The Use of Hyperbaric Oxygen Therapy for Ear Reconstruction: A Case Series

Introduction: The unique anatomy of the ear makes the reconstruction more challenging. Microtia and auricula hematomas are deformities or defects that can occur in the ear. Treating traumatic injury and congenital malformations of the ears needs some technique and expertise. Hyperbaric Oxygen Therapy is an additional therapy that makes a significant contribution and is effective in wound healing. Case Series: In our first case, a 52-year-old man presented with a traumatic right cauliflower ear due to a traffic accident two weeks before hospital admission. The second case involves a boy 14-year-old who has a Microtia in the right ear with total ear construction performed using autologous costochondral cartilage techniques in a two-stage. Results: Both cases following hyperbaric oxygen therapy, yield good results with good scars, no sign of infection nor tissue necrosis Summary: The combination therapy of reconstructive surgery and administration of oxygen therapy gave satisfactory results in both cases. Five sessions of hyperbaric treatment showed promising results. There is no infection, rapid wound healing, and cessation of flap compromise.

Spinal cord decompression sickness in an inside attendant after a standard hyperbaric oxygen treatment session

Medical personnel in hyperbaric treatment centres are at occupational risk for decompression sickness (DCS) while attending patients inside the multiplace hyperbaric chamber (MHC). A 51-year-old male hyperbaric physician, also an experienced diver, was working as an inside attendant during a standard hyperbaric oxygen therapy (HBOT) session (70 minutes at 253.3 kPa [2.5 atmospheres absolute, 15 metres’ seawater equivalent]) in a large walk-in MHC. Within 10 minutes after the end of the session, symptoms of spinal DCS occurred. Recompression started within 90 minutes with an infusion of lignocaine and hydration. All neurological symptoms resolved within 10 minutes breathing 100% oxygen at 283.6 kPa (2.8 atmospheres absolute) and a standard US Navy Treatment Table 6 was completed. He returned to regular hyperbaric work after four weeks of avoiding hyperbaric exposures. Transoesophageal echocardiography with a bubble study was performed 18 months after the event without any sign of a persistent (patent) foramen ovale. Any hyperbaric exposure, even within no-decompression limits, is an essential occupational risk for decompression sickness in internal hyperbaric attendants, especially considering the additional risk factors typical for medical personnel (age, dehydration, tiredness, non-optimal physical capabilities and frequent problems with the lower back).

Definitive Treatment of Neurological Decompression Sickness in a Resource Limited Location

BACKGROUND: While Fairbanks, AK, USA, is a remote location with significant constraints on medical resources and specialty care, a small U.S. Air Force clinic was able to provide a pilot with definitive care for neurological decompression sickness.CASE REPORT: A 31-yr-old female patient presented to her flight surgeon in Anchorage, AK, USA, with migrating polyarthropathy and headaches 48 h after a flight which included planned aircraft decompression for high altitude low opening (HALO) jump operations. In order to get definitive treatment in a hyperbaric chamber, the patient typically would have to be flown to Seattle, WA, USA. This transfer of care would cost the Air Force approximately 150,000 and may have led to more complicated disease. Fortunately, Eielson Air Force Base (AFB) in Fairbanks had previously procured a Hyperlite hyperbaric chamber specifically for this situation. After consultation with a hyperbaric specialist, the team decided that the most appropriate course of action was to transfer her by car 6 h north from Anchorage to Fairbanks. On initiation of the Hart treatment table, she experienced immediate reduction in joint pain with a reversal of neurological symptoms.DISCUSSION: This patients care could not have been done without the procurement of a hyperbaric chamber. This case demonstrates the utility and necessity for these capabilities at more facilities that manage significant flying operations. Military bases should ensure that hyperbaric treatment capabilities are available within a close proximity.Petruso MJ, Philbrick SM. Definitive treatment of neurological decompression sickness in a resource limited location. Aerosp Med Hum Perform. 2021; 92(1):4749.

Cerebral Gas Embolism in the Course of Mildly Symptomatic Pulmonary Barotrauma in a Scuba Diver

The paper presents a case of pulmonary barotrauma in a scuba diver. Swallowing water and respiratory arrest during the ascent caused the trauma. Symptoms from the respiratory system (including the Behnke’s symptom) appeared several minutes after the completion of the dive and were not severe. However, symptoms from the peripheral nervous system, which appeared later, increased rapidly until the seizure episode and loss of consciousness. Hyperbaric treatment was applied in a decompression chamber on board the ship from which the dive was conducted. The treatment resulted in complete remission of symptoms without any consequences.

Hyperbaric Normoxia Improved Glucose Metabolism and Decreased Inflammation in Obese Diabetic Rat

Hyperbaric treatment improves hyperglycemia and hyperinsulinemia in type 2 diabetes associated with obesity. However, its mode of action is unknown. The purpose of the present study was to investigate the influences of regular hyperbaric treatment with normal air at 1.3 atmospheres absolute (ATA) on glucose tolerance in type 2 diabetes with obesity. The focus was directed on inflammatory cytokines in the adipose tissue and skeletal muscle. Otsuka Long-Evans Tokushima Fatty (OLETF) rats were used as models of type 2 diabetes with obesity and Long-Evans Tokushima Otsuka (LETO) rats served as healthy controls. The rats were randomly assigned to untreated or hyperbaric treatment groups exposed to 1.3 ATA for 8 h d-1 and 5 d wk-1 for 16 wks. Glucose levels were significantly higher in the diabetic than in the healthy control rats. Nevertheless, glucose levels at 30 and 60 min after glucose administration were significantly lower in the diabetic rats treated with 1.3 ATA than in the untreated diabetic rats. Insulin levels at fasting and 120 min after glucose administration were significantly lower in the diabetic rats treated with 1.3 ATA than in the untreated diabetic rats. Hyperbaric treatment also increased interleukin-10 (IL-10) expression in the skeletal muscle and decreased tumor necrosis factor α (TNFα) expression in adipose tissue. These results suggested that TNFα downregulation and IL-10 upregulation in diabetic rats subjected to hyperbaric treatment participate in the crosstalk between the adipose and skeletal muscle tissues and improve glucose intolerance.

Hyperbaric treatment of air or gas embolism: current recommendations

Gas can enter arteries (arterial gas embolism, AGE) due to alveolar-capillary disruption (caused by pulmonary over-pressurization, e.g. breath-hold ascent by divers) or veins (venous gas embolism, VGE) as a result of tissue bubble formation due to decompression (diving, altitude exposure) or during certain surgical procedures where capillary hydrostatic pressure at the incision site is subatmospheric. Both AGE and VGE can be caused by iatrogenic gas injection. AGE usually produces stroke-like manifestations, such as impaired consciousness, confusion, seizures and focal neurological deficits. Small amounts of VGE are often tolerated due to filtration by pulmonary capillaries; however VGE can cause pulmonary edema, cardiac “vapor lock” and AGE due to transpulmonary passage or right-to-left shunt through a patient foramen ovale. Intravascular gas can cause arterial obstruction or endothelial damage and secondary vasospasm and capillary leak. Vascular gas is frequently not visible with radiographic imaging, which should not be used to exclude the diagnosis of AGE. Isolated VGE usually requires no treatment; AGE treatment is similar to decompression sickness (DCS), with first aid oxygen then hyperbaric oxygen. Although cerebral AGE (CAGE) often causes intracranial hypertension, animal studies have failed to demonstrate a benefit of induced hypocapnia. An evidence-based review of adjunctive therapies is presented.

Hyperbaric treatment for decompression sickness: current recommendations

Rationale Decompression sickness (DCS, “bends”) is caused by formation of bubbles in tissues and/or blood when the sum of dissolved gas pressures exceeds ambient pressure (supersaturation) [1]. This may occur when ambient pressure is reduced during any of the following: • ascent from a dive; • depressurization of a hyperbaric chamber; • rapid ascent to altitude in an unpressurised aircraft or hypobaric chamber; • loss of cabin pressure in an aircraft [2] and • during space walks.