Håkan Sandler

CPR-related injuries after manual or mechanical chest compressions with the LUCAS™ device: A multicentre study of victims after unsuccessful resuscitation ☆

AIM The reported incidence of injuries due to cardiopulmonary resuscitation using manual chest compressions (manual CPR) varies greatly. Our aim was to elucidate the incidence of CPR-related injuries by manual chest compressions compared to mechanical chest compressions with the LUCAS device (mechanical CPR) in non-survivors after out-of-hospital cardiac arrest. METHODS In this prospective multicentre trial, including 222 patients (83 manual CPR/139 mechanical CPR), autopsies were conducted after unsuccessful CPR and the results were evaluated according to a specified protocol. RESULTS Among the patients included, 75.9% in the manual CPR group and 91.4% in the mechanical CPR group (p=0.002) displayed CPR-related injuries. Sternal fractures were present in 54.2% of the patients in the manual CPR group and in 58.3% in the mechanical CPR group (p=0.56). Of the patients in the manual CPR group, there were 64.6% with at least one rib fracture versus 78.8% in the mechanical CPR group (p=0.02). The median number of rib fractures among patients with rib fractures was 7 in the manual CPR group and 6 in the mechanical CPR group. No CPR-related injury was considered to be the cause of death. CONCLUSION In patients with unsuccessful CPR after out-of-hospital cardiac arrest, rib fractures were more frequent after mechanical CPR but there was no difference in the incidence of sternal fractures. No injury was deemed fatal by the pathologist.

Fatal intoxication by dextromethorphan: A report on two cases

A report is given of two young people who died after intake of dextromethorphan, one by suicide and the other for uncertain reasons. To our knowledge this is the first reported fatal intoxications with this drug.

Effect of stable fish oil on arterial thrombogenesis, platelet aggregation, and superoxide dismutase activity

We examined the influence of dietary stable fish oil on aortic thrombosis, platelet aggregation, and superoxide dismutase (SOD) activity in a rat model. Twenty-nine Sprague-Dawley rats were fed regular chow supplemented with stable fish oil preparation (for 1 or 3 weeks), and 37 rats fed regular chow served as controls. The abdominal cavity was opened, and the abdominal aorta isolated. Whatman paper impregnated with 35% FeCl3 was wrapped around the surface of the aorta, and aortic flow was continuously recorded. In control rats, an occlusive platelet-fibrin-rich thrombus was formed in 21 +/- 3 min. Dietary fish oil in a time-dependent fashion delayed time to thrombus formation (24 +/- 2 min in rats fed fish oil for 1 week and 31 +/- 2 min in rats fed fish oil for 3 weeks), inhibited platelet aggregation (21 +/- 5% vs. 45 +/- 6%; p < 0.01) and increased SOD activity (p < 0.01). We conclude that dietary supplementation with stable fish oil delays formation of arterial thrombus, probably by reducing platelet aggregation and oxidative stress-associated arterial injury.

Alzheimer changes are common in aged drivers killed in single car crashes and at intersections

With increasing age, diseases affecting the cognitive functions are more frequent. These diseases may increase the risk for fatal car crashes. We analyzed the frequency of neuropathological alterations characteristic of Alzheimers disease (i.e. neuritic and diffuse plaques, and neurofibrillary tangles) in two association areas of the brain, parietal and frontal cerebral cortex, from 98 fatally injured aged drivers. In the age groups of 65-75 and over 75 years of age, 50% and 72% of the drivers, respectively, had neuritic plaques in either parietal and/or frontal cortex. In 14% of all killed drivers the number of neuritic plaques reached the Consortium to Establish a Registry for Alzheimers Disease (CERAD) age-related histologic score C, which indicates the diagnosis of Alzheimers disease (AD), and an additional 33% had score B, which suggests the diagnosis of AD. Neuropathological AD changes were most common in the brains of drivers killed in single vehicle crashes, followed by multivehicle crashes at intersections and least common in multivehicle crashes elsewhere, but the differences did not reach statistical significance. In a great majority (80-85%) of cases the killed aged driver was the guilty party of the crash. The results imply, that incipient AD may contribute to fatal crashes of aged drivers, and therefore the forensic autopsy of these victims should include neuropathological examination.

Comparison of computed tomography and autopsy in detection of injuries after unsuccessful cardiopulmonary resuscitation.

AIM Computed tomography (CT) has been suggested as an aid or even a replacement for autopsy. The aim of this trial was to study the conformity of the two methods in finding injuries in non-surviving patients after unsuccessful cardiopulmonary resuscitation. METHODS In this prospective study, 31 patients were submitted to a CT prior to autopsy after unsuccessful resuscitation attempts. Pathological findings were noted by both the radiologist and the pathologists in a specified protocol. The pathologists and radiologist were blinded from each others results. RESULTS CT and autopsy revealed rib fractures in 22 and 24 patients respectively (kappa=0.83). In 8 patients, CT revealed more rib fractures than autopsy; and in 12 patients, autopsy revealed more rib fractures than CT. In 7 patients, neither method showed any rib fractures. The mean difference between the two methods in detecting rib fractures was 0.16 (S.D.: ± 3.174, limits of agreement: -6.19 to 6.51). The kappa value for sternal fractures was 0.49. A total of 260 pathological findings were noted by CT and 244 by autopsy. The average patient showed a median of 9 injuries (every fracture counted as one injury), independent of the method used in detecting the injuries. CONCLUSIONS There was a strong concordance between the two methods in finding rib fractures but not sternal fractures and these results support the concept of CT as a valuable complement to autopsy in detecting rib fractures after unsuccessful cardiopulmonary resuscitation but not as a replacement. Other injuries did not show the same concordance.

Effect of a synthetic leukocyte elastase inhibitor on thrombin-induced pulmonary edema in the rat.

The effect of a synthetic leukocyte elastase inhibitor on thrombin-induced pulmonary edema was studied in rats. The chloromethylketone human neutrophil elastase inhibitor, ICI 200,355, blunted rat leukocyte elastase activity in rat lung tissue. Administration of thrombin produced a significant increase (p < .01) in lung weight. The wet weight to dry weight ratio (WW/DW) and relative water contents were also significantly elevated (p < .01). Pretreatment with ICI 200,355 (200 micrograms/kg h-1) resulted in significant reductions (p < .05) in lung weight and a tendency to decrease WW/DW and water content compared with animals given thrombin alone. It is possible that the elastase inhibitor effectively reduced the rate of thrombin-induced pulmonary edema by attenuation of increased vascular permeability.

The importance of nonlinear tissue modelling in finite element simulations of infant head impacts

Despite recent efforts on the development of finite element (FE) head models of infants, a model capable of capturing head responses under various impact scenarios has not been reported. This is hypothesized partially attributed to the use of simplified linear elastic models for soft tissues of suture, scalp and dura. Orthotropic elastic constants are yet to be determined to incorporate the direction-specific material properties of infant cranial bone due to grain fibres radiating from the ossification centres. We report here on our efforts in advancing the above-mentioned aspects in material modelling in infant head and further incorporate them into subject-specific FE head models of a newborn, 5- and 9-month-old infant. Each model is subjected to five impact tests (forehead, occiput, vertex, right and left parietal impacts) and two compression tests. The predicted global head impact responses of the acceleration–time impact curves and the force–deflection compression curves for different age groups agree well with the experimental data reported in the literature. In particular, the newly developed Ogden hyperelastic model for suture, together with the nonlinear modelling of scalp and dura mater, enables the models to achieve more realistic impact performance compared with linear elastic models. The proposed approach for obtaining age-dependent skull bone orthotropic material constants counts both an increase in stiffness and decrease in anisotropy in the skull bone—two essential biological growth parameters during early infancy. The profound deformation of infant head causes a large stretch at the interfaces between the skull bones and the suture, suggesting that infant skull fractures are likely to initiate from the interfaces; the impact angle has a profound influence on global head impact responses and the skull injury metrics for certain impact locations, especially true for a parietal impact.

Studies on the role of thromboxane in thrombin-induced pulmonary insufficiency in the rat.

During infusion of thrombin in rats pulmonary arterial pressure rose from 15 +/- 2 to 35 +/- 3 mmHg and mean arterial pressure fell from 120 +/- 6 to 49 +/- 27 mmHg. Plasma thromboxane B2 (TxB2) increased from 0.3 +/- 0.04 to 3.6 +/- 0.5 ng/ml. Ninety minutes later the lung weight and albumin concentration in the lung were increased (2.21 +/- 0.13 g and 22.7 +/- 4.7 mg/g) compared with controls (1.12 +/- 0.14 g and 8.5 +/- 0.9 mg/g). An inhibitor of thromboxane synthetase, Dazoxiben R, reduced the elevated pulmonary arterial pressure and the elevated plasma TxB2 concentration following infusion of thrombin. Ninety minutes after infusion of thrombin, the in vitro synthesis of TxB2 in lung tissue was increased. Dazoxiben and antineutrophil serum reduced this synthesis of TxB2 in vitro. The lung weight (2.18 +/- 0.20 g) and lung albumin concentration (21.4 +/- 3.4 mg/g) was not affected by Dazoxiben. The results indicate that TxA2 is an important mediator of the pressure changes in the early phase after infusion of thrombin and that neutrophils are associated with thromboxane formation in the lung tissue.

A non-fatal intoxication and seven deaths involving the dissociative drug 3-MeO-PCP

INTRODUCTION 3-methoxyphencyclidine (3-MeO-PCP) appeared on the illicit drug market in 2011 and is an analogue of phencyclidine, which exhibits anesthetic, analgesic and hallucinogenic properties. In this paper, we report data from a non-fatal intoxication and seven deaths involving 3-MeO-PCP in Sweden during the period March 2014 until June 2016. CASE DESCRIPTIONS The non-fatal intoxication case, a 19-year-old male with drug problems and a medical history of depression, was found awake but tachycardic, hypertensive, tachypnoeic and catatonic at home. After being hospitalized, his condition worsened as he developed a fever and lactic acidosis concomitant with psychomotor agitation and hallucinations. After 22h of intensive care, the patient had made a complete recovery. During his hospitalization, a total of four blood samples were collected at different time points. The seven autopsy cases, six males and one female, were all in their twenties to thirties with psychiatric problems and/or an ongoing drug abuse. METHODS 3-MeO-PCP was identified with liquid chromatography (LC)/time-of-flight technology and quantified using LC-tandem mass spectrometry. RESULTS In the clinical case, the concentration of 3-MeO-PCP was 0.14μg/g at admission, 0.08μg/g 2.5h after admission, 0.06μg/g 5h after admission and 0.04μg/g 17h after admission. The half-life of 3-MeO-PCP was estimated to 11h. In the autopsy cases, femoral blood concentrations ranged from 0.05μg/g to 0.38μg/g. 3-MeO-PCP was the sole finding in the case with the highest concentration and the cause of death was established as intoxication with 3-MeO-PCP. In the remaining six autopsy cases, other medications and drugs of abuse were present as well. CONCLUSION Despite being scheduled in January 2015, 3-MeO-PCP continues to be abused in Sweden. Exposure to 3-MeO-PCP may cause severe adverse events and even death, especially if the user does not receive life-supporting treatment.

Decreased lung hyaluronan in a model of ARDS in the rat: Effect of an inhibitor of leukocyte elastase

Abstract Background. Hyaluronan (HA) is a component of the extracellular matrix in lung tissue and is normally present at low concentrations in blood. HA is rapidly cleared from blood by the liver. Increased concentrations of plasma HA have been found in patients with acute respiratory distress syndrome (ARDS). We investigated changes in HA levels in plasma, bronchoalveolar lavage fluid (BALF), and lung, and their relationship to pretreatment with a leukocyte elastase inhibitor in a rat model of ARDS. Methods. Rats were randomly assigned to three groups: control, thrombin, and thrombin plus elastase inhibitor. By use of a radiometric assay, HA was measured in lungs, BALF, and plasma. Tissue samples from the lungs were stained for HA and examined microscopically. Liver circulation and cardiac output were monitored using radiolabeled microspheres. Results. Infusion of thrombin produced a pronounced increase in wet weight to dry weight ratio, and relative lung water content. This increase was blunted by a leukocyte elastase inhibitor. A decrease in lung HA and increases in both BALF and plasma HA were found. The leukocyte elastase inhibitor counteracted not only the decrease in lung tissue HA, but also the increase in plasma HA. Histologically, there was decreased HA-staining of peribronchial and perivascular areas in the injured rat lung. Decreased liver perfusion was observed after infusion of thrombin. Conclusions. The decrease in lung HA may be involved in the development of pulmonary edema in this ARDS model, and leukocyte elastase may be one cause of this decrease. In addition, an elevated plasma HA level may be an indicator of lung injury.