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Confirmation of cerebral air embolism with computerized tomography.

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Confirmation of
Cerebral Air Embolism
with Computerized
Te-Long Hwang, MD,” Richard Fremaux, MD,F
E. Simon Sears, MD,* Bruce MacFadyen, MD,’
Brian Hills, DSc, ScD,” Jon T. Mader, MD,?
and Bruce Peters, M D t
Paradoxical cerebral air embolism is an unusual complication following insertion of a subclavian intravenous catheter. W e report an ultimately fatal case in a 75-year-old man
in whom the diagnosis was confirmed by computerized tomographic (CT) scanning. W e postulate that air passed
through a physiologically closed but anatomically patent
foramen ovale.
A 75-year-old black man with an ileocutaneous fistula
had an alimentation catheter inserted into the right subclavian vein while in the Trendelenburg position. After
completion of the maneuver and assumption of a sitting
position, the patient became unresponsive in midsentence.
Neurological evaluation revealed right conjugate gaze
preference with full conjugate excursion to the left upon
left caloric stimulation with cold water. T h e patient was not
responsive to verbal stimulation; noxious stimulation
caused decerebrate posturing on the right. All extremities
were rigid. Deep tendon reflexes were symmetrically
hyperactive and plantar responses were bilaterally extensor.
A chest radiograph showed neither pneumothorax nor
hemothorax, and the tip of the central venous catheter lay
in the region of the superior vena cava. An unenhanced
brain CT scan performed o n a GE 8800 unit, employing a 1
cm collimator, reveaied multiple small, well-defined collections of markedly decreased attenuation within both
cerebral hemispheres. Attenuation coefficients of the lesions were equivalent to that of air in the left frontal sinus.
Presumably, the abnormalities represented intrahemispheric collections of air, probably within and around
small-caliber arteries (Figure).
Three hours later the patient was placed on 10056 oxygen
and transferred to a monoplace hyperbaric recompression
(HBR) chamber. One hundred percent oxygen given at 3
atm absolute pressure for 4 5 minutes elicited no improvement. H e was then transferred to a multiplace H B R
chamber where the treatment protocol of the US Navy
Diving Manual, Table GA, was followed [ 5 ] . N o improvement occurred, and the patient remained in a vegetative
state until his death eight weeks later. CT scans performed
four and six weeks postictus revealed poorly defined areas
of infarction density scattered throughout both cerebral
hemispheres. Investigation for the mechanism of paradoxical embolization by the indocyanine green test and the
technetium 99m-labeled macroaggregated albumin test
failed to show major right-to-left shunts in either the heart
o r lungs.
Systemic air embolism is almost invariably iatrogenic ex-
2 14
/A)Nonenhunced C T scun cut IGE 8800) above the Iuterul
ventricleJ of the bruin showing multiple diisrrete foci of deci*easeddensitji and varying Jize (arrows) in both henziJrheres.
tB) Magnified ( 3 XI vieu ofthefiontul region Jeen in A .
Jhowing a .rimilar absorption coefficient in the right frontirl
sinus (open square) and the le.iion (arrow).
cept for cases of penetrating trauma to the thorax, lungs, o r
major vessels or in decompression sickness. It may complicate surgical procedures, including thoracic, cardiovascular,
and neurosurgical operations; and it can be associated with
abortion, hemodialysis, thoracentesis, needle biopsy of
lung, and perirenal air insufflation.
There has been only one report of an autopsydocumented cerebral infarction secondary to disconnection
of an administration set from a central venous pressure
catheter. An intracardiac septa1 defect in the form of a patent foramen ovale was the presumed mechanism in that
instance [6]. The diagnosis in other reported cases of cerebral air embolism related to placement of central venous
pressure catheters was based on clinical observations aione
[ l , 3, 41. In our patient, air was probably introduced into
the subclavian vein during the interval between catheter
insertion and connection of the administration set while the
patient inspired. Air at atmospheric pressure was sucked
into the catheter along the differential pressure gradient,
collecting in the chambers of the right heart and in the
pulmonary arterial tree. Subsequently the pressure in the
right heart rose above that of the left by reflex constriction
of the pulmonary vasculature. Thus, a physiologically
closed but anatomically patent foramen ovale transiently
opened, providing passage of air from the right to the left
heart. Air entered the aorta and systemic arterial circulation when the patient sat up. This conclusion remains
speculative inasmuch as postmortem examination was not
permitted. However, the presumption is based on the 359%
incidence of patent foramen ovale found at autopsy [ 7 ] .
Oxygen supplementation and HBR are well-established
specific treatments for cerebral air embolism. Although the
repeat C T scan following completion of H B R therapy
showed resolution of the air densities, the patient did not
benefit clinically, probably because HBR therapy was not
initiated soon enough (6 hours after the ictus). Response to
HBR therapy is variable, in that resolution of neurological
deficits has been reported when HBR was delayed as long
as 29 hours after the onset of symptoms [2].
CT scanning provides the most direct method for
confirming the diagnosis of cerebral air embolism, but obtaining the test creates some delay in initiating prompt
therapy. Should a CT scan reveal, in an undiagnosed patient, multiple small, well-defined low-density areas in the
brain that share the same absorption coefficients as air in
the frontal sinus, the diagnosis of air embolism should be
strongly suspected and appropriate therapy instituted.
When the diagnosis of cerebral air embolism is evident on
clinical grounds, diagnostic C T can be dispensed with if
immediate HBR therapy is possible. However, as is often
the case, if transfer to another medical facility for H B R
therapy is necessary, an emergency noncontrast CT scan
should be obtained while the transfer is being arranged. If
possible, the scan should be performed in a large-aperture
CT unit with the left head-down position maintained.
“Univenity of Texas Medical School at Houston
643 1 Fannin
Houjton, T X 77030
J-UniverJity of Texas Medical School at GalveJton
Galveston T X 7 7550
1. Grace DM: Air embolism with neurologic complications: a
potential hazard of central venous catheters. Can J Surg
20151-53, 1977
2. Mader JT, Hulet WH: Delayed hyperbaric treatment of cere-
bral air embolism: report of a case. Arch Neurol 36:504-505,
3. McGoon MD, Benedeto PW, Greene BM: Complications of
percutaneous central venous catheterization: a report of two
cases and review of the literature. Johns Hopkins Med J
145:l-6, 1979
4. Menkin M, Schwartzman RJ: Cerebral air embolism. Arch
Neurol 34168-170, 1977
5. Minimal recompression oxygen breathing method for treatment of decompression sickness and gas embolism. US Navy
Diving Manual, Table GA, Navy Department, Washington,
DC, 1973, pp 8-26
6. Ponsky JL, Pories WJ: Paradoxical cerebral air embolism. N
Engl J Med 284:985, 1971
7. Thompson T, Evans W: Paradoxical embolism. Q J Med
23: 135-1 50, 1030
“Lhermitte’s Sign” as a
Presenting Symptom of
Subacute Combined
Degeneration of the Cord
R. Sandyk, MD, and M. J. W. Brennan, MB BCh, PhD‘
“Lhermitte’s sign,” consisting of a sensation resembling
electric current radiating from the head to the upper limbs
and legs and induced by forward flexion of the head, was
first described by Babinski and Dubois [l] and emphasized
by Lhermitte [2] as a symptom of multiple sclerosis. We
recently examined a woman in whom the phenomenon BCcompanied subacute combined degeneration of the spinal
The patient was 60 years old and for three months had
experienced “shooting sensations” radiating from the head
to the shoulders, upper limbs, and toes. The sensation was
described as resembling an electric shock and was provoked by even the slightest flexion of the neck, a movement that she carefully avoided. On examination, there was
no local tenderness or limitation of neck movement. Adson’s test was negative, and there was no sensory deficit in
the upper limbs or atrophy of the intrinsic hand muscles.
Roentgenograms of the cervical spine revealed no skeletal
abnormalities. Motor system examination showed mild
distal weakness in the lower limbs associated with increased
knee jerks, absent ankle jerks, and Babinski responses
bilaterally. Her gait was unsteady and Romberg’s sign was
present. Vibration sense, light touch, and proprioception
were impaired symmetrically in the lower limbs. Examination of the fundi showed early primary optic atrophy bilaterally. Routine serum electrolyte estimations were within
the normal ranges. She had a hemoglobin concentration of
10.7 gmidl and red cell indices indicative of a macrocytic
anemia (mean cell volume, 110 femtoliters; mean cell
hemoglobin, 2 5 pg). Bone marrow examination showed
generalized marrow depression with megaloblasts. Serum
cyanocobalamin concentration was 189 pgiml (normal
“Present address: Neurological Unit, Boston City Hospital, Boston, MA 02 118.
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air, computerized, confirmation, tomography, embolism, cerebral
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