Reducing Aortic Barotrauma and Vascular Extracellular Matrix Degradation by Pacemaker-Mediated QRS Widening.

Background The extent of pressure-related damage might be related to acceleration rate of the applied pressure (peak dP/dt) in the vascular system. In this study, we sought to determine whether dP/dt applied to the aortic wall (aortic dP/dt) and in turn vascular extracellular matrix degradation can be mitigated via modulation of left ventricular (LV) contractility (LV dP/dt) by pacemaker-mediated desynchronization. Methods and Results First, in 34 patients, changes in aortic dP/dt values in 3 aortic segments in response to pacemaker-mediated stepwise QRS widening leading to gradual desynchronization of the LV contraction by means of steadily changed atrioventricular delay (AVD) with temporary dual-chamber pacing was examined before and after beta-blocker (15 mg IV metoprolol) administration. Second, serum matrix metalloproteinase-9 levels were measured in the 20 patients with permanent pacemaker while they were on sinus rhythm with normal QRS width and 3 weeks after wide QRS rhythm ensured by dual pacing, dual sensing, and dual response to sensing with short AVD. LV dP/dt substantially correlated with dP/dt measured in ascending (r=0.83), descending (r=0.89), and abdominal aorta (r=0.96). QRS width strongly correlated with dP/dt measured in ascending (r=-0.95), descending (r=-0.92), and abdominal (r=-0.96) aortic segments as well. In patients with permanent pacemaker, wide QRS rhythm led to a significant reduction in serum matrix metalloproteinase-9 levels (from 142.5±32.9 pg/mL to 87.5±32.4 pg/mL [P<0.001]) at the end of 3 weeks follow-up. Conclusions QRS prolongation by short AVD dual pacing, dual sensing, and dual response to sensing results in concomitant decreases in peak dP/dt values in the LV and in all aortic segments with or without background beta-blocker administration, which in turn led to a significant reduction in circulating matrix metalloproteinase-9 levels. Registration URL: https://www.clini​caltr​ials.gov; Unique identifier: NCT03665558.

A Fire Extinguisher Death: The Macklin Effect.

We present the case of an adult white man found dead in a psychiatric institution with fine white powder (monoammonium phosphate) deposited over the entire face after he insufflated the contents of a dry chemical fire extinguisher. Fine white powder was present within the mouth and sinuses and lined the upper airways. On opening the thoracic cavity, approximately 500 g of fine white powder was present within the right thoracic cavity. The esophagus was ruptured. Traumatic emphysema of the posterior sternum wall was present (pneumomediastinum). The ethmoid bones were fractured by the barotrauma. On polarization of the lung tissue, birefringent material was noted deposited along the bronchovascular sheaths and in a subpleural distribution. Death was probably due to a combination of barotrauma and asphyxia.This case study provides strong evidence in support of the etiology and pathophysiology of the Macklin effect. It also provides for the first visual evidence of the phenomenon.

Scuba diving death: Always due to drowning? Two forensic cases and a review of the literature.

Scuba diving is an increasingly common recreational activity. We describe the physiopathology of barotrauma in two cases where death was caused by pulmonary barotrauma while diving. An inspection and autopsy were carried out in both cases. The autopsy data were supported by post-mortem radiological investigation. Histological and toxicological analyses were also carried out, and dive computer and tank manometer analysis performed. In both cases, the cause of death was attributable to arterial gas embolism, resulting from pulmonary barotrauma subsequent to pulmonary over-distension. The dive computer analysis and the tank manometer allowed us to understand what happened underwater. In our opinion, a multidisciplinary approach is crucial in order to clarify the cause of death. Some pathological conditions and risk factors should be considered before diving.

Death of a seven-month-old child in a washing machine: a case report.

The authors present a case which brings out a unique modality of child homicide by placing the baby in a washing machine and turning it on. The murder was perpetrated by the baby's mother, who suffered from a serious depressive disorder. A postmortem RX and then a forensic autopsy were performed, followed by histologic examinations and toxicology. On the basis of the results of the autopsy, as well as the histology and the negative toxicological data, the cause of death was identified as acute asphyxia. This diagnosis was rendered in light of the absence of other causes of death, as well as the presence of typical signs of asphyxia, such as epicardial and pleural petechiae and, above all, the microscopic examinations, which pointed out a massive acute pulmonary emphysema. Regarding the cause of the asphyxia, at least two mechanisms can be identified: drowning and smothering. In addition, the histology of the brain revealed some findings that can be regarded as a consequence of the barotrauma due to the centrifugal force applied by the rotating drum of the washing machine. Another remarkable aspect is that we are dealing with a mentally-ill assailant. In fact, the baby's mother, after a psychiatric examination, was confirmed to be suffering from a mental illness-a severe depressive disorder-and so she was adjudicated not-guilty-by-reason-of-insanity. This case warrants attention because of its uniqueness and complexity and, above all, its usefulness in the understanding of the pathophysiology of this particular manner of death.

Airway pressure release ventilation during ex vivo lung perfusion attenuates injury.

OBJECTIVE: Critical organ shortages have resulted in ex vivo lung perfusion gaining clinical acceptance for lung evaluation and rehabilitation to expand the use of donation after circulatory death organs for lung transplantation. We hypothesized that an innovative use of airway pressure release ventilation during ex vivo lung perfusion improves lung function after transplantation. METHODS: Two groups (n = 4 animals/group) of porcine donation after circulatory death donor lungs were procured after hypoxic cardiac arrest and a 2-hour period of warm ischemia, followed by a 4-hour period of ex vivo lung perfusion rehabilitation with standard conventional volume-based ventilation or pressure-based airway pressure release ventilation. Left lungs were subsequently transplanted into recipient animals and reperfused for 4 hours. Blood gases for partial pressure of oxygen/inspired oxygen fraction ratios, airway pressures for calculation of compliance, and percent wet weight gain during ex vivo lung perfusion and reperfusion were measured. RESULTS: Airway pressure release ventilation during ex vivo lung perfusion significantly improved left lung oxygenation at 2 hours (561.5 ± 83.9 mm Hg vs 341.1 ± 136.1 mm Hg) and 4 hours (569.1 ± 18.3 mm Hg vs 463.5 ± 78.4 mm Hg). Likewise, compliance was significantly higher at 2 hours (26.0 ± 5.2 mL/cm H2O vs 15.0 ± 4.6 mL/cm H2O) and 4 hours (30.6 ± 1.3 mL/cm H2O vs 17.7 ± 5.9 mL/cm H2O) after transplantation. Finally, airway pressure release ventilation significantly reduced lung edema development on ex vivo lung perfusion on the basis of percentage of weight gain (36.9% ± 14.6% vs 73.9% ± 4.9%). There was no difference in additional edema accumulation 4 hours after reperfusion. CONCLUSIONS: Pressure-directed airway pressure release ventilation strategy during ex vivo lung perfusion improves the rehabilitation of severely injured donation after circulatory death lungs. After transplant, these lungs demonstrate superior lung-specific oxygenation and dynamic compliance compared with lungs ventilated with standard conventional ventilation. This strategy, if implemented into clinical ex vivo lung perfusion protocols, could advance the field of donation after circulatory death lung rehabilitation to expand the lung donor pool.

Traumatic lung injury attributed to tornadic activity-induced barometric pressure changes in two dogs.

CASE DESCRIPTION A 7-year-old castrated male Italian Greyhound (dog 1) and an approximately 1-year-old female Labrador Retriever (dog 2) were evaluated because of respiratory distress 8 and 10 days, respectively, after a tornado. CLINICAL FINDINGS No obvious external injuries were identified auscultation revealed decreased bronchovesicular sounds in the affected hemithorax of both dogs. Clinicopathologic changes were mild, with evidence of inflammation in both dogs. Thoracic radiography of both dogs revealed pneumothorax and pleural effusion with effacement of the diaphragm; findings on CT included severe pulmonary atelectasis of affected lung lobes with normal bronchial tree configurtion and no evidence of diaphragmatic hernia. TREATMENT AND OUTCOME Exploratory thoracotomy of both dogs confirmed CT findings Pulmonary parenchymal damage consistent with a large rupture was found in both patients. A large hematoma was adhered to the ruptured lung lobe of dog 1. Grossly affected lung tissue was removed; histologic examination revealed atelectasis, pulmonary fib osis, thrombosis, and minimal (dog 1) to marked (dog 2) inflammation Microbial culture of lung tissue yielded no growth for dog 1 and Streptococcus spp and Escherichia coli susceptible to amoxicillin-clavulanic acid for dog 2. Dog 1 had a recurrence of pneumothorax treated by drainage with a thoracostomy tube 1 month after surgery. Eighteen months after surgery, both dogs were reportedly doing well. CLINICAL RELEVANCE Development of clinical signs after a tornado, together with clinical, diagnostic imaging, surgical, and histologic findings led to a presumptive diagnosis of pulmonary barotrauma for both dogs. Long-term outcome for these dogs, treated at a referral hospital, was good.

A Dynamic Rabbit Model of Sinus Barotrauma and Its Related Pathology.

BACKGROUND: This study was undertaken to establish a dynamic animal model of sinus barotrauma (SB). METHODS: The right nasal cavities of 65 rabbits were filled with sponges to obstruct the right ostiomeatal complex (OMC), while in the left nasal cavities, the left OMC was kept clear. The rabbits were exposed to hypobaric chamber simulation. The right sinuses were assigned as the model group, randomly divided into 13 subgroups with 5 in each subgroup, while the left sinuses were assigned as the control group. The hypobaric chamber simulation involved 6 pairs of ascending/descending speeds (100 m · s(-1), 75 m · s(-1), 50 m · s(-1)) to 2 altitudes (13,123 ft or 6562 ft). The ascending/descending speed for Model Group 13 was 15 m · s(-1) to an altitude of 13,123 ft. The control group was not exposed to hypobaric chamber simulation or obstruction of the OMC. All rabbits were monitored for behavior and via nasal endoscopy, MRI, and mucosal pathology, and statistically analyzed. RESULTS: SB appeared at the ascending/descending speeds of 50 m · s(-1), 75 m · s(-1), and 100 m · s(-1). SB was more obvious at 100 m · s(-1) than at 50 m · s(-1) and 75 m · s(-1), and SB happened mainly at altitudes between 0-6562 ft. Based on behavior during hypobaric chamber simulation and the results of endoscopic morphology, imaging, and cell pathology, SB could be divided into mild, moderate, and severe. DISCUSSION: By obstructing the OMC and using hypobaric chamber simulation at high ascending/descending speeds and altitude, a dynamic rabbit model of SB at various degrees was established. The severity of SB was proportional to the ascending/descending speeds and mainly seen below 6562 ft.

Experimental modeling of pulmonary barotrauma.

The main causes of pulmonary barotrauma include loss of consciousness or panic attack of a diver and emergence from underwater with a constricted glottis. However, numerous publications and our observations indicate that the majority of fully symptomatic cases of pulmonary barotrauma develop without any evident errors in the ascending technique. Therefore, an attempt was made to examine such cases using the experimental model of pulmonary barotrauma designed by the authors. The experiment was conducted on 32 rabbits divided into three groups: Group C--not subjected to any treatment; Group E--with induced pulmonary barotrauma; and Group CT--subjected only to compression followed by quick decompression. In Groups E and CT, the same morphological markers of pulmonary barotrauma were detected in the lungs, although their severity varied. Morphological markers of pulmonary barotrauma were observed both in the group where the tube was not ob-structed (E) and in animals exposed only to rapid decompression (CT)

Macroscopic barotrauma caused by stiff and soft-tipped airway exchange catheters: an in vitro case series.

BACKGROUND: Many airway management guidelines include the use of airway exchange catheters (AECs). There are reports, however, of harm from their use, from both malpositioning and in particular from the administration of oxygen via an AEC leading to barotrauma. METHODS: We used an in vitro pig lung model to investigate the safety of administering oxygen at 4 different flow rates from a high-pressure source via 2 different AECs: a standard catheter and a soft-tipped catheter. Experiments were performed with the catheters positioned either above the carina or below it at the first point of resistance to advancement (hold-up). The experiments were then repeated to produce a series of 32 cases. RESULTS: With an AEC positioned above the carina, we did not observe macroscopic lung damage after the administration of oxygen. The administration of oxygen through an AEC positioned below the carina resulted in macroscopic barotrauma regardless of the rate of oxygen delivery. Increasing speed of oxygen flow led to faster and more extensive damage. Use of an "injector" at 2.5 or 4 bar led to instantaneous macroscopic lung damage and advancement of the AEC through the lung tissue. Our observations were the same when both types of AECs were used. CONCLUSIONS: Our results are consistent with reports of harm during the use of AECs and demonstrate the risk of administering oxygen through these devices when they are positioned below the carina. An indicator, ideally made on an AEC at the time of manufacture and designed to lie at the same level as the teeth, may be useful in preventing the insertion of that AEC beyond the level of the carina and improve the safety of using such devices.

Diving fatality investigations: recent changes.

Modifications to the investigation procedures in diving fatalities have been incorporated into the data acquisition by diving accident investigators. The most germane proposal for investigators assessing diving fatalities is to delay the drawing of conclusions until all relevant diving information is known. This includes: the accumulation and integration of the pathological data; the access to dive computer information; re-enactments of diving incidents; post-mortem CT scans and the interpretation of intravascular and tissue gas detected. These are all discussed, with reference to the established literature and recent publications.

Lower neurocognitive function in U-2 pilots: Relationship to white matter hyperintensities.

OBJECTIVE: Determine whether United States Air Force (USAF) U-2 pilots (U2Ps) with occupational exposure to repeated hypobaria had lower neurocognitive performance compared to pilots without repeated hypobaric exposure and whether U2P neurocognitive performance correlated with white matter hyperintensity (WMH) burden. METHODS: We collected Multidimensional Aptitude Battery-II (MAB-II) and MicroCog: Assessment of Cognitive Functioning (MicroCog) neurocognitive data on USAF U2Ps with a history of repeated occupational exposure to hypobaria and compared these with control data collected from USAF pilots (AFPs) without repeated hypobaric exposure (U2Ps/AFPs MAB-II 87/83; MicroCog 93/80). Additional comparisons were performed between U2Ps with high vs low WMH burden. RESULTS: U2Ps with repeated hypobaric exposure had significantly lower scores than control pilots on reasoning/calculation (U2Ps/AFPs 99.4/106.5), memory (105.5/110.9), information processing accuracy (102.1/105.8), and general cognitive functioning (103.5/108.5). In addition, U2Ps with high whole-brain WMH count showed significantly lower scores on reasoning/calculation (high/low 96.8/104.1), memory (102.9/110.2), general cognitive functioning (101.5/107.2), and general cognitive proficiency (103.6/108.8) than U2Ps with low WMH burden (high/low WMH mean volume 0.213/0.003 cm(3) and mean count 14.2/0.4). CONCLUSION: In these otherwise healthy, highly functioning individuals, pilots with occupational exposure to repeated hypobaria demonstrated lower neurocognitive performance, albeit demonstrable on only some tests, than pilots without repeated exposure. Furthermore, within the U2P population, higher WMH burden was associated with lower neurocognitive test performance. Hypobaric exposure may be a risk factor for subtle changes in neurocognition.

A forensic investigation into the etiology of bat mortality at a wind farm: barotrauma or traumatic injury?

Migrating bats have increased mortality near moving turbine blades at wind farms. The authors evaluated competing hypotheses of barotrauma and traumatic injury to determine the cause. They first examined the utility of lungs from salvaged bat carcasses for histopathologic diagnosis of barotrauma and studied laboratory mice as a model system. Postmortem time, environmental temperature, and freezing of carcasses all affected the development of vascular congestion, hemorrhage, and edema. These common tissue artifacts mimicked the diagnostic criteria of pulmonary barotrauma; therefore, lung tissues from salvaged bats should not be used for barotrauma diagnosis. The authors next compared wind farm (WF) bats to building collision (BC) bats collected near downtown Chicago buildings. WF bats had an increased incidence in fracture cases and specific bone fractures and had more external lacerations than BC bats. WF bats had additional features of traumatic injury, including diaphragmatic hernia, subcutaneous hemorrhage, and bone marrow emboli. In summary, 73% (190 of 262) of WF bats had lesions consistent with traumatic injury. The authors then examined for ruptured tympana, a sensitive marker of barotrauma in humans. BC bats had only 1 case (2%, 1 of 42), but this was attributed to concurrent cranial fractures, whereas WF bats had a 20% (16 of 81) incidence. When cases with concurrent traumatic injury were excluded, this yielded a small fraction (6%, 5 of 81) of WF bats with lesions possibly consistent with barotrauma etiology. Forensic pathology examination of the data strongly suggests that traumatic injury is the major cause of bat mortality at wind farms and, at best, barotrauma is a minor etiology.

[Case report: fatal diving-accident. Or: accident while diving?]. / Tödlicher Tauchunfall. Oder: Unfall während des Tauchens mit Todesfolge?

This example of a fatal diving accident shows how challenging such cases can be in pre-hospital and clinical care. There is no common mechanism in diving fatalities and more than one group of disorders coming along with decompression sickness. Diving medicine is not an element of medical education, which results in insecurity and hampers adequate therapy of diving incidents. This is aggravated by an insufficient availability of hyperbaric chambers in Germany.

Effects of barotrauma and mitigation methods on released Australian bass Macquaria novemaculeata.

The effects of barotrauma on the short-term mortality and physical condition of Australian bass Macquaria novemaculeata were investigated after being: (1) conventionally angled and released during two tournaments in deep impoundments and (2) released untreated or subjected to venting or recompression during a manipulative experiment. All fish were released into two 20 m deep bathy-cages and monitored for 3 days. Of 238 M. novemaculeata angled during the tournaments, 43 (18·1%) had clinical signs of barotrauma or were vented and five of these later died (11·6% mortality). Catch histories varied significantly between both barotrauma and non-barotrauma fish and tournaments, but only hook ingestion significantly influenced mortality (P < 0·05). During the manipulative experiment, venting significantly influenced mortality (13·3%) compared to no treatment or recompression (no deaths). Magnetic resonance images and dissections of barotrauma fish indicated large variation among clinical signs. On the basis of these results, wherever possible M. novemaculeata suffering barotrauma should be immediately released with no treatment. Fish that are unable to resubmerge should be recompressed, while those held in live wells and released in shallow water should be vented.

Ventilator-induced lung injury: the anatomical and physiological framework.

Since its introduction into the management of the acute respiratory distress syndrome, mechanical ventilation has been so strongly interwoven with its side effects that it came to be considered as invariably dangerous. Over the decades, attention has shifted from gross barotrauma to volutrauma and, more recently, to atelectrauma and biotrauma. In this article, we describe the anatomical and physiologic framework in which ventilator-induced lung injury may occur. We address the concept of lung stress/strain as applied to the whole lung or specific pulmonary regions. We challenge some common beliefs, such as separately studying the dangerous effects of different tidal volumes (end inspiration) and end-expiratory positive pressures. Based on available data, we suggest that stress at rupture is only rarely reached and that high tidal volume induces ventilator-induced lung injury by augmenting the pressure heterogeneity at the interface between open and constantly closed units. We believe that ventilator-induced lung injury occurs only when a given threshold is exceeded; below this limit, mechanical ventilation is likely to be safe.

Ovine smoke/burn ARDS model: a new ventilator-controlled smoke delivery system.

BACKGROUND: Our current ovine smoke/burn acute respiratory distress syndrome (ARDS) model utilizes a manual bee smoker. This smoke delivery system lacks standardization and reproducibility, with 20% of sheep failing to meet ARDS criteria. Time to reach ARDS criteria and survival time are also variable. The mild volutrauma (15 mL/kg) applied after smoke/burn injury may also fail to induce ARDS within 24 h. We hypothesized that these inconsistencies were associated with the bee smoker and the mild volutrauma. In the current study, we addressed these problems to improve the consistency of the smoke/burn ARDS model. METHODS: Adult female sheep (n = 10) were given a 40% total body surface area third degree cutaneous burn and 48 breaths (4 × 12) of cotton smoke under general anesthesia. A modified ventilator was then used to deliver a precise and consistent smoke volume (tidal volume) to the sheep. Additional barotrauma was induced by pressure control ventilation (40 cm H(2)0). When ARDS criteria (PaO(2)/FiO(2) < 200) were met, the ARDS Network low tidal volume ventilation protocol (6-8 mL/kg ideal body weight) was used. RESULTS: Carboxyhemoglobin levels were 81.4% ± 5.6% immediately following smoke injury. All sheep met ARDS criteria within 24 h (12.5 ± 4.9 h). Mean survival time post-injury was 62.1 ± 26.4 h. White blood cells and granulocytes were significantly elevated at 24 h post-smoke/burn injury. Lung tissue at necropsy was consistent with ARDS. CONCLUSIONS: The refinements made to the original ovine smoke/burn ARDS model produce a more reliable time to ARDS onset, injury severity, and time of death.