Sepsis is one of the leading causes of mortality during the first weeks of life in canine neonates, and early diagnosis is essential to reduce these rates. This study aimed to evaluate changes in clinical, hematological, biochemical, and biomarker parameters (procalcitonin, C-reactive protein, and troponin I levels) in neonatal sepsis in dogs. Descriptive statistics, normality testing, group comparisons, and Pearson or Spearman correlations were performed, with significance set at p < 0.05. Biomarker cut-off values were determined using ROC curve analysis based on sensitivity and specificity above 80%. Thirty-one neonates were included, with 17 animals in the sepsis group (SG) and 14 in the control group (CG). In the assessment of clinical parameters, signs of systemic infection, such as diarrhea, erythema of the body, omphalitis, ecchymoses or hematomas, and cyanosis or necrosis of the extremities, were observed. Neonates in the SG showed bradycardia (p<0.05), hypothermia (p<0.05), and reduced neurological reflexes (p<0.05). Leukopenia (p<0.05), hyperlactatemia (p<0.01), hyperkalemia (p<0.05), and increased cardiac troponin I (p<0.01) were observed in the SG. A negative correlation was detected between the leukocyte count and the lactate concentration (r = -0.59; p<0.01) and between the neutrophil count and the troponin I concentration (r = -0.57; p<0.01). A positive correlation was observed between body temperature and leukocytes (r = 0.54, p < 0.01). Additionally, there was a trend toward thrombocytopenia, hypoglycemia, and increased CRP in the SG, although these findings did not reach statistical significance. The origin of the infections was predominantly maternal (intrauterine or via mastitis), with isolation of beta-hemolytic Streptococcus from uterine swabs (41.2%), Staphylococcus sp. from uterine swabs and milk (35.3%), and Streptococcus sp. from milk only (23.5%). Future serial studies are needed to characterize biomarker kinetics during infection. Early diagnosis of neonatal canine sepsis relies on litter monitoring, clinical signs and laboratory tests, including leukopenia, bacterial culture, lactate (≥3mmol/L), and cardiac troponin I (≥0.1ng/dL).

This study evaluated the effects of underbody warming and heated IV fluids on maternal and neonatal outcomes during cesarean delivery. In a university hospital, 105 pregnant patients were randomized into three groups that dictated heating methods applied during their cesarean delivery: underbody warmer only, underbody warmer plus heated IV fluids, or passive heating with blankets. Primary outcomes were maternal and neonatal body temperatures. Secondary maternal outcomes included intraoperative blood loss, analgesic use, and time to first gas and urination. Secondary neonatal outcomes included cord blood cortisol levels, glucose levels, and Apgar scores. Neonatal temperature, Apgar scores, and maternal intraoperative temperature were significantly higher in the intervention groups. Active warming was associated with lower cortisol levels, reduced analgesic use, and faster recovery. In total, active warming improved maternal recovery and neonatal adaptation, and its routine use as a simple, safe, and effective strategy to enhance perioperative outcomes may be warranted.

Severe acute hypermagnesemia from excessive magnesium (Mg[2+]) exposure is rare but life-threatening and requires prompt recognition. We report a 54-year-old previously healthy man who presented to the emergency department with acute altered consciousness and generalized weakness. Physical examination showed stupor, hypothermia, hypotension, and generalized areflexia. Initial laboratory testing demonstrated mixed respiratory and metabolic acidosis, a normal serum creatinine concentration, and severe hypermagnesemia (serum Mg[2+] concentration, 15.8 mg/dL). The initial 12-lead ECG demonstrated diffuse ST-segment depression, and an artificial intelligence-enabled electrocardiography (AI-ECG) model identified an estimated mortality risk above the 99th percentile. Nasogastric decompression retrieved minimal gastric contents, and initial treatment with intravenous calcium, saline, and a loop diuretic did not produce meaningful neurological improvement. Emergent hemodialysis resulted in rapid recovery of consciousness and a decrease in serum Mg[2+] to 4.9 mg/dL during treatment, together with neurological improvement and a marked decline in AI-ECG-predicted mortality risk. Subsequent history-taking indicated inadvertent ingestion of approximately 100 mL of a private-label artificial hot-spring mineral preparation, for which spa personnel reported a nominal formulation of 30% magnesium chloride, 33% magnesium sulfate, and 10% potassium sulfate. He recovered without residual complications. This case emphasizes that a normal serum creatinine concentration at presentation does not preclude life-threatening magnesium toxicity after a large acute Mg[2+] exposure. Timely hemodialysis should be considered when severe symptoms persist despite initial therapy.

Seasonally recurring hibernation-like states are exceptionally rare in humans, and their neural substrates remain unknown. We investigated the brain of a 57-year-old woman with a > 30-year history of winter-associated hypothermia, neuroendocrine instability, psychomotor suppression and circannual rhythmicity. Postmortem neuropathological analysis revealed preserved hypothalamic and basal forebrain anatomy but profound neurochemical abnormalities. Key peptidergic neuronal populations involved in circadian and neuroendocrine regulation, including arginine vasopressin (AVP), oxytocin (OXT), corticotropin-releasing hormone (CRH) and thyrotropin-releasing hormone (TRH) neurons, showed near-complete loss of immunoreactivity in the SCN, SON and PVN. Immunoreactivity for vasoactive intestinal peptide (VIP) and neurotensin (NT) in the SCN was markedly reduced. These changes were accompanied by markedly reduced synaptophysin immunoreactivity in all hypothalamic regions examined, whereas catecholaminergic neurons were relatively preserved in the PVN and SON. Beyond the hypothalamus, cholinergic neurons in the NBM showed a moderate reduction without evidence of Alzheimer-related pathology. Microglial immunoreactivity was nearly absent in the hypothalamic and extrahypothalamic regions examined, contrasting with preserved GFAP and AQP4 immunoreactivity. Moreover, myelination and microvascular architecture also remained intact. These findings identify a selective hypothalamic and microglial suppression associated with a rare human hibernation-like phenotype and indicate markedly reduced output of core neuroendocrine and circadian circuits during long-standing hypometabolic states. The case also illustrates that recurrent, profound hypothermia can be tolerated over decades without systemic organ failure, highlighting an unexpected degree of human metabolic resilience.

Severe traumatic brain injury (TBI) is a leading cause of death and long-term disability worldwide. Therapeutic hypothermia may lower intracranial pressure (ICP) and reduce metabolic demand. This study aims to compare mild therapeutic hypothermia with controlled normothermia in adult TBI patients undergoing Barbiturate Coma Therapy (BCT), and to explore artificial intelligence (AI)-assisted prognostic models.

Neonatal hypoxic-ischemic encephalopathy (HIE) is a common severe neurological disorder following perinatal asphyxia and a leading cause of neonatal mortality and long-term neurodevelopmental impairments, including cerebral palsy, epilepsy, and cognitive and behavioral deficits. It remains one of the primary causes of death and disability in newborns, imposing a substantial burden on families and society. Although therapeutic hypothermia is currently recognized as an effective intervention, its narrow treatment window, limited patient eligibility, and the persistence of significant sequelae in some affected infants underscore the urgent need for adjunctive therapeutic strategies targeting novel mechanisms. In recent years, short-chain fatty acids (SCFAs), which are metabolites of the gut microbiota, have garnered considerable attention due to their neuroprotective effects via the gut-brain axis. This article systematically reviews the potential mechanisms and therapeutic prospects of SCFAs in neonatal HIE, focusing on their modulation of mitochondrial dysfunction and endoplasmic reticulum stress (ERS).

Critically ill patients often suffer from alterations in body temperature either from disease, injury, exposure, or therapeutic interventions. Therefore, nurses must use evidence to guide decisions in choosing the most appropriate thermometer, route, and technique that accurately and consistently reflects core body temperature. This article will review the evidence for measuring body temperature for critically ill patients. Practical recommendations for measuring body temperature will follow.

Background: Therapeutic hypothermia has significantly improved the prognosis of infants with hypoxic-ischemic encephalopathy (HIE), shifting the focus of follow-up toward the identification of early predictors of preschool neurodevelopmental outcome. This study aimed to evaluate the predictive value of early neurological, developmental and neuroradiological assessments in children with HIE treated with therapeutic hypothermia. Methods: We conducted a prospective longitudinal study including 105 children with HIE treated with therapeutic hypothermia between 2015 and 2022 at a tertiary neonatal center. Early neurological examination using the Hammersmith Infant Neurological Examination (HINE), Griffiths Mental Development Scales at 24 months, brain magnetic resonance imaging (MRI), and neonatal clinical variables were evaluated as predictors of preschool neurodevelopmental outcome. Outcome was classified as favourable or adverse according to cognitive performance and the presence of major neurodevelopmental impairment. Results: Of the 105 children included in the preschool follow-up, 84 (80.0%) had a favourable neurodevelopmental outcome and 21 (20.0%) an adverse outcome. Moderate-to-severe neonatal MRI abnormalities were observed in 11/84 (13.1%) children with favourable outcome and 12/21 (57.1%) with adverse outcome (p < 0.001). Children with adverse outcomes had lower HINE scores at 12 months (p < 0.001) and lower Griffiths Global Developmental Quotients at 24 months (p < 0.001). ROC analyses showed high discrimination for HINE (AUC 0.920), Griffiths Global Developmental Quotient (AUC 0.917), and Griffiths Hearing and Speech Scale (AUC 0.915). Conclusions: Most children with moderate-to-severe HIE treated with therapeutic hypothermia achieved favorable preschool outcomes. Neonatal MRI, followed by standardized neurological and developmental assessments during infancy and toddlerhood, provides complementary information that may progressively refine neurodevelopmental prognostication.

Many animals utilize a survival strategy of hypothermia, inactivity, and a dramatic decrease in their energy metabolism when faced with a shortfall in energy supplies. Mice, for example, show daily torpor that may last several hours to bridge the lack of energy availability in a cold environment. While our recent studies identified a population of neurons in the median preoptic nucleus (MnPO) necessary for fasting-induced torpor regulation, the specific brain circuits that trigger energy conservation in response to food restriction are unknown. We show here that the energy state of the animal is conveyed to preoptic neurons by inputs from the arcuate nucleus (ARC), a region known to be indispensable for driving metabolic and behavioral adaptations to the fasted state. We first found that the activity of ARC neurons expressing Agouti-Related Peptide (ARC AgRP ) is required for the generation of fasting-induced torpor. Then, we showed that torpor-active ARC AgRP neurons innervate the preoptic area of the hypothalamus (POA), including the MnPO. Using optogenetic methods, we also found that activating the ARC AgRP →MnPO pathway induces key features of torpor: decreased body temperature, bradycardia, reduction of energy expenditure, and suppression of brown adipose tissue thermogenesis. Remarkably, we also show that inhibition of the ARC AgRP →MnPO brain circuit entirely prevents fasting-induced torpor. Furthermore, we identified that both NPY and GABA are neuromodulators used by ARC AgRP neurons to enable hypothermic responses during starvation. Our studies provide a detailed view of a hypothalamic pathway enabling energy conservation, a survival mechanism in conditions of low energy availability.

BackgroundAccidental hypothermia is an unintentional drop in core temperature below 35 °C, typically resulting from exposure to cold environmental conditions. Clinical presentations may vary widely depending on the severity of hypothermia and the presence of coexisting conditions complicating diagnosis and treatment. We report a case of accidental hypothermia caused by environmental exposure and associated with cardiogenic shock from a myocardial infarction with complete heart block.Case PresentationA group of ski tourers found a 62-y-old male skier at 3000 m in severe distress with abdominal pain, shivering, and profound exhaustion. On arrival at a mountain hut, he was agitated, then became unconscious and bradycardic with a weak femoral pulse. Once advanced medical equipment reached the hut, a 12-lead electrocardiogram showed an inferior ST-elevation myocardial infarction (STEMI) with complete third-degree atrioventricular block and a ventricular escape rhythm. The first measurable axillary temperature was 32.2 °C. Consciousness progressively improved, but bradycardia persisted during rewarming. The patient was evacuated 6 h after the diagnosis of acute STEMI. He underwent percutaneous coronary intervention and was successfully treated with a stent.ConclusionsThis case illustrates that hypothermia and environmental factors can complicate the diagnosis of atypical presentations of life-threatening conditions, such as STEMI, and how unexpected clinical findings not fully explained by hypothermia may indicate the presence of an underlying condition. In such situations, hypothermia staging systems should be used with caution. Early electrocardiography, awareness of cognitive biases, and the use of safe rewarming practices are essential to ensure timely diagnosis and prevent complications.