A Case of Mixed Decompression Illness Manifestations in a Commercial DC-8 Cargo Jet Pilot
S.J.H. Veronneau
FAA Civil Aerospace Medical Institute, Oklahoma City, OK 73125-5066
A.A. Pilmanis
Armstrong Laboratory/CFTS
Brooks AFB TX, 78235-5104
Stanley R. Mohler
Wright State University
Aerospace Medicine Residency Program
Dayton, OH, 45401-0927
Introduction
This case documents a case of signs and symptoms from both air gas embolism (AGE) and venous gas embolism (VGE) decompression illness and may represent the first reporting of either the simultaneous onset of both conditions or an overlap in symptomatology.
Sequence of Events
After an otherwise normal departure a DC-8 cargo flight experienced pressurization problems at flight level FL 80. The Capt. ordered the donning of masks, use of 100% O2 , and wanted FL 350, to complete the mission, despite the repeated objections of the crew. Following an 18 minute climb and 4 min of level flight at FL 330 the captain suffered a fairly rapid incapacitation over a minute or two, communicating by hand his intention to descend but being unable to effect it. A 5000 fpm, 8 minute descent to FL 80 while on oxygen did not result in any improvement.
Medical Findings
After diverting into CVG the pilot was taken to a local hospital able to move and speak, with difficulty, and demonstrating some varying left sided neurological signs. After diagnosing dysbarism, the pilot was transferred by helicopter to receive HBO. He was hypertensive but stable in aeromedevac, and at a tertiary care hospital the diagnosis was changed to dissecting aortic aneurysm.
Physical exam documentation is incomplete, but tests showed evidence of noncardiogenic pulmonary edema, normal echocardiogram, normal pulmonary and arch aortogram, no hyperacute EKG changes, mild-moderate CPK serum enzyme elevations (4% MB), normal dipyridamole stress test, and later abnormal pulmonary scan positive for pulmonary emboli.
Consistent with DCS II: At least 40 LB overweight, BMI 34, no prebreath, no improvement with descent, hematocrit to 63% transiently, leucocytosis, CXR showing pulmonary edema, second CT of head showed edema. Consistent with AGE: very rapid onset of neurological deficits, smoker with likely air trapping, no improvement with descent, 3rd CT scan of head showed widespread distribution of watershed infarcts, CPK enzyme spike with elevated MB fraction.
Discussion
This case report highlights a commercial pilot who experienced decompression illness with a mixed picture of DCS and AGE features. The pilot experienced a rapid onset neurological problem after a rapid unpressurized climb to FL 330, on oxygen, which did not improve on descent and in fact evolved into pulmonary edema, cerebral edema, circulatory collapse and cerebral infarctions. Fortunately treatment is the same for both once the diagnosis of decompression illness can be made. Hospitals need to maintain a higher awareness of decompression illness and the illnesses that mimic it. The case will be discussed in detail in light of recent findings in the decompression illness literature.
FAA Civil Aerospace Medical Institute, Oklahoma City, OK 73125-5066
A.A. Pilmanis
Armstrong Laboratory/CFTS
Brooks AFB TX, 78235-5104
Stanley R. Mohler
Wright State University
Aerospace Medicine Residency Program
Dayton, OH, 45401-0927
Introduction
This case documents a case of signs and symptoms from both air gas embolism (AGE) and venous gas embolism (VGE) decompression illness and may represent the first reporting of either the simultaneous onset of both conditions or an overlap in symptomatology.
Sequence of Events
After an otherwise normal departure a DC-8 cargo flight experienced pressurization problems at flight level FL 80. The Capt. ordered the donning of masks, use of 100% O2 , and wanted FL 350, to complete the mission, despite the repeated objections of the crew. Following an 18 minute climb and 4 min of level flight at FL 330 the captain suffered a fairly rapid incapacitation over a minute or two, communicating by hand his intention to descend but being unable to effect it. A 5000 fpm, 8 minute descent to FL 80 while on oxygen did not result in any improvement.
Medical Findings
After diverting into CVG the pilot was taken to a local hospital able to move and speak, with difficulty, and demonstrating some varying left sided neurological signs. After diagnosing dysbarism, the pilot was transferred by helicopter to receive HBO. He was hypertensive but stable in aeromedevac, and at a tertiary care hospital the diagnosis was changed to dissecting aortic aneurysm.
Physical exam documentation is incomplete, but tests showed evidence of noncardiogenic pulmonary edema, normal echocardiogram, normal pulmonary and arch aortogram, no hyperacute EKG changes, mild-moderate CPK serum enzyme elevations (4% MB), normal dipyridamole stress test, and later abnormal pulmonary scan positive for pulmonary emboli.
Consistent with DCS II: At least 40 LB overweight, BMI 34, no prebreath, no improvement with descent, hematocrit to 63% transiently, leucocytosis, CXR showing pulmonary edema, second CT of head showed edema. Consistent with AGE: very rapid onset of neurological deficits, smoker with likely air trapping, no improvement with descent, 3rd CT scan of head showed widespread distribution of watershed infarcts, CPK enzyme spike with elevated MB fraction.
Discussion
This case report highlights a commercial pilot who experienced decompression illness with a mixed picture of DCS and AGE features. The pilot experienced a rapid onset neurological problem after a rapid unpressurized climb to FL 330, on oxygen, which did not improve on descent and in fact evolved into pulmonary edema, cerebral edema, circulatory collapse and cerebral infarctions. Fortunately treatment is the same for both once the diagnosis of decompression illness can be made. Hospitals need to maintain a higher awareness of decompression illness and the illnesses that mimic it. The case will be discussed in detail in light of recent findings in the decompression illness literature.
Last updated: Monday, March 2, 2009