2. Dressler’s syndromeDressler’s syndrome
• AKA postpericardiotomy syndrome (PPCS)
• Fever and pleuropericardial disease days or months
after cardiac injury i.e. combination of pleuritis and
pericarditis
• Pathogenesis: An immune response to damaged
cardiac tissue immune complexes deposit onto the
pleura, lungs, and pericardium, eliciting an
inflammatory response
• Timeline: typically 1+ week after myocardial injury
• Sx: chest pain, pericardial rub, fever, leukocytosis,
pulmonary infiltrates, pleural effusions
• Tx: aspirin or other NSAIDs. Colchicine is sometimes
given for primary prevention after cardiac surgery
o Prednisone, HOWEVER, in patients s/p MI there is a greater incidence of
ventricular aneurysm formation and free wall rupture
3. What else you should know about pleural effusionsWhat else you should know about pleural effusions
Diagnosis Comment
Common Causes
Heart failure Most common cause of transudative
effusion; diuresis can cause borderline
exudative chemical characteristics
Atelectasis Small effusion caused by negative
transpleural pressure
Hepatic hydrothorax Most are right-sided; occurs in 6%-12% of
patients with end-stage liver disease and
clinical ascites; can occur in the absence of
ascites
Hypoalbuminemia Small bilateral effusions with evidence of
generalized anasarca, from decreased
intravascular oncotic pressure
Constrictive pericarditis Usually bilateral with normal heart size;
95% have jugular venous distention
Trapped lung Unilateral as a result of remote pleural
inflammation and resultant unexpandable
lung; caused by negative transpleural
pressure
Uncommon Causes
Cerebrospinal fluid leak into pleural space
(duropleural fistula)
Caused by trauma or thoracic spinal
surgery
Urinothorax Unilateral effusion caused by ipsilateral
obstructive uropathy; the only low-pH
transudate
Iatrogenic Caused by a central venous catheter
misdirected into the pleural space
Superior vena cava obstruction From acute systemic venous hypertension
or lymphatic congestion
Peritoneal dialysis Massive effusion; develops within 48 hours
of initiating dialysis due to dialysate
crossing into the chest because of
congenital or acquired defects
• No thoracentesis if < 1 cm*
• Gradients if transudative
• TP > 3.1 g/dL OR Alb > 1.2 g/dL*
• Exudative if
• Pleural TP : Serum TP > 0.5 OR Pleural LDH >
2/3 ULN
• > 10,000 WBC typically suggests infection
• Uncomplicated parapneumonic: influx of
PMNs and fluid that resolves with treatment
• Complicated parapneumonic : bacterial
invasion drain for faster recovery & less risk
of complications
• Empyema: Pus drainage
• Other causes
• Pancreatitis, PE, Subphrenic abscess, TB,
rheumatoid, lupus pleuritis
• Eosinophilia: meds, fungi, parasites,
eosinophilic pneumonia, Churg-Strauss,
benign asbestos pleural effusions
* Not always
4. Pleural fluid quizPleural fluid quiz
• Adenosine deaminase
• Triglycerides
• Magic cut-off for pleural triglyceride level
• NT ProBNP
• % of caner positive cells after first thoracentesis
• % of caner positive cells after second thoracentesis
• % of caner positive cells after third thoracentesis
• Magic cut-off for pleural glucose
• Magic cut-off for pleural pH
*you don’t tend to see a low pH in uncomplicated effusions
5. Other things to considerOther things to consider
• Erosion of a central venous catheter through
venous structures into the pleural space pleural
fluid accumulation and mediastinal widening
(mediastinal hygroma)
• Disruption of the thoracic duct or its intrathoracic
lymphatic tributaries chylothorax
• Infectious mediastinitis : usually bilateral effusions.
Managed with debridement and irrigation
6. Other things to considerOther things to consider
• Erosion of a central venous catheter through
venous structures into the pleural space pleural
fluid accumulation and mediastinal widening
(mediastinal hygroma)
• Disruption of the thoracic duct or its intrathoracic
lymphatic tributaries chylothorax
• Infectious mediastinitis : usually bilateral effusions.
Managed with debridement and irrigation