Disorders of the Pleura and Mediastinum
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Transcript of Disorders of the Pleura and Mediastinum
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Disorders of the Pleura and Mediastinum
Dr. Gerrard Uy
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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Other Causes of pleural effusion
• Esophageal rupture• Pancreatitis• Intraabdominal
abscess• Meig’s Syndrome –
benign ovarian tumor + ascited and pleural effusion
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Pneumothorax
• Presence of gas in the pleural space• 4 categories– Spontaneous pneumothorax– Secondary pneumothorax– Traumatic pneumothorax– Tension pneumothorax
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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
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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
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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
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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
2nd anterior ICS
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ARDS(Acute Respiratory Distress Syndrome)
Dr. Gerrard Uy
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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) PO2 (in mmHg)/FIO2 (inspiratory O2
fraction) <200 mmHg is characteristic of ARDS• Acute lung injury (ALI) is a less severe form – a PaO2/FiO2 ratio between 200-300 identifies patients
who are likely to benefit from aggressive therapy
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ARDS
• caused by diffuse lung injury from many underlying medical and surgical disorders
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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
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ARDS
• Natural history is marked by 3 phases:
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• 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
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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
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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
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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
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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