[abstract] A MECHANISM FOR EXPLAINING THE PATHOPHYSIOLOGY OF PAIN ONLY (LIMB) BENDS.

Rubicon Research Repository/Manakin Repository

[abstract] A MECHANISM FOR EXPLAINING THE PATHOPHYSIOLOGY OF PAIN ONLY (LIMB) BENDS.

Show full item record


Title: [abstract] A MECHANISM FOR EXPLAINING THE PATHOPHYSIOLOGY OF PAIN ONLY (LIMB) BENDS.
Author: Strauss, MB
Abstract: Pain only, Type I Decompression Sickness (DCS), appears to be a distinct clinical entity from the more serious Type II DCS. Although invascular bubbles and secondary ischemic changes to vital tissues is the accepted mechanism for Type II DCS, there is no presently accepted mechanism for explaining the pathophysiology of limb bends. The diving profiles, clinical presentations, and dramatic responses to recompression therapy (with or without increased oxygen percentages) suggest Type I DCS is a mechanical problem and its pathophysiology is due entirely to the distention of pain sensitive structures. However, to date, such a structure or the presence of bubbles within tissues in Type I DCS has defied discovery. The orthopaedic literature (Halatha, et al. Ultra-structure of sensory nerve endings in monkey [Macaca fascicularis] knee joint capsule. J Ortho Res 2:169-176, 1984) discusses an organelle, the Ruffini Type II corpuscle, which is an ideal model for explaining the pathophysiology of Type II DCS. The organelle is embedded in joint capsules. It is pain sensitive, responding to stretch when its thick peripheral perineural capsule is distended. Its central fluid intracapsular space is a site for bubble formation when the inert gas pressure differential is great enough to precipitate bubble formation. Once bubbles form in the microscopic intracapsular space, the perineural capsule becomes distended and pain without other detectable signs occurs. The dramatic response to recompression in this proposed model is due to the physical reduction or collapse of the bubble and the immediate relaxation of the pain sensitive perineural cpasule. No contemporary model exists that better explains the pathophysiology of Type I DCS. This paper is presented to share this hypothesis with the individuals interested in undersea and hyperbaric medicine and promote studies to verify it.
Description: Abstract of the Undersea and Hyperbaric Medical Society, Inc. Joint Annual Scientific Meeting with the International Congress for Hyperbaric Medicine and the European Undersea Biomedical Society held 11-18 August 1990. Okura Hotel, Amsterdam, The Netherlands (http://www.uhms.org)
URI: http://archive.rubicon-foundation.org/7024
Date: 1990

Files in this item

Files Size Format View
abstract.txt 193bytes Text file View/Open

This item appears in the following Collection(s)

  • UHMS Meeting Abstracts
    This is a collection of the published abstracts from the Undersea and Hyperbaric Medical Society (UHMS) annual meetings.

Show full item record

Browse

My Account