Pulmo/Crit Flashcards
Pleural effusion in patients on Diuretics
Light’s criteria are nearly 100% sensitive but only 83% specific for identifying exudates, and the specificity decreases in the setting of diuretic use.
Up to 20% of heart failure patients with pleural effusion may fulfill criteria for exudative effusion after receiving diuretics.
In this case, a serum-effusion protein difference >3.1 g/dL or serum- effusion albumin gradient >1.2 g/dL suggests a true transudative effusion.
Newly diagnosed bronchiectasis approach
Patients with high resolution chest CT findings suggestive of bronchiectasis should undergo functional assessment with pulmonary function testing and identification of potentially reversible causes. Initial diagnostic evaluation includes a complete blood count with differential, immunoglobulin quantitation (i.e., IgA, IgG, and IgM), and sputum culture and smear (bacteria, fungi, and mycobacteria).
Lofgren syndrome
Risk groups
African descent, Scandinavians, Irish, Puerto Ricans
Clinical features
Bilateral ankle arthritis, Erythema nodosum, Hilar adenopathy
Treatment
Often self-limited,NSAIDs for symptom control
ABPA
History
Asthma, cystic fibrosis
Chest Imaging
X-ray: Infiltrates (often fleeting)
CT: Central bronchiectasis
Diagnostic testing
Skin test positive for Aspergillus fumigatus
Eosinophilia >500/μL
IgE >417 IU/mL
Specific IgG & IgE for A fumigatus.
Treatment
Corticosteroids + Itraconazole
Benign asbestos related pleural effusion
Benign asbestos- related pleural effusions (BAPE) are an early pleural manifestation of asbestos- related lung disease, usually occurring between 10-15 years postexposure. They are usually small (<500 mL), often bloody, and exudative, with eosinophilic predominance (>10% of nucleated cells, frequently >50%). BAPE may be asymptomatic or present with dyspnea, low-grade fever, and pleuritic chest pain. Spontaneous resolution over weeks to months is the norm. BAPE usually predates asbestos-related pleural plaques and may be a marker for future development of diffuse pleural thickening
Fat embolism
Causes:
-Fracture of long bone
-pancreatitis
-sickle cell disease
-Orthopedic surgery
Classical triad:
Respiratory distress, Altered mental status, petecheal rash
Treatment: supportive
Acute bronchitis management
Many patients develop a persistent cough due to bronchospasm with transient airway obstruction.
Inhaled beta-2 adrenergic agonists can relieve the obstruction and provide symptomatic relief in those with significant symptoms.
routine use of antibiotics is not recommended and purulent sputum production has not been shown to reflect bacterial infection. Even among those patients who test positive for atypical bacterial respiratory pathogens (eg, Mycoplasma pneumoniae, Chlamydia pneumoniae), there is no evidence that antibiotics provide benefit over supportive care.
Effect of NIPPV in Cardiogenic pulmonary edema
Noninvasive positive-pressure ventilation in cardiogenic pulmonary edema patients enhances oxygenation via improvements in respiratory (Decrease dead space ventilation, increase tidal volume, increase alveolar/minute ventilation)
cardiac indices (Decrease preload, Decrease afterload).
Malignant pleural effusion
Repeated thoracentesis can detect up to 90% of malignant cells in high-risk patients. If there is still a suspicion of malignancy despite repeated negative thoracentesis, thoracoscopy should be performed
Approach to increased peak pressure on the vent.
Normal plateau pressure
-Bronchospasm
-Mucus plug
-biting the tube
Increased plateau pressure
- pneumothorax
- Pneumonia
- Atelectasis
- pulmonary edema
- Rt main stem intubation
Chylothorax
Chylothorax is a relatively rare cause of pleural effusion, usually due to traumatic or non-traumatic disruption of the thoracic duct.
The most common non-traumatic cause is thoracic duct obstruction due to malignancy, sarcoidosis, or retrosternal goiter, and infections such as tuberculosis and filariasis. Traumatic disruption most commonly occurs in central venous catheter placement (subclavian approach) and esophageal surgery.
When associated with cirrhosis, congestive heart failure, or nephritic syndrome, the chylothorax may be transudative.
Aspirin-exacerbated respiratory disease
Usually presents with the classic triad of nasal polyposis, asthma, and aspirin (or NSAID) sensitivity.
The reaction is not an IgE-mediated allergic response but is likely a shift in the arachidonic acid metabolic pathway causing excessive leukotriene production.
These patients should be treated with leukotriene antagonists and optimal asthma management.
Acute eosinophilic pneumonia
Diagnosis
🔴 a BAL with 25% eosinophils or a lung biopsy showing an eosinophilic pneumonia.
+ the absence of other cause of pulmonary eosinophilia including drugs, toxins, and infectious pathogens
Sarcoidosis poor prognostic factors
black race, osseous involvement, lupus pernio (disfiguring nasolabial cutaneous lesions), chronic hypercalcemia, and chronic pulmonary sarcoidosis
Lymphangiomyomatosis (LAM)
LAM is a rare disorder affecting exclusively women that is characterized by hamartomatous proliferation of atypical smooth muscle along lymphatics in the lung, thorax, abdomen, and pelvis
• Mean age of onset is between 30 and 45 years.
• Progressive airflow obstruction, pneumothorax (50-80%), hemoptysis, or chylothorax.
• LAM can complicate tuberous sclerosis complex (TSC)
• Radiology: numerous thin-walled cysts, ranging in size from a few millimeters to 6 cm throughout both lungs; the intervening lung parenchyma is normal. Hyperinflation. Pneumothorax, effusion (chylothorax)
• PFT: Obstructive pattern, hyperinflation/airtrapping, reduced DLCO
• The course of LAM is indolent, but most patients ultimately die of respiratory failure.
• Treatment: LTX. Medications (Tamoxifen? Sirolimus?)
Desquamative Interstitial Pneumonia (DIP)
• DIP is a histologic syndrome characterized by dense collections of alveolar macrophages within air spaces.
• Radiology: Homogeneous pattern, preserved alveolar architecture, and minimal or absent fibrosis or honeycombing.
• More than 90% of patients with DIP are smokers.
Pulmonary Langerhan’s cell histocytosis
🔴 is a rare disorder usually seen in smokers.
🔴Age: 20-50
🔴PLCH is almost exclusively seen in Caucasian patients
🔴 presentation: cough and dyspnea. Pneumothoraces occurs in 6 to 20% of patients and may be the presenting feature.
🔴Extrapulmonary involvement occurs in 20% of patients with PLCH. Solitary punched-out lesions of bone and diabetes insipidus (from involvement of the pituitary) are the most common sites of extrapulmonary involvement.
🔴Radiologically: CT shows cystic and nodular lesions, with a proclivity to involve the upper lobes, strongly suggests PLCH.
🔴PFT: Obstructive, restrictive or mixed
🔴Treatment: Smoking cessation, Steroids, Lung Transplant
Pulmonary Alveolar Proteinosis (PAP)
🔴A rare parenchymal lung disease characterized by an accumulation of lipoproteinaceous material in the alveoli.
🔴Most cases (90%) are idiopathic; remaining cases consist of congenital and secondary forms of PAP.
🔴most patients are between 20 and 60 years of age.
🔴Radiology’crazy-paving”
🔴The diagnosis of PAP may be made by BAL, which typically yields a milky effluent
🔴Transbronchial biopsy: accumulation of granular, PAS positive, lipoproteinaceous material within the alveolar spaces with preserved alveolar architecture.
🔴The standard treatment for PAP is whole lung lavage.
🔴GM-CSF: favorable responses in 40% to 65% of patients, some enjoying a complete response.
Chronic Eosinophilic Pneumonia
🔴usually affects middle-aged atopic women
🔴Progressive
🔴Asthma is present in 50 to 60% of patients
🔴Increased IgE levels, and the levels may correspond to the clinical activity.
🔴Peripheral eosinophilia occurs in up to 88%.
🔴CXR: photographic negative of pulmonary edema
🔴Treatment and prognosis
10% of patients will have spontaneous resolution
Good response to steroids, can relapse
Causes of lymphocytic pleural effusion
• Primary effusion lymphoma or systemic lymphoma.
• Tuberculous pleurisy
• Sarcoidosis
• Chronic rheumatoid pleurisy
• Yellow nail syndrome
• Chylothorax
Pulmonary hypertension reversibility
Definition
🔴Pulmonary vasoreactivity testing is only recommended in patients with Ideopathic PAH, Hereditary PAH, or Drug induced PAH.
🔴 A positive acute response is defined as a reduction in mPAP by ≥10 mmHg to reach an absolute value <40 mmHg, with increased or unchanged Cardiac output.
🔴 Treat with high dose CCB.
Pulmonary hypertension
Genetics
The various mutations associated with idiopathic PAH and hereditary PAH are BMPR2 (most common), SMAD1, SMAD 9, KCNK3, CAV 1, and SOX17,
Pulmonary arterial hypertension medications during pregnancy
🔴Safe: Prostacyclin and PDE-5 inhibitor
🔴Unsafe: Endothelin receptor antagonist and sGC stimulator (Riociguat)
Pulmonary arterial hypertension
Approach to treatment
🔴In treatment-naïve patients with low or intermediate risk, the preferred treatment is dual combination with an endothelin receptor antagonist (ERA) and a phosphodiesterase-5 (PDE5) inhibitor.
🔴Calcium channel blockers are indicated for vasoreactive patients.
🔴Triple therapy is reserved for high-risk patients including parenteral prostacyclin therapy