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?
Wednesday, December 19, 2007
Friday, November 30, 2007
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?
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?
He was considering waiting 2 weeks to help decrease the risk to those in the bronchoscopy suite.
What do you think?
Monday, November 12, 2007
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?
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?
Thursday, October 25, 2007
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.
Tuesday, October 23, 2007
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).
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).
Monday, October 15, 2007
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?
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?
Saturday, October 13, 2007
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?
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?
Tuesday, September 18, 2007
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.
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.
Monday, September 10, 2007
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?
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.
Sunday, September 09, 2007
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.
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.
Wednesday, September 05, 2007
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?
Monday, September 03, 2007
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?
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?
Friday, August 31, 2007
More data on "Abnormal CxR"
This is the 64-year-old man with progressive, worsening dyspnea described below.
Initial blood cultures and sputum culture were non-revealing. His ESR was 75 with a positive ANA screen but essentially negative titers (<1:40); U/A was unimpressive, renal function was normal, initial CBC had mild anemia (Hgb 12.6) but normal WBC (7.6 with 90% PMNs) and normal platelets.
What other tests/info would you like next?
Initial blood cultures and sputum culture were non-revealing. His ESR was 75 with a positive ANA screen but essentially negative titers (<1:40); U/A was unimpressive, renal function was normal, initial CBC had mild anemia (Hgb 12.6) but normal WBC (7.6 with 90% PMNs) and normal platelets.
What other tests/info would you like next?
Tuesday, August 28, 2007
Abnormal CxR
This is a very pleasant, 64-year-old man with progressive worseningdyspnea over the past couple of months. He states that up until maybe six months ago he had been in his usual state of health and had no persistentdyspnea. For the past 3-4 months he has had insidious onset of dyspnea on exertion, which has been worsening. He has had no associated cough, no chest pain, no fever, no chills and no night sweats. He denies any significant paroxysmal nocturnal dyspnea, though he does have some component of orthopnea. He has never had hemoptysis. His weight has been stable. He actually has gained some weight in the past couple of years. He has had no previous label of severe chronic lung disease.
PAST MEDICAL HISTORY: Significant for some hypertension.He had been diagnosed with mediastinal and hilar adenopathy some 15 yearsago, according to the patient. He actually underwent a bronchoscopy atthat time, but was not found to have any significant evidence ofmalignancy. He has never had a sleep study. The films and reports on his adenopathy are in a Mississippi and not available...
SOCIAL HISTORY: He used to smoke, but quit about 15 years ago when he was diagnosed with the mediastinal and hilar adenopathy. He worked in freight mostly at docks and driving transport. No alcohol abuse, no illicit drug use. He used to live in Mississippi (now here in TN). He has no exposure to sick contacts. He lives with his wife and they have no pets. No alcohol abuse, no illicit drug use.
FAMILY HISTORY: Is remarkable for his sister having pulmonary fibrosis, but we are not sure as to what type. She apparently is on oxygen 24/7.
REVIEW OF SYSTEMS is otherwise fairly unremarkable.
PHYSICAL EXAMINATION: Afebrile. Only pertinent positives are some faint right basilar crackles which actually cleared withcough. He has slightly diminished breath sounds at the bases. I could not appreciate any wheezing. He has no edema, no clubbing and no cyanosis.
CxR and CT as below. What do you think and how would you work him up?
SOCIAL HISTORY: He used to smoke, but quit about 15 years ago when he was diagnosed with the mediastinal and hilar adenopathy. He worked in freight mostly at docks and driving transport. No alcohol abuse, no illicit drug use. He used to live in Mississippi (now here in TN). He has no exposure to sick contacts. He lives with his wife and they have no pets. No alcohol abuse, no illicit drug use.
FAMILY HISTORY: Is remarkable for his sister having pulmonary fibrosis, but we are not sure as to what type. She apparently is on oxygen 24/7.
REVIEW OF SYSTEMS is otherwise fairly unremarkable.
PHYSICAL EXAMINATION: Afebrile. Only pertinent positives are some faint right basilar crackles which actually cleared withcough. He has slightly diminished breath sounds at the bases. I could not appreciate any wheezing. He has no edema, no clubbing and no cyanosis.
CxR and CT as below. What do you think and how would you work him up?
Monday, August 27, 2007
Hemoptyis and bilateral infiltrated UPDATE
The case below was posted last week. Since that time I obtained a high res CT and autoimmune panel. The ANCA and ANA were normal. The BAL (clear non-bloody) was negative for any infection. The cell count of about 500 was predominantly macrophages. He is still short of breath (mostly on exertion but to a lesser extent at rest). He has no fevers or other constitutional symptoms. No more hemoptysis.
CT (no hilar adenopathy, by the way):
63 year old man with one week of hemoptysis. The hemoptysis is described as streaks of blood with the underlying sputum being slighltly light green or white. No malaise. Just some shortness of breath. No fevers or night sweats. No anorexia or weight loss. He feels pretty well except for the mild increase in SOB.
He is a 48 pack year smoker now quit. No significant exposure or travel history. For what its worth (if anything), he was cleaning out his gutters about a week before the symptoms. Lots of decayed leaves etc.
On exam he is WNWD and NAD. Vitals and pulsox are normal. No LAD and the lungs are clear to auscultation.
His WBC is 14 and in June it was 7.
His xray from 3 years ago:
The xray from today is seen here:
He has persistent dyspnea despite a course of azithro for presumed mycoplasma. The BAL was negative for virus or fungi.
His new cxr is here:
What is your differential dx?
CT (no hilar adenopathy, by the way):
63 year old man with one week of hemoptysis. The hemoptysis is described as streaks of blood with the underlying sputum being slighltly light green or white. No malaise. Just some shortness of breath. No fevers or night sweats. No anorexia or weight loss. He feels pretty well except for the mild increase in SOB.
He is a 48 pack year smoker now quit. No significant exposure or travel history. For what its worth (if anything), he was cleaning out his gutters about a week before the symptoms. Lots of decayed leaves etc.
On exam he is WNWD and NAD. Vitals and pulsox are normal. No LAD and the lungs are clear to auscultation.
His WBC is 14 and in June it was 7.
His xray from 3 years ago:
The xray from today is seen here:
He has persistent dyspnea despite a course of azithro for presumed mycoplasma. The BAL was negative for virus or fungi.
His new cxr is here:
What is your differential dx?
Wednesday, August 08, 2007
TB pericarditis
Submitted by IS:
What are your opinions regarding the use of adjuvant steroids for presumed TB pericarditis? Do you think a pericardial biopsy is a must if we have a positive PPD, negative cytology of fluid, low glucose on fluid studies, and good clinical history? Thanks.
What are your opinions regarding the use of adjuvant steroids for presumed TB pericarditis? Do you think a pericardial biopsy is a must if we have a positive PPD, negative cytology of fluid, low glucose on fluid studies, and good clinical history? Thanks.
Thursday, July 26, 2007
Steroid responsive adenopathy?
65-year-old woman presented initially for evaluation of shortness of breath. A CT thorax revealed some patchy airspace opacification RUL (see below) . She underwent bronchoscopic evaluation and it demonstrated some interstitial inflammation with hyperplastic type 2 pneumoctyes. No granulomas seen. No fungal or AFB elements on BAL. A cell count was not sent.
She was begun on a course of steroids 40mg and felt her breathing improved significantly while on them, but once she stopped them, her shortness of breath recurred. Her cough has also recurred, though it's mostly non-productive. A CT was repeated 5 monts later and is shown below.
Question: What ILD had adenopathy and is steroid responsive? The only 2 I can think of are sarcoid and berrylliosis, but the interstial inflammation would be inconsistent with that. Any thoughts out there?
She was begun on a course of steroids 40mg and felt her breathing improved significantly while on them, but once she stopped them, her shortness of breath recurred. Her cough has also recurred, though it's mostly non-productive. A CT was repeated 5 monts later and is shown below.
Question: What ILD had adenopathy and is steroid responsive? The only 2 I can think of are sarcoid and berrylliosis, but the interstial inflammation would be inconsistent with that. Any thoughts out there?
Tuesday, July 24, 2007
A man with weakness and a some minor CT abnormalities
From Doug:
53 yo man with an 80 pack yr smoking hx and history of Etoh abuse was admitted
with a 5 week hx of progressive ataxia, diplopia, dysarthria,
and dysphagia. Initially w/u revealed unremarkable MRI brain, and a CT
C/A/P showing prevascular lymph nodes with some calcifications and left hilar borderline enlarged lymph nodes, and a renal cyst not further characterized on that study.
DDx included subacute cerebellar degeneration and progressive supranuclear palsy.
Multiple CSF and serum labs were pending at time of discharge
He was readmitted a week later for progressive dysphagia for liquids in addition to solids, worsening gait s/p falls, and continued dysarthria and diplopia. IV IgG was given empirically without improvement. Repeat LP and additional infectious
serologies were negative. A dedicated renal CT was done to further characterize the indeterminate lesion on the previous CT, showing only a
simple cyst.
What would you do next? <<<>>>
Addendum added after case presented:
These are the EBUS images from the bronch including and the core biopsy from the TBNA. The answer was that these little lymph nodes were small cell carcinoma. The special stain is a cytokeratin stain of the malignant cells.
53 yo man with an 80 pack yr smoking hx and history of Etoh abuse was admitted
with a 5 week hx of progressive ataxia, diplopia, dysarthria,
and dysphagia. Initially w/u revealed unremarkable MRI brain, and a CT
C/A/P showing prevascular lymph nodes with some calcifications and left hilar borderline enlarged lymph nodes, and a renal cyst not further characterized on that study.
DDx included subacute cerebellar degeneration and progressive supranuclear palsy.
Multiple CSF and serum labs were pending at time of discharge
He was readmitted a week later for progressive dysphagia for liquids in addition to solids, worsening gait s/p falls, and continued dysarthria and diplopia. IV IgG was given empirically without improvement. Repeat LP and additional infectious
serologies were negative. A dedicated renal CT was done to further characterize the indeterminate lesion on the previous CT, showing only a
simple cyst.
What would you do next? <<<
Addendum added after case presented:
These are the EBUS images from the bronch including and the core biopsy from the TBNA. The answer was that these little lymph nodes were small cell carcinoma. The special stain is a cytokeratin stain of the malignant cells.
Friday, June 22, 2007
Shortness of breath with phrenic nerve paralysis
Submission
60 year old woman with sarcoidosis by mediastinal biopsy 1978 doing well, never requiring steroids. 2 mos prior developed SOB - smothering type of feeling even at rest but also on exertion. A CXR during a routine physical showed a left paralyzed hemidiaphragm.
Pmhx
sarcoid as above
NQWMI 1991 Echo on f/u showed torn chordae and LV "contractile abnormality" on a thallium test.
Three fluorouscopies revealed unilateral paralysis. Scheduled for EMG studies
Patient also adds:
"I am 60 y/o and live a quiet life but my legs are now getting weak and I am unable to bend down in a sitting position and get up. I failed to mention that I had a lumbar puncture which was normal. MRI showed cervical problems but nothing serious I guess. The pons area of my brain showed vascular changes due to aging. I also had strabismus during all of this and had a prism put in my glasses because of a convergence problem with my eyes. Could this all be connected? Myasthenia gravis I guess has been ruled out and they are calling this idiopathic phrenic nerve paralysis. Should I pursue this any further?I have about 40% function of my left lung."
Note: please consider adding a comment to help keep this blog going!
60 year old woman with sarcoidosis by mediastinal biopsy 1978 doing well, never requiring steroids. 2 mos prior developed SOB - smothering type of feeling even at rest but also on exertion. A CXR during a routine physical showed a left paralyzed hemidiaphragm.
Pmhx
sarcoid as above
NQWMI 1991 Echo on f/u showed torn chordae and LV "contractile abnormality" on a thallium test.
Three fluorouscopies revealed unilateral paralysis. Scheduled for EMG studies
Patient also adds:
"I am 60 y/o and live a quiet life but my legs are now getting weak and I am unable to bend down in a sitting position and get up. I failed to mention that I had a lumbar puncture which was normal. MRI showed cervical problems but nothing serious I guess. The pons area of my brain showed vascular changes due to aging. I also had strabismus during all of this and had a prism put in my glasses because of a convergence problem with my eyes. Could this all be connected? Myasthenia gravis I guess has been ruled out and they are calling this idiopathic phrenic nerve paralysis. Should I pursue this any further?I have about 40% function of my left lung."
Note: please consider adding a comment to help keep this blog going!
Friday, June 15, 2007
Shortness of breath
Submission from outside reader:
Hi I have been looking at this blog for since 2005 on a weekly basis and wonder if you take questions from patients. Your site is informative it is a pity you are not getting the hits.
I am a 38yo M and I have a chronic symptoms now for many years with NO DIAGNOSIS despite pressing for one.
I have a hacking cough with some sputum in the morning, I also have nearly constant SOB with an inability to get a deep breath. A feeling of stiffness in my lungs. I feel constantly like my breathing is not good. This has been with me since 2003. Excercise tolerance is ok i.e. I could run a mile in 10min but I struggle to breathe throughout.
Pleurisy type pain on and off weekly, specifically located in same location at upper left back. Lower rib pain on left.
Asthma as a child, allergic rhinitis as a teenager and young adult, smoked in college (10 a day) and socially (30 at weekend) till I was 33. On and off asthma meds since 1994. Tried Singulair, Symbicort, Spiriva etc. Tried also extensive courses of Zoton, Nasocort etc.
Have been evaluated many times over the years by 3 pulmos spent '000$ and the best they can give me as a diagnosis is " a chronic inflammation similar to chronic bronchitis with little or no asthma but we are reluctant to give it a title "
Here is the dilemma, all tests normal my FEV1 is 4.45…101%, FVC 5.8…104%, FEV/FVC 76. DLCO Normal. FEF25-75 83% Lung Vols Normal
Here is the question:
Why do I have symptoms if all tests are normal. What do you guys think.. have you seen this before, normal tests but chronic symptoms with dyspnea.
Chest xray x 4 Normal
2 x HRCT (1 year between) Normal, Body Ples Normal. Methacholine Normal
ECG Stress Test Normal
Echo Cardio Normal
Bloods Normal, 2 x HRCT (1 year between) Normal, Body Ples Normal. Methacoline Normal
MRI ordered by Rheumo .. Normal
Not in my brain either!! I have loads of other stuff to worry about like kids, my stressful job as a broker, mortgages etc
Hi I have been looking at this blog for since 2005 on a weekly basis and wonder if you take questions from patients. Your site is informative it is a pity you are not getting the hits.
I am a 38yo M and I have a chronic symptoms now for many years with NO DIAGNOSIS despite pressing for one.
I have a hacking cough with some sputum in the morning, I also have nearly constant SOB with an inability to get a deep breath. A feeling of stiffness in my lungs. I feel constantly like my breathing is not good. This has been with me since 2003. Excercise tolerance is ok i.e. I could run a mile in 10min but I struggle to breathe throughout.
Pleurisy type pain on and off weekly, specifically located in same location at upper left back. Lower rib pain on left.
Asthma as a child, allergic rhinitis as a teenager and young adult, smoked in college (10 a day) and socially (30 at weekend) till I was 33. On and off asthma meds since 1994. Tried Singulair, Symbicort, Spiriva etc. Tried also extensive courses of Zoton, Nasocort etc.
Have been evaluated many times over the years by 3 pulmos spent '000$ and the best they can give me as a diagnosis is " a chronic inflammation similar to chronic bronchitis with little or no asthma but we are reluctant to give it a title "
Here is the dilemma, all tests normal my FEV1 is 4.45…101%, FVC 5.8…104%, FEV/FVC 76. DLCO Normal. FEF25-75 83% Lung Vols Normal
Here is the question:
Why do I have symptoms if all tests are normal. What do you guys think.. have you seen this before, normal tests but chronic symptoms with dyspnea.
Chest xray x 4 Normal
2 x HRCT (1 year between) Normal, Body Ples Normal. Methacholine Normal
ECG Stress Test Normal
Echo Cardio Normal
Bloods Normal, 2 x HRCT (1 year between) Normal, Body Ples Normal. Methacoline Normal
MRI ordered by Rheumo .. Normal
Not in my brain either!! I have loads of other stuff to worry about like kids, my stressful job as a broker, mortgages etc
Monday, June 11, 2007
Pulmicort discontinued?
Has anyone else heard that Astra Zeneca will be discontinuing pulmicort? Were they not making a profit on this? Anecdotally, I see a lot of patients on Pulmicort.
This is from The FDA site:
NDA 20-441, PULMICORT TURBUHALER 200 mcg (budesonide inhalation powder) will no longer be available at AstraZeneca.
The introduction of PULMICORT FLEXHALER (budesonide inhalation powder, 90 & 180 mcg), NDA 21-949, will be accompanied by the phasing out of PULMICORT TURBUHALER so as to minimize confusion in the marketplace.
AstraZeneca has no further plans to manufacture NDA 20-441, PULMICORT TURBUHALER 200 mcg (budesonide inhalation powder).
This is from The FDA site:
NDA 20-441, PULMICORT TURBUHALER 200 mcg (budesonide inhalation powder) will no longer be available at AstraZeneca.
The introduction of PULMICORT FLEXHALER (budesonide inhalation powder, 90 & 180 mcg), NDA 21-949, will be accompanied by the phasing out of PULMICORT TURBUHALER so as to minimize confusion in the marketplace.
AstraZeneca has no further plans to manufacture NDA 20-441, PULMICORT TURBUHALER 200 mcg (budesonide inhalation powder).
Worsening dyspnea in a patient with IPF
71 year olf woman with idiopathic pulmonary fibrosis diagnosed by open lung 2004 (UIP on biopsy). Since that time she has been stable with good exercise tolerance, and able to get around with little difficulty. PFT's also stable during that time frame with FVC in low 80% since 2004. Over the last 2 months she reports increased dyspnea on exertion and fatigue. Her ambulation has decreased over the last 3 or 4 months because of pain of her left hip, which for the last 6 months she had been getting injections for. She is due to get left total hip replacement. She has difficulty getting out of the chair because of pain in her hip. She does still try to get around, but her ambulation she does admit has decreased over the last 3 months because of this pain. She denies any nocturnal shortness of breath or orthopnea. She has no chest pain. There is no fevers, chills, night sweats. No appreciable weight gain subjectively. No anorexia. No cough.
Her physical exam is a pleasant woman sitting in a chair, in no acute distress. Blood pressure 123/59, pulse is 77, respiration is 20, O2 sat is 97% on room air, her weight is 228 pounds. Her weight in March 21st on another scale at another clinic was 221 pounds and her weight on our scale in January 2007 was 231 pounds. HEENT: Trachea midline, no lymphadenopathy. The JVP seems to be about 4 to 5 cm. The lungs have crackles basilarly and laterally about the third of the way up. Heart is regular rate and rhythm with a positive S3, no murmurs or rubs. Abdomen: Benign. There is trace pitting edema bilaterally at the ankles.
Spirometry shows the ratio of 84%. FEV1 of 1.87 (83% of predicted), FVC of 2.21 (74% of predicted). DLCO 65% of predicted. In May 2006 FVC was 80% of predicted and DLCO 74% of predicted.
CXR this visit:
CXR from 2 years ago:
What are your thoughts and/or what would you do next?
Her physical exam is a pleasant woman sitting in a chair, in no acute distress. Blood pressure 123/59, pulse is 77, respiration is 20, O2 sat is 97% on room air, her weight is 228 pounds. Her weight in March 21st on another scale at another clinic was 221 pounds and her weight on our scale in January 2007 was 231 pounds. HEENT: Trachea midline, no lymphadenopathy. The JVP seems to be about 4 to 5 cm. The lungs have crackles basilarly and laterally about the third of the way up. Heart is regular rate and rhythm with a positive S3, no murmurs or rubs. Abdomen: Benign. There is trace pitting edema bilaterally at the ankles.
Spirometry shows the ratio of 84%. FEV1 of 1.87 (83% of predicted), FVC of 2.21 (74% of predicted). DLCO 65% of predicted. In May 2006 FVC was 80% of predicted and DLCO 74% of predicted.
CXR this visit:
CXR from 2 years ago:
What are your thoughts and/or what would you do next?
Thursday, June 07, 2007
Acute on chronic Blogemia
Sorry there have been no new posts. Baleeiro and I are essentially the last surviving members of the blog (functionally, not literally - the others are not dead; they just lost interest) and our motivation for daily posts has somewhat diminished given lack of participation from outside readers, previous contributors and anyone else who might come across this blog. I will most likely leave a post or two a week and we will see where this goes. We have been steadily building a database over 2 years of pulmonary cases (with discussion) and all categorized, so it is a bit of a shame that it goes this way. Hopefully we can wean the blog off of the proverbial vent and not proceed to comfort care measures....
-JJ
-JJ
Friday, April 20, 2007
low DLCO in runner
Submission from Hal :
15 y/o WF distance runner on track team c/o SOB. No improvement in the past year as perceived inability to breathe. She is is 5 7 tall, 115 pounds. All State, All American runner in 1600M and 800M.
PFTs showed DLCO 71% pred (18.9 with ref 26.6), DL Adj 80% (18.9 with 23.5 ref).
VA 5.09 L
FVC 106%, FEV1 100%, FEF25-75 96%.
Chest xray showed...ordered but not done yet.
Normal CBC
Any thoughts on etiology and suggestions for further work-up?
15 y/o WF distance runner on track team c/o SOB. No improvement in the past year as perceived inability to breathe. She is is 5 7 tall, 115 pounds. All State, All American runner in 1600M and 800M.
PFTs showed DLCO 71% pred (18.9 with ref 26.6), DL Adj 80% (18.9 with 23.5 ref).
VA 5.09 L
FVC 106%, FEV1 100%, FEF25-75 96%.
Chest xray showed...ordered but not done yet.
Normal CBC
Any thoughts on etiology and suggestions for further work-up?
Friday, April 13, 2007
Cavitary mass
86 year old man with history of dementia brought by his caretaker for mental status changes and lethargy. He lives in an assisted living facility, but has no TB risk factors otherwise (He has his own apartment-like structure, but I beleive there is a common area).
His CT:
There was no hilar or mediastinal adenopathy.
The thickest wall area on that lesion was 4-5 mm.
Someone placed a PPD and it was 11 mm. It was reportedly negative 6 months ago.
He is not productive of sputum, so 3 gastric lavages were done and they were all negative. What would you do next? Are you worried about active tb? Here are my thoughts
1. How sensitive is gastric lavage for afb?
2. location of the cavitary mass is not where tb should be.
3. is he a ppd converter, or was he anergic or are we seeing a booster effect
4. His family does not want an aggressive w/u for cancer, but on the other hand one would not want to send someone home to hospice with active tb....
His CT:
There was no hilar or mediastinal adenopathy.
The thickest wall area on that lesion was 4-5 mm.
Someone placed a PPD and it was 11 mm. It was reportedly negative 6 months ago.
He is not productive of sputum, so 3 gastric lavages were done and they were all negative. What would you do next? Are you worried about active tb? Here are my thoughts
1. How sensitive is gastric lavage for afb?
2. location of the cavitary mass is not where tb should be.
3. is he a ppd converter, or was he anergic or are we seeing a booster effect
4. His family does not want an aggressive w/u for cancer, but on the other hand one would not want to send someone home to hospice with active tb....
Wednesday, April 11, 2007
Dose of T-PA - Part Deux
I didn't get much feedback or interest on the post below on T-PA and empyemas so I contacted our T-PA rep and we got some references on the matter.
The dose varies widely and it seems you just can't go wrong...
In the Chest abstract I had listed in the original post the authors used 10 mg per instillation.
In a brief review/case report in Hospital Pharmacy in 2003 (vol 38 (11); pp: 1024-29) the authors used 16mg/100ml NSS infused daily. They derived the dose by extrapolating the ratio of Streptokinase usually used in empyemas to the dose for MI's.
In another Chest abstract, the initial dose was 10mg for complicated hemothoraces and that was increased to 25mg, still with good tolerability.
The pediatric literature was a bit more consistent and usually 0.1mg/kg was used in various trials.
Any other suggestions?
The dose varies widely and it seems you just can't go wrong...
In the Chest abstract I had listed in the original post the authors used 10 mg per instillation.
In a brief review/case report in Hospital Pharmacy in 2003 (vol 38 (11); pp: 1024-29) the authors used 16mg/100ml NSS infused daily. They derived the dose by extrapolating the ratio of Streptokinase usually used in empyemas to the dose for MI's.
In another Chest abstract, the initial dose was 10mg for complicated hemothoraces and that was increased to 25mg, still with good tolerability.
The pediatric literature was a bit more consistent and usually 0.1mg/kg was used in various trials.
Any other suggestions?
Monday, April 09, 2007
Dose of T-PA
There is a wealth of articles on using fibrinolytics in empyema (with mixed results) listing the doses for urokinase and streptokinase. I have had trouble finding a narrower consensus on T-PA dosing though. The Pediatric literature suggests ~4mg/kg and there is a dose of 2mg for clotted central venous access. I also found an abstract from Chest where doses of 10 mg were used but couldn't find a good consensus.
Have you used T-PA in empyemas? And how much?
Have you used T-PA in empyemas? And how much?
Wednesday, April 04, 2007
Lung mass(es)
Unfortunately, our computer is not letting me retrieve the PET images on this patient so I'll try and describe it without puppets.
This is a 71 y/o man with long TOB Hx but still good mechanics (FEV1~78%) with a new lung mass. He was found to have a 2.5-cm mass in the RML and had a CT-guided Bx which was + for adenoCa. He then had a PET and came to see us: the mass was obviously hot but he had FDG-avid subcarinal and L hilar nodes and a 1-cm FDG-avid LUL peripheral lesion. I bronch'ed him and sampled his nodes and got lots of giant cells and lymphocytes but no malignancy (from both sites). A LUL BAL was non-Dx.
Would you Bx the LUL separately? And if so how would you approach this (synchronous vs metastatic lesions, etc.)?
This is a 71 y/o man with long TOB Hx but still good mechanics (FEV1~78%) with a new lung mass. He was found to have a 2.5-cm mass in the RML and had a CT-guided Bx which was + for adenoCa. He then had a PET and came to see us: the mass was obviously hot but he had FDG-avid subcarinal and L hilar nodes and a 1-cm FDG-avid LUL peripheral lesion. I bronch'ed him and sampled his nodes and got lots of giant cells and lymphocytes but no malignancy (from both sites). A LUL BAL was non-Dx.
Would you Bx the LUL separately? And if so how would you approach this (synchronous vs metastatic lesions, etc.)?
Thursday, March 29, 2007
Tongue lesions followed by dyspnea?
From AK:
22 year old with recurrent dyspnea, usually preceded by pea-sized painless denuded areas on the tongue (see picture). Episodes of dyspnea have landed her in the ER multiple times, where she's treated with nebs and steroids. No ulcers anywhere else on her body, but she has had some easy bruising lately. Others describe wheezing on exam and I've heard inspiratory stridor during an episode. Normal VC movement on laryngoscopy. PFTs with mild flattening of inspiratory portion of flow-volume loop, otherwise unremarkable. Normal soft tissue film of the neck. Methacholine challenge normal. CXR normal. Allergy skin testing negative. IgE 5. TSH normal. CRP 0.4. Liver and kidney function normal. U/A normal. CBC with diff normal.
Also had an unexplained episode of weight loss last fall, approx. 20 lbs. Resolved spontaneously and weight came back.
I'm temped to call this VC dysfunction, but other docs claim definite peripheral wheezing on exam, and these tongue lesions don't ring any bells.
Any ideas?
22 year old with recurrent dyspnea, usually preceded by pea-sized painless denuded areas on the tongue (see picture). Episodes of dyspnea have landed her in the ER multiple times, where she's treated with nebs and steroids. No ulcers anywhere else on her body, but she has had some easy bruising lately. Others describe wheezing on exam and I've heard inspiratory stridor during an episode. Normal VC movement on laryngoscopy. PFTs with mild flattening of inspiratory portion of flow-volume loop, otherwise unremarkable. Normal soft tissue film of the neck. Methacholine challenge normal. CXR normal. Allergy skin testing negative. IgE 5. TSH normal. CRP 0.4. Liver and kidney function normal. U/A normal. CBC with diff normal.
Also had an unexplained episode of weight loss last fall, approx. 20 lbs. Resolved spontaneously and weight came back.
I'm temped to call this VC dysfunction, but other docs claim definite peripheral wheezing on exam, and these tongue lesions don't ring any bells.
Any ideas?
Tuesday, March 27, 2007
Where is Waldo (or the line)?
Wednesday, March 21, 2007
Rheumatoid arthritis and effusions
From one of our readers. Edited a slight bit.
Found your site and thought I‘d run some of this by you to get your take on the situation so we might be more well-equipped to talk to our local doctors.
Husband is a 52 yr old smoker (about a pack and a half a day) with advanced rheumatoid arthritis. He is on:
Methotrexate for ten years (20 mg a week, currently)
Had a five-year stint on enbrel/etanercept - discontinued six months ago)
Recently moved to remicade.
Other meds: folic acid, indomethacin, prednisone 30 mg, QD, and hydrochlorthiazide (12.5 mg, daily).
February 2005, he started feeling “full” in his torso. Blood tests were “normal”. But he gained 9 pounds in a day. In the ER he was fpund to have fluid around his heart and in his pleural cavity. They withdrew 31 ounces of fluid off the heart. All seemed well....for a time.
Had another bout with all this in March, 2005.
Around Christmas 2005, he started feeling full again, and the doctor said go to the Emergency Room. Hubby said he didn’t want to go through all that again, so they told him to take prednisone (40 mg a day). Gave him relief. Started to step-down the dosage of prednisone...got down to 10mg/day, and started feeling full, again.
HRCT was ordered and showed:
Clinical Information: Pleural effusion.
Findings: Standard and high resolution chest CT images demonstrate moderate centrilobular and paraseptal emphysema. No focal consolidating process. Mild ground glass with traction bronchiectasis involving the peripheral aspect of the lung fields, with upper lung zone predominance. The findings are nonspecific, and may represent sequela of chronic hypersensitive pneumonotis. There is evidence of prior granulomatous disease. There is a 5-mm hyperdense pulmonary nodule in the right upper lobe; this nodule may be partially calcified. There is also an 8-mm, not obviously calcified nodule in the right middle lobe. Small left and trace right pleural effusions are noted. There is no lymphadenopathy. The heart is not enlarged. There is not significant pericardial effusion. The adrenal glands are not enlarged. There is a focal 3-cm mass lesion involving the pancreatic tail. The lesion demonstrates slightly higher attenuation relative to the remaining pancreatic parenchyma. Central low attenuation is noted, suggestive of cystic components. No significant surrounding inflammation is identified. There is not pancreatic ductal dilatation.
I have been reading as much as I can to try and understand what this means. Originally, when I started research, I had not began with the idea that all of these are tied to his rheumatoid arthritis; however, the more I read, a correlation seems to be drawn between many of these conditions and either rheumatoid arthritis, or prolonged exposure to methotrexate.
I had read one of the posts on the pulmonaryroundtable.com site title BAL eosinophilia in a patient with rheumatoid arthritis which seemed to resemble some of my husband’s case.
I wanted to ask what you thought of these results and to see if you thought that my supposition / correlations drawn in my own mind are simply that (suppositions on my part), or if you think that these links are founded, possible, and real.
I am also concerned about the noted lesion on the pancreas, as I do not seem to be able to find much regarding pancreatic mass lesions. It is very confusing reading
Found your site and thought I‘d run some of this by you to get your take on the situation so we might be more well-equipped to talk to our local doctors.
Husband is a 52 yr old smoker (about a pack and a half a day) with advanced rheumatoid arthritis. He is on:
Methotrexate for ten years (20 mg a week, currently)
Had a five-year stint on enbrel/etanercept - discontinued six months ago)
Recently moved to remicade.
Other meds: folic acid, indomethacin, prednisone 30 mg, QD, and hydrochlorthiazide (12.5 mg, daily).
February 2005, he started feeling “full” in his torso. Blood tests were “normal”. But he gained 9 pounds in a day. In the ER he was fpund to have fluid around his heart and in his pleural cavity. They withdrew 31 ounces of fluid off the heart. All seemed well....for a time.
Had another bout with all this in March, 2005.
Around Christmas 2005, he started feeling full again, and the doctor said go to the Emergency Room. Hubby said he didn’t want to go through all that again, so they told him to take prednisone (40 mg a day). Gave him relief. Started to step-down the dosage of prednisone...got down to 10mg/day, and started feeling full, again.
HRCT was ordered and showed:
Clinical Information: Pleural effusion.
Findings: Standard and high resolution chest CT images demonstrate moderate centrilobular and paraseptal emphysema. No focal consolidating process. Mild ground glass with traction bronchiectasis involving the peripheral aspect of the lung fields, with upper lung zone predominance. The findings are nonspecific, and may represent sequela of chronic hypersensitive pneumonotis. There is evidence of prior granulomatous disease. There is a 5-mm hyperdense pulmonary nodule in the right upper lobe; this nodule may be partially calcified. There is also an 8-mm, not obviously calcified nodule in the right middle lobe. Small left and trace right pleural effusions are noted. There is no lymphadenopathy. The heart is not enlarged. There is not significant pericardial effusion. The adrenal glands are not enlarged. There is a focal 3-cm mass lesion involving the pancreatic tail. The lesion demonstrates slightly higher attenuation relative to the remaining pancreatic parenchyma. Central low attenuation is noted, suggestive of cystic components. No significant surrounding inflammation is identified. There is not pancreatic ductal dilatation.
I have been reading as much as I can to try and understand what this means. Originally, when I started research, I had not began with the idea that all of these are tied to his rheumatoid arthritis; however, the more I read, a correlation seems to be drawn between many of these conditions and either rheumatoid arthritis, or prolonged exposure to methotrexate.
I had read one of the posts on the pulmonaryroundtable.com site title BAL eosinophilia in a patient with rheumatoid arthritis which seemed to resemble some of my husband’s case.
I wanted to ask what you thought of these results and to see if you thought that my supposition / correlations drawn in my own mind are simply that (suppositions on my part), or if you think that these links are founded, possible, and real.
I am also concerned about the noted lesion on the pancreas, as I do not seem to be able to find much regarding pancreatic mass lesions. It is very confusing reading
Tuesday, March 20, 2007
RADS
A 70 year old man has reactive airways dysfunction syndrome from a previous inhalant. He was seen in 2005 for dyspnea but primary did not initiate any steroids. At that time his fev1 was 2.05, 66% predicted. When we saw him in January where there was obstruction with an FEV1 of 2.34 (72% predicted). 20 mg of steroids were given (higher doses resulted in his fingers "locking") and a repeat spiro this month shows no change in the obstruction (2.27 l, 69% predicted).
How many would continue the steroids? How many would stop the steroids for apparent lack of efficacy?
Symptomatically he has mild dyspnea with exertion that is less than prior to the steroids.
How many would continue the steroids? How many would stop the steroids for apparent lack of efficacy?
Symptomatically he has mild dyspnea with exertion that is less than prior to the steroids.
Monday, March 19, 2007
Vasoreactivity testing in PH
Two cases today (pop an ibuprofen and read on...)
This comes to us from "IS"
After a R heart cath confirms pulm HTN and a vasodilator test with IV Flolan or inhaled NO confirms a responder, what do you guys start with? Do you start with calcium channel blocker sustained release or short acting? Do you leave the right heart cath in and monitor the hemodynamics as you titrate the dose of CCB? Just wondering as we are trying to start a PH program here and it seems that there isn't a standardized protocol. Thanks for your input.
This comes to us from "IS"
After a R heart cath confirms pulm HTN and a vasodilator test with IV Flolan or inhaled NO confirms a responder, what do you guys start with? Do you start with calcium channel blocker sustained release or short acting? Do you leave the right heart cath in and monitor the hemodynamics as you titrate the dose of CCB? Just wondering as we are trying to start a PH program here and it seems that there isn't a standardized protocol. Thanks for your input.
Mediastinal adenopathy, hypoxia
Dr.Carrillo submitted a case for your enjoyment/pontification:
49yo Hx of ETOH and presumptive cirrhosis. Exposed to birds through his early years. 2000 had abnormal CT thorax with interlobular septal thickening, Pleural thickening encasing the lungs and multiple adenopathy in the med. Mediatinoscopy report says multiple venous collaterals may be early SVC.Thickened fat through the mediastinum.Bx of LN neg,no Cx sent. 2003 - Same CT findings.
Now presents with hypoxia and CT findings similar as before. The radiologist describes that the mediatinum looks abnormal with strading. I think this guy probably has histo with some fibrosis of the medistinum. I wonder if he has compression of the thoracic duct with causing his lymphatics to be prominent and show like interlobular septal thickening on CT and he had previous Chylo?. I was going to do broncoscopy with TBBX and TBNA and serologies. Any other idea or opinion about this case. Do you think I should further investigate the possible thoracic duct obstruction?
49yo Hx of ETOH and presumptive cirrhosis. Exposed to birds through his early years. 2000 had abnormal CT thorax with interlobular septal thickening, Pleural thickening encasing the lungs and multiple adenopathy in the med. Mediatinoscopy report says multiple venous collaterals may be early SVC.Thickened fat through the mediastinum.Bx of LN neg,no Cx sent. 2003 - Same CT findings.
Now presents with hypoxia and CT findings similar as before. The radiologist describes that the mediatinum looks abnormal with strading. I think this guy probably has histo with some fibrosis of the medistinum. I wonder if he has compression of the thoracic duct with causing his lymphatics to be prominent and show like interlobular septal thickening on CT and he had previous Chylo?. I was going to do broncoscopy with TBBX and TBNA and serologies. Any other idea or opinion about this case. Do you think I should further investigate the possible thoracic duct obstruction?
Tuesday, March 13, 2007
2-year-old mass
This is a 67 y/o male with a 75 p/y Hx of TOB but still good lung function (his FEV1 is 2.06L).
2 years ago he was told he had a "quarter-sized" nodule on his RML (at a different facility so I don't have those films) and he decided not to show up for his scheduled Bx or further follow-up visits. The lesion has clearly grown and I'd be surprised if it is anything other than a malignancy. Does the time of "follow-up" with growth but no spread in 2 years change your w/up sequence?
For example, if the PET shows no other disease, would you consider going straight to resection without a Bx?
2 years ago he was told he had a "quarter-sized" nodule on his RML (at a different facility so I don't have those films) and he decided not to show up for his scheduled Bx or further follow-up visits. The lesion has clearly grown and I'd be surprised if it is anything other than a malignancy. Does the time of "follow-up" with growth but no spread in 2 years change your w/up sequence?
For example, if the PET shows no other disease, would you consider going straight to resection without a Bx?
Monday, March 12, 2007
Pulmonary HTN question
case comments: This is just a question: Are most of you still routinely performing a right heart catheterization prior to treatment initiation in patients with pulmonary hypertension - even in those associated with collagen vascular disease, etc? What do you use as your drug of choice for vasodilatory testing? Do you routinely perform a left heart cath as well?
Friday, March 09, 2007
Xigris and platelets
Yesterday I got consulted on this 63 y/o woman with abdominal sepsis: she had been on chronic prednisone for SLE and presented with perforated colon diverticuli with peritonitis. She has developed mild renal failure (creat up to 2.4 from 1.5), resp. failure (PaO2/FiO2 ~80) and is still requiring pressors after VERY vigorous fluid replacement. She had good post-op hemostasis and platelets around 100K. In addition to the usual care (ABTx, vent, etc). We started her on Xigris. ~8 hours into it her platelets dropped to ~10K. We held the Xigris and this am they are 26K. Would you continue to hold it, monitor and resume it, transfuse platelets and resume it or just forget about Xigris in her?
Monday, March 05, 2007
Interferon-gamma trial for IPF is discontinued
Well, the press-release was today so it is public info: the phase 3 trial testing IFN-gamma vs. placebo in patients with IPF has been discontinued. The independent data monitoring committee did an interim analysis and found no difference between IFN-gamma and placebo for mortality (14.5% in the Actimmune group as compared to 12.7% in the placebo). The adverse reactions were consistent with prior clinical experience(constitutional symptoms, neutropenia and possibly pneumonia).
“The interim results of the INSPIRE trial and our decision to discontinue the trial are disappointing,” said Steve Porter, M.D., Ph.D., Chief Medical Officer at InterMune.
I'm not sure what this means for the company, but they are also running the perfenidone trial, but not so sure this will fare any better...
To me, this is not so surprising, but it really does illustrate the importance of being careful not to read too much into sub group analysis before the next study is done- the original study found that patients with more "mild" IPF (FVC 55-90% predicted) might have a survival advantage and the current study was powered to test that hypothesis. Ultimately it was found not to be the case after all.
People currently taking the IFN-g as part of the study will be instructed to stop it, and everyone will then pack up their bags and move on to the next latest and greatest...
Does anyone have any patients enrolled int his trial?
“The interim results of the INSPIRE trial and our decision to discontinue the trial are disappointing,” said Steve Porter, M.D., Ph.D., Chief Medical Officer at InterMune.
I'm not sure what this means for the company, but they are also running the perfenidone trial, but not so sure this will fare any better...
To me, this is not so surprising, but it really does illustrate the importance of being careful not to read too much into sub group analysis before the next study is done- the original study found that patients with more "mild" IPF (FVC 55-90% predicted) might have a survival advantage and the current study was powered to test that hypothesis. Ultimately it was found not to be the case after all.
People currently taking the IFN-g as part of the study will be instructed to stop it, and everyone will then pack up their bags and move on to the next latest and greatest...
Does anyone have any patients enrolled int his trial?
Bronch equipment
Our hospital is looking into updating the bronch equipment. We have tested the Pentax and the Olympus equiment and are waiting for bids.
What equipment do you use at your facility? What has your experience been with either (or both)?
What equipment do you use at your facility? What has your experience been with either (or both)?
Tuesday, February 27, 2007
SPN
Friday, February 23, 2007
Digging for gold
This nice woman with mild asthma lost a tooth crown and aspirated it as she was about to have lunch.
Check out the CxR. It was lodged at the first branching of the R bronchus intermedius with the smooth side (the shiny top of the crown) up towards us. Unfortunately I was using an optic (as opposed to digital, I know they are all "optic") scope and couldn't take a picture. I did snap a picture of the crown after removal with the basket on the side.
We did not have a bronch basket handy so an OR gallstone basket was just the perfect sixe.
Thursday, February 22, 2007
BAL in suspected VAP
A few years ago, Fagon et al published a large trial of BAL for evaluation of VAP in over 400 ICU patients in France. Compared to a noninvasive strategy, an invasive strategy was significantly associated with fewer deaths at 14 days, earlier attenuation of organ dysfunction, and less antibiotic use in patients suspected of having ventilator-associated pneumonia.
Recently a trial was published on the NEJM comparing quantitative BAL to endotracheal aspiration with nonquantitative culture of the aspirate. They found no significant difference in the primary outcome (28-day mortality rate), the rates of targeted therapy, days alive without antibiotics, maximum organ-dysfunction scores, length of stay in the ICU or hospital.
What is your routine practice in the ICU for VAP? Do you bronch everybody with suspected VAP?
(Dr. Kollef had an interesting editorial on the Canadian trial in the same issue of the NEJM).
Recently a trial was published on the NEJM comparing quantitative BAL to endotracheal aspiration with nonquantitative culture of the aspirate. They found no significant difference in the primary outcome (28-day mortality rate), the rates of targeted therapy, days alive without antibiotics, maximum organ-dysfunction scores, length of stay in the ICU or hospital.
What is your routine practice in the ICU for VAP? Do you bronch everybody with suspected VAP?
(Dr. Kollef had an interesting editorial on the Canadian trial in the same issue of the NEJM).
TORCH trial
The TORCH trial is the lead article on today's NEJM. No statistically significant change in mortality with Advair but reduced annual rate of exacerbations and improved health status and spirometric values. There was also an increase in pneumonias in the fluticasone-treated groups (FP alone or Advair).
How do you think this data will affect your prescribing patterns for ICS in COPD?
How do you think this data will affect your prescribing patterns for ICS in COPD?
Wednesday, February 21, 2007
Propofol for bronchs
I had posted a long time ago on sedation for bronchs and our preference for propofol. I am at a new hospital and looking to implement a similar protocol (propofol is now generic and much cheaper than a Versed/opiate combo) and in my experience provides more predictable and reliable sedation.
1. Have you used propofol for bronchs?
2. If not what is your default?
3. Do you have any data on either? I have found the following references in support of propofol is somewhat more obscure sources:
1: Acta Anaesthesiol Scand. 2003 Apr;47(4):411-5. Should patients undergoing a bronchoscopy be sedated? Gonzalez R, De-La-Rosa-Ramirez I, Maldonado-Hernandez A, Dominguez-Cherit G.
2: Anasthesiol Intensivmed Notfallmed Schmerzther. 2004 Oct;39(10):597-602. Sedation for fiberoptic bronchoscopy: fewer adverse cardiovascular effects with propofol than with midazolam. Ozturk T, Cakan A, Gulerce G, Olgac G, Deren S, Ozsoz A.
3: Anesth Analg. 2002 May;94(5):1212-6, table of contents. Target-controlled versus manually-controlled infusion of propofol for direct laryngoscopy and bronchoscopy. Passot S, Servin F, Allary R, Pascal J, Prades JM, Auboyer C, Molliex S.
1. Have you used propofol for bronchs?
2. If not what is your default?
3. Do you have any data on either? I have found the following references in support of propofol is somewhat more obscure sources:
1: Acta Anaesthesiol Scand. 2003 Apr;47(4):411-5. Should patients undergoing a bronchoscopy be sedated? Gonzalez R, De-La-Rosa-Ramirez I, Maldonado-Hernandez A, Dominguez-Cherit G.
2: Anasthesiol Intensivmed Notfallmed Schmerzther. 2004 Oct;39(10):597-602. Sedation for fiberoptic bronchoscopy: fewer adverse cardiovascular effects with propofol than with midazolam. Ozturk T, Cakan A, Gulerce G, Olgac G, Deren S, Ozsoz A.
3: Anesth Analg. 2002 May;94(5):1212-6, table of contents. Target-controlled versus manually-controlled infusion of propofol for direct laryngoscopy and bronchoscopy. Passot S, Servin F, Allary R, Pascal J, Prades JM, Auboyer C, Molliex S.
Thursday, February 15, 2007
Allergy shots
The Cochrane database recently published this review on allergy shots for rhinitis. They retrieved 1111 publications of which 51 satisfied their inclusion criteria (looking for RCTs with placebo-control) and in total there were 2871 participants (1645 active, 1226 placebo), each receiving on average 18 injections.
Duration of immunotherapy varied from three days to three years. Symptom score data from 15 trials were suitable for meta-analysis and showed an overall reduction in the immunotherapy group and medication score data from 13 trials also showed an overall reduction in the immunotherapy group.
It is good to see some good quality data on that. However, I was amazed by the number of shots. Where I was in practice patients would be on weekly or monthly shots for 3, 4, 7 years and would be way over these limited numbers.
What has your experience been with allergy shots?
Duration of immunotherapy varied from three days to three years. Symptom score data from 15 trials were suitable for meta-analysis and showed an overall reduction in the immunotherapy group and medication score data from 13 trials also showed an overall reduction in the immunotherapy group.
It is good to see some good quality data on that. However, I was amazed by the number of shots. Where I was in practice patients would be on weekly or monthly shots for 3, 4, 7 years and would be way over these limited numbers.
What has your experience been with allergy shots?
Tuesday, February 13, 2007
Low DLCO
Here is a submission from John B: It is interesting that it is close to the very first post of this blog.
I continually test a low (60% I think) DLCO on a PFT. All other parts of that test are normal.
I have dizziness, lightheadedness, sob (random- at rest or exertion). Palpitations at times, but not nearly as often as in the past.
Occasional feeling of pressure in chest. Echo was normal, but imo it looks like values have been increasing over the past 2 years- still in normal ranges, but I do show some trace/mild tricuspid regurg and trace mitral regurg.
Two times I have done a cardiopulmonary stress test, and both times it shows a cardiovascular limitation evidenced by crossing of the anaerobic threshold earlier than I should- metabolic acidosis after exertion.
Nuclear stress test shows no blockages.
Also, my own testing with a pulse oximeter seems to indicate occasional drops in my O2 to as low as 92, but then quickly recovering to 96-98. This has never happened in doctor's office with their oximeters, so I don't know if mine is accurate (however, when testing my wife as a control subject, she always shows 96-98).
high-res CT scan of chest - normal (6 months ago)
non-invasive ct angiography (body scan) - normal lungs / lung blood vessels (1+ year ago)
- calcium score was 0 (2 years ago)
multiple echocardiograms are in normal range but show trace / mild regurgitation
- cardiopulmonary stress test shows a cardiovascular limitation evidenced by a metabolic acidosis at peak exercise
- low DLCO (+-60% of predicted - 1 month ago)
- nuclear stress test shows no blockages (1.5 years ago)
- triglycerides 270 - vldl 56 - ldl 240 - hdl 36)
- lyme disease- treated with abx in past
No one knows what to make of this. I was thinking of requesting a stress echo, to see if there is more regurgitation after exercise.
Any other tests I should have done? Would really appreciate some assistance. I can provide more specific data if needed.
-John
I continually test a low (60% I think) DLCO on a PFT. All other parts of that test are normal.
I have dizziness, lightheadedness, sob (random- at rest or exertion). Palpitations at times, but not nearly as often as in the past.
Occasional feeling of pressure in chest. Echo was normal, but imo it looks like values have been increasing over the past 2 years- still in normal ranges, but I do show some trace/mild tricuspid regurg and trace mitral regurg.
Two times I have done a cardiopulmonary stress test, and both times it shows a cardiovascular limitation evidenced by crossing of the anaerobic threshold earlier than I should- metabolic acidosis after exertion.
Nuclear stress test shows no blockages.
Also, my own testing with a pulse oximeter seems to indicate occasional drops in my O2 to as low as 92, but then quickly recovering to 96-98. This has never happened in doctor's office with their oximeters, so I don't know if mine is accurate (however, when testing my wife as a control subject, she always shows 96-98).
high-res CT scan of chest - normal (6 months ago)
non-invasive ct angiography (body scan) - normal lungs / lung blood vessels (1+ year ago)
- calcium score was 0 (2 years ago)
multiple echocardiograms are in normal range but show trace / mild regurgitation
- cardiopulmonary stress test shows a cardiovascular limitation evidenced by a metabolic acidosis at peak exercise
- low DLCO (+-60% of predicted - 1 month ago)
- nuclear stress test shows no blockages (1.5 years ago)
- triglycerides 270 - vldl 56 - ldl 240 - hdl 36)
- lyme disease- treated with abx in past
No one knows what to make of this. I was thinking of requesting a stress echo, to see if there is more regurgitation after exercise.
Any other tests I should have done? Would really appreciate some assistance. I can provide more specific data if needed.
-John
Monday, February 12, 2007
Chest tube care
We are re-vamping our group's chest tube standard orders and I was wondering how people like their chest tubes handled.
What do you use for sedation/pre-medication for a non-emergent chest tube placement?
How often do you like the dressing changed?
What do you tell the nursing staff to do in case of CTs accidentally coming out?
I thought about calling this post "Zen and the art of chest tube maintenance" but I didn't know if the joke would go well...
What do you use for sedation/pre-medication for a non-emergent chest tube placement?
How often do you like the dressing changed?
What do you tell the nursing staff to do in case of CTs accidentally coming out?
I thought about calling this post "Zen and the art of chest tube maintenance" but I didn't know if the joke would go well...
Wednesday, February 07, 2007
C. diff, C. diff run, run diff run
This is more of a critical care (or general care, if you will) than true pulmonary.
I have been seen a lot of docs (including some ID) treating uncomplicated C. diff colitis with PO vanco up front instead of Flagyl. Have recommendations changed? Do you use much PO vanco?
I have been seen a lot of docs (including some ID) treating uncomplicated C. diff colitis with PO vanco up front instead of Flagyl. Have recommendations changed? Do you use much PO vanco?
Tuesday, February 06, 2007
Alternatives to surgery
Following Jeff's question on therapy for lung Ca in octogenarian (see post below) I just saw a patient in a similar situation. This is an 85 y/o woman with a recent spiro revealing an FEV1 of 600 ml. She was just diagnosed with a 2-cm LUL adenoCa with no adenopathy and no other distant disease on PET. She is still fairly active but stated that even if her lung function improved, she would not want surgery.
With such a low FEV1 and with some risk of further loss of function with radiation, what would you suggest? And following on JJ's question, what are your alternatives for octogenarians (or anybody else) who can't or won't have surgery?
With such a low FEV1 and with some risk of further loss of function with radiation, what would you suggest? And following on JJ's question, what are your alternatives for octogenarians (or anybody else) who can't or won't have surgery?
Tuesday, January 30, 2007
This is an 89 year old previous smoker with a probably stage 1b cancer:
No adenopathy.
She looks younger than her stated age but has emphysema on CXR:
We dont have PFT's but she has good exercise tolerance.
How would you proceed assuming the patient was willing to go with whatever the doctor recommends:
1. surgery (is age alone an absolute contraindication, even if she would otherwise be a surgical candidate)?
2. CT-guided bx (but what would you do with this info? it is obviously a cancer. Would you offer this 89 year old chemo?)
3. Do nothing.
4. Other.
Looking for all opinions - use anonymous or make up a name if you wish, but all comments encouraged.
No adenopathy.
She looks younger than her stated age but has emphysema on CXR:
We dont have PFT's but she has good exercise tolerance.
How would you proceed assuming the patient was willing to go with whatever the doctor recommends:
1. surgery (is age alone an absolute contraindication, even if she would otherwise be a surgical candidate)?
2. CT-guided bx (but what would you do with this info? it is obviously a cancer. Would you offer this 89 year old chemo?)
3. Do nothing.
4. Other.
Looking for all opinions - use anonymous or make up a name if you wish, but all comments encouraged.
Thursday, January 18, 2007
Solitary pulmonary nodule
I recently saw a 62-year-old woman with a past medical history of fibromyalgia who received a CT scan for chest pain, which picked up an incidental pulmonary nodule.
She is asymptomatic; no shortness of breath or cough. She is a 35 pack-year smoker and has not been able to quit. Her spirometry is normal.
A CT is shown here
What would you do?
1. refer to CTS for resection
2. Get a PET (and what would you do with that info?)
3. Follow radiographically, say, with a repeat CT in 3 months?
I'll tell you what I did after comments.
Feel free to enter your name as "anonymous".....
She is asymptomatic; no shortness of breath or cough. She is a 35 pack-year smoker and has not been able to quit. Her spirometry is normal.
A CT is shown here
What would you do?
1. refer to CTS for resection
2. Get a PET (and what would you do with that info?)
3. Follow radiographically, say, with a repeat CT in 3 months?
I'll tell you what I did after comments.
Feel free to enter your name as "anonymous".....
Monday, January 15, 2007
Follow up to vocal cord paralysis
A new question from anonymous regarding the case on vocal cord paralysis
Has anyone scoped his GI tract to R.O esophageal disease?
Has anyone scoped his GI tract to R.O esophageal disease?
multiple pulmonary nodules in system lupus
Case from slkanowitz:
57 y.o. white female with SLE for 20+yrs presents with multiple small non calcified nodules on chest CT. CT was done for evaluation of asthma. Pt. symptomatic only with her usual migratory pleuritic pain associated with her lupus, and mild, intermittent asthmatic symptoms present since young adulthood. Asthma is treated prn with albuterol inhaler. Largest nodule is 6mm, most are peripheral and they are bilateral. Follow up chest CT scan 4 mos. later shows resolution of some of the nodules, the remaining ones show no growth. PFT are normal, O2 sat. normal. There has been no change in symptoms and no change in treatment for her lupus during that time. Other pertinent medical problems include allergic rhinitis, chronic sinusitis, S/P antral windows, and chronic bronchitis. Negative for pneumonia, SLE pneumonitis, RA, ANCA, anti-phospholipid AB. Recent echo WNL. No hx malignancy.
Hx significant for living in Ohio River Valley prior to 1973 and Southern Calif. during 1990, but no history unusual respiratory infections.
1998 chest xray normal. No xrays done until CT scan of chest and sinuses in 09/06.
SLE confirmed without evidence of other connective tissue disease. Pt. on Placquenil 200mg BID and Methotrexate 22.5 mg/week.
She did not pose a question but I assume it is what to do about the multiple nodules.
Since the nodules decreased in size over 4 months, this is likely inflammatory and a repeat CT in 6 months for that last nodule would be what I would do. I'm not sure what her smoking history is, but pretest prob for malignancy is low here. Any one else wish to comment?
57 y.o. white female with SLE for 20+yrs presents with multiple small non calcified nodules on chest CT. CT was done for evaluation of asthma. Pt. symptomatic only with her usual migratory pleuritic pain associated with her lupus, and mild, intermittent asthmatic symptoms present since young adulthood. Asthma is treated prn with albuterol inhaler. Largest nodule is 6mm, most are peripheral and they are bilateral. Follow up chest CT scan 4 mos. later shows resolution of some of the nodules, the remaining ones show no growth. PFT are normal, O2 sat. normal. There has been no change in symptoms and no change in treatment for her lupus during that time. Other pertinent medical problems include allergic rhinitis, chronic sinusitis, S/P antral windows, and chronic bronchitis. Negative for pneumonia, SLE pneumonitis, RA, ANCA, anti-phospholipid AB. Recent echo WNL. No hx malignancy.
Hx significant for living in Ohio River Valley prior to 1973 and Southern Calif. during 1990, but no history unusual respiratory infections.
1998 chest xray normal. No xrays done until CT scan of chest and sinuses in 09/06.
SLE confirmed without evidence of other connective tissue disease. Pt. on Placquenil 200mg BID and Methotrexate 22.5 mg/week.
She did not pose a question but I assume it is what to do about the multiple nodules.
Since the nodules decreased in size over 4 months, this is likely inflammatory and a repeat CT in 6 months for that last nodule would be what I would do. I'm not sure what her smoking history is, but pretest prob for malignancy is low here. Any one else wish to comment?
Tuesday, January 09, 2007
Hypersensitivity Pneumonitis
Anonymous M.D. asks if anyone knows of alternative immunotherapy for the treatment of chronic hypersensitivity pneumonitis in a patient who is not responding to steroids. Her FVC has remained in the mid 50% range regardless of predxnisone does (range 0 to 40 mg). The HRCT shows fairly extensive ground glass to indicate an active alveolitis. Of note, this patient has an open lung bx that was consistent with the diagnosis of HP).
Tuesday, January 02, 2007
Follow-up to PAP case
I had posted a while ago on this patient with alveolar changes and a Bx consistent with PAP. We had also initiated a discussion on PAP and anti-GM-CSF antibodies.
I did send the Pt's blood to the Cleveland Clinic and her titers were 1:12,800 (1:400 or less is the usual normal level).
She is still asymptomatic and doing well.
Have you checked anti-GM-CSF ABs in your PAP Pts? Would you start treatment at this point (she is asymptomatic with normal PFTs) or just monitor?
I did send the Pt's blood to the Cleveland Clinic and her titers were 1:12,800 (1:400 or less is the usual normal level).
She is still asymptomatic and doing well.
Have you checked anti-GM-CSF ABs in your PAP Pts? Would you start treatment at this point (she is asymptomatic with normal PFTs) or just monitor?
Post-thoracotomy pain
One of my patients has had persistent post-thoracotomy pain following a RULobectomy in 9/05. She has been on gabapentin and narcotics; tried nerve root blocks (with short-lived results) and is not a drug-seeker. She has now undergone a dorsal rhizotomy (confirmed by path of the dorsal root ganglion) and after a 1-week improvement is now having even more pain.
What do you usually do for these cases of persistent post-thoracotomy pain that extend for months and years?
What do you usually do for these cases of persistent post-thoracotomy pain that extend for months and years?
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