Dysbaric Osteonecrosis Review Short Update on Dysbaric Osteonecrosis: Concepts and Decompression Management Niladri Kumar Mahato1 Abstract Dysbaric osteonecrosis (DON) is caused by inadequate decompression after exposure to very high ambient air pressures. Different pathological events have been shown to occur in conjunction to result in DON. New observations from clinical and experimental data in this field have led investigators to reformat the etiology, pathogenesis and modify existing modalities of treatment of DON. This short review revisits concepts related to pathophysiology of DON occurring as a part of generalized decompression sickness and discusses newer therapeutic insights stemming from recent advancements in DON research. Keywords: Decompression; Dysbarism; Embolism; Hyperbaric Juxta-articular; Metaphysis; Rhizomelic J Bangladesh Soc Physiol. 2015, December; 10(2): 76-81 For Authors Affiliation, see end of text. http://www.banglajol.info/index.php/JBSP Introduction ysbarism or musculoskeletal pointed towards several etiologies of DON8-13. decompression sickness (DCS) is Given the typical anatomy of vasculature around Dusually observed in people who undergo the end of long bones, it seems plausible that deep-sea diving or are exposed to environments DON is linked to occurrence of micro-embolisms of high air pressures1-5. Dysbarism or Caisson with gas or lipid bubbles following a rapid Disease (CD) is characterized by an array of decrease in surrounding air pressure at those systemic complications involving soft tissues, the sites3,10,14-17. Other investigators have proposed cardio-pulmonary, nervous, renal and external compression of blood flow in such musculoskeletal systems when individuals or vessels due to similar bubbles arising in structures experimental animals are brought back to normal around an artery or a vein to induce external pressure. Intra- or extravascular compressions atmospheric pressures without adequate disrupting blood flow usually follow creation of decompression, even after a single hyperbaric bubbles typically arising from nitrogen gas that exposure1,6,7. Dysbaric osteonecrosis (DON), is less soluble in the plasma and also expand one of the primary constituents of DCS, has been rapidly to induce morbid symptoms of DCS, once a subject of prolonged investigations to determine released rapidly from tissues11,12,16,,18-20. the precise patho-physiology of the affliction, and its prevalence and relationship with DCS. Recent research suggests that an increased Evidences obtained from patients and data hypercoagulability due to increased levels of collected from experimental CD animals have serum plasminogen activator inhibitor plays a decisive role in active occurrence and prognosis Received June 2015; Accepted August 2015 of DON11,12,19,,21. The role of lipid dissolution 76 J Bangladesh Soc Physiol. 2015, December; 10(2): 76-81 Dysbaric Osteonecrosis Niladri Kumar Mahato in the bone marrow cavity and events of localized shoulders and /or hips more frequently than other and systemic activation of platelet aggregates are joints6,19,27. There are more than a few variables also being probed for their purported association that link DCS to DON and the correlation with DON. Treatment strategies are being between these two conditions is controversial1. evolved in the lines of our current understanding DON can be thought of as a condition that may of DON to prevent its occurrence and to combat arise independently with triggering specific long term extremely debilitating osseous damage patho-physiological events immediately after resulting from rapid and flawed decompression. decompression, or a long term sequel of DCS. This paper would briefly review the patho- In light of this background, it would be physiologic concepts associated with DON, worthwhile if one questioned if re-compressive discuss current research findings, and outline treatment strategies (used for all CD patients) directions of new therapeutic considera-tions for would have the same desired effect for different its management1,2,5,12,15,19,22,23. pathologies operating simultaneously in CD10,11. Methods This scenario becomes more complicated as Primary scientific literature on dysbaric newer etiological mechanisms are being osteonecrosis was accessed as journal articles identified for DCS – devoted to clinical studies and experimental (i) It all starts with the ‘bends’: Bends in DCS models of DON. Online databases were searched are characterized by acute pain at or near the limb using a set of specific search terms and keywords joints following rapid decompression. Nitrogen including the ones mentioned in this text. is more soluble in fat than in non-fatty tissue. Databases searched included Pubmed®, Google Therefore fat in the bone marrow acts as Scholar® and MEDLINE® resources. Special reservoirs of nitrogen, as more nitrogen gets attention was paid to screen and analyze absorbed within the marrow cavity when a person information on the current concepts surrounding is subjected to adequate air compression. The the pathogenesis and clinical course of DCS, bubble threshold is defined as the limit of air DON, CD, and current management strategies compression when fat stores are supersaturated and future research areas defined in this field. by inert gases beyond which point gas bubbles start to form inside the body, at a given pressure Discussion and for a given period of time2-4. Slow Features of DON observed in ‘dysbarically’ decompression and adequate blood flow in the injured subjects is thought to be a part of the vessels allows almost all the accumulated gases 1,12 spectrum of CD symptomatology . DON does to diffuse out of the tissues, enter capillary not feature as an immediate complication in networks and eventually exhaled via the lungs. persons presenting with symptoms of generalized Since the solubility of nitrogen is poor, rapid decompression sickness9. The specific lesions of decompression creates aggregates of large, bone necrosis, per se, are not detected by even symptomatic bubbles. Accordingly, the ‘bends’ sophisticated MRI evaluation at the early stages have been thought to occur predominantly due of the dysbaric injury8,11,16,22. However, gas to stretching and irritation of the nerve endings bubbles in the marrow can be picked up using of the marrow sinusoids and the endosteum by MR techniques8,22. Other causes of aseptic bone the expanding nitrogen bubbles1. Bends of DCS necrosis being ruled out, lesions specific to DON is treated by re-compressive hyperbaric oxygen can take months to develop1,17,21,23-26. Almost treatment (HBO) that induces a back-diffusion all cases of DCS (including prospective cases of of gases into the tissues thereby preventing DON) invariably report pain, the ‘bends’, at their embolism. Slowly released gas moving from J Bangladesh Soc Physiol. 2015, December; 10(2): 76-81 77 Dysbaric Osteonecrosis Niladri Kumar Mahato tissues to capillaries do not form bubbles, travel to fatal local or disseminated intravascular in solution and can be slowly cleared out by the coagulation cascades. Even a small increase in lungs. However, recent investigators have intramedullary pressure gradients above the questioned the effectiveness of re-compressive systemic venous pressure may cause fat treatment applied across all symptomatic CD embolism with its deleterious effects 9. This may patients5, 9, 10, 28. They have proposed that happen with rapid and unregulated HBO therapy, application of HBO should be careful and should as may be seen with some decompression not result in critically elevated intra-medullary treatment. Though recompression of a fat coated pressure causing death of the marrow cells. nitrogen bubble may reduce the size of the bubble Additionally, the intensity of HBO should not by diffusion of the trapped nitrogen (thereby be so high that it accentuates pain during relieving pain symptoms of DCS), the residual treatment and be very specific in the timing of fat bubble still remains a potential source of its application and the duration of its exposure producing DON through occlusion of finer blood to tissues. vessels. A fair degree of research focus is currently being directed towards understanding (ii) What happens to the fat cells (adipocytes) in different thrombogenetic events related to DON rapid decompression ?: Lipid degeneration has with relation to modulation of lipid and platelet been implicated as the starting point of several linked enzyme activity9-12. systemic pathological cascades seen in DCS. Data from animal experiments and human (iii) Role of blood coagulation in DON: There autopsy studies show that rapid decompression has been a growing body of evidence that results in significant enlargements in the size of connects DON patho-physiology mechanisms to adipocytes2, 9. On further decompression, these derailment of physiologic intrinsic blood cells rupture spilling their contents to forms larger coagulation pathways in the body. Studies related coalesced intracellular aggregates of fat bubbles, to blood-bubble interface show presence of in combination with other cell lytic debris. These fibrinogen in the vicinity of the bubble, a decrease fat bubbles, in combination with air bubbles, may in antithrombin III activity, and accelerated cause extravascular compression on the tiny platelet aggregation at sites of accumulated epiphyseal or diaphyseal vessels at juxta-articular intravascular fat and air bubbles9-12. Autopsy areas of long bones. Fat bubbles often have been materials