DISCUSSION: Cerebral arterial air embolism has been described with cardiac surgery, mechanical ventilation, underwater diving and bronchoscopic laser operations. Arterial embolization results from direct passage of air into the arterial circulation or from paradoxical embolization. The effect of an air embolus depends on its size as well as its rate of entry into the circulation. Arterial embolization is dangerous in that it can cause ischemic damage to organs. Because absorption of arterial emboli is inversely related to the arterial pressure of nitrogen, treatment with hyperbaric oxygen has been effective. This treatment also helps reduce the air bubble size and increases the oxygen content of blood. In our patient, no bubbles were detected in the right heart chambers, which makes paradoxical embolization unlikely. A plausible biological mechanism is cerebral air embolism through bronchovenous fistula, with possible pathogenetic implication of either micrometastases to the lung or the prior thoracic radiation therapy, but this remains to be proven. Recognize the possibility of multiple opportunistic infections in immunocompromised patients. CASE INFORMATION: A 40-year-old man presented to a hospital with a 5-month history of progressive dyspnea on exertion, productive cough, and gradual weight loss. He had a 52 packyear history of smoking. He was treated with several courses of antimicrobials for bronchitis and was maintained on high-dose prednisone (60 mg daily) for several months. He presented to an outside hospital with respiratory distress, requiring 50% FiO2. Chest x-ray showed bilateral alveolar infiltrates, and on computed tomography (CT), the chest had a diffuse ground-glass appearance. Bronchoscopy was nondiagnostic, so he underwent an open lung biopsy, which showed pulmonary alveolar proteinosis. He was transferred to our tertiary care facility where he was given normal saline lavage (17 L per lung) under general anesthesia. His respiratory status improved and he was discharged home on 6 L/min of oxygen and tapering doses of prednisone. He returned few days later with worsening dyspnea, fever, and increased cough, now productive of copious brown rusty sputum. His vitals: T 101.08F, BP 95/56 mm Hg, Pulse 120, and RR 30/min. His lung auscultation revealed diffuse crackles. His PaO2 on 6 L of oxygen was 57 mm Hg. He was intubated and started on broad-spectrum antibiotics. Sputum staining showed branching gram-positive filaments with weak acid-fast stain, and intravenous Bactrim (trimethoprim and sulfamethoxazole) was added for treatment of Nocardia pneumonia. Ophthalmologic exam and CT of the abdomen and brain showed no evidence of nocardial dissemination. His sputum stain subsequently showed septate hyphae, which was targeted with amphotericin B. The fungus was identified as Trichosporon beigellii. The patient eventually died of septic shock. Autopsy showed panlobar bilateral necrotizing pneumonia and the presence of silver-positive organisms consistent with Nocardia, Trichosporon, and Aspergillus. DISCUSSION: Pulmonary alveolar proteinosis (PAP) is a diffuse lung disease characterized by dense accumulation of PAS-positive (periodic acid-Sciff) phospholipid material in the alveoli, with preservation of the lung architecture and absence of inflammation. Patients usually present with a subacute prodrome of cough and progressively decreasing exertional tolerance. Tissue biopsy, by open lung or thoracoscopy, is the gold standard for diagnosis, though transbronchial biopsy and fluid obtained by bronchoalveolar lavage may also be used. Whole lung lavage is the treatment of choice, and recently interest has grown about the potential therapeutic role of GM-CSF (granulocyte/macrophage colony stimulating factor) because defective alveolar macrophages are involved in the pathophysiology. There is no role for immunosuppressants in treatment, and, in fact, some suspect that corticosteroids may increase mortality. The association of pulmonary nocardiosis with PAP has been described frequently. Nocardia asteroides tends to disseminate from a pulmonary or cutaneous focus to any organ, notably the central nervous system, retina, heart, kidneys, and joints. The new onset of fever and change in the quality of sputum in our immunocompromised patient prompted us to think of superimposed opportunistic infections. A thirty-three year old Caucasian man presented with history of recurrent spells. He described episodes of palpitations and hot flushes, followed by tunnel vision, pre-syncopal feeling, and loss of consciousness. He had spontaneous recoveries, with no incontinence or postictal state. He reported loose stools, intermittent urticarial rash, and occasional wheezings associated with these episodes. He had an AICD (automatic implantable cardioverter-defibrillator)placed after the second spell for complete heart block that degenerated into ventricular fibrillation. Subsequent interrogation of the AICD showed no evidence of dysrrhytmias despite recurrent spells. 24-hour EEG monitoring showed no epileptiform activity. He underwent a cardiac catherization, which showed normal coronary arteries. CT scans of the head and the abdomen were non-revealing. Pulmonary angiography showed no evidence of pulmonary embolism. On presentation, his physical exam, including neurological exam, was completely normal, except for urticarial rash on the dorsum of his hands. Telemetry monitoring didn't reveal any arrhythmia. A tilt table test showed asymptomatic postural tachycardia. Urine metanephrine and 5-HIAA levels were within normal. Echocardiography showed no valvular lesions. Glucose levels and CBC were normal. A MIBG scan was also negative. The patient was discharged home on a beta-blocker. His spells recurred. Further work up included a twenty-four hour urine histamine collection, which was normal. Punch biopsy of his urticarial skin lesions, revealed urticaria pigmentosa, with perivascular and interstitial mast cells infiltration of the superficial dermis. Colonoscopy showed mast cells infiltration of the lamina propria of the ileum and right colon. A bone marrow aspirate revealed 15% mast cell cellularity. The diagnosis was consistent with systemic mastocytosis. The patient was switched to a combination of H1 and H2 blockers, and later had a leukotriene receptor antagonist added to his regimen. He remained spell-free afterwards. DISCUSSION: One needs to exclude other causes of spells, like cardiovascular, neurologic, endocrine, pharmacologic, and psychologic etiologies. Systemic mastocytosis is a disease characterized by mast cell infiltration of multiple organs. It presents with episodic flushing, diarrhea, abdominal pain, bronchospasm, alcohol intolerance, and syncope. Triggers include emotional stress, iodinated contrast agents, aspirin, and exercise. Urticaria pigmentosa is a characteristic skin lesion. Therapeutic armamentorium includes H1 and H2 blockers, cromolyn sodium and prostaglandin synthesis inhibitors. Epinephrine is used in severe cases associated with anaphylaxis, while interferon therapy is reserved for proliferative disease. Our patients had a dramatic presentation and a dramatic response after addition of a leukotriene antagonist. -old white woman presented with a 4-week history of progressive shortness of breath and persistent dull right-sided chest pain. She had never been a smoker. On admission, she was afebrile, RR 14, and had oxygen saturation of 95% on room air. Lung auscultation in the right lower lung fields found decreased breath sounds and decreased tactile fremitus. Chest x-ray confirmed the presence of right pleural effusion. Thoracentesis showed a milky fluid consistent with chylothorax (pH = 7.26, RBC = 79, WBC = 4.4, LDH = 398 u/l, protein = 1.6 g/dl, glucose = 51 mg/dl, triglyceride = 715 mg/dl, cholesterol = 26 mg/dl, and positive chylomicron screen). CT of the chest and abdomen revealed a large pleural mass emanating from the posterior hemithorax, with extension below the right diaphragm. Thoracoscopic biopsy of the mass revealed malignant mesothelioma. The patient had no occupational exposure to asbestos, but her father (who had no lung disease) had worked in the steel industry. The patient was switched to a medium-chain fatty acid diet, and her pleural drainage became serous, although it persisted. Eventually, a Pleurex catheter was inserted for self-administered therapeutic drainage as needed, and the patient was discharged home with hospice care. DISCUSSION: Malignant mesothelioma is an insidious neoplasm that usually afflicts patients in their fifth to seventh decades of life. Patients usually present with dyspnea, nonpleuritic chest pain, and unilateral pleural effusion. Exposure to asbestos is elicited in only 70% to 90% of cases. Domestic exposure to asbestos through family members is well documented and could have been the cause in our patient. Multimodality therapeutic approaches (surgery with chemotherapy +/-radiotherapy) produce a slight improvement in quality of life and survival. Our patient' tumor extended across the diaphragm and was therefore nonresectable (stage IV). Chylothorax is usually due to either trauma such as surgery or nontraumatic causes such as malignancies, with lymphoma accounting for the majority of cases. Prolonged chyle loss can lead to nutritional depletion and immunologic deficiency. A triglyceride level above 110 mg/dL in a pleural effusion is very suggestive of chylothorax, and the presence of chylomicrons confirms the diagnosis. The presentation of a young patient with no asbestos exposure, with malignant mesothelioma and a chylothorax is extremely rare.