Myointimal hyperplasia and sympathetic reinnervation following local cold injury and rapid rewarming in the rabbit central ear artery.

BACKGROUND: Functional and pathological improvements following rapid rewarming in 42 degrees C water was compared with alterations following slow thawing at room temperature (22 degrees C) after frostbite (-9 degrees C, 15 minutes) in vivo of the rabbit central ear artery. METHODS: Following two to ten weeks of in vivo regeneration, vascular segments were tested in vitro. Maximal and dose-dependent isometric contractions were induced by exogenous noradrenaline. Sympathetic nerves in the vascular wall were stained with glyoxylic acid. Vascular ring segments were stained with haematoxylin and eosin. RESULTS: Following slow thawing, the total uptake, the K+ evoked and the spontaneous release of [3H]noradrenaline in the sympathetic nervous system were strongly reduced two weeks after freezing, with a subsequent increase to control level within 3-4 weeks. After rapid rewarming the total uptake, the spontaneous release and the K+ evoked release of [3H]noradrenaline commenced earlier such that after ten weeks the level was twice as high as following slow rewarming. The glyoxylic acid induced catecholamine fluorescence in sympathetic nerves, revealed an earlier regeneration after rapid rewarming. Haematoxylin and eosin-stained segments revealed less intimal hyperplasia three to 20 weeks after rapid rewarming than after slow thawing. CONCLUSION: Rapid rewarming of in vivo frozen arteries in warm water (42 degrees C) did not prevent immediate vasoparalysis and degeneration of sympathetic nerves. However, nerve regeneration occurred earlier and with higher tissue nerve densities as compared to tissue that had been slowly rewarmed. Myointimal hyperplasia was less pronounced after rapid rewarming. Abnormal sympathetic nerve function and myointimal hyperplasia, as observed in this study, may contribute to a greater understanding of sequelae in the human body following frostbite.

Early and late functional and histopathological perturbations in the rabbit ear-artery following local cold injury.

BACKGROUND: These experiments aimed to study the in vivo short and long term neurovascular regeneration after frostbite. METHODS: The rabbit central ear-artery was used as the experimental model. The effects on the noradrenergic innervation of the artery were measured in isolated vascular ring segments the first day and 2, 3-4, and 8-10 or 10-20 weeks following freezing at -9 degrees C or -18 degrees C for 15 min with slow rewarming for 7 min at room temperature. RESULTS: Two days after freezing the sympathetic nerves were completely degenerated, as observed with glyoxylic acid-induced fluorescence. The vascular isometric tension responses to exogenous noradrenaline and endogenously released noradrenaline by electrical stimulation in vitro were abolished. A varying degree of necrosis of the vascular wall was observed. Two weeks after freezing at -18 degrees C in vitro responses to exogenous noradrenaline and electrical stimulation were still abolished, then gradually approaching control levels after 10-20 weeks of in vivo regeneration. Eight and 10 weeks after injury at -9 degrees C increased vascular tension responses to exogenous noradrenaline was found. In spite of a long regeneration period the total uptake and the spontaneous and K+ (75 mM) evoked releases of [3H]noradrenaline were persistently decreased after frostbite at -18 degrees C, but they were regenerated to control levels already 10-20 weeks after -9 degrees C. Regeneration of noradrenergic nerve function, expressed as [3H]noradrenaline uptake and release and responsiveness to electrical stimulation, expressed as vascular contraction, was slower than the regeneration of the vascular smooth muscle. Myointimal hyperplasia developed in response to -9 degrees C and -18 degrees C frostbite. The uptake and the K+ evoked release of [3H]noradrenaline were particularly sensitive parameters for autonomic nerve function. CONCLUSIONS: The present findings may demonstrate important neurovascular reactions to local frostbite and may explain human sequelae following frostbite.

Nerve conduction velocity in human limbs with late sequelae after local cold injury.

Cold-induced neuropathy may play a dominant role in the long-term sequelae with cold sensitivity after local cold injuries (LCIs). Somatosensory functions were assessed and nerve conduction velocity (NCV) and motor distal delay (MDD) were measured in the limbs of 31 Norwegian former soldiers with persistent cold intolerance 3-4 years after the primary LCI. NCV measurements were performed in 24 lower and 16 upper extremities. NCV was related to degree of overall subjective complaints quantified by means of a visual analogue scale (VAS). Motor (MNCV) and sensory conduction velocity (SNCV) in the lower extremities and SNCV in the hands were significantly decreased compared with controls. MDD was pathologically increased in the feet. NCV of the forearms ranged from normal to significant reduction. The more pronounced effect on the lower extremities may be caused by deeper cooling of the calves compared with forearms for several reasons. No significant associations were found between VAS and NCV except for the right median nerve. NCV measurements may provide objective findings in cold-injured patients and in those with few or no conspicuous clinical signs.

Skin microcirculation in patients with sequelae from local cold injuries.

The microcirculation in the skin was assessed in 31 patients with sequelae from local cold injuries (LCI) in the extremities. All patients reported cold intolerance 3-4 years after the primary cold injury, which they sustained during military service. The used methods were laser Doppler fluxmetry, transcutaneous oxygen tension (TCpO2) and vital capillaroscopy. Neurovascular reflexes were stimulated by deep inspiration, digital cuff occlusion of venous and arterial circulation, neck cooling with an ice bag and water immersion at 5 and 15 degrees C. Unaffected lower or upper extremities were also investigated as part of a search for generalized effects of LCI. During immersion in ice water the cold-induced vasodilation (CIVD or Lewis' 'hunting' reaction) was profoundly delayed or abolished in the affected limbs. These also showed the lowest skin temperatures after 15-20 min of immersion. Additionally, a delayed CIVD was found in the unaffected feet of patients with a previous hand injury. TCpO2 resting values were decreased in the patients, but oxygen reappearance time, oxygen recovery index, postocclusive reactive hyperemia and the venoarterial reflex were normal. No capillary abnormalities were found. In conclusion, LCI induces disturbances in the CIVD, impairs cold tolerance and increases the risk of future cold injuries. These data demonstrate disturbances of reflex mechanisms mediated by the central nervous system. Neurophysiologic factors seem to be more important than ischemic mechanisms in the pathophysiology of late sequelae from LCI.

[Contents and updating of disaster plans]. / Katastrofeplaners innhold og oppdatering.

The disaster contingency plans of 62 hospitals with surgical, acute emergency functions were evaluated. Most plans were incomplete with regard to continued and extended activity or evacuation of the entire hospital in the event of war. Only 13% had adequate plans for internal accidents or situations with reduced of lost supply of vital resources such as water, medical gases or electricity. Plans for serious accidents in peacetime were to some degree deficient with regard to important aspects of the organization of the hospital in an emergency situation. Efforts to improve this crucial planning work are discussed.

[Form and readability of disaster plans]. / Katastrofeplaners form og lesbarhet.

We have evaluated the disaster contingency plans for 62 out of 69 Norwegian hospitals with surgical, acute emergency functions. Page volume varied from 2-115, mean 33 pages. Only nine hospitals had pocket size printed documents (A5). At the rest of the hospitals the plans had an A4-format and consisted of photocopied pages. Illustrations were few and of low quality. Too much text contained general information with no practical relevant instruction. Readability varied for different groups of health workers. Doctors received the best instructions for their tasks. Hospitals should seek professional assistance to edit, illustrate and produce the plans, and a certain degree of standardization of the plans should be aimed at. National health authorities should encourage the hospitals in this work.

Local cold injuries sustained during military service in the Norwegian Army.

The series comprises 40 soldiers who sustained 49 local cold injuries during their service in The Norwegian Army. Twenty-one cold injuries were classified as first degree, 15 as second degree and 13 as third degree. No difference in ambient temperature at the time of injury was observed between the three categories of injuries, but the duration of cold exposure was significantly longer in those suffering third degree injury. Thirty-eight of the 40 soldiers experienced sequelae. The trend was that the severity of sequelae was most pronounced in third degree injuries. However, soldiers with first degree injury may suffer from significant sequelae, while those with third degree injury may exhibit a more benign clinical course. Overall degree of distress from sequelae was mild to moderate with exacerbation of symptoms and signs upon cold exposure. Although the influence on civilian occupational activity was minor, a substantial negative impact on performance in the field or combat setting may be anticipated. Soldiers as well as commanders must be thoroughly informed about prophylactic measures, symptoms and signs of an impending cold injury. Rewarming of the skin must be initiated without delay.