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Compartmental pressure measurements during application of the pneumatic antishock garment
The Journal of Emergency Medicine, Vol.
1,pp. 377485,1994
Printed in the USA
Copyright 0 1984 Pergamon Press Ltd
??
COMPARTMENTAL PRESSURE MEASUREMENTS DURING APPLICATION OF THE PNEUMATIC ANTISHOCK GARMENT Jerris R. Hedges,
MD, FACEP,
Paul 6. Baker,
MD,
and William C. Dalsey,
MD
The Department of Emergency Medicine, University of Cincinnati Medical Center, Cincinnati, Ohio Reprint address: Jerris R. Hedges, MD, FACEP, Division of Emergency Medicine (ML 769), University of Cincinnati Medical Center, 234 Goodman Street, Cincinnati OH 45267
0 Abstract-Recent case reports have implicated the pneumatic antishock garment (PASG) in the development of the compartment syndrome in the lower extremities. The present study used the anterolateral compartment of the canine hindlimb to model the effect of the PASG on tissue pressure within the compartment (P,). Prior to inflation of the garment, baseline Pe was 5.3 mm Hg. PASG inflation to 60 mm Hg for 20 minutes resulted in an increase in Pe of 75.0 mm Hg over baseline values. The rise in P, was reduced significantly following hemorrhage of the animal, measuring 65.8 mm Hg at a mean arterial pressure of 70 to 80 mm Hg and 62.5 mm Hg at a mean arterial pressure of 40 to 50 mm Hg. In the immediate postarrest state, PErise after a five-minute inflation of the garment was 57.5 mm Hg. In all cases, PC promptly returned to baseline values when the PASG was deflated, and there was no significant change in P, following deflation of the garment under conditions of normotension, hemorrhagic hypotension, and in the immediate postarrest state. Our results suggest that the level of arterial pressure may contribute to P, rise during PASG inflation. 0 Keywords -PASG; compartment pressure; ischemic necrosis
Introduction The pneumatic antishock garment (PASG) has gained increasing acceptance as a valuable adjunct in the initial management of hypovolemic shock. During the past decade, the PASG has received widespread use in the prehospital and emergency department setting, both to maintain an adequate blood pressure and to control hemorrhage resulting from pelvic, abdominal, or lower extremity trauma. With proper patient selection and correct application of the garment, the PASG has been associated with few complications. ’ Several case reports have appeared in the recent literature linking prolonged application of the PASG with subsequent development of the compartment syndrome in the lower extremity.*-6 Although the pathogenesis of the compartment syndrome in such clinical situations is not completely understood, it may be the result of abruptly elevating compartmental pressures in already ischemic, and in some cases, traumatized muscle. There have been few studies documenting changes in com-
Original Contributions presents papers of interest to both academic and practicing physicians. This section of JEM is coordinated by John A. Marx, MD, of Denver General
m
Hospital.
RECEIVED:
29 August 1983; ACCEPTED: 19 December 1983 377
0736-4679/84 $3.00 + .OO
378
Jerris R. Hedges, Paul B. Baker, William C. Dalsey
partmental pressure that occur during external pneumatic compression of an extremity. Chisholm and Clark measured the effect of the PASG on intramuscular pressures within the anterior tibia1 compartment of eight normotensive volunteers’ using the wick catheter technique of Mubarak et al.8 Compartmental pressures were found to roughly parallel externally applied PASG pressure during inflation, with prompt return to baseline values following deflation of the garment.’ It must be emphasized that the PASG is most frequently used under conditions of hemorrhagic hypotension, where the effects of external compression on potentially ischemic muscle compartments are not known. In order to assess the potential of the PASG to induce the compartment syndrome in the lower extremity, the present study was designed, using the canine hindlimb as a model. Objectives of the study were twofold: first, to measure changes in compartmental pressure during inflation and deflation of the PASG and second, to observe such changes under conditions of normal hemodynamics, during hemorrhagic hypotension, and in the immediate postarrest state.
Methods Animal Preparation Six nonsplenectomized dogs, weighing 18 to 25 kg, were anesthetized with 30 mg/kg pentobarbital intravenously (IV), intubated, and placed on a mechanical ventilator (Harvard pump) at a respiratory rate of 15/min and a tidal volume of 20 mL/kg. Supplemental dosages of 2 to 4 mg/kg pentobarbital were given periodically to maintain anesthesia throughout the experimental protocol. An 1%gauge catheter @-inch Intracath) was placed via cutdown into the left brachial artery for measurement of arterial pressure. A large-bore catheter (modified IV tubing) was placed in the superior vena cava (SVC) via cutdown on the right
external jugular vein to provide ready access for hemorrhage or volume infusion. A slit catheter was prepared, using PE 60 polyethylene tubing following the method of Rorabeck et a1.9 The anterolateral hindlimb of the animal was shaved, and a 1Cgauge catheter (Angiocath) was inserted percutaneously 2 to 3 cm into the muscle belly at a 45” angle. The needle was withdrawn, and the remaining catheter sheath carefully observed for signs of bleeding. If bleeding was noted, an altemative site in the same compartment was chosen. If no hemorrhage was present, the slit catheter was introduced into the muscle compartment through the catheter sheath, the sheath slowly withdrawn, and the slit catheter secured in place with adhesive tape wrapped over the insertion site in a circumferential, nonconstricting fashion. Both arterial and slit catheters were connected to pressure transducers (Statham P23) using high-pressure, nondistensible tubing. During in vitro testing, inflation of the PASG was found to produce no measurable pressure rise as a result of pressure applied directly to the tubing or the attached slit catheter. All pressure measurements were monitored on a multichannel chart recorder (Hewlett Packard 7758). The animal was turned to the left lateral decubitus position. Once all lines were secured, the animal was given 2,000 units of heparin IV. A canine model PASG (Jobst, Inc, Toledo, OH) was carefully placed on the animal, covering the hindlegs and lower third of the abdomen. The garment was custom fitted for medium-sized dogs and was equipped with pressure gauges for monitoring pressures within the garment. Both the PASG gauges and the pressure transducers were calibrated with a mercury manometer immediately prior to the beginning of the experiment.
Experimental Technique Baseline levels of mean arterial blood pressure (BP) and compartmental pressure (P,)
379
Compartmental Pressure
were recorded with the garment deflated (PASG = 0 mm Hg). Slit catheter placement and function were verified by squeezing the hindlimb and observing the expected rise in compartmental pressure. The garment was inflated to 60 mm Hg according to a three phase protocol (Figure l), while BP and PC were continuously monitored. Phase I: Normotensive inflation. The PASG was inflated to 60 mm Hg in 5 mm Hg increments over one minute. Initially, the garment was kept at 60 mm Hg for five minutes, then rapidly deflated to 0 mm Hg over 15 seconds. After a five-minute recovery period at a PASG of 0 mm Hg, the garment was, in previous fashion, inflated to 60 mm Hg and maintained at that level of external pressure for 20 minutes. The PASG was then deflated to 0 mm Hg for another 20-minute recovery period. Throughout Phase I, no attempt was made to control BP. Phase II: Inflation during hemorrhagic hypotension. At the end of the 20-minute deflation period, hemorrhage of the animal was initiated via the SVC catheter. The animal was hemorrhaged to a BP of 70 to 80 mm Hg, and stabilized at that pressure for three to five minutes. Incremental inflation to a PASG pressure of 60 mm Hg was performed as before, and the garment was kept at that level for 20 minutes. BP was maintained at 70 to 80 mm Hg throughout the PASG inflation period by further hemorrhage when necessary. At the end of the 20-minute inflation period, the PASG was rapidly deflated to 0 mm Hg for an additional 20-minute recovery period. At the end of the deflation period, the BP was established at the 40 to 50 mm Hg level for three to five minutes using either further hemorrhage or crystalloid infusion. The PASG was again inflated to 60 mm Hg for 20 minutes, during which time the pressure was maintained at a BP of 40 to 50 mm Hg. At the end of the inflation period, the garment was deflated to 0 mm Hg for five minutes.
Phase Ill: Inflation during the postarrest state. At the end of the last five-minute deflation period, all surviving animals were sacrificed with high-dose barbiturate (Socumb 0.2 ml/kg). The PASG was again inflated to 60 mm Hg for two 5-minute inflation/deflation cycles. Correct placement of the slit catheter within the anterolateral compartment and the absence of significant compartmental hemorrhage were confirmed by postmortem examination of each animal.
Statistical Analysis Values for PC and rise in pressure associated with PASG inflation (APJ were tabulated at the following times: immediately prior to inflation of the PASG (T,); at 0, 5, and 20 minutes of full 60 mm Hg inflation (T,, T,, T,,,); and after 5 and 20 minutes of deflation of the PASG to 0 mm Hg (T,, TFJ. Mean values were compared using the Student’s i test for paired data. The criterion for significance was a P-value of .05 or less. All values are listed as mean f 1 standard deviation.
Results Baseline Values Initial values are listed in Table 1. PC within the anterolateral compartment measured 5.3 f 2.4 mm Hg at the beginning of the experiment. BP prior to inflation of the PASG was 104.2 f 7.4 mm Hg. Vigorous squeezing of the muscle compartment resulted in an abrupt rise in PC of 50 to 100 mm Hg, whereas maximal manual traction of the animal’s hindlimb elevated PCby 10 to 20 mm Hg. Values immediately returned to baseline levels following release of tension. Phase I: Normotensive inflation. Inflation of the PASG to 60 mm Hg resulted in a rise
Jerris R. Hedges, Paul B. Baker, William C. Dalsey
380
70
Garment Pressure
Phase I
Phase II
Phase Ill
60 50 40 30 20 10 o-
~=5
Normotensive
Hemorrhage BP 70-80 mmHg
Hemorrhage BP 40-50 mmHg
Post-Arrest
min > Time
Figure 1. PASG inflation schedule.
Table 1. Baseline Measurements Prior to Inflation. Mean arterial blood pressure 104.2b7.4 mm Hg (W) Compartmental pressure (PJ 5.3h2.4 mm Hg Change in BP with PASG inflation (Am) 37.5 * 16.5 mm Hg AP, With compartment squeeze 50-100 mm Hg AP, With hindlimb traction lo-20 mm Hg
in BP of 37.5 f 16.5 mm Hg over the 20minute inflation period. Values of P, immediately before inflation (T,), and at 5 and 20 minutes following PASG deflation to 0 mm Hg (Tz, Tz) were not significantly different (Table 2). P, increased in parallel fashion with garment inflation, rising an average of 75.0 & 16.1 mm Hg over baseline pressure after 20 minutes of PASG at 60 mm Hg (Table 3). Comparison of APc during the two normotensive inflation periods after five minutes of PASG (74.3 f 13.3 mm Hg and 73.6hl4.5 mm Hg at T,) showed no significant differences (Figure 2). Values obtained during Phase I were significantly higher (PC .05) than those re-
corded during Phases II and III. Other comparisons were not statistically significant (Table 3). Phase II: Inflation during hemorrhagic hypotension. Inflation of the PASG to 60 mm Hg following hemorrhage to a i!%Pof 70 to 80 mm Hg was associated with a significantly smaller rise in the P, (65.8 f 10.3 mm Hg), measured after 20 minutes of inflation, than found with normal mean blood pressure PASG inflation. Further hemorrhage to a BP of 40 to 50 mm Hg resulted in an additional small decrease in the AP, at T,, to 62.5* 12.7 mm Hg. Comparison of PCmeasurements after deflation at T,, Tz, and Tz again showed no significant changes following either level of hemorrhagic hypotension. Phase Ill: Inflation during the postarrest state. In the immediate postarrest state, two 5-minute inflations of the garment to 60 mm Hg resulted in PC rises of 57.5 f 13.8 mm Hg and 56.5 f 15.6 mm Hg. These values of APc were significantly lower than those obtained in the normoten-
Compartmental
381
Pressure
Table 2. Mean Compartmental Pressure (P,) Before and After PASG Inflation/ Deflation Compartmental Pressure (P,) (mm Hg)
Phase I Normotensive (N=6) Phase II wotensive at BP = 70-80 mm Hg (N=6) 2potensive at BP = 40-50 mm Hg (N=4*) Phase Ill First inflation (N=6) Second inflation (N=6)
5.3zt2.4
6.6zt2.2
6.6h2.7
6.3h2.7
6.5kl.8
6.3 k2.4
6.5 h4.5
7.0 ~4.5
t
5.7h3.0
5.8zk4.4
$
5.2h4.0
4.7b5.3
$
T = before inflation; T_s, Tz= 5- and 20-min deflation p;riod, respectively. p% .05. ‘N = 4 because two of the original six animals died before the completion of the full 20-minute PASG inflation. tDeflation period was five minutes only. Slnflation and deflation periods were five minutes only.
sive state, but not significantly different from each other nor from similar measurements obtained during hemorrhagic hypotension. Again, no significant change was noted in baseline PC before and after PASG inflation during the postarrest state. P, values following inflation of the PASG for 20 minutes are shown in Figure 3. Values were measured before inflation (T,), at 0, 5, and 20 minutes of full inflation to 60 mm Hg (T,, T,, T,,,), and following 5 and 20 minutes of deflation (TZ, T;;iii). Phase I values were significantly higher 0, < .05) than Phase II and III values measured at T, and T,,. Other comparisons were not statistically significant.
Discussion
The anterolateral compartment of the canine hindlimb has well defined and relatively impermeable osseofascial boundaries and provides an excellent model for experimental studies of the compartment syn-
drome.“’ The slit catheter is a simple and easily constructed device for monitoring PC. The accuracy of this technique compares favorably with other established methods of pressure measurement, such as the wick catheter.” The present investigation used the slit catheter in a canine model to study PC changes during application of the PASG and observed such changes under conditions simulating clinical use of the garment, i.e., hemorrhagic hypotension. Results of the current investigation can be summarized as follows. First, PC rises simultaneously with increases in externally applied pressure generated by inflation of the PASG and, perhaps more importantly, promptly returns to baseline pressure values on deflation of the garment. The lack of significant changes in baseline PC readings on deflation of the PASG was also reported by Chisholm and Clark in their work with normotensive human volunteers.’ Furthermore, the absence of sustained PC elevation following deflation of the garment was also substantiated under conditions of hemorrhagic hypotension used in our study. Second, the amount of PC rise (APJ during PASG inflation may be dependent on the level of arterial BP since a significantly smaller EC was seen following hemorrhage to a BP of 70 to 80 mm Hg. Further hemorrhage to a BP of 40 to 50 mm Hg further decreased APc, although the AP, was not significantly different than with a BP of 70 to 80 mm Hg for the sample size studied. When BP was reduced to zero in the postarrest state, the PC was found to be approximately equal to externally applied PASG pressure. The finding of a relationship between P, and systemic arterial pressure is not without precedence: Hargens and co-workers, in their study of fluid balance within the canine anterolateral compartment, found that PCmeasurements were responsive to variations in arterial pressure.12 Also of interest is the clinical report of the development of the compartment syndrome following revascularization surgery and the resumption of increased arterial perfusion
382
Jerris R. Hedges, Paul B. Baker, William C. Dalsey
All values are listed + 1 S.D.
Normotensive Inflation
Hypotensive Inflation BP= 70-80 MO
Phase I Figure 2. P, rise (AP,) following
-
Post-Arrest Inflation
BP =40-50 mmf+3
Phase II
Phase Ill
PASG inflation for five minutes.
Table 3. Change in Compartmental Pressure (APJ During Inflation of the PASG to 00 mm Hg
AP,
at T,
Phase I
Phase II
Normotensive Inflation (N=6)
Hemorrhage to Hemorrhage to m of 70-80 m of 70-80 mm Hg (N=6) mm Hg (N=4*)
73.6hl4.5
mm Hg APc at T,,
75.Oh16.1
mm Hg
64.2~10.2 mm Hg 65.8~ 10.3 mm Hg
59.0116.9 mm Hg 62.5zt 12.7 mm Hg
Phase Ill First Postarrest (N=6)
Second Postarrest (N=6)
57.5zt13.8 mm Hg t
56.5+15.6 mm Hg t
Tg, TB = 5- and P&min inflation period, respectively. Phase I values were significantly higher @C .05) than those of Phases II and III. Other comparisons were not statistically significant. ‘N=4 because two of the dogs died before full completion of the 20-minute PASG inflation. tlnflation of the PASG was for five minutes only.
in a previously ischemic extremity.” The finding of values of APC in excess of 60 mm Hg external PASG pressure deserves further comment. One possible mechanism for the unexpectedly high readings is the anatomy of the dog’s hindlimb. The angulation of the canine hindlimb is such that inflation of the PASG may result in some degree of straightening of the ex-
tremity and subsequent stretching of the anterolateral compartment. The tension developed would elevate PC within the compartment, independent of any externally applied pressure. Vigorous passive straightening of the animal’s hindlimb during deflation periods, consistently produced a AP, of 10 to 20 mm Hg. Although this factor is difficult to quantitate and var-
Compartmental
383
Pressure
PC A
80
WNormotensive Inflation WHypotensive Inflation BP at 70-80mm A=Hypotensive Inflation BP at 40-50 mm
60
50
All values are listed?1 SD.
40
30
20
10 1
0
-
3 To
T20
Ti PASG Inflation
Figure 3. P, values following
TPS
TPZO
to 6OmmHg
PASO inflation for 20 minutes.
ies from animal to animal, it could account for some of the additional pressure developed during inflation of the PASG. It is interesting to note that this elevation was unaffected by administration of succinylcholine or additional pentobarbital. This indicates that any stretching of the compartment is the result of passive muscle loading rather than active contraction. Several of the volunteers in the study of Chisholm and Clark also developed PC rises in excess of externally applied pressure.’ In conscious human volunteers, active contraction of muscles within the compartment in response to pain or discomfort from the garment may have contributed to the elevation of PC to levels above the PASG inflation pressure. Dynamic PCelevations in excess of 75 mm Hg have been measured in the anterior tibia1 compartment of man during active flexion and extension of the foot.“’ Careful review of the literature regard-
ing PASG use and development of the compartment syndrome reveals several important points. In all seven patients reported, the PASG was inflated for prolonged periods: from a minimum 2% hour? to a maximum of 48 hours.* The most common location for the compartment syndrome following PASG use is the anterior tibia1 compartment, although a recent report describes two cases of compartment syndromes involving both the thigh and lower leg, following garment inflation for greater than 12 hours.6 Although the exact intragarment pressure was seldom monitored in the case reports, the maximum PASG pressure (when the Velcro straps begin to slip) was frequently used. Some of the patients in these case reports had sustained severe injuries to the lower extremity that could have produced the compartment syndrome even if the PASG had not been used. Another patient developed the compartment syndrome fol-
384
Jerris R. Hedges,
lowing improper use of the PASG, i.e., with deflation of the leg segments of the garment while the abdominal segment was still inflated.4 Nevertheless, the compartment syndrome can develop following prolonged PASG use even when the garment is properly applied and in the absence of detectable trauma to the lower extremity.3.5 A sustained increase in tissue pressure is thought to be the central element in the pathogenesis of the compartment syndrome, resulting in markedly decreased tissue perfusion, ischemia, and eventual death of muscle cells.15 The importance of the transient elevations in P, seen during inflation of the PASG to any subsequent development of the compartment syndrome is not fully known. It is necessary to distinguish between PCelevations that spontaneously develop in severely traumatized and ischemic muscle compartments and those occurring in healthy muscle as a result of external compression devices such as the PASG. In the absence of external compression, resting P, readings of 30 mm Hg or more have been associated with major muscle necrosis and may necessitate fasciotomy; the threshold for muscle damage may occur at even lower levels of P, in hypotensive individuals.9 Yet, much higher levels of PC are transiently generated during routine use of the PASG and are tolerated by the vast majority of individuals without long-term damage to the lower extremities. The critical factors in the development of permanent injury with external compression appear to be the duration of the P, elevation and perhaps the presence of associated lower extremity trauma. At least 12 hours of tourniquet ischemia is re-
Paul B. Baker, William C. Dalsey
quired to reliably produce the compartment syndrome in the hindlimb of healthy normotensive dogs.16 Reversible functional changes in the extremity (owing to ischemia), however, may be seen well before this time. Matsen and co-workers noted significant depression of nerve-conduction velocity and muscle action potential amplitude in the legs of normotensive human volunteers after 80 minutes of external compression by an air splint inflated from 40 to 80 mm Hg.” The ability of the PASG to cause considerable ischemic pain is frequently underestimated in a trauma patient, who is often unable to express his discomfort. Most volunteers in PASG studies report that inflation of the garment to higher pressures is a fairly painful experience.18 Although no elevations of compartmental pressure were found following deflation of the PASG in our study of normotensive and hypotensive dogs, the effects of prolonged hypotension were not evaluated. Furthermore, the possibility of a delayed elevation is P, following a relatively brief (20 minutes) period of hypotension and PASG inflation was not ruled out. Additional studies of PC changes with PASG use are needed with monitoring of pressures for longer periods of time. AcknowledgmentsWe would like to thank the Jobst Institute of Toledo, Ohio, for providing a canine version of the PASG. We also gratefully acknowledge the technical advice provided by Marjorie Gabel and Cooper Lewis and thank the Division of Cardiology, University of Cincinnati Medical Center, for use of their laboratory facility.
REFERENCES 1. Wayne MA, MacDonald SC: Clinical evaluation of the antishock trouser: Retrospective analysis of five years of experience. Ann Emerg Med 1983; 12:342-347. 2. Maul1 KI, Capehart JE, et al: Limb loss following Military Anti-Shock Trouser (MAST) Application. J Trauma 1981; 21:60-63. 3. Williams TM, Knopp R, Ellyson JH: Compart-
ment syndrome after anti-shock use without lower extremity trauma. J Trauma 1982; 22: 595-597. 4. Brotman S, Browner BD, Cox BF: MAST-trousers improperly applied causing a compartment syndrome in lower extremity trauma. J Trauma 1982; 22:598-599. 5. Johnson BE: Anterior tibia1 compartment syn-
Compartmental
385
Pressure
drome following use of MAST suit. Ann Emerg Med 1981; 10:209-210. 6. Bass RR, Allison EJ, Reines JD, et al: Thigh compartment syndrome without lower extremity trauma following application of pneumatic antishock trousers. Ann Emerg Med 1983; 12:382384. 7. Chisholm CD, Clark DE: The effect of the pneu-
slit catheter: A comparison with the wick catheter in the measurement of compartment pressure. Injury 1981; 13:404-408. 12. Hargens AR, Akeson WHm, et al: Fluid balance within the canine anterolateral compartment and its relationship to compartment syndromes. J Bone Joint Surg 1978; 6OA:499-505.
21:446-449. 10. Zweifach SS, Hargens AR, et al: Skeletal muscle
13. Coupland GA: Anterior tibia1 syndrome following restoration of arterial flow. Aust NZ J Surg 1972; 41:338-341. 14. McDermott AGP, Marble AE, et al: Monitoring dynamic anterior compartmental pressures during exercise. Am J Sports Med 1982; 10:83-89. 15. Matsen FA: Compartmental syndromes-A unified concept. C/in Orthop 1975; 113:8-14. 16. Hutton M, Rhodes RS, Chapman G: The lowering of postischemic compartment pressures with Mannitol. J Sum Res 1982: 32~239-242. 17. Matsen FA, Mayo LA, et al: A model compartmental syndrome in man with particular reference to the quantification of nerve function. J Bone
necrosis in pressurized compartments associated with hemorrhagic hypotension. J Trauma 1980;
Joint Surg 1977; 59A:648-653. 18. Gaffney FA, Thal ER, et al: Hemodynamic effects
matic antishock garment on intramuscular pressure. Presented at the 13th Annual Meeting of the University Associates for Emergency Medicine, June 1983, Boston, MA. 8. Mubarak SJ, Owen GA, et al: Acute compartmental syndromes: Diagnosis and treatment with the aid of the wick catheter. J Bone Joint Surg 1978; 60A:1091-1095. 9. Rorabeck CH, Castle GSP, et al: Compartmental pressure measurements: An experimental investigation using the slit catheter. J Trauma 1981;
20:941-947.
11. Shakespeare DT, Henderson MJ, Clough G: The
of medical anti-shock trousers (MAST garment). J Trauma 1981; 21:931-937.
1,pp. 377485,1994
Printed in the USA
Copyright 0 1984 Pergamon Press Ltd
??
COMPARTMENTAL PRESSURE MEASUREMENTS DURING APPLICATION OF THE PNEUMATIC ANTISHOCK GARMENT Jerris R. Hedges,
MD, FACEP,
Paul 6. Baker,
MD,
and William C. Dalsey,
MD
The Department of Emergency Medicine, University of Cincinnati Medical Center, Cincinnati, Ohio Reprint address: Jerris R. Hedges, MD, FACEP, Division of Emergency Medicine (ML 769), University of Cincinnati Medical Center, 234 Goodman Street, Cincinnati OH 45267
0 Abstract-Recent case reports have implicated the pneumatic antishock garment (PASG) in the development of the compartment syndrome in the lower extremities. The present study used the anterolateral compartment of the canine hindlimb to model the effect of the PASG on tissue pressure within the compartment (P,). Prior to inflation of the garment, baseline Pe was 5.3 mm Hg. PASG inflation to 60 mm Hg for 20 minutes resulted in an increase in Pe of 75.0 mm Hg over baseline values. The rise in P, was reduced significantly following hemorrhage of the animal, measuring 65.8 mm Hg at a mean arterial pressure of 70 to 80 mm Hg and 62.5 mm Hg at a mean arterial pressure of 40 to 50 mm Hg. In the immediate postarrest state, PErise after a five-minute inflation of the garment was 57.5 mm Hg. In all cases, PC promptly returned to baseline values when the PASG was deflated, and there was no significant change in P, following deflation of the garment under conditions of normotension, hemorrhagic hypotension, and in the immediate postarrest state. Our results suggest that the level of arterial pressure may contribute to P, rise during PASG inflation. 0 Keywords -PASG; compartment pressure; ischemic necrosis
Introduction The pneumatic antishock garment (PASG) has gained increasing acceptance as a valuable adjunct in the initial management of hypovolemic shock. During the past decade, the PASG has received widespread use in the prehospital and emergency department setting, both to maintain an adequate blood pressure and to control hemorrhage resulting from pelvic, abdominal, or lower extremity trauma. With proper patient selection and correct application of the garment, the PASG has been associated with few complications. ’ Several case reports have appeared in the recent literature linking prolonged application of the PASG with subsequent development of the compartment syndrome in the lower extremity.*-6 Although the pathogenesis of the compartment syndrome in such clinical situations is not completely understood, it may be the result of abruptly elevating compartmental pressures in already ischemic, and in some cases, traumatized muscle. There have been few studies documenting changes in com-
Original Contributions presents papers of interest to both academic and practicing physicians. This section of JEM is coordinated by John A. Marx, MD, of Denver General
m
Hospital.
RECEIVED:
29 August 1983; ACCEPTED: 19 December 1983 377
0736-4679/84 $3.00 + .OO
378
Jerris R. Hedges, Paul B. Baker, William C. Dalsey
partmental pressure that occur during external pneumatic compression of an extremity. Chisholm and Clark measured the effect of the PASG on intramuscular pressures within the anterior tibia1 compartment of eight normotensive volunteers’ using the wick catheter technique of Mubarak et al.8 Compartmental pressures were found to roughly parallel externally applied PASG pressure during inflation, with prompt return to baseline values following deflation of the garment.’ It must be emphasized that the PASG is most frequently used under conditions of hemorrhagic hypotension, where the effects of external compression on potentially ischemic muscle compartments are not known. In order to assess the potential of the PASG to induce the compartment syndrome in the lower extremity, the present study was designed, using the canine hindlimb as a model. Objectives of the study were twofold: first, to measure changes in compartmental pressure during inflation and deflation of the PASG and second, to observe such changes under conditions of normal hemodynamics, during hemorrhagic hypotension, and in the immediate postarrest state.
Methods Animal Preparation Six nonsplenectomized dogs, weighing 18 to 25 kg, were anesthetized with 30 mg/kg pentobarbital intravenously (IV), intubated, and placed on a mechanical ventilator (Harvard pump) at a respiratory rate of 15/min and a tidal volume of 20 mL/kg. Supplemental dosages of 2 to 4 mg/kg pentobarbital were given periodically to maintain anesthesia throughout the experimental protocol. An 1%gauge catheter @-inch Intracath) was placed via cutdown into the left brachial artery for measurement of arterial pressure. A large-bore catheter (modified IV tubing) was placed in the superior vena cava (SVC) via cutdown on the right
external jugular vein to provide ready access for hemorrhage or volume infusion. A slit catheter was prepared, using PE 60 polyethylene tubing following the method of Rorabeck et a1.9 The anterolateral hindlimb of the animal was shaved, and a 1Cgauge catheter (Angiocath) was inserted percutaneously 2 to 3 cm into the muscle belly at a 45” angle. The needle was withdrawn, and the remaining catheter sheath carefully observed for signs of bleeding. If bleeding was noted, an altemative site in the same compartment was chosen. If no hemorrhage was present, the slit catheter was introduced into the muscle compartment through the catheter sheath, the sheath slowly withdrawn, and the slit catheter secured in place with adhesive tape wrapped over the insertion site in a circumferential, nonconstricting fashion. Both arterial and slit catheters were connected to pressure transducers (Statham P23) using high-pressure, nondistensible tubing. During in vitro testing, inflation of the PASG was found to produce no measurable pressure rise as a result of pressure applied directly to the tubing or the attached slit catheter. All pressure measurements were monitored on a multichannel chart recorder (Hewlett Packard 7758). The animal was turned to the left lateral decubitus position. Once all lines were secured, the animal was given 2,000 units of heparin IV. A canine model PASG (Jobst, Inc, Toledo, OH) was carefully placed on the animal, covering the hindlegs and lower third of the abdomen. The garment was custom fitted for medium-sized dogs and was equipped with pressure gauges for monitoring pressures within the garment. Both the PASG gauges and the pressure transducers were calibrated with a mercury manometer immediately prior to the beginning of the experiment.
Experimental Technique Baseline levels of mean arterial blood pressure (BP) and compartmental pressure (P,)
379
Compartmental Pressure
were recorded with the garment deflated (PASG = 0 mm Hg). Slit catheter placement and function were verified by squeezing the hindlimb and observing the expected rise in compartmental pressure. The garment was inflated to 60 mm Hg according to a three phase protocol (Figure l), while BP and PC were continuously monitored. Phase I: Normotensive inflation. The PASG was inflated to 60 mm Hg in 5 mm Hg increments over one minute. Initially, the garment was kept at 60 mm Hg for five minutes, then rapidly deflated to 0 mm Hg over 15 seconds. After a five-minute recovery period at a PASG of 0 mm Hg, the garment was, in previous fashion, inflated to 60 mm Hg and maintained at that level of external pressure for 20 minutes. The PASG was then deflated to 0 mm Hg for another 20-minute recovery period. Throughout Phase I, no attempt was made to control BP. Phase II: Inflation during hemorrhagic hypotension. At the end of the 20-minute deflation period, hemorrhage of the animal was initiated via the SVC catheter. The animal was hemorrhaged to a BP of 70 to 80 mm Hg, and stabilized at that pressure for three to five minutes. Incremental inflation to a PASG pressure of 60 mm Hg was performed as before, and the garment was kept at that level for 20 minutes. BP was maintained at 70 to 80 mm Hg throughout the PASG inflation period by further hemorrhage when necessary. At the end of the 20-minute inflation period, the PASG was rapidly deflated to 0 mm Hg for an additional 20-minute recovery period. At the end of the deflation period, the BP was established at the 40 to 50 mm Hg level for three to five minutes using either further hemorrhage or crystalloid infusion. The PASG was again inflated to 60 mm Hg for 20 minutes, during which time the pressure was maintained at a BP of 40 to 50 mm Hg. At the end of the inflation period, the garment was deflated to 0 mm Hg for five minutes.
Phase Ill: Inflation during the postarrest state. At the end of the last five-minute deflation period, all surviving animals were sacrificed with high-dose barbiturate (Socumb 0.2 ml/kg). The PASG was again inflated to 60 mm Hg for two 5-minute inflation/deflation cycles. Correct placement of the slit catheter within the anterolateral compartment and the absence of significant compartmental hemorrhage were confirmed by postmortem examination of each animal.
Statistical Analysis Values for PC and rise in pressure associated with PASG inflation (APJ were tabulated at the following times: immediately prior to inflation of the PASG (T,); at 0, 5, and 20 minutes of full 60 mm Hg inflation (T,, T,, T,,,); and after 5 and 20 minutes of deflation of the PASG to 0 mm Hg (T,, TFJ. Mean values were compared using the Student’s i test for paired data. The criterion for significance was a P-value of .05 or less. All values are listed as mean f 1 standard deviation.
Results Baseline Values Initial values are listed in Table 1. PC within the anterolateral compartment measured 5.3 f 2.4 mm Hg at the beginning of the experiment. BP prior to inflation of the PASG was 104.2 f 7.4 mm Hg. Vigorous squeezing of the muscle compartment resulted in an abrupt rise in PC of 50 to 100 mm Hg, whereas maximal manual traction of the animal’s hindlimb elevated PCby 10 to 20 mm Hg. Values immediately returned to baseline levels following release of tension. Phase I: Normotensive inflation. Inflation of the PASG to 60 mm Hg resulted in a rise
Jerris R. Hedges, Paul B. Baker, William C. Dalsey
380
70
Garment Pressure
Phase I
Phase II
Phase Ill
60 50 40 30 20 10 o-
~=5
Normotensive
Hemorrhage BP 70-80 mmHg
Hemorrhage BP 40-50 mmHg
Post-Arrest
min > Time
Figure 1. PASG inflation schedule.
Table 1. Baseline Measurements Prior to Inflation. Mean arterial blood pressure 104.2b7.4 mm Hg (W) Compartmental pressure (PJ 5.3h2.4 mm Hg Change in BP with PASG inflation (Am) 37.5 * 16.5 mm Hg AP, With compartment squeeze 50-100 mm Hg AP, With hindlimb traction lo-20 mm Hg
in BP of 37.5 f 16.5 mm Hg over the 20minute inflation period. Values of P, immediately before inflation (T,), and at 5 and 20 minutes following PASG deflation to 0 mm Hg (Tz, Tz) were not significantly different (Table 2). P, increased in parallel fashion with garment inflation, rising an average of 75.0 & 16.1 mm Hg over baseline pressure after 20 minutes of PASG at 60 mm Hg (Table 3). Comparison of APc during the two normotensive inflation periods after five minutes of PASG (74.3 f 13.3 mm Hg and 73.6hl4.5 mm Hg at T,) showed no significant differences (Figure 2). Values obtained during Phase I were significantly higher (PC .05) than those re-
corded during Phases II and III. Other comparisons were not statistically significant (Table 3). Phase II: Inflation during hemorrhagic hypotension. Inflation of the PASG to 60 mm Hg following hemorrhage to a i!%Pof 70 to 80 mm Hg was associated with a significantly smaller rise in the P, (65.8 f 10.3 mm Hg), measured after 20 minutes of inflation, than found with normal mean blood pressure PASG inflation. Further hemorrhage to a BP of 40 to 50 mm Hg resulted in an additional small decrease in the AP, at T,, to 62.5* 12.7 mm Hg. Comparison of PCmeasurements after deflation at T,, Tz, and Tz again showed no significant changes following either level of hemorrhagic hypotension. Phase Ill: Inflation during the postarrest state. In the immediate postarrest state, two 5-minute inflations of the garment to 60 mm Hg resulted in PC rises of 57.5 f 13.8 mm Hg and 56.5 f 15.6 mm Hg. These values of APc were significantly lower than those obtained in the normoten-
Compartmental
381
Pressure
Table 2. Mean Compartmental Pressure (P,) Before and After PASG Inflation/ Deflation Compartmental Pressure (P,) (mm Hg)
Phase I Normotensive (N=6) Phase II wotensive at BP = 70-80 mm Hg (N=6) 2potensive at BP = 40-50 mm Hg (N=4*) Phase Ill First inflation (N=6) Second inflation (N=6)
5.3zt2.4
6.6zt2.2
6.6h2.7
6.3h2.7
6.5kl.8
6.3 k2.4
6.5 h4.5
7.0 ~4.5
t
5.7h3.0
5.8zk4.4
$
5.2h4.0
4.7b5.3
$
T = before inflation; T_s, Tz= 5- and 20-min deflation p;riod, respectively. p% .05. ‘N = 4 because two of the original six animals died before the completion of the full 20-minute PASG inflation. tDeflation period was five minutes only. Slnflation and deflation periods were five minutes only.
sive state, but not significantly different from each other nor from similar measurements obtained during hemorrhagic hypotension. Again, no significant change was noted in baseline PC before and after PASG inflation during the postarrest state. P, values following inflation of the PASG for 20 minutes are shown in Figure 3. Values were measured before inflation (T,), at 0, 5, and 20 minutes of full inflation to 60 mm Hg (T,, T,, T,,,), and following 5 and 20 minutes of deflation (TZ, T;;iii). Phase I values were significantly higher 0, < .05) than Phase II and III values measured at T, and T,,. Other comparisons were not statistically significant.
Discussion
The anterolateral compartment of the canine hindlimb has well defined and relatively impermeable osseofascial boundaries and provides an excellent model for experimental studies of the compartment syn-
drome.“’ The slit catheter is a simple and easily constructed device for monitoring PC. The accuracy of this technique compares favorably with other established methods of pressure measurement, such as the wick catheter.” The present investigation used the slit catheter in a canine model to study PC changes during application of the PASG and observed such changes under conditions simulating clinical use of the garment, i.e., hemorrhagic hypotension. Results of the current investigation can be summarized as follows. First, PC rises simultaneously with increases in externally applied pressure generated by inflation of the PASG and, perhaps more importantly, promptly returns to baseline pressure values on deflation of the garment. The lack of significant changes in baseline PC readings on deflation of the PASG was also reported by Chisholm and Clark in their work with normotensive human volunteers.’ Furthermore, the absence of sustained PC elevation following deflation of the garment was also substantiated under conditions of hemorrhagic hypotension used in our study. Second, the amount of PC rise (APJ during PASG inflation may be dependent on the level of arterial BP since a significantly smaller EC was seen following hemorrhage to a BP of 70 to 80 mm Hg. Further hemorrhage to a BP of 40 to 50 mm Hg further decreased APc, although the AP, was not significantly different than with a BP of 70 to 80 mm Hg for the sample size studied. When BP was reduced to zero in the postarrest state, the PC was found to be approximately equal to externally applied PASG pressure. The finding of a relationship between P, and systemic arterial pressure is not without precedence: Hargens and co-workers, in their study of fluid balance within the canine anterolateral compartment, found that PCmeasurements were responsive to variations in arterial pressure.12 Also of interest is the clinical report of the development of the compartment syndrome following revascularization surgery and the resumption of increased arterial perfusion
382
Jerris R. Hedges, Paul B. Baker, William C. Dalsey
All values are listed + 1 S.D.
Normotensive Inflation
Hypotensive Inflation BP= 70-80 MO
Phase I Figure 2. P, rise (AP,) following
-
Post-Arrest Inflation
BP =40-50 mmf+3
Phase II
Phase Ill
PASG inflation for five minutes.
Table 3. Change in Compartmental Pressure (APJ During Inflation of the PASG to 00 mm Hg
AP,
at T,
Phase I
Phase II
Normotensive Inflation (N=6)
Hemorrhage to Hemorrhage to m of 70-80 m of 70-80 mm Hg (N=6) mm Hg (N=4*)
73.6hl4.5
mm Hg APc at T,,
75.Oh16.1
mm Hg
64.2~10.2 mm Hg 65.8~ 10.3 mm Hg
59.0116.9 mm Hg 62.5zt 12.7 mm Hg
Phase Ill First Postarrest (N=6)
Second Postarrest (N=6)
57.5zt13.8 mm Hg t
56.5+15.6 mm Hg t
Tg, TB = 5- and P&min inflation period, respectively. Phase I values were significantly higher @C .05) than those of Phases II and III. Other comparisons were not statistically significant. ‘N=4 because two of the dogs died before full completion of the 20-minute PASG inflation. tlnflation of the PASG was for five minutes only.
in a previously ischemic extremity.” The finding of values of APC in excess of 60 mm Hg external PASG pressure deserves further comment. One possible mechanism for the unexpectedly high readings is the anatomy of the dog’s hindlimb. The angulation of the canine hindlimb is such that inflation of the PASG may result in some degree of straightening of the ex-
tremity and subsequent stretching of the anterolateral compartment. The tension developed would elevate PC within the compartment, independent of any externally applied pressure. Vigorous passive straightening of the animal’s hindlimb during deflation periods, consistently produced a AP, of 10 to 20 mm Hg. Although this factor is difficult to quantitate and var-
Compartmental
383
Pressure
PC A
80
WNormotensive Inflation WHypotensive Inflation BP at 70-80mm A=Hypotensive Inflation BP at 40-50 mm
60
50
All values are listed?1 SD.
40
30
20
10 1
0
-
3 To
T20
Ti PASG Inflation
Figure 3. P, values following
TPS
TPZO
to 6OmmHg
PASO inflation for 20 minutes.
ies from animal to animal, it could account for some of the additional pressure developed during inflation of the PASG. It is interesting to note that this elevation was unaffected by administration of succinylcholine or additional pentobarbital. This indicates that any stretching of the compartment is the result of passive muscle loading rather than active contraction. Several of the volunteers in the study of Chisholm and Clark also developed PC rises in excess of externally applied pressure.’ In conscious human volunteers, active contraction of muscles within the compartment in response to pain or discomfort from the garment may have contributed to the elevation of PC to levels above the PASG inflation pressure. Dynamic PCelevations in excess of 75 mm Hg have been measured in the anterior tibia1 compartment of man during active flexion and extension of the foot.“’ Careful review of the literature regard-
ing PASG use and development of the compartment syndrome reveals several important points. In all seven patients reported, the PASG was inflated for prolonged periods: from a minimum 2% hour? to a maximum of 48 hours.* The most common location for the compartment syndrome following PASG use is the anterior tibia1 compartment, although a recent report describes two cases of compartment syndromes involving both the thigh and lower leg, following garment inflation for greater than 12 hours.6 Although the exact intragarment pressure was seldom monitored in the case reports, the maximum PASG pressure (when the Velcro straps begin to slip) was frequently used. Some of the patients in these case reports had sustained severe injuries to the lower extremity that could have produced the compartment syndrome even if the PASG had not been used. Another patient developed the compartment syndrome fol-
384
Jerris R. Hedges,
lowing improper use of the PASG, i.e., with deflation of the leg segments of the garment while the abdominal segment was still inflated.4 Nevertheless, the compartment syndrome can develop following prolonged PASG use even when the garment is properly applied and in the absence of detectable trauma to the lower extremity.3.5 A sustained increase in tissue pressure is thought to be the central element in the pathogenesis of the compartment syndrome, resulting in markedly decreased tissue perfusion, ischemia, and eventual death of muscle cells.15 The importance of the transient elevations in P, seen during inflation of the PASG to any subsequent development of the compartment syndrome is not fully known. It is necessary to distinguish between PCelevations that spontaneously develop in severely traumatized and ischemic muscle compartments and those occurring in healthy muscle as a result of external compression devices such as the PASG. In the absence of external compression, resting P, readings of 30 mm Hg or more have been associated with major muscle necrosis and may necessitate fasciotomy; the threshold for muscle damage may occur at even lower levels of P, in hypotensive individuals.9 Yet, much higher levels of PC are transiently generated during routine use of the PASG and are tolerated by the vast majority of individuals without long-term damage to the lower extremities. The critical factors in the development of permanent injury with external compression appear to be the duration of the P, elevation and perhaps the presence of associated lower extremity trauma. At least 12 hours of tourniquet ischemia is re-
Paul B. Baker, William C. Dalsey
quired to reliably produce the compartment syndrome in the hindlimb of healthy normotensive dogs.16 Reversible functional changes in the extremity (owing to ischemia), however, may be seen well before this time. Matsen and co-workers noted significant depression of nerve-conduction velocity and muscle action potential amplitude in the legs of normotensive human volunteers after 80 minutes of external compression by an air splint inflated from 40 to 80 mm Hg.” The ability of the PASG to cause considerable ischemic pain is frequently underestimated in a trauma patient, who is often unable to express his discomfort. Most volunteers in PASG studies report that inflation of the garment to higher pressures is a fairly painful experience.18 Although no elevations of compartmental pressure were found following deflation of the PASG in our study of normotensive and hypotensive dogs, the effects of prolonged hypotension were not evaluated. Furthermore, the possibility of a delayed elevation is P, following a relatively brief (20 minutes) period of hypotension and PASG inflation was not ruled out. Additional studies of PC changes with PASG use are needed with monitoring of pressures for longer periods of time. AcknowledgmentsWe would like to thank the Jobst Institute of Toledo, Ohio, for providing a canine version of the PASG. We also gratefully acknowledge the technical advice provided by Marjorie Gabel and Cooper Lewis and thank the Division of Cardiology, University of Cincinnati Medical Center, for use of their laboratory facility.
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drome following use of MAST suit. Ann Emerg Med 1981; 10:209-210. 6. Bass RR, Allison EJ, Reines JD, et al: Thigh compartment syndrome without lower extremity trauma following application of pneumatic antishock trousers. Ann Emerg Med 1983; 12:382384. 7. Chisholm CD, Clark DE: The effect of the pneu-
slit catheter: A comparison with the wick catheter in the measurement of compartment pressure. Injury 1981; 13:404-408. 12. Hargens AR, Akeson WHm, et al: Fluid balance within the canine anterolateral compartment and its relationship to compartment syndromes. J Bone Joint Surg 1978; 6OA:499-505.
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necrosis in pressurized compartments associated with hemorrhagic hypotension. J Trauma 1980;
Joint Surg 1977; 59A:648-653. 18. Gaffney FA, Thal ER, et al: Hemodynamic effects
matic antishock garment on intramuscular pressure. Presented at the 13th Annual Meeting of the University Associates for Emergency Medicine, June 1983, Boston, MA. 8. Mubarak SJ, Owen GA, et al: Acute compartmental syndromes: Diagnosis and treatment with the aid of the wick catheter. J Bone Joint Surg 1978; 60A:1091-1095. 9. Rorabeck CH, Castle GSP, et al: Compartmental pressure measurements: An experimental investigation using the slit catheter. J Trauma 1981;
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11. Shakespeare DT, Henderson MJ, Clough G: The
of medical anti-shock trousers (MAST garment). J Trauma 1981; 21:931-937.