5/4/18 Intern Morning Report – Shortness of Breath, Cough, Unintentional Weight Loss, Bloody Pleural Effusion, Asbestosis, Malginancy

CC: Shortness of breath and cough for 2 weeks

HPI: This is a 65-year old female with no past medical history presenting with two weeks of shortness of breath and cough as well as three weeks of generalized malaise.  She received a five day course of azithromycin prescribed by her primary care physician with no improvement in symptoms.  She is from Northeastern China and moved to Los Angeles in the 1990s.  She works at and owns a pencil manufacturing factory for ten years . She denies any smoking or alcohol use. Review of systems is pertinent for unintentional weight loss of 10 lbs over the last month.  Physical exam shows the patient to be afebrile, heart rate in the 130s, tachypneic to 22, and sat’ing 96% on room air.  Her rhythm is regular and pulmonary exam demonstrates evidence of a pleural effusion (decreased breath sounds in left lung base, dullness to percussion in the left lung field with decreased tactile fremitus).



CT Chest: Bilateral calcified pleural plaques are present with left pleural thickening.


Pleural fluid is grossly bloody with the following studies:

  • Glucose 72
  • LDH 1100
  • Protein 5.3
  • Color: Red
  • Markedly bloody
  • 902 nucleated cells
  • 84% segmented neutrophils
  • 16% lymphocytes
  • Pathology did not show malignant cells

Body Fluid Comparison

  • Glucose 90
  • LDH 161
  • Protein 6.6

Initial cytology is negative, so the favored diagnosis at the time is BAPE.  However repeat cytology done, showing atypical cells most consistent with Invasive Ductal Carcinoma primary site likely breast.  Patient is eventually diagnosed with breast cancer that is ER+/PR+/HER2 negative.

Morning Report Pearls:

Grossly bloody pleural effusions can narrow your differential to: Malignancy, Trauma, Asbestos, Pulmonary infarct, and Infection


Hemothorax is when the Hct in the pleural fluid is >50% of serum.  Important to know because chest tube placement would be indicated.


Benign Asbestos Pleural Effusion came up on this differential given the fluid being bloody, exudative and with a CT showing calcified pleural plaques.  Just remember that BAPE is a diagnosis of exclusion!  Malignancy should be ruled out first particularly given the elevated risk with asbestos exposure.


Risk Factors to know with regards to asbestos exposure include construction, automotive servicing, mining workers and shipbuilding industries.  When exposed the shorter fibers are typically cleared from the lungs however the longer fibers are transported to the interstitium or to the lymphatics where they can reach the pleura.  Most common finding in asbestos related pleural diseases is parietal plaques followed by pleural fibrosis and pleural effusion.  Pleural fibrosis can cause a restrictive disease if diffuse.  BAPE is almost always hemorrhagic as mentioned above and eosinophils can be elevated in 1/3.  Mesothelioma is a potential cancer that can be difficult to exclude in cases suspicious for BAPE given the low sensitivity of cytology so pleuroscopy may be needed.


Lung cancer is the most common malignancy to cause a pleural effusion and asbestos exposure does increase the risk of lung cancer.  Other cancers that can commonly lead to pleural effusion to consider are breast cancer and lymphoma.

2/2/18 Intern Morning Report – Shortness of Breath, Generalized Weakness, Dysphagia, New Onset Atrial Fibrillation, Hypoxia, Normal A-a Gradient, Myasthenia Gravis

CC: Shortness of Breath

HPI: 80 year old Chinese female with no past medical history presented to the emergency department with shortness of breath and dyspnea on exertion over the past week. She noted orthopnea with an inability to sleep and continued worsening exercise intolerance.  She denies fevers, chills, nausea, vomiting, or diarrhea. At baseline, she is usually independent and active without limitations.  On review of systems, she additionally reports dysphagia and generalized weakness.  On exam, her heart rate is 142 and irregularly irregular. She is hypoxic to 82% on room air and has poor inspiratory effort but lungs are clear.  There is evidence of left eye ptosis on exam which she says has been chronic in nature.  Basic labs are normal, EKG demonstrates atrial fibrillation, and CXR shows small lung volumes with bronchovascular crowding.  No initial ABG drawn.




Hospital Course:  Patient admitted for rate control of her atrial fibrillation and diuresis for which patient received metroprolol and lasix IV as well as initiation of a heparin drip.  A couple days into her hospitalization, patient became lethargic and was found to have the following ABG: 7.10/107/97/33 while on 5L NC, requiring intubation.  Post-extubation, she had recurrent episodes of hypoxia necessitating intermittent BiPAP.   Though patient only had unilateral ptosis, with this reported symptom as well as report of dysphagia, and hypercapnic respiratory failure with no obvious etiology,  suspicion for MG was high.  See the work up below that confirmed the diagnosis.


Work up for Myasthenia Gravis:

Acetylcholine Receptor Binding Ab – 124.5 (H)

Acetylcholine Receptor Modulating Ab – 88% binding inhibition (H)

Acetylcholine Receptor Blocking Ab – 51% of inhibition (H)

Striated Muscle Ab – Positive


EMG: positive for post-synaptic neuromuscular junction disease.

Morning Report Pearls:

Hypercapnic Respiratory Failure has only a hand full of etiologies that can be broken down into whether there is a A-a gradient or not:

  1. Extra thoracic Causes (Normal A-a gradient)
    1. Decrease respiratory drive (medication induced or CNS lesion like mass or stroke)
    2. Neuromuscular Disease (Myasthenia, GBS, ALS, spinal cord disease, myopathy)
    3. Chest wall compliance issues (kyphoscoliosis, obesity)
  2. Intrathoracic Causes (High A-a gradient)
    1. Pulmonary fibrosis (late stage usually)
    2. Athma
    3. COPD
    4. Bronchiectasis

Using your ABG to differentiate the two in addition to a great history and exam can be helpful!


Very important in MG patients is avoiding medications that exacerbate their condition.  This patient likely decompensated due to the cardiac medications given to her to control her atrial fibrillation.

Medications that unmask or worsen MG are extensive but here are a few:

-Antibiotics like aminoglycosides, clindamycin, fluoroquinolones, vancomycin

-Cardiovascular drugs like beta blockers, quinidine



Lastly, one unique feature of this case is the cardiac manifestation of her MG, atrial fibrillation.  A variety of arrhythmias have been documented in MG cases including sinus bradycardia, atrial premature beats, and atrial fibrillation.  Other cardiac manifestations include Takostubo’s cardiomyopathy and giant cell myocarditis.

1/30/18 Resident Morning Report – Shortness of Breath, Hemoptysis, Fever, Anemia, Bilateral Infiltrates, Hypoxemia, and Diffuse Alveolar Hemorrhage

CC: Shortness of Breath, Hemoptysis


HPI: This is a 23 year-old male with no past medical history who presents with progressive fatigue, pleuritic chest pain, shortness of breath, and hemoptysis for 2 months.  Initially his cough was productive with occasional blood-streaked sputum but progressed to frank hemoptysis in the last 3-4 weeks. Additionally, he reports subjective intermittent fevers and chills for 3-4 weeks.  Also notable is a 30 lbs unintentional weight loss over 2 months.  Exam shows patient saturating at 78% on room air, tachypneic to 30, febrile to 38.6, and tachycardic to 128.  Patient has diffuse crackles and wheezes from bases to mid lung fields but no rashes or joint findings.  His labs were notable for a normocytic anemia and leukocytosis with left shift.  CXR showed bilateral diffuse disease (see below) with CT demonstrating ground-glass opacities in a central distribution.   On BAL,  diffuse blood and secretions throughout all segments of lobes on both side of the lungs were visualized.  A diagnosis of Diffuse Alveolar Hemorrhage was made with the underlying etiology being Systemic Lupus Erythematosus based off other findings of nephritic syndrome with renal biopsy demonstrating Lupus Nephritis Class 3, +ANA, +dsDNA, low complements.


Morning Report Pearls:

Clinical suspicion for Diffuse Alveolar Hemorrhage should always be present when diffuse infiltrates on Chest X-ray are seen in the setting of anemia, respiratory failure and hemoptysis.  Of note, one third of patients will not have hemoptysis!


Diagnosis is made on BAL when it demonstrates serial samples that are progressively hemorrhagic.   Yield is higher if performed within the first 48 hours of symptoms.


There are many causes of DAH with overlapping pathophysiology.  DAH can result from small vessel inflammation resulting in alveoli necrosis followed by leakage of RBCs into the lung, bleeding into the alveolar space as a result of diffuse alveolar damage (ARDS pathologies), or bland hemorrhage resulting from etiologies like coagulopathies.


Pulmonary Capillaritis Conditions:

  • Systemic Vasculitis (GPA, MPA, Cryoglobunemia, HSP, IgA vasculitis)
  • Connective Tissue Disorders (SLE, MCTD, RA, APLS)
  • Drugs like Retinoic acid or PTU
  • Lung transplant rejection


Bland Pulmonary Hemorrhage Conditions:

  • Left sided heart failure
  • Mitral stenosis or mitral regurgitation
  • Anticoagulants or coagulopathies like DIC
  • Pulmonary Veno-occlusive Disease
  • Endocarditis
  • Drugs like Marcobid


Diffuse Alveolar Damage Conditions:

  • Anything that can cause ARDS like infections
  • Bone marrow transplantation
  • Crack cocaine inhalation
  • SLE


When having a patient with DAH, always consider the Pulmonary-Renal Syndromes which is defined as DAH with Glomerulonephritis.  This is one of many reasons to always obtain a urinalysis on these patients.  The pulmonary-renal syndromes really narrow the above list to Vasculitis and Connective Tissue Disorders if present.