This post highlights in-depth breakdowns of my favorite clinical cases from May 2026. I then provide some commentary and build on the lessons from my own experience, where appropriate.
I’ve broken these cases into multiple parts to keep the length of each post more digestable.
Case Summary
An 81F with AFib on apixaban, mod-severe MR who is 16 days post-hip arthroplasty presented with exertional dyspnea. She was hypoxic and tachycardic in AFib with RVR. BNP was elevated. CTPE confirmed a segmental PE with e/o right heart strain. It also noted diffuse GGOs. A POCUS showed no signs of acute severe RV dysfunction but did show diffuse bilateral B lines. The diagnosis was acute on chronic decompensated heart failure precipitated by A-fib with RVR, which was itself likely triggered by the PE. Given the above, the right heart strain called on the CT was likely related to overload and not hemodynamic compromise from an otherwise stable PE. The patient was managed with diuresis, rate control, and continued anticoagulation.
Hemodynamically Stable Pulmonary Embolism with Acute-on-Chronic Decompensated Heart Failure
This case highlights the importance of differentiating a hemodynamically significant PE from other causes of dyspnea and hypoxia. This can be challenging in patients with underlying cardiopulmonary disease. CTA can identify a thrombus and suggest RV strain by comparing ventricular diameters. However, a functional assessment with echo is essential to guide management.
In acute hemodynamically significant PE, elevated BNP and troponin can reflect myocardial stretch and injury.
POCUS or ECHO is the most critical tool for assessing the physiologic impact of the PE. Signs of acute RV pressure, overload, and failure include RV dilatation based on RV:LV ratio >1, interventricular septal flattening (the “D-sign”), and McConnell’s sign (RV mid-free wall akinesis with apical hyperkinesis), which is highly specific. Other findings can include a depressed RV systolic function (TAPSE <1.6 cm), significant tricuspid regurgitation (TR), and a dilated non-collapsible IVC.
Advanced Doppler findings, like the “6060 sign,” which is defined by pulmonary artery acceleration time < 60 ms and a TR gradient < 60 mmHg, are also highly specific for acute PE. This is because a chronically strained RV can often generate higher pressures than this.
A hemodynamically stable PE without RV dysfunction is treated with AC alone. A hemodynamically significant PE with evidence of RV dysfunction requires consideration of advanced therapies like systemic thrombolysis or catheter-directed thrombectomy.
Pearls
Though valuable in some cases, a CTA report of “right heart strain” must be correlated with a functional assessment via POCUS or echo.
The absence of classic echo signs of acute RV failure argues against a hemodynamically significant PE, even if a clot is present on imaging.
In a patient with multiple potential diagnoses causing dyspnea, a POCUS can rapidly identify the primary derangement. In this case, diffuse B-lines confirmed pulmonary edema was the main driver of hypoxia.
AFib with RVR can both be a consequence of a PE due to acute artery strain and a cause of decompensated heart failure, especially in patients with preexisting valvular disease and diastolic dysfunction
Hypercoagulable structures in the right heart are not always caught in transit. True clots are typically mobile and serpiginous, whereas fixed structures are more likely normal variants, such as Chiari network or other pathology.
My Commentary
This case is excellent because it’s a reminder that all clinicians should be trained on POCUS. Though formal echos can often be done quickly in a hospital setting, decisions on patients that are intermediate-risk may be delayed which can be consequential. B-lines are one of the more satisfying things to identify on a POCUS, as this finding can certainly swing your clinical judgment in uncertain cases. This especially comes in handy in patients with multiple comorbidities presenting with dyspnea and you’re unsure whether it is driven by overload from ADHF vs another etiology. Everyone should feel comfortable with a the basic cardiac views, assessing for B-lines, and assessing for lung sliding. POCUS is best when used in addition to your usual focused workup.
Case Summary
A 56F with breast cancer on tamoxifen presented with several months of fatigue, shifting joint pains (migratory polyarthritis) with significant morning stiffness and subjective fevers. Her workup is notable for a positive COVID-19 test, a low TSH, an ANA 1:640, positive RF. ESR and CRSP were normal. Her physical exam was normal. On further history, the patient was found to be taking biotin supplements, and thus the TSH was favored to be spuriously low. Given she was not having objective fevers during subjective experiences, these experiences were re-characterized as hot flashes. These hot flashes in combination with prominent joint pains led to a diagnosis of tamoxifen-induced adverse effect. The medication was discontinued, and her symptoms completely resolved. The ANA and RF were felt to be red herrings.
Tamoxifen Adverse Effects
Tamoxifen-induced arthralgia is a common MSK side effect of treatment with selective estrogen receptor modulators (SERMs) which are used for hormone-positive breast cancer. The pathophysiology is thought to relate to estrogen deprivation, which is similar to what is seen with aromatase inhibitors.
Common presentations can include vasomotor symptoms such as hot flashes and MSK complaints. The arthralgia seen is often symmetric, affecting both small and large joints, and can be accompanied by significant morning stiffness that can closely mimic an inflammatory condition like RA or lupus. Fatigue is also frequently noted.
Understandably, the diagnosis of one of exclusion is made largely based on history. Key for your chart include the absence of inflammation on labs and a lack of objective synovitis or joint swelling, despite reports of severe pain and stiffness autoantibodies can be coincidentally positive and are common in the age group of women often taking tamoxifen. Positive serology alone does not indicate an underlying connective tissue disease.
Management is primarily symptomatic with analgesics such as NSAIDs. If symptoms are severe and impact quality of life, the definitive intervention is a discussion with the patient’s oncologist about discontinuing or changing therapy. The diagnosis is confirmed after a “de-challenge” where the drug is stopped and symptoms subsequently resolve.
Pearls
It’s important to consider the difference between discomfort and dysfunction. This patient had significant subjective discomfort, including arthralgias and fatigue, but did not have any objective dysfunction since they had a normal exam, labs, and organ function
Tamoxifen is a classic mimic of rheumatologic disease, since it can cause arthralgias and prominent morning stiffness.
Biotin supplementation can interfere with many lab values and can classically cause spurious hyperthyroidism by falsely suppressing TSH and elevating free thyroid hormones
A positive autoantibody does not equal a diagnosis. Without a compatible clinical syndrome, there are often incidental findings that can lead to a misdiagnosis if not interpreted in the appropriate context.
Over time and depending on how it is asked, a patient’s description of symptoms can evolve. In this case, “subjective fevers” were later reframed as hot flashes, which was a key clue pointing towards a hormonal or medication-related etiology.
My Commentary
This case is great not only because it includes my favorite lab pearl (biotin producing spurious hyperthyroidism), but also because it includes a number of common pitfalls. The first pitfall taking vocabulary used by patients at face value instead of further questioning to better reinterpret the actual symptoms or sensations that the patient is experiencing. Patients use the terminology that they know, not necessarily the appropriate medical terminology that fits the situation. It’s a good starting point, and it’s valuable to mirror language that the patient uses. However, clinicians should always investigate further what patients mean by the terms that they use. I also loved the lab red herrings - I can’t tell you how many times unexpected abnormal labs that don’t seem to fit a specific clinical picture has led my teams astray. The last major takeaway is to remember that medications have side effects. I have a pet theory that the average complex patient on countless medications is almost certainly having some sort of side effect or nagging symptom that is either a consequence of one of the medications they take or a combination of multiple medications. While we certainly learn about common side effects of commonly prescribed medications, the reality is that it’s simply impossible to know, given it’s unlikely that I’m going to be de-prescribing medications in an inpatient setting unless there’s a clinical reason to do so.
Case Summary
A 61M with T2DM and HTN presented with five days of fevers, diarrhea, cough, and RUQ discomfort. Shortly after presentation, he clinically deteriorated, developing hypoxemia, confusion, AKI, transaminitis, and rhabdomyolysis. Imaging was notable for a right basilar opacity that progressed to bilateral infiltrates. There was a strong clinical suspicion for Legionnaires disease, however, the urine Legionella antigen test was negative. Given clinical suspicion, a bronchoscopy was performed that showed a positive PCR for Legionella species. It was attributed to a non-serogroup one strain from a recent potting soil exposure. He was treated with azithromycin and improved significantly.
Legionnaires’ Disease
Legionella species are gram-negative intracellular bacteria that can cause an atypical pneumonia known as Legionnaires disease. Transmission occurs via inhalation of aerosolized contaminated water. Sources can include cooling towers, plumbing systems, hot tubs, and, less commonly, soil or compost. The classic presentation is a severe pneumonia that’s accompanied by prominent extrapulmonary manifestations.
Patients often present with high fever, dry cough, and shortness of breath. Diarrhea, nausea, and abdominal pain are very common. Neurological symptoms like headache and confusion are also classic. Relative bradycardia (also known as Faget sign) can also be a clue.
Hyponatremia is also a classic finding. Inflammatory markers such as CRP and ferritin are typically elevated.
Chest imaging usually shows patchy unilobar consolidation that can rapidly progress to bilateral involvement and pleural effusions.
The urine antigen test is rapid and widely used but primarily detects the serogroup 1, which is the most common cause. A negative test does not rule out disease from other serogroups or species. Definitive diagnosis can be made by culture on buffered charcoal yeast extract agar or, more commonly, by PCR on respiratory specimens such as sputum or BAL fluid.
Legionnaires disease is treated with a macrolide (azithromyin), or a respiratory fluoroquinolone such as levofloxacin. In cases where there’s clinical suspicion, they should be started empirically, waiting for confirmatory results.
Pearls
A negative Legionella urinary antigen does not rule out the diagnosis. It is insensitive for non-serogroup one species like L. longbeachae.
A detailed exposure history can be invaluable. You should ask beyond water exposure and ask about gardening and exposure to potting soil or compost.
A sputum gram stain showing many neutrophils but few or no visible organisms is a classic clue for an intracellular pathogen such as Legionella.
In patients with suspected atypical pneumonia and a negative urine antigen, proceeding to a bronchoscopy for PCR and culture can be a critical diagnostic step.
Relative bradycardia in a febrile patient should prompt consideration of intracellular pathogens, including Legionella, Salmonella, Chlamydia
My Commentary
What I like about this case is the clinical gumption to feel strongly about a disease despite a negative test. It also brings to mind the importance of covering for atypical infections when there’s concern for a pulmonary source of sepsis. I’ve seen a number of times patients coming in starting cap antibiotics, and when the patient starts to decompensate they are broadened to a regimen such as vancomycin and cefepime, without the inclusion of a medication that will treat atypicals. There are numerous types of atypical infectious processes that can lead to patients deteriorating and having evidence of end-organ dysfunction. Always be mindful of what you are covering for and what the suspected source is! Lastly, I’ve seen conflicting data on whether hyponatremia is actually attributable to Legionnaires specifically, or if it’s just more likely an SIADH related to severe illness and pneumonia. I’d say the most important takeaway is that the absence of hyponatremia shouldn’t dissuade you from thinking about Legionnaires, even though that’s one of the classic associations. Instead, its presence can just be one more data point consistent with the diagnosis.
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