Acute Hypertension Traumatic
as a Diagnostic
Rupture
of the Thoracic
EUGENE G. LAFORET, M.D., Boston,
From the Departmentsof Thoracic Surgery, Boston University School of Medicine, Massachusetts Memorial Hospitals, Boston City Hospital, and Newton- Wellesley Hospital, Boston, Massachusetts.
method
to determine
patient
who
has
matic rupture When
A
should
mentally even
be
fatal study
which
there rupture
tinctly
of
of the thoracic
the diagnosis
is no effective
long
technics.
enough Since
ment demands diagnosis is the clinical
to
paper
of persistent
may
constitute
ble
10 will
dence.
manage-
often
to describe
Accidents
resulting
diag-
OF TRAUMATIC
rupture injuries
of the thoracic of the chest”
which
rupture
origin
of the
from a height, involve
from abrupt associated
occurs left
aorta.
are the classic variety usually
just
falls may
root.
When
artery.
in the
In
the aortic
subclavian
beyond
on the other hand, rupture the aortic
and immediate
tion
a subadventitial
is prevented, develops.
cause fatal rupture chronic
traumatic
“Steering-wheel
ture is incomplete hematoma
deceleration
with
“traumatic
(Fig.
rup-
exsanguinaperiaortic
1.) This may either
secondarily aneurysm.”
or progress There
traumatic
frequency
has
are compati-
rupture
of
enlargement
increases been
the
in a patient the
of the
diagnostic
aortography,
and
upon
of a shadow
confi-
of course, employed
is
with
in recent years. CASE REPORT
RUPTURE OF THE THORACIC AORTA
are most commonly
becomes
year old man was admitted to Newton-Wellesley Hospital one hour after the car he had been driving ran into a ditch. He had been hurled violently against the steering wheel, receiving injury to the anterior part of the chest. Although there was clinical evidence of shock, the patient was coherent and oriented. Injuries included facial lacerations, left anterior rib fractures, and fractures of the left clavicle, left forearm, and left femur. Blood pressure, which had been unobtainable, rose to 80/40 mm. Hg with blood transfusion and other resuscitative measures. When the clinical status stabilized, a portable anteroposterior chest roentgenogram was obtained. This showed widening of the superior mediastinum to the left and displacement of the trachea to the right (Fig. 2) in addition to rib fractures on the left. As often happens, the mediastinal changes were ascribed to technical factors involved in obtaining a chest roentgenogram in a severely injured patient. Proteinuria and microscopic hematuria were present. Blood pressure the day after A
nostic clue. PATHOGENESIS
of
Progressive
shadow
the
hyperten-
an important
depends
and clinical findings
Emergency decisive
greater
it
diagnosis
demonstration
those aorta.
mediastinal
and since such
acute
will follow. to be estab-
intervention
with hemomediastinum
with
thoracic
modern
a high index of suspicion,
of this
finding
by
the
whose history
Spencer
surgical
precise diagnosis,
purpose
sion, which
salvable
consistent
dis-
that
essence
roentgenographic
Trau-
with this injury
be
In
for
quite
category.
appropriate
requires
not,
have estimated
to 20 per cent of patients live
aorta
aorta
a
trau-
DIAGNOSIS
sophis-
treatment.
of the thoracic
for example,
or
survived
is considered
surgical
lesions,
in the
lethal
of these courses
funda-
curable
than
diseases,
in
which
momentarily
mandatory.
physician
interested
falls into the former [I],
the
potentially
uncommon,
matic et al.
more but
though
ticated
pragmatist
Aorta
Massachusetts
lished, therefore,
s a benevolent
Clue in
to a is no 948
forty-two
American
Journal
of Surgery
Rupture
of Thoracic
FIG. 1. A, diagrammatic representation of traumatic rupture of the aorta distal to the origin of the left subclavian artery, with compression of the aorta by periaortic hematoma and partial obstruction of lumen by the clot. Kate shift of the trachea to the right by the mediastinal hematoma. B, complete transection of aorta, with the exception of adventitia. There is distraction of the ends and total obstruction of the lumen by clot. (Both illustrations modified from Zehnder [IZ] .)
was lW/lOO mm. Hg and three days after injury was 200/120 mm. Hg. As far as could be determined there had been no prior hypertension. The patient showed persistent tachycardia, oliguria, falling hemoglobin and hematocrit values despite transfusions, and increas ng azotemia. Serial chest roentgenograms suggested regression of the mediastinal enlargement. It was postulated that a retroperitoneal hematoma had compromised the renal arterial inflow. resulting in acute renal ischemia (“Goldblatt phenomenon”) with mounting hypertension, oliguria, and nitrogen retention PI. Elevated blood pressure persisted between 150/100 and 190/l 10 mm. Hg. Femoral pulses unfortunately were not examined. Although the patient’s condition seemed stable, it was never entirely satisfactory, and tachycardia, apprehension, and evidence of continuing blood loss were present. His major problem, however, was thought to be a renal one. On the morning of the seventh hospital day he suddenly died. Autopsy disclosed traumatic rupture of the aorta immediately beyond the origin of the left subclavian artery, with massive left extrapleural hemorrhage and left hemothorax. Both kidneys showed hypoxic nephrosis. The apparent regression of the mediastinal hematoma as demonstrated roentgenographically was probably due to extrapleural sequestering of the blood which could not be delineated on portable chest roentgenogram. With intrapleural
injury
Vol. 110. DPcembc+r 1965
.iorta
! l-i! I
of thi5 collection the tamponin:: cfl‘cct L\;IS lost and tht’ patient cssanguinated.
rupture
COMMENTS
The insistent emphasis on travel at high speeds makes it likely that traumatic rupture of the thoracic aorta will increase in frequency. Simultaneously the outlook for the patient who survives the initial injury has brightened [S]. This is the result not only of improved surgical technics for managing the lesion but also, and perhaps particularly, of greater reliance on angiographic methods of establishing a definitive diagnosis. The decision to employ aortography in a severely injured patient, however, may be a difficult one. Consequently, any clinical clue that may help to reinforce this decision might be welcome. In the case previously detailed herein, persistent hypertension was incorrectly assigned a renal cause. If its true significance had been understood, death may possibly have been averted. Rice and m’ittstruck [4] were probably first in calling attention to the association of acute hypertension with traumatic rupture of the thoracic aorta. The diagnostic value of this finding has nevertheless been generally unrecognized, although Jahnke, Fisher, and Jones [3] have recently stated that, “Significant hypertension developing shortly after trauma in a previously normotensive individual is believed to be an important confirmatory finding.” It may, of course, be difficult to ascertain from a
Laforet TABLE I OCCURRENCEOF HYPERTENSIONIN FIFTEEN PATIENTS WITH PROVEDTRAUMATICRUPTUREOF THE THORACIC AORTA
Reference
Rice and Wittstruck [4] Wyman [j] Jay and French [6] Passaro and Pace [7] Spencer et al. [I] Malm [8] Dobell, MacNaughton, and Crutchlow [9] Fleischaker, Mazur, and Baisch [IO] Jahnke, Fisher, and Jones
[31
Age hr. 1 and Sex
20, 49, 20, 30, 24, *,
F F M M M M
[ill
180/120 170/90 160/90 150/70 140/100 210/110
39, M
160/90
17, M 20, M 25, M 23,M 33, M 36, M
180/80 142/84 180/90 200/90 180/72 210/110
19, M 42, M
200/120
Stoney, Roe, and Redington Present case
Blood Pressure (mm. Hg)
*
* Not recorded.
severely injured patient whether blood pressure was normal prior to trauma, but factors such as youth or active military status may be helpful in this regard. In Table I the basic data are recorded in fifteen instances of significant hypertension associated with proved traumatic rupture of the thoracic aorta. The finding of hypertension in a severely injured patient, particularly if coupled with evidence of continuing blood loss, is somewhat of a paradox. The patient reported on by Rice and Wittstruck [4] was a twenty year old woman who, in the last month of pregnancy, was involved in an accident as a passenger in a taxicab. These writers state, “The occurrence of a severe intractable hypertension is explained on the possible basis of (a) local segmental spasm of the aorta as the result of trauma, or (b) reflex irritation of cardiac accelerator nerves aggregated in the superficial cardiac plexus at the site of the laceration. The presence of previous mild hypertension and pressor instability is believed to have formed the etiological background.” On the basis of the findings in later cases, without the complicating factors of mild antecedent hypertension and of pregnancy, it may be possible to invoke a more mechanistic cause. Figure 1 suggests that some degree of
aortic obstruction occurs in these cases. This may result from extrinsic compression by the periaortic hematoma, intraluminal blockage by clot, or from both. Operative confirmation of this thesis has been obtained by other writers [8,11]. The situation, then, is essentially one of acute coarctation of the aorta, and hypertension in the upper extremities is thus inevitable. Aortic obstruction is further suggested if there is concomitant diminution in the volume of the femoral pulses, quantitated by sphygmomanometer if possible. SUMMARY
Traumatic rupture of the thoracic aorta is a fundamentally lethal but potentially curable lesion. It is due to accidents involving abrupt deceleration. Acute hypertension in the upper extremities may constitute an important clue in the diagnosis, and results from what is basically an acute aortic coarctation. REFERENCES 1. SPENCER, F. C., GUERIN, P. F., BLAKE, H. A., and BAHNSON, H. T. A report of fifteen patients with traumatic rupture of the thoracic aorta. J. Thoracic & Cardiooasc. Sarg., 41: 1, 1961. 2. LAFORET, E. G. Malignant hypertension associated with unilateral renal artery occlusion: three cases. Ann. Int. Med., 38: 667, 1953. 3. JAHNKE, E. J., JR., FISHER, G. W., and JONES, R. C. Acute traumatic rupture of the thoracic aorta: report of six consecutive cases of successful early repair. J. Thoracic b Cardiovasc. Surg., 48: 63, 1964. 4. RICE, W. G. and WITTSTRUCK, K. P. Acute hypertension and delayed traumatic rupture of the aorta. J.A.M.A., 147: 915, 1951. 5. WYMAN, A. C. Roentgenologic diagnosis of traumatic rupture of the thoracic aorta. Arch. Swg., 66: 656, 1953. 6. JAY, J. B. and FRENCH, S. W., III. Traumatic rupture of the thoracic aorta: review of literature and case report. Arch. Surg., 68: 657, 1954. 7. PASSARO. E.. TR. and PACE, W. G. Traumatic rupture of the aorta. Surgerj, 46: 787, 1959. 8. MALM, J. R. In discussion of reference [I]. 9. DOBELL, A. R. C., MACNAUGHTON, E. A., and CRUTCHLOW, E. F. Successful early treatment of subadventitial rupture of the thoracic aorta. New England J. Med., 270: 410, 1964. 10. FLEISCHAKER, R. J.. MAZUR, J. H., and BAISCH, B. F. Surgical treatment of acute traumatic rupture of the thoracic aorta. J. Thoracic & Cardiovast. Surg., 47: 289, 1964. 11. STONEY, R. J., ROE, B. B., and REDINGTON, J. V. Rupture of thoracic aorta due to closed-chest trauma. Arch. Surg., 89: 840, 1964. 12. ZEHNDER, M. A. Aortenruptur bei stumpfem Thoraxtrauma: retrospektive Auswertung der Kasuistik und zukiinftige chirurgische Mijglichkeiten. Helvet. chir. acta, 26: 442, 1959. American Journal of Surgery