Frozen sections are unreliable for the diagnosis of necrotizing soft tissue infections.

Necrotizing soft tissue infections are rare but are associated with high rates of morbidity and mortality. The use of bedside or intraoperative frozen sections has been reported to be associated with faster diagnosis and better outcomes; however, to date no large studies have been published to determine the sensitivity and specificity of frozen sections in this setting. Twenty years of cases suspicious for necrotizing soft tissue infection at a large academic referral center were reviewed, blinded to the final clinical diagnosis (gold standard). Cases were assessed for the number of neutrophils, extent of necrosis, presence of thrombi, bacteria, karyorrhexis, and fibrin, and concordance with permanent sections. A total of 166 cases suspicious for necrotizing soft tissue infection had frozen section slides available for review. Sixty-three cases were clinically determined to be positive and 103 negative. Neutrophils, necrosis, thrombi, bacteria, karyorrhexis, and fibrin were present in both positive and negative cases; however, no histological feature or combination of features was found to be both sensitive and specific for necrotizing soft tissue infection. The combined presence of necrosis and frequent neutrophils was 73% sensitive and 68% specific, with a 58% positive predictive value and 80% negative predictive value. The additional observation of bacteria decreased sensitivity to 32%, whereas raising specificity to 91%, with 69% positive predictive value and 68% negative predictive value. Thirty-two cases (19%) contained findings identified on permanent sections (eg, bacteria) not observed on frozen section slides, highlighting the risk of false negatives owing to technical limitations or sampling errors. Frozen sections in necrotizing soft tissue infections and negative cases may show similar histological findings. Combined with the risk of false negatives, these results suggest that frozen sections are likely to be of limited clinical utility due to lack of sensitivity and specificity, and risk for delayed diagnosis and treatment.

2012 Liver resections in the 21st century: we are far from zero mortality.

OBJECTIVES: Recent improvements in surgical technique have extended the indications for liver resection. The aims of this study were to assess whether this extension is associated with a changing patient profile and to evaluate how this potential shift has influenced mortality after liver resection in order to define standard expectations for hepatectomy. METHODS: The characteristics and postoperative outcomes of all patients undergoing elective hepatectomy from 2000 to 2009 were reviewed retrospectively. Multivariate analysis was conducted to determine the factors associated with mortality in the subgroup of patients with malignant disease. RESULTS: Among the 2012 patients in whom hepatectomies were performed, the percentage of patients operated for malignancy increased from 66.4% in 2000 to 82.3% in 2009 (P < 0.001). These patients experienced higher mortality (4.5% versus 0.7%; P < 0.001), were significantly older, and displayed greater comorbidity and underlying parenchymal disease compared with those with benign lesions. Mortality over the entire study period was 3.5% and was fairly stable, dropping from 3.8% in 2000 to 3.1% in 2009 (P = 0.686). On multivariate analysis, age of >60 years, an American Society of Anesthesiologists score of ≥3, major resection, vascular procedure, severe fibrosis (F3-F4) and steatosis of >30% were associated with increased mortality in patients with malignant disease. CONCLUSIONS: The profile of patients undergoing liver resection has changed and now includes more high-risk patients with diseased parenchyma undergoing major hepatectomy for malignancy. This change in patient profile is responsible for the stability in mortality rates over the years.

Essay on Being a Doctor: Patient Mentor.

Through the generosity of Charles R. Millikan, D. Min., vice president for Spiritual Care and Values Integration, an annual award competition was established at Houston Methodist Hospital among the resident staff. To enter the writing competition, residents must submit a poem or essay of 1,000 words or less on the topic, "On Being a Doctor." A committee of seven was selected from Houston Methodist Hospital Education Institute to establish the judging criteria and select the winning entries. The following is the second-place winning entry for 2018; the third-place entry will be published in the next issue of this journal.

Ontogeny of purinergic receptor-regulated Ca2+ signaling in mouse cortical collecting duct epithelium.

Changes in ATP-induced increase in [Ca2+](i) during collecting duct ontogeny were studied in primary monolayer cultures of mouse ureteric bud (UB) and cortical collecting duct (CCD) cells by Fura-PE3 fluorescence ratio imaging. In UB (embryonic day E14 and postnatal day P1) the ATP-stimulated increase (EC(50) approximately 1 microM) in fluorescence ratio (DeltaR(ATP)) was independent of extracellular Ca2+ and insensitive to the P2 purinoceptor-antagonist suramin (1 mM). From day P7 onward when CCD morphogenesis had been completed DeltaR(ATP) increased and became dependent on extracellular Ca2+. This ATP-stimulated Ca2+ entry into CCD cells was non-capacitative and suramin (1 mM)-insensitive, but sensitive to nifedipine (30 microM) and enhanced by Bay K8644 (15 microM), a blocker and an agonist of L-type Ca2+ channels, respectively. Quantitative RT-PCR demonstrated similar mRNA expression of L-type Ca2+ channel alpha1-subunit, P2Y(1), P2Y(2), and P2X(4b) purinoceptors in UB and CCD monolayers while the abundance of P2X(4) mRNA increased with CCD morphogenesis. In conclusion, both embryonic and postnatal cells express probably P2Y(2)-stimulated Ca2+ release from intracellular stores. With development, the CCD epithelium acquires ATP-stimulated Ca2+ entry via L-type Ca2+ channels. This pathway might by mediated by the increasing expression of P2X(4)-receptors resulting in an increasing ATP-dependent membrane depolarization and activation of L-type Ca2+ channels.