Biomedical subjects
Publications and source records attributed to T J Francis.
A case of neurapraxia of the infraorbital nerve occurring as a result of maxillary sinus barotrauma in a diver is presented. Existing reports of a similar nature are reviewed and the pathogenesis of cranial nerve involvement in barotrauma is discussed. Guidelines for treatment are suggested.
The period from 1 January 1980 to 31 December 1989 produced a total of 244 training and operational diving accident reports involving Royal Navy and Royal Marines personnel. Because the incidence figures fluctuated widely year by year, a clear trend over the decade failed to emerge. However, the incidence of Type II decompression sickness, as a percentage of total decompression sickness, was greater in the second half of the decade than in the first, a trend similar to, although more moderate than, recent experience of dysbaric illness amongst sport divers. Student divers were disproportionately highly represented in the statistics, particularly with regard to pulmonary barotrauma and near-drowning.
Decompression illness was formerly an occupational hazard confined to professional divers and compressed-air workers. With the increasing popularity of recreational diving it has come to involve a wider cross-section of the population. Furthermore, the proportion of cases presenting with the more serious manifestations of the disease appears to be rising.
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Five anesthetized dogs undertook a chamber dive, on air, to 300 feet of seawater for 15 min. After the dive, spinal cord decompression sickness was detected by recording a reduced amplitude of the somatosensory evoked potential compared with predive base-line values. After the diagnosis of decompression sickness and rapid perfusion fixation of the animal, the spinal cord was removed and examined histologically. Numerous space-occupying lesions (SOL) that disrupted the tissue architecture were found in each cord, mainly in the white matter. The size and distribution of the SOL were determined using computerized morphometry. Although SOL occupied less than 0.5% of the white matter volume, we tested a number of algorithms to assess whether the SOL may have been directly involved in the loss of spinal cord function that followed the dive. We determined that the loss of somatosensory evoked potential amplitude may be attributed to the SOL if 30-100% of the spinal cord fibers that they displaced were rendered nonconducting. A number of possible mechanisms by which SOL may interfere with spinal nerve conduction are discussed.
A continuous infusion of air (1.0 ml.min-1) was delivered via a fine aortic cannula into the arterial circulation of 7 anesthetized dogs until no spinal cord function could be elicited by somatosensory evoked potentials. The animals were then rapidly perfusion-fixed and the spinal cords removed for histological examination. The appearance of the embolized cords differed substantially from eight spinal cords injured by fulminant decompression sickness (DCS). The embolized cords appeared essentially normal whereas the DCS cords featured extravascular, nonstaining, space-occupying lesions (SOLs) scattered throughout the cord, mainly in the white matter. Two spinal cords injured by DCS with a delayed onset (30 min from surfacing) appeared similar to the embolized cords. These findings are compatible with the hypothesis that two mechanisms are involved in the onset of spinal cord DCS. Fulminant disease is associated with SOLs, which are probably caused by the in situ evolution of a gas phase. Disease with a delayed onset is more likely to be caused by an ischemic mechanism, which in the acute phase is histologically indistinguishable from gas embolism.
Sixteen anesthetized dogs undertook a chamber dive that was designed to induce decompression sickness. Somatosensory evoked potentials (SEP) were used to diagnose and quantify the outcome of spinal cord involvement in the disease. Following diagnosis, 8 animals were treated with methyl prednisolone (MP), 20 mg.kg-1 ("megadose"), as an adjuvant to recompression on an abbreviated U.S. Navy Treatment Table 6. Eight control animals were recompressed in a similar manner, but received the MP diluent only as an adjuvant. Analysis of the SEP at the conclusion of treatment showed that there was no significant difference in outcome for the 2 groups of animals. However, if all the SEP recorded during the treatment period are compared, the MP-treated animals experienced a significantly worse outcome than the diluent-treated controls. The risks and benefit of using corticosteroids in the treatment of human spinal cord DCS are discussed.
Histological examination by light and electron microscopy of the spinal cords of four dogs rapidly perfusion-fixed after the onset of decompression sickness revealed the presence of numerous non-staining, space-occupying lesions that were absent in similarly prepared sections of control or ischemic spinal cords. We propose the hypothesis that these lesions are caused by the liberation of a gas phase. The possible significance of these lesions in the evolution of spinal cord dysfunction is discussed with reference to the principal theories of the pathogenesis of spinal cord decompression sickness.
Many aspects of central nervous system (CNS) decompression sickness (DCS) are poorly understood, including the temporal pattern of its presentation and the pathogenic mechanisms involved in the development of the disease. Using case histories and clinical series published in the literature and retrieved from treatment center records, this study is an attempt to define the interval between surfacing from a hyperbaric exposure and the onset of symptoms of CNS DCS. The results of 1070 cases of human CNS DCS were included in the study. The results show that the disease generally occurs rapidly: over 50% became symptomatic within 10 min of returning to 1 ATA, and in only 15% of cases was the onset of symptoms delayed for more than 1 h. Cerebral DCS had a more rapid onset than spinal cord disease: 50% of cerebral cases became apparent within about 3 min and a similar proportion of spinal cord cases within about 9 min from surfacing. The influence of these results on the diagnosis and treatment of dysbaric illness, on the safety of certain diving practices, and on possible pathogenic mechanisms is discussed.
Twenty-eight dogs underwent a 300 fsw chamber dive designed to generate spinal cord decompression sickness (DCS), which was detected by observing a reduction in the amplitude of the spinal somatosensory evoked potential (SEP). After an interval of 15 min on the surface following diagnosis, the animals received a therapeutic recompression. The latency was defined as the time between surfacing from the dive and the diagnosis of DCS, the severity as the minimum SEP amplitude, and the outcome as the amplitude of the SEP after 2 h of treatment. Significant correlations between latency and severity (P less than 0.05), latency and outcome (P less than 0.01), and severity and outcome (P less than 0.05) were found. Canine spinal cord latency is shown to be very similar to that found in man up to a surface interval of 30 min. The association between latency, severity, and outcome of spinal cord DCS is discussed with reference to the possible mechanisms involved in this disease.
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Blood flow in the right foot of 11 subjects was measured simultaneously by a strain gauge placed around the mid metatarsal circumference of the foot and a water displacement plethysmograph in which the foot was resting. A close linear correlation (r = 0.88) between the results of the two methods existed over a wide range of blood flows. It was apparent however that blood flow at the mid metatarsal region of the foot was only about 30% of the total foot blood flow measured by the plethysmograph. The likely cause of this finding is the varying proportion of bone to soft tissue along the length of the foot. It was observed that the strain gauge estimates of blood flow increased two to three fold when the plethysmograph was emptied, an effect that was abolished by refilling the plethysmograph. These changes were highly statistically significant (P less than 0.01) in all ten subjects in whom this comparison was made. The application of progressively increasing hydrostatic pressure in a further 4 subjects demonstrated that the reduction in blood flow was proportional to the pressure applied. Explanations for this effect based upon small temperature and pressure changes altering strain gauge performance are excluded. Three mechanisms are proposed, based upon an increase in venous leakage, a reduction in arterial inflow and the consequence of increased capillary filling occurring as a result of hydrostatic pressure within the plethysmograph.
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In a preliminary report, Adkisson et al. (Lancet 1989; 2:119-121) used 99Tcm-hexamethylpropylene amine oxime (HMPAO) single photon emission computed tomography (SPECT) to provide evidence for cerebral perfusion deficits in 28 cases of dysbarism. The report caused concern because these deficits were found even in cases in which the clinical manifestations were limited to the spinal cord. To address this issue further, a case-control study of cerebral perfusion using 99Tcm-HMPAO SPECT is reported. Four groups of 10 subjects were studied: a) divers scanned on average 11 days after treatment of neurologic decompression illness, b) divers scanned 3-5 yr after treatment for neurologic decompression illness, c) diver controls, and d) population controls. All groups were matched for age, and the divers were further matched for general diving experience. The scans were randomized and reported blind to history. Despite a trend toward larger numbers of deficits in individuals with decompression illness, the 4 groups were statistically indistinguishable. Furthermore, no correlation was found between the location of the perfusion deficits and the clinical presentation. These results indicate that 99Tcm-HMPAO SPECT scanning requires further evaluation before clinical significance can be ascribed to perfusion deficits found in divers.