Breath-Hold Diving Injuries - A Primer for Medical Providers.

ABSTRACT: Breath-hold divers, also known as freedivers, are at risk of specific injuries that are unique from those of surface swimmers and compressed air divers. Using peer-reviewed scientific research and expert opinion, we created a guide for medical providers managing breath-hold diving injuries in the field. Hypoxia induced by prolonged apnea and increased oxygen uptake can result in an impaired mental state that can manifest as involuntary movements or full loss of consciousness. Negative pressure barotrauma secondary to airspace collapse can lead to edema and/or hemorrhage. Positive pressure barotrauma secondary to overexpansion of airspaces can result in gas embolism or air entry into tissues and organs. Inert gas loading into tissues from prolonged deep dives or repetitive shallow dives with short surface intervals can lead to decompression sickness. Inert gas narcosis at depth is commonly described as an altered state similar to that experienced by compressed air divers. Asymptomatic cardiac arrhythmias are common during apnea, normally reversing shortly after normal ventilation resumes. The methods of glossopharyngeal breathing (insufflation and exsufflation) can add to the risk of pulmonary overinflation barotrauma or loss of consciousness from decreased cardiac preload. This guide also includes information for medical providers who are tasked with providing medical support at an organized breath-hold diving event with a list of suggested equipment to facilitate diagnosis and treatment outside of the hospital setting.

Mapping the functional brain state of a world champion freediver in static dry apnea.

Voluntary apnea showcases extreme human adaptability in trained individuals like professional free divers. We evaluated the psychological and physiological adaptation and the functional cerebral changes using electroencephalography (EEG) and functional Magnetic Resonance Imaging (fMRI) to 6.5 min of dry static apnea performed by a world champion free diver. Compared to resting state at baseline, breath holding was characterized by increased EEG power and functional connectivity in the alpha band, along with decreased delta band connectivity. fMRI connectivity was increased within the default mode network (DMN) and visual areas but decreased in pre- and postcentral cortices. While these changes occurred in regions overlapping with cerebral signatures of several meditation practices, they also display some unique features that suggest an altered somatosensory integration. As suggested by self-reports, these findings could reflect the ability of elite free divers to create a state of sensory dissociation when performing prolonged apnea.

Prolonged syncope with multifactorial pulmonary oedema related to dry apnoea training: Safety concerns in unsupervised dry static apnoea.

Many competitive breath-hold divers use dry apnoea routines to improve their tolerance to hypoxia and hypercapnia, varying the amount of prior hyperventilation and lung volume. When hyperventilating and exhaling to residual volume prior to starting a breath-hold, hypoxia is reached quickly and without too much discomfort from respiratory drive. Cerebral hypoxia with loss of consciousness (LOC) can easily result. Here, we report on a case where an unsupervised diver used a nose clip that is thought to have interfered with his resumption of breathing after LOC. Consequently, he suffered an extended period of severe hypoxia, with poor ventilation and recovery. He also held his breath on empty lungs; thus, trying to inhale created an intrathoracic sub-atmospheric pressure. Upon imaging at the hospital, severe intralobular pulmonary oedema was noted, with similarities to images presented in divers suffering from pulmonary barotrauma of descent (squeeze, immersion pulmonary oedema). Describing the physiological phenomena observed in this case highlights the risks associated with unsupervised exhalatory breath-holding after hyperventilation as a training practice in competitive freediving.

Anterior sacral pseudomeningocele following minimal trauma: case report.

Sacral fractures are rare and seldom result in formation of a sacral pseudomeningocele. Treatment of these pseudomeningoceles usually consists of conservative management with flat bedrest or open operative management. The authors describe the case of a 55-year-old woman with an anterior sacral pseudomeningocele that was successfully treated using a lumbar drain for temporary continuous CSF drainage. The patient first presented to an outside institution several days after sacral trauma from an ice skating fall. Initial symptoms included throbbing headaches relieved by lying flat. Head and cervical spine CT demonstrated no abnormality. As symptoms worsened, she presented to another institution where MRI of the lumbar spine indicated sacral fracture with pseudomeningocele. The patient subsequently transferred to the authors' facility, where symptoms included headaches and occasional mild sacral pain. Given her headaches and the authors' concern for CSF leak, another head CT scan was performed. This revealed no subdural hematoma or other abnormality. A subsequent CT myelogram revealed an anterior sacral pseudomeningocele at S3-4 with an anterior irregular linear filling defect, likely representing torn dura. Treatment included placement of a lumbar drain (10 ml/hr) and flat bedrest. Resolution of the CSF leak occurred on postprocedure Day 9. At the 4-week follow-up visit, the patient had no clinical symptoms of CSF leak and no neurological complaints. To our knowledge, this is the first description of temporary continuous CSF drainage used to treat a posttraumatic sacral pseudomeningocele. This technique may reduce the need for potentially complicated surgical repair of sacral fractures associated with CSF leak in select patients.

Schmorl's nodes.

INTRODUCTION: First described in 1927, a Schmorl's node (SN) is the herniation of nucleus pulposus (NP) through the cartilaginous and bony end plate into the body of the adjacent vertebra. SNs are common findings on imaging, and although most SNs are asymptomatic, some have been shown to become painful lesions. In this manuscript, we review the literature regarding the epidemiology, clinical presentation, pathogenesis, imaging, and management of SNs. MATERIALS AND METHODS: Using databases from the US National Library of Medicine and the National Institutes of Health, relevant articles were identified. RESULTS: While several theories regarding the pathogenesis of SNs have been proposed, an axial load model appears to have the greatest supporting evidence. Symptomatic SNs are thought to be due to the inflammatory response solicited by the herniation of NP into the well-vascularized vertebral body. Management options for symptomatic SNs vary, ranging from medical management to surgical fusion. CONCLUSION: SNs are common lesions that are often asymptomatic. In certain cases, SNs can cause back pain. No consensus on pathogenesis exists. There is no established treatment modality for symptomatic SNs.

Tarlov cysts: a controversial lesion of the sacral spine.

The primary aim of our study was to provide a comprehensive review of the clinical, imaging, and histopathological features of Tarlov cysts (TCs) and to report operative and nonoperative management strategies in patients with sacral TCs. A literature review was performed to identify articles that reported surgical and nonsurgical management of TCs over the last 10 years. Tarlov cysts are often incidental lesions found in the spine and do not require surgical intervention in the great majority of cases. When TCs are symptomatic, the typical clinical presentation includes back pain, coccyx pain, low radicular pain, bowel/bladder dysfunction, leg weakness, and sexual dysfunction. Tarlov cysts may be revealed by MR and CT imaging of the lumbosacral spine and must be meticulously differentiated from other overlapping spinal pathological entities. They are typically benign, asymptomatic lesions that can simply be monitored. To date, no consensus exists about the best surgical strategy to use when indicated. The authors report and discuss various surgical strategies including posterior decompression, cyst wall resection, CT-guided needle aspiration with intralesional fibrin injection, and shunting. In operative patients, the rates of short-term and long-term improvement in clinical symptoms are not clear. Although neurological deficit frequently improves after surgical treatment of TC, pain is less likely to do so.