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1.
Vet Anaesth Analg ; 50(4): 315-324, 2023 Jul.
Article in English | MEDLINE | ID: mdl-37142463

ABSTRACT

OBJECTIVE: To evaluate the sleep quality, prevalence of fatigue and depressive symptoms in veterinary anaesthesia personnel. STUDY DESIGN: Anonymous online voluntary survey. METHODS: Sleep quality, fatigue, depressive symptoms and self-perceived burnout were scored using the Pittsburgh Sleep Quality Index (PSQI), Fatigue Severity Scale (FSS), Patient Health Questionnaire-9 (PHQ-9) and single-item burnout measure, respectively. Demographic data and questions about work-related fatigue, out-of-hours duty, transport and rest periods were included. PSQI, FSS and PHQ-9 scores were compared using Spearman rank correlation tests. RESULTS: Responses from 393 participants were obtained from an estimated population of 1374 including diplomates of the American and European Colleges of Veterinary An(a)esthesia and Analgesia (43.9%), residency-trained veterinarians (15.6%), residents-in-training (13.8%) and veterinary technicians and nurses (12.0%), from 32 countries. Most were employed in clinical university teaching hospitals (54.2%) or clinical private practice (41.5%). PSQI scores > 5 were reported by 71.2% of respondents, with 52.4% reporting insufficient sleep to meet their job demands. Many showed high or borderline fatigue (56.4%), and 74.7% reported mistakes due to work-related fatigue. Major depressive symptoms (PHQ-9 score ≥ 10) were found in 42.7%, with 19.2% reporting they had thought about suicide or self-harm in the previous 2 weeks. Over half (54.8%) met the criteria for burnout and more veterinary nurses and technicians suffered from burnout than other roles, with 79.6% of this group affected (p < 0.001). Scores for PSQI and FSS [r (388) = 0.40, p < 0.001]; PSQI and PHQ-9 [r (389) = 0.23, p < 0.001]; and FSS and PHQ-9 [r (387) = 0.24, p < 0.001] were all positively correlated. CONCLUSIONS AND CLINICAL RELEVANCE: This survey demonstrates a high prevalence of poor sleep, fatigue, depressive symptoms and burnout in veterinary anaesthesia personnel, and more should be done to improve the health of those in the profession.


Subject(s)
Anesthesia , Depressive Disorder, Major , Animals , Mental Health , Cross-Sectional Studies , Fatigue/epidemiology , Fatigue/etiology , Fatigue/veterinary , Sleep , Surveys and Questionnaires , Anesthesia/adverse effects , Anesthesia/veterinary
2.
PLoS One ; 10(5): e0128076, 2015.
Article in English | MEDLINE | ID: mdl-26018205

ABSTRACT

Acute liver failure is a rare but catastrophic condition which can progress rapidly to multi-organ failure. Studies investigating the onset of individual organ injury such as the liver, kidneys and brain during the evolution of acute liver failure, are lacking. MicroRNAs are short, non-coding strands of RNA that are released into the circulation following tissue injury. In this study, we have characterised the release of both global microRNA and specific microRNA species into the plasma using a porcine model of acetaminophen-induced acute liver failure. Pigs were induced to acute liver failure with oral acetaminophen over 19h±2h and death occurred 13h±3h thereafter. Global microRNA concentrations increased 4h prior to acute liver failure in plasma (P<0.0001) but not in isolated exosomes, and were associated with increasing plasma levels of the damage-associated molecular pattern molecule, genomic DNA (P<0.0001). MiR122 increased around the time of onset of acute liver failure (P<0.0001) and was associated with increasing international normalised ratio (P<0.0001). MiR192 increased 8h after acute liver failure (P<0.0001) and was associated with increasing creatinine (P<0.0001). The increase in miR124-1 occurred concurrent with the pre-terminal increase in intracranial pressure (P<0.0001) and was associated with decreasing cerebral perfusion pressure (P<0.002). Conclusions: MicroRNAs were released passively into the circulation in response to acetaminophen-induced cellular damage. A significant increase in global microRNA was detectable prior to significant increases in miR122, miR192 and miR124-1, which were associated with clinical evidence of liver, kidney and brain injury respectively.


Subject(s)
Acetaminophen/adverse effects , Chemical and Drug Induced Liver Injury/blood , Liver Failure, Acute/blood , Liver Failure, Acute/chemically induced , MicroRNAs/blood , Animals , Disease Models, Animal , Intracranial Pressure/drug effects , Swine
3.
Vet Anaesth Analg ; 42(1): 39-49, 2015 Jan.
Article in English | MEDLINE | ID: mdl-24984762

ABSTRACT

OBJECTIVE: To examine the cardiopulmonary effects of two anesthetic protocols for dorsally recumbent horses undergoing carpal arthroscopy. STUDY DESIGN: Prospective, randomized, crossover study. ANIMALS: Six horses weighing 488.3 ± 29.1 kg. METHODS: Horses were sedated with intravenous (IV) xylazine and pulmonary artery balloon and right atrial catheters inserted. More xylazine was administered prior to anesthetic induction with ketamine and propofol IV. Anesthesia was maintained for 60 minutes (or until surgery was complete) using either propofol IV infusion or isoflurane to effect. All horses were administered dexmedetomidine and ketamine infusions IV, and IV butorphanol. The endotracheal tube was attached to a large animal circle system and the lungs were ventilated with oxygen to maintain end-tidal CO2 40 ± 5 mmHg. Measurements of cardiac output, heart rate, pulmonary arterial and right atrial pressures, and body temperature were made under xylazine sedation. These, arterial and venous blood gas analyses were repeated 10, 30 and 60 minutes after induction. Systemic arterial blood pressures, expired and inspired gas concentrations were measured at 10, 20, 30, 40, 50 and 60 minutes after induction. Horses were recovered from anesthesia with IV romifidine. Times to extubation, sternal recumbency and standing were recorded. Data were analyzed using one and two-way anovas for repeated measures and paired t-tests. Significance was taken at p ≤ 0.05. RESULTS: Pulmonary arterial and right atrial pressures, and body temperature decreased from pre-induction values in both groups. PaO2 and arterial pH were lower in propofol-anesthetized horses compared to isoflurane-anesthetized horses. The lowest PaO2 values (70-80 mmHg) occurred 10 minutes after induction in two propofol-anesthetized horses. Cardiac output decreased in isoflurane-anesthetized horses 10 minutes after induction. End-tidal isoflurane concentration ranged 0.5%-1.3%. CONCLUSION AND CLINICAL RELEVANCE: Both anesthetic protocols were suitable for arthroscopy. Administration of oxygen and ability to ventilate lungs is necessary for propofol-based anesthesia.


Subject(s)
Blood Pressure/drug effects , Dexmedetomidine/pharmacology , Horses , Isoflurane/pharmacology , Ketamine/pharmacology , Propofol/pharmacology , Animals , Body Temperature/drug effects , Cross-Over Studies , Dexmedetomidine/administration & dosage , Female , Heart Rate/drug effects , Isoflurane/administration & dosage , Ketamine/administration & dosage , Male , Propofol/administration & dosage
4.
Liver Int ; 33(4): 544-51, 2013 Apr.
Article in English | MEDLINE | ID: mdl-23331547

ABSTRACT

BACKGROUND: A clinically relevant, translational large animal model of acute liver failure (ALF) is required for testing of novel therapies to prolong survival in acute liver failure, to permit spontaneous liver recovery or to act as a bridge to transplantation. AIMS: The aim was to establish a pig model of acetaminophen-induced ALF that mimics the human clinical syndrome, is managed as in a human intensive care unit and has a predictable survival time. METHODS: Nine female pigs were anaesthetised and instrumented for continuous intensive care monitoring and management using: target-driven protocols for treatment of cardiovascular collapse, metabolic acidosis and electrolyte abnormalities; intermittent positive pressure ventilation; and continuous renal replacement therapy. Six animals were induced to ALF with acetaminophen (paracetamol). Three animals acted as controls. RESULTS: Irreversible acute liver failure, defined as rise in prothrombin time >3 times normal, occurred 19.3 ± 1.8 h after the onset of acetaminophen administration. Death occurred predictably 12.6 ± 2.7 h thereafter, with acute hepatocellular necrosis in all animals. Clinical progression of liver failure mimicked the human condition including development of coagulopathy, intracranial hypertension, hyperammonaemia, cardiovascular collapse, elevation in creatinine, metabolic acidosis and hyperlactataemia. In addition, cardiovascular monitoring clearly demonstrated progressive cardiac dysfunction in ALF. CONCLUSIONS: A reproducible, clinically relevant, intensively managed, large animal model of acute liver failure, with death as a result of multi-organ failure, has been successfully validated for translational studies of disease progression and therapies designed to prolong survival in man.


Subject(s)
Chemical and Drug Induced Liver Injury/therapy , Critical Care , Liver Failure, Acute/therapy , Liver , Acetaminophen , Acid-Base Equilibrium , Acidosis/etiology , Acidosis/physiopathology , Acidosis/therapy , Animals , Biomarkers/metabolism , Cardiovascular Diseases/etiology , Cardiovascular Diseases/physiopathology , Cardiovascular Diseases/therapy , Chemical and Drug Induced Liver Injury/blood , Chemical and Drug Induced Liver Injury/etiology , Chemical and Drug Induced Liver Injury/pathology , Chemical and Drug Induced Liver Injury/physiopathology , Critical Care/methods , Disease Models, Animal , Disease Progression , Female , Hemodynamics , Intracranial Pressure , Liver/metabolism , Liver/pathology , Liver/physiopathology , Liver Failure, Acute/blood , Liver Failure, Acute/chemically induced , Liver Failure, Acute/pathology , Liver Failure, Acute/physiopathology , Monitoring, Physiologic , Multiple Organ Failure/etiology , Multiple Organ Failure/physiopathology , Multiple Organ Failure/therapy , Necrosis , Renal Replacement Therapy , Reproducibility of Results , Respiration, Artificial , Swine , Time Factors
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