Pneumosiderosis

What causes Pneumosiderosis? Try doing a search on that you won't find anything.
It is a 64 year old patient presenting with some weight loss and a bit of a dry cough. CT showed bilateral reticulonodular opacities and no lymphadenopathy. We sent him for a bronch to assess for things like MAC. The TBBx came back as Pneumosiderosis (iron in the lung). The micro was negative. He was a welder as an occupation. The metal was steel.

intermittent oxygen in hydropneumothorax with Bronchopleural fistula(BPF)?

Here is an interesting question submitted by "zolt"

OK we all know that oxygen accelerates the rate of absorption of pneumothorax by about 4 times and so is of value in patients with pneumothorax being managed conservatively. Now in patients with hydropneumothorax with collapse with BPF with tube thoracostomy, is there any role of intermittent oxygen? how will be the diffusion mechanics in such patients or will all the oxygen come out through BPF?

Follow-up to pulmonary infiltrates

This is the case below with worsening infiltrates. She had diffuse alveolar hemorrhage and we checked an ANCA that was + at 1:640. She was started on steroids and Cytoxan but has developed hematuria and worsening renal failure. Her pulmonary hemorrhage is much improved but her kidneys continue to worsen.

D-dimer testing to determine the duration of anticoagulant therapy

What do you all think about using the d-dimer test in the decision to stop or continue anticoagulation in patients with a first idiopathic thrombotic event?
Here is the abstract from Current Opinion in Pulmonary Medicine. 13(5):393-397, September 2007.

Abstract

Purpose of review: The optimal duration of oral anticoagulation after a first idiopathic venous thromboembolism is uncertain. Recent prospective observational studies show that D-dimer levels have a predictive value for the risk of recurrence. D-dimer testing may help in assessing the individual need for prolonged anticoagulation.

Recent findings: The recently published Prolong study investigated 608 patients with a first unprovoked venous thromboembolism who had received oral anticoagulation for at least 3 months. D-dimer testing was performed 1 month after anticoagulation withdrawal. Patients with normal D-dimer (n = 385) did not resume anticoagulation. Patients with abnormal D-dimer were randomized to resume (n = 103) or not resume (n = 120) anticoagulation. All patients were followed for an average of 1.4 years. Study outcomes occurred in 6.2% of patients with normal D-dimer, and in 15.0% and 2.9% of those with abnormal D-dimer who were allocated to stop or to resume anticoagulation, respectively.

Summary: Patients with an abnormal D-dimer measured 1 month from anticoagulation withdrawal have a significant incidence of recurrent venous thromboembolism which is reduced by resumption of anticoagulation. The risk of recurrence in patients with normal D-dimer is significantly lower. D-dimer testing can be used to regulate the duration of anticoagulation.

Pulmonary infiltrates

This is a 77-year-old woman who presented with significant cough, dyspnea and hypoxemia and was found to have pulmonary infiltrates. She has been started on aggressive good antibiotic therapy, but continued to have an elevated white blood cell count, dyspnea and cough so we were consulted. No previous label of COPD; never smoked; no heart disease; no odd exposures.

She had not been able to produce significant amounts of sputum. She was also found to be hyponatremic with significant fluctuation of her sodium during her initial hospital stay. Urine and serum Osms were consistent with some SIADH and she improved with fluid restriction. Unremarkable U/A and normal renal function.

She then developed some respiratory distress, mild hemoptysis, worsening hypoxemia and had to be intubated and had the changes seen on the second CxR. (Some cuts from the CT from that day are included).

What would you want to know/do next?

Abnormal CxR

This is a follow-up to the case below of the 64 y/o man with dense pulmonary infiltrates.
Cultures were all negative. His ANCA was positive with an atypical pattern. A mediastinoscopy revealed large benign nodes with sinus histiocytosis with no diagnostic evidence of metastatic carcinoma, granulomata, or lymphoma.
His VATS lung Bx revealed necrotizing vasculitis and fibrosis most consistent with Wegener's granulomatosis (the Bx slides were sent out for a second opinion and were reviewed by Dr. Katzenstein).
How would you treat him?