On Tuesday, 12 April 1726, Robert Worger fell from his horse at Barnham Down, Kent, hitting his head on the ground ‘with strong Force’. Unconscious, he was taken to Bridge, a nearby village, and laid out at the home of Sarah Knot, ‘Nurse and Landlady to the Patient’, bled several times, given ‘volatile mixture’ (ammonia, salt, opium) and treated with purgatives and clysters. He vomited as many as five times over the course of his illness and delivered ‘half a score [of] very foul, stinking, loose Stools’. Worger died, ‘without … Agony’, at 5 am, Thursday, 21 April 1726, after living for 8 days in the care of Knot, his wife, two surgeons, an assistant, an apothecary and two physicians, Christopher Packe and John Gray. An autopsy was performed – the next night, by the light of a single candle – and, although there was little extravasation and no severe fractures or depressions in the skull, slight abnormalities were found: the cerebellum ‘Turgid with Blood’, two small fissures appeared on the os frontis. Worger’s illness and death spurred months of rebarbative public controversy: in order to exonerate themselves, both physicians published pamphlets and letters, secured affidavits, importuned surgeons and Worger’s relatives for support, vied for authority and mastery over the circumstances of the case and argued about propriety, professionalism and conduct. This paper explores Worger’s case – controversy about diagnosis and prognosis, concern with ‘knowledge and deportment’, with the status of medical offices and medical jurisprudence and with relationships between physicians, patients, surgeons – as an instance of learned medical controversy in early eighteenth-century England.

Introduction: Pulse check by manual palpation (MP) is an unreliable skill even in the hands of healthcare professionals. In the context of cardiac arrest, this may translate into inappropriate chest compressions when a pulse is present, or conversely omitting chest compressions when one is absent. To date, no study has assessed the utility of B-mode ultrasound (US) for the detection of a carotid pulse. The primary objective of this study is to assess the time required to detect a carotid pulse in live subjects using US compared to the standard MP method. Methods: This is a prospective randomized controlled cross-over non-inferiority trial. Health care professionals from various backgrounds were invited to participate. They attended a 15 minute focused US workshop on identification of the carotid pulse. Following a washout period, they were randomized to detect a pulse in live subjects either by MP first or by US first. Both pulse check methods were timed for each participant on 2 different subjects. The primary outcome measure was time to carotid pulse detection in seconds. Secondary outcome measures included comfort levels of carotid pulse detection measured on a 100mm visual analog scale (VAS), and rates of prolonged pulse checks (greater than 5 or 10 seconds) for each technique. Mean pulse detection times were compared using Students t-test. The study was powered to determine whether US was not slower than MP by greater than 2 seconds. Results: A total of 93 participants completed the study. Time to detect pulse was 4.2 (SD=3.4) seconds by US compared with 4.7 (SD=6.5) seconds by MP (P=0.43). Seventeen (18%) participants took >5 seconds to identify the carotid pulse using US compared to 19 (20%) by MP (P=0.74). Eight (9%) candidates took >10 seconds to identify the pulse using US compared to 9 (10%) by MP (P=0.81). Prior to training, participants had a higher comfort level using MP than US pulse checks (67 vs 26 mm, P<0.001). Following the study, participants reported higher comfort levels using US than MP (88 vs 78 mm, P<0.001). Conclusion: Carotid pulse detection in live subjects was not slower using US as compared to MP in this study. A brief teaching session was sufficient to improve confidence of carotid pulse identification even in those with little to no previous US training. The preliminary results from this study provide the groundwork for larger studies to evaluate this pulse check method for patients in actual cardiac arrest.

Excited delirium syndrome (ExDS) is defined by marked agitation and confusion with sympathomimetic surge and incessant physical struggle, despite futility, which may lead to profound pathophysiologic changes and sudden death. Severe metabolic derangements, including lactic acidosis, rhabdomyolysis, and hyperthermia, occur. The pathophysiology of excited delirium is a subject of ongoing basic science and clinical research. Positive associations with ExDS include male gender, mental health disorders, and substance abuse (especially sympathomimetics).

Excited delirium syndrome patients often exhibit violent, psychotic behavior and have “superhuman” strength which can result in the patient fighting with police and first responders. Continued struggle can cause a patient with ExDS to experience elevated temperature (T) and acidosis which causes enzymes to fail, leading to sudden death from cardiovascular collapse and multi-system organ failure. Therefore, effective early sedation is optimal to stop this fulminant process.

Treatment of ExDS must be focused on rapidly, safely, and effectively sedating the patient and providing intensive, supportive care. Benzodiazepines, like midazolam, may not be ideal to sedate ExDS patients since their onset takes several minutes, and their side effects include loss of airway control and respiratory depression. Injectable antipsychotic medications have a relatively slow onset and may cause prolongation of the QTc interval. Ketamine is the ideal medication to sedate patients with ExDS. Ketamine has a rapid, predictable onset within three to four minutes when given by intramuscular (IM) injection. It does not adversely affect airway control, breathing, heart rate, or blood pressure (BP).

In this retrospective case series, prehospital scenarios in which ExDS patients received ketamine by paramedics for sedation, and their subsequent treatment in the emergency department (ED) and hospital, are described. It is demonstrated that ketamine administered by paramedics in the prehospital setting of a community hospital based Emergency Medical Services (EMS) system is a safe and effective treatment for ExDS.

ScaggsTR, GlassDM, HutchcraftMG, WeirWB. Prehospital Ketamine is a Safe and Effective Treatment for Excited Delirium in a Community Hospital Based EMS System. Prehosp Disaster Med. 2016;31(5):563–569.

In this paper we investigate the role of spatial effects in determining thedynamics of a subclass of signalling pathways characterised by their ability todemonstrate oscillatory behaviour. To this end, we formulate a simple spatial model of thep53 network that accounts for both a negative feedback and a transcriptional delay. We show that the formation of protein density patterns can depend on the shape of the cell, position of the nucleus, and the protein diffusion rates. Thetemporal changes in the total amounts of protein are also subject to spatial influences. The level of DNA damage required to induce sustained oscillations, forinstance, depends on the morphology of the cell. The model also provides a newinterpretation of experimentally observed undamped oscillations in p53 levels in single cells.Our simulations reveal that alternate sequences of high- and low-amplitudeoscillations can occur. We propose that the digital pulses may correspond to snap-shots ofour high-amplitude sequences. Shorter waiting-times between subsequent time-lapse fluorescence microscopy images in combination with lower detection thresholds may reveal the irregular high-frequency oscillations suggested by our spatialmodel.