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Ischemia-reperfusion injury can occur with any injury that involves the interruption of vascular flow. Potential causes include soft tissue crush injuries, myocardial ischemia, and stroke. Hyperbaric oxygen treatment is not only an adjunctive treatment aimed at reducing ischemic tissue damage but, when used early enough post-injury, may mitigate the ischemia-reperfusion response by modulating inflammation, supporting microcirculatory function, maintaining metabolic function in affected tissues, and decreasing the production of reactive oxygen species and oxidative tissue damage. Due to a paucity of available hyperbaric chambers in many regions and a lack of experience or knowledge regarding its indications, hyperbaric oxygen therapy is an often missed therapeutic option. This topic discusses the etiology and pathophysiology of ischemia-reperfusion injuries, reviews the treatment of these injuries with hyperbaric oxygen, and highlights the interprofessional team's role in managing patients with this condition. Objectives: Identify patients at risk of or presenting with ischemia-reperfusion injury. Implement hyperbaric oxygen therapy as an adjunctive treatment for ischemia-reperfusion injury, following established guidelines and protocols. Review the potential adverse effects of treating ischemia-reperfusion injury with hyperbaric oxygen. Collaborate with an interprofessional healthcare team to manage patients with ischemia-reperfusion injuries, including coordinating the timing and duration of hyperbaric oxygen therapy and other treatment modalities. Access free multiple choice questions on this topic.

Ischemia-reperfusion injury (IRI) is a well-recognized phenomenon potentially occurring following nearly any ischemic insult to tissue. Upon restoring blood flow, a secondary reperfusion injury can further damage tissue.[1][2] If initiated early, hyperbaric oxygen therapy (HBOT) can help ameliorate the damaging effects of reperfusion by modulating inflammation, supporting microcirculation, maintaining metabolic function in affected tissues, and decreasing the production of reactive oxygen species and oxidative tissue damage.[1][3] Hyperbaric oxygen therapy involves the administration of 100% oxygen at an atmospheric pressure greater than 1 atmosphere absolute and elevates the partial pressure of oxygen in the blood and tissues. One atmosphere absolute (ATA) is the average atmospheric pressure exerted at sea level. The resulting 20-fold increase in dissolved oxygen in the blood reaches all body tissues, providing excess oxygen to tissues suffering from a lack of delivered oxygen. Often, the secondary reperfusion injury is more severe than the initial insult. Injuries leading to possible IRI are: direct traumatic tissue injuries; pressure-induced injuries; cold injuries or burns; and embolic, thrombotic, and inflammatory occlusive insults.[1] Clinical scenarios where IRI may manifest are: following thrombolytic therapy for cerebrovascular accidents; massive trauma resuscitations; fasciotomy for compartment syndrome; restoration of blood flow to transplanted organs; and invasive cardiovascular interventions.[1][4] The severity of the IRI that results following an ischemic event is a function of multiple factors, including the duration of ischemia, the size of the ischemic territory, and the metabolic function of the ischemic tissue.[1] The time at which irreversible tissue damage occurs varies based on the metabolic activity of the affected area, with sensitive tissues such as the brain showing evidence of irreversible damage after as little as 20 minutes.[5][6] The subsequent IRI pattern of injury shares many common pathological features regardless of the tissue or organ involved. The common pathological features are: oxidative stress; reactive oxygen species (ROS) production; inflammation; increased neutrophil-endothelial interaction with subsequent neutrophil infiltration of affected tissue; microvascular dysfunction; and tissue necrosis.[1][7]

Ischemia-reperfusion injury has the potential to occur in multiple clinical scenarios. Reperfusion after myocardial infarction, cerebrovascular accident, organ transplantation, and compartment syndrome are all common clinical scenarios encountered in modern medical practice. Reperfusion may result in tissue injury worse than the original ischemic insult. To improve patient care and reduce morbidity and mortality associated with IRI, healthcare professionals must understand the mechanisms underlying IRI and the benefits of HBOT. Clinicians across all specialties should know the clinical scenarios in which IRI occurs and the associated clinical findings. Hyperbaric oxygen treatment is not only an adjunctive treatment aimed at reducing ischemic tissue damage but, when used early enough post-injury, may help to mitigate the ischemia-reperfusion response. Patients affected by IRI often have healthcare professionals from multiple specialties involved in their care. The complexity necessitates a collaborative approach among clinicians to ensure patient-centered care and improve overall outcomes. Clinicians must contribute individual expertise while providing effective interprofessional communication to provide the best patient care and reduce morbidity and mortality. Initiation of HBOT will reduce the amount of lost tissue while improving the patient's quality of life.

Clinicians and members of interprofessional teams need to be fully aware of the specific indications for hyperbaric oxygen therapy (HBOT) and the practical aspects of its administration. To enhance the process of administering HBOT, treatment teams can take specific steps before sending patients to an HBOT facility. Early communication with a hyperbaric team is critical to facilitate these steps. For instance, for patients with an endotracheal tube (ET) in place, filling the cuff of an ET tube with fluid instead of air may be necessary to prevent pressure-related complications in the HBOT chamber. An air-filled cuff can lose volume during chamber compression, leading to air leaks, improper endotracheal tube positioning, and compromised ventilation. Moreover, when patients require intravenous infusions and HBOT simultaneously, special pressure-rated tubing and pumps capable of withstanding the higher pressures of HBOT are necessary. Regular and early communication between the primary and hyperbaric teams can streamline care coordination, address the logistical aspects of hyperbaric treatment, and improve patient outcomes.

The interprofessional team overseeing hyperbaric therapy must actively monitor potential risks associated with the treatment. These risks include central nervous system and pulmonary oxygen toxicity, barotrauma to the inner ear, sinuses, and lungs, and confinement anxiety or claustrophobia. Vigilance regarding oxygen toxicity of the central nervous and pulmonary systems is essential, as the risk for these conditions increases with 100% oxygen pressurized above atmospheric pressure. Immediate symptom recognition is critical. The symptoms of central nervous system oxygen toxicity are: Headache Tinnitus Visual changes Paresthesias Seizures Pulmonary oxygen toxicity symptoms are: Tickle or burning sensation with inhalation Hemoptysis Dyspnea Early identification of these adverse effects by the interprofessional team facilitates timely interventions, improving patient outcomes. Additionally, the team should be aware of the heightened risk of fire associated with hyperbaric oxygen due to the high oxygen concentrations used. A fire within a hyperbaric chamber can be catastrophic. Removing flammable materials from chambers and prohibiting electronics help mitigate these risks and can help prevent accidents. Enforcing the hyperbaric team's policies on fire reduction strategies and promptly recognizing fires, if they occur, are ways the interprofessional team can contribute to reducing the risk of fire incidents.