Arterial Gas Embolism
I understand that arterial gas embolism (AGE) can manifest like a stroke, with facial droop and cognitive problems. It makes sense that bubbles in the brain could cause such serious symptoms, but I have also heard about facial droop occurring with much less severe dive injuries. How could this happen?
This phenomenon is illustrated by a recent case involving a 46-year-old male diving in Ambon Island, Indonesia. The diver was doing several days of repetitive diving using 32 percent enriched air nitrox. Recent diving days included 50- to 90-foot dives that lasted 60 to 90 minutes. He typically did two or three dives per day. On his fourth day of diving, he did a dive to 93 feet for a total dive time of 51 minutes and then, following a five-hour surface interval, he did a second dive to 50 feet for 41 minutes.
Ten minutes after surfacing from this second dive, he experienced left facial weakness and a contracture of his left hand. He also described his tongue as feeling "numb" and "thick." Upon further questioning the diver stated that he experienced a significant reverse ear squeeze earlier that day. He was immediately administered oxygen via a mask on the dive boat.
By chance, a neurologist was present on the dive boat and performed a medical evaluation. The physician found that the left facial muscle weakness involved the forehead as well as the lower face. All of the diver's symptoms except for the "thick" tongue sensation resolved within 30 minutes of breathing 100 percent oxygen. Because of his symptoms and multiday diving history, the dive staff were concerned about decompression illness (DCI) and recommended evaluation by a physician trained in dive medicine.
The differential diagnosis in this case encompasses many nondiving- and diving-related diseases. Given the multiday diving history and rapid onset of symptoms, it is certainly prudent to consider DCI. The anatomical distribution and type of symptoms are not typical for decompression sickness (DCS), however, and without a rapid or uncontrolled ascent, AGE is not likely. Possible non-diving-related maladies include a cerebral vascular accident (CVA) and a transient ischemic attack (TIA), commonly referred to as a stroke and mini-stroke, respectively. These conditions, however, would likely spare the forehead area of weakness and paralysis. Bell's palsy and inner-ear DCS are also possible, yet this diver's history of a significant reverse ear squeeze combined with his pattern of symptoms is highly suspicious for another much less commonly discussed diving illness.
Facial baroparesis, also known as alternobaric facial palsy, is an ischemic neurapraxia (a temporary paralysis) of cranial nerve VII. It is caused by impaired Eustachian tube function that leads to persistent overpressurization of the middle ear following a reduction in ambient pressure — i.e., an ascent. The seventh cranial nerve, or facial nerve, runs through a bony canal as it travels through the middle ear. In most people a small part of the nerve enters the middle-ear cavity unprotected by the bony facial canal. As a result, overpressurization in the middle ear can lead to a localized reduction in blood flow to the exposed portion of the nerve. If the reduction in blood flow is severe or persists, the nerve suffers from ischemia. As a result of this ischemia, the motor and sensory functions of the facial nerve are inhibited. The seventh cranial nerve controls the muscles of facial expression and relays taste sensation from part of the tongue. An appreciation of this anatomy and nerve function along with careful consideration of the symptoms and diving history facilitate diagnosis of this condition.
Facial baroparesis is not DCI. Thus, there is no role for hyperbaric oxygen therapy. In fact, treatment in a hyperbaric chamber might further exacerbate the ischemia and symptoms. Rather, conservative treatment and follow-up with a dive-medicine specialist or otolaryngologist (ear, nose, throat physician) is recommended. If symptoms persist, the treating physician might elect to perform a myringotomy (piercing the eardrum) to decompress the middle ear. To prevent this condition, avoid diving when congested, and equalize early and often. Finally, keep in mind that not all medical problems encountered in diving environments stem from DCI.
Ten minutes after surfacing from this second dive, he experienced left facial weakness and a contracture of his left hand. He also described his tongue as feeling "numb" and "thick." Upon further questioning the diver stated that he experienced a significant reverse ear squeeze earlier that day. He was immediately administered oxygen via a mask on the dive boat.
By chance, a neurologist was present on the dive boat and performed a medical evaluation. The physician found that the left facial muscle weakness involved the forehead as well as the lower face. All of the diver's symptoms except for the "thick" tongue sensation resolved within 30 minutes of breathing 100 percent oxygen. Because of his symptoms and multiday diving history, the dive staff were concerned about decompression illness (DCI) and recommended evaluation by a physician trained in dive medicine.
The differential diagnosis in this case encompasses many nondiving- and diving-related diseases. Given the multiday diving history and rapid onset of symptoms, it is certainly prudent to consider DCI. The anatomical distribution and type of symptoms are not typical for decompression sickness (DCS), however, and without a rapid or uncontrolled ascent, AGE is not likely. Possible non-diving-related maladies include a cerebral vascular accident (CVA) and a transient ischemic attack (TIA), commonly referred to as a stroke and mini-stroke, respectively. These conditions, however, would likely spare the forehead area of weakness and paralysis. Bell's palsy and inner-ear DCS are also possible, yet this diver's history of a significant reverse ear squeeze combined with his pattern of symptoms is highly suspicious for another much less commonly discussed diving illness.
Facial baroparesis, also known as alternobaric facial palsy, is an ischemic neurapraxia (a temporary paralysis) of cranial nerve VII. It is caused by impaired Eustachian tube function that leads to persistent overpressurization of the middle ear following a reduction in ambient pressure — i.e., an ascent. The seventh cranial nerve, or facial nerve, runs through a bony canal as it travels through the middle ear. In most people a small part of the nerve enters the middle-ear cavity unprotected by the bony facial canal. As a result, overpressurization in the middle ear can lead to a localized reduction in blood flow to the exposed portion of the nerve. If the reduction in blood flow is severe or persists, the nerve suffers from ischemia. As a result of this ischemia, the motor and sensory functions of the facial nerve are inhibited. The seventh cranial nerve controls the muscles of facial expression and relays taste sensation from part of the tongue. An appreciation of this anatomy and nerve function along with careful consideration of the symptoms and diving history facilitate diagnosis of this condition.
Facial baroparesis is not DCI. Thus, there is no role for hyperbaric oxygen therapy. In fact, treatment in a hyperbaric chamber might further exacerbate the ischemia and symptoms. Rather, conservative treatment and follow-up with a dive-medicine specialist or otolaryngologist (ear, nose, throat physician) is recommended. If symptoms persist, the treating physician might elect to perform a myringotomy (piercing the eardrum) to decompress the middle ear. To prevent this condition, avoid diving when congested, and equalize early and often. Finally, keep in mind that not all medical problems encountered in diving environments stem from DCI.
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