Today our amazing PGY-2, Dr. Alexis Quade, led us through an interesting case of an elderly woman who initially came in with some knee pain but was found to have an AKI and sepsis in the ED. We found out that she had untreated psoriasis, a bioprosthetic valve and a recent Staph Aureus UTI. Her exam was notable for extensive, near full body, erythematous desquamating lesions sparing mucosal membranes, with a yellowish crust but otherwise hemodynamically stable that was concerning for erythroderma. Our expert discussant from dermatology, Dr. Nell Haddock, helped us learn about the pathophysiology of erythroderma and the most common disease processes that will cause this condition. Dr. Quade reminded us that erythroderma, given the large degree of vasodilation and shunting of blood flow, can be a cause of high-output heart failure. Ultimately, the patient was diagnosed with impetiginized psoriasis and staph bacteremia and greatly improved with IV antibiotics and topical steroids.
1) Remember to look for possible bacteremia and occult infection in patients with Staph bacteruria
2) Erythroderma is a dermatologic emergent condition that is defined by an exfoliative dermatitis that covers over 90% of the body and is caused by a number of disease states.
3) Treatment includes aggressive wound care and hemodynamic monitoring given large degree of insensible losses and control of underlying disease process. Remember, do not use oral steroids for psoriasis flares, start with topical steroids +/- immunologics!
Thank you again, Dr. Quade, for the great case and to Dr. Haddock, for your amazing teaching!
Today we were joined by our dermatology colleague (and UCSD IM alumnus!) Dr. Brittany Yee as we discussed the case of a middle-aged woman presenting with subacute blistering lesions with mucocutaneous involvement. After describing her lesions and discussing the differential, we consulted dermatology for biopsy, confirming pemphigus vulgaris (PV)! We then discussed some of the key distinguishing features of the two most common autoimmune bullous diseases (PV and bullous pemphigoid). Thank you Dr. Yee for your insight into this rare but life-threatening disease!
Take Away Points:
Auto-immune bullous diseases may be life-threatening and should always be considered when blistering is present
The history and physical are very helpful for narrowing the diagnosis. Ultimately, a biopsy is required
There is not much data on therapeutics, but many patients will need high dose steroids and long-term immunosuppression
We were lead today through some interesting high yield Osteoporosis learning objectives by our RACE track resident Dr. Kusuma Pokala and endocrinologist Dr. Gina Woods. Our residents took on the challenge of teaching each other and we took our newfound knowledge through a Jeopardy game to solidify this information! We then learned about common dermatologic conditions that general internists may encounter with the help of Drs. Natasha Carter, Laura Romero and Joyce Yuan. Thank you all for helping our residents with our virtual learning experiences!
Today our excellent 2nd year resident Kevin Wang presented a case of an elderly woman who was coming in with acute on chronic blistering rash and vision changes. We walked through a diagnostic schema for vesicular/bullae and went over pertinent questions to ask to determine the etiology of the lesions. We then practiced going over our descriptions of bullous lesions. Our patient had noted uncontrolled bullous foliaceous (an autoimmune cause of superficial bullae) but was experiencing an additional painful vesicular facial rash that lead the team to suspect that her rash was caused by more than one process. She was ultimately found to have a super-imposed HSV infection, and was treated with IV acyclovir as well as high-dose steroids with gradual improvement of her symptoms.
Thanks for an interesting case, Dr. Wang!
1) Always remember to assess for vision changes/ocular involvement in patients with generalized bullous skin conditions
2) Bullous skin conditions can be delineated into tense vs flaccid bullae depending on the depth of skin involvement: subepidermal lesions will produce tense blisters!
3) You may need to involve dermatology for a skin biopsy to figure out the etiology of the bullae, if autoimmune in nature start oral steroids with ultimately steroid sparing immunomodulators for maintenance. Burn surgery might also need to be involved depending on the extent of surface area involved.
Today our wonderful PGY-2 Dr. Dan Corbally led us through a case of a young woman who came in with a concerning cluster of symptoms of subacute fever and chills and diarrhea and an acute rash after receiving ciprofloxacin. We took a moment to review how to describe various concerning skin lesions with the help of our expert dermatology discussant Dr. Nancy Habib. We then learned that the patient had hemodynamic instability about 3 days into her admission and was found to have 4/4 group A strep in her blood cultures! The patient’s skin biopsy ultimately revealed possible toxic shock syndrome, when examined in context with her clinical findings. We then reviewed the management for toxic shock- remember to use both a beta-lactam and clindamycin for best efficacy!
Thank you, Dr. Corbally for the interesting case and Dr. Habib for your teaching!
Today, Dr. Lizzy Hastie presented a case of an elderly gentleman who presented to the ED with worsening bilateral lower extremity swelling and erythema. Although the ED was concerned for cellulitis, we discussed that bilateral cellulitis is very uncommon, and thus decided to take a step back to broaden our differential.
We discussed that when approaching “the red leg,” we can break-up etiologies by laterality and mechanism (bugs, barrier, and blood). Using this approach, we narrowed our diagnosis dramatically! Our expert discussants Drs. Jassal and Habib then helped us to describe the patient’s exam findings (see below), and provided their respective approach to “the red leg.” Dr. Jassal noted that in the clinic, the most common diagnoses to consider include cellulitis (unilateral, fevers, chills) vs stasis dermatitis (bilateral, underlying venous stasis). We then discussed that dermatology should step in if there is no resolution after treating the common conditions or if concerning systemic findings are present. Ultimately, a KOH preparation was performed (see below), and the diagnosis of tinea corporis was made! His symptoms improved with topical and oral terbinafine (Think Terbinafine for Tinea!).
Thank you, Drs. Hastie, Jassal, and Habib for a great case and interesting discussion!
Dr. Leverone presented a case of rash today. He started by telling us this patient presented to the ER for a rash after having been discharged for an admission during which he was told he had EtOH cirrhosis and CKD. We paused to review some rash descriptors (other than maculopapular) that we should all be using when we encounter rashes. Below are some examples: Back to our case… the patient turned out to have leukocytosis and his rash was described as progressive, diffuse, erythematous rash. So then we thought about the differential for diffuse erythematous rash and came up with the following: Note that our expert discussant Dr. Goldenberg reminded us to think of what could be deadly and then what is most common This patient later developed worsening rash and fever, had a mild eosinophilia and was diagnosed with DRESS. Below are some more informative slides on DRESS: Dr. Goldenberg told us to think of dangerous reactions like this
This morning, Dr. Jack Strutner (med-peds PGY2) presented a case of a patient presenting with subacute proximal muscle weakness and photodistributed rash, who was ultimately diagnosed with dermatomyositis. Remember, dermatomyositis is one of the idiopathic inflammatory myopathies: Dr. Soo In Choi, stellar rheumatologist, was our expert discussant. She reminded us that Gottron’s Papules and a Heliotrope Rash are pathognomonic for dermatomyositis. Other cutaneous manifestations that may be seen with dermatomyositis are a photodistributed rash (shawl sign or V sign) and Raynaud’s phenomenon.
We had a joint IM-neuro case conference this morning at the VA with Dr. Chamindra Konersman (neuro guru) as our expert discussant. One of our stellar PGY3’s, Dr. Amit Pandey, presented a case of a patient who presented with a facial droop, ipsilateral hearing loss and vesicular rash, found to have Ramsay-Hunt Syndrome (AKA: herpes zoster oticus). We reviewed a mnemonic to help remember the cranial nerve functions (see left). Remember that the facial nerve (CN VII) also innervates the anterior 2/3 of the tongue, so patients with Ramsay-Hunt Syndrome may have a rash there (example below). Dr. Konersman reminded us that a single physical exam maneuver can really help to guide your diagnostic approach to facial droop. If a patient is unable to raise their eyebrow on the affected side, then it suggests a lower motor neuron lesion in the facial nerve itself. If the patient is able to raise their eyebrow, then it suggests an upper motor neuron
This morning, Masha Barsky presented a classic case of a severe cutaneous drug reaction: Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS). The patient was a middle-aged gentleman who was receiving IV antibiotics for osteomyelitis. Approximately one month after starting antibiotics (Vancomycin, and CTX then Zosyn), he developed acute onset rash, fevers and facial swelling. We reviewed a variety of severe rashes (see slideshow) and focused on the diverse presentation of drug reactions including: exanthematous drug reaction (the typical maculopapular rash we often think of), fixed drug reaction (violacious, severe), Acute Generalized Exanthematous Pustulosis (AGEP) and DRESS. We identified key features of this case that were classic for DRESS including: Onset 2-6 weeks after drug initiation Facial swelling Lymphadenopathy +/- Eosinophilia or “atypical lymphocytes” End-organ damage (transaminase elevation, AKI, etc) We then discussed that the key to treatment is to identify and stop the offending agent and then, if the case is severe, a long taper of systemic steroids can