Case Presentation:
A 75–year–old female with a history of schizophrenia and diabetes mellitus was transferred to our hospital for sepsis and worsening rash. The rash first appeared on the flexor surfaces of her upper extremities, progressing to her entire body over 3 months. At the referring hospital, she was empirically started on vancomycin, cefepime, and fluconazole. Upon admission, vital signs revealed hypothermia (35.5°C), HR 81, and BP 100/62. Exam revealed confluent, thick, hyperkeratotic plaques with fissures involving 80% of her entire body surface area, including the scalp and face. Laboratory results revealed: hgb 10.7 g/dl, wbc 5.1 mm3, plt 67,000 mm3, cr 1.3 mg/dl, with normal liver functions test, PT, PTT. The outside hospital blood cultures were positive for E. coli. Dermatology was consulted and skin scrapings with oil prep revealed Sarcoptes scabiei (scabies). Treatment was started with oral ivermectin, permethrin cream and urea cream. Vancomycin and fluconazole were discontinued. Underlying immune deficiencies were ruled out. Her skin desquamated and she developed acute leukopenia, thrombocytopenia and anemia. On hospital day 3, she became acutely hypotensive and hypothermic (29°C) despite resuscitation with heated fluids and antibiotic broadening. She became more hypotensive and hypoxic and next of kin opted for comfort care measures only. She died on hospital day 10. Hospital staff that were exposed to this patient were contacted by infection control to monitor for signs and symptoms of scabies.
Discussion:
Crusted scabies (also known as Norwegian scabies) is a rare presentation of ordinary scabies (Sarcoptes scabiei) and is highly contagious. While a typical scabies infection will manifest with only a few mites on skin scrapings, patients with crusted scabies will have thousands to millions of mites. Skin lesions can mimic a wide variety of skin diseases such as eczema, psoriasis, keratosis follicularis, and drug eruption, thus recognition can be difficult and often delayed. Patients with cognitive deficiencies or with a compromised immune system are at higher risk for developing crusted scabies. For those patients with extensive skin involvement, there is increased mortality due to risk of infection and sepsis. Given the highly contagious nature of crusted scabies, this remains an important diagnosis for hospital infection control management. Prompt recognition, determination of outbreak magnitude, employing immediate infection control strategies, education and reassurance are essential.
Conclusions:
Crusted scabies is a rare diagnosis with high morbidity and mortality. Due to its atypical presentation and highly contagious nature, hospitalists need to have high clinical suspicion for this diagnosis. We speculate that the incidence of crusted scabies may rise due to increased numbers of immunocompromised patients admitted to hospitals. Hospital infection control remains paramount for coordinated efforts for prevention and treatment of this diagnosis.