and pulmonary vasoconstriction can lead to progressive pulmonary hypertension, increased pulmonary artery after load resulting in right ventricular hypertrophy and enlargement leading to RV dysfunction. Smokers with accelerated pulmonary vasoconstriction and COPD can have an acceleration of this process. In the patient with asthma and peripheral edema , OSA with cardiac dysfunction should be considered in the differential diagnosis. In this case, patient showed dramatic improvement in nocturnal and daytime asthmatic symptoms and in the quality of life after treatment with nasal controlled positive air pressure (CPAP) with great decrease in the apneic events and improved quality of life. A study by Shu chan et al ., confirmed that CPAP therapy can be used safely in treating patients with OSA and coexisting asthma. It is possible that recurrent upper airway obstruction and snoring may be important triggering mechanisms of nocturnal asthmatic attacks. In summary, aggressive evaluation and treatment of sleep apnea in patients with asthma can improve the outcome and quality of life and prevent cardiac complications.


Metastatic Thyroid Cancer with a Histologically Normal Thyroid

Vipul Brahmbhatt, MD, Richard Jordon, M.D, Patrick Costello, M.D., Alan Peiris, M.D., East Tennesse State University

Thyroid carcinoma is the most common endocrine malignancy and it is estimated that as many as 10% of population may have histologic evidence of this tumor at autopsy. We discuss a case of papillary thyroid carcinoma that was presented with cervical lymphadenopathy with the thyroid gland clinically, radiologically and histologically entirely normal.

The patient is a 38-year man who was presented with cervical lymphadenopathy and had an excision biopsy, which showed a mixture of metastatic, well differentiated papillary thyroid carcinoma with diffuse sheets of poorly differentiated carcinoma. Immunohistochemistry showed a strong expression of thyroglobin in the papillary component and weaker patchy expression in the poorly differentiated area. Thyroid transcription factor-1 (TTF-1) was expressed in both the components. Thyroid ultrasound was unremarkable for any structural abnormality of the thyroid. Total thyredectomy was done and the thyroid gland was completely examined with no histologic abnormality. Two of nine lymph nodes removed showed metastatic papillary thyroid cancer. Whole body I123 scan was done with patients thyroid stimulating hormone (TSH) elevated to 135 mIU/ml and no activity was noted within the neck or elsewhere. Three months after his surgery he developed recurrent cervical lymphadenopathy with similar histology. One month later a new lymph node appeared. This raised a question of ectopic thyroid tissue harboring an occult thyroid cancer. The Patient remained asymptomatic throughout the course of illness.

Ectopic thyroid tissue can be seen anywhere from the foramen caecum to the lower neck. Ectopic thyroid tissue has been reported in carotid triangle, submandibular region and within the heart. This is usually diagnosed with I131 whole body scan. Even with whole body I131 scan no ectopic thyroid tissue was identified in our case.

Conclusion-This is unique because patient had multiple recurrences of cervical lymph node metastates with the same histology even after total thyredectomy and radioactive iodine I131 therapy with no clinical, radiological or histological evidence of cancer in thyroid. The patient also presents a challenging diagnostic and therapeutic dilemma as he may have ectopic thyroid cancer at unknown site and this tumor does not concentrate I131.


EFFUSIVE-CONSTRICTIVE PERICARDITIS: AN UNUSUAL MENIFESTATION OF ACUTE LEUKAMIA.

Vipul Brahmbhatt, MD, Jeffrey Schoondyke, MD, Joseph Peters, MD, Israel Garcia, MD. East Tennessee State University, Johnson City, Tennessee-37601.

Leukemia involves all organs and tissue of the body. Effusive-constrictive pericarditis is an uncommon condition where pericardial constriction and pericardial effusion presents simultaneously. Effusive constrictive pericarditis is rare in acute leukemia, although leukemia infiltration of pericardium is reported in 37% of autopsy. Pericardial effusion as the presenting feature of acute leukemia is still rare. Considering potential severity one should remember this association and start therapy early to get good result. Although the cause of this condition is many, we described a unique case of effusive-constrictive pericarditis caused by acute myeloid leukemia. Management option for pleuro-pericardial effusion and rare association of leukemia is discussed.

A 77-year male patient with past medical history of well controlled DM and Htn was admitted to the hospital with complaint of syncope and newly diagnosed atrial fibrillation. Patient was feeling weak, fatigue and anorexic since 2 month. On examination he had distant heart sound and bilateral pitting edema with jugular venous distension. His blood pressure of 90/53 with a pulsus paradoxus of 16mmhg. X ray chest showed cardiomegaly with bilateral pleural effusion. Patient had abdominal distension and ultrasound showed minimal ascites. Transthorasic echocardiography showed pericardial effusion, calcified pericardium with uneven pericardium surface with scattered fibrinous material consistent with constrictive pericarditis without any temponade physiology. Inferior vana cava was dilated with minimal collapse on inspiration consistent with elevated right atrial pressure. On routine lab WBC count was elevated (63000) with thrombocytopenia (58000) and anemia (Hgb 7.9). Peripheral smear showed blast with morphological feature consistent with myelomonocytic leukemia (M4) which was confirmed on Bone marrow biopsy and cytogenetic analysis. During hospitalization patient had myocardial infarction and acute MI in leukemia has been reported with normal coronary artery. He also had acute renal failure of unknown etiology with creatinine ranging from 2.5 to 3.5. Considering his comorbid condition it was decided to treat patient conservatively with cytoreduction therapy with hydroxuurea. Thoracocentesis was done which showed numerous blasts with morphology similar to peripheral blood smear. He was not a surgical candidate for pericardiotomy because of poor survival and bleeding tendency. Patient had repeated admission with worsening dyspnoe and pedal edema and he was treated symptomatically with repeated thoracocentesis. During one hospitalization he had subarachnoid hemorrhage and died from complication of it. Our patient had multiple unusual and rare associated conditions of acute leukemia including myocardial infarction, renal failure and effusive-constrictive pericarditis. He was treated with hydroxyurea and effusive-constrictive pericarditis and bilateral pleural effusion with hydroxyurea is not reported. Constrictive pericarditis in leukemia may result from infiltration of pericardium with blast cell or chemotherapy. Pleuro-pericardial effusion can be treated successfully with chemotherapy. Pericardiocentesis or pericardiotomy is leukemia pericardial effusion is recommended when the pericardial effusion is resistant to chemotherapy. Radiotherapy may have to be considered in resistant case of pericardial effusion.


First Case Report of Chloroquine induced Non-obstructive Hypertrophic Cardiomyopathy

Vipul Brahmbatt MD, Anil K.Goli MD, Sujatha A. Goli MD, Hiren Patel MD, Ann S. Jackson MD, Stephen Fahrig MD

Chloroquine an antimalarial drug, frequently used to treat autoimmune diseases such as Systemic lupus erythematosus, Sarcoidosis, and Rheumatoid arthritis for several decades. The most common irreversible complication associated with long term use of Chloroquine are retinopathy, skeletal myopathy and neuropathy. Cardiac complication are very rare and are often fatal. Conduction disturbances and congestive heart failure has been reported sporadically in cardiology literature due to chronic Chloroquine treatment. We present the first case report of massive non-obstructive hypertrophic cardiomyopathy in a 53 year old female with history of systemic lupus erythematosus treated with Chloroquine for over 10 years. In addition our patient also had conduction disturbances such as right bundle branch block and first degree atrioventricular block due to Chloroquine. We emphasis that careful cardiac monitoring is necessary in patient on long-term chlroquine.


Desquamative Interstitial Pneumonia and Hepatitis C Virus Infection: A Rare Association

Said B. Iskandar, MD, Lisa A. McKinney, DO, Lata Shah, MD, Thomas M. Roy MD, Ryland P. Byrd, Jr., MD.

Affiliations: The Veterans Affairs Medical Center, Mountain Home, TN and the Division of Pulmonary Diseases and Critical Care Medicine, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN

Hepatitis C virus (HCV) is a common infecting agent. It is estimated that 2.7 million people in the United States (US) have chronic HCV infection. Ten to 15% of the HCV infected patients progress to liver cirrhosis. Data from death certificates indicate that at least 10,000 deaths a year result from chronic HCV in the US.

While liver disease typically dominates the clinical picture of patients with chronic HCV, 38% of patients will manifest at least one extrahepatic symptom. Autoimmune, hematological, dermatological, and rheumatic disorders with or without mixed cryoglobulinemia have been associated with HCV infection.This multisystem expression of HCV infection is thought to be due to the viruss effect upon the lymphoproliferative system, ultimately causing chronic stimulation of the immune system. Respiratory complications of HCV infection include pulmonary vasculitis, alveolitis, decreased diffusing capacity, broncholitis obliterans organizing pneumonia, and mixed cryoglobulinemia associated with the acute respiratory distress syndrome. The medical literature suggests evidence linking HCV to idiopathic pulmonary fibrosis (IPF). Some studies have found an increased prevalence of antibodies to HCV in patients diagnosed with IPF, while other researchers have failed to confirm such a relationship. Desquamative interstitial pneumonitis (DIP) has been described in two patients with HCV infection. We present an additional patient with HCV who developed acute respiratory failure due to biopsy proven DIP.

A 46 year-old male complained of dyspnea, cough, and pleuritic chest pain of 10 days duration. He denied hemoptysis, weight loss, nausea, vomiting, and loss of consciousness. He had no arthralgias and skin rash. The patient could not recall a recent viral or bacterial infection. The patient smoked cigarettes. He denied exposure to other fumes, vapors, and dusts. He had been diagnosed with chronic HCV infection one year prior to presentation but had received no therapy for this disorder. On admission, Patient was hemodynamically stable with positive crackles over the left lower lobe. His status though did not get better with antibiotic therapy and he needed to be Intubated. His chest X-ray was getting worse with left sided infiltrates. A bronchoalveolar lavage was done and the pathology was positive for DIP. Patient was started on steroids and antibiotics were stopped. This was followed my an extraordinary amelioration of his clinical status and patient was extubated 3 days later and discharged home in a stable condition on prednisone.

Two prior cases were found reporting an association between HCV and DIP. Our patient was the only patient with HCV associated DIP documented to have received corticosteroid therapy. He responded well to this treatment. Moreover, his viral load, as ascertained by quantitative HCV RNA polymerase chain reaction, did not increase. One patient had slow progression of his DIP despite alpha interferon therapy for his HCV infection. The third patients DIP remained stable without therapy for either her DIP or HCV infection The prognosis of DIP is generally good. Most patients improve with smoking cessation and corticosteroid therapy. The overall 10-year survival for patients with DIP is 70 percent. However, further studies are needed to determine the exact relationship between HCV infection and DIP, the effectiveness of alpha interferon and ribavirin therapy on DIP in patients with HCV, and the prognosis of HCV associated DIP.


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