Livedoid Vasculopathy with Severe Debilitating Neuropathy in a Prior Professional Athlete.

Livedoid vasculopathy (LV) can be a challenging diagnosis with an interesting pathophysiology. LV is an uncommon diagnosis that can be easily mistaken for more common skin conditions, especially in a person of color who may be underrepresented in pathology images used in medical education. LV has an average of five years from initial presentation to diagnosis, possibly due to providers not having it on their differential for lower extremity ulcerations. Prolonged time to diagnosis can potentially lead to life-changing complications. We present a case of a former professional sprinter who became debilitated by neuropathy secondary to complications from LV. He was seen multiple times and had an extensive work-up exploring a broad differential including autoimmune etiologies, hypercoagulable disorders, neuropathies, and other vascular disorders before reaching the diagnosis. This case emphasizes the importance of early diagnosis and treatment with a multidisciplinary team to help prevent the progression of these symptoms. We break down an extensive work-up that involves a multidisciplinary team including dermatology, hematology, neurology, rheumatology, and vascular surgery. This case will also highlight examples of LV in a patient with a dark skin complexion, which can be challenging to find in current literature. We additionally show images that demonstrate many of the classic pathologic findings associated with LV and how those can help lead to the diagnosis along with detailed descriptions of those findings. Classic physical exam findings including atrophic blanche and lower extremity ulcerations are highlighted. We also review LV's history, diagnosis, and treatment to help readers achieve a better understanding of the disease.

Cefepime-Induced Generalized Fixed Drug Eruption With Morbilliform Rash.

Fixed drug eruption (FDE) is a cutaneous reaction that characteristically recurs in the same locations upon re-exposure to the offending drug(s). The typical presentation of FDEs is single or multiple violaceous plaques with hyperpigmentation due to inflammation. The causative agents for FDEs include antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, barbiturates, and anticonvulsants. We present an interesting case of a generalized fixed drug eruption secondary to cefepime that resolved with the cessation of the offending drug and the institution of antihistamines and topical steroids.

Relaxation of H2O from its /04>- vibrational state in collisions with H2O, Ar, H2, N2, and O2.

We report rate coefficients at 293 K for the collisional relaxation of H2O molecules from the highly excited /04>(+/-) vibrational states in collisions with H2O, Ar, H2, N2, and O2. In our experiments, the mid R:04(-) state is populated by direct absorption of radiation from a pulsed dye laser tuned to approximately 719 nm. Evolution of the population in the (/04>(+/-)) levels is observed using the combination of a frequency-quadrupled Nd:YAG laser, which selectively photolyses H2O(/04>(+/-)), and a frequency-doubled dye laser, which observes the OH(v=0) produced by photodissociation via laser-induced fluorescence. The delay between the pulse from the pump laser and those from the photolysis and probe lasers was systematically varied to generate kinetic decays. The rate coefficients for relaxation of H2O(/04>(+/-)) obtained from these experiments, in units of cm3 molecule(-1) s(-1), are: k(H2O)=(4.1+/-1.2) x 10(-10), k(Ar)=(4.9+/-1.1) x 10(-12), k(H2)=(6.8+/-1.1) x 10(-12), k(N2)=(7.7+/-1.5) x 10(-12), k(O2)=(6.7+/-1.4) x 10(-12). The implications of these results for our previous reports of rate constants for the removal of H2O molecules in selected vibrational states by collisions with H atoms (P. W. Barnes et al., Faraday Discuss. Chem. Soc. 113, 167 (1999) and P. W. Barnes et al., J. Chem. Phys. 115, 4586 (2001).) are fully discussed.