CURIOUS CASE OF CAISSON DISEASE

Abstract

SESSION TITLE: Medical Student/Resident Critical Care SESSION TYPE: Med Student/Res Case Report PRESENTED ON: October 18-21, 2020 INTRODUCTION: Decompression sickness is caused by rapid changes in breath air pressure and increased amounts of oxygen and nitrogen in different body tissues. As stated by Henry’s law, at a constant temperature the amount of gas dissolved is proportional to its partial pressure above the liquid. As the diver rapidly ascends, the air pressure substantially decreases creating air bubbles that can obstruct different blood vessels creating a wide variety of complications, including ischemia. With more than 9.5 million licensed divers, only 1,000 approximate cases of decompression sickness are reported per year, making it a rare diagnosis. CASE PRESENTATION: A 33 years-old male scuba diver was brought to the ED by ambulance after being found unconscious on the beach shore. Medical history consistent with MDD and cocaine dependence. While en route to the ED, developed neck pain, loss of muscle strength with preserved consciousness. Symptoms developed after five consecutives dives at 115 feet of sea water (fsw) without safety stops nor surface intervals. Spinal MRI was performed with findings consistent with acute isquemia at C6-T2 level. At this point the diagnosis of severe Caisson’s disease was made. Physical exam consisted of severe sensory neurologic impairment at level of T4-T5 dermatome accompanied by motor deficit in the lower extremities and left upper extremity motor deficit at level C8-T1. Initial laboratories showed increased coagulation factors and serum pH of 7.2. Immediately after diagnosis Hyperbaric Oxygen Therapy (HBO) was initiated. During his first session the patient developed respiratory distress and required endotracheal intubation. Follow up spinal MRI showed significant improvement of edema, however, patient’s neurological deficit persisted despite receiving corticosteroids and five HBO sessions. At this point the decision to continue HBO was made. By day 10 in the hospital the patient’s respiratory symptoms improved significantly and MV was discontinued. The patient completed a total of 20 sessions and regained complete movement and sensation in his body. He was discharged for inpatient rehabilitation where he completed therapy. DISCUSSION: This case illustrates the potential complications of decompression sickness and the importance of a prompt identification and rapid treatment to diminish the neurological sequelae and irreversible damage. Identifying precipitant factors that could further aggravate the ischemic symptoms are essential to decide whether the patient will benefit from an extended treatment. The decision to lengthen therapy with hyperbaric oxygen was conclusively beneficial despite delayed neurological improvement. Ultimately minimizing the tissue damage and increasing the odds of motor and sensory function recovery. CONCLUSIONS: Prolonged hyperbaric oxygen therapy could be beneficial in some patients. However, decisions should be made case by case. Reference #1: Hallenbeck, J. M., A. A. Bove, and D. H. Elliott. "Mechanisms underlying spinal cord damage in decompression sickness." Neurology 25.4 (1975): 308-308. Reference #2: Bühlmann, Albert A. Decompression—Decompression Sickness. Springer Science & Business Media, 2013. Reference #3: Weathersby, P. K., L. D. Homer, and E. T. Flynn. "On the likelihood of decompression sickness." Journal of Applied Physiology 57.3 (1984): 815-825. DISCLOSURES: No relevant relationships by Felix Aponte Santos, source=Web Response No relevant relationships by Rosa Marrero-Fernandez, source=Web Response No relevant relationships by Nikita Rabelo-Pagán, source=Web Response No relevant relationships by Nicole Rassi, source=Web Response No relevant relationships by Jean Rodriguez/Agramonte, source=Web Response