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

Abstract

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 T2-weighted 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. DiscussionWith an increase in diving to greater depths, decompressionassociated injury is becoming more frequent [1]. According to the accepted decompression protocols, after deep submersion the pressure must be reduced gradually to avoid serious possibly life-threatening complications.Insufficient washout of excess inert gas during rapid ascent may result in bubble formation due to the relatively low ambient pressure [2].In the case reported here the patient went up very fast from a depth of at least 15 m. Furthermore he stated that he had made repetitive dives within a few hours, which increases the risk of decompression sickness [3].Decompression sickness is classified into two groups: type I includes joint pain, skin marbling, small patchy

Breath-Hold Diving-Related Decompression Sickness with Brain Involvement: From Neuroimaging to Pathophysiology

“…This facilitating effect of the development of DCS, related to the right-to-left shunt, has also been suggested in some cases in breath-hold divers [ 14 ]. On the other hand, in DCS affecting the spinal cord, injury is thought to involve obstruction and congestion of venous drainage, in addition to direct injury by bubble formation within the cord itself [ 5 , 8 , 9 , 15 ]. Finally, in the case of neurological involvement of breath-hold diving-related DCS, knowledge of the pathophysiology is even less well understood, as this is a rarer pathology, with most published work on acute DCS in scuba divers and fewer reports on DCS in breath-hold diving [ 4 , 7 , 16 , 17 , 18 , 19 ].…”

Neuroimaging of Diving-Related Decompression Illness: Current Knowledge and Perspectives

“…9 Second, several histopathologic studies have demonstrated venous obstruction and white matter congestion. 45,46 Third, vasogenic edema, appearing as high signal on both DWI and ADC maps, was observed by Vollmann et al in 2011 47 in a case of spinal cord decompression sickness, also suggesting a venous rather than arterial pathologic process.…”

“…48,49 Authors of MR imaging studies of decompression illness frequently report that the different clinicoradiologic patterns mentioned above overlap in the same patient, thereby suggesting that no single unifying pathophysiologic mechanism could completely explain this complex condition. 14,16,47 Some have argued that there is a greater participation of arterial occlusion in brain lesions because they are more frequently described in cases of arterial gas embolism, while venous occlusion may play a greater role in spine lesions and may even be favored by local mechanical cord compression. 11,15 Whatever the preponderant mechanism involved, the treatment is urgent hyperbaric therapy to allow nitrogen to dissolve and be expelled via the lungs.…”

“…Most of the authors used a 1.5T system, 11,47,49,55 and some even used a 0.5T system, which has a very low sensitivity. 8,56 Second, with the exception of Vollmann et al, 47 no previously published MR imaging studies of decompression sickness used DWI and ADC maps. The use of these sequences could conceivably increase MR imaging sensitivity and even provide additional data on the pathophysiology of brain damage in divers.…”