Mr 432014
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Transcript of Mr 432014
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MR MR 4/3/144/3/14
Dressler’s syndrome &
pleural effusions
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Dressler’s syndrome Dressler’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 surgeryo Prednisone, HOWEVER, in patients s/p MI there is a greater incidence of
ventricular aneurysm formation and free wall rupture
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What else you should know about pleural What else you should know about pleural
effusionseffusionsDiagnosis 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
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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
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Other things to Other things to considerconsider
• 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