Transcript ARDS (Acute Respiratory Distress Syndrome)

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
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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
2nd 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) 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
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:
Exudative Phase
• 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
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