Recent Papers
Recent Papers
Gianvincenzo Sparacia, Aurelia Banco, Maria Accardi, *Benedetta Sparacia, Roberto Lagalla
Institute of Radiology "P. Cignolini" and *Institute of Anaesthesiology, Hyperbaric Oxygen Therapy Section - University of Palermo, Italy
Presented at the XXII Congress of the European Society of Neuroradiology, Milan September 1996
Neuroradiology 38, Suppl. 2: S87 (P78), 1996.
Introduction
Decompression sickness (DCS) is a clinical syndrome caused by alterations in environmental
pressure, which result in the liberation into tissue or blood of inert gas bubbles
previously loaded within tissues as a soluble phase. Sport divers generally use compressed
air as the breathing mixture, and in their case, the inert gas that may be liberated
during decompression is nitrogen.
Pathophysiological changes of DCS are attributable to bubble formation and to the
damage caused by the bubbles to tissues and blood supply.
Based on clinical manifestations, the generally accepted classification of DCS is
type I or II. Type I includes joint pain, skin marbling, small patchy hemorrhages,
and lymphatic obstruction, while type II is dominated by injury to the central nervous
system, mainly spinal, and inner ear and lung involvement.
Scuba diving is associated with risk of severe decompression sickness with primarily
spinal cord involvement (DCS type II).
The population at risk includes, in addition of sport divers, naval and commercial
divers, high-altitude personnel exposed to hypobaric decompression, and compressed-air
workers.
Hyperbaric oxygen therapy provided in specially designed pressure chambers is currently
the treatment of choice for decompression sickness. Until the patient reaches a hyperbaric
medical facility, the treatment for DCS includes proper hydration and the administration
of oxygen at the highest possible concentration.
Purpose
This exhibit discuss the value of MR imaging in the detection of pathologic changes
of spinal cord decompression sickness, that were previously undetectable by other
neuroimaging methods.
Subjects and Methods
10 patients (8 men and 2 women; 16-38 years old, mean 32 years) were referred
to the Hyperbaric Oxygen Therapy Center of our Institution for diving-related injuries.
Neurologic examinations were performed by a staff neurologist to characterize the
extent of clinical compromise. 8 patients had minor symptoms whereas 2 patients had
symptoms of spinal cord dysfunction alone suggesting spinal decompression sickness.
All patients underwent MR examination of the spinal cord (0.5-T, surface coil) and
were treated with therapeutic hyperbaric recompressions and auxiliary therapy.
Results
MR demonstrated patchy areas of increased signal intensity in the white-matter
tracts on both GRE T2*-weighted and fast SE T2-weighted images in the 2 patients
with symptoms of spinal cord dysfunction, corresponding to an area of the cord believed
to be clinically involved (Case 1 - cervical and dorsal tract; Case
2 - cervical tract).
In one patient (Case 1), after a course of therapeutic hyperbaric recompressions, MRI revealed
a decreased extension of areas of increased signal intensity (not showed) and the
patient was able to stand and walk a short distance.
Conclusion
MRI has proved to be reliable in the detection of intramedullary lesions due
to a decompression accident that were previously undetectable by other neuroradiological
investigations (such as myelography, CT, angiography, isotopic tests).
Further MRI has proved to be useful to make decision on how to structure a prompt
hyperbaric treatment and for the follow-up during therapeutic hyperbaric recompressions.
Acknowledgment
We thank Dr. G. Brancatelli (from the Institute of Radiology; University of Palermo),
who contributed to the gathering of the data in this study.
References
1) Warren LP, Djang WT, Moon RE, et al. Neuroimaging of scuba diving injuries
to the CNS. AJR 1988;151:1003-1008
2) Ahron-Peretz J, Adir Y, Gordon CR, et al. Spinal cord decompression sickness in sport diving. Arch Neurol 1993;50:753-756
3) Dick APK, Massey EW. Neurologic presentation of decompression sickness and air embolism in sport divers. Neurology 1985;35:667-671
4) Kizer KW. The role of Computed Tomography in the management of dysbaric diving accidents. Radiology 1981;140:705-707
5) Hallenbeck JM, Bove AA, Elliot DH, et al. Mechanism underlying spinal cord damage in decompression sickness. Neurology 1975;25:308-316
6) Levin HS, Goldstein FC, Norcross K, et al. Neurobehavioral and Magnetic Resonance Imaging findings in two cases of decompression sickness. Aviat Space Environ Med 1989;60:1204-1210
7) Hodgson M, Beran RG, Shirtley G. The role of Computed Tomography in the assessment of neurologic sequelae of decompression sickness. Acrh Neurol 1988;45:1033-1035
8) Calder IM, Palmer AC, Hughes JT. Spinal cord damage found at autopsy in divers. In EUBS 87, diving and hyperbaric medicine. Proceedings of the XIIIth annual meeting of the European Undersea Biomedical Society, Palermo, Italy, September, 1987:310-314
Address your comments by e-mail to Dr. G. Sparacia at: sparacia@mbox.unipa.it
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