Objective: To measure the relationship between lactate and mortality in hospital inpatients. Main outcomes of interest were 3-day, 30-day, and 1-year all-cause mortality. Design: Retrospective cohort study, October 2011 to September 2013. Setting: University-affiliated US Veterans Affairs Hospital. Patients: All inpatients with lactate level measured during the study period. Measurements: Analysis of peak lactate level (mmol/L) during the most recent admission for patients who died, and peak lactate level during an admission for surviving patients. Covariates including sepsis, ICU admission, code blue and rapid response calls, medical vs surgical ward, liver disease, kidney disease, and hospice status were recorded. Results: In total, 3325 inpatients were included; 564 patients had sepsis. Median lactate 1.7 mmol/L (interquartile range [IQR] 1.2-2.6). The 3-day, 30-day, and 1-year mortality were 2.5%, 10%, and 24%, respectively. A lactate level cutoff of ⩾4 mmol/L had best test characteristics (sensitivity 52.4%, specificity 91.4%) to predict increased 3-day mortality. Unadjusted risk ratio of death in 3 days for lactate ⩾4 was 10.3 (95% confidence interval [CI] 6.8-15.7). Patients with sepsis had a consistently higher risk of death compared with patients without sepsis for any given level of lactate. Adjusted odds ratio (OR) of 3-day mortality for lactate ⩾4 was 7.6 (95% CI 4.6-12.5); 30-day mortality was 2.6 (95% CI 1.9-3.6); and 1-year mortality was 1.8 (95% CI 1.4-2.6). Lactates in the normal range (<1.7) were also independently associated with 30-day and 1-year mortality. Conclusions: Lactate predicts risk of death in all patients, although patients with sepsis have a higher mortality for any given lactate level. We report the novel finding that serum lactate, including normal values, is associated with long-term mortality.

Clevidipine-induced pulmonary shunting is a little-reported adverse effect, manifesting as refractory hypoxemia, which may cause significant patient harm. We present the case of a mechanically ventilated patient admitted to the intensive care unit following a neurosurgical procedure. He was treated postoperatively with clevidipine for blood pressure management, and within 16 hours, he developed profound refractory hypoxemia, requiring increased ventilatory support. A workup for other causes was negative. The hypoxemia recovered within 1 hour of clevidipine discontinuation. Though other calcium channel blockers have been reported to cause pulmonary shunting from vasodilation, this is a novel case report for clevidipine-induced hypoxemia.

Penetrating trauma from sea urchin (Echinoidea) spines has been shown to cause numerous cutaneous reactions, ranging from initial pain that rapidly dissipates and resolves to chronic inflammation and formation of characteristic sea urchin granulomas. Many of these skin-colored or violaceous papules and nodules form weeks to months after injury, and may be surgically excised. Histopathologic examination commonly shows well-defined granulomas, the majority of which represent sarcoidal-type granulomas. Other microscopic patterns, such as foreign body reactions and chronic inflammation, have also been shown. Retained spine fragments are birefringent on polarized microscopic examination and are most likely found in the dermal layer. Herein, we describe a case of traumatic sea urchin cutaneous injury with a unique early cutaneous trauma reaction in a young male who lived in Hawaii. Histopathologic exam was significant for retained spines in the layer of the stratum corneum, but no signs of granulomatous inflammation were observed. This case report emphasizes the unique features of our case and reviews the common clinical and histopathologic features of sea urchin cutaneous reactions.

Contaminated surfaces in a hospital serve as reservoirs for pathogen spread. The aim of this study was to evaluate UV lights in preventing the spread of a DNA tracer in an intensive care unit (ICU) through sterilization of highly touched surfaces. In a prospective trial, a non-pathogenic DNA virus was inoculated onto surfaces in an ICU patient room. Investigators swabbed frequently touched surfaces in non-inoculated ICU rooms at 24, 48, and 96 h post inoculation. Culture specimens were analyzed for the presence of viral DNA via PCR. After baseline data were obtained, UV lights were deployed in a standardized fashion onto vitals monitors, ventilators, keyboards, and intravenous (IV) pumps. Inoculation and culturing were then repeated. Prior to UV implementation, the DNA tracer disseminated to 10.10% of tested surfaces in non-inoculated rooms at 48 h. Post UV light deployment, only 1.20% of surfaces tested positive for the DNA tracer after 48 h. UV decontamination significantly retarded the spread of the virus DNA, with a relative reduction of 90% at 48 h from 10.10% of surfaces pre UV to 1.20% of surfaces post UV (p < 0.0001). UV decontamination holds the potential to confer protection to patients by reducing the number of surfaces that can serve as a nidus for transfer.