Both coronavirus disease 2019 (COVID‐19) and heat stroke have symptoms of fever or hyperthermia and the difficulty in distinguishing them could lead to a strain on emergency medical care. To mitigate the potential confusion that could arise from actions for preventing both COVID‐19 spread and heat stroke, particularly in the context of record‐breaking summer season temperatures, this work offers new knowledge and evidence that address concerns regarding indoor ventilation and indoor temperatures, mask wearing and heat stroke risk, and the isolation of older adults. Specifically, the current work is the second edition to the previously published guidance for handling heat stroke during the COVID‐19 pandemic, prepared by the “Working group on heat stroke medical care during the COVID‐19 epidemic,” composed of members from four organizations in different medical and related fields. The group was established by the Japanese Association for Acute Medicine Heatstroke and Hypothermia Surveillance Committee. This second edition includes new knowledge, and conventional evidence gleaned from a primary selection of 60 articles from MEDLINE, one article from Cochrane, 13 articles from Ichushi, and a secondary/final selection of 56 articles. This work summarizes the contents that have been clarified in the prevention and treatment of infectious diseases and heat stroke to provide guidance for the prevention, diagnosis, and treatment of heat stroke during the COVID‐19 pandemic.
Background Vasopressin is a second-line vasoactive agent for refractory septic shock. Vasopressin loading is not generally performed because of the lack of evidence for its effects and safety. However, based on our previous findings, we hypothesized it can predict the responsibility to vasopressin infusion with safety, and prospectively examined it in the present study. Methods Vasopressin loading was performed via the intravenous administration of a bolus of 1 U, followed by its continuous infusion at 1U/h in patients with septic shock treated with ≥ 0.2 μg/kg/min noradrenaline. An arterial pressure wave analysis was conducted, and endocrinological tests were performed immediately prior to vasopressin loading. We classified patients into responders/non-responders based on mean arterial pressure (MAP) changes after vasopressin loading. Based on our previous findings, the lower tertile of MAP changes was selected as the cut-off. The change in the catecholamine index (CAI) after 6 h was assigned as the primary outcome. Digital ischemia, mesenteric ischemia, and myocardial ischemia during the admission period were prospectively and systematically recorded as adverse events. Results Ninety-two patients were registered during the study period and examined. Sixty-two patients with a MAP change > 22 mmHg were assigned as responders and the others as non-responders. Blood adrenocorticotropic hormone levels were significantly higher in non-responders. Stroke volume variations were higher in responders before loading, while stroke volume and dP/dtmax were higher in responders after loading. Median CAI changes were − 10 in responders and 0 in non-responders, which was significantly lower in the former (p < 0.0001). AUROC of MAP change with vasopressin loading to predict CAI change < 0 after continuous infusion was 0.843 with sensitivity of 0.92 and specificity of 0.77. Ischemia events were observed in 5 cases (5.4%). Conclusions Vasopressin loading may be safely introduced for septic shock. Vasopressin loading may be used to predict responses to its continuous infusion and select appropriate strategies to increase blood pressure.
Adequate protein delivery is recommended in the acute phase of critical illness with kidney dysfunction. However, the influence of the protein and nitrogen loads has not yet been clarified. Patients admitted to the intensive care unit were included. In the former period, patients received standard care (0.9 g/kg/day protein). In the latter, patients received the intervention of active nutrition therapy with high protein delivery (1.8 g/kg/day protein). Fifty patients in the standard care group and 61 in the intervention group were examined. Maximum blood urea nitrogen (BUN) on days 7-10 were 27.9 (17.3, 38.6) vs 33 (26.3, 51.8) (mg/dl) (p = 0.031). The maximum difference in BUN increased [31.3 (22.8, 55) vs 50 (37.3, 75.9) mg/dl (p = 0.047)] when patients were limited to an estimated glomerular filtration rate (eGFR) <50 ml/min/1.73 m 2 . This difference increased further when patients were limited to eGFR <30 ml/min/1.73 m 2 . No significant differences were observed in maximum Cre or in the use of RRT. In conclusion, the provision of 1.8 g/kg/day protein was associated with an increase in BUN in critically ill patients with kidney dysfunction; however, it was tolerated without the need for RRT.
Diarrhea is one of the most common complications associated with enteral nutrition in hospitalized patients. Oligomeric enteral nutrition has been considered to reduce the incidence of diarrhea. We herein introduced and examined the effects of a specific oligomeric enteral nutrition with the low-molecular-weight whey peptides, Peptino ® in critically ill patients with refractory diarrhea or at high risk of mesenteric ischemia. A retrospective study of a consecutive case series was conducted. Patients were divided into two groups: enteral nutrition products were switched to Peptino ® (switching group) and Peptino ® was the initial enteral nutrition product (first initiation group). Sixty-eight patients were administered Peptino ® in the ICU. Diarrhea occurred in 28.3% of patients in the switching group and 13.3% in the first initiation group. EN failure with gastrointestinal intolerance was observed in 6 patients (8.8%). Diarrhea resolved in 29 out of the 35 patients (82.9%) with diarrhea prior to the switch to Peptino ® . Diarrhea cessation within 24 h of the initiation of Peptino ® was achieved in 11 patients (31.4%) and within 24-48 h in 12 (34.3%). Mesenteric ischemia was not detected in any patients. In conclusion, Peptino ® may be effective against diarrhea and gastrointestinal intolerance in critical care nutrition.
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