Nosocomial COVID-19 infection in the era of vaccination and antiviral therapy.

BACKGROUND AND AIMS: Coronavirus disease 2019 (COVID-19) vaccination and antiviral therapies have altered the course of the COVID-19 pandemic through mitigating severe illness and death. However, immunocompromised, elderly and multimorbid patients remain at risk of poor outcomes and are overrepresented in hospital populations. The aim of this study was to describe the characteristics and outcomes of patients with nosocomial COVID-19 infection. METHODS: This was a retrospective, observational study of patients who acquired COVID-19 after 7 days of hospital admission within the Southern Adelaide Local Health Network (SALHN) in South Australia between 1 June 2022 and 30 November 2022. Data were ascertained from the electronic medical record and the South Australian registry of births, deaths and marriages. RESULTS: Of 1084 COVID-19 inpatient cases managed in SALHN, 295 (27%) were nosocomial, with 215 included in the study. The median age of patients was 80 years (interquartile range [IQR], 68-88 years), the median Charlson Comorbidity Index score was 5 (IQR, 4-7) and 6% were immunocompromised. Most nosocomial COVID-19 infections were of mild severity (81%). The 30-day all-cause mortality rate following COVID-19 infection was 6%, and, in most cases, a cause of death other than COVID-19 was recorded on the death certificate. CONCLUSION: The majority of cases of nosocomial COVID-19 infection were mild, with a lower mortality rate than in earlier studies. This finding is likely attributable to immunity through vaccination and prior infection, early antiviral therapy and attenuated severity of the Omicron variant. The high proportion of nosocomial infections supports ongoing infection control measures.

Does pre-injury clopidogrel use increase the risk of intracranial haemorrhage post head injury in adult patients? A systematic review and meta-analysis.

BACKGROUND: Several current guidelines do not include antiplatelet use as an explicit indication for CT scan of the head following head injury. The impact of individual antiplatelet agent use on rates of intracranial haemorrhage is unclear. The primary objective of this systematic review was to assess if clopidogrel monotherapy was associated with traumatic intracranial haemorrhage (tICH) on CT of the head within 24 hours of presentation following head trauma compared with no antithrombotic controls. METHODS: Eligible studies were non-randomised studies with participants aged ≥18 years old with head injury. Studies had to have conducted CT of the head within 24 hours of presentation and contain a no antithrombotic control group and a clopidogrel monotherapy group.Eight databases were searched from inception to December 2020. Assessment of identified studies against inclusion criteria and data extraction were carried out independently and in duplicate by two authors.Quality assessment and risk of bias (ROB) were assessed using the Newcastle-Ottawa Quality Assessment tool and Risk Of Bias In Non-randomised Studies of Interventions (ROBINS-I) tool. Meta-analysis was conducted using a random-effects model and reported as an OR and 95% CI. RESULTS: Seven studies were eligible for inclusion with a total of 21 898 participants that were incorporated into the meta-analysis. Five studies were retrospective. Clopidogrel monotherapy was not significantly associated with an increase in risk of tICH compared with no antithrombotic controls (OR 0.97, 95% CI 0.54 to 1.75). Heterogeneity was high with an I2 of 75%. Sensitivity analysis produced an I2 of 21% and did not show a significant association between clopidogrel monotherapy and risk of tICH (OR 1.16, 95% CI 0.87 to 1.55). All studies scored for moderate to serious ROB on categories in the ROBINS-I tool. CONCLUSION: Included studies were vulnerable to confounding and several were small-scale studies. The results should be interpreted with caution given the ROB identified. This study does not provide statistically significant evidence that clopidogrel monotherapy patients are at increased risk of tICH after head injury compared with no antithrombotic controls. PROSPERO REGISTRATION NUMBER: CRD42020223541.

Deep and profound hypothermia in haemorrhagic shock, friend or foe? A systematic review.

INTRODUCTION: Survival in exsanguinating cardiac arrest patients is poor, as is neurological outcome in survivors. Hypothermia has traditionally been seen as harmful to trauma patients and associated with increased mortality; however, there has been speculation that cooling to very low temperatures (≤20°C) could be used to treat haemorrhagic trauma patients by the induction of a suspended animation period through extreme cooling, which improves survival and preserves neurological function. This has been termed emergency preservation and resuscitation (EPR). METHODS: A systematic review of the literature was used to examine the evidence base behind the use of deep and profound hypothermia in haemorrhagic shock (HS). It included original research articles (human or animal) with cooling to ≤20°C after HS or an experimental model replicating it. Normovolaemic cardiac arrest, central nervous system injury and non-HS models were excluded. RESULTS: Twenty articles using 456 animal subjects were included, in which 327 were cooled to ≤20°C. All studies describing good survival rates were possible using EPR and 19/20 demonstrated that EPR can preserve neurological function after prolonged periods of circulatory arrest or minimal circulatory flow. This additional period can be used for surgical intervention to arrest haemorrhage in HS that would otherwise be lethal. CONCLUSIONS: The outcomes of this review have significant implications for application to human patients and the ongoing human clinical trial (EPR for Cardiac Arrest from Trauma). Current evidence suggests that hypothermia ≤20°C used in the form of EPR could be beneficial to the HS patient.

Hypothermia in trauma.

Hypovolaemic shock that results through traumatically inflicted haemorrhage can have disastrous consequences for the victim. Initially the body can compensate for lost circulating volume, but as haemorrhage continues compensatory mechanisms fail and the patient's condition worsens significantly. Hypovolaemia results in the lethal triad, a combination of hypothermia, acidosis and coagulopathy, three factors that are interlinked and serve to worsen each other. The lethal triad is a form of vicious cycle, which unless broken will result in death. This report will focus on the role of hypothermia (a third of the lethal triad) in trauma, examining literature to assess how prehospital temperature control can impact on the trauma patient. Spontaneous hypothermia following trauma has severely deleterious consequences for the trauma victim; however, both active warming of patients and clinically induced hypothermia can produce particularly positive results and improve patient outcome. Possible coagulopathic side effects of clinically induced hypothermia may be corrected with topical haemostatic agents, with the benefits of an extended golden hour given by clinically induced hypothermia far outweighing these risks. Active warming of patients, to prevent spontaneous trauma induced hypothermia, is currently the only viable method currently available to improve patient outcome. This method is easy to implement requiring simple protocols and contributes significantly to interrupting the lethal triad. However, the future of trauma care appears to lie with clinically induced therapeutic hypothermia. This new treatment provides optimism that in the future the number of deaths resulting from catastrophic haemorrhaging may be significantly lessened.