Abstract
Background: This study was undertaken to determine
whether alveolar dead space increases during intramedullary nailing
of femoral shaft fractures and whether alveolar dead space predicts
postoperative pulmonary dysfunction in patients undergoing intramedullary
nailing of a femoral shaft fracture.
Methods: All patients with a femoral shaft fracture
were prospectively enrolled in the study unless there was evidence
of acute myocardial infarction, shock, or heart failure. Arterial
blood gases were measured at three consecutive time-periods after
induction of general anesthesia: before intramedullary nailing and ten
and thirty minutes after intramedullary nailing. The end-tidal carbon-dioxide
level, minute ventilation, positive end-expiratory pressure,
and percent of inspired and expired inhalation agent were recorded
simultaneously with the blood-gas measurement. Postoperatively,
all subjects were monitored for evidence of pulmonary dysfunction,
defined as the need for mechanical ventilation or supplemental oxygen (at
a fraction of inspired oxygen of >40%) in the
presence of clinical signs of a respiratory rate of >20
breaths/min or the use of accessory muscles of respiration.
Results: Seventy-four patients with a total
of eighty femoral shaft fractures completed the study. Fifty fractures
(62.5%) underwent nailing after reaming, and thirty fractures
(37.5%) underwent nailing with minimal or no reaming. The
mean alveolar dead-space measurements before canal opening and at
ten and thirty minutes after canal opening were 14.5%, 15.8%,
and 15.2% in the total series of seventy-four
patients (general linear model, p = 0.2) and 20.5%,
22.7%, and 24.2% in the twenty patients with postoperative
pulmonary dysfunction (general linear model, p = 0.05).
Of the twenty-one patients with an alveolar dead-space
measurement of >20% thirty minutes after nailing,
sixteen had postoperative pulmonary dysfunction. According to univariate
and multivariate analysis, the alveolar dead-space measurement was
strongly associated with postoperative pulmonary dysfunction.
Conclusions: According to our data, intramedullary
nailing of femoral shaft fractures did not significantly increase
alveolar dead space, and the amount of alveolar dead space can predict which
patients will have pulmonary dysfunction postoperatively.
Long-bone fractures, especially femoral shaft fractures,
can contribute to lung damage in patients who have sustained a traumatic
injury1-5. Fractures disrupt both
the medullary vessels and the marrow matrix, creating the potential
for extrusion of marrow contents into the venous system4-6. A large bolus of embolized marrow
can block perfusion to a portion of the well-ventilated lung, resulting
in a high ventilation-to-perfusion ratio or increased alveolar dead
space7-17.
The method used to prepare the medullary canal may determine
the amount of bone marrow extrusion during intramedullary nailing3,18-20. Pape et al. proposed that
reaming of the femoral canal may exacerbate lung damage in patients
with chest injury2-4. Reaming
of the medullary canal may increase the risk of fat emboli and the
prevalence of adult respiratory distress syndrome in patients with
concurrent pulmonary injury. Although the findings of Pape et al.2-4,20 have not been corroborated by
other investigators21, concern
remains regarding the effect of intramedullary nailing of femoral
shaft fractures on the pulmonary function of patients with multiple
injuries. If objective physiologic or clinical measures of pulmonary
dysfunction were to show an adverse effect of nailing or reaming,
then a compelling argument could be made against performing one
or both procedures.
Previous investigators have used intraoperative echocardiography
to demonstrate echogenic material passing through the right ventricle
during femoral nailing; however, the findings were not correlated
with pulmonary function6. We are
aware of only one recent study in which pulmonary physiologic consequences
of femoral nailing and/or intramedullary reaming were documented
in humans22. In that study, the
alveolar dead space and alveolar-arterial gradient were
evaluated before, during, and after nailing. However, few patients
had an adverse pulmonary outcome, limiting the conclusions of the
study. Measurement of alveolar dead space provides a clinical measure
of pulmonary vascular occlusion, regardless of the etiology, because
it accurately reflects the difference between measurements of alveolar
and arterial carbon dioxide8,10-12,14-16,23.
In healthy patients, the ratio should approach 1.0, as carbon dioxide
rapidly debonds from the hemoglobin molecule at the alveolar level.
Few clinical conditions affect the ratio acutely; pulmonary embolic
events and extremely low cardiac flow states (shock) are the most
common conditions that do affect the ratio. Therefore, measurement
of this ratio should help to identify variables that affect the
pulmonary system in patients with a femoral shaft fracture. Several
questions may be addressed and hopefully answered with evaluation
of the alveolar dead space: Do patients with a femoral shaft fracture
have increased alveolar dead space as a result of the fracture?
Does femoral nailing increase alveolar dead space? Does intramedullary
reaming affect alveolar dead space? Moreover, a large alveolar dead
space (as estimated by a high Vd/Vt [ratio of physiologic
dead space to tidal volume]) measured intraoperatively
may influence postoperative management. The hypotheses of the present
study were (1) the amount of alveolar dead space changes with intramedullary
nailing of femoral shaft fractures, (2) reaming alters the amount
of alveolar dead space, (3) measurement of alveolar dead space can
predict postoperative pulmonary dysfunction, and (4) other variables such
as the Injury Severity Score, pulmonary injury, and pulmonary comorbidities
may more accurately predict pulmonary dysfunction following intramedullary
nailing of femoral shaft fractures.
Study Enrollment
This study was conducted at the University of Tennessee College
of Medicine in Chattanooga, Tennessee, from January 1997 to January
1998, and at the Carolinas Medical Center in Charlotte, North Carolina,
from February 1996 to June 1996. The study was approved by the institutional
review boards of both hospitals. To be included in the study, a
patient had to be an adult with a femoral shaft fracture that had
occurred 5 cm distal to the level of the lesser trochanter and 5
cm proximal to the knee joint and was amenable to treatment with
an intramedullary nail. Exclusion criteria included acute myocardial
infarction, circulatory shock, and heart failure. An acute myocardial
infarction was defined as an active injury current on electrocardiogram
or biochemical evidence of acute cardiac muscle injury. Circulatory
shock was defined as systolic blood pressure of <90 mm
Hg together with base deficits (a measure of anaerobic metabolism
secondary to poor tissue perfusion) of less than —5 mN.
Heart failure was defined as the presence of pulmonary rales on
physical examination together with the appearance of alveolar edema
on a chest radiograph as well as a cardiac index (if available)
of <2.5 L/min/m2.
Initially, six patients were excluded from the study because of
shock; however, these patients were later enrolled after the hemodynamic
instability had been corrected. No patient was excluded because
of myocardial infarction or heart failure.
Collection of Preoperative, Intraoperative,
and Postoperative Data
Data for each patient were prospectively logged on a standardized
form that included demographic information, time to fixation of
the femoral fracture, associated injuries, Injury Severity Score,
pulmonary injury (defined as a pneumothorax, hemothorax, or pulmonary
contusion), pulmonary comorbidity (defined as asthma or chronic
obstructive pulmonary disease), and smoking status. Additional data
included intraoperative surgical technique (nail insertion technique
and number of canal passes) and parameters associated with mechanical
ventilation (fraction of inspired oxygen, minute ventilation, positive
end-expiratory pressure, and percent of inspired and expired
inhalation agent). We recorded the presence or absence of postoperative
pulmonary dysfunction, which was defined as the need for mechanical
ventilation or clinical signs of respiratory distress (the need
for supplemental oxygen administration at a fraction of inspired
oxygen of >40% as well as a respiratory rate of >20
breaths/min or the use of accessory muscles of respiration).
Accessory muscle use was defined as visible retraction of the sternocleidomastoid
and intercostal muscles on physical examination. The fraction of
inspired oxygen was calculated with the assumption of a 0.03 increase
in the fraction of inspired oxygen per liter of supplemental oxygen
per minute in a nonintubated patient. The specific guidelines for
the use of mechanical ventilation were determined by the attending
physicians but, in general, included clinical evidence of inadequate
gas exchange and respiratory distress.
All subjects were evaluated during the first twenty-four-hour postoperative
period for development of pulmonary dysfunction. Additional evaluations
were performed at the request of the trauma team or the nurse treating
the patient. All pulmonary evaluations and measurements were performed
by either the authors or the orthopaedic trauma service without
knowledge of the intraoperative pulmonary gas-exchange data. Arterial
blood-gas levels, chest radiographs, and other clinically important
data were obtained when the patient’s condition warranted
it. Other important outcomes that we recorded included readmittance
to an intensive-care unit and death during hospitalization.
Pulmonary Gas-Exchange Indexes
Arterial blood-gas measurements were performed at three time-points:
(1) after induction of anesthesia but before the beginning of the
procedure, (2) ten minutes after the opening of the femoral canal,
and (3) thirty minutes after the opening of the femoral canal. At
the time of the arterial blood-gas measurement, end-tidal
carbon-dioxide concentration, positive end-expiratory pressure,
minute ventilation, and percent of inspired and expired volatiles
(halothane, fluorane, and isoflurane) were also recorded. Anesthesia
personnel who had been instructed about the ongoing study performed
the intraoperative pulmonary measurements. Capnometers (model 1025B;
Hewlett-Packard, Atlanta, Georgia) were calibrated and
maintained by hospital bioengineering personnel. The alveolar dead
space was calculated with use of the Enghoff modification of the
Bohr equation: Vd/Vt = (PaCO2 — PetCO2)/(PaCO2)
100%, where PaCO2 is the arterial partial pressure of
carbon dioxide (obtained from the arterial blood-gas measurement)
and PetCO2 is the steady-state end-tidal carbon-dioxide
concentration measured by capnometry at each of the three time-points24.
Operative Technique
Patients were placed under general anesthesia with endotracheal
intubation and with use of volume-controlled ventilation prior to
any manipulation of the fracture. They were then positioned either
supine on a fracture-table or supine with a hip-bump and the leg
free on a radiolucent table. Associated injuries and the preference
of the attending orthopaedic surgeon determined the positioning
of the patient. All surgery was performed by orthopaedic surgery
residents with the supervision of attending faculty. The femoral
shaft fractures were fixed with the Synthes intramedullary nail
(Paoli, Pennsylvania). A standard lateral hip incision was made
proximal to the level of the greater trochanter, and a c-arm
was used to visualize the proximal femoral starting point on both
the anteroposterior and the lateral image. A 2.8-mm guide-pin was
drilled through the piriformis fossa and into the medullary canal.
The proximal part of the femur was then opened with a 13-mm cannulated
reamer, and a femoral nail was placed with extensive reaming or
with minimal or no reaming. The decision whether to ream was left
to the attending surgeon. A single canal pass was recorded whenever
an object (a guide-rod, awl, reamer, or nail) was passed into the
opened canal, distal to the level of the isthmus, and then removed. Locking
of the nail was performed on the basis of the fracture configuration
and the preference of the attending surgeon. Patients were monitored
postoperatively by the orthopaedic trauma service, and all complications
were recorded. Postoperative mobilization and rehabilitation of
the patients were advanced on the basis of the fracture configuration
and the associated injuries.
Data Analysis
Data were entered on an Excel spreadsheet (version 4.0; Microsoft,
Redmond, Washington, 1992). Analyses were performed with use of
SPSS software (version 8.0.0; SPSS, Chicago, Illinois, 1997). Means,
ranges, standard deviations, and frequency distributions for continuous
variables were examined; proportions were used to describe categorical
variables. The continuous variables were normally distributed; therefore,
parametric methods were used for our analyses.
The primary study hypothesis (that the physiologic measure of
alveolar dead space changes during nailing) was tested by evaluating
alveolar dead space over time with repeated measures of analysis
of variance. The second study hypothesis (that reaming of the femoral
canal is associated with a change in alveolar dead space) was tested
by examining the association between the extent of reaming and the
change in alveolar dead space over time with use of a general linear
model. The third study hypothesis (that increased alveolar dead
space prior to or after surgical fixation is associated with postoperative
pulmonary dysfunction) was tested with logistic regression analysis,
with postoperative pulmonary dysfunction treated as the dependent
variable. The following variables were examined for possible association
with postoperative pulmonary dysfunction: alveolar dead space measured
preoperatively and ten and thirty minutes after opening of the femoral
canal, reaming, the Injury Severity Score, pulmonary comorbidity,
smoking status, and age. Correlation between variables was examined
with use of the Pearson method. Because odds ratios and confidence
intervals are a clinically meaningful way to present these data,
we converted beta coefficients (and standard error of beta) to respective
odds ratios with 95% confidence intervals, in order to
describe the association between predictors of postoperative pulmonary
dysfunction and outcome. Finally, to test the fourth hypothesis,
we used multivariate logistic regression analysis to evaluate the potential
importance of other covariates, such as Injury Severity Score and
the presence of pulmonary injury or comorbidity, by testing the
association between these covariates and postoperative pulmonary
dysfunction, with postoperative pulmonary dysfunction again treated
as the dependent variable. Odds ratios and 95% confidence
intervals were generated for the results of these multivariate models.
We also examined the discriminate ability of our final model for
predicting postoperative pulmonary dysfunction.
Clinical Data
Seventy-four patients with a total of eighty femoral
shaft fractures enrolled in and completed the study. The mean age
of the patients was thirty-two years (range, sixteen to
seventy-seven years). Six patients (8%) had a preinjury
history of pulmonary comorbidity. Nineteen patients (26%)
had a history of pulmonary injury. Eleven of them had a pulmonary
contusion (as diagnosed by chest radiography), and eight had a hemothorax,
a pneumothorax, or a hemopneumothorax; all eight patients required
placement of a chest tube. Twenty-five patients (34%)
reported a history of smoking. Thirty-nine patients (53%)
had multiple injuries, and thirty-five (47%) had
an isolated fracture. Seventy-four fractures in sixty-eight patients
(92%) were treated with intramedullary nailing less than
twelve hours after the injury. Three fractures in three patients
(4%) initially were treated with external fixation, which
was later converted to intramedullary nailing. Three patients with
three fractures were managed with distal traction and then underwent
nailing more than twelve hours after the injury. The mean Injury
Severity Score was 17 points, with a range of 9 to 43 points. We
compared baseline risk factors for postoperative pulmonary dysfunction
between the patients who had extensive reaming and those who had
minimal or no reaming. The patients with extensive reaming were
more likely to have a history of smoking than were the patients
with minimal or no reaming (p = 0.01, chi square), but
the two groups were similar with regard to the presence of pulmonary injury
(p > 0.05, chi square) and the Injury Severity Score (p > 0.05).
Intraoperative Data
No patient was excluded from the study because of preoperative
or postoperative hemodynamic instability. The mean minute ventilation
for all subjects was 7.8 L. We observed no significant association
between the alveolar dead-space measurements and minute ventilation,
positive end-expiratory pressure, or percent inspired and
expired volatiles (anesthetic agents). Fifty fractures (62.5%)
were treated with extensive reaming and the placement of a 12-mm-diameter
femoral nail, and thirty (37.5%) were treated with minimal
or no reaming and the placement of a 9 or 10-mm-diameter femoral
nail. The mean number of canal passes for these two subgroups was
seven (range, five to eleven) and three (two, three, or four), respectively.
Pulmonary Gas-Exchange Indexes
Table I summarizes
the alveolar dead-space (Vd/Vt) data. The mean alveolar
dead-space measurements before canal opening, ten minutes after
canal opening, and thirty minutes after canal opening were 14.5%,
15.8%, and 15.2%, respectively (general linear
model, p = 0.2), for the seventy-four patients.
No significant change in the alveolar dead space occurred between measurements.
Thus, our data do not support the first hypothesis that intramedullary
nailing of femoral shaft fractures alters alveolar dead space.
The mean alveolar dead-space measurements before canal opening,
ten minutes after canal opening, and thirty minutes after canal
opening were 14.8%, 16.1%, and 13.9% for
the patients who had nailing with extensive reaming and 13.5%, 15.0%,
and 17.2% for those who had nailing with minimal or no
reaming. The increase in the mean alveolar dead space over time
among the patients who had minimal or no reaming was significantly
greater than the increase in those with extensive reaming (p = 0.03).
Therefore, our data do not support the second hypothesis that extensive
intramedullary reaming of femoral shaft fractures increases alveolar
dead space.
Postoperative Data
According to our criteria, postoperative pulmonary dysfunction
developed in twenty patients (27%). Fifteen of these patients
required mechanical ventilation postoperatively. Three of them were
reintubated after attempted extubation following surgery. Other
reasons for the mechanical ventilation included severe head injury
(three patients), poor pulmonary mechanics (four patients), facial
fractures (two patients), failure to extubate as ordered (one patient),
and impending operative procedures by specialists in other fields
of surgery (two patients). The mean alveolar dead-space measurements before
canal opening, ten minutes after canal opening, and thirty minutes
after canal opening were 20.5%, 22.7%, and 24.2%,
respectively, in patients with postoperative pulmonary dysfunction.
These values were significantly greater (p = 0.05) than
those for the patients without postoperative pulmonary dysfunction.
As described above, eight patients remained intubated for reasons
possibly unrelated to pulmonary dysfunction. Six of these patients
had been treated with extensive reaming while two had been treated
with minimal reaming. When these patients were excluded from the
analysis, the remaining patients with postoperative pulmonary dysfunction had
no significant change in the mean alveolar dead space over time,
although a trend was noted (p < 0.08). This finding suggests
that patients in whom pulmonary dysfunction develops after operative
treatment of a femoral shaft fracture have an increased alveolar
dead space prior to that treatment, supporting our third hypothesis.
In twenty-one patients, the alveolar dead-space measurement at
thirty minutes was >20%. Sixteen (76%)
of these patients had evidence of postoperative pulmonary dysfunction,
and one patient with a measurement of 52% died during the
study period. Postmortem examination confirmed fat emboli in the lungs.
Risk of Postoperative Pulmonary Dysfunction
Univariate and multivariate analyses were performed to look for
any association between the development of postoperative pulmonary
dysfunction and alveolar dead space, Injury Severity Score, pulmonary
injury or comorbidity, smoking status, or age (Table II). We examined
the correlation between postoperative pulmonary dysfunction and
the predictor variables included in the multivariate models and
found significant correlations with the measures of alveolar dead
space at the three time-intervals (p < 0.001 for all correlations)
as well as with lung injury or comorbidity and the Injury Severity
Score (p < 0.001). In the univariate analysis, one of the
factors most strongly associated with the development of postoperative
pulmonary dysfunction was the alveolar dead-space measurement at
thirty minutes. No significant association was noted with the extent of
reaming, the smoking status, or age. After controlling for important
covariables, we found that the most important predictors of postoperative
pulmonary dysfunction in the multivariate model were again the alveolar
dead-space measurement at thirty minutes and the Injury Severity
Score. The discriminant ability for this model correctly identified 80% of
patients in whom postoperative pulmonary dysfunction would develop.
There was no additional significant contribution from reaming, pulmonary
injury or comorbidity, or a history of smoking. We re-examined the
multivariate model after excluding patients who remained intubated
for reasons possibly unrelated to pulmonary dysfunction. Similarly,
the alveolar dead-space measurement at thirty minutes (p = 0.005)
and pulmonary injury or comorbidity (p = 0.01) were the
most important predictors of postoperative pulmonary dysfunction,
despite the fact that the majority (six) of the eight excluded patients
had had extensive reaming.
Intramedullary nailing has evolved over the last forty years
to become the preferred treatment for fractures of the femoral shaft,
and it has been found to be associated with low morbidity rates
and excellent clinical outcomes25,26.
However, in a retrospective study of patients with femoral shaft
fracture and thoracic injury who had undergone intramedullary nailing,
Pape et al. found a higher prevalence of adult respiratory distress
syndrome and a higher mortality rate in patients treated with reaming
less than twenty-four hours after injury compared patients
who had not had reaming3. Furthermore,
Pape et al. compared the effects of intramedullary nailing with
and without reaming in a prospective investigation of a small group
of thirty-one patients with femoral shaft fracture but without thoracic
injury20. They found a persistent
and significant decrease in the oxygenation ratio in patients who
underwent reaming, and they concluded that a nailing technique that
does not involve reaming is indicated for patients with preexisting
lung injury20. The results of
this work led to other changes as well, including the use of small-diameter
solid nails and alterations in the reamer design2-4.
Bosse et al.21 contradicted
the work of Pape et al. In a retrospective study at two large metropolitan
trauma centers, intramedullary nailing was compared with plate fixation
for the treatment of femoral shaft fractures in patients with and
without lung injury. There were no significant differences in the
rates of adult respiratory distress syndrome or mortality between
any of the groups, including patients with associated pulmonary
injury. Bosse et al. concluded that the treatment of femoral shaft
fractures with reaming and intramedullary nailing did not worsen
the clinical or pulmonary outcome of patients with multiple injuries.
Despite this positive report, there is a scarcity of data documenting
pulmonary gas exchange and/or early pulmonary outcomes
in this patient population22.
The rationale for measuring alveolar dead space to demonstrate
a functional consequence of pulmonary embolization has been well
documented7-9,11,12,14. In an
experimental study involving glass-bead embolization, alveolar dead
space increased proportionate to the degree of pulmonary vascular
obstruction in mechanically ventilated goats15.
Other animal studies have suggested that an increase in the alveolar
dead space occurs simultaneously with the onset of pulmonary vascular
occlusion15,16. Measurement of
alveolar dead space in humans has been examined as a method of screening
for acute pulmonary embolism7,19.
In 1990, Burki found measurement of physiologic dead-space fraction
comparable, in terms of sensitivity and specificity, to radioisotope
lung-scanning in the diagnosis of pulmonary embolism7.
Furthermore, experimental studies on the effect of pulmonary embolism
have demonstrated an increase in alveolar dead space secondary to
a reduction in perfusion of the affected lung16.
Measurement of alveolar dead space is a sensitive screening test
(sensitivity of 88%) for acute pulmonary emboli in ambulatory
patients12, and it has a high
sensitivity and specificity for detection of pulmonary emboli in
mechanically ventilated patients with intrinsic lung disease (asthma,
chronic obstructive pulmonary disease, and so on)9,11.
Thus, there is ample evidence suggesting that pulmonary gas exchange—specifically,
alveolar dead space—should change if a large embolic burden
is routinely induced by reaming and/or nailing of a fractured
femoral shaft.
Recently, Weresh et al. sought to determine if nailing of femoral
shaft fractures produces immediate worsening of pulmonary gas exchange22. They found no significant change
in the alveolar dead space during or shortly following nailing,
and they concluded that intramedullary nailing of femoral shaft
fractures does not routinely produce a large enough burden of pulmonary
embolization to significantly change pulmonary gas exchange (specifically,
alveolar dead space).
We prospectively studied a consecutive series to determine intermediate-term
pulmonary and clinical outcomes in patients with a femoral shaft
fracture treated with intramedullary nailing. We believe that we
are the first to define an important relationship between alveolar
dead space and specific pulmonary clinical outcomes in such patients.
Our definition of postoperative pulmonary dysfunction was chosen
to identify patients who would clearly benefit from reevaluation by
a physician or from intensive-care monitoring postoperatively. Thus,
the fifty-four patients in our series who had no signs of postoperative
pulmonary dysfunction could have been safely managed on a nonmonitored
orthopaedic ward. This study’s strength lies in our ability
to evaluate several important confounding variables that affect
pulmonary function, such as pulmonary contusion, hemothorax, pneumothorax,
chronic obstructive pulmonary disease, asthma, and smoking. Unlike
in previous studies, the number of patients with postoperative pulmonary
dysfunction in our study provided adequate statistical power for
us to evaluate several important predictors of this outcome. The
most controversial of these, extensive reaming of the medullary
canal, was not associated with postoperative pulmonary dysfunction.
Other, more important predictors of postoperative pulmonary dysfunction—that
is, alveolar dead space, Injury Severity Score, and concomitant
pulmonary injury—were identified. These data should be
validated in a prospective fashion. Furthermore, we examined the
impact of excluding from the analysis eight patients who had remained
intubated for reasons not attributed to known pulmonary dysfunction.
The results of our predictive model were robust; again, alveolar
dead space and lung injury were the major predictors of postoperative
pulmonary dysfunction.
Our study had several weaknesses. Although the sample size allowed
evaluation of several important predictor variables, a larger sample
might have increased our ability to identify other factors contributing
to postoperative pulmonary dysfunction. We could not control for
the selection of patients for either minimal or extensive reaming.
Other, unmeasured factors may play a role in this decision and thus
in patient outcome. Nevertheless, we identified the association
between the objective score for overall patient injury and the outcome, which
may partially address this concern. Validation of our results in
a separate study would be useful.
Alveolar dead-space measurements did not increase significantly
over time in patients who underwent extensive femoral reaming. We
interpreted these findings to indicate that extensive reaming of
the femoral canal does not pose an increased threat to pulmonary
function in patients with a femoral fracture. Furthermore, the addition
of reaming did not increase the risk of postoperative pulmonary
dysfunction according to univariate or multivariate analysis. This
was true regardless of potential confounding variables, including
associated pulmonary injury, preexisting pulmonary disease, and
a positive smoking history. These results suggest that the concern
that the process of reaming the femoral canal will worsen pulmonary
function in a patient with multiple injuries may be unfounded.
Additionally, we found that an increased alveolar dead space prior
to nailing is predictive of postoperative pulmonary dysfunction.
Even more important is the alveolar dead-space measurement obtained
thirty minutes after opening of the femoral canal. This single measurement,
if increased by >20%, is highly predictive of
postoperative pulmonary dysfunction.
Finally, our study results suggest that patients who undergo minimal
reaming of the femoral canal have greater alveolar dead space and
greater risk for the development of postoperative pulmonary dysfunction
than do those who undergo extensive reaming. We speculate that a
selection bias may have occurred in our study. At our institution,
femoral nailing with minimal reaming is reserved for severely injured
or clinically unstable patients. It is likely that the condition
of these patients was considered to be more unstable than that of
the patients who underwent extensive reaming. However, on analysis
of such covariables as the Injury Severity Score, the degree of
pulmonary injury, and pulmonary comorbidities, no difference was
noted between the group treated with reaming and that treated without
reaming. This finding suggests that other variables, unknown and
uncontrolled, likely influenced the attending physician’s
decisions regarding reaming in the treatment of the femoral shaft
fractures in these patients with multiple injuries.
Boulanger BR, Stephen D,Brenneman FD. Thoracic trauma and early intramedullary nailing of femur fractures:
are we doing harm?. J Trauma,1997;43: 24-8. 4324
1997
[PubMed]
Pape HC, Regel G, Dwenger A, Sturm
JA,Tscherne H. Influence of thoracic trauma and primary femoral intramedullary
nailing on the incidence of ARDS in multiple trauma patients. Injury,1993;24 Suppl 3: 82-103. 24 Suppl 382
1993
Pape HC, Regel G, Dwenger A, Krumm
K, Schweitzer G, Kretteck C, Sturm JA,Tscherne H. Influences of different methods of intramedullary femoral nailing
on lung function in patients with multiple trauma. J Trauma,1993;35: 709-16. 35709
1993
[PubMed]
Pape HC, Auf’m’Kolk
M, Paffrath T, Regel G, Sturm JA,Tscherne H. Primary intramedullary femur fixation in multiple trauma patients
with associated lung contusion—a cause of posttraumatic
ARDS?. J Trauma,1993;34: 540-7. 34540
1993
[PubMed]
Talucci RC, Manning J, Lampard
S, Bach A,Carrico JC. Early intramedullary nailing of femoral shaft fractures:
a cause of fat embolism syndrome. Am J Surg,1983;146: 107-11. 146107
1983
[PubMed]
Pell AC, Christie J, Keating JF,Sutherland
GR. The detection of fat embolism by transesophageal echocardiography
during reamed intramedullary nailing. A study of 24 patients with
femoral and tibial fractures. J Bone Joint Surg Br,1993;75: 921-5. 75921
1993
[PubMed]
Burki NK. Diagnosing pulmonary embolism. Chest,1990;98: 777-8. 98777
1990
[PubMed]
Carroll GC. Capnographic trend curve monitoring can detect 1-ml
pulmonary emboli in humans. J Clin Monit,1992;8: 101-6. 8101
1992
[PubMed]
Chopin C, Fesard P, Mangalaboyi
J, Lestavel P, Chambrin MC, Fourrier F,Rime A. Use of capnography in diagnosis of pulmonary embolism
during acute respiratory failure of chronic obstructive pulmonary disease. Crit Care Med,1990;18: 353-7. 18353
1990
[PubMed]
Elliott CG. Pulmonary physiology during pulmonary embolism. Chest,1992;101(4 Suppl): 163S-71S. 101(4 Suppl)163
1992
Hatle L,Rokseth R. The arterial to end-expiratory carbon dioxide
tension gradient in acute pulmonary embolism and other cardiopulmonary
diseases. Chest,1974;66: 352-7. 66352
1974
[PubMed]
Kline JA, Meek S, Boudrow D, Warner
D,Colucciello S. Use of the alveolar dead space fraction (Vd/Vt)
and plasma D-dimers to exclude acute pulmonary embolism
in ambulatory patients. Acad Emerg Med,1997;4: 856-63. 4856
1997
[PubMed]
Santolicandro A, Prediletto R, Fornai
E, Formich B, Begliomini E, Gianella-Neto A,Giuntini C. Mechanisms of hypoxemia and hypocapnia in pulmonary embolism. Am J Respir Crit Care Med,1995;152: 336-47. 152336
1995
[PubMed]
Sasahara AA, Cannilla JE, Morse
RL, Sidd JJ,Tremblay GM. Clinical and physiologic studies in pulmonary
thromboembolism. Am J Cardiol,1967;20: 10-20. 2010
1967
[PubMed]
Schreiner MS, Leksell LG, Gobran
SR, Hoffman EA, Scherer PW,Neufeld GR. Microemboli reduce phase III slopes of CO2 and invert
phase III slopes of infused SF6. Respir Physiol,1993;91: 137-54. 91137
1993
[PubMed]
Severinghaus JW,Stupfel M. Alveolar dead space as an index of distribution of blood
flow in pulmonary capillaries. J Appl Physiol,1957;10: 335-48. 10335
1957
[PubMed]
Wilson RF, Tyburski JG, Kubinec
SM, Warsow KM, Larky HC, Wilson SR,Schermerhorn T. Intraoperative end-tidal carbon dioxide levels
and derived calculations correlated with outcome in trauma patients. J Trauma,1996;41: 606-11.. 41606
1996
[PubMed]
Duwelius PJ, Huckfeldt R, Mullins
RJ, Shiota T, Woll TS, Lindsey KH,Wheeler D. The effects of femoral intramedullary reaming on pulmonary function
in a sheep lung model. J Bone Joint Surg Am,1997;79: 194-202. 79194
1997
[PubMed]
Heim D, Regazzoni P, Tsakiris DA, Aebi
T, Schlegel U, Marbet GA,Perren SM. Intramedullary nailing and pulmonary embolism: does unreamed
nailing prevent embolism? An in vivo study in rabbits. J Trauma,1995;38: 899-906. 38899
1995
[PubMed]
Pape HC, Dwenger A, Grotz M, Kaever
V, Negatsch R, Kleeman W, Regel G, Sturm JA,Tscherne H. Does the reamer type influence the degree of lung dysfunction after
femoral nailing following severe trauma? An animal study. J Orthop Trauma,1994;8: 300-9. 8300
1994
[PubMed]
Bosse MJ, MacKenzie EJ, Riemer
BL, Brumback RJ, McCarthy ML, Burgess AR, Gens DR,Yasui Y. Adult respiratory distress syndrome, pneumonia, and mortality
following thoracic injury and a femoral fracture treated either
with intramedullary nailing with reaming or with a plate. A comparative
study.. J Bone Joint Surg Am,1997;79: 799-809. 79799
1997
[PubMed]
Weresh MJ, Stover MD, Bosse MJ, Jeray
K, Kellam JF, Sims SH,Kline JA. Pulmonary gas exchange during intramedullary fixation
of femoral shaft fractures. J Trauma,1999;46: 863-8. 46863
1999
[PubMed]
Domsky M, Wilson RF,Heins J. Intraoperative end-tidal carbon dioxide values
and derived calculations correlated with outcome: prognosis and
capnography. Crit Care Med,1995;9: 1497-503. 91497
1995
Enghoff H. Volumen ineffeicax. Bemerkungen zur Frage des schädlichen Raumes. Upsala: Läkaref Förhandl,1938;44: 191-218. 44191
1938
Winquist RA, Hansen ST Jr,Clawson
DK. Closed intramedullary nailing of femoral fractures. A
report of five hundred and twenty cases. J Bone Joint Surg Am,1984;66: 529-39. 66529
1984
[PubMed]
Winquist RA,Hansen ST Jr. Comminuted fractures of the femoral shaft treated by intramedullary
nailing. Orthop Clin North Am,1980;11: 633-48. 11633
1980
[PubMed]