1. science
2. medicine
3. surgery

British Journal of Anaesthesia 1997; 79: 440–445
Prognosis of intraoperative brachial plexus injury: a review of 22 cases
B. BEN-DAVID AND S. STAHL
Summary
A retrospective review over 6 yr of patients
presenting to the hand clinic was performed to
identify cases of postoperative brachial plexopathy
(PBP) and to assess both prognosis and early
indices of prognosis. Over this period (1989–1995),
22 patients were referred by the hospital’s surgical
departments to the hand clinic because of PBP.
Eight cases followed open heart surgery (OHS) and
14 followed non-cardiac surgery (NCS). Median full
recovery took 10 (range 4–16) weeks and 20 (8–50)
weeks, respectively. Long-term follow-up revealed
one OHS patient with residual tingling and
three NCS patients with residual weakness.
Brachial plexopathy after median sternotomy was
characterized by a predominance of sensory
complaint in the lower roots of the plexus. Injury
after non-cardiac surgery was reflected by a
predominance of motor deficit in the upper and
middle roots. Brachial plexus injury after cardiac
surgery carries an excellent prognosis for full
functional recovery. Although the limited number
of cases precludes statistical substantiation, the
data suggest that the prognosis of PBP after noncardiac surgery may be worse in males, diabetics,
those with injury to all roots of the plexus and,
when in addition to the motor deficit there is
sensory loss and pain or dysaesthesia. At a 1 week
“prognostic milestone”, 79% of NCS patients with
significant symptomatology enjoyed complete
recovery although this took as long as 5 months to
1 yr in 50% of patients. At a 6–8 week “prognostic
milestone”, 50% of those who had not yet had
improvement in the motor deficit suffered residual
neurological deficit. All patients recovered to a
significant extent even when recovery was not
complete and none suffered from late deterioration or chronic pain. (Br. J. Anaesth. 1997; 79:
440–445).
Key words
Complications, brachial plexus injury. Nerve, damage (postoperative).
Postoperative brachial plexopathy (PBP) has been
documented in the literature for more than 100 yr.
PBP is generally believed to be a result of traction
injury of the nerves with compression a contributing
factor.1 Both stretching and compression of the
nerve ultimately lead to ischaemia of the vasa
nervorum and subsequent injury to the nerve.2–4 In
addition, there may be rupture of intraneural
capillaries and haematoma formation with further
compression.1 Several factors have been associated
with intraoperative brachial plexus injury, including
concomitant patient disease, anatomical variations,
positioning of the patient, surgical factors and
physiological factors (table 1).
The prevalence of PBP has been estimated at
0.02–0.06%.1 5 6 A recent review of 1541 closed
anaesthesia malpractice claims included 227 (15%)
for nerve injury. Of these, brachial plexus injury
represented 23% and was second only to ulnar
neuropathy (34%) in frequency.7 Insofar as these
cases draw from insurance claim files, they almost
certainly represent cases of residual loss and
dysfunction. Yet previous authors have suggested
that the long-term outcome in cases of intraoperative
brachial plexus injury is almost invariably good—an
apparent contradiction.1 8–10 Review of the literature
regarding prognosis and outcome of PBP reveals a
relatively sparse published data base.1 6 10 11 This is
particularly true if one considers separately those
cases occurring after non-cardiac surgery.
It is reasonable to assume that an awareness of the
potential for brachial plexus and other nerve injuries
together with a knowledge of the pertinent anatomy,
pathogenesis and associated risk factors should
reduce the incidence of these injuries. However,
this information is of little practical value when
confronted with such a patient after operation.
Foremost among the patient’s anxious questions will
be with regard to prognosis. This retrospective
review was undertaken in order to specifically
address the question of prognosis of PBP.
Patients and methods
The records of the Rambam Medical Center Hand
Clinic were searched for all cases of introperative
brachial plexus injury occurring during the period
1989–1995. Both clinic and inpatient hospital charts
were reviewed thoroughly and the patients, where
possible, were contacted for long-term follow-up.
All patients included in this review were those who
presented after operation to the hand clinic following
surgery at this institution. The data do not include
BRUCE BEN-DAVID, MD, Department of Anesthesia, HerzliyaHaifa (Horev) Medical Center, 15 Horev Street, Haifa, Israel.
SHALOM STAHL, MD, Hand Unit, Rambam Medical Center,
Haifa, Israel. Accepted for publication: May 8, 1997.
Correspondence to B. B.-D.
Prognosis of intraoperative brachial plexus injury
441
Table 1 Factors associated with intraoperative brachial plexus
injury
Each patient’s injury was described by a specific
description of the involved nerve roots and by a
description of the initial presentation in terms of
pain, motor and sensory impairment. For the
purposes of this review these disturbances were
classified on three-point scales. These scales were:
motor: 1paralysis, 2paresis, 3no weakness;
sensory: 1anaesthesia, 2hypoaesthesia, 3
normal sensation; and pain: 1 frank pain, 2
dysaesthesia, 3no pain. Electromyography (EMG)
was not performed in the early postoperative period
as this would only be indicated to validate suspicion
of a pre-existing neurological condition.12 Electrophysiological studies were performed 6–8 weeks
after operation, but only in those patients who had
yet to demonstrate significant clinical improvement.
The purpose of the study was to establish nerve
continuity and to serve as a baseline for further
evaluation and decision making regarding other
intervention (e.g. surgical neurolysis).
All patients were treated in a similar manner. To
prevent contractures, occupational therapy was
undertaken for splinting of the wrist and fingers
where indicated. Weakness resulting in shoulder
subluxation or difficulty in elbow flexion was treated
with a supportive sling. Active and passive physical
therapy was conducted agressively in all patients.
Particular attention was paid to full passive range of
motion exercises several times a day to maintain
joint motion and prevent contractures.
Concomitant disease
Diabetes mellitus
Hypothyroidsim
Pernicious anaemia
Alcoholism
Pre-existing neuropathy
Herpes zoster
Polyarteritis nodosa
Peripheral vascular disease
Coagulopathy
Concomitant anatomical predisposition
Cervical rib
Scalene muscle hypertrophy
Deformity (e.g. post-traumatic) of shoulder region
Anomalous derivation of plexus
Positioning
Steep Trendelenburg
Steep Trendelenburgshoulder braces
Steep Trendelenburgwrist suspension
Excessive abduction of arm (990⬚)
Dorsal extension at shoulder
Posterior shoulder displacement
External rotation of arm
Excessive rotation of head
Surgical
Prolonged operative time
Median sternotomy
Physiological
Hypothermia
Hypotension
those patients who had in-hospital consultations
unless the patient went on to receive care through
the outpatient hand clinic. No patient presented to
the clinic sooner than 1 week after operation.
Patients were seen at monthly intervals for 2–3
months after achieving maximum recovery. Longterm follow-up to verify residual injuries and to
eliminate the possibility of late deterioration was
provided by phone contact during the gathering of
data for this review.
Evaluation of all patients included a detailed
history covering concomitant diseases and predisposing factors, a clinical history regarding upper
extremity pain, paraesthesia, numbness and
weakness, and physical examination of all motor and
sensory functions supplied by the brachial plexus.
Results
A total of 22 cases of PBP were identified; 14 of
these had undergone non-cardiac surgery (NCS)
(table 2) and eight had undergone open heart
surgery (OHS) with median sternotomy (table 3). In
the NCS group there were six women and eight
men, with mean ages of 52 and 57 yr, respectively. In
the OHS group there were seven males (mean age
62 yr) and one female (aged 45 yr). Both groups had
patients with possible contributing factors. Hospital
inpatient chart reviews revealed that all patients had
undergone general anaesthesia, but none of the
charts contained information on the specifics of
Table 2 Cases of postoperative bracial plexopathy following open heart surgery. Initial presentation: motor, 1paralysis, 2paresis,
3no weakness; sensory, 1anaesthesia, 2hypoaesthesia, 3normal sensation; pain, 1frank pain 2dysaesthesia, 3no pain.
CABGcoronary artery bypass grafts, MVRmitral valve replacement
Patient
No.
Possible
Presented
contributory
Age Onset of
to clinic
pre-existing
Sex (yr) Sx postop. (weeks) Surgery condition
1
4
7
14
M
M
M
M
61
50
60
58
1 day
Immediate
2 days
1 day
16
17
F
M
45
58
1 day
2
Immediate 1.5
MVR
CABG
20
21
M
M
72
76
1 day
1 day
CABG
CABG
5
2
2
2
4
2
CABG
CABG
CABG
CABG
Injury Not
Time to
to
improved max. recovery Degree of
recovery
Motor Sensory Pain roots at 6–8 wks (weeks)
Initial presentation
2
3
2
Ulnar cubital 2
syndrome
Cervical rib 3
History of
2
brachial
plexus
injury
3
Diabetes
3
2
3
2
2
3
2
3
1
C8–T1
C8–T1
C8–T1
C8–T1
13 wks
4 wks
8 wks
10 wks
Full
Full
Full
Full
1
1
2
1
C7–T1
C7–T1
16 wks
10 wks
Full
Full
2
2
3
2
C8–T1
C8–T1
7 wks
40 wks
Full
Residual
tingling
Full
10
C5–7
3
3
2
Residual weakness
32
2
2
2
54
2 days
3
F
22
3
1 day
38
M
Road trauma pinning femur, tibia fxs,
laparotomy
Hysterectomy
Carpal tunnel
Thoracic outlet syndrome
C5–8
24
48
26
C5–8
C5–T1
C7–T1 3
3
3
3
3
2
1
2
2
Immediate 1
1 day
4
2 days
1.5
55
48
55
F
M
M
Shoulder replacement
Nephrectomy
Hemicolectomy
16
50
8
15
29
20
16
56
56
C6–8
C5–T1
C5–6
C5–7
C5–7
C5–8
C5–6
C5–T1
C5–7
3
1
3
3
2
3
3
1
2
2
2
3
3
2
3
3
2
2
2
2
2
2
2
2
2
2
2
Hysterectomy
Diabetes
Aorto-bifemoral
Alcoholism
Cholecystectomy
Carpal tunnel
Abd.-perineal resection
Sigmoidectomy
Aorto-bifemoral
Heavy smoke rperiph. vasc. disease
Road trauma laparotomy, splenectomy
Hemicolectomy
Pancreas transplant
Diabetes
1 day
1 day
1 day
Immediate
Immediate
1 day
3 days
1 day
1 day
3
3
2
2
1
1
1
3
2
55
62
48
64
70
72
32
70
46
F
M
F
M
F
M
F
M
M
Patient
No.
2
3
5
6
8
9
10
11
12
loss
13
15
18
weeks)
19
Not
improved
at
6–8 wks
Initial presentation
Injury
---------------------------------------- to
Motor Sensory Pain roots
Possible
contributory
pre-existing
condition
Presented
to clinic
Age Onset of
Sex (yr) Sx postop (weeks) Surgery
Full
Full
Full (scalenectomy at 18
Table 3 Cases of postoperative brachial plexopathy following non-cardiac surgery. Initial presentation: motor, 1paralysis, 2paresis, 3no weakness; sensory, 1 anaesthesia, 2hypoaesthesia, 3
normal sensation; pain, 1frank pain 2dysaesthesia, 3no pain
intraoperative positioning or arm positioning. None
of the patients had undergone regional anaesthesia
of the neck or upper extremity. All operations were
of more than 2 h duration but there was no correlation between duration and long-term outcome.
Because of the retrospective nature of the study and
the limited method of case collection, no attempt
was made to estimate incidence data from the total
number of surgical cases over this period.
In the OHS group, seven of eight patients
achieved full recovery over a median of 10 (range
4–16) weeks. One patient, a diabetic, suffered from a
persistent tingling sensation in the affected hand. All
had suffered injury to the roots of the lower trunk
(C8, T1) with two also having injury to the middle
trunk (C7). In the NCS group, three of 14 patients
failed to achieve full recovery although all patients
improved substantially. Injuries included roots of
upper and middle trunks in all but one patient (No.
18). Three patients (Nos 3, 11 and 15) had injury
inclusive of all roots of the plexus. For patients who
recovered fully, the median time to recovery was 20
(range 8–50) weeks after operation. Six patients had
no evidence of motor improvement by 6–8 weeks
after operation and were studied by EMG. This continued evaluation, and a prior history of thoracic
outlet syndrome, led to scalenectomy in patient No.
18, the result of which was complete neurological
recovery. Age had no apparent influence on the
likelihood of residual injury. All four patients with
residual injury were male. While suggestive of an
influence of gender on outcome (non-significant by
Fisher’s exact test) the small number of patients precluded meaningful statistical analysis. The same was
true for the influence of “predisposing factors”; nine
of 22 patients had some predisposing factor (see
table 1) and two had a history of prior carpal tunnel
release. It is uncertain if this is any different from the
incidence of such factors in the general population of
surgical patients. Of the four patients with residual
injury, two had no predisposing factors and two were
diabetic. That two of three diabetics with PBP had
residual injury may suggest a poorer prognosis
among diabetics.
The clinical presentation differed between OHS
and NCS groups. In the former, sensory impairment
and pain–dysaesthesia were the prominent and
consistent features. No patient had isolated or predominant motor loss and six of eight patients had
sensory–pain disturbance without motor loss or of
greater degree than the motor loss. In the NCS
group the opposite was true. Here, motor deficit was
the prominent and consistent feature. There appears
to be no indication of prognosis in the particular
degree and features of the initial presentation. The
one exception to this was for NCS-PBP where
patients with pain–dysaesthesia tended to have a
prolonged recovery. Further, all three patients with
residual injury had pain–dysaesthesia. Also, patients
with injury to all roots tended to have incomplete or
prolonged recovery.
Six NCS-PBP patients had no motor recovery by
6–8 weeks. This group included all three patients
with residual injury; that is 50% of patients with no
motor recovery by 6–8 weeks ultimately had a
Full
Full
Full
Full
Full
Full
Full
Residual weakness
Residual motor and sensory
British Journal of Anaesthesia
Time to.
max
recovery Degree of
(weeks) recovery
442
Prognosis of intraoperative brachial plexus injury
residual deficit. There were several other observations related to recovery; motor recovery proceeded
in a caudad–cepahalad direction with the lower roots
recovering sooner. Sensory recovery appears to
precede motor recovery and failure to observe any
sensory recovery by 3–4 weeks may also be an
ominous prognostic milestone. All patients exhibited
significant recovery even if recovery was not
complete; temporal progression was always in the
direction of recovery with no patient exhibiting
deterioration. No patient in this series suffered
chronic pain.
Discussion
The most striking finding of this study was the
disparate outcomes for the OHS compared with the
NCS group. Although there was no significant
difference in the quantitative incidences of residual
injury (one of eight patients compared with three of
14 patients) there was a qualitative difference. In the
OHS group, one of eight patients suffered a mild
residual tingling sensation whereas in the NCS
group, three of 14 suffered residual weakness. These
values are in contrast with existing opinion that
nearly all intraoperative brachial plexus injuries
recover, and perhaps explains the prevalence of this
complication in the insurance industry data.
It must be acknowledged that our methodology
of case collection skewed the prognostic significance of
these data to the pessimistic. A retrospective review of
only those cases presenting to the hand clinic more
than 1 week after operation eliminates those cases of
mild and transient injury and may preferentially
select those cases of motor complaint over those with
sensory complaint. It has been reported that most
cases of PBP after sternotomy are already asymptomatic at the time of hospital discharge.13 Parks6
reported 25 cases of PBP of whom eight suffered
mild injury and recovered in an average time of 9
days. Of the remaining 17 patients, 14 recovered
within 6 months and three had residual injury.
Presumably our method of data collection would
have missed 94% (if not all) of the cases of
Tomlinson and colleagues13 and 32% of Parks’
cases.6 It is therefore impossible to judge what
fraction of all cases of PBP actually went on to referral to the hand clinic. The prognostic significance of
our data therefore does not relate to all patients presenting immediately after operation with PBP, but
rather to some subset of “worst cases”. As a
prognostic indicator these data are more representative of those patients with significant symptomatology 1 week after operation or at hospital
discharge.
In the OHS cases of PBP the fact that all patients
achieved full functional recovery in spite of this
“worst case” selection suggests an extraordinarily
good prognosis for this subset of cases. While most
authors concur with this optimistic outlook for
OHS-PBP, a prospective study of 1000 cardiac
surgery patients found 55 cases of postoperative
upper extremity disturbance of whom 28 recovered
within several days, 19 recovered within 3 months
and eight were still symptomatic 3 months after
443
operation.14 However, as follow-up did not extend
beyond 3 months it is impossible to know the final
disposition of these eight patients, and it is incorrect
to assume that they suffered permanent injury. In
our own series, three of eight OHS-PBP patients
required 3 months or more to achieve full recovery.
Plexus injury after median sternotomy differs from
PBP after NCS in several critical ways. First, PBP
after OHS is far more common. As opposed to
an incidence of 0.02–0.06% for NCS-PBP, the
incidence of OHS-PBP in various prospective
studies has ranged from a low of 1.9%15 to 18.3%.16
Electrophysiological evidence suggests the existence
of subclinical injury in the majority of cardiac
surgery patients.17 Roy, Stafford and Charlton18
summarized six prospective studies totalling 1772
patients undergoing OHS. The overall incidence of
nerve injuries in these studies was 7.6% of which
80% (6.1%) were PBP. In their own prospective
analysis of 162 cardiac surgery patients there were 12
(7.4%) cases of PBP.
OHS-PBP also differed from NCS-PBP in the
distribution of the injury. Nearly all of the former
involved lower roots of the plexus whereas the latter
were typically lesions of the upper and middle roots.
This generalization holds true throughout the literature and our data are consistent. The mechanism of
injury in OHS-PBP is different (anatomically and
mechanically) from that of NCS-PBP. The positioning of sternal retractors (cephalad placement
promotes injury), extent of sternal retraction (excessive retraction promotes injury) and the wide, asymmetric sternal traction necessary for harvesting of an
internal mammary artery graft pedicle have been
associated with PBP.14 Sternal retraction forces the
clavicle into the retroclavicular space rotating the
first rib superiorly and stretching the lower plexus.19
Persistent changes in somatosensory evoked potentials associated with sternal retraction predict postoperative deficits.20 On occasion, rib fracture may
occur with the possibility of nerve penetration.16 21
These fractures are common when evaluated by
radionuclide bone scan although they are usually not
detected by x-ray.22 This mechanism may explain
the more severe cases of OHS-PBP.
Another difference between OHS-PBP and NCSPBP is in the clinical expression of the injury. Apart
from the different anatomical distributions of the
injuries, the presentation in NCS-PBP has been
described as that of a relatively painless motor deficit
which is greater in degree than sensory loss.8 Our
data supported the relative emphasis on the motor
deficit in NCS-PBP. Where sensory deficit or
pain–dysaesthesia presented in the NCS group it
appeared to herald prolonged or incomplete
recovery and an association with injury to the roots
of the lower trunk in addition to those of the upper
and middle trunks. For OHS-PBP the relative
emphasis is on sensory disturbance as opposed to
motor loss.13 14 Our OHS-PBP patients also had
primarily sensory complaints and 50% had no motor
deficit.
An important difference between these two
categories of PBP is that of prognosis. Although
there are reported cases of persistent deficit after
444
OHS, the literature indicates a high likelihood of full
recovery.14 23–25 Our finding of seven patients with
full recovery and one with only mild residual tingling
(in spite of the “worst case” selection) is consistent
with this. This compares with a less encouraging
prognosis in the case of NCS-PBP.
Regarding the prognosis of OHS-PBP, most
patients are already asymptomatic within several
days.13 14 In the study of Tomlinson and colleagues,13
94% were asymptomatic by the time of hospital discharge. Hudson, Boome and Sanpera26 reported an
incidence of 0.2% of OHS patients in their centre
being referred to the hand clinic for PBP. Using the
incidence data from prospective studies this implies
that in their institution 96–98% of patients with
OHS-PBP enjoyed rapid recovery. We estimate
therefore that 90–95% of patients will be wholly or
substantially improved within 1 month of surgery
(with full recovery forthwith). Of those patients who
have not substantially recovered by the 1 week “prognostic milestone” (our presumed criteria for referral
to the hand clinic) our data suggest complete or nearcomplete recovery is highly likely. Most patients
recover within several months, although on occasion
recovery may be protracted (up to 1 yr) and, only
rarely, incomplete.
In the case of NCS-PBP there are no prospective
studies to allow a valid estimate of what percentage
of patients have transient injury. Using the “1 week
milestone” criteria, our data suggest that of those
NCS-PBP patients with significant symptoms at
1 week, 79% (11 of 14) recover fully. This compares
closely with Parks’ finding of 82% (14 of 17 patients)
full recovery. In assessing the individual patient there
are no absolute markers of prognosis. However, this
study suggests several possible portents to a slower
recovery and worse outcome, including male gender,
diabetes, injury to all roots of the plexus, and the
presence of sensory deficit and pain or dysaesthesia.
Absence of sensory recovery by 3–4 weeks and
motor recovery by 6–8 weeks are further negative
“prognostic milestones”. Half of those patients with
no motor recovery at 6–8 weeks ultimately suffered
residual deficit. We stress that the data of this study
are only suggestive and that the small number of
patients involved precludes statistically significant
conclusions. On the positive side, all patients
achieved substantial, if not full, recovery. The role
of physical therapy in this recovery cannot be
overemphasized.
In summary, brachial plexus injury occurring after
cardiac and non-cardiac surgery are two separate
entities. The former is characterized by a predominance of sensory complaint in the lower roots of the
plexus and the latter by a predominance of motor
deficit in the upper and middle roots. The former is
far more frequent than the latter, with an excellent
prognosis for recovery. The prognosis of brachial
plexopathy after non-cardiac surgery may be worse
in males, diabetics, those with injury to all roots of
the plexus and when, in addition to the motor
deficit, there is sensory loss and pain or dysaesthesia.
At a 1 week “prognostic milestone” 79% of symptomatic patients enjoyed complete recovery, although
this took as long as 5 months or more in 50% of
British Journal of Anaesthesia
patients. In some, recovery took up to 1 yr. At the
6–8 week “prognostic milestone” 50% of those who
had not yet shown evidence of improvement in the
motor deficit suffered residual neurological deficit.
However, all patients recovered to a significant
extent even when recovery was not complete and
none suffered from late deterioration or chronic
pain. The relative infrequency of this serious complication and the paucity of our literature data base
imply the need for further such series and perhaps
ultimately their compilation through meta-analysis.
References
1. Cooper DE, Jenkins RS, Bready L, Rockwood CA. The
prevention of injuries of the brachial plexus secondary to
malposition of the patient during surgery. Clinical Orthopaedic
and Related Research 1988; 228: 33–41.
2. Denny-Brown D, Brenner C. Paralysis of nerve induced by
direct pressure and tourniquet. Archives of Neurology and
Psychiatry 1944; 51: 1.
3. Denny-Brown D, Doherty MM. Effects of transent stretching of peripheral nerve. Archives of Neurology and Psychiatry
1945; 54: 116.
4. Lundburg G, Rydevik B. Effects of stretching of the tibial
nerve of the rabbit: a preliminary study of the intraneural
circulation and the barrier function of the perineurium.
Journal of Bone and Joint Surgery (Br) 1973; 55: 390–401.
5. Dhuner KG. Nerve injuries following operations: A survey of
cases occurring during a six year period. Anaesthesia 1950;
11: 289–293.
6. Parks BJ. Postoperative peripheral neuropathies. Surgery
1973; 74: 348–357.
7. Kroll DA, Caplan RA, Posner K, Ward RJ, Cheney FW.
Nerve injury associated with anesthesia. Anesthesiology 1990;
73: 202–207.
8. Leffert RD. Postanesthetic brachial plexus palsy. In: Leffert
RD, ed. Brachial Plexus Injuries. New York: Churchill
Livingstone, 1985; 121–129.
9. Jackson L, Keats AS. Mechanism of brachial plexus palsy
following anaesthesia. Anaesthesia 1965; 26: 190–194.
10. Kwaan JHM, Rappaport I. Postoperative brachial plexus
palsy. Archives of Surgery 1970; 101: 612–615.
11. Po BT, Hansen HR. Iatrogenic brachial plexus injury: a
survey of the literature and of peritnent cases. Anesthesia and
Analgesia 1969; 18: 915–922.
12. Leffert RD. Clinical diagnosis, testing, and electromyographic study in brachial plexus traction injuries. Clinical
Orthopedics (US) 1988; 237: 24–31.
13. Tomlinson DL, Hirsch IA, Kodali SV, Slogoff S. Protecting
the brachial plexus during median sternotomy. Journal of
Thoracic and Cardiovascular Surgery 1987; 94: 297–301.
14. Vahl CF, Carl I, Müller-Vahl H, Struck E. Brachial plexus
injury after cardiac surgery. Journal of Thoracic and
Cardiovascular Surgery 1991; 102: 724–729.
15. Keates JRW, Innocenti DM, Ross DN. Mononeuritis multiplex: a complication of open-heart surgery. Journal of Thoracic
and Cardiovascular Surgery 1975; 69: 816–819.
16. Vander Salm TJ, Cereda J-M, Cutler BS. Brachial plexus
injury following median sternotomy. Journal of Thoracic and
Cardiovascular Surgery 1980; 80: 447–452.
17. Marganitt B, Shemesh Y, Golan M, Lin E, Engel J.
Subclinical
brachial
plexopathy
following
median
sternotomy. Orthopedic Review 1986; 15: 305–310.
18. Roy RC, Stafford MA, Charlton JE. Nerve injury and
musculoskeletal complaints after cardiac surgery: influence of
internal mammary artery dissection and left arm position.
Anesthesia and Analgesia 1988; 67: 277–279.
19. Kirsh MM, Magee KR, Gago O, Kahn DR, Sloan H.
Brachial plexus injury following median sternotomy incision.
Annals of Thoracic Surgery 1971; 11: 315–319.
20. Hickey C, Gugino LP, Aglio LS. Intraoperative somatosensory evoked potential monitoring predicts peripheral nerve
injury during cardiac surgery. Anesthesiology 1993; 78: 29–35.
Prognosis of intraoperative brachial plexus injury
21. Vander Salm TJ, Cutler BS, Okike ON. Brachial
plexus injury following median sternotomy. Part II.
Journal of Thoracic and Cardiovascular Surgery 1982; 83:
914–917.
22. Woodring JH, Royer JM, Todd EP. Upper rib fractures
following median sternotomy. Annals of Thoracic Surgery
1985; 39: 355–357.
23. Hanson MR, Breuer AC, Furlan AJ, Lederman RJ, Wilbourn
AJ, Cosgrove DM, Loop FD, Estafanous FG. Mechanisms
and frequency of brachial plexus injury in open-heart surgery:
a prospective analysis. Annals of Thoracic Surgery 1983; 36:
675–679.
445
24. Shaw PJ, Bates D, Cartlidge NEF, Heaviside D, Julian DG,
Shaw DA. Early neurological complications of coronary
artery bypass surgery. British Medical Journal 1985; 291:
1384–1387.
25. Lederman RJ, Breuer AC, Hanson MR, Hanson MR,
Furlan AJ, Loop FD, Cosgrove DM, Estafanous FG,
Greenstreet RL. Peripheral nervous system complications of
coronary artery graft surgery. Annals of Neurology 1982; 12:
297–301.
26. Hudson DA, Boome R, Sanpera I. Brachial plexus injury
after median sternotomy. Journal of Hand Surgery 1993; 18A:
282–284.