Pulmonary Flashcards
Elderly smoker with FEV1/FVC 0.35 presents with: Fever Dyspnea Worsening cough CXR: Lobar consolidation, in addition to chronic changes Sputum Gram stain: Gram-negative cocci What is the diagnosis?
Moraxella community-acquired pneumonia (CAP). Explanation Clues: COPD and the bacterial morphology. There are only a couple of clinically significant gram-negative cocci: Neisseria species and Moraxella. Dx: Clinical + microbiologic (Gram stain and/or culture); perfectly acceptable to treat pneumonia empirically. Targeted Tx: Amoxicillin/clavulanic acid, macrolide (azithromycin or clarithromycin), tetracycline, or cephalosporin.
There are only a couple of clinically significant gram-negative cocci: ___ species and ___.
There are only a couple of clinically significant gram-negative cocci: Neisseria species and Moraxella.
Rx: Moraxella community-acquired pneumonia (CAP).
Amoxicillin/clavulanic acid, macrolide (azithromycin or clarithromycin), tetracycline, or cephalosporin.
Nonsmoking patient presents with 4 months of: Weight loss Fever Progressive cough, productive of profuse watery sputum with a salty taste
Bronchoalveolar adenocarcinoma alias: adenocarcinoma in situ. Explanation - associated with profuse sputum production, termed “bronchorrhea” (which by definition is > 100 cc of sputum/day). - Occasionally, the bronchorrhea is associated with salt-wasting and can cause electrolyte imbalances. Dx: Lung imaging + PET scan + tissue biopsy. Tx: Variable, based on extent of disease.
Dx-criteria: Bronchoalveolar adenocarcinoma
Lung imaging + PET scan + tissue biopsy.
Bronchioloalveolar carcinoma (BAC)
- a subset of adenocarcinoma - peripheral - well-differentiated histology - lepidic growth pattern - potential for both aerogenous and lymphatic spread.
Female in her 40s presents with:
Exertional syncope
Exam: JVD, large v waves, a loud P2, holosystolic murmur at LLSB, and normal lungs
PFTs: Normal except for ↓ DLCO
VQ scan: Low probability
What is the diagnosis?
Idiopathic pulmonary arterial hypertension (IPAH).
Explanation: Murmur of TR
Dx: Echo followed by right heart catheterization, extensive evaluation. Confirmed by PASP is ≥25 mmHg at rest
Tx: O2 + diuretics + CCBs ± endothelin receptor antagonists (bosentan) ± PDE-5 inhibitors (sildenafil) +warfarin ± prostacyclins (iloprost) ± lung transplant.
Pulmonary hypertension: which group benefits from anti-coagulation?
Group 4 PH (eg, chronic thromboembolic pulmonary hypertension [CTEPH])
Anticoagulation in patients with group 1 PAH is controversial.
Group 1 pulmonary arterial hypertension (PAH) have idiopathic pulmonary arterial hypertension (IPAH, formerly called primary pulmonary hypertension), hereditary PAH, or PAH due to diseases that localize to small pulmonary arterioles, such as connective tissue diseases, HIV infection, portal hypertension, congenital heart disease, schistosomiasis, and drug use.
Asthma exacerbations every 2 months while on an inhaled and LABA + medium-dose ICS
± Eosinophilia
Sputum: Branching hyphae
CXR: central bronchiectasis with “fingers in glove” pattern
What is the diagnosis?
Allergic bronchopulmonary aspergillosis (ABPA).
Dx: Clinical (history of asthma) + positive prick test + evidence of fungus (fungal elements in the sputum or antibodies against Aspergillus in the serum).
Tx: Systemic glucocorticoids + itraconazole.
Explanation: presence of fungal elements in the sputum of a patient with uncontrolled asthma = ABPA.
Alternative: prick test is positive and that the patient has an increased IgE level.
Nonsmoking female presents with:
Intermittent cough with hemoptysis
Long bone pain
Clubbing
Pain with palpation of the anterior tibias
What is the diagnosis?
Adenocarcinoma of the lung with hypertrophic pulmonary osteoarthropathy (HPOA).
Dx: Clinical.
Tx: NSAIDs + treatment of underlying disorder.
digital clubbing + periostosis of tubular bones and synovial effusions, which are most prominent in the large joints: Trigger.
Hypertrophic osteoarthropathy (HOA)
is a syndrome characterized by abnormal proliferation of the skin and osseous tissue at the distal parts of the extremities.
Look for lung neoplasm, primary or secondary.
oundry worker with h/o cough and “hilar eggshell calcifications” on CXR presents with 3 months of:
Weight loss
Night sweats
Productive cough
Occasional hemoptysis
Sputum: +Acid-fast organisms
Diagnosis is ______________________ associated with ______________________.
tuberculosis associated with silicosis.
Explanation
Dx: Clinical and of exclusion + abnormal chest radiograph ± HRCT of the chest.
Mx: Avoidance + yearly TB screening (induration of ≥ 10 mm using the PPD test or positive IGRA) + lung transplant in young patients with severe disease.
Patient with months of bilateral hand and knee pain presents with:
Dyspnea
Exudative pleural effusion
Active synovitis of bilateral MCPs, PIPs, and elbows
Soft tissue nodular lesions over the olecranon bursa
Pleural fluid glucose: < 30 mg/dL
TB skin test: Nonreactive
What is the cause of the pleural effusion?
Pleural effusion is caused by rheumatoid arthritis (RA).
Ex: Very low pleural fluid glucose, exudative
Dx: Clinical and of exclusion.
Tx: Treat underlying RA.
Male presents with:
Dyspnea
Productive cough
Occasional hemoptysis
Nasal ulcer
↓ Hgb and Hct with normal MCV and MCHC
U/A: Protein, RBCs, RBC casts
CXR: Cavitary lesions and nodules
+Anti-PR3 and c-ANCA
What is the diagnosis?
GPA
Dx: Clinical + biopsy of tissue showing vasculitis.
GPA: Rx
Limited disease: Steroid and methotrexate + rituximab?
Severe disease: Steroid and (daily) cyclophosphamide, controversial. Some authors/editors favor a cyclophosphamide-based regimen as initial therapy, while others choose a rituximab-based regimen for the majority of patients.
Disease appears to accelerate when serum creatinine begins to rise; detection of renal involvement signals medical emergency that must be treated swiftly
ANCA serologies useful in making diagnosis, but serial testing of ANCA titers not useful
Reflecting dramatic improvements in treatment, there is now 90% survival at 5 years
GPA: Rx in severe disease controversy
approach to initial therapy depends upon the severity of the disease and the organ systems involved:
- Non-organ-threatening and non-life-threatening disease – This group of patients has no evidence for “active” glomerulonephritis (ie, normal serum creatinine and no red cell casts or proteinuria) and no organ-threatening or life-threatening manifestations (eg, absence of pulmonary hemorrhage, cerebral vasculitis, progressive neuropathy, orbital pseudotumor, gastrointestinal bleeding, pericarditis, or myocarditis). Such patients may have rhinosinusitis, arthritis, and/or pulmonary nodules. Non-organ-threatening and non-life-threatening disease can still result in substantial disease burden and long-term damage.
- Organ-threatening or life-threatening disease – Other patients with GPA or MPA are classified into this group for the purpose of initial therapy. Such patients may have ma
Some authors/editors favor a cyclophosphamide-based regimen as initial therapy, while others choose a rituximab-based regimen for the majority of patients.
Nonsmoking hunter from Alabama develops:
An indolent productive cough
CXR: Mass-like lesion
Sputum KOH: Broad-based budding yeasts
What is the diagnosis?
blastomycosis.
Dx: Definitive diagnosis requires growth of the organism from a clinical specimen. Unlike Candida and Aspergillus spp, colonization or contamination with B. dermatitidis does not occur, which means that visualizing the organism on histology or obtaining a positive culture confirms the diagnosis of blastomycosis. Presumptive diagnosis of blastomycosis may be made by visualization of the characteristic yeast form in clinical specimens, such as sputum, tissue, or purulent material.
Visualization may justify beginning empirical antifungal therapy. Serology is not useful
Tx: Itraconazole or amphotericin B (for severe infections and any involving the CNS).
Asthmatic on montelukast and omalizumab who is weaning from high-dose prednisone develops:
Allergic rhinitis
Tender upper extremity nodules or other forms of skin rash
Chronic cough and dyspnea
CBC: ↑ Eosinophils
U/A: Protein and RBC casts
What is the diagnosis?
EGPA
4 or more of these criteria had a sensitivity of 85 percent and a specificity of 99.7 percent:
●Asthma
● > 10 percent eosinophils
● Mononeuropathy (including multiplex) or polyneuropathy
●Migratory/transient pulmonary opacities
●Paranasal sinus abnormality
●Biopsy: blood vessel + eosinophils in extravascular areas
Rx:
Anca and EGPA: why is not useful?
Low sensitivity and specificity
There are no laboratory tests that are specific for EGPA, although eosinophilia is characteristic. For patients who have suspected EGPA, we typically obtain a complete cell count with differential, a total eosinophil count, and an IgE level. We also usually obtain an ANCA test, although the sensitivity and specificity are low.
CGD vs CVID
CGD: first 2 years of life + abscess
The functional residual capacity is comprised of two lung volumes:
ERV + RV
The expiratory reserve volume represents the additional volume of air that can be exhaled from the lungs when acted upon by the respiratory muscles of exhalation. The residual volume is the volume of air that remains in the lung following a complete exhalation and is determined by the closing pressure of the small airways.
At what lung volume does the outward recoil of the chest wall equal the inward elastic recoil of the lung?
Expiratory reserve volume
Functional residual capacity
Residual volume
Tidal volume
Total lung capacity
Functional residual capacity
The functional residual capacity of the lung refers to the volume of air that remains in the lung following a normal tidal respiration.
This volume of air represents the point at which the outward recoil of the chest wall is in equilibrium with the inward elastic recoil of the lungs. The lungs would remain at this volume if not for the actions of the respiratory muscles.
The functional residual capacity is comprised of two lung volumes: the expiratory reserve volume and the residual volume.
The expiratory reserve volume represents the additional volume of air that can be exhaled from the lungs when acted upon by the respiratory muscles of exhalation. The residual volume is the volume of air that remains in the lung following a complete exhalation and is determined by the closing pressure of the small airways.
A 65-year-old man has progressive dyspnea on exertion over past 3 months. History of necrotizing pancreatitis that resulted in multiorgan failure and ARDS., requiring mechanical ventilation for 6 weeks prior to his recovery.
Examination: a low-pitched inspiratory and expiratory wheeze is heard that is loudest over the mid-chest area. FEV1 is 2.5 L (78% predicted), forced vital capacity is 4.00 L (94% predicted), FEV1/FVC ratio is 62.5%. Most likely cause?
Aspirated foreign body
Chronic obstructive pulmonary disease
Idiopathic pulmonary fibrosis
Subglottic stenosis
Unilateral vocal cord paralysis
Flow volume: box-like appearance
Fixed central airflow obstruction
results in flattening of the flow-volume loop in both inspiration and expiration, yielding the characteristic boxlike effect.
Examples of fixed airflow obstruction include tracheal stenosis and an obstructing central airway tumor
Fixed airway obstruction: causes
- tracheal stenosis
- obstructing central airway tumor
Fixed central airflow obstruction results in flattening of the flow-volume loop in both inspiration and expiration, yielding the characteristic boxlike effect.
Examples of fixed airflow obstruction include tracheal stenosis and an obstructing central airway tumor
Patterns of airflow obstructoin
- Fixed
- Variable
- intra-thoracic: eg: tracheomalacia
- extra-thoracic: eg: VCD paralysis or tumor
Examples of fixed airflow obstruction include tracheal stenosis and an obstructing central airway tumor.
Variable obstruction: In these situations, flattening of the flow-volume curve occurs on only one limb of the flow-volume loop, and the pattern of flattening can be explained by the dynamic changes in pressure that affect the trachea.
A variable intrathoracic obstruction causes flattening of the flow-volume curve only on expiration. During inspiration the pleural pressure is more negative than the tracheal pressure, and the trachea remains unimpeded to flow. However, when pleural pressure rises on expiration relative to tracheal pressure, there is collapse of the trachea and flattening of the flow-volume curve. An example of a variable intrathoracic obstruction is tracheomalacia.
In contrast, the variable extrathoracic defect leads to flattening of the flow-volume loop on inspiration but not expiration. The relevant pressure acting on airflow in the trachea in an extrathoracic obstruction is atmospheric pressure. During inspiration, the tracheal pressure drops below atmospheric pressure, leading to compromised airflow and the characteristic flattening of the flow-volume loop. However, tracheal pressure rises above atmospheric pressure during expiration, leading to a normal expiratory curve.
Flow volume loops
A = lower airway obstruction (COPD/asthma) B = fixed upper airway obstruction (tracheal stenosis) C = variable intrathoracic upper airway obstruction (tumour in lower trachea) D = variable extrathoracic upper airway obstruction (vocal cord tumour or paralysis, enlarged thyroid)
A 32-year-old woman presents to the emergency department in her 36th week of pregnancy complaining of acute dyspnea. Blood pressure 128/78, heart rate 126 beats/min, respiratory rate 28 breaths/min, and oxygen saturation is 96% on room air. Afebrile. Her lung and cardiac examinations are normal. There is trace bilateral pitting pedal edema.
CXR: normal, ECG: sinus tachycardia. ABG: pH is 7.52, PaCO2 is 26 mmHg, and PaO2 is 85 mmHg.
Management
CTPA
The normal arterial blood gas in pregnancy shows a chronic respiratory alkalosis with a pH ranging as high as 7.47 and PaCO2 between 30 and 32 mmHg. Calculation of the alveolar-arterial gradient (A-a gradient) can be helpful in this situation. It is easy to be fooled by the presence of a normal oxygen saturation and partial pressure of oxygen on arterial blood gas, but the A-a gradient may still be elevated in the presence of respiratory alkalosis.
To calculate the A-a gradient, one first must calculate the alveolar oxygen tension with the alveolar gas equation shown below:
PaO2 = PiO2 − (PaCO2/R) where,
PiO2 = inspired partial pressure of oxygen = FiO2 × (Pbar − PH2O), and
R = respiratory quotient = carbon dioxide production/oxygen consumption = ∼0.8
In this patient, calculation of the PaO2 = [0.21 × (760 − 47)] − (26/0.8) = 117.23 mmHg. At the same time the measured arterial partial pressure of oxygen was 85. Thus, the A-a gradient is elevated at 32 mmHg and should prompt the physician to perform further workup for pulmonary embolism.
The choice of test for diagnosis of pulmonary embolism in pregnant patients is most commonly CT pulmonary angiography, although ventilation-perfusion scanning may also be used.
ABG on room air: pH is 7.52, PaCO2 is 26 mmHg, and PaO2 is 85 mmHg.
What is the AA gradient?
- aa_gradient == (alveolar_pO2 - arterial_pO2)
- alveolar_pO2= inspired_pO2 - (1.25*arterial_pco2) //
- inspired_pO2 = FiO2 × (atmospheric_pressure − partial_pressure_o2)
If we are at sea level, inspired_pO2 = FiO2 * (760 - 47) = FiO2 * (710)
PaO2 = PiO2 − (PaCO2/R) where,
PiO2 = inspired partial pressure of oxygen = FiO2 × (Pbar − PH2O), and
R = respiratory quotient = carbon dioxide production/oxygen consumption = ∼0.8
In this case:
PaO2 = [0.21 × (760 − 47)] − (26/0.8) = 117.23 mmHg.
Measured arterial partial pressure of oxygen was 85. Thus, the A-a gradient is elevated at 32 mmHg and should prompt the physician to perform further workup for pulmonary embolism. T
Alveolar gas equation
alveolar_oxygen_partial_pressure = FiO2*(atmospheric_pressure - partial_pressure_water) - arterial_co2_partial_pressure*(1/respiratory_exchange_ratio)
Typically:
alveolar_oxygen_partial_pressure = FiO2*710 - pCO2*1.25
AA_gradient = FiO2*710 - pCO2*1.25 - arterial_pO2
The 1.25 comes from the inverse of the respiratory_exchange_ratio.
The partial pressure of oxygen (pO2) in the pulmonary alveoli is required to calculate both the alveolar-arterial gradient of oxygen and the amount of right-to-left cardiac shunt, which are both clinically useful quantities. However it is not practical to take a sample of gas from the alveoli in order to directly measure the partial pressure of oxygen. The alveolar gas equation allows the calculation of the alveolar partial pressure of oxygen from data that is practically measurable.
- pAO2: 107
- FIO2: 0.21
- PATM: 760
- pH2O: 47
- paCO2: 40
- RER: 0.8
Assumptions:
Inspired gas contains no carbon dioxide (CO2) or water
Nitrogen (and any other gases except oxygen) in the inspired gas are in equilibrium with their dissolved states in the blood
Inspired and alveolar gases obey the ideal gas law
Carbon dioxide (CO2) in the alveolar gas is in equilibrium with the arterial blood i.e. that the alveolar and arterial partial pressures are equal
The alveolar gas is saturated with water
High AA gradient: Cx
- V/Q mismatch
- Alveolar membrane diseases
- Interstitial diseases
Hypoxemia + normal AA gradient
Hypoventilation with displacement of alveolar O2 by CO2 or other substance.
Normal AA Gradient
Aa_gradient = 2.5 + 0.21 x age
PaO2 vs PAO2
“A” denotes alveolar and “a” denotes arterial oxygenation
Hypoxia: mechanisms
- Hypoventilation
- V/Q mismatch
- Right-to-left shunt
- Diffusion limitation
- Reduced inspired oxygen tension
Hypoventilation induced hypoxemia: mechanism
- once the partial pressure of one gas rises, the other must decrease.
- Both arterial and alveolar carbon dioxide pressures increase during hypoventilation,
- which causes the alveolar oxygen tension (PAO2) to decrease.
- As a result, diffusion of oxygen from the alveolus to the pulmonary capillary declines with a net effect of hypoxemia and hypercapnia.
- Because the respiratory quotient (Defined as CO2 eliminated/O2consumed) is assumed to be 0.8, hypoventilation affects PaCO2 more than O2.
Hypoxemia due to pure hypoventilation: characteristics
- Easily corrects with a small increase in FiO2
- paCO2 is elevated.
An exception exists when the hypoventilation is prolonged because atelectasis can occur, which will increase the A-a gradient
V/Q mismatch
imbalance of blood flow and ventilation. It causes the composition of alveolar gas to vary among lung regions.
V/Q mismatch in the normal lung
- Both ventilation and perfusion are greater in the bases than in the apices.
- However, the difference between apical and basilar ventilation is smaller than the difference between apical and basilar perfusion.
- As a result, the V/Q ratio is higher in the apices than in the bases.
- V/Q mismatch is responsible for the normal A-a gradient.
Normal AA gradient: cause
Physiologic V/Q mismatch
Both ventilation and perfusion are greater in the bases than in the apices (when in an upright position). However, the difference between apical and basilar ventilation is smaller than the difference between apical and basilar perfusion. As a result, the V/Q ratio is higher in the apices than in the bases. V/Q mismatch is responsible for the normal A-a gradient.
Hypoxemia due to V/Q mismatch: causes
- obstructive lung diseases
- pulmonary vascular diseases
- interstitial diseases.
Hypoventilation: causes
- CNS depression: eg drug overdose
- Obesity hypoventilation (Pickwickian) syndrome
- Neuropathy: eg ALS, GBS high cervical spine injury, phrenic nerve paralysis, or aminoglycoside blockade
- Muscular weakness, such as myasthenia gravis
- Poor chest wall elasticity: eg kyphoscoliosis
Right-to-left shunt
blood passes from the right to the left side of the heart without being oxygenated.
Right-to-left shunt: types
- Anatomic shunts. Eg: intracardiac shunts, pulmonary AVMs, and hepatopulmonary syndrome.
- Physiologic shunts exist when non-ventilated alveoli are perfused. Eg: atelectasis and diseases with alveolar filling (eg, pneumonia, acute respiratory distress syndrome).
Right to left shunt: commonest example
Pneumonia
- Anatomic shunts: Examples include
- intracardiac shunts,
- pulmonary AVMs
- hepatopulmonary syndrome.
- Physiologic shunts: exist when non-ventilated alveoli are perfused. Examples
- atelectasis
- diseases with alveolar filling (eg, pneumonia, ARDS).
Mechanism of hypoxemia in pneumonia
Right-to-left shunt
IPF: mild to moderate; RX
- Mild to moderate: pirfenidone or nintedanib
- Advanced: sildenafil
- Mild or moderate IPF (PFTs) who do not have underlying liver disease start with either. Patient preference, SideFx profile guides choice.
- Advanced IPF, a diffusing capacity (DLCO) <35 percent of predicted, right ventricular dysfunction, and no contraindications to sildenafil, a trial of sildenafil.
Hantavirus-pulmonary-syndrome.Transmission
Aerosolized rat excreta
Hantavirus, seen mostly in the southwestern United States, is a rare cause of viral pneumonia that quickly evolves to acute respiratory distress in previously health individuals and is associated with a high mortality rate
Pulmonary-embolism.chronic.Mx
Proximal arterial filling defects: Mx
Thrombectomy
Successful pulmonary thromboendarterectomy removes obstructive, whitish, hardened thromboembolic material and markedly improves the hemodynamic measures of mean pulmonary-artery pressure, pulmonary vascular resistance, and cardiac output (Fig. 4).29,30 Improvement in hemodynamics causes reverse right ventricular remodeling, with reductions in tricuspid regurgitation and the return of right ventricular systolic and diastolic function toward normal levels.
http://www.nejm.org/doi/pdf/10.1056/NEJMra0910203?ssource=kplus
Specific test for rheumatoid interstitial lung disease
ACPA
ost patients have already had serologic testing for rheumatoid factor (RF) and anti-cyclic citrullinated peptide antibodies (ACPA), but full assessment of other autoantibodies should be performed, including antinuclear antibodies and anti-double stranded DNA antibodies, and also cryoglobulins to assess for coexistent rheumatic disease that may be contributory in the appropriate clinical setting, such as when purpura, Raynaud phenomenon, skin ulcers, or renal disease are present.
Bronchiectasis.BestTest
HRCT
Common cause: CVID
Status-asthmaticus.Ventilated
Evidence of auto-peep
Mx
Disconnect ventilator from tube
PEEP.Auto-PEEP
Causes
- high minute ventilation
- expiratory flow limitation, and
- expiratory resistance
There are three common situations during which auto-PEEP develops: high minute ventilation, expiratory flow limitation, and expiratory resistance. (See ‘Causes’ above.)
Critical-Care.Ventilation
Auto-PEEP: Problems caused by
- Reduces cardiac output
- Barotrauma
Auto-PEEP increases intrathoracic pressure, which can decrease venous return, reduce cardiac output, and potentially cause hypotension. It can also cause alveolar overdistension, increasing the likelihood of pulmonary barotrauma and ventilator-associated lung injury. Finally, auto-PEEP increases the work required for a patient to trigger a ventilator breath if pressure-triggering is being used. (See ‘Potential sequelae’ above.)
Why is moxifloxacin a good choice in CAP in a solid organ transplant recepient 6 months post-transplant?
6 months post-transplant: standard community organisms
Early post-transplant: need to cover for nosocomial organisms
Endobronchial mass: why is the wheezing monophonic, expiratory?
Intra-thoracic airways become smaller with expiration
Non-response to asthma therapy in spite of adherence in a young woman
DDx
VCD
Vocal cord dysfunction
Septic shock
Need for vasopressors to keep MAP > 65
or
Lactate > 2 in the absence of hypovolemia
Nitrogen narcosis: prevention
Helium-oxygen
Nitrogen narcosis is caused by the raised partial pressure of nitrogen in nervous system tissue, and usually occurs at depths greater than 100 feet. It has been called “rapture of the depths” because it induces signs and symptoms similar to alcohol or benzodiazepine intoxication, such as impairment of intellectual and neuromuscular performance and changes in behavior and personality. Hallucinations and loss of consciousness can occur at depths greater than 300 feet.
A diver’s susceptibility to nitrogen narcosis is increased by other factors that have an opioid effect on the central nervous system, such as, hypercarbia, fatigue, alcohol, and hypothermia (core temperature less than 35ºC) induced by cold water. Divers recover rapidly upon ascent to a shallower depth. The main danger of this condition stems from impairment of the diver’s judgment, which can lead to drowning accidents.
ABPA vs aspergillus infection
- ABPA: allergic response, IgE levels are up.
- Aspergillus infection: + Galactomannan
Filamentous, weakly Gram +ve organism
Nocardia
Nocardiosis is caused by an aerobic actinomycete in the genus Nocardia, an unusual gram-positive bacteria. Nocardial infection most often occurs in immunocompromised patients. (See ‘Introduction’ above.)
●The most common disease sites are the lung, central nervous system (CNS), and skin. There are no pathognomonic signs or symptoms for nocardiosis. It should be suspected in any patient who presents with brain, soft tissue, or cutaneous lesions and a concurrent or recent pulmonary process. (See ‘Introduction’ above.)
Pulmonary alveolar proteinosis: Rx
whole lung lavage
Spontaneous hemopneumothorax in a young woman: Dx
Catamenial hemopneumothorax
Bilateral pleural effusions, ascites, peripheral edema: abrupt onset; female of reproductive age; recent fertility treatment
Ovarian hyperstimulation syndrome
Asthma: pregnant: mild-persistent: rx
low dose budenoside
