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PubMed2006

Pathophysiology and natural history of avascular necrosis of bone.

Avascular necrosis of bone (AVN) occurs as two main variants, local and systemic. Local AVN is usually caused by trauma or microtrauma; examples include primary osteonecrosis of the medial condyle, vertebral osteonecrosis, necrosis after meniscectomy, and osteonecrosis of the mandible or small bones. Systemic AVN manifests as epiphyseal necrosis or bone infarction, which is often multifocal. Little is known about the factors that trigger AVN. One possible mechanism is intraluminal obliteration of blood vessels by microscopic fat emboli, sickle cells, nitrogen bubbles (caisson disease), or focal clotting due to procoagulant abnormalities. Extraluminal obliteration may result from elevated marrow pressure or increased marrow fat. Cytotoxicity and genetic factors may be involved also. Many factors are probably capable of inducing AVN, and combinations of factors may be required, although the final mechanism is always critical ischemia. The natural history of AVN is better understood than the early triggering factors. AVN becomes detectable 1-6 months after exposure to an easily identifiable risk factor such as high-dose glucocorticoid therapy or femoral neck fracture. Later on, AVN is uncommon even when the patient remains exposed to the risk factor. The turning point in the natural history of AVN is subchondral plate fracture, which leads to collapse of the necrotic segment of the epiphysis, usually within the first 2 years. The risk of collapse depends chiefly on the initial size and location of the necrotic segment, which can be determined accurately by magnetic resonance imaging (MRI). This natural history has obvious clinical implications.

Bone and Bones↗
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↗
PubMed1977

[Bone and joint changes due to compressed air in divers and Caisson workers (author's transl)].

The radiological and morphological changes of Caisson disease in the skeleton are well known. The findings of interest to radiologists are described. Because of its position, its was possible to review a large number of divers in Kiel; these have been under observation for years, and even decades. The development, manifestation and course of chronic skeletal changes due to compressed air are described to compressed air are described and, according to severity, are classified into types 1 to 4. Late changes are discussed in detail, since these are of importance in relation to compensation.

Bone Diseases↗
PubMedDate not supplied

Interfacility transport of patients with decompression illness: literature review and consensus statement.

OBJECTIVE: Decompression illness (DCI) is a potentially lethal complication of diving and may occur far from hyperbaric facilities. The need for prompt transport to a hyperbaric facility often involves air medical transport, but this may exacerbate DCI. The authors reviewed available literature to establish evidence-based transport strategies utilizing safe altitudes for patients, with DCI. METHODS: MEDLINE, EMBASE, and materials from organizations with expertise in diving medicine were searched for the following terms: decompression sickness, caisson disease, hyperbaric oxygenation, depth intoxication, or diving. Two reviewers independently selected relevant citations involving patients with DCI and air medical transport for review and consensus statement development by an expert working group. RESULTS: A total of 341 citations were identified, and 53 unique citations were reviewed. Nine relevant citations were selected for consensus statement development. There were no clinical trials or prospective cohort studies. Only two retrospective case series, including nine patients, specifically examined the effect of altitude on patients with DCI during transport. No symptom recurrence occurred when the cabin altitude remained within 500 feet of ground level. Seven citations were either letters or statements of expert opinion, recommending a maximum cabin altitude of 500-1000 feet (152-305 meters). CONCLUSIONS: The working group identified the paucity of clinical studies and evidence-based recommendations for air medical transport of patients with DCI. Transport selection should be based on minimizing total transport time and, when transporting by air, ensuring that a cabin altitude of the transporting vehicle does not exceed 500 feet (152 meters) above the departure point.

Air Ambulances↗
PubMed1992

[Work history, health conditions and hearing loss of Ishigaki fishermen].

Based on our previous health survey among Ishigaki fishermen in 1979, this study aimed at clarifying the relations of their work histories to physical characteristics, physiological functions, blood conditions and hearing levels. Medical examination was conducted in 1987 on 118 fishermen inclusive of 33 followed-up fishermen, and in 1989 noise-level and noise-induced temporary threshold shift of hearing was measured for different fishing methods. The results were as follows; 1) Fishing history was not specifically associated with any physical characteristics. 2) High HDL cholesterol, which was observed among divers using diving apparatus, was considered to be a survival effect for divers, since HDL cholesterol is amplified by intensive muscle work. 3) Abnormalities of ECG except for a high R wave were notably observed among the divers, who once changed from unassisted diving to diving with apparatus and then to fishing lines. The main reason for switching jobs was claimed to be caisson disease, and it was suggested that diving with apparatus was related to a high risk of health hazards in the central nervous system and/or respiro-circulatory system. 4) Acoustic acuity greatly declined with aging, and which was commonly observed in groups with different work histories. By way of explanation, exposure to ship engine sounds during daily travelling was the most likely cause. It was also revealed that several hours' exposure to the engine sounds was needed to detect a temporary threshold shift of hearing before and after work.

Cardiovascular Diseases↗
PubMed2001

[Osteonecrosis].

In orthopedic pathology, the pathologist is most commonly faced with the study of resected femoral heads for osteonecrosis. Such a study necessitates a knowledge of clinical findings, of physiopathology and chiefly of radiological findings. Osteonecrosis of the femoral head following fracture has been reported with four morphological stages which are very precisely described. In the same way, idiopathic, non traumatic, or primary osteonecrosis is covered, stressing the putative etiological factors and the most important findings of imaging. The review includes also the skeletal manifestations of decompression sickness as well as bone infarctions not associated with caisson disease, and spontaneous osteonecrosis of the knee. From the recruitment of the Hospital for Special Surgery, NY, it has been recently reported that a significant number of patients regarded as cases of osteonecrosis, either in the femoral head or in the knee, are actually cases of subchondral insufficiency fractures.

Decompression Sickness↗
PubMed2004

[Transtrochateric rotational osteotomy for osteonecrosis of the femoral head].

OBJECTIVE: To explore the indications, operative technique and clinical results of the transtrochanteric rotational osteotomy (TRO) for osteonecrosis of the femoral head (ONFH). METHODS: Nineteen patients (23 hips) with ONFH underwent TRO from October 1992 to May 2001 were reviewed. There were 14 males and 5 females. The age was ranging from 22 to 43 years old with an average age of 33.4 years old. The etiology were as followed: alcoholism 10 cases (12 hips); steroid 6 cases (7 hips); trauma 2 cases (2 hips); caisson disease 1 case (2 hips). Ficat stage: II 8 cases 8 hips; III 11 cases 15 hips. Harris hip score 46 to 74 with mean score 56 preoperatively. In order to determine the location and extent of osteonecrosis, A-P view and accurate lateral view (the film should be placed parallel to the femoral neck with the hip in precisely 90 degrees and flexion 45 degrees of abduction and neutral rotation) were taken in both hips preoperatively. The surgical technique described by Sugioka were used in all patients. RESULTS: Seventeen patients (19 hips) were followed up ranging from 18 to 11 years with mean 54 months. The Harris hip score was from 55 to 94 with mean 80.5. Fourteen hips score more than 80 and good to excellent rate was 73.2%. Harris score were less than 79 in 5 cases and 4 hips of these 5 hips were revised by total hip arthroplasty. The rotation angle was from 55 degrees to 80 degrees with mean 60 degrees . COMPLICATIONS: The circumflex femoral medial artery injury was found in 1 hip; subtrochanteric fracture was found in 2 hips and 1 osteotomy site nonunion occurred. CONCLUSION: TRO can be used to treat ONFH. The indications include: (1) younger patients (less than 45 years old). (2) Ficat stage II and III with more than one third intact articular surface of the femoral head. The better results could be obtained using posterior rotation and lager rotational angle. The Sugioka osteotomy should be used carefully because of its complicated surgical technique.

Adult↗
PubMed1978

[Etiological assessment of aseptic femoral head necrosis from blood serum metabolic parameters (author's transl)].

The etiological assessment of aseptic femoral head necrosis in adults is facilitated by investigation of the uric acid level and of fat metabolism parameters. From 98 of our own patients it appears that femoral head necrosis after trauma, irradiation therapy and caisson disease and after massive doses of cortisone only exceptionally shows pathological serum levels. Femoral head necrosis with manifest metabolic diseases shows 53.3% hyperuricemias and hyperlipemias or dyslipidemias. Of femoral head necroses without concomitant diseases, prior physical effects and administration of cortisone, 91% had hyperuricemia and 65% hyperlipemia or dyslipidemia.

Adult↗
PubMed1998

Avascular necrosis.

There are multiple conditions associated with the development of osteonecrosis including trauma, hemoglobinopathies, Caisson disease, local infiltrative lesions, hypercortisolism, alcohol consumption, chronic renal failure, and autoimmune disease.

Angiography↗
PubMed2002

[Osteonecrosis of the femoral head].

The femoral head is the main location of avascular osteonecrosis. The lesion remains asymptomatic for several months or years before causing non specific hip pain. Risk factors have been identified, mainly femoral neck fractures, corticosteroid therapy and related conditions (lupus erythematosus, organ transplantations), alcohol abuse, dyslipidemia, sickle cell disease, HIV infection, caisson workers, Gaucher's disease, male sex. When typical radiological signs are lacking, MRI is the best investigation. Progression toward hip joint damage highly depends on the necrotic volume assessed at MRI. The combination of plain radiographs which help staging the severity of osteonecrosis, and MRI which indicates the prognosis of the lesion, determines the therapeutic options: symptomatic pain relief therapies or surgical treatment (core decompression, osteotomy or total hip replacement).

Adrenal Cortex Hormones↗
PubMed2002

Internal carotid artery dissection in stroke from SCUBA diving: a case report.

Although diving with compressed air is generally safe, neurological problems resulting from infarction in SCUBA diving are well known, including arterial gas embolism and decompression sickness (caisson's disease, bends) involving the brain and spinal cord. While air gas embolism forms the overwhelming majority of causes for stroke in divers, internal carotid artery (ICA) dissection is another potential mechanism for central nervous system infarction in the setting of SCUBA diving. A 38 year-old female, who presented with complaints of headache, nausea, vomiting, and left sided hemiparesis after rapid ascent to the surface from a depth of 120 feet of seawater was initially treated for decompression illness in a hyperbaric chamber. Further neurological workup revealed a right ICA dissection. This case demonstrates the dangers of ICA dissection following rapid ascent to the surface from underwater and emphasizes an interesting presentation of stroke associated with SCUBA diving.

Adult↗