A healthy 32-year-old scuba diver was taken to the emergency department (ED). He had lost consciousness following a dive in which he had held his breath during a rapid ascent to the surface and had performed the Valsalva maneuver to clear his ears.
A healthy 32-year-old scuba diver was taken to the emergency department (ED). He had lost consciousness following a dive in which he had held his breath during a rapid ascent to the surface and had performed the Valsalva maneuver to clear his ears. In the ED, the patient was alert with normal speech; he complained of extremity weakness and paresthesias but denied nausea, vertigo, diplopia, and oscillopsia. A chest film, an ECG, and serum metabolic study results were normal. Pulse oximetry was 99% without dyspnea. A CT scan of the brain showed no cerebral hemorrhage. There was no evidence of cervical spine injury. Drs Paul W. Buza and Lauren E. Romeo of Melbourne, Fla, suspected arterial gas embolism of the brain stem and high cervical spinal cord. Maximum oxygen support (non-rebreather), aggressive intravenous hydration, famotidine, aspirin, and high-dose decadron were given in the ED, where the patient’s condition stabilized. He was transferred to a hyperbaric treatment center within 6 hours of the injury. The patient had diffuse weakness and profound gait ataxia; he was unable to stand. Profound loss of proprioception of all joints was present, with loss of light touch and temperature sensations across the lower neck, upper and lower extremities, thorax, and abdomen. Vibratory sensation was absent. Toes were up-going bilaterally with crossed adductor responses. Spontaneous triple flexion signs were noted. Umbilicus reflexes and rectal tone were absent. Deep tendon reflexes showed diffuse hyperreflexia with sustained ankle clonus. Cerebellar examination revealed severe dysmetria on finger pursuit with right worse than left. The patient’s speech was normal. MRI scans of the brain and spinal cord revealed a C2-4 infarct, right cerebellar infarct (A, arrow) and a smaller left parietal-occipital internal capsular infarct. A fast spin echo T2-weighted image without fat saturation demonstrated the infarct within the right cerebellar hemisphere (B, arrow). These lesions share a common arterial supply through the vertebral basilar arteries (posterior cerebral circulation). The patient embolized gas through the vertebral artery, which ascended to the anterior median spinal artery (just proximal to the basilar artery) that supplies the superior region of the cervical spinal cord. Additional gas emboli ascended to the right inferior cerebellar artery and caused the cerebellar infarct. The remaining remnants of gas emboli ascended to the bifurcation of the basilar artery crossing to the left posterior cerebral artery, which gives rise to the medial lenticulostriate vessels and explains the lacunar infarct within the left hemisphere. No evidence of cerebral edema was noted. The patient received daily recompression treatments in the ICU. After his condition improved, he was transferred out of the ICU. During the 5 weeks he spent in the hospital, he started to walk with assisting devices and his bladder function and sensation of light touch and temperature began to recover. He was transferred to a neurologic rehabilitation facility. The diver’s history of breath-holding on rapid ascent with subsequent loss of consciousness suggested arterial gas embolism.1 Pulmonary overpressurization from the Valsalva maneuver with rapid pulmonary air expansion on ascent is a common cause of arterial gas embolism.2 Arterial gas embolism needs to be distinguished from decompression illness, which tends to manifest over several hours and is associated with multiple joint pain, patchy dysesthesias, and other related symptoms. Patent foramen ovale, which is present in nearly 30% of the general population, is usually not a health problem. However, in the setting of rapid pressure changes, this relatively benign condition can predispose a person to arterial gas embolism and its associated high risk of morbidity and mortality.3 In this patient, a Doppler echocardiogram showed no patent foramen ovale or other abnormalities. Arterial gas embolism may occur from iatrogenic causes that include intravenous and central venous catheter placement, arterial line placement, mechanical positive pressure ventilation, air contrast salpingography, air insufflation with pneumatic otoscope, needle biopsy of the lung, and hemodialysis.2 Intraoperative complications that can arise during cardiac surgery with extracorporeal circulation and peripheral vascular surgery may cause a gas embolism. Endobronchial resection of lung tumors using Nd:YAG laser, cesarean section, and pelvic surgery in the Trendelenburg position also can induce these embolisms. In addition, trauma encountered during rapid submarine escape, rapid decompression from loss of cabin pressure during flight, pulmonic barotrauma during cardiopulmonary resuscitation, and head and neck injury can lead to these embolisms.4 Maintain a high index of suspicion for iatrogenic arterial gas embolism, particularly in the sedated patient. Emergent therapy is needed to compress the gas emboli and provide hyperbaric oxygen to ischemic tissues. Early recompressive treatment can improve patient outcome.2,5,6 Recompression treatment provides oxygen to ischemic tissues and protects against leukocyte-mediated reperfusion injury by inhibiting inflammatory mediators that lead to leukocyte adhesion and migration into infarcted tissue.3,7 Corticosteroids can be considered for acute spinal cord and posterior fossa lesions; these agents may be less effective for cerebral lesions. Rehydration with volume expansion can maximize microcirculation perfusion. Aspirin or heparin may be given to avoid platelet aggregation and clot formation. This patient is home and receives outpatient physical therapy. His quadriparesis and sensory dysesthesias have almost completely resolved, although significant proprioceptive loss that compromises his gait remains. Outpatient and occupational therapy will continue.
Diagnosis and treatment of gas embolism. In: Shilling CW, Cariston CB,Mathias RA, Undersea Medical Society, eds.
The Physician’s Guide to Diving Medicine
.Flagstaff, Ariz: Best Publishing Company; 1984:349-361.
Gas embolism. In: Oriani G, Marroni A, Waftel F, eds.
Handbook on HyperbaricMedicine
. Berlin: Springer; 1996:229-243.
Pathogenesis of the decompression disorders. In: Bennett PB, Elliot DH, eds.
The Physiology and Medicine of Diving
. 4th ed. Philadelphia: WB Saunders Company;1993:454-473.
Cerebral air embolism. In: Jain KK, ed.
Textbook of Hyperbaric Medicine
. 3rded. Seattle: Hogrefe & Huber; 1999:143-152.
Gas embolism. In: Kindwall EP, ed.
Hyperbaric Medicine Practice
. Flagstaff,Ariz: Best Publishing Company; 1995:328-341.
Treatment of decompression sickness and arterial gas embolism. In: BoveAA, Davis JC, eds.
. 2nd ed. Philadelphia: WB Saunders Company;1990:249-260.
Decompression illness. In: Hill K, ed.
Preferred Practice Protocols for HyperbaricMedicine
. Houston: The American College of Hyperbaric Medicine; 1997:86-101.