Volkmann 1 described 1881 myonecrosis and secondary contracture after prolonged muscle
ischemia. He suspected that splints caused muscle cell death due to diminished arterial
blood flow describing an untreated compartment syndrome. Bardenheuer 2 described 1911
the first forearm compartment decompression for impending compartment syndrome and
Griffiths 3 described 1940 patients developping Volkmann’s contractures after embolectomy
of the brachial artery. He was the first to introduce the “5 P’s” of compartment syndrome (pain,
pallor, paresthesias, paralysis, pulselessness) in clinical practice. Bywaters and Beall 4 described
during the second world war several victims with a “crush syndrome”. Thereafter, Bentley et
al. 5 made similar reports describing crushed extremities leading to multiorgan system failure
suggesting that myoglobin precipitation in renal tubules led to mechanical obstruction and
consecutive renal failure. Only in the 1970s, the focus was put on basic science and treatment
of compartment syndrome. Rorabeck 6-8 described compartment syndrome following arterial
insufficiency or venous obstruction showing that the clearance of radioactive technetium
from a compartment was inversely related to compartment pressures and directly related
to blood flow and a normal blood flow after fasctiotomy of this compartment.
ROLE OF MENINGEAL FIBROBLASTS AND MAST CELLS
IN OPIATE INDUCED INFLAMMATORY MASSES
Tony L. Yaksh, Ph.D.
Department of Anesthesiology, University of California,
San Diego, La Jolla, CA, USA
Spinal opiates yield a potent naloxone reversible analgesia. The first report of continuous
intrathecal morphine delivery to manage chronic pain was in 1978. (Onofrio, et al, 1978).
Aside from anticipated opiate effects, no evidence of untoward effects on spinal function
were reported. Beginning in 1991, numerous clinical case series describe patients receiving
intrathecal morphine infusion who present with neurologic signs secondary to a local
compressive lesion. Retrospective data indicate an overall incidence of 0.1% although
estimates in limited populations have been as high as 43% (Deer et al., 2017c).