Question came in today:
"What could be the possible etiology for a pleural effusion that
started after chest pain in a 59 year old; it is exudative, has 480
WBC with 51% PMNs, no micro grew out and the glucose was 183. A
PE-protocol CT was negative. The echo shows normal EF but there is a
small free-flowing pericardial effusion. He had arthoscopic knee
surgery in May but there are no xrays until he came in with CP in
July, where the b/l effusion L>R was found. A CT shpwed bibasilar
airspace disease and atelectasis and the effusion.
How would you put this together, especially with pericardial
involvement. Oh, also he has a high anticardiolipan antibody, but
again, the PE prot CT was negative for PE (and now the effusion is
still there for the past month, and there are no eosinophils in there
either."
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That is very interesting, especially with the perssitence of the effusion. A couple quick questions: What did the fluid look like? Do you have an LDH? Any adenopathy on the CT? Did the lung re-expand with the thoracentesis?
Since he does have air space disease infection would be a concern. It would be unusual for this to be a "typical" bacterial pneumonia with a persistence effusion for so long. However, less common infections may act so. Tb pleuritis (unlike Tb empyema) can prenetl acutely (3/4s with sharp pleuritic pain) and have a more subacute course. Furthermore it is usually smear negative and Cxs are + in less than 50% of patients. PPD may be helpful as would the sampling (bronch if needed) of the air space disease. One of the telltale signs is the low or absent number of mesothelial cells in the fluid: >15% meso's and it is not TB pleuritis.
Since the effusion has been there for a month, more aggressive agents, and more acute conditions with infection such as an esophageal rupture (glucose would be lower and amylase would be high) are less likely.
There is no Hx of trauma or surgical/invasive manipulations so those would not be considered.
He does have a +Anticardiolipin, which can be associated with various autoimmune disorders (50% of Pts with + lupus anticoagulant will have SLE). His effusion is not described as the "characteristic" rheumatoid effusion with low pH, low glucose and yellow-greenish almost like sterile pus aspect but they are not al like that. Since the pathophysiology in many of those is a serositis, pain would be expected as in this case. It would also account for the pericardial involvement. An ESR, ANA, RF would be a good initial screening.
Chylothoraces are usually chronic (because of some of their underlying conditions) and may be tricky to diagnose. If the patient had been NPO/fasting prior to the thoracentesis, the fluid will not appear milky and will look like an ordinary exudative effusion (though usually with far fewer PMNs...) and re-tapping shortly after a lipid-rich meal may be necessary to make a diagnosis.
I will leave some of the other DDx to some of the other bloggers.
BTW, does (or did) he smoke?
I was wondering what would be int he differential or exluded, specifically related to the fact that there is a pericardial effusion. Is there anything that can be taken off the list with the presence of pericardial effusion?
I am still concerned for pulmonary embolism in the setting of anticardiolipan syndrom. I found out later that the 1st PE protocol CT had poor blous and could opnly evaluate the more proximal system, but since he needs lifelong coumadin for the a-CL antibody *anyway*, I won't move on to angiogram since it wouldn't change management.
The TB thought is good but there's nothing on history to suggest it.
The autoimmune diseases would fit really well with the coexisting pericardial fluid. Particularly with the ACL I would check other serologies.
I have had a recent similatr case (I'll have to post it later) where the patient had a parapneumonic effusion, +Staph in the sputum and nothing on Hx to suggest Tb. The fluid reaccumulated despite ABTx and a bronch found AFB (MTb) in the BAL... sometimes we get surprised. Because of the disseminated nature of Tb, it could also cause pericardial disease.
The combination of pericardial and pleural effusion in the setting of a positive anticardiolipin antibody should make one consider the ACL antibody syndrome. Usually you will get small bilateral pleural effusions. If the effusion is unilateral and coincides with the chest pain, a pulmonary embolism in the setting of a positve ACL should be considered. If the ACL is a red herring to the presentation, then I agree with considering things like TB and cancer.
If the CT-PE study was sub-optimal, I agree with re-studying the Pt, whether with a V/Q and/or dopplers or a repeat scan.
I did not mention malignancy since there was nothing too obvious from the history but lymphomas, leukemias, melanomas and lung cancer are common causes of malignant pericardial effusions (+breast in women) and could explain the combination of effusions if there is any other clue on CT or Hx.
For the sake of completion, I would also add hypothyroidism to the above, and would check TSH.
Hypothyroidism is a great thought. People can actually have quite large pericardial effusions with few symptoms from that.
Wouldn't expect as many PMNs though.
The effusion had 17% mesothelial cells. There were only 11% lymphocytes. TB Cx no growth x 19 days so far (or any other micro). His serum LDH was 304 and the pleural was 130. The effusion TP was 3.4 and the serum was 5.4.
I think it must be anticardiolipan syndrome, but maybe you all have other opinions. Don't you have to anticoagulate just based on the fact that he has a high titer of the ACL antibody *anyway*?
You do NOT need to anticoagulate a patient with an ACL antibody unless they have evidence of either arterial thrombotic disease or venous thromboembolic disease. The IgM antibody is typically the on that makes you hypercoagulable because it is the largest antibody. However, without clotting, no anticoagulation is needed.
Did anyone diurese this patient prior to you seeing him? As most of the rest of his numbers are benign, you can transform a transudate to an exudate by diuresis. The only light criteria that is met is the fluid/serum protein ratio.
If your patient has a transudate, you may want to consider an echo to r/o an intracardiac source of your pleural and pericardial fluid. Constrictive pericarditis could cause chest pain and pleural/pericardial effusions.
Also the % of meso's virtually rules out Tb though the negative Cxs help as well.
A few months ago the patient had acute loss of vision in 1 eye that spontaneously resolved. The opthamologist's impression was that this was an arterial thrombotic event. Subsequent w/u revealed a high ACL antibody titer. He was put on an aspirin only. A few months later he presents with acute onset of left anterior pleuritic chest pain that woke him at 2am. In ER an echo showed normal EF, PAP not assessed but RV and RA sizes normal. There was a small pericardial effusion as well. Rest of cardiac w/u negative. No I do not believe he was given any lasix because there was no evidence of failure and the effusionw as an exudate (pre-diuresis).
With this added info, would you anticoagulate? Then I will leave you guys alone. :)
His TSH was normal.
Well, with with a previous thrombotic event I would probably add anticoagulation. APS/ACL requires a higher target INR though I found one reference for "lower" (2-3) INR with ASA for prevention of re-thrombosis: ita was better than ASA or low-dose warfarin but not as good as a higher INR (N Engl J Med 1995 Apr 13;332(15):993-7).
And please do share more cases. This was a very interesting case and pleural disease can be very challenging.
I agree with Carlos'suggestion re: anticoagulation.
I will also reiterate his request that you post more cases.
This was a nice review for me/all of us. Pleural diseases are among the most challenging pulmonary cases.
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