AN UNUSUAL CAUSE OF CHEST PAIN: SPONTANEOUS PNEUMOTHORAX. S. Daud 1 , R. Granieri 1 ; 1 University of Pittsburgh, Pittsburgh, PA (Tracking ID #73682) LEARNING OBJECTIVES: 1) Recognize spontaneous pneumothorax as an etiology of chest pain. 2) Describe the typical presentation of spontaneous pneumothorax 3) Recognize the treatment options and prognosis of spontaneous pneumothorax. CASE INFORMATION: A previously healthy seventeen year-old male was seen in the emergency department for complaints of chest pain. His pain was described as a sharp pain above his nipples, bilaterally, which initially had occurred at rest. The pain was neither exacerbated nor relieved by movement or deep inspiration. There were no associated palpitations nor diaphoresis or vomiting. He was taking no medications, but smoked marijuana weekly for the past few months. He occasionally smoked cigarettes, but never consumed alcoholic beverages. There was no family history of coronary artery disease, hypercoagulable states, or vasculitis. Examination revealed a 5 H 11 HH young man in mild distress. His weight was 60 kg, his respiratory rate was 16, and his heart rate was 84. He had no oral lesions and had normal dentition. The cardiac exam revealed normal heart sounds and no murmurs. The lungs were clear to auscultation and had a normal percussion note. The abdomen was scaphoid and non-tender. There was no peripheral edema. Electrocardiogram and pulse oximetry were normal. A chest roentgenogram revealed bilateral apical pneumothoraces. They were estimated to be 10% each. Bilateral apical drainage catheters were placed and the patient's symptoms resolved. The patient was admitted to the hospital for observation. IMPLICATIONS/DISCUSSION: Primary spontaneous pneumothorax is defined as a pneumothorax without a precipitating factor such as trauma, in a patient without clinically evident lung disease. It typically occurs in tall, thin males between 10 and 30 years of age. The use of smoking tobacco has been reported to increase the risk in men by as much as a factor of 20 in a dose dependent manner. Subpleural bullae are found in virtually all patients; their mechanism of formation is not completely understood, but is thought to be related to degradation of elastic fibers in the lung. This process is thought to be accelerated by smoking. The primary spontaneous pneumonthorax results in a decrease in vital capacity, and an increase in the alveolar-arterial oxygen gradient, leading to hypoxemia. Because underlying lung function is normal, hypercapnia is not usually seen. Most patients present with ipsilateral pleuritic chest pain occurring at rest. Tachycardia is frequently the only abnormal physical finding. The diagnosis is confirmed by the identification of a thin, visceral pleural line displaced from the chest wall on chest roentgenography. Treatment with observation, needle aspiration, or drainage through a chest tube all have been advocated. The average rate of recurrence is about 30%, with pulmonary fibrosis, asthenic habitus, and history of smoking all thought to be risk factors for recurrence. (Tracking ID #73698) LEARNING OBJECTIVES: 1) Recognize the common causes and workup of diffuse pulmonary infiltrates. 2) Recognize the usual presentation of desquamative interstitial pneumonitis. CASE INFORMATION: A 45 year-old male with a history of COPD and multiple pneumonias within the past year was admitted to the hospital for complaints of cough productive of yellow sputum, fevers, chills, and worsening shortness of breath. He was found to be febrile and hypoxemic, and have a leukocytosis with a predominance of neutrophils. A chest x-ray showed the presence of diffuse interstitial infiltrates. He was admitted to the hospital and treated for pneumonia with antibiotics and bronchodilators for 11 days without significant improvement. Sputum and blood cultures were negative for bacterial pathogens. Computed tomography (CT) of the thorax showed ground-glass opacities in all lung fields, worse on the right. Pulmonary function testing revealed mild restrictive disease with decreased lung volumes and decreased DLCO. He did not improve clinically and was scheduled for open lung biopsy. Pathology revealed the diagnosis of desquamative interstitial pneumonitis. He was started on Prednisone 60mg daily, had significant clinical improvement and was discharged from the hospital. CT of the thorax performed one month later showed near-complete resolution of the ground-glass infiltrates. IMPLICATIONS/DISCUSSION: The differential diagnosis of a patient with diffuse pulmonary infiltrates is broad. Acute diffuse lung diseases (less than 4±6 weeks in duration) include infection, pulmonary edema, pulmonary hemorrhage, hypersensitivity pneumonitis, and acute eosinophilic pneumonia. Chronic diffuse lung diseases include idiopathic pulmonary fibrosis, sarcoidosis, pneumoconioses, and interstitial lung disease associated with connective tissue diseases. Desquamative interstitial pneumonitis (DIP) is one of the distinct clinical and histopathological entities belonging to the family of idiopathic interstitial pneumonias. The average age of onset is about 45 years of age, and a male preponderance has been noted. Cigarette smoking has been linked consistently to this diagnosis. The typical presentation is an insidious onset of dyspnea and cough. Chest roentgeography often shows a diffuse pattern of reticulonodular opacities, with CT showing a ground-glass appearance. Pulmonary function testing shows a restrictive pattern. Diagnosis is best made with lung biopsy demonstrating the characteristic appearance of alveolar filling by mononuclear cells and thickening of the alveolar septa. Pateints are generally treated with corticosteroids until symptoms are improved at which point they are tapered slowly. Data are lacking regarding the optimal duration of treatment and prognosis of DIP. A 44 year old African American woman presented with the acute onset of shortness of breath and substernal chest pain with radiation of the pain to the neck and left arm. She was diagnosed with acute myocardial infarction with positive CK and isoennymes and troponin-T. Initial ECG did not indicate an acute injury pattern, however ST-T wave change in V5 and V6 suggested lateral ischemia. Platelet count on initial presentation was 36,000. Her initial Hgb was 9.2. No previous laboratory data were available to review. She was initially treated with aspirin, low molecular weight heparin, and GIIB/IIIA inhibitors. Subsequent to this her blood count was repeated and platelet count had dropped to 11,000. At this time her peripheral smear was reviewed and 20±25 schistocytes were identified per high power field. The case was discussed with the Hematology division and plasmapheresis was initiated within 12 hours. After two double volume exchange transfusions, her platelet count had rebounded to 50,000 and her LDH was falling as well. Her platelet count slowly continued to improve over the course of her hospitalization. At discharge on hospital day #8, her platelet count was 236,000. At no point did the patient have renal dysfunction, neurologic symptoms, or fever. IMPLICATIONS/DISCUSSION: TTP is characterized by arteriolar lesions in various organs that contain platelets and fibrin. This results in MHA, and thrombocytopenia. The tissue hypoxia that ensues is responsible for the symptoms. Myocardial vessel involvement may be a cause of sudden death in some patients. However the isolated involvement of myocardial vessels is rare, especially when there is no of involvement of renal and cerebral vessels. TTP is treated with plasmapheresis initially. The disease is now 90% survivable if therapy is initiated promptly. Before this therapy was available, TTP had a 90% mortality. Plasmapheresis is conducted until platelet count, LDH, and MHA resolves. At that time, pheresis is gradually weaned. Those patients who relapse can be treated with corticosteroids, cyclophosphamide, or vincristine. Splenectomy is also an option. LEARNING OBJECTIVES: 1. Diagnose B12 deficiency on clinical grounds 2. Recognize the relationship between H. pylori infection and B12 deficiency 3. Assess potential complications of B12 deficiency. CASE INFORMATION: A 65 year old male was admitted to our hospital with a two month history of progressive gait instability, weakness and bilateral lower extremity numbness. He was unable to walk without assistance, was totally dependant for activities of daily living, had recently become incontinent of urine and had developed severe constipation. He also complained of mild numbness, tingling and weakness in his upper limbs, and had difficulties with hand motor control. He denied fevers, myalgias, pain, involuntary limb movements, headaches, or trauma, however he did have a forty pound weight loss over the previous three months. He had no significant past medical history and was on no medications. Physical exam showed no cranial nerve defects, mild proximal weakness and proprioceptive loss, with severe, diminished lower extremity strength, proprioception, vibration and sensation. Lower extremity tendon reflexes were brisk with positive Babinskis. Bilateral crackles at mid lung fields were evident on chest exam. Laboratory values on admission were significant for hemoglobin of 10.8 g/dl, mean corpuscular volume of 106.8 fL, and B12 of 75 ng/L (190±900). Arterial blood gas on 2L of oxygen showed pH of 7.456, PCO2 of 40.4, and PO2 of 69.0. With the laboratory diagnosis of B12 deficiency, a homocysteine level was obtained and was significantly elevated at 188 mmol/L (0±13). Chest X-ray showed extensive bilateral reticular infiltrates and small bilateral effusions. Due to these findings, a computed tomography of the chest was done which revealed left apical bullae, extensive ground glass opacities, and multiple filling defects in the interlobar and branch arteries consistent with pulmonary emboli. Lower extremity Doppler ultrasound confirmed deep vein thrombosis (DVT). An esophagogastroduodenoscopy was ordered to help determine the cause of the B12 deficiency. This showed mild chronic gastritis and H. pylori organisms. Serum studies for intrinsic factor and parietal cell antibodies were negative. He was treated with intravenous B12, triple therapy for H. pylori, anti-coagulation and oxygen support, however his respiratory status declined over the next three to four weeks and he died approximately one month after admission. Autopsy confirmed sub acute combined degeneration in the spinal cord and organizing thromboemboli with diffuse alveolar damage of the lungs. IMPLICATIONS/DISCUSSION: This case demonstrates a cascade of events that most likely began with the relatively common finding of H. pylori gastritis. Our patient then developed B12 deficiency, which has a known association with this infection. This in turn contributed to elevated homocysteine by interfering with its conversion to methionine. This contributed to a hypercoagulable state and in combination with immobility from the B12 deficiency induced sub acute combined degeneration, led to the DVT and pulmonary emboli. This directly contributed to the patient's respiratory decline. This case demonstrates that when H. pylori gastritis is confirmed, the association between this infection, B12 deficiency and hyperhomocysteinemia should be considered, as this can have profound consequences. 3) Discriminate between opiate dependence and addiction. CASE INFORMATION: A 29-year-old male with a history of hemophilia and hepatitis C presented with recurrent episodes of crampy abdominal pain over the past seven months. He denied fevers, chills, nausea, vomiting. There was no change in bowel habits or alteration of the pain with food or defecation. He denied previous surgeries or intravenous drug use. Physical exam showed no fever, heart rate 106, dilated pupils, diaphoresis, and a soft abdomen with voluntary guarding. The patient had undergone an extensive prior workup for these symptoms including CT scanning, colonoscopy, and upper endoscopy-all of which were normal. On our further review we learned that the patient had been taking two narcotic medications prescribed from different doctors. He described occasionally taking these medications for pain control, but was unaware both were narcotics. His symptoms completely resolved after starting a low dose methadone taper, and the patient was grateful for ending a seven-month cycle of pain. IMPLICATIONS/DISCUSSION: The symptoms of opiate withdrawal can include sweating, headache, nausea/vomiting, abdominal cramping, diarrhea, dilated pupils, piloerection, insomnia, agitation, and anxiety. Opiate withdrawal can occur from chronic prescription narcotic use, but may go unrecognized by patients and physicians. In our patient with hemophilia, prescription narcotics rather than NSAIDS were given for minor pains. His abdominal pain along with dilated pupils and diaphoresis suggested withdrawal leading to a more extensive review of his medication use. Despite using his medications as prescribed, his chronic use led to physical dependence. Addiction is defined as the compulsive use of a substance despite negative consequences. Dependence, however, does not usually have the psychological associations that are seen in addiction, making it harder to recognize. Nonetheless, patients with physical dependence can experience severe distress, as did our patient. Opiate withdrawal causing abdominal pain remains a diagnosis of exclusion and other serious causes should always be ruled out. LEARNING OBJECTIVES: 1. Discuss approach to fever in travelers 2. Recognize Dengue fever presentation 3. Realize importance of controlling mosquito vectors. CASE INFORMATION: 23 year old male with no prior history presents with 3 days of fever, malaise, headache and body aches. He returned to the US 6 days prior after a month-long backpacking trip in Brazil. His fever has no pattern and is relieved with Ibuprofen. His headache is bitemporal with some associated photophobia and neck pain. His body aches are generalized but most severe in the lower back. He denied HIV risk factors and review of systems is negative. He did not receive any vaccines or prophylactic medications. His bp is normal, pulse 70, and temperature 38.6 degrees Centigrade with malaise and a maculopapular rash over the trunk. Otherwise exam was negative. At this point the differential included flu, malaria, typhoid fever, leptospirosis, acute HIV, and Dengue fever. Laboratory investigation revealed a mild leukopenia with normal platelet count. CSF, HIV p24 Ag, thick and thin smear, RPR were all negative. Dengue titer came back positive for serum ELISA IgM. He was treated symptomatically with resolution of symptoms within a week's time. IMPLICATIONS/DISCUSSION: Dengue fever is caused by a single stranded RNA virus in the family Flaviviridae (found throughout the tropics) and transmitted to humans by the Aedes aegyptia mosquito. With urbanization and subsequent inadequate waste and water management, Dengue incidence is increasing in South America and the Caribbean. There is a disease spectrum with Dengue ranging from a relatively non-specific illness, to Dengue fever (acute illness with leukopenia, headache, malaise, myalgias/arthralgias) to Dengue hemorrhagic fever (the above plus positive tourniquet sign, thrombocytopenia, and increase vascular permeability) to Dengue shock syndrome (the above plus hypotension and narrow pulse pressure). Diagnosis of Dengue is usually by isolation of the virus or serologic testing such as ELISA for IgM. Dengue fever is typically self-limited with symptoms lasting appoximately 7 days. Warning signs for Dengue shock syndrome include sustained abdominal pain, persistent vomiting, change of level of consciousness, and a sudden decrease in platelet count. Dengue has 4 serotypes and repeat infection with another serotype is more likely to casue severe disease. In addition to improved mosquito control, a vaccine is currently being developed.