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Biomedical subjects

D R Leitch

Publications and source records attributed to D R Leitch.

At least 19 recordsLinked to original sources
PubMed1987

Twenty years of treating decompression sickness.

Twenty years of treatment records were searched for cases of serious decompression sickness (DCS). Spinal cord DCS was the most common presentation. The efficacy of various treatment tables were compared. Oxygen tables were found to be as effective as long air tables in treating cases presenting within 12 h of the onset of symptoms and were superior for cases presenting later. Using RN 61 (USN 5) to treat serious decompression sickness resulted in a high post-treatment relapse rate. Other inappropriate practices such as in-water air treatment and nontreatment of spontaneously recovering cases resulted in a high incidence of deterioration or relapse.

Air↗
PubMed1986

Spinal cord decompression sickness: a comparison of recompression therapies in an animal model.

Somatosensory evoked potentials (SEP) were used in an animal model to measure spinal cord electrophysiological function. Animals were submitted to a dive profile resulting in spinal cord decompression sickness (DCS). The animals were treated after a delay allowing the lesion to consolidate. Serial measurements of SEP documented the onset, duration, and outcome of treatment. Physiological data were recorded throughout each experiment. Group A (n = 10) was recompressed to 60 fsw (feet of sea water) breathing 100% oxygen (2.8 ATA) and Group B (n = 8) was treated at 66 fsw breathing 66% oxygen (2.0 ATA). No differences were found between groups in the severity, surface interval before treatment, or the maximum effect of treatment. The maximum effect of treatment was seen by 25 min of treatment. Animals were regrouped into responders and nonresponders. The latter displayed a more rapid onset, a more severe insult, and more adverse physiological effects than the responders. The possibility of a different etiology was considered together with the failure to differentiate between the treatment groups. It was concluded that treatment B was safer but the problems of introducing a new therapeutic table outweighed the safety advantage.

Animals↗
PubMed1986

Pulmonary barotrauma in divers and the treatment of cerebral arterial gas embolism.

A review of case records spanning 20 years revealed 140 cases of decompression pulmonary barotrauma (PBT) in divers. There were 23 cases of uncomplicated PBT and 117 cases of cerebral arterial gas embolism (AGE), of which 58 had respiratory manifestations. Details of presentation and precipitating factors were analysed. Half of AGE cases improved spontaneously, including 21% which recovered completely. The 89 treated cases of AGE (including 2 iatrogenic cases) were used to study the efficacy of different treatments. An overall success rate of 65% was seen with 62% of cures occurring within 25 min of arrival at pressure. The remaining cures occurred in equal numbers during decompression and after surfacing. No cases receiving steroids relapsed. Increasing the time to treatment reduced the likelihood of cure. Comparison of treatments proved difficult and it was concluded that, although most cases would probably respond satisfactorily to 2.8 bar (2100 mm Hg) of oxygen, there were no compelling reasons for altering the current treatment practice of beginning treatment of acute cases with a 30-min period at 6.0 bar (165 fsw) before returning to 2.8 bar (60 fsw) to complete the therapy.

Barotrauma↗
PubMed1986

Recurrent pulmonary barotrauma.

Twenty years of diving incident records were searched to find the 12 cases of recurrent pulmonary barotrauma (PBT) reported. The trend observed was that recurrences tended to be worse than the first incident and more likely to include arterial gas embolism (AGE). It is concluded that the Royal Navy policy of preventing all divers who suffer PBT from further diving is justified, regardless of the cause or mild nature of the injury. The incidence of AGE was low at 1 per 19,800 to 1 per 34,000 dives and was similar to United States Navy incidence. There was no evidence that routine screening by simple spirometry had influenced the PBT rate and, therefore, its usefulness is questioned.

Adult↗
PubMed1986

Pulmonary barotrauma in submarine escape trainees and the treatment of cerebral arterial air embolism.

The reports of all dysbaric incidents occurring during submarine escape training at the Royal Navy's training facility in HMS Dolphin during 1954-84 were reviewed. All cases treated for unequivocal arterial gas embolism were used to assess the effectiveness of various treatments. Presentation and accident rates were analysed. As training techniques and treatments have varied over the years, the data were not uniform thus making comparison of treatments difficult. Both long air tables and RN Table 63 (USN6A) appear to offer effective treatment. There was insufficient data to assess the efficacy of prophylactic steroids in preventing relapse. It was concluded that the current recommendations for treating AGE by commencing on RN Table 63 with a change to RN Table 54 in the event of no response or of relapse should remain unchanged.

Accident Prevention↗
PubMed1985

Complications of saturation diving.

The experience of 458 man-dives with 731 excursions between 50 m and 300 m carried out by Royal Navy saturation divers is summarized. During saturation decompression there were 6 treated bends and 33 reported niggles. Two bends occurred in dives deeper than 249 m and the remaining 4 bends occurred in dives where decompression began in much less than the saturation stop time after completion of downward excursions. There was one case of vestibular system decompression sickness after an excursion to 300 m. It is concluded that the decompression table is effective in use shallower than 150 m but that the risk increases with greater depth. There is, however, only limited experience in the deeper range. There is no evidence that chamber compression with air to 10 m adversely affects decompression from deeper than 50 m. An account of the medical and physiological conditions affecting divers in these dives is given.

Decompression Sickness↗
PubMed1985

Oxygen in the treatment of spinal cord decompression sickness.

Twenty-five anesthetized dogs were used to find the optimum Po2 for the delayed treatment of spinal cord decompression sickness (DCS). They were instrumented for the measurement of physiological variables and somatosensory spinal evoked potentials (SEP) given an air dive of 15 min at 10 bar (300 ft) and decompressed in under 6 min. At the surface SEP were observed for signs of DCS. Fifteen minutes after cord DCS was observed in the SEP, the dogs were compressed to 5.0 bar breathing one of 5 gas mixtures giving a Po2 of 1.0, 1.5, 2.0, 2.5, or 3.0 bar. At the start of therapy all groups were in a similar physiological state with a similar loss of SEP. Between 40 and 120 min, recovery was significantly different (P less than 0.05) between the groups, most SEP recovery having occurred within 15 min. The treatments ended with 22, 32, 70, 66, and 42% recovery, respectively. It would appear that the optimum Po2 is around 2.0 bar.

Animals↗
PubMed1985

Pressure in the treatment of spinal cord decompression sickness.

Previous work had shown that a Po2 of about 2.0 bar was the optimal Po2 for the treatment of spinal cord decompression sickness (DCS). With 20 anesthetized dogs the hypothesis was tested that pressures in excess of a threshold, taken as 3 bar, did not enhance recovery of spinal cord DCS. Dogs were subjected to a 15-min air dive at 10 bar (300 ft) and decompressed over 5.5 min. At the surface, spinal cord evoked potentials (SEP) were observed for changes indicating DCS. Fifteen minutes after DCS was first detected the dogs were recompressed to 3, 5, 7, or 2.8 bar breathing 66, 40, 29, or 100% oxygen which gave a Po2 of 2.0 bar except in the 2.8 bar group. The recovery of the SEP over 2 h was observed. Group mean recoveries at 67, 62, 29, and 42% were not significantly different after 120 min. As the hypothesis was supported, a tentative proposal for changing current therapy was made.

Animals↗
PubMed1985

Electrocardiographic changes in serious decompression sickness.

Electrocardiographic changes observed in 21 dogs suffering from spinal cord decompression sickness (DCS) are described. Changes seen included P wave peaking and P-R depression compatible with right heart strain; S-T segment and T wave changes suggestive of myocardial ischemia; and ventricular arrhythmias ranging from unifocal premature ventricular contractions to ventricular tachycardia. Compression therapy did not always restore the ECG changes promptly to normality. The changes are discussed in association with concurrent physiological events. These included pulmonary hypertension, systemic hypertension and hypotension, and cerebral DCS. Possible mechanisms ranging from local cardiac DCS or coronary gas embolism to autonomic nervous system disturbances arising from cerebral and spinal cord DCS are reviewed. It is concluded that ECG recordings should be made more often when treating clinical DCS.

Animals↗
PubMed1985

Additional pressurisation for treating nonresponding cases of serious air decompression sickness.

In this study, 20 years of decompression sickness (DCS) treatment records were reviewed to establish whether or not compression to 50m (165 fsw) was a useful response to serious DCS cases which failed to respond satisfactorily at 18m (60 fsw) breathing oxygen. It was concluded from 14 cases that further compression rarely altered the recovery of cases which were not already recovering at 18m or were of a relatively mild nature. The only case with motor deficits to recover at 50m later relapsed. In general, cases without motor deficits were more likely to be cured, and then only slowly. The only real justification for compression to 50m is rapid deterioration at 18m. This does not guarantee to stop or prevent deterioration as four cases of deterioration at 50m are reported. Nine cases of compression beyond 50m to as deep as 76m (250 fsw) on air are reported with the conclusion that it provides little or no benefit.

Atmospheric Pressure↗
PubMed1984

Somatosensory evoked potentials and neuraxial blood flow in central nervous system decompression sickness.

Seven adult, conditioned dogs were anesthetized with pentobarbital sodium and prepared for measurement of upper lumbar, mid-thoracic and lower cervical spinal evoked potentials (SEPs), cortical evoked potential (CEP), and aortic, right ventricular, and cerebrospinal fluid pressures. Following preparation, one animal was monitored by means of repeated evoked potentials for 2 h, at which time a [14C]iodoantipyrine autoradiographic blood flow study was performed. The 6 other animals were exposed to simulated dives in a compression chamber while anesthesia was maintained through a chamber penetration. These animals developed decompression sickness (DCS) of varying severity upon returning to the surface, and the corresponding decrements in neuronal function of the cord and the brain were measured by means of serial SEP and CEP recording. Following this evoked potential recording, [14C]iodoantipyrine autoradiographic blood flow studies were performed. The results indicated that clear reductions in SEP and CEP amplitude were associated with very low blood flows, which were in the 'neuron-disabling' range. Spinal and cortical somatosensory evoked potentials provide a valuable index with which to monitor and manage a model of spinal cord DCS.

Animals↗
PubMed1984

Several new aspects of bubble-induced central nervous system injury.

Ischaemia is a major mechanism underlying central nervous system (c.n.s.) damage in decompression sickness. Some recent experimental observations on the effect of bubble-induced ischaemia on c.n.s. tissue sharpen and extend our understanding of the pathophysiology of decompression sickness. After bubble-induced brain ischaemia, a measurable increase in 111In-labelled leucocytes occurs in the injured hemisphere. By 4 h into the recovery period the cells are concentrated in zones of low blood flow, as measured by the [14C]iodoantipyrine technique. The presence of these cells during the critical early hours of c.n.s. ischaemia suggests that they may contribute to the evolution of neuronal damage. Oedema is often cited as the cause of clinical deterioration after c.n.s. ischaemia or trauma. Recent evidence indicates that the presence and degree of circumscribed brain oedema is not a good predictor of the amount of nerve cell recovery (by using cortical sensory evoked response) after bubble-induced brain ischaemia. This brings into question the role of circumscribed oedema of the c.n.s. in dysfunction of post-ischemic nerve cells.

Animals↗
PubMed1984

Remote monitoring of neuraxial function in anesthetized dogs in compression chambers.

This paper describes the development of an electrophysiological model using spinal and cortical evoked potentials (SEP, CEP), for the diagnosis and monitoring of spinal cord decompression sickness (DCS) in anesthetized dogs. A comparison of alpha-chloralose with sodium pentobarbital showed that the latter caused a reduction in CEP amplitude. Continuous observation of EPs over 5 h showed a small reduction and an increasing variance of amplitude with time. The effectiveness of the method in the diagnosis of DCS and in studies of the adequacy of treatment is illustrated with several examples.

Anesthesia↗
PubMed1984

A model of spinal cord dysbarism to study delayed treatment: I. Producing dysbarism.

This paper reports the development of a model of spinal cord decompression sickness (DCS) which lends itself to studies of treatment in anesthetized dogs. Models tried early in this development could be used in the future to study blow-up and cerebral decompression sickness. We found that a dive with a bottom time of 12-15 min at 300 ft breathing air and decompressed in 5.5 min produced a high incidence of cord DCS, as diagnosed by changes in spinal evoked potentials (SEP). Furthermore the animals could generally be sustained on the surface using intravenous fluids, without going into shock, before treatment by compression was begun. The findings are discussed in the light of previous studies.

Anesthesia, Intravenous↗
PubMed1984

A model of spinal cord dysbarism to study delayed treatment: II. Effects of treatment.

Using the spinal cord decompression sickness model described in Part I, we explored the effects of delay to treatment on the recovery of spinal evoked potentials (SEP). The primary treatments of oxygen at 60 fsw (2.8 bar) and air at 165 fsw (6.0 bar) were studied. In this exploratory study the results were surprisingly poor in all treatments applied. There is evidence that in this model a delay of 15-18 min between diagnosis and start of therapy would generally allow some recovery of SEP, which would rarely be complete. Supporting experiments involving cord ischemia are described. The results from this study enabled us to design a set of practicable experimental criteria for the purpose of discovering the optimal combinations of oxygen and pressure for the treatment of spinal cord decompression sickness.

Animals↗
PubMed1984

Cerebral arterial air embolism: I. Is there benefit in beginning HBO treatment at 6 bar?

A method for studying treatment of cerebral arterial gas embolism in dogs is described. The model produces severe cortical dysfunction and cerebral blood flow deficits. The efficacy of treatment was assessed using median nerve somatosensory cortical evoked potentials (CEP), [14C]iodoantipyrene autoradiographic cerebral blood flow studies, brain water content, and various physiological parameters. A direct comparison of modified U.S. Navy Treatment Tables 6 and 6A is reported. Complete recovery of CEP was not seen after 90 min of treatment. The maximum rate of CEP recovery occurred in the first 15 min of treatment. Recovery continued out to 60 min. Thereafter, some dogs on treatment 6A showed signs of deterioration. The cerebral blood flow studies were the same in both groups and showed no sign of pathologically low levels of flow. It appeared that there was no advantage in preceding 2.8-bar (60-ft) oxygen treatments with compression to 6 bar (165 ft) on air for the treatment of arterial air embolism in this model.

Animals↗