Disorders of the Pleura and Mediastinum Dr. Gerrard Uy

Pleural Effusion Presence of an excess quantity of fluid in the pleural space – The pleural space lies between the lungs and chest wall and normally contains a very thin layer of fluid

Etiology Pleural fluid accumulates when pleural fluid formation exceeds absorption Normally, pleural fluid enters the pleural space from the capillaries in the parietal pleura and removed via the lymphatics

Approach to Patient Determining the cause is essential 2 types of effusion – Transudate Occurs when systemic factors that influence the formation and absorption of pleural fluid are altered Leading cause: heart failure and cirrhosis – Exudate Occurs when local factors that influence the formation and absorption of pleural fluid are altered Leading cause: pneumonia, malignancy, pulmonary embolism

Light’s Criteria Used to determine the type of pleural fluid Criteria: – Pleural fluid protein/serum protein > 0.5 – Pleural fluid LDH/serum LDH > 0.6 – Pleural fluid LDH > 2/3 normal upper limit for serum Misidentify ~25% of transudates as exudates

Effusion Due to Heart Failure Most common cause of pleural effusion is left ventricular failure Isolated right sided pleural effusions are more common than left sided pleural effusion If diagnosis is established, patients are best treated with diuretics NT pro BNP > 1500 pg/ml is diagnostic of effusion secondary to congestive heart failure

Hepatic Hydrothorax Occurs in ~5% of patients with cirrhosis and ascites Direct movement of peritoneal fluid through small openings in the diaphragm into the pleural space Effusion is usually right sided

Parapneumonic effusion Most common cause of exudative pleural fluid in the united states Empyema refers to a grossly purulent effusion the presence of free pleural fluid can be demonstrated with a lateral decubitus radiograph, CT scan, or ultrasound – If free fluid > 10mm, a therapeutic thoracentesis should be performed

Parapneumonic effusion Indications for considering CTT insertion – Loculated pleural fluid – Pleural fluid ph<7.2 – Pleural fluid glucose<3.3mmol/L(<60mg/dl) – Positive gram stain or culture of the pleural fluid – Presence of gross pus in the pleural space

Effusion secondary to Malignancy Secondary to metastatic disease Second most common type of exudative pleural effusion Most common tumors causing malignant pleural effusion: – Lung carcinoma – Breast carcinoma – lymphoma

Effusion secondary to Malignancy Diagnosis is usually made via cytology of the pleural fluid If cytology is negative, thoracoscopy is the best next procedure if malignancy is highly suspected If unavailable, needle biopsy of the pleura is the alternative

Mesothelioma Primary tumors arising from mesothelial cells that line the pleural cavities Related to asbestos exposure Thoracoscopy or open pleural biopsy is usually necessary to establish the diagnosis

Chylothorax Accumulation of chyle in the pleural space Occurs when the thoracic duct is disrupted Most common cause is trauma Thoracentesis reveals a milky fluid with a triglyceride level > 110 gm/dl Treatment of choice is CTT insertion and administration of octreotide

Hemothorax Blood in the pleural space Hematocrite should be obtained from the pleural fluid True hemothorax if hematocrit is greater than half of the peripheral blood CTT insertion, thoracoscopy and thoracotomy

Other Causes of pleural effusion Esophageal rupture Pancreatitis Intraabdominal abscess Meig’s Syndrome – benign ovarian tumor + ascited and pleural effusion

Pneumothorax Presence of gas in the pleural space 4 categories – Spontaneous pneumothorax – Secondary pneumothorax – Traumatic pneumothorax – Tension pneumothorax

Spontaneous Pneumothorax Occurs in the absence of an underlying disease Usually due to rupture of small apical blebs, small cystic spaces that lie immediately under the visceral pleura Occurs almost exclusively in smokers Simple aspiration, thoracoscopy and thoracotomy with stapling of blebs, CTT insertion

Secondary Pneumothorax Most are due to COPD Pneumothorax in patients with lung disease are more life threatening than it is in normal individuals Usually treated with CTT

Traumatic Pneumothorax Can result from both penetrating or non penetrating chest trauma Traumatic pneumothorax should be treated with CTT unless very small Iatrogenic pneumothorax most commonly caused by needle aspiration, thoracentesis and insertion of a central IV catheter

Tension Pneumothorax Usually occurs during mechanical ventilation or resuscitative efforts Diagnosis is made by P.E. showing enlarged hemithorax with no breath sounds, hyperresonace to percussion, and shift of the mediastinum to the contralateral side Treated as a medical emergency A large bore needle should be inserted at the 2 nd anterior ICS

ARDS (Acute Respiratory Distress Syndrome) Dr. Gerrard Uy

ARDS clinical syndrome of severe dyspnea of rapid onset, hypoxemia, and diffuse pulmonary infiltrates leading to respiratory failure Caused by diffuse lung injury The arterial (a) P O2 (in mmHg)/FI O2 (inspiratory O 2 fraction) <200 mmHg is characteristic of ARDS Acute lung injury (ALI) is a less severe form – a PaO2/FiO2 ratio between identifies patients who are likely to benefit from aggressive therapy

ARDS caused by diffuse lung injury from many underlying medical and surgical disorders

ARDS >80% are caused by severe sepsis syndrome and/or bacterial pneumonia (~40–50%), trauma, multiple transfusions, aspiration of gastric contents, and drug overdose older age, chronic alcohol abuse, metabolic acidosis, and severity of critical illness

ARDS Natural history is marked by 3 phases:

alveolar capillary endothelial cells and type I pneumocytes (alveolar epithelial cells) are injured Edema fluid Cytokines first 7 days of illness after exposure to a precipitating ARDS risk factor Dyspnea develops Chest radiograph reveals alveolar and interstitial opacities involving at least ¾ of the lung fields Exudative Phase

Proliferative Phase lasts from day 7 to day 21 Most recover rapidly, off ventilation many still experience dyspnea, tachypnea, and hypoxemia first signs of resolution Shift of neutrophil to lymphocytes proliferation of type II pneumocytes along alveolar basement membranes

Fibrotic Phase Many patients with ARDS recover lung function 3-4 weeks after the initial pulmonary injury require long-term support on mechanical ventilators and/or supplemental oxygen extensive alveolar duct and interstitial fibrosis emphysema-like changes with large bullae

Treatment General Principles – (1) the recognition and treatment of the underlying medical and surgical disorders (e.g., sepsis, aspiration, trauma); – (2) minimizing procedures and their complications; – (3) prophylaxis against venous thromboembolism, gastrointestinal bleeding, and central venous catheter infections; – (4) the prompt recognition of nosocomial infections; and – (5) provision of adequate nutrition

Prognosis Recent mortality estimates for ARDS range from 41-65% Mortality is largely attributable to nonpulmonary causes Sepsis and nonpulmonary organ failure account for >80% of deaths Risk fasctor for mortality includes: – Advance age – Preexsiting medical condition