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Mr 432014

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Mr 432014

  1. 1. MRMR 4/3/144/3/14 Dressler’s syndrome & pleural effusions
  2. 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. 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. 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. 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. 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

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