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C D Hutter

Publications and source records attributed to C D Hutter.

9 recordsLinked to original sources
PubMed2000

Dysbaric osteonecrosis: a reassessment and hypothesis.

Dysbaric osteonecrosis is associated with exposure to large ambient pressure changes, and comprises necrotic lesions in the fatty marrow-containing shafts of the long bones, and the ball and socket joints (hips and shoulders). The fundamental causes are still in question and the illness remains a significant health hazard. Radiological and pathological features of both dysbaric and non-dysbaric osteonecrosis are indistinguishable and both are characterized by intramedullary venous stasis, ischemia and necrosis of bone. It has been generally accepted that gas bubbles (probably by initiating intramedullary venous stasis) are the prime cause of dysbaric osteonecrosis, as well as being responsible for Type 1 Decompression Sickness or 'the bends'. Importantly, however, not all series have found a correlation between dysbaric osteonecrosis and 'the bends'. Thus even though it is likely that gas bubbles remain the prime cause of dysbaric osteonecrosis, workers have proposed that in some cases there is another etiological factor which may exaggerate the pathologic effects of gas bubbles, making the bone more susceptible to necrosis. It is proposed that rapid compression by impeding venous drainage from bone initiates intramedullary venous stasis. In the presence of intramedullary gas bubbles, this may progress to thrombosis, ischemia and bone necrosis. The review offers an explanation for total sparing of the knee joint in dysbaric osteonecrosis, and sole involvement of the hip and shoulder (in terms of sub-articular lesions and subsequent joint collapse). In addition to continued observance of proper decompression procedures, a slower rate of compression may further reduce the incidence of dysbaric osteonecrosis. Bone death or osteonecrosis is a concept which Hippocrates put forward in antiquity (1), but it was not until 1794 that James Russell of Edinburgh wrote the first modern-day descriptions. In these cases infection was the predominant etiology (1,2). In 1888 Konig described necrosis of the adult femoral head without infection (3) (aseptic necrosis of bone) and in the same year Twynam reported a case of osteonecrosis in a caisson worker (4) in which there was still a significant infective component. In 1911 Bornstein and Plate, followed later and independently by Bassoe in 1913, presented radiological confirmation of aseptic necrosis of bone in compressed air workers (5). The first report of aseptic necrosis in an underwater diver subsequently appeared in 1936 (6). The condition of aseptic necrosis of bone in association with exposure to raised ambient pressure (previously referred to as caisson disease, pressure-induced osteoarthropathy (7), 'bone rot' (8) and other synonyms (6)) is now generally known as dysbaric osteonecrosis (6). Despite detailed examination of this problem by many authorities, dysbaric osteonecrosis still remains a significant occupational hazard with serious medico-legal consequences (5-13). This suggests that preventative measures are being based upon an incomplete understanding of the pathophysiology of the disease, and that other etiological factors are perhaps being overlooked.

Adult↗
PubMed2000

The Woolley and Roe case.

Albert Woolley and Cecil Roe were healthy, middle-aged men who became paraplegic after spinal anaesthesia for minor surgery at the Chesterfield Royal Hospital in 1947. The spinal anaesthetics were given by the same anaesthetist, Dr Malcolm Graham, using the same drug on the same day at the same hospital. The outcome for the patients and their families was devastating, as it was for the use of spinal anaesthesia in the UK. At the trial 6 yr later, and against the opinion of leading neurologists, the judge accepted Professor Macintosh's suggestion that phenol, in which the ampoules of local anaesthetic had been immersed, had contaminated the local anaesthetic through invisible cracks. In an interview 30 yr after the verdict, Dr Graham believed tha the tragedy was caused by contamination of the spinal needles or syringes during the sterilization process. The subsequent explanation that, on the day in question, descaling liquid in the sterilizing pan had not been replaced by water, supported his belief and finally offered a credible explanation. We review the Woolley and Roe case, the status of spinal anaesthesia before and after 1947, and the relevant medico-legal judgments in claims for negligence in the early days of the National Health Service.

Anesthesia, Spinal↗
PubMed1996

Multiple sclerosis: sunlight, diet, immunology and aetiology.

Multiple sclerosis is more common in temperate latitudes, and migration studies indicate the involvement of an aetiological environmental factor in pre-pubertal life; the precise nature of this factor has never been identified and may perhaps have been overlooked. Here we suggest a simple explanation for the latitude gradient of multiple sclerosis, i.e. that it can be explained by the immunosuppressant effects of sunlight mediated via suppression of the secretion of the immunostimulatory neurohormone melatonin from the pineal gland. The effects of dietary fatty acids in multiple sclerosis also indicate the involvement of anti-inflammatory eicosanoids in its pathogenesis. We further suggest that the exceptions to the latitude gradient (e.g. Japan), which have previously been attributed to genetic factors, may in fact have a dietary basis. Since sunlight also influences the metabolism of fatty acids in the retina, it may also influence the development of retrobulbar optic neuritis-a common antecedent of multiple sclerosis. We suggest a re-examination of the epidemiology of multiple sclerosis based on an understanding of the immunological consequences of illumination of the retina by sunlight.

Autoimmunity↗
PubMed1996

Carbon monoxide--does fetal exposure cause sudden infant death syndrome?

The epidemiological features of sudden infant death syndrome (cot death) include a peak incidence between 8 and 13 weeks of age, a time of death or conception occurring during the winter months and an excess of deaths in infants born to young multiparous women of low socioeconomic status who smoke. We suggest that, through hypoxia, carbon monoxide in tobacco smoke and in the home exerts a noxious effect on the developing central respiratory control mechanism of the fetal brain which then remains particularly susceptible to further insults in the early postnatal period from infection and hyperthermia, resulting in death from central respiratory dysfunction.

Brain↗
PubMed1990

The Woolley and Roe case. A reassessment.

In 1953, two patients, Cecil Roe and Albert Woolley, sued their anaesthetist for alleged negligence because they had developed painful spastic paraparesis after spinal anaesthesia. The court found that phenol, which was used to sterilise the outside of the ampoules of local anaesthetic, had percolated the glass through invisible cracks, contaminating the solution, but that the anaesthetist could not have been aware of this risk. The case was important, despite the fact that judgement was in favour of the anaesthetist, because of the fears that it generated over the incidence of paralysis after spinal anaesthesia. The 'invisible crack' theory has been the subject of much scepticism. New information has been obtained, and the case re-examined objectively. The most probable source of contamination, which led to paralysis in the two patients, and in a third who received spinal anaesthesia on the same day, has been identified. A similar explanation may lie behind a number of other episodes of paralysis associated with spinal anaesthesia.

Aged↗