Extravascular Gas Research Articles

Incidental findings of soft tissue gas in canine and feline thoracic computed tomographic examinations.

Computed tomography (CT) is a commonly used modality in small animal veterinary medicine. Anecdotally, gas bubbles are frequently identified in small animals undergoing thoracic CT examination. The aim of this retrospective observational study was to record the occurrence and prevalence of vascular and extravascular gas in routine thoracic CT examinations in dogs and cats. Patients with any clinical signs of diseases related tosoft tissue gas were excluded. A total of 84 canine studies and 90 feline studies were included, detecting gas in 66.7% of all studies, with gas more likely to be detected in canine studies (75.0%) than in feline cases (58.9%) (P=0.009). Canine studies were more likely to have gas detected in postcontrast studies than in precontrast studies (P=0.016). Intravascular gas was detected in 65.5% of all included studies (75% canine and 56.7% feline). Extravascular gas was detected in 13.8% of all studies (14.3% canine, 13.3% feline), with gas detected in the vertebral canal of 8.62% of all studies (canine 11.9%, feline 5.56%) and within fascial planes in 5.75% of all studies (canine 2.38%, feline 8.89%). In conclusion, gas bubbles were identified in the majority of canine and feline thoracic CT studies without clinical evidence of a pathologic etiology.

Microscopic Findings in the Cardiac Muscle of Stranded Extreme Deep-Diving Cuvier's Beaked Whales (Ziphius cavirostris).

Considerable information has been gained over the last few decades on several disease processes afflicting free-ranging cetaceans from a pathologist's point of view. Nonetheless, there is still a dearth of studies on the hearts of these species. For this reason, we aimed to improve our understanding of cardiac histological lesions occurring in free-ranging stranded cetaceans and, more specifically, in deep-diving Cuvier's beaked whales. The primary cardiac lesions that have been described include vascular changes, such as congestion, edema, hemorrhage, leukocytosis, and intravascular coagulation; acute degenerative changes, which consist of contraction band necrosis, wavy fibers, cytoplasmic hypereosinophilia, and perinuclear vacuolization; infiltration of inflammatory cells; and finally, the presence and/or deposition of different substances, such as interstitial myoglobin globules, lipofuscin pigment, polysaccharide complexes, and intra- and/or extravascular gas emboli and vessel dilation. This study advances our current knowledge about the histopathological findings in the cardiac muscle of cetaceans, and more specifically, of Cuvier's beaked whales.

Establishment of a fish model to study gas-bubble lesions

Decompression sickness (DCS) is a clinical syndrome caused by the formation of systemic intravascular and extravascular gas bubbles. The presence of these bubbles in blood vessels is known as gas embolism. DCS has been described in humans and animals such as sea turtles and cetaceans. To delve deeper into DCS, experimental models in terrestrial mammals subjected to compression/decompression in a hyperbaric chamber have been used. Fish can suffer from gas bubble disease (GBD), characterized by the formation of intravascular and extravascular systemic gas bubbles, similarly to that observed in DCS. Given these similarities and the fact that fish develop this disease naturally in supersaturated water, they could be used as an alternative experimental model for the study of the pathophysiological aspect of gas bubbles. The objective of this study was to obtain a reproducible model for GBD in fish by an engineering system and a complete pathological study, validating this model for the study of the physiopathology of gas related lesions in DCS. A massive and severe GBD was achieved by exposing the fish for 18 h to TDG values of 108–109%, characterized by the presence of severe hemorrhages and the visualization of massive quantities of macroscopic and microscopic gas bubbles, systemically distributed, circulating through different large vessels of experimental fish. These pathological findings were the same as those described in small mammals for the study of explosive DCS by hyperbaric chamber, validating the translational usefulness of this first fish model to study the gas-bubbles lesions associated to DCS from a pathological standpoint.

Decompressive Pathology in Cetaceans Based on an Experimental Pathological Model.

Decompression sickness (DCS) is a widely known clinical syndrome in human medicine, mainly in divers, related to the formation of intravascular and extravascular gas bubbles. Gas embolism and decompression-like sickness have also been described in wild animals, such as cetaceans. It was hypothesized that adaptations to the marine environment protected them from DCS, but in 2003, decompression-like sickness was described for the first time in beaked whales, challenging this dogma. Since then, several episodes of mass strandings of beaked whales coincidental in time and space with naval maneuvers have been recorded and diagnosed with DCS. The diagnosis of human DCS is based on the presence of clinical symptoms and the detection of gas embolism by ultrasound, but in cetaceans, the diagnosis is limited to forensic investigations. For this reason, it is necessary to resort to experimental animal models to support the pathological diagnosis of DCS in cetaceans. The objective of this study is to validate the pathological results of cetaceans through an experimental rabbit model wherein a complete and detailed histopathological analysis was performed. Gross and histopathological results were very similar in the experimental animal model compared to stranded cetaceans with DCS, with the presence of gas embolism systemically distributed as well as emphysema and hemorrhages as primary lesions in different organs. The experimental data reinforces the pathological findings found in cetaceans with DCS as well as the hypothesis that individuality plays an essential role in DCS, as it has previously been proposed in animal models and human diving medicine.

Iatrogenic cerebral gas embolism-A systematic review of case reports.

Cerebral gas embolism is a complication of several medical procedures and occurs when gas enters the cerebral circulation. Knowledge about etiology and outcome in affected patients is limited, and prospective trials on management and treatment are hardly feasible. Case reports are therefore an important source of information. A systematic literature search was conducted in June 2016 and May 2018, supplemented by a manual search. Titles and abstracts were systematically assessed for eligibility, followed by full-text screening for included papers. Screening and data extraction were performed independently by two researchers. Cases of cerebral gas embolism due to any iatrogenic cause were included. Criteria for exclusion were: animal studies, non-cerebral localization, extravascular gas only, and non-iatrogenic causes. 264 cases reported in 189 papers were included. A broad range of procedures leading to iatrogenic cerebral gas embolism (ICGE) were identified and a comprehensive list is presented in this article. Procedures were mostly reported as conducted correctly, but procedure related error, patient activity, or defective equipment were also reported as causes. Neurological, neuropsychological, and cardiopulmonary symptoms were common. The diagnosis was frequently based on or confirmed by radiology, usually CT. Hyperbaric oxygen therapy was applied in a large number of cases. The reported causes, symptoms and signs, and outcomes of ICGE vary significantly, and awareness of the condition in the medical community is essential. A standardized method of reporting could facilitate higher quality research in the field.

Bubbles Quantified In vivo by Ultrasound Relates to Amount of Gas Detected Post-mortem in Rabbits Decompressed from High Pressure

The pathophysiological mechanism of decompression sickness is not fully understood but there is evidence that it can be caused by intravascular and autochthonous bubbles. Doppler ultrasound at a given circulatory location is used to detect and quantify the presence of intravascular gas bubbles as an indicator of decompression stress. In this manuscript we studied the relationship between presence and quantity of gas bubbles by echosonography of the pulmonary artery of anesthetized, air-breathing New Zealand White rabbits that were compressed and decompressed. Mortality rate, presence, quantity, and distribution of gas bubbles elsewhere in the body was examined postmortem. We found a strong positive relationship between high ultrasound bubble grades in the pulmonary artery, sudden death, and high amount of intra and extra vascular gas bubbles widespread throughout the entire organism. In contrast, animals with lower bubble grades survived for 1 h after decompression until sacrificed, and showed no gas bubbles during dissection.

Acute kidney injury due to decompression illness.

Decompression illness is a rare but serious complication of diving caused by intravascular or extravascular gas bubble formation. We report the first case of acute kidney injury in a 27-year-old diver following three rapid ascents. He presented with transient neurological symptoms and abdominal pain followed by rapidly progressive acute kidney injury (creatinine peak 1210 µmol/L) due to arterial air emboli. He received supportive care and 100% oxygen followed by hyperbaric therapy and recovered fully. Arterial air emboli caused by rapid decompression can affect multiple organs including the kidneys. Early transfer to a hyperbaric unit is important as complications may present delayed.

Simulation of Gas Bubble Growth and Dissolution in Human Tissues During Dives and Recompression

As is known, there are many cases when symptoms of decompression sickness (DCS) in divers appear extremely late (> 15 h after completion of diving) and there is much evidence for unsuccessful treatment of DCS by means of recompression. In this study, we have tried to gain insight into the roots of these phenomena. Using the mathematical model of extravascular gas bubble dynamics, we have analyzed the time history of such bubbles under typical air dives and recompression procedures used for DCS treatment. If the parameters defining the bubble dynamics remained invariable, the bubbles formed in different body tissues would reach their maximal sizes within the well-known latency time range for DCS onset, and later these bubbles would dissolve completely during standard recompression procedures. Actually, the parameters defining the processes of bubble growth and dissolution vary with time. The symptoms of DCS that arise with abnormal latency may be induced by bubbles that grow a very long time in some tissues when the rate of nitrogen washout from them is reduced significantly due to vascular bubbles blocking the microcirculation. An abnormal latency of DCS onset may also appear when the negative effects of the initially asymptomatic bubbles are detected during the very slow process of their dissolution. The failure of recompression to resolve this DCS probably happens when the previously formed bubbles are large and located in tissues with less permeability so that they dissolve very slowly.

Role of Extravascular Gas Bubbles in Spinal Cord Injury Induced by Decompression Sickness in the Rat

We have evaluated the contribution of extravascular gas bubbles to spinal cord injury in decompression sickness. For this purpose, a model of decompression sickness was developed by subjecting rats to simulated dives using compressed air. Various diving profiles were tested and the presence of spinal cord injury was demonstrated by electrophysiologic measurements. To evaluate the space occupying lesions induced by gas bubbles in the white matter, the spinal cord was fixed by perfusion with 10% buffered formalin. Tissue blocks from cervical, thoracic, and lumbar spinal cords were embedded in paraffin. Tissue sections were double stained with luxol fast blue and hematoxylin and eosin. The space occupying lesions were quantified with a digitizer tablet. The fractional area of the lesions was 0.009% in controls and 0.026% in rats subjected to diving. We conclude that the volume of extravascular free gas present in the cord of rats with spinal decompression sickness is small and that artifacts of tissue preparation contribute to the volume estimate. As far as can be judged from the results in this animal model, the contribution of extravascular gas bubbles to spinal cord decompression injury is minor.

Therapeutic arterial embolisation of the spleen: a new cause of free intraperitoneal gas

Case histories of two patients are presented in whom splenectomy was required for haematological disorders, but because surgery was contraindicated had therapeutic arterial embolisation of the spleen performed as an initial alternative. A significant improvement in the haematological state was achieved in both cases but one of the patients required drainage of a splenic abscess three months later. In both patients the embolisation caused the early appearances of extravascular gas in the spleen and in one patient a pneumoperitoneum also occurred. The possible aetiological factors involved in this phenomenon are discussed, together with the potential role of splenic embolisation. It is concluded that therapeutic embolisation may be a useful alternative to splenectomy in selected poor-risk patients, but carries a significant risk of inducing a splenic abscess. Intrasplenic or intraperitoneal gas may appear as an apparently benign incidental finding in the early post-embolisation period.

Dysbaric Osteonecrosis

Dysbaric osteonecrosis appears to be independent of decompression sickness. The 2 conditions, however, may share etiologic and pathogenetic factors. The incidence of osteonecrosis is influenced by the number of hyperbaric exposures, extent of pressure, decompression profile and possibly by the rate of compression and degree of obesity. Though etiology and pathogenesis are unclear, osteonecrosis is probably due to ischemia, with gas bubbles causing direct or indirect circulatory impairment. In vitro experiments, as well as human and animal studies, suggest multiple pathogenetic mechanisms: intraosseous vessel compression by extravascular bubbles; vessel obstruction by bubbles, fibrin thrombi, platelet aggregates, clumped erythrocytes or coalesced lipids; and narrowing of arterial lumina by bubble-induced myointimal thickening. Obstructing materials, whether autochthonous or embolic, may result from blood-bubble interface reactions. Rheologic changes and blood flow redistribution could play contributing roles. It seems likely that multiple pathogenetic factors act in concert or sequentially. Proposed nonischemic changes, such as hyperoxic injury gas-induced osmosis, or autoimmunity, lack sufficient supporting evidence. The peculiar vulnerability of bone may be related to gas supersaturation of the fatty marrow; sensitivity to extravascular gas pressure because of tissue rigidity; poor vascularization; and the presence of uranium 238 which promotes nucleation and subsequent gas bubble formation.

Intrafetal gas.

The earliest stage in pregnancy at which intrafetal gas can be demonstrated radiographically is the eighth month (2). Stewart (9, 10) in in vitro experiments found no relationship between the degree of maceration, the quantity of gas present, and the interval between fetal death and the radiographic examination. Gas has been seen in the retroperitoneal area prenatally and postnatally (8, 10), the peritoneal cavity prenatally and postnatally (5, 10), the thoracic wall antenatally and postnatally (10), the cranial cavity antenatally (6), the shoulder joint postnatally (1), and the vertebral canal prenatally (1). Case Material and Methods The radiographs of 53 cases of intrauterine fetal death, in which intravascular gas was demonstrated, were carefully reviewed with special reference to the possible coexistence of extravascular gas. All patients were examined by Edholm's method (3). We wished to investigate (a) the incidence of extravascular gas; (b) whether it is possible to distinguish intrafetal gas from maternal gas or from translucent tissue such as fetal fat, and (c) whether it is possible to determine radiographically in which vessels the gas is contained. In 2 of the 53 cases, gas was seen in the vertebral canal, and these were the only cases in which extravascular gas was identified. Case I: W. U., aged twenty-seven years, gravida III, Para 2. The patient was Rh-positive. The two previous pregnancies were uncomplicated; the present one had proceeded normally, the expected date of delivery being April 7. On April 13 fetal movements ceased, and on April 16 radiography disclosed intravascular gas and gas in the lumbosacral portion of the vertebral canal (Fig. 1). A second roentgen examination on April 17 demonstrated only the intravascular gas. Following medical induction of labor, the patient was delivered of a full-term, stillborn infant. Postmortem examination performed on April 18 showed gross maceration. Case II. K. E., aged twenty-three years, gravida II, Para 1. The previous pregnancy had been uneventful. During the present pregnancy Rh antibodies were demonstrated. The expected date of delivery was Aug. 18. Fetal movements ceased on July 7. Radiography on Aug. 7 disclosed gas in the lumbosacral portion of the vertebral canal coexisting with intravascular gas (Fig. 2). Following medical induction of labor, the patient was delivered of a full-term, stillborn infant. Postmortem examination performed twelve days after the radiographic study showed gross maceration. With Edholm's method the maternal intestines are displaced and not superimposed on the fetal shadows, thereby permitting a differential diagnosis between intrafetal and maternal gas to be made with confidence. To make certain that the streak of translucency in the fetal vertebral canal actually represented gas (Figs. 1 and 2), the lateral films taken prenatally by Edholm's method in 90 cases of intrauterine pregnancy, in which the fetus was alive, were also carefully reviewed.