What do you see?

The patient is a 59-year-old female with history of hepatitis C, currently on dual therapy with pegylated interferon and ribavirin for last 2 months presented with complaint of cough.
PAST MEDICAL HISTORY:
1. Hepatitis C, liver cirrhosis.
2. Childhood asthma.
3. History of positive PPD more than 10 years ago, which was positive, at
that time with negative chest x-ray.

stage iiia?

Would this PET scan be enough to convince you that this is IIIa or would you have the surgeon go after that node for staging purposes?
A corollary: if that node is negative, would he be a surgical candidate (assuming lung function etc. not issue)

post thoracotomy pain

One more post today. How do you best deal with post-thoracotomy pain. I admit I see it fairly often as well.

Patient writes in a recent comment

I have acute persistent pain in my right breast and along the six inch incision at the base of my breast. I have tried gabapentin, Lyrica, and Topimate. I am on my third round of corticosteroid injections into the intercostals. I am reluctant to use narcotics, but if the steroids do not work, I am at a loss. I cannot move my right arm without pain. Any suggestions would be greatly appreciated.

ABPA without steroids

A reader writes:

I am 48 years old female, and lived with asthma for the last 25 years. I am not under great control. I have had blood work done recently, and found out I have severe allergies. I have an IgE of 1700, my aspergillus allergen is 2.05 ku/l. I recently had a chest ct which showed nonspecific infiltrates with ground glass appearance. A sinus ct showed acute maxillary sinusitis. my physician says she is not sure of a diagnosis of ABPA, and is hesitant to treat me with steroids. In the past year I have been diagnosed with avascular necrosis of both hips, and my right knee as well as severe cataracts in both eyes. I was told probably from the use of steroids to treat my asthma. My concern is I never feel great, and why is this so hard to diagnose, and if I have ABPA what will ahappen if it goes untreated.

What types of steroid-sparing therapies do you use for ABPA (or asthma)?

Acute ILD

This 77 year old man has had a bit of honeycombing at the bases since at least 2004. Radiographically c/w UIP. Biopsies not done and he has been stable for years (and FVC normal at 84% predicted).
In February he developed worsenign cough and SOB. He was admitted and was hypoxic with the CT shown below. A cath was done showing normal wedge, normal CO/CI.
A BAL showed only 184 cells half of which were macrophages. A TBBX was not done because he's on coumadin for afib and we didn't think it would add much to determining the diagnosis.
SH, desk job all his life. In January, routine maintenance change of the humidifier pipes in his furnace. This may be a red herring but throwing it out there. No one else in household sick.



Was going to send him for open lung/VATs, but what do you think are possible etiologies?
I also repeated autoimmune chemistries that had been negative in 2004.

lesion in a 45 year old woman

A 45 y/o woman presented with atypical chest pain that led to a ct showing the following:


Although a benign lesion/resolving pneumonia were possibilities, I was concerned about bronchoalveolar carcinoma in this young non-smoker. A bronch was done - BAL cytology and tbbx were negative. We were in the right area (posterior segment RUL) and Fluoro did support this, but the biopsies came back as unremarkable pulmonary parenchyma.

What would you do next? Some options would be follow with serial CT's - q 3 months, open lung, repeat bronch, or another course.

What's your line?

A resident put in a left subclavian line and maybe went a little too far. An xray shows that it went into the right atrium and into the IVC and up to the IVC filter. When it was removed (with help from vascular), the filter had migrated up 2 vertebrae... Click image to enlarge. It is a bit dark.

Fibrosis

A submission from a reader: "34 year old, non-smoking African American female presenting with a recurring (for three years now), chronic (lasts for several weeks up to a few months) dry, non productive cough. No other symptoms (though the attached CT report says wheezing). No response to a variety of drug treatments over the years, including steroid shot, Levaquin, OTC Mucinex, OTC Claritin, Tussionex, Nasacort, OTC Prilosec, 6-day regimen of Metrol (4mg), Advair and Albuterol. First pulmonologist (who performed no diagnostic tests) diagnosed asthma and allergies. Nothing indicated on chest x-ray. Internal medicine doctor ordered CT scan (report attached). Second pulmonologist said subpleural cysts exist, which he indicated exist with UIP patients, but he said this was not UIP. Also said it's not tuberculosis or sarcoidosis. Prescribed 20 mg of Prednisone twice a day to get rid of cough, said we will proceed once cough is gone. Said a lung biopsy or thoracic biopsy may be in order.

CT reading:
Helical CT images through the chest were obtained following
intravenous contrast administration.

Within both lungs and involving both the upper and lower lung zones,
there are areas of subpleural macrocystic change with some
associated subpleural interstitial thickening. There are no
particular areas of ground-glass opacity associated with these
findings. No significant nodularity is seen. The central and midlung
zones are spared. No pleural fluid or lymphadenopathy is seen. These
findings can be seen in patients with usual interstitial pneumonia
(UIP) although this would be somewhat atypical in a patient of this
age group. Does the patient have a smoking history? Other
interstitial lung disease in its early stages may give a similar
appearance.

41 year old with HIV and fever

This is a 41 year old man with AIDS, CD4 below 10, who presented with shortness of breath and fever. He was admitted to a general ward but trasnferred to the unit a few days later for tachypnea. On the general floor, his vitals were normal except for some tachycardia. He was 97% on 2 l NC. CXR:



a full workup was done to look for infectious source.
sputums: AFB negative x 3, fungal negative. PCP negative (no PCR, no bacteria
CSF - negative for infection.

What kinds of things could be causing these findings and what would you do?

Lymphocytic effusion

Since another question from a doc is related to TB, I'll post that here as well:

55 y old gentleman presented with few weeks history of progressive dyspne and right sided pleuritic chest pain, with history of contact with a case of pulmonary TB, no symptoms of toxemia, clinically the patient got signs of right sided pleural effusion which was aspirated and shown to be lymphocytic exudate,because the patient also presented with hoaseness of voice CT chest was done showed no lung masses or lymphadenopathy, BAL showed no malignant cells, PPD test was highly positive, laryngeal examination showed cordal polyp. culturing the fluid and sputum for TB was negativethe patient was started on antituberculous ttt , 1st 2 months quadrible therpy and then dual therapy and the patient still have re accumulating effusion? any suggestions?

TB treatment and a followup BAL

A physcian from Florida recently asked how one should approach the following. A younger man from a TB-endemic area with cavitary upper lobe lesions. He is not productive of sputum. Obviously, the physician elected to treat empirically for TB. In terms of getting sensitivities, a BAL should be done, but his question was, how long after initiation of 4-drug therapy would the BAL give a false positive. By false positive, I guess you could view that as as either afb negative, or culture negative (if the former represents dead TB bugs).

He was considering waiting 2 weeks to help decrease the risk to those in the bronchoscopy suite.
What do you think?

need for lymph node biopsy?

Question submitted by anonymous:

24 year old Asian female presented with chronic productive cough of green/yellow sputum for the last year. Travelled to Malaysia and Pakistan in the last year. Some mild episodes of haemoptysis. CXR when the patient initially presented was NAD. Bloods all normal, barring a bilirubin of 16.

A CT a year after initial presentation showed right upper lobe collapse with a 2cm mass. Left upper lobe bronchiectasis. Also widespread mediastinal adenopathy.

Sputum cultures negative. Bronchoscopy showed a sputum plug sent for MC+S - negative. Nil else on bronchoscopy.

Why is there mediastinal adenopathy? Should a biopsy be performed in order to aid diagnosis?

Lung cancer letter

Very interesting letter to the editor on lung cancer, that puts things into perspective and that is often overlooked. Written by someone who also has left many comments on this site, so check it out.

IPF treatment - worse than the "cure"

Here's another anecdote on a patient started on prednisone/azathioprine/NAC for IPF. He was started on this for a variety of reasons, but one was that the biopsy had a bit more inflammatory changes even though there was ample fibroblastic foci and heterogeneity, so I thought a 3-6 month trial would be reasonable. By the time his imuran was up to 75 mg, I saw him. A repeat spiro was unchanged (FVC 43% predicted) but his DLCO went from 35% to 45% so I continued the meds. However he had mouth pain and the tongue showed possible thrush so I kept the Imuran at 75, gave some nystatin swish and sent him out to be followed up in 2 months and repeat the HRCT with the sprio/DLCO. However, his mouth pain did not go away and worsened, and he started developing malaise and a fever. I saw him in clinic that day. He looked fairly sick but vitals ok. He had a soft palate lesion. I got derm to KOH it and there are some non-budding hyphae so he's to get clotrimazole . Then almost as an afterthought I added on amylase and lipase to the repeat LFT's and low and behold the lipase is 800.
Of note his WBC was 13 and now down to 6....
This side effect is likely going to be self-limiting as he stays off the imuran. As I tell him to go light on PO intake, I am adding a creatinine to make sure he is not volume depleted (he's an outpatient).

Precedex?

Redneck Crit Care (nice name) submitted this question:

One of our CT surgeons has been using Precedex for postop sedation for vent patients with good success.
www.ptjournal.com/ptjournal/fulltext/30/3/PTJ3003158.pdf

according to information in that article, it appears to be a very attractive option. It is a short-acting alfa2 agonist and you do not have to discontinue this before, during or after extubation because it does not cause respiratory depression. Are many intensivists already using this in medical ICU?

Tuberculosis

Interesting question submitted from Nasia:

18 year old man migrated from Thailand in 2005. Father in 2004-2205 had active pulmonary TB, treated for six months with standard regimen and responded. Patient does not recall whether he had PPD done then or not and was not treated for LTBI. Now is asymptomatic but CXR done for other reasons was abnormal.chest CT shows 5 very small (largest is 2.5 mm) scattered nodules. sputum AFBs are negative including cultures. current PPD negative and quantiferon test negative as well. Physical exam unrevealing. would you treat for latent TB given exposure?

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.