Tissue injury due to the use of inotropic and vasopressor agents is a challenging clinical scenario marked by impaired perfusion, delayed wound healing, and increased risk of infection. The occurrence is relatively infrequent, documented to be below 2% in certain case reports, but it can manifest in critically ill patients receiving life-saving vasopressor therapy [1]. The severity of a wound can be categorized using the Society for Vascular Surgery (SVS) WIfI (wound, ischemia, and foot infection) score, which was introduced in 2013. This scoring system assesses the degree of tissue engagement, encompassing ischemic alterations, necrosis, infection, and ulceration in the affected digits [2]. Treatment approaches involve early recognition and the withdrawal of vasopressors, application of topical nitroglycerin ointment, administration of intravenous prostaglandin E1, wound debridement, and (in severe cases) vascular surgery or amputation [3]. Hyperbaric oxygen therapy (HBOT) has recently been suggested to enhance tissue oxygenation, stimulate angiogenesis, and accelerate wound repair [4]. This case report highlights the effectiveness of HBOT in a patient with severe peripheral tissue injury following inotropic and vasopressor administration.

A 64-year-old female patient with diabetes mellitus and a recent history of epidural steroid injection (L2 level) visited the emergency center due to severe dyspnea, lumbago, and xerostomia. She was diagnosed with septic shock due to hypervirulent Klebsiella pneumoniae, iatrogenic emphysematous osteomyelitis at L2, and a paravertebral abscess of the right psoas. The patient was immediately admitted to the emergency intensive care unit (EICU) to manage her hemodynamic instability. During her EICU stay, the patient underwent continuous renal replacement therapy and mechanical ventilation care, as well as intravenous multiantibiotic therapy. An inotropic agent and vasopressor (norepinephrine at a highest dose of 60 mcg/min, vasopressin at a highest dose of 5 IU/hr) were initiated to maintain adequate blood pressure and cardiac output. The vasopressin was tapered on the 1st day of hospital admission, and norepinephrine was fully tapered by the 11th day of hospitalization.

On her 12th hospital day, the patient developed peripheral tissue injury on the bilateral lower extremities, characterized by dusky skin and decreased capillary refill time (Fig. 1). The wound was considered grade 2 in the SVS WIfI classification system and clinically was described as major tissue loss. The gangrenous change in both feet was further evaluated with the ankle-brachial index (ABI) to rule out peripheral arterial disease, which is characterized by reduced blood flow to the lower limbs due to atherosclerosis or other vascular conditions. The ABI results revealed normal values, with a left ABI of 1.33 and a right ABI of 1.30 (Fig. 2). This outcome strongly suggested that the manifestation in both feet stemmed from the iatrogenic administration of vasoconstrictors.

Given the compromised perfusion and risk of tissue necrosis, the decision was made to initiate a series of HBOT sessions as soon as the patient’s medical condition allowed in-ward management. The patient underwent a total of 27 mono chamber HBOT sessions, each lasting 130 minutes, administered at a pressure of 2.5 atmospheres absolute and 100% oxygen. The treatments were well-tolerated, and the patient's vitals remained stable throughout the sessions.

A noticeable improvement in skin perfusion was not directly observed following the 27 HBOT sessions. Furthermore, when her medical condition was recovered enough for outpatient follow-up, she revisited our orthopedic outpatient department every 1 or 2 months to check on her peripheral tissue injuries, which still did not show evident improvement. Amputation was recommended for the foot lesions in the lower extremities, but the patient refused.

Ten months following the patient's previous outpatient appointment, she returned to the orthopedics department, and significant progress had been made in the healing of her foot lesions (Fig. 3). No additional treatment was administered during the period of follow-up loss, and the patient reported that she had independently performed self-debridement of hardened skin tissues. The previous areas of necrotic skin showed enhanced capillary refill and a gradual return of normal skin coloration. Also, the follow-up x-ray image revealed partial self-amputation of the distal phalanx in regions where the skin was previously necrotic, following the restoration of normal skin coloration (Fig. 4). The patient reported decreased pain and discomfort associated with the peripheral tissue injury. The total progress of the case report is shown in Fig. 5.

This case report highlights the usefulness of HBOT in improving skin perfusion in a patient with peripheral tissue injury due to inotrope and vasopressor use. The limitation of this case was the restricted assessment of wound healing after the patient was discharged from the hospital. It is assumed that the HBOT sessions played a preventive role in halting additional ischemia below the joint level, resulting in autoamputation of the tip of the distal phalanx and revascularization of the remaining wounds. Further research, including controlled trials, is needed to establish standardized protocols and to confirm the broader applicability of HBOT in similar clinical scenarios.

The improvement in skin perfusion observed in this case suggests that HBOT has the potential to enhance tissue oxygenation and angiogenesis in peripheral tissue injuries related to compromised perfusion caused by the administration of inotropes and vasopressors. HBOT involves breathing 100% oxygen under increased atmospheric pressure, leading to elevated oxygen levels in plasma and tissues. This increased oxygen availability directly supports cellular metabolism and promotes wound healing [5]. HBOT also augments the diffusion of oxygen in tissues with compromised blood flow, which is crucial for providing oxygen to areas with limited circulation. HBOT triggers the release of growth factors such as vascular endothelial growth factor, promoting the formation of new blood vessels (angiogenesis) to improve tissue perfusion [6]. Moreover, HBOT can attenuate inflammation by reducing proinflammatory cytokines and oxidative stress. This anti-inflammatory effect prevents vasoconstriction and helps maintain blood vessel patency. HBOT can reverse microvascular constriction caused by hypoxia and ischemia. This vasodilation improves blood flow and nutrient delivery to tissues. Lastly, HBOT encourages the development of collateral circulation, compensating for compromised blood vessels and contributing to improved skin perfusion [7]. The combined effects of increased oxygen availability, angiogenesis stimulation, inflammation reduction, and vascular dilation offer a comprehensive explanation for the observed improvements in wound healing and tissue repair.