Spinal Decompression Sickness Research Articles

Case report: Reassessing guidelines for safe resumption of diving after spinal decompression sickness: insights from a challenging case

BackgroundRecreational divers who have experienced Spinal Decompression Sickness (DCS) often aspire to return to their diving activities. Traditionally, it is recommended to observe a waiting period of several months before contemplating a return to unrestricted diving, particularly when clinical symptoms are absent, spinal cord Magnetic Resonance Imaging shows no anomalies, and the evaluation for Patent Foramen Ovale (PFO) returns negative results.MethodsThis article presents a compelling case study involving a 51-year-old recreational scuba diver who encountered two episodes of spinal decompression illness within a two-year timeframe. Notably, the search for a PFO produced negative results. The primary objective of this article is to underscore the critical importance of a meticulously planned approach to resuming diving after DCS incidents, emphasizing the potential for recurrence and the essential preventive measures.ConclusionWe delve into the intricate decision-making process for returning to diving, emphasizing the significance of clinical evaluations, PFO assessments, spinal cord Magnetic Resonance Imaging, and the absence of clinical symptoms. By recognizing the risk of recurrence and the need for proactive prevention measures, we provide recommendations for both medical professionals and divers, with the ultimate goal of enhancing safety and informed decision-making within the diving community.

Hyperbaric treatment deviations for U.S. Navy divers: Spinal DCS

Introduction The United States Navy (USN) developed and refined standardized oxygen treatment tables for diving injuries, but USN tables may not address all situations of spinal decompression sickness (DCS). We describe a detailed recompression treatment regimen that deviated from standard USN protocol for an active-duty USN diver with a severe, delayed presentation of spinal cord DCS. Case Report A USN diver surfaced from his second of three dives on a standard Navy ‘no-Decompression’ Air SCUBA dive (Max depth 101 fsw utilizing a Navy Dive Computer) and developed mid-thoracic back pain, intense nausea, paresthesias of bilateral feet, and penile erection. Either not recognizing the constellation of symptoms as DCS and after resolution of the aforementioned symptoms, he completed the third planned dive (essentially an in-water recompression). Several hours later, he developed paresthesias and numbness of bilateral feet and legs and bowel incontinence. He presented for hyperbaric treatment twenty hours after surfacing from the final dive and was diagnosed with severe spinal DCS. Based on the severity of clinical presentation and delay to treatment, the initial and follow-on treatments were modified from standard USN protocol. MRI of the spine four days after initial presentation demonstrated a 2∙2 cm lesion at the T4 vertebral level extending caudally. Follow-up examinations over two years demonstrated almost complete return of motor and sensory function; however, the patient continued to suffer fecal incontinence and demonstrated an abnormal post-void residual urinary volume. An atypical presenting symptom, a discussion of MRI findings, and clinical correlations to the syndrome of spinal DCS are discussed throughout treatment and long-term recovery of the patient.

Relationship between clinical and radiologic findings of spinal cord injury in decompression sickness.

Decompression sickness may involve the central nervous system. The most common site is spinal cord. This study was conducted to determine the relationship between magnetic resonance(MR) imaging findings of spinal damage. We conducted a retrospective review of 12 patients (male=10, female=2) who presented with spinal cord symptoms. We investigated their clinical features, neurological findings and radiologic findings. The depth and bottom time of the dive were 34.5 meters (range 22-56) and 22.7 minutes (range 10-55) respectively. Most divers ascended within appropriate time frame as shown by the decompression tables. The most frequent initial symptoms were lower limb weakness (n=12), followed by sensory disturbances (n=10) and bladder dysfuction (n=5). The chief radiologic abnormalities were continuous (n=3), or non-continuous (n=5) high-signal intensity on T2-weighted images at posterior paramedian portion of the spinal cord, mainly thoracic level. There were no abnormal findings in the remaining four (4) patients, and they showed good prognosis. All patients were treated with hyperbaric oxygen therapy and some received high-dose dexamethasone. On discharge, five (5) patients had made a full recovery, seven (7) had some residual neurological sequelae, and all patients except one (1) regained normal bladder function. Spinal cord decompression sickness is a neurological emergency. Early recognition and treatment may minimize neurological damage. Initial normal finding in MR imaging was a good predictor for prognosis in spinal decompression sickness.

Norman Keith Ian McIver

Norman Keith Ian McIver (“Nick”) was the key UK diving physician during the early years of the North Sea oil industry. He pioneered clinical treatments, medical support for the offshore...

06-3 Rehabilitation to residual functional disorders in spinal decompression sickness resulting from recreational scuba diving

06-3 Rehabilitation to residual functional disorders in spinal decompression sickness resulting from recreational scuba diving

Spinal Cord Injury in Decompression Sickness: A Case Report

Abstract Study Design Case report. Objective To describe an unusual case of deep diving followed by spinal cord injury due to decompression sickness (DCS). Setting Princess Royal Spinal Injuries Centre, Sheffield Teaching Hospitals NHS Foundation Trust, England. Method Description and observation of management and outcomes, of spinal decompression sickness (DCS). Results The patient's symptoms and signs developed after she surfaced after a deep sea diving event. She was managed and treated in a tertiary level care hospital. MRI performed within 24 hours, showed signs of increased signal intensity in the cervical and thoracolumbar regions. She was treated with hyperbaric oxygen which improved her pain symptoms but there was no immediate resolution in motor sensory deficits. Repeat MRI done after a week showed resolution if hyperintensity in the cervical region but not in the thoracolumbar region. Patient progressed to have significant neurological recovery in the next 6 months. She became ambulant with unilateral ankle foot orthotic and a pair of crutches, she continued to have bladder incontinence at 1 year follow-up interval. Conclusion Central nervous involvement is not uncommon in decompression sickness in divers. Early diagnosis and proper management can reduce acute symptoms and prevent further complications of permanent neurological disability. Primary prevention by education and adhering to standard diving guidelines is needed to reduce mortality and morbidity in decompression sickness.

Magnetic Resonance Imaging of the Spine in a Patient with Decompression Sickness

The case of a 60-year-old male patient who was admitted to hospital because of a scuba diving accident is reported. The patient initially complained about dizziness and pain in the shoulders. The exact rate of ascent from diving was not known, however, the patient said that he had had a panic attack and went up very fast from a depth of at least 15 m. despite a rapid recompression the patient developed hypesthesia of the right upper limb 2 days later. To rule out a stroke magnetic resonance imaging (MrI) of the brain and the whole spinal column was performed.MrI examinations were carried out with a 1.5 Tesla system (siemens Magnetom espree). The imaging protocol included a diffusionweighted (dW) single-shot spin echo echoplanar sequence acquired from the anterior commissure-posterior commissure. For dW MrI, the diffusion gradients were successively and separately applied in three orthogonal directions for a total acquisition time of 97 s. Trace images were then generated and apparent diffusion coefficient (ADC) maps calculated with a dedicated software tool (syngo; siemens). These studies revealed signal alterations in the cervical spinal cord with an increased signal in diffusion and T2weighted images at the level of the fourth and fifth cervical vertebral body, affecting both grey and white matter (Fig. 1). diffusion-weighted imaging at the same level detected some bright lesions (Fig. 2), which could be correlated with signal alterations in T2-weighted sequences and the ADC maps also revealed a high signal in these regions (Fig. 3). The MrI scans of the brain did not detect any abnormalities. Because of these finding the diagnosis of spinal decompression sickness was made. After treatment in the decompression chamber with hyperbaric oxygen for 5 days the pain in the shoulders and the dizziness disappeared, however, the hypesthesia remained.

Spinal decompression sickness presenting as partial brown-sequard syndrome and treated with robotic-assisted body-weight support treadmill training

To describe the rehabilitation outcome of a case of spinal decompression sickness presenting as partial Brown-Sequard syndrome treated with robotic-assisted body-weight support treadmill training. Case report. Type II decompression sickness patients commonly suffer from myelopathy with gait disturbances necessitating rehabilitation. Robotic-assisted body-weight support treadmill training has been shown to improve the rehabilitation outcome of incomplete spinal cord injury. Its usefulness has not been described in decompression sickness myelopathy. Robotic-assisted body-weight support treadmill training was administrated using the Lokomat. Primary outcomes were American Spinal Cord Association scale, Spinal Cord Independence Measurement, Berg Balance Test, and Walking Index for Spinal Cord Injury. The patient was admitted 3 weeks after the diving injury, with severe paraparesis and a T11 sensory neurological level, resembling partial Brown-Sequard syndrome. After 3 months of rehabilitation including 18 Lokomat sessions, American Spinal Cord Association score improved from C to D, Spinal Cord Independence Measurement improved from 50 to 90 out of 100. Berg Balance Test improved from 35 to 43 out of 56 and Walking Index for Spinal Cord Injury improved from 1 to 15 out of 20. Upon discharge he could walk with one crutch for more than 1 km. Robotic-assisted body-weight support treadmill training for spinal decompression sickness rehabilitation might be beneficial.

MRI Findings and Clinical Outcome in 45 Divers with Spinal Cord Decompression Sickness

Decompression sickness (DCS) affecting the spinal cord is the most dangerous form of diving-related injury with potential sequelae. This study was conducted to evaluate the relationship between spinal cord lesions on MRI and clinical findings in divers with spinal DCS. We studied 45 cases of DCS that were referred to our hyperbaric facility with clinical evidence of spinal involvement during the period 2002-2007. The study included only patients who underwent MRI within 10 d of injury. The severity of spinal DCS for each patient was rated numerically for both the acute event and 1 mo later. The presence or absence of back pain was also noted. Spinal cord lesions were significantly more frequent in divers with severe DCS, and did not occur in any diver who experienced a favorable outcome (sensitivity = 67%, specificity = 100%, negative predictive value = 77%, positive predictive value = 100%). The presence of vertebral degenerative changes that impinged on the spinal cord was strongly associated with MRI abnormalities, but not with a negative outcome. Acute back pain was associated with hyperintense lesions and persistence of neurological sequelae [OR = 14 (95% CI, 3.1 to 63.5)]. The results show that MRI could be helpful in predicting clinical outcome in divers with spinal cord DCS. The presence of medullary compressive factors and vertebral back pain after surfacing indicate increased likelihood of severe myelopathy with incomplete recovery.

Delayed spinal decompression sickness after air flight

Delayed spinal decompression sickness after air flight

Plongée à l'air avec la table de décompression MN 90. Bilan de 12 années d'utilisation par la Marine française : à propos de 61 accidents de désaturation de 1990 à 2002

Objective. – Decompression MN 90 Table is used for air diving by military divers and both sports divers in France. In the aim to confirm MN 90 safety, we studied 61 decompression sicknesses observed in the French Navy for 1990–2002. Method. – Each year 1800 divers carry out 150 000 dives ± 10%. Divers are 1600 ship divers (dives less than 35 m-sub-water) and 200 mine clearance divers (dives up to 60 msw max). Each accident must be notified and data are recorded into a database. Results. – The total risk is estimated at 1 accident/30 000 dives. We observed no death and only 2 divers with persistent neurological deficits. We found spinal decompression sickness: 66%, cerebral 23%, inner ear 8% and joint bends 3%. Neurological accidents are purely sensitive for 65%. The evolution was favourable for 97% after early hyperbaric recompression at 400 kPa. One hundred percent respected the MN90 procedure. Water temperature, age, effort during diving, repetitive dive were not found as risk factors. A right-to-left shunt was present for only 30% of type II accident. The main result of the study is that 54% of accidents concerned only 200 mine clearance divers with a risk estimated at 1 accident/3000 dives for 45–60 msw depths. Conclusion. – MN90 decompression procedure is safe for a young population of trained military divers with a low risk of accident. The major risk factor seems to be the depth. Studies are necessary to optimize the decompression for deep air diving.

Magnetic Resonance Imaging and Neuropathology Findings in the Goat Nervous System following Hyperbaric Exposures

Divers may be at risk of long-term CNS damage from non-symptomatic hyperbaric exposure. We investigated the effect of severe, controlled hyperbaric exposure on a group of healthy goats with similar histories. Thirty goats were exposed to various dive profiles over a period of 5 years, with 17 experiencing decompression sickness (DCS). Brains were scanned using magnetic resonance (MR) imaging techniques. The animals were then culled and grossly examined, with the brain and spinal cord sent for neuropathological examination. No significant correlation was found between age, years diving, DCS or exposure to pressure with MR-detectable lesions in the brain, or with neuropathological lesions in the brain or spinal cord. However, spinal scarring was noted in 3 animals that had suffered from spinal DCS.

Patent foramen ovale and decompression sickness in sports divers.

Patency of the foramen ovale (PFO) may be a cause of unexplained decompression sickness (DCS) in sports divers. To assess the relationship between PFO and DCS, a case-control study was undertaken in a population of Belgian sports divers. Thirty-seven divers who suffered from neurological DCS were compared with matched control divers who never had DCS. All divers were investigated with transesophageal contrast echocardiography for the presence of PFO. PFO size was semiquantified on the basis of the amount of contrast passage. Divers with DCS with lesions localized in the high cervical spinal cord, cerebellum, inner ear organs, or cerebrum had a significantly higher prevalence of PFO than divers with DCS localizations in the lower spinal cord. For unexplained DCS (DCS without commission of any diving procedural errors), this difference was significant for large PFOs only. We conclude that PFO plays a significant role in the occurrence of unexplained cerebral DCS, but not of spinal DCS. We further stress the importance of standardization and semiquantification of future PFO studies that use transesophageal contrast echocardiography.

Role of Extravascular Gas Bubbles in Spinal Cord Injury Induced by Decompression Sickness in the Rat

We have evaluated the contribution of extravascular gas bubbles to spinal cord injury in decompression sickness. For this purpose, a model of decompression sickness was developed by subjecting rats to simulated dives using compressed air. Various diving profiles were tested and the presence of spinal cord injury was demonstrated by electrophysiologic measurements. To evaluate the space occupying lesions induced by gas bubbles in the white matter, the spinal cord was fixed by perfusion with 10% buffered formalin. Tissue blocks from cervical, thoracic, and lumbar spinal cords were embedded in paraffin. Tissue sections were double stained with luxol fast blue and hematoxylin and eosin. The space occupying lesions were quantified with a digitizer tablet. The fractional area of the lesions was 0.009% in controls and 0.026% in rats subjected to diving. We conclude that the volume of extravascular free gas present in the cord of rats with spinal decompression sickness is small and that artifacts of tissue preparation contribute to the volume estimate. As far as can be judged from the results in this animal model, the contribution of extravascular gas bubbles to spinal cord decompression injury is minor.

Spinal decompression sickness with delayed onset, delayed treatment, and full recovery.

Spinal decompression sickness with delayed onset, delayed treatment, and full recovery.

Spinal cord degeneration in a case of "recovered" spinal decompression sickness

Spinal cord degeneration in a case of "recovered" spinal decompression sickness