Open Tibia Fracture with Compartment Syndrome

Open Tibia Fracture with
Compartment Syndrome
JESSE
c. DELEE,M.D.,* AND JAMES B. STIEHL, M . D . * *
Compartment syndromes in the leg associated with closed fracture of the tibia are
well documented.7.15.17.20.22.23.26.28 However,
the existence of compartment syndrome in
open fractures of the tibia has received little
recognition. 17.2'.26 It is generally believed
that open fractures adequately decompress
the compartments and hence prevent the
accumulation of pressure.14s26
The goals of
this paper are to emphasize that open tibia
fractures can produce compartment syndromes and that the associated compartment
syndrome greatly increases patient morbidity.
MATERIALS AND METHODS
During the period between January 1975 to
January 1979, 104 open tibia fractures were
treated at the University of Texas Health Science
Center in San Antonio, of which six developed
compartment syndromes involving all four compartments of the lower leg. During the same period, 41 l closed tibia fractures were treated, five
developing compartment syndromes.
Initial treatment for fractures consisted of intravenous administration of antibiotics, debridement and irrigation of the wound, followed by
immobilization with the Hoffman external fixation device or a long leg cast until clinical and
roentgenographic union was evidenced.
The diagnosis of compartment syndrome was
based on the following clinical signs: ( 1 ) pain disproportional to injury; (2) palpably swollen compartments; (3) pain on passive stretching of the
involved muscles; (4) diminished simple touch
perception; (5) decreased strength of the involved
compartment muscles; and (6) hypesthesias or
anesthesia in the sensory distribution of nerves in
the involved compartment. Distal pulses were palpable unless there was an associated vascular injury.
In each case, a four-compartment fasciotomy
was executed either through combined anterolatera1 and posteromedial incisions2' or a single posterolateral incision." All wounds were initially left
open. Closure was later performed by the delayed
primary technique or by skin grafting. Five of the
six patients were examined postoperatively for
joint range of motion, sensory and motor function,
drainage, and fracture union. One patient had
changed residence after initial fracture care and
was unavailable for personal interview.
RESULTS
Our study included six patients (five men,
one woman) ranging in age from 18 to 42
years (mean, 25 years). In the five patients
contacted, time from injury to follow-up was
16 months (range, eight to 25 months). No
patient had a previous history of injury to
the lower extremity.
Of the six fractures, four were sustained
in motorcycle accidents, and two on impact
with an automobile. The open wounds were
small, measuring an average of 4 cm in
length (range, 2 to 7 cm) and would correspond to Grade I1 injuries.'' The fibular
fractures were segmental and displaced in
four cases; the tibia fractures comminuted
in five (Table I ) . Initial examination re-
Assistant Professor. Division of Orthopaedics, University of Texas Health Science Center, 7703 Floyd Curl
Drive, San Antonio. Texas 78284.
** 12255 de Paul Drive. Suite 250. de Paul Professional Office Building, Bridgeton, Missouri 63044.
Reprint requests to Jesse C. DeLee, M.D.
Received: August 19. 1980.
0009-921X/81/1000/175%0l.00
QJ. B. Lippincott Co
175
TABLE 1.
sex1
Case No.
ARC
Tibia Fx
Fibula Fx
Time: Injury 10
Onser Sx
Wound Debridement and Fasciotomy
Time: Initial
Dcbridemenr
10 Onser of
Sx
Time: Onser Sx ro
Fascioromy
Signs and Sex
A
L
PIS and DI
Wound debridement and
fasciotomy
simultaneously
1
MI42
Tibia: D/3
Spiral oblique
Fibula:
Segmental and
displaced
2 hr.
7 hr.
F/32
Tibia: M/3
Comminuted
Fibula:
Segmental and
displaced
2 hr.
5% hr.
Mf 22
Tibia: M/3
Comminuted
Fibula: Segmental and displaced
6 hr.
Insulindependent
diabetic
2
*Extensive soft tissue
infection resulted in
debridement of
peroneal (sup. and
deep) nerves
Wound debridement
with fasciotomy
later
3
1 hr.
8 hr.
Follo*~upTime and
Findings
Fx at FIU (Union.
Nonunion. Osreomye!irisJ
Fascioromy
A: Weak EHL and EDL
lDPN and SPN sensation
Pain on passive PF
L Swollen tense lateral
compartment
I peroneal strength
P IPTN sensation
Painful passive
DF toes
FfU: 24 mos.
Sensation: ISPN,
DPN, PT
Motor: 1 Ankle, toe
DF ankle and toc
PF
Ankle ROM:
Active: 0"DF20°PF
Passive: 1O"DF3OoPF
Clawing of toe-Yes
Union: 19 mos.
Fibulectomy: 5
mos.
Bone graft: 13
m a . (healed)
Osteomyelitis:
Yes
Combined
A: Weak EHL and EDL
lDPN and SPN sensation
Pain on passive PF
L: 1 peroneal strength
P Weakness of PF toes; lPTN
sensation
Pain passive DF toes
FfU: 8 m a .
Sensation: ISPN,
DPN
Motor: 1 ankle, toe.
DF
Ankle ROM:
Active: OODF1O"PF
Passive: 2OODF30'PF
Clawing-yes
Union: no
Fibulectomy: no
Bone graft: no
Delayed union: 8
mos., post Fx.
Osteomyelitis:
Yes
Combined
A: IEHL, AT & EDL
lDPN and SPN sensation
Pain passive P F toes
L Very weak peroneals; ISN
sensation.
F/U: 25 mos.
Sensation: ISPN.
DPN. PTN, S N
Motor: 1 Ankle, toe
DF. ankle P F
Union: 16 mos.
Fibulectomy: 7
mos.
Bone graft: none
Nonunion: no
Lateral
only
M/19
6
Tibia: D/3 Comminuted
Fibula: Segmental and displaced
Tibia: M/3
Comminuted
Fibula: Comminuted
Tibia: M/3
Comminuted
Fibula: Comminuted
14 hr
9 hr.
8 hr.
AT = anterior tibial muscle
EHL = extensor hallucis longus
EDL = extensor digitorum longus
DPN = deep peroneal nerve
SPN = superficial peroneal nerve
M/18
5
M = male
F = female
M
- = mid-third
3
D
- = distal third
3
M/22
4
17 hr.
I5 hr.
10 hr.
A: IEHL, EDL; lDPN and
SPN sensation
Pain with passive PF
L: ISN sensation swollen tense
compartment
P 1 P F toes and ankle
JPTN sensation
Pain passive DF toes
A: IEHL. EDL. A T
ISPN, DPN sensation
Pain with passive
PF ankle
L: 1 strength peroneals; ISN
sensation; painful passive; inversion.
P 1 strength of toe flexors
A: IEHL, EDL. lDPN and
SPN sensation
Pain passive PF toes
L: ISN sensation tense and
swollen compartment
P IPF toe and ankle
JPTN sensation. pain passive
DF toes
PTN = posterior tibial nerve
S N = sural nerve
DF = dorsiflexion
PF = plantarflexion
I2 hr.
5 hr.
I hr.
P Ankle and toe PF absent:
lPTN sensation.
~~~~~~
~
~
F/U: 2 mos. (moved)
Sensation: ISPN.
DPN. PTN. S N
Motor: I Ankle PF
Ankle, toe DF
Ankle ROM:
Active: None
Passive: DF0"PF2O"
Clawing-no
F/U: 9 mos.
Sensation: ISPN,
DPN. PTN. S N
Motor: 1 Ankle, toe
DF; Ankle, toe PF
Ankle ROM:
Active: 0
Passive: DF0"PF20"
Clawing-no
F/U: 16 mos.
Sensation: ISPN,
DPN, PTN. S N
Motor: 1 Ankle and
toe DF, ankle PF.
Ankle ROM:
Active: PF20°-300
Passive: PF2OO3OoPF
Clawing-no
Ankle ROM:
Active: 2OOPF30"PF
Passive: 2OoPF3OoPF
Clawing-yes
Moved
Union: no
Fibulectomy: no
Bone graft: no
Nonunion: 9
mos., post
fracture
Osteornyelitis: no
Union: no
Fibulectomy: no
Bone graft: no
Nonunion: 16
mos.
Osteomyelitis:
yes
Ostcomyelitis:
yes
Combined
Combined
Combined
178
DeLee and Stiehl
vealed no evidence of sensory deficit in the
posterior tibial, sural, superficial or deep peroneal nerves. Due to pain from the comminuted tibial fractures, individual muscle
strength was not gradable. However, no leg
muscles were found to be totally lacking in
motor function (Table 1).
Patients’ charts were reviewed to determine the time of onset of the compartment
syndrome. In two cases, the compartment
syndrome was diagnosed prior to debridement (Table 1). The average time between
injury and onset of symptoms was two hours;
the average time from onset of symptoms to
debridement-fasciotomy was six hours. In
the other four cases, the diagnosis of compartment syndrome was made after initial
wound debridement and fracture reduction.
In none of these patients was the wound
closed primarily. The average time from debridement to the development of symptoms
was 4.75 hours (Table 1). Fasciotomy was
accomplished within eight to 17 hours (averaging 12.5 hours after the onset of symptoms).
Prior to fasciotomy, all patients were
noted to have a tense, swollen leg with
marked pain on muscle palpatation in all
compartments, and diminished sensation of
the superficial and deep peroneal nerves.
Five patients had decreased sensation in the
posterior tibial nerve and four in the sural
nerve (Table 1). Muscle testing revealed extensor hallucis longus and extensor digitorum communis function to be weak or absent
in all cases. Marked weakness of the toe flexors was evidenced in five cases. Although
muscle strength had not been gradable on
initial examination, progressive weakness in
these muscles was evident. Muscle pain on
passive plantar flexion of the toes was present in all six cases, whereas pain on passive
dorsiflexion was present in only four. Review
of patient records revealed that serial neurologic examinations were inadequate in
three cases.
Vascular surgery consultation was obtained in all six cases (Table 1). Only one
patient had early loss of palpable pulses;
Clinical Orthopaedios
and Related Research
arteriography demonstrated vessel spasm
with no evidence of disruption.
When last seen, all six patients demonstrated absent dorsiflexion of the ankle and
toes; five patients evidenced weakened plantar flexion. Superficial and deep peroneal
sensation was decreased or absent in all six
cases, posterior tibial nerve sensation was
decreased but protective in five, and sural
nerve sensation was diminished in four.
The mean length of hospitalization was
25 days (range, 14 to 42 days). An average
of six surgical debridements per case were
required (range, two to 13). The Hoffmann
external fixation device was employed in five
of six cases, and long-leg cast immobilization
in one. Patellar tendon-bearing casts of orthoplast were employed after adequate soft
tissue stability developed.
At six months’ follow-up, fractures had
not healed in any of the five patients (Table
1). Fibular ostectomy, to encourage tibial
union, was performed in two of the five cases,
of which one healed without further surgical
intervention. One patient required a posterolateral bone grafting 13 months postoperation and subsequently healed by 19
months. All five of these cases were characterized by significant soft tissue loss and
exposed bone. Chronic osteomyelitis and
small draining sinuses developed in four of
these cases.
Five cases had fasciotomy of the four compartments of the lower leg using combined
anterolateral and posteromedial incision^.^^.^^
One patient had decompression through a
single posterolateral incision.” Delayed
wound closure of the fasciotomy incisions
was performed in all cases. Soft tissue loss
from necrosis was severe in four cases, requiring multiple debridements in the operating room, subsequent whirlpool debridement, and eventual skin coverage with splitthickness grafts. In four cases where large
areas of muscle necrosis had occurred, requiring subsequent debridement, return of
ankle motion was neglible. None of the three
patients with a follow-up of more than one
year had active dorsiflexion past neutral
Number 180
October. 1981
Compartment Syndrome
179
FIG. I A . Cross-sectional view of the four
compartments of the
lower leg.
(Table 1). Four of the six patients now have
some degree of active plantar flexion. Two
patients developed equinus contractures of
the foot and required heel elevation for satisfactory gait; both had significant anterior
compartment injuries and were unable to
actively dorsiflex the foot. None of the six
patients was noted to have varus deformities
of the forefoot. Clinically, clawing of the toes
was evident in three of the six patients.
DISCUSSION
V ~ l k m a n n ,in~ ~his report of a case involving a contracture in the leg, drew attention to the development of ischemic injury
following trauma as early as 1872. The key
etiologic factor of ischemic injury is the development of increased tissue pressure
inside closed fascial-osseous compartments,
hence, “compartmental syndromes.”’6 Burton’ demonstrated that if tissue pressure
rises, or arteriolar pressure decreases, the
transmural pressure difference decreases.
Blood flow decreased until, at a critical tissue
pressure, there is no transmural difference,
and arterioles close.’ This causes prolonged
ischemia and muscle anoxia which in turn
promote the formation of histamine substances that dilate the capillary bed and increase endothelial permeabilit~.~
This increases intramuscular edema and swelling
(expansion is limited by the fascia1 envelope), and causes a rise in tissue pressure.
Thus a viscious ischemia-edema cycle develops which will ultimately result in necro-
sis of all elements in the involved compartment.
DIAGNOSIS
This study illustrates that, even in the
presence of an open fracture, development
of compartment syndromes is possible. Physical examination, including neurologic and
vascular tests, immediately on arrival at the
emergency room is essential for documenting a developing compartment syndrome.
The identification of the “patient at risk”
will aid in early diagnosis. The minimal size
of the open wound may be misleading; indeed, the small wounds may be the reason
that these fractures do not spontaneously
d e c ~ m p r e s s . ’Comminution
~-~~
of tibia1 diaphyseal fractures implies a great amount
of energy absorbed at this fracture site.8 In
addition, the association of displaced, segmental fibular fractures in four of our six
cases stresses the presense of high energy
trauma. Displacement of the fibular fracture
confirms disruption of the interosseous membrane with associated severe soft tissue injury” (Figs. 1A and 1B). This allows the
fracture hematoma to extend into the posterior and lateral compartments with resultant increased pressure. A displaced fibula
fracture can result in peroneal artery laceration, another cause of increased compartment pressure (Fig. 1B). We conclude
that a displaced, comminuted fibula fracture
should suggest high energy trauma and pos-
180
Clinical Orthopaedice
and Related Research
DeLee and Stiehl
Tibia
Fibula
Peruneal A.
sible compartment syndrome in patients with
open tibia fractures. (Fig. 2).
Several methods have been advocated to
accurately determine interstitial fluid pressure and ultimately diagnose compartment
syndromes in the clinical ~etting.'~.'*.'~''
However, tissue pressures were not used in
our study. It was decided that increasing
pain in muscle groups that was exaggerated
with stretching, a definite loss of sensation,
and a decrease in muscle strength as noted
by the physician were sufficient to establish
the diagnosis in these cases. In all six of our
patients, results from the initial sensory examination were normal. Muscle strength,
although initially ungradable due to pain at
the fracture site, had decreased prior to fasciotomy.
It is recognized that diminished arterial
pulses are seen late in the development of
compartment
Rarely does
the tissue pressure rise high enough to completely obliterate the pulses. One patient in
our study had early loss of palpable pulses;
however, an arteriogram revealed vascular
integrity. We believe that the absence of
pulses should be an absolute indication for
arteriography.
TREATMENT
In five cases, fasciotomy was performed
through two inci~ions.~".~~
The two posterior
compartments were released through the
FIG.1 B. Cross-section
of the leg with open fracture of the tibia. Displaced fibula fracture can
tear the interosseous
membrane and possibly
other compartmental
septae resulting in a four
compartment syndrome.
medial incision,2" and the anterior and lateral compartments through the lateral incision (Fig. IA). Mubarak and Owen2"recommend that both incisions be 15 cm long;'"
however, we feel that the fascia should be
released through the entire leg length. Incisions shorter than 15 cm may result in inadequate decompression. Gaspardghas shown
that with massive swelling the skin itself may
become constricting. In one patient, we released all four compartments through a single posterolateral incision as described by
Matsen.' ' Epimysiotomy, sometimes necessary to decompress tight, individual muscles,
was utilized in four cases in this ~ e r i e s . ~
Due to the swelling which occurs after
fasciotomy, all six cases required split thickness skin grafting to cover the gaping wounds.
Fibulectomy-fasciotomy and decompression of all four compartments through a lateral approach has been rec~rnmended;~
however, we think that the presence of an intact
fibula may be necessary for later posterolateral bone grafting. The peroneal and posterior tibia1 arteries are more vulnerable in
this approach and, if injured, could cause
further ischemia.
Duration of hospitalization is usually less
than two weeks for uncomplicated open tibia
fractures. No patient in this series was discharged earlier than 14 days; the majority
required more than three weeks of treatment. The most important factor prolonging
Number 1 8 0
October, 1081
Compartment Syndrome
181
dence injury after eight hours of ischemia.
Sheridan and M a t ~ e n ’have
~
reported 92%
residual functional impairment after 12 hours
of ischemia. In our series, ischemia for a
duration longer than six hours led to irreversible changes and permanent necrosis of
tissues. Our poorest results occurred in the
four patients where fasciotomy was performed after the initial debridement (there
was an average delay of 12.5 hours from
onset of clinical symptoms to fasciotomy).
Patients evidenced marked sensory deficit
and a total active motion at the ankle of less
than 20”. In all patients, active dorsiflexion
of the toes or ankle was absent, and plantar
flexors either weak or absent. Such losses can
be secondary to direct muscular injury at the
time of fracture or to ischemic necrosis postfracture. Inability to document the degree
of muscle weakness in a fractured limb
makes it difficult to determine the cause of
postfracture motor weakness.
NEUROLOGIC
DEFICIT
Fic. 2. A displaced segmental fibula fracture
suggests high energy trauma and the possibility
of a compartment syndrome.
morbidity was the management of the large
open wounds required for decompressing the
compartments.
PROBLEMS
ISCHEMICNECROSIS
Harmon and Guinn” and Whitesides et
al.” found that 90% of muscle fibers evi-
Functional neurologic changes occur after
30 minutes of ischemia, and irreversible
changes after 12 to 24 hour^.'^**^ Although
permanent sensory changes resulted in all
six patients in this series, they were more
severe in the four who evidenced ischemia
12.5 hours (average time) before decompression. Of the other two, one case had severe
involvement of the anterior and lateral compartments in which both the superficial peroneal and deep peroneal nerves were necrosed and subsequent debridement required.
In all patients, plantar sensation was sufficient to prevent ulceration.
OPENWOUNDS
The effects of creating large open wounds
in grossly unstable tibia1 fractures should not
be taken lightly. The posteromedial incision
employed to decompress both posterior compartments may have contributed to the morbidity rate in this series. In open fractures,
the anteromedial skin is often compromised,
and fasciotomy in this area may lead to ad-
182
Clinical Orthopaadlca
and Related Renoarch
DeLee and Stiehl
ditional skin necrosis. Morever, if the skin
incision is too long, much of the soft tissue
support is lost. The muscles arising from the
posterior tibia will tend to “hang” and often
pull away from the tibia. This results in further compromise of bone circulation and exposure of more bone as was seen in four of
the five patients who had a double incision
fasciotomy. In the one patient who had decompression performed through the posterolateral approach,” soft tissues did not tend
to “hang” off the tibia, exposed bone was
not a problem, and union occurred in 16
months without difficulty. We have since
used this approach on three patients and
have found it to be much easier to manage.
Skin coverage of swollen, edematous muscle and soft tissue becomes preeminent after
limb viability is assured. Of greater importance is coverage of bone at the fracture site.
We found necrosis of skin and muscle at the
level of the fracture site to be present, particularly in the four cases with prolonged
ischemia from the compartment syndrome.
In this situation, multiple operative debridements were necessary to remove all nonviable tissue before a granulating bed capable
of accepting a skin graft could be established. Since the tibia is subcutaneous in
most of its diaphyseal portion, debridement
of the anterior compartment leaves most of
the lateral aspect of the tibia exposed.
Hence, exposed bone was drilled to encourage granulation tissue formation as a base
for later skin grafting. After soft tissue healing and bone coverage were achieved (usually by six weeks), the Hoffmann device was
discontinued and full weight bearing was
c~mmenced.~
Once marked stability was regained, an orthoplast gaiter was employed
until union occurred.
SKELETAL
STABILITY
The Hoffmann external fixation device
obviated the problem of fracture instability.
Since many patients were debrided on a
daily basis early in the course of treatment,
the external fixator simplified measures dramatically. We were unwilling to use internal
fixation in the face of these grossly contaminated wounds.”
DELAYED
UNION
Nicoll” notes that displacement, comminution, loss of bone, infection, and soft tissue
wounds are the main determinants causing
an increase in the rate of delayed or nonunion. In our study, union was delayed over
six months in all patients with follow-up.
This rate is greater than in most series
whereby delayed union in open tibia fractures treated by external means varied from
10% to 33%” The amount of soft tissue injury and the fasciotomy itself were major
contributors to delayed healing. In five patients, the bone ends were devoid of all soft
tissue for up to 1% inches. This degree of
soft tissue disruption about the fracture site
must play a significant role in decreasing the
vascularity of the bone ends.
Posterolateral bone grafting was done late
in one case and proved successful. At present, one patient (Case 4) is under treatment
with a transcutaneous electrostimulation
unit. Two patients are still in orthoplast gaiters (Case 2 and Case 5 ) .
Our approach to delayed union has been
to perform a fibulectomy early (within six
months), particularly if we can demonstrate
hypertrophic callus or the possibility of a
healed fibular fracture distracting the fracture site. Fibulectomy, a simple and effective
method for enhancing compression at the
fracture site,6 was successful in treating one
of two cases in this series.
INFECTION
Patzakis and Harvey” demonstrated that
open tibia fractures treated with Cephalothin became infected in 2.3% of cases. We
discontinued intravenous antibiotics (Cephalothin) early as we felt the presence of
local commensal organisms would be preferable to more resistant strains. Although
no patient in our series required treatment
for an acute wound infection, 66% of our
cases (four out of six) harbored infections
Number 180
October. 198 1
Compartment Syndrome
as evidenced by chronic osteomyelitis with
draining wounds. This high incidence of osteomyelitis underlines the severity of the soft
tissue and bone injuries.
FUNCTIONAL
DEFICIT
Ankle stiffness and decreased range of
motion occurred in all patients. One patient
had passive range of motion of 10" dorsiflexion to 30" plantar flexion, but active
motion from neutral to 20" plantar flexion.
The other patients had less than 20" of active
or passive total motion and two of these patients had fixed equinus contractures. One
may ask whether or not internal fixation and
early motion may have prevented the degree
of ankle stiffness in our patients. Nicoll"
found that severity of soft tissue damage
with fibrosis of muscles, ligaments, and fascia1 planes was more important than immobilization in causing residual stiffness.
It is also important to emphasize that
muscle strength improvement due to hypertrophy and regeneration, will continue for
up to one year postinjury." This was encouraging to the patients in our series (two
have been followed for less than one year).
In spite of the complications (nonunion,
infection, limited range of ankle motion, and
loss of muscle function) no amputations have
been indicated. To our knowledge no other
series of patients has been reported with
compartment syndromes involving all four
compartments in the lower extremity. However, Matsen and Clawson" reported two
cases of four-compartment syndrome, one of
which had not recovered at two months and
the other required amputation. This reinforces the fact that four-compartment syndromes are high-energy injuries. The prognosis for significant recovery, especially with
delay in diagnosis, is poor.
SUMMARY
In a series of 104 open tibia fractures, six
patients developed compartment syndromes
involving all four compartments of the lower
leg, four of which developed after initial debridement and reduction. The presence of
183
an open tibia fracture with a displaced, comminuted, fibula fracture should suggest the
possibility of a developing compartment syndrome.
Clinical symptoms include: increasing
muscle pain which can be exaggerated by
stretching; loss of sensation; decrease in muscle strength; and palpably swollen compartments. Double fasciotomy incisions may lead
to adequate decompression, but result in
marked loss of soft tissue support for the
fracture. To sustain stability, a single posterolateral incision is recommended for compartmental decompression.
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DeLee and Stiehl
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