Pleural Effusion, Pulmonary Embolism, Hemoptysis, ARDS. Pulmonary embolism is the fourth leading cause of pleural effusion. The possibility of pulmonary embolus should be evaluated for all patients who have an undiagnosed pleural effusion. The mechanism of pleural effusion caused by a pulmonary embolus is usually increased interstitial fluid in the lungs as a result of ischemia or the release of vasoactive cytokines. Approximately 75% of patients with pulmonary emboli and pleural effusion have pleuritic chest pain.
A 68 year-old male with a history of hypertension, diabetes, hyperlipidemia, chronic obstructive pulmonary disease and congestive heart failure (CHF) with depressed ejection fraction presents via ambulance with a chief complaint of shortness of breath. EMS reports that the patient was tachypneic and saturating 80% on ambient air on their arrival. En route, he received nebulized albuterol, nitroglycerin and was started on non-invasive positive pressure ventilation (NI-PPV).
On arrival, he remains uncomfortable-appearing with a respiratory rate of 35 breaths/min and accessory muscle use. His heart rate is 136bpm, blood pressure is 118/85mmHg, and he is saturating 95% on an FiO2 of 100%. Attempts to obtain a history are limited due to difficulty comprehending his responses with the PPV mask on, and prompt desaturation with it off. Lung auscultation is similarly challenging due to ambient and transmitted sounds, although basilar crackles and diffuse expiratory wheezing are appreciated. Cardiovascular examination reveals a rapid and irregularly irregular rhythm. Assessment of jugular venous distension is limited due to the patient’s body habitus and the presence of mask straps around the patient’s neck. Lower extremities demonstrate 2+ pitting edema, symmetric bilaterally. Intravenous access is established and laboratory tests are sent. The ECG technician and portable chest x-ray are called.
The case presentation above demonstrates a common emergency department scenario: a critically-ill patient with undifferentiated dyspnea. Specifically, the scenario reveals a situation where the physical examination is either obfuscated by technical challenges or otherwise indeterminate. The patient is at risk for deterioration and targeted intervention is mandatory. If a COPD exacerbation is assumed, additional nebulized breathing treatments are indicated – a potentially costly jolt of beta agonists if the patient’s atrial fibrillation and rapid ventricular response are the consequence of decompensated systolic heart failure. Take the route of decompensated CHF and prompt afterload reduction with diuresis would be next – if incorrect, not only would the primary cause go untreated, but his tenuously-maintained blood pressure may suffer.
Algorithm for the Use of Ultrasound in the Evaluation of Dyspnea
1. Lung Ultrasound
An approach incorporating point-of-care ultrasonography may be useful. First, a thoracic ultrasound is performed where certain causative etiologies might be identified immediately – for example absent lung sliding suggesting pneumothorax, or signs of generalized or subpleural consolidation.
The POCUS Atlas
The ultrasound images and videos used in this post come from The POCUS Atlas, a collaborative collection focusing on rare, exotic and perfectly captured ultrasound images.
2. Cardiac Ultrasound
Other findings on lung ultrasound may point to causes that are not primarily pulmonary. For example, if diffuse B-lines are encountered a focused cardiac ultrasound can be performed to grossly evaluate ejection fraction and estimate right atrial pressure.
3. Venous Ultrasound
Finally, if the lung ultrasound is largely unremarkable (A-lines), a sequence of ultrasonographic findings including right ventricular dilation and the presence of a deep venous thrombosis would point to pulmonary embolism as the diagnosis.
Decreased BS, subQ emphysema, JVD and tracheal deviation if tension
Dietary indiscretion, medication non-adherence
JVD, S3/S4, peripheral edema
Tobacco use, personal/family history
Retractions, accessory muscle use, wheezing
US (distinguish from fluid overload)
Tobacco use, weight loss
64F with a history of CAD, MI, CHF, CLL and rheumatoid arthritis who presented to the emergency department after transfer from a rehabilitation facility for respiratory distress. The patient reported several days of progressive shortness of breath with dyspnea on exertion. She also noted some associated orthopnea and lower extremity edema. The patient was recently hospitalized for similar symptoms and was diagnosed with CHF at the time. At the rehab facility, the patient became hypoxemic and hypertensive, reporting shortness of breath and chest pain prior to presentation.
The patient was initially managed with BiPAP and nitroglycerin continuous infusion, but was then stable on supplemental O2 via nasal cannula and was transitioned to long-acting nitrates and anti-hypertensives. The patient’s hypoxemic respiratory failure was initially attributed to acute exacerbation of left-ventricular heart failure, and the patient was managed with spot diuresis. However, there was no symptomatic improvement and the patient became hypernatremic so diuresis was held as alternative diagnoses were explored.
A transthoracic echocardiogram showed preserved LVEF (50-55%), but some diastolic dysfunction and elevated PAP/RAP. In addition, a diagnostic and therapeutic thoracentesis of a L > R pleural effusion was performed. Pleural fluid studies were suggestive of a transudative process, though with some abnormal characteristics (including lymphocyte predominance, as well as presence of signet cells).
Rheumatology and pulmonology services were consulted for input and recommendations for further evaluation were appreciated. Per rheumatology, the patient’s diagnosis of rheumatoid arthritis may not be consistent with her presentation or prior serologic studies. Her pleural fluid analysis was also not consistent with rheumatoid disease. According to pulmonary consult, the patient’s hypoxemia remains most consistent with left ventricular dysfunction though primary pulmonary processes cannot be excluded (and would warrant further evaluation with imaging and pulmonary function testing).
No family history of autoimmune disease.
Denies tobacco/EtOH/drug use
Lives at home, at SNF since discharge
Furosemide 20mg p.o. daily
Gabapentin 300mg p.o. t.i.d.
Hydralazine 50mg p.o. t.i.d.
Hydrochlorothiazide 25mg p.o. b.i.d.
Hydroxychloroquine 200mg p.o. daily
Levothyroxine 25mcg p.o. daily
Minoxidil 2.5mg p.o. b.i.d.
Pantoprazole 40mg p.o. daily
Prednisone 15mg p.o. daily
Elderly female, alert and oriented to self and place, responding appropriately to questions.
Mucous membranes moist, sclera anicteric, no cervical lymphadenopathy.
Regular rate and rhythm, normal S1/S2, no additional heart sounds. III/VI mid-systolic murmur heard best at LLSB with diastolic component, no radiation appreciated. Non-displaced PMI. JVP measured to 14cm.
Decreased breath sounds in left lung field to inferior 2/3 with crackles above, on right crackles to inferior 1/2 of lung fields posteriorly. Dullness to percussion of inferior left lung field posteriorly.
Soft, non-tender, non-distended, no hepatosplenomegaly, no appreciable fluid wave.
Bilateral lower extremities with 2+ pitting edema to knees, some hyperpigmentation to right lower extremity.
There is a large left pleural effusion obscuring the lower half of the left hemi thorax. The cardiac silhouette is also obscured. There is pulmonary venous vascular congestion. There is also a right pleural effusion with fluid tracking into the minor fissure. Pulmonary interstitial edema is also noted.
CT Chest (High-Resolution):
Bilateral, left greater than right, pleural effusions with adjacent atelectasis and collapse versus consolidation of the left lower lobe.
Prominent main pulmonary artery measuring 3.3 cm in diameter, which can be seen with pulmonary arterial hypertension.
LVEF is 50-55%.
Impaired left ventricular relaxation, which is associated with grade I/IV or mild diastolic dysfunction.
Moderate aortic stenosis with mild regurgitation (AVA 1.4 cm3, mean gradient 14mmHg, peak velocity 2.4 m/s).
Severe pulmonary hypertension (est PASP 52-62mmHg).
The inferior vena cava appeared dilated and decreased <50% with respiration (RAP 10-20 mmHg).
Minimal pericardial effusion without echocardiographic evidence of tamponade.
64F with history of CAD (prior MI), CHF, hypertension, CLL, hypothyroidism presented from a SNF with progressive shortness of breath, orthopnea and LE swelling, found to have bilateral (L>R) pleural effusion now s/p thoracentesis with transudative fluid.
#Acute hypoxic respiratory failure: Large pleural effusions, s/p thoracentesis with pleural fluid suggestive of transudative process. Most likely secondary to left ventricular diastolic dysfunction. Improved after thoracentesis and diuresis. High-resolution CT chest performed without evidence of autoimmune-related pulmonary fibrosis or ILD (though persistent pleural effusions, pulmonary vascular congestion).
#Pleural fluid signet cells: Identified on cytology, potentially related to history of untreated CLL or alternative primary malignancy.
#Left ventricular diastolic dysfunction, decompensated: Associated with pleural effusions and hypoxemic respiratory failure. Management with diuresis.
#Pulmonary Hypertension: Severe, noted on transthoracic echocardiography, may be secondary to hypoxemia associated with pleural effusions, consider repeat imaging once euvolemic or right-heart catheterization.
#Microscopic Hematuria: No evidence of infection, no symptoms suggestive of nephrolithiasis. No casts identified or significant proteinuria. Plan for renal ultrasound.
#Rheumatoid Arthritis: History of rheumatoid arthritis, on prednisone and hydroxychloroquine. Imaging without evidence of inflammatory arthropathy, RF elevated but CCP negative. Per rheumatology, the patient’s symptoms are not consistent with RA, continuing home medications while evaluation is ongoing. Pleural effusions unlikely associated with RA as transudative, and without monocyte predominance or low glucose.
Case 2: Malignant Pleural Effusion
Within the lungs there are ground-glass opacities bilaterally, and a left pleural effusion with adjacent consolidation vs compressive atelectasis.
Protein: 2.6 (serum: 4.9)
LDH: 1275 (serum: 219)
Cytology: Malignant cells
Case 3: Traumatic Thoracentesis
Moderate right pleural effusion, some fluid in non-dependent portions suggestive of loculation. Diffuse nodules and opacification in right lung with compressive atelectasis. Left pleural effusion with high density material at the posterior costophrenic angle. Left chest tube.
Protein: 2.7 (serum 6.4)
LDH: 344 (serum 236)
Cell count: 100,000 RBC
Case 4: Pneumonia
Loculated right pleural effusion with foci of atelectasis and consolidative changes concerning for pneumonia. Minimal left-sided pleural effusion with consolidative changes. Enlarged mediastinal lymph nodes, possibly reactive.
Protein: 4.3 (serum 6.7)
LDH: 377 (serum 108)
Etiology of Pleural Effusions:
Clinical Features in the Diagnosis of Pleural Effusions and Identifying Etiology: 1,2
Pleural effusions can be easily identified on chest radiography, physical examination findings include dullness to percussion, decreased tactile fremitus and decreased (or absent) breath sounds.
Hemoptysis: Malignancy, PE, TB
Weight Loss: Malignancy, TB
Ascites: Cirrhosis, ovarian cancer
Unilateral Leg Swelling: PE
Bilateral Leg Swelling: CHF, cirrhosis, nephrotic syndrome
Jugular Venous Distension: CHF
Differential Diagnosis of Pleural Effusions: 1,2,3,4
Pulmonary Embolism in Hospitalized Patients
Brief Progress Note
Notified by nursing of abnormal vital signs, SpO2 91%. Briefly, this patient is a 52-year-old G1P1 with no prior medical history who is post-operative day three status post total abdominal hysterectomy, bilateral salpingo-oophorectomy as well as tumor debulking and staging for suspected primary ovarian adenocarcinoma based on peritoneal fluid cytology.
On evaluation, the patient denied shortness of breath, chest pain, pleuritic chest pain, cough/hemoptysis, or calf/thigh pain. She states that she had been ambulating around the ward prior to having her vital signs assessed.
No acute distress, speaking in full sentences.
No jugular venous distension.
RRR, normal S1/S2, no prominent P2, no additional heart sounds.
Decreased breath sounds at inferior 1/3 posterior lung fields bilaterally, faint crackles above, no wheezing. Dullness to percussion in inferior lung fields.
Warm, well-perfused. Sequential compression devices on bilateral lower extremities, removed revealing trace pitting edema symmetric bilaterally, no tenderness to palpation of posterior leg, no pain with passive dorsiflexion.
Lovenox 40mg s.q. daily
Norco 5-325mg p.o. q.4.h. p.r.n. pain
Morphine 2mg i.v. q.3.h. p.r.n. breakthrough pain
Colace 100mg p.o. b.i.d. p.r.n. constipation
Zofran 4mg i.v. q.6.h. p.r.n. nausea/vomiting
No evidence of pulmonary embolism, study performed 5 days prior to onset of symptoms.
Significant peritoneal carcinomatosis, ascites delineates peritoneal from retroperitoneal spaces.
Assessment and Plan:
52yo G1P1 with likely primary ovarian adenocarcinoma with extensive peritoneal involvement, complicated by malignant ascites and pleural effusions with hypoxemia. The primary concern in this post-operative patient with a history of malignancy is venous thromboembolism, particularly pulmonary embolism. Aside from hypoxemia, this patient had no symptoms suggestive of pulmonary embolism (denied dyspnea, chest pain, cough, or lower extremity pain). Her examination had some signs infrequently associated with pulmonary embolism which were otherwise adequately explained by known bilateral pleural effusions (including decreased breath sounds, rales, and tachypnea), she was not tachycardic, had no evidence of jugular venous distension, nor a prominent P2. In addition, she was receiving appropriate VTE prophylaxis (both pharmacological and mechanical). The application of the Modified Wells clinical decision rule suggests low likelihood of pulmonary embolism (with 2.5 points assigned for recent surgery and history of malignancy). The patient had a recent CT chest without evidence of pulmonary embolism, and given that an elevated D-dimer was virtually assured which would have necessitated repeat imaging (and the associated risks of radiation exposure and contrast injury), the episode was ascribed to ventilation/perfusion mismatch secondary to large pleural effusions. Hypoxemia resolved after several minutes at rest and no further testing was performed.
LMWH prevents approximately ½ of VTE events (including PE, symptomatic and asymptomatic DVT)
Acute Respiratory Distress Syndrome
25M with a history of mild asthma transferred from an outside hospital after 10 days in the intensive care unit for continued management of ARDS.
The patient was well until one week prior to admission when he developed intermittent subjective fevers and general malaise associated with a non-productive cough and nausea/vomiting. He presented to the emergency department of an outside hospital with difficulty breathing and was noted to have respiratory distress and was subsequently admitted. Initial CT at the outside hospital revealed pneumomediastinum but no evidence of pulmonary embolism. Results from the outside hospital reveal a wide array of bacterial/fungal cultures and viral serologies including bronchoscopy but no obvious infectious source. The patient was treated with broad spectrum antibiotics for several days but his condition worsened requiring intubation, mechanical ventilation and transfer to the ICU. Further imaging was suggestive of ARDS, and the patient was transferred for additional management.
The patient was well until one week prior to admission when he reported development of malaise and fatigue. On the day of hospitalization, the patient presented to primary care doctor with complaint of cough and shortness of breath and was found to be in respiratory distress and was admitted. The patient received IV antibiotics (cefepime, vancomycin) and was intubated when respiratory distress worsened. Found to have evidence of ARDS on CXR.
Mild asthma, not requiring medication
MRSA skin abscess
Lives with family and works at a local supermarket. Rare alcohol use and no prior tobacco or drug use.
No recent travel or sick contacts.
ciprofloxacin 400mg i.v. q12h
linezolid 600mg i.v. q12h
meropenem 1g i.v. q8h
heparin 5000units s.q. q8h
PRVC, VT 320, RR 35, PEEP 6, FiO2 95%
Young male, thin-appearing, intubated and sedated and not responding to verbal commands
PERRL, unable to assess EOM, ET tube in place
RRR, normal S1/S2, no murmurs
Coarse breath sounds bilaterally
Normoactive bowel sounds, soft, non-distended, no hepatosplenomegaly
No clubbing, cyanosis, edema
Unable to assess
Blood/sputum/urine cultures: Negative
Aspergillus, crypto, cocci: Negative
EBV, HIV, influenza, RSV: Negative
CT Chest: Evidence of pneumomediastinum and pneumopericardium. Bilateral pulmonary infiltrates, but no pulmonary embolism.
25M with ARDS transferred from outside hospital for further management.
# ARDS: Severe (P/F ratio <100). Etiology unclear, thorough infectious workup without obvious source. Consider autoimmune or allergic cause.
Ventilator: PRVC lung-protective ventilation
Consider NMB for dyssynchrony despite sedation
Monitor strict I/O, maintain net negative fluid balance.
# Sepsis: Leukocytosis, tachycardia. Continue broad-spectrum antibiotics and monitor cultures.
# Acidosis: Largely respiratory, place dialysis catheter if acute need arises.
# Pneumomediastinum: Possible Boerhaave syndrome given reports of nausea/vomiting.
Pathophysiology of Acute Respiratory Distress Syndrome (ARDS):
ARDS represents a stereotyped response to multiple insults. It is characterized by damaged capillary endothelium and alveolar epithelium resulting in increased permeability and the accumulation of fluid in the alveolar space. This causes diffuse alveolar damage and triggers the release of various cytokines (TNF, IL-1, IL-6) which recruit and activate neutrophils causing oxidative cell damage.
Definition of ARDS (Berlin):
Acute in onset (<1 week)
Origin of pulmonary edema
Not explained by heart failure or fluid overload (assessed with echocardiography)
Causes of ARDS:
An Introduction to Mechanical Ventilation:
This is a simplification of the general principles underlying the most common ventilator modes. For more detail, see the articles cited in the references.
Continuous Mandatory Ventilation (CMV)
All breaths controlled by ventilator, no triggered breaths.
Assist-Control Ventilation (AC)
Every patient-triggered breath is fully supported, a backup rate is set. In the absence of patient-triggered breaths, AC acts like CMV.
Preset minimum mandatory breaths are “synchronized” to patient’s efforts. The patient is allowed to breathe spontaneously between supported breaths.
Pressure Support (PS)
All breaths are triggered by the patient and each is supported by preset pressure.
Continuous Positive Airway Pressure (CPAP)
Spontaneous breathing at elevated baseline pressure
Volume Control (VC)
Volume is set, pressure is variable. With a drop in compliance, the preset minimum volume is maintained with an increase in pressure.
Pressure Control (PC)
Pressure is set, volume is variable. With a drop in compliance, a smaller volume is delivered to maintain pressures at the preset limit.
Pressure-Regulated Volume Control (PRVC)
Pressure is targeted with a set minimum volume. The ventilator makes breath-to-breath adjustments of pressure to maintain minimum volumes. Breath mechanics are therefore comparable to pressure-control as a defined pressure is delivered based on prior breath’s respiratory mechanics (note pressure and flow tracings for PRVC/PC vs. VC)
Volume Control (VC)
Pressure Control (PC)
Pressure-Regulated Volume Control (PRVC)
Linear IgG deposits consistent with anti-GBM disease.
61yo African American female w/hx of HTN presenting with 1mo of persistent cough productive of green-yellow sputum, noticed streaks of blood for the past 5 days. She came to the ED today because she has been feeling increasingly fatigued. She reports subjective fevers at the onset of symptoms which has resolved. She denies shortness of breath, chest pain, chills, night sweats. She sought medical care for this problem 2wk ago and was treated with amoxicillin and a cough suppressant. She recalls a coworker was ill one month ago. She is US-born, had a negative PPD in the past and has no known exposures to tuberculosis.
Of note, the patient reports her urine had a foamy appearance and has been darker in color beginning 3 weeks ago, but this had resolved. She denied dysuria, or frank hematuria.
UA: brown, trace LE, – nitrites, 2+ protein, 81 RBC
Right mid-lung zone consolidation is present, suggests pneumonia if acute.
Mild asymmetric right parenchymal increased density is seen diffusely as well.
65AAF w/hx HTN presents with persistent productive cough, recently with hemoptysis.
# Cough: Symptoms and physical findings of abnormal breath sounds (crackles, though no strict consolidation) concerning for community-acquired pneumonia. Addition of hemoptysis raises concern for TB, particularly when taking into consideration the duration of cough and presence of constitutional symptoms. CBC shows leukocytosis with left shift, CXR with right mid/lower lob infiltrates consistent with pneumonia. Recommend admission and isolation to rule out TB, start empiric therapy for community acquired pneumonia with ceftriaxone, azithromycin. Obtain induced sputum samples for culture, AFB smear and culture.
# Abnormal urine: Patient describes changes in urine suggestive of proteinuria and hematuria. Acuity of onset and apparent spontaneous resolution suggests a chronic kidney injury 2/2 hypertension is unlikely. Absence of dysuria, or tenderness (suprapubic, costovertebral) suggests complicated UTI unlikely. Urinalysis notable for 2+ protein and significant RBC’s, possible nephritic syndrome. In the setting of hemoptysis, this raises concern for anti-GBM disease vs. vasculitis.
# Anemia: Normocytic anemia. No evidence of acute, life-threatening hemorrhage as patient is currently hemodynamically stable. Possible sites of blood loss include alveoli, glomeruli. Given that patient sought care today for worsening fatigue, will monitor hemoglobin closely and consider transfusion. Obtain iron studies.
# HTN: BP stable, hold home medications.
The patient was admitted for management of community-acquired pneumonia and isolation to rule out TB. Empiric therapy with CTX + azithromycin was continued. On HOD1, the patient was transfused two units of PRBC’s. On HOD2, the patient underwent CT chest/abdomen/pelvis due to worsening respiratory status despite antimicrobial therapy. On HOD3, the patient went into atrial fibrillation with RVR which was converted to sinus rhythm with metoprolol 5mg IV x3. On HOD5, nephrology consult recommended starting steroid therapy, plasmapheresis and obtaining a renal biopsy, however the biopsy was delayed due to worsening respiratory status.
Iron studies: Fe 8, TIBC 203, Ferritin 468, haptoglobin 333, retics 2.7
LFT: AST 34, ALT 29, ALP 52, protein 6.3, albumin 2.4, T.bil 0.8, D.bil 0.2
Anti-GBM 1.2 (nl <1.0)
p-ANCA: positive 1:640, [ELISA pending]
ANA: positive 1:320, speckled
Diffuse right lung, tree and bud opacities, ground-glass opacities and areas of confluence with scattered air bronchograms. Less severe similar pattern in the left lung as well particular at the base.
Right paratracheal, subcarinal and perihilar LAD.
Findings concerning for primary TB in the right clinical setting. DDx nonspecific bacterial PNA and fungal PNA.
Mild nonspecific R > L perinephric stranding.
# Acute respiratory failure: Unlikely simple CA-PNA given worsening status while on appropriate antibiotic therapy. Active tuberculosis possible given history of chronic productive cough with hemoptysis, constitutional symptoms and imaging findings. IGRA’s of limited utility in diagnosis of active disease, further, while three negative sputum AFB smears decreases the likelihood of TB, additional testing with NAAT and culture is required. Another possibility is a vasculitic process given concomitant hematuria and acute renal failure, with respiratory symptoms now 2/2 alveolar hemorrhage. This was evaluated with ANCA assay which was positive for p-ANCA with high titer. This is often suggestive of primary vasculitis (in this case likely microscopic polyangiitis vs. Churg-Strauss), however ELISA for target antigen is of particular importance as p-ANCA with specificity for antigens other than MPO can be associated with another condition on the differential: Goodpasture’s syndrome. This patient was found to have elevated anti-GBM antibodies which are highly suggestive of Goodpasture’s syndrome, and can be associated with ANCA-positivity (often suggesting a poorer prognosis with decreased likelihood of recovery of renal function).1
# Acute kidney injury: The patient had significant elevation of serum creatinine compared to last-recorded baseline. She also described darkening and foamy appearance of urine 3 weeks prior to admission, suggestive of proteinuria/hematuria of relatively acute onset. This was supported by urinalysis findings of protein and RBC’s (with casts). Given presence of anti-GBM antibodies, high specificity of such findings, and correlation with glomerulonephritis with evidence of pulmonary alveolar hemorrhage, this appears to be the most likely cause at this time. Definitive diagnosis with renal biopsy to be obtained following stabilization of respiratory status. Patient will be started on plasmapheresis and immunosuppressive therapy (corticosteroids, cyclophosphamide).
# Normocytic Anemia: Likely combination of acute blood loss (2/2 hematuria, pulmonary alveolar hemorrhage) and chronic disease. Normocytic anemia with some reticulocytosis suggestive of acute blood loss, however iron studies with low Fe, TIBC and elevated ferritin suggest chronic disease as an associated factor.
Differential Diagnosis of Hemoptysis:
A System for the Diagnosis of Tuberculosis:
A System for Vasculitides:
Interpretation of antineutrophil cytoplasmic autoantibodies (ANCA): 10
Granulomatosis with polangiitis (Wegener’s)
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
Infection (HIV, fungal)
Differential Diagnosis of Anemias:
Quick Case: Pleuritic Chest Pain
30yo male presenting with forearm cellulitis, also complaining of right-sided sharp chest pain worse with deep inspiration and some movements of the ipsilateral shoulder. Found to have multiple pulmonary nodules (suggestive of metastasis) with the largest being a subpleural nodule in the superior/anterior portion of the RUL (roughly the location of the patient’s pain).
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