INTRODUCTION

Diving accidents include several entities varying in severity. Decompression accidents (DA) represent 30-60% of diving accidents (1) . They may vary from minor accidents (cutaneous and musculoskeletal accidents or simple malaise) to very severe accidents involving the neurological system, the vestibilum and the respiratory system. The spinal cord is the most a€ected in severe accidents (2). Although it is rare in DA, air pulmonary embolism, should be suspected in the presence of some suggestive diagnostic clues. is diagnosis could be explained by, on one hand, the excessive importance of degassing which exceeded the victim’s pulmonary ltering abilities (on account of the abruptness of the accident and of the important depth leading to the formation of real gaseous mantles and, on another hand, by activation of the clotting process. Prolonged and continuous immobilization of the paraplegic patient, in addition to the increased blood viscosity are in the present case some associated factors. In our review of the literature we found only one similar case, but pulmonary embolism occurred on the 6th day after the accident. The mechanism seems, therefore, to be di€erent (2)

CASE REPORT 

This case in about a 33-year-old professional diver from the north west of Tunisia who dived at a depth of 105 meters using a tri-mixture at 35% of helium. After 18 minutes at this depth, his lower limbs opened and he came back up to the surface. As his lower limbs immediately afterwards felt heavy, the patient was rapidly enclosed in a home-made hyperbaric chamber for 7½ hours but the patient’s condition did not improve and he was rushed to hospital. History taking revealed that the patient had no relevant medical history. It also revealed that while in the hyperbaric chamber, the patient had a feeling of pressure in the chest and urinary retention.

The physical examination yielded the following ndings: GCS 15/15, T=37°c, pulse 100 pm, BP 130/70 mmHg, FR at 22 cpm and SPO2 at 94%. The patient also had a distended bladder. The neurologic examination revealed a #abby paralysis of the lower limbs with a syndrome of funiculus posterior medullar spinalis, thermal and algesis hypoesthesia with a sensitivity at D8, a pyramidal syndrome at the upper limbs associated with a bilateral Ho€man’s sign and a plantar re#ex on both side laboratory tests showed D-dimeres at 9320 ng/ml and blood gas analysis revealed a hypoxia at 69 mmHg and a hypocapnia at mmHg. The patient received 250 mg of aspirin. He was hydrated and put on broadband normobaric oxygen therapy.

On arrival at the Emergency Department, the patient had a 60-minute session of hyperbaric oxygen therapy (Hbo) at 2.2 ATA because he arrived late (more than 12 hours after the accident). In view of the feeling of pressure in the chest, polypnea, of the tachycardia, the results of blood gas analysis, the normal ndings of chest X-ray (g A) of Well’s score (4.5 indicating an intermediate probability and the raised D-dimeres, a chest CT scan was performed. It revealed a sub-segmental antero and postero basal pulmonary embolism at the right lower lobe (FigB).

Considering the neurological manifestations which were suggestive of the spinal medulla-involvement, an MRI of the brain and spine was ordered (Fig C). It revealed hypersignal
T2 intramedullary ischemic lesions spreading from C3 to C7 with a swollen dorsal medulla the patient was admitted to the Neurology Department where he was put on aspirin and HBPM. Ten sessions of HBO were also prescribed as a consolidation treatment. Neurologically, the course was unfavourable since the decits in the lower limbs persisted and were complicated by other problems related to the supine position. THe patient was then referred to a rehabilitation centre. He did not go back to work.

CONCLUSION

During serious diving accidents spinal involvements are usually the most frequent. They are feared very much due to the neurological deficits that may follow (1,2,3). 

Symptomatic degassing in the intravascular area is much less frequent and should be looked for systematically whenever there are presenting symptoms or signs suggestive of arterial
or venous embolism (3,4). Pulmonary air embolism is very rare in DA(2,). At an early stage, HbO therapy permits an important reduction in the size of the air bubbles and thereby in the consequences of their formation. In fact, beyond 12 hours, the expected benefit derived from HbO therapy is much less on account of the transformation of the air emboli into combined emboli, air and fibrinocruoric emboli (2)