Propranolol, post-traumatic stress disorder, and intensive care: incorporating new advances in psychiatry into the ICU.

Post-traumatic stress disorder (PTSD) is a common complication of an ICU admission. Rarely is there a continuation of care, which is aimed at screening for and treating this debilitating disease. Current treatment options for PTSD are held back by inconsistent efficacy, poor evidence, and a lack of understanding of its psychopathology. Without 'gold standard' assessment techniques to diagnose PTSD after an ICU admission, the development of care pathways is hindered. This paper advocates for two interwoven advances in psychiatric care (specifically for PTSD) after ICU: (1) incorporate the monitoring and treating of psychiatric co-morbidities during extended patient follow-up, and (2) rapidly adopting the latest research to maximize its benefit. The discovery that memories were not fixed, but malleable to change, set off a sequence of experiments that have revolutionized the approach to treating PTSD. It is hoped that the phenomenon of reconsolidation can be exploited therapeutically. In the act of remembering and re-storing traumatic memories, propranolol can act to dissociate the state of sympathetic arousal from their recollection. Often, ICU patients have multiple physical co-morbidities that may be exacerbated, or their treatment disrupted, by such a pervasive psychological condition. The rapid uptake of new techniques, aimed at reducing PTSD after ICU admission, is necessary to maximize the quality of care given to patients. Increasingly, the realization that the role of intensive care specialists may extend beyond the ICU is changing clinical practice. As this field advances, intensivists and psychiatrists alike must collaborate by using the latest psychopharmacology to treat their patients and combat the psychological consequences of experiencing the extremes of physiological existence.

The benefits of tight glycemic control in critical illness: Sweeter than assumed?

Hyperglycemia has long been observed amongst critically ill patients and associated with increased mortality and morbidity. Tight glycemic control (TGC) is the clinical practice of controlling blood glucose (BG) down to the "normal" 4.4-6.1 mmol/L range of a healthy adult, aiming to avoid any potential deleterious effects of hyperglycemia. The ground-breaking Leuven trials reported a mortality benefit of approximately 10% when using this technique, which led many to endorse its benefits. In stark contrast, the multi-center normoglycemia in intensive care evaluation-survival using glucose algorithm regulation (NICE-SUGAR) trial, not only failed to replicate this outcome, but showed TGC appeared to be harmful. This review attempts to re-analyze the current literature and suggests that hope for a benefit from TGC should not be so hastily abandoned. Inconsistencies in study design make a like-for-like comparison of the Leuven and NICE-SUGAR trials challenging. Inadequate measures preventing hypoglycemic events are likely to have contributed to the increased mortality observed in the NICE-SUGAR treatment group. New technologies, including predictive models, are being developed to improve the safety of TGC, primarily by minimizing hypoglycemia. Intensive Care Units which are unequipped in trained staff and monitoring capacity would be unwise to attempt TGC, especially considering its yet undefined benefit and the deleterious nature of hypoglycemia. International recommendations now advise clinicians to ensure critically ill patients maintain a BG of <10 mmol/L. Despite encouraging evidence, currently we can only speculate and remain optimistic that the benefit of TGC in clinical practice is sweeter than assumed.

Injury-Reduction Programs Containing Neuromuscular Neck Exercises and the Incidence of Soccer-Related Head and Neck Injuries.

CONTEXT: Concern is growing among soccer players, coaches, and parents regarding head and neck injuries, including concussion, particularly from heading a ball. Thus, we need to explore soccer-specific head injury risk-reduction initiatives. One such initiative is to condition the neck musculature of young players by adding neuromuscular neck exercises to existing injury-reduction exercise programs. OBJECTIVE: To investigate the effect of neuromuscular neck exercises completed as part of an injury risk-reduction exercise program on the incidence of soccer-related head and neck injuries in adolescent soccer players. DESIGN: Prospective cohort study. SETTING: Two sports high schools and 6 soccer clubs during the 2021 soccer season. PATIENTS OR OTHER PARTICIPANTS: A total of 364 male and female soccer players, aged 12 to 18 years. INTERVENTION(S): Members of 1 sports high school and 2 soccer clubs performed neuromuscular neck exercises as part of an injury-reduction program during training (neck training group). Members of another sports high school and 4 soccer clubs performed an injury-reduction program but without neck exercises (comparison group). MAIN OUTCOME MEASURE(S): Self-reported injury data were collected from each player at the end of the season and used to calculate incidence rate ratios (IRRs) with 95% CIs. RESULTS: In total, 364 players completed the study, including 146 players in the neck training group and 218 players in the comparison group. Despite players in the neck training group being less likely to self-report a concussion (IRR = 0.23; 95% CI = 0.03, 1.04) and pain on heading a ball (IRR = 0.62; 95% CI = 0.34, 1.07), only a lower incidence of possible concussive events (IRR = 0.38; 95% CI = 0.14, 0.90; P < .05) was significant. CONCLUSIONS: Integrating neuromuscular neck exercises into injury-reduction exercise programs has the potential to reduce the risk of adolescent soccer players sustaining a possible concussive event, concussion, or pain on heading a ball.

A case of type B lactic acidosis as a complication of chronic myelomonocytic leukaemia: a case report and review of the literature.

INTRODUCTION: Type B lactic acidosis represents a rare and often lethal complication of haematological malignancy. Here, we present a patient who developed a type B lactic acidosis presumably due to a concurrent chronic myelomonocytic leukaemia. Upon swift initiation of cytoreductive chemotherapy (doxorubicin), the lactic acidosis was rapidly brought under control. This case adds to the literature reporting other haematological malignancies that can cause a type B lactic acidosis and its successful treatment. CASE PRESENTATION: We report the case of a 77-year-old Caucasian man brought to our Accident and Emergency department following an unwitnessed collapse; he was found surrounded by coffee-ground vomit. Although haemodynamically stable on admission, he rapidly deteriorated as his lactic acid rose. An initial arterial blood gas revealed a pH of 7.27 and lactate of 18mmol/L (peaking at 21mmol/L). CONCLUSIONS: A high degree of clinical suspicion for haematological malignancy should be held when presented with a patient with lactic acidosis in clinical practice, even without evidence of poor oxygenation or another cause. Treatment with emergency chemotherapy, in lieu of a definitive diagnosis, was rapidly successful at lowering lactate levels within 8 hours. This may suggest a causal and perhaps direct relationship between lactic acid production and the presence of leukemic cells. Veno-venous haemofiltration had no apparent effect on reducing the lactic acidosis and therefore its benefit is questioned in this setting, especially at the cost of delaying chemotherapy. In the face of a life-threatening lactic acidosis, pragmatic clinical judgement alone may justify the rapid initiation of chemotherapy.