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Diving and Hyperbaric Medicine Sep 2022Respiratory injury during or following hyperbaric oxygen treatment (HBOT) is rare, but associated pressure changes can cause iatrogenic pulmonary barotrauma with... (Review)
Review
Respiratory injury during or following hyperbaric oxygen treatment (HBOT) is rare, but associated pressure changes can cause iatrogenic pulmonary barotrauma with potentially severe sequelae such as pneumothoraces. Pulmonary blebs, bullae, and other emphysematous airspace abnormalities increase the risk of respiratory complications and are prevalent in otherwise healthy adults. HBOT providers may elect to use chest X-ray routinely as a pre-treatment screening tool to identify these anomalies, particularly if a history of preceding pulmonary disease is identified, but this approach has a low sensitivity and frequently provides false negative results. Computed tomography scans offer greater sensitivity for airspace lesions, but given the high prevalence of incidental and insignificant pulmonary findings among healthy individuals, would lead to a high false positive rate because most lesions are unlikely to pose a hazard during HBOT. Post-mortem and imaging studies of airspace lesion prevalence show that a significant proportion of patients who undergo HBOT likely have pulmonary abnormalities such as blebs and bullae. Nevertheless, pulmonary barotrauma is rare, and occurs mainly in those with known underlying lung pathology. Consequently, routinely using chest X-ray or computed tomography scans as screening tools prior to HBOT for low-risk patients without a pertinent medical history or lack of clinical symptoms of cardiorespiratory disease is of low value. This review outlines published cases of patients experiencing pulmonary barotrauma while undergoing pressurised treatment/testing in a hyperbaric chamber and analyses the relationship between barotrauma and pulmonary findings on imaging prior to or following exposure. A checklist and clinical decision-making tool based on suggested low-risk and high-risk features are offered to guide the use of targeted baseline thoracic imaging prior to HBOT.
Topics: Adult; Humans; Barotrauma; Hyperbaric Oxygenation; Lung Diseases; Lung Injury
PubMed: 36100931
DOI: 10.28920/dhm52.3.197-207 -
Brain Injury 2017It has been shown that there is an increased risk for impaired auditory function following traumatic brain injury (TBI) in Veterans. Evidence is strongest in the area of... (Review)
Review
It has been shown that there is an increased risk for impaired auditory function following traumatic brain injury (TBI) in Veterans. Evidence is strongest in the area of self-report, but behavioural and electrophysiological data have been obtained that are consistent with these complaints. Peripheral and central dysfunction have both been observed. Historically, studies have focused on penetrating head injuries where central injury is more easily documented than in mild closed head injuries, but several recent reports have expanded the literature to include closed head injuries as well. The lack of imaging technology that can identify which closed head injuries are likely to impact auditory function is a significant barrier to accurate diagnosis and rehabilitation. Current behavioural and electrophysiological measures are effective in substantiating the auditory complaints of these patients but leave many questions unanswered. One significant limitation of current approaches is the lack of clear data regarding the potential influence of those mental health comorbidities that are very likely to be present in the Veteran population. In the area of rehabilitation, there are indications that hearing aids and other assistive listening devices may provide benefit, as can auditory training programmes, yet more research needs to be done.
Topics: Blast Injuries; Brain Injuries, Traumatic; Hearing Loss; Hearing Tests; Humans; Self Report; Veterans
PubMed: 28981349
DOI: 10.1080/02699052.2016.1274781 -
European Annals of Otorhinolaryngology,... Nov 2020
Topics: Barotrauma; Diving; Humans; Orbital Diseases; Pain
PubMed: 32335000
DOI: 10.1016/j.anorl.2020.03.011 -
Minerva Anestesiologica Oct 2019Our understanding of decompression physiopathology has slowly improved during this last decade and some uncertainties have disappeared. A better understanding of anatomy... (Review)
Review
Our understanding of decompression physiopathology has slowly improved during this last decade and some uncertainties have disappeared. A better understanding of anatomy and functional aspects of patent foramen ovale (PFO) have slowly resulted in a more liberal approach toward the medical fitness to dive for those bearing a PFO. Circulating vascular gas emboli (VGE) are considered the key actors in development of decompression sickness and can be considered as markers of decompression stress indicating induction of pathophysiological processes not necessarily leading to occurrence of disease symptoms. During the last decade, it has appeared possible to influence post-dive VGE by a so-called "preconditioning" as a pre-dive denitrogenation, exercise or some pharmacological agents. In the text we have deeply examined all the scientific evidence about this complicated but challenging theme. Finally, the role of the "normobaric oxygen paradox" has been clarified and it is not surprising that it could be involved in neuroprotection and cardioprotection. However, the best level of inspired oxygen and the exact time frame to achieve optimal effect is still not known. The aim of this paper was to reflect upon the most actual uncertainties and distil out of them a coherent, balanced advice towards the researchers involved in gas-bubbles-related pathologies.
Topics: Decompression Sickness; Diving; Embolism, Air; Foramen Ovale, Patent; Humans; Oxygen Inhalation Therapy
PubMed: 31238641
DOI: 10.23736/S0375-9393.19.13618-8 -
BMJ Case Reports Mar 2016A body of a 91-year-old donor underwent whole-body CT scanning before being transferred for use in an anatomical dissection course. Metallic objects were detected in the...
A body of a 91-year-old donor underwent whole-body CT scanning before being transferred for use in an anatomical dissection course. Metallic objects were detected in the thigh muscles, extensive bone abnormalities were found in the left femur and the diaphysis of the left femur was 50% wider than that of the right diaphysis. History revealed that the body donor had been seriously wounded at the end of World War II by a rocket explosion. His multiple fractures and lesions had not been surgically treated either in an Austrian military hospital or in a French prisoner of war camp. The patient suffered for almost 70 years from this violation of the Geneva Conventions. In the light of current armed conflicts, the present case is an example of how one injustice can result in severe, lifelong medical consequences. It also shows that the history behind a wounded thigh can have an enormous impact on teaching ethics to today's medical students.
Topics: Aged, 80 and over; Anatomy; Blast Injuries; Cadaver; Femur; Humans; Male; Military Personnel; World War II
PubMed: 27216934
DOI: 10.1136/bcr-2015-212909 -
Diving and Hyperbaric Medicine Sep 2019There are few issues that generate as much confusion in diving medicine as the nomenclature of bubble-induced dysbaric disease. Prior to the late 1980s, the diagnosis...
There are few issues that generate as much confusion in diving medicine as the nomenclature of bubble-induced dysbaric disease. Prior to the late 1980s, the diagnosis 'decompression sickness' (DCS) was invoked for symptoms presumed to arise as a consequence of bubble formation from dissolved inert gas during or after decompression. These bubbles were known to form within tissues, and also to appear in the venous blood (presumably after forming in tissue capillaries). A second diagnosis, 'arterial gas embolism' (AGE) was invoked for symptoms presumed to arise when bubbles were introduced directly to the arterial circulation as a consequence of pulmonary barotrauma. This approach was predicated on an assumption that the underlying pathophysiology could usually be inferred from the nature and tempo of resulting symptoms. DCS was considered to exhibit a slower more progressive onset, symptoms were protean (including pain, rash, paraesthesias, subcutaneous swelling, and neurological symptoms), and the neurological manifestations were mainly attributable to spinal cord or inner ear involvement. In contrast, AGE was considered to exhibit a more precipitous onset (often immediately on surfacing), and the principal manifestation was stroke-like focal neurological impairment suggestive of cerebral involvement. In 1989 an association between a large persistent ('patent') foramen ovale (PFO) and serious neurological DCS was independently reported by two groups, and subsequently corroborated for neurological, inner ear, and cutaneous DCS by multiple studies. The assumed pathophysiological role of a PFO in this setting was to allow bubbles formed from inert gas in the venous blood to avoid removal in the pulmonary circulation and to enter the arterial circulation. These bubbles could then pass to the microcirculation of vulnerable target tissues where inward diffusion of supersaturated inert gas from the surrounding tissue could cause them to grow. This emergence of 'arterialisation' of venous bubbles as an important vector of harm in some forms of DCS resulted in a challenge to the use of traditional 'DCS/AGE' terminology. It was suggested that very early onset of cerebral symptoms after diving could be explained not only by arterial bubbles introduced by pulmonary barotrauma, but also by venous bubbles crossing a PFO into the arterial circulation. Moreover, once venous bubbles had entered the arterial circulation they were then technically 'arterial gas emboli'; thus creating confusion with arterial gas emboli from pulmonary barotrauma. To many commentators, it made little sense to use diagnostic labels (DCS and AGE) that implied a particular pathophysiology when the two disorders might be difficult to tell apart, and had mechanistic processes in common. An alternative approach derived at a UHMS workshop in 1991 was to shift from nomenclature that implied a particular pathophysiology, to a descriptive system that lumped both DCS and AGE together under the label "decompression illness" (DCI). Using this system, terms to describe the organ system(s) involved and the progression of symptoms were applied. For example, a diver with worsening upper arm pain after a dive could be suffering 'progressive musculoskeletal DCI'; and a diver who lost consciousness immediately on surfacing but regained consciousness minutes later would be considered to be suffering 'remitting cerebral DCI'. Classifying cases in this manner made considerable sense at a clinical level, particularly given that there was an emerging consensus that manifestations of DCS and AGE that potentially overlapped did not require different approaches to recompression treatment. This descriptive classification of bubble-induced dysbaric disease gained substantial traction in the community, though not always with a full appreciation by users of the intended nuances of its application. Indeed, it became increasingly common over time to see the terms DCS and DCI used interchangeably; for example, authors using the term DCI to specifically infer the consequences of bubble formation from dissolved gas. This highlights one of the shortcomings of the DCI terminology: it becomes confusing when discussing dysbaric disease at a theoretical or experimental level when the nature of the insult is known or there is a specific intent to discuss bubble formation either from dissolved gas or from pulmonary barotrauma. The potential for confusion between mechanisms and manifestations of DCS and AGE as one of the principle drivers for adopting the DCI terminology deserves further discussion. It is tempting to suggest that if venous bubbles cross a PFO into the arterial blood then any resulting symptoms should be considered a manifestation of 'AGE'. However, there seems little sense in re-naming the primary pathophysiological event (DCS caused by bubble formation from inert gas) just because the bubbles have distributed elsewhere; especially using a name that commonly infers a completely different primary event (bubble formation from pulmonary barotrauma). Moreover, there are grounds for suggesting that these two processes may not be as difficult to distinguish as previously believed. Venous inert gas bubbles are small, and of a similar size distribution to those used as bubble contrast during PFO testing. Decades of experience in testing thousands of divers (and other patients) for PFO using bubble-contrast echocardiograpy have shown that even when strongly positive (that is, large showers of bubbles enter the arterial circulation), symptoms of any sort are very rare. There are sporadic reports of evanescent visual or cerebral symptoms, but (to this author's knowledge) reports of the focal or multifocal cerebral infarctions that can be caused by large arterial bubbles introduced iatrogenically or by pulmonary barotrauma are lacking. One could argue that in the context of PFO testing the brain is not supersaturated with inert gas (which might cause small arterial bubbles to grow), but being such a 'fast tissue' nor is it likely to be after diving. Thus, while sustained showers of small inert gas bubbles crossing a PFO after diving appeal as a plausible cause of transient visual symptoms or dysexecutive syndromes after diving, they are less likely to be the cause of dramatic stroke-like events occurring early after surfacing. In the final edition of Bennett and Elliott it was suggested that one editorial approach to the terminology conundrum would be to utilise the traditional terminology (DCS and AGE) when referring specifically to the pathophysiology and manifestations of bubble formation from dissolved inert gas or pulmonary barotrauma respectively, and to utilise the descriptive (DCI) terminology in clinical discussions when a collective term is useful, or when discussing individual patients where there is either ambiguity about pathophysiology or no need to attempt a distinction. Diving and Hyperbaric Medicine recommends a similar approach. The journal is reluctant to attempt to generate or apply hard 'rules' in relation to terminology of bubble-induced dysbaric disease, but we strongly discourage use of the term 'arterial gas emboli(ism)' to characterise venous inert gas bubbles that cross a right-to-left shunt such as a PFO. The pathophysiological consequences of bubble formation from dissolved inert gas should be regarded as decompression sickness (DCS). There is an expectation that authors are cognisant of the above issues and attempt to adopt terminology that reflects these considerations and best suits the circumstances of their manuscript.
Topics: Decompression; Decompression Sickness; Diving; Embolism, Air; Foramen Ovale, Patent; Humans
PubMed: 31523788
DOI: 10.28920/dhm49.3.152-153 -
Journal of the Royal Army Medical Corps Jun 2019Blast-associated traumatic brain injury (TBI) has become one of the signature issues of modern warfare and is increasingly a concern in the civilian population due to a... (Review)
Review
Blast-associated traumatic brain injury (TBI) has become one of the signature issues of modern warfare and is increasingly a concern in the civilian population due to a rise in terrorist attacks. Despite being a recognised feature of combat since the introduction of high explosives in conventional warfare over a century ago, only recently has there been interest in understanding the biology and pathology of blast TBI and the potential long-term consequences. Progress made has been slow and there remain remarkably few robust human neuropathology studies in this field. This article provides a broad overview of the history of blast TBI and reviews the pathology described in the limitedscientific studies found in the literature.
Topics: Blast Injuries; Brain Injuries, Traumatic; History, 20th Century; History, 21st Century; Humans; Military Medicine; Military Personnel
PubMed: 29326126
DOI: 10.1136/jramc-2017-000867 -
Journal of Otolaryngology - Head & Neck... Nov 2018Hemotympanum refers to both the presence of blood in the middle ear cavity and to ecchymosis of the tympanic membrane (TM), and a systematic study of intra-TM (iTM)...
BACKGROUND
Hemotympanum refers to both the presence of blood in the middle ear cavity and to ecchymosis of the tympanic membrane (TM), and a systematic study of intra-TM (iTM) hemorrhage without bleeding in the middle ear cavity has not been conducted. The goals of our study were to analyze the causes of iTM hemorrhage without TM perforation or bleeding in the middle ear cavity, and to demonstrate the clinical characteristics of the disease.
METHODS
This Case series study included five patients with iTM hemorrhage between August 2014 and August 2017. An iTM hemorrhage was diagnosed when otoendoscopic examination demonstrated minor bleeding behind the intact TM, a hemorrhage was observed between the TM annulus and the epidermal layer, and temporal bone computed tomography revealed thickening of the TM without soft tissue density within the tympanic cavity or temporal bone fracture. Initial symptoms, and serial findings of otoendoscopy and pure tone audiometry (PTA) were investigated.
RESULTS
iTM hemorrhage developed due to blunt head trauma in two patients, descent barotrauma during scuba diving in two patients, and spontaneous epistaxis in one patient. Otalgia and ear fullness were the most common symptoms, but PTA showed no or minimal conductive hearing loss in all patients.
CONCLUSIONS
An iTM hemorrhage may develop after blunt head trauma, barotrauma due to scuba diving, or spontaneous epistaxis; otological symptoms included otalgia, tinnitus, and aural fullness. An iTM hemorrhage resolved spontaneously without specific treatment, usually within 1 month.
Topics: Adult; Barotrauma; Cohort Studies; Craniocerebral Trauma; Earache; Female; Hemorrhage; Humans; Male; Middle Aged; Otoscopy; Prognosis; Remission, Spontaneous; Retrospective Studies; Risk Assessment; Severity of Illness Index; Temporal Bone; Tomography, X-Ray Computed; Tympanic Membrane; Tympanic Membrane Perforation; Wounds, Nonpenetrating; Young Adult
PubMed: 30400952
DOI: 10.1186/s40463-018-0300-0 -
PloS One 2020The effects of neuromuscular blocking agents (NMBAs) on adult patients with acute respiratory distress syndrome (ARDS) remain unclear. We performed a meta-analysis of... (Meta-Analysis)
Meta-Analysis
BACKGROUND
The effects of neuromuscular blocking agents (NMBAs) on adult patients with acute respiratory distress syndrome (ARDS) remain unclear. We performed a meta-analysis of randomized controlled trials (RCTs) to evaluate its effect on mortality.
METHODS
We searched the Cochrane (Central) database, Medline, Embase, the Chinese Biomedical Literature Database (SinoMed), WanFang data and ClinicalTrials from inception to June 2019, with language restriction to English and Chinese. We included published RCTs and eligible clinical trials from ClinicalTrials.gov that compared NMBAs with placebo or usual treatment in adults with ARDS. We pooled data using random-effects models. The primary outcome was mortality. The secondary outcomes were the ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen (PaO2/FIO2), total positive end expiratory pressure (PEEP), plateau pressure (Pplat), days free of ventilator at day 28, barotrauma and ICU-acquired weakness.
RESULTS
We included 6 RCTs (n = 1557). Compared with placebo or usual treatment, NMBAs were associated with lower 21 to 28-day mortality (RR 0.72, 95% CI 0.53-0.97, I2 = 59%). NMBAs significantly improved oxygenation (Pao2:Fio2 ratios) at 48 hours (MD 27.26 mm Hg, 95% CI 1.67, 52.84, I2 = 92%) and reduced the incidence of barotrauma (RR 0.55, 95% CI 0.35, 0.85, I2 = 0). However, NMBAs had no effect on oxygenation (Pao2:Fio2 ratios) (MD 18.41 mm Hg, 95% CI -0.33, 37.14, I2 = 72%) at 24 hours. We also found NMBAs did not affect total PEEP, plateau pressure, days free of ventilation at day 28 and ICU-acquired weakness.
CONCLUSIONS
In patients with moderate-to-severe ARDS, the administration of NMBAs could reduce 21 to 28-day mortality and barotrauma, and improve oxygenation at 48 hours, but have no significant effects on 90-day/ICU mortality, days free of ventilation at day 28 and the risk of ICU-acquired weakness. Further large-scale, high-quality RCTs are needed to confirm our findings. Registration: PROSPERO (ID: CRD 42019139656).
Topics: Adult; Barotrauma; Female; Humans; Male; Neuromuscular Blocking Agents; Oxygen; Randomized Controlled Trials as Topic; Respiration, Artificial; Respiratory Distress Syndrome; Time Factors; Treatment Outcome
PubMed: 31961896
DOI: 10.1371/journal.pone.0227664 -
Annals of African Medicine 2024Hyperbaric therapy is generally considered a safe therapy for the treatment of wounds, mucormycosis, and orthopedic injuries. It is fraught with complications such as... (Review)
Review
Hyperbaric therapy is generally considered a safe therapy for the treatment of wounds, mucormycosis, and orthopedic injuries. It is fraught with complications such as barotrauma, pulmonary toxicity, fire hazards, and claustrophobia. This article discusses the safety protocols and preventive aspects on usefulness of this new emerging therapy.
Topics: Humans; Hyperbaric Oxygenation; Barotrauma
PubMed: 38358163
DOI: 10.4103/aam.aam_16_22