The Clinical Problem Solvers

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**The Clinical Problem Solvers**

The Clinical Problem Solvers is a multi-modal venture that works to disseminate and democratize the stories and science of diagnostic reasoning
Twitter: @CPSolvers
Website: clinicalproblemsolving.com

Latest Episodes:

Episode 84 – RLR – Hoarseness May 05, 2020

Show notes

https://clinicalproblemsolving.com/wp-content/uploads/2017/05/RLR-Episode-2_Hoarseness.mp3

Episode description

Reza and Rabih talk through a case

RLR #2 – Hoarseness
A 54-year-old man with a history of PTSD, depression, and a recent diarrheal illness presented with acute dysphagia to liquids and solids. Neurologic exam was initially unremarkable, but the patient returned the next day with diplopia and ataxia. Exam was notable for new bilateral cranial nerve III palsies and areflexia. Laryngoscopy revealed unilateral vocal cord paralysis. Cerebrospinal fluid analysis was notable for elevated protein and positive GQ1b antibody testing. He was diagnosed with Miller Fisher’s syndrome, a variant of Guillain-Barre Syndrome.

Teaching Points:

Miller Fisher’s Syndrome(MFS) is a rare variant of Guillain-Barre syndrome (acute inflammatory demyelinating polyneuropathy) that primarily affects the bulbar nerves. MFS is suggested by the classic triad of acute-onset ophthalmoplegia, ataxia, and areflexia and often occurs following a prodromal illness (upper respiratory infection or gastroenteritis). Diagnosis is supported by elevated cerebrospinal fluid protein as well as demonstration of GQ1b ganglioside autoantibodies (which are positive in 85% of cases). Prognosis is typically favorable, and most cases are self-limited.

Episode 83 – RLR – Lymphadenopathy May 05, 2020

Show notes

https://clinicalproblemsolving.com/wp-content/uploads/2017/05/RLR-Diffuse-LAD.mp3

Episode description

Reza and Rabih talk through a case

RLR #1 – Lymphadenopathy
A woman in her 20’s with a history of prior possible thrombotic thrombocytopenic purpura (TTP) and recently treated secondary syphilis was transferred to a tertiary referral center for evaluation of generalized lymphadenopathy, new anemia, and thrombocytopenia. Laboratory workup was concerning for a Coombs-positive autoimmune hemolytic anemia, possible immune thrombocytopenia, and polyclonal gammopathy. Core and excisional lymph node biopsies were unrevealing for either infection or malignancy. Ultimately, anti-nuclear, anti-dsDNA, and anti-Sm autoantibodies were grossly positive and the patient was diagnosed with systemic lupus erythematosus.

Teaching Points:

Systemic Lupus Erythematosus(SLE) is a complex autoimmune disease that most frequently presents with inflammatory arthritis, malar rash, and nephropathy.Hematologic abnormalities are common in SLE and are components of both the American College of Rheumatology (ACR) and Systemic Lupus International Collaborating Clinics (SLICC) diagnostic criteria. Common features include leukopenia (both neutropenia and lymphopenia), autoimmune hemolytic anemias (generally Coombs-positive, warm-type), and thrombocytopenia. SLE is a recognized cause of secondary thrombotic thrombocytopenic purpura (TTP), which may present concurrently with or, in some instances, precede the diagnosis of SLE.

Episode 82: Virtual Morning Report unknown with student Dr. Jean-Claude Guidi and Drs. Kushal Vaishnani & Ramya Ramachandran – hypoxemia Apr 29, 2020

Show notes

https://clinicalproblemsolving.com/wp-content/uploads/2017/05/VMR-15-4-26-20-5.52-PM.mp3

Dr. Kushal Vaishnani presents a clinical unknown on Virtual Morning Report to student Dr. Jean-Claude Guidi and Dr. Ramya Ramachandran.

Case Overview & Teaching Points

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Problem Representation
A 53-year-old woman with a history of rheumatoid arthritis and amiodarone-induced lung injury on immunosuppression presented with acutely progressive hypoxic respiratory failure and hypotension, found to have a serpiginous truncal rash, acute anemia, and elevated beta-d-glucan.
Schemas
In this episode, we revisit the schemas for fever and rash (which highlights first addressing the life-threatening causes) and diffuse alveolar hemorrhage (which focuses on differentiating vasculitis from other etiologies).
Diagnosis
The patient underwent bronchoscopy with bronchoalveolar lavage fluid demonstrating elevated leukocytes with a neutrophilic predominance as well as progressively bloody fluid, consistent with diffuse alveolar hemorrhage. Silver stain was diagnostic for Pneumocystis jiroveci, and pathology revealed helminthic larvae consistent with Strongyloides stercoralis. The patient was diagnosed with both Pneumocystis pneumonia and Strongyloides hyperinfection syndrome!

Teaching Points:

Beta-D-glucan(BDG) is a cell wall polysaccharide found in many fungal organisms (with notable exceptions including Cryptococcus, the zygomycetes, and Blastomyces dermatitidis) and is frequently used as a laboratory marker for invasive fungal infections. Caution is advised when interpreting this test, as it is imperfectly sensitive and false positives have been reported in association with certain hemodialysis filters, immunoglobulins (e.g., IVIG), albumin, and beta-lactam antimicrobials (thought to be more of an issue with older formulations).
Strongyloides stercoralisis an important human pathogen in tropical and subtropical areas throughout the world. While many cases of chronic strongyloidiasis are mild and may go unrecognized, severe manifestations can include the strongyloides hyperinfection syndrome and disseminated strongyloidiasis. Hyperinfection occurs when there is accelerated autoinfection (i.e., the ability to complete the parasitic life cycle entirely within the host – a trait relatively unique to Strongyloides among human helminthiases) and most commonly occurs in the setting of immune dysregulation or exogenous immunosuppression.
Pneumocystis jiroveciis an important opportunistic infection in immunosuppressed patients. Originally identified by Carlos Chagasin 1909, who believed it to represent a pulmonary manifestation of the parasite Trypanosoma cruzi, it was later reclassified as a fungus in 1988. The most frequent symptoms include subacute dyspnea, nonproductive cough, and low-grade fever, with hypoxemic respiratory failure being the most common manifestation of severe decompensation.