SCIENTIFIC PAPERS

Effect of Micropore Filtration on Pulmonary Function After Massive Transfusion

M. B. Durtschi, MD, Seattle, Washington C. E. Maisch, MD, Seattle, Washington L. Reynolds, PhD, Seattle, Washington E. Pavlin, MD, Seattle, Washington T. Ft. Kbhler, MD, Seattle, Washington D. M. l-kimbach, MD, Seattle, Washington C. J. Carrico, MD, Seattle, Washington

The adult respiratory distress syndrome (ARDS) has been associated with multiple clinical conditions including sepsis, shock, trauma, and massive blood transfusion [I]. Its precise pathogenesis remains uncertain. Many investigators suggest that one cause is pulmonary microembolism [1-4] from either endogenously generated [5,6] or exogenously administered [2,3,7,8] microaggregates of platelets, leukocytes, and fibrin [5,9]; however, the validity of this concept has been questioned [10,11]. Disruption of the pulmonary structure at the alveolar level was demonstrated in animals given large transfusions of microaggregate-rich blood [6,12,13]. Similarly, postmortem studies in patients who received massive blood transfusions revealed pulmonary and anatomic changes associated with ARDS, that is, multiple microemboli and thrombi in pulmonary arterial capillaries, intraalveolar hemorrhage, small vessel debris, atelectasis, and widespread patchy hemorrhage [7,8]. A number of workers believe that the use of either a 20 P [2,4,14] or a 40 /J [15,16] filter protects the pulmonary microvasculature from these changes. At least one clinical study that was carefully performed, however, failed to demonstrate From

a beneficial

effect

of filter

use [I 71. Fi-

the Departments of Surgery and Anesthesiology, University of Washington School of Medicine, and the Department of Electrical Engineering. University of Washington, Seattle, Washington. Reprint requests should be addressed to C. James Carrico, MD, Department of Surgery, Harborview Medical Center, 325 Ninth Avenue, Seattle, Washington 98104. Presented at the 50th Annual Meeting of the Pacific Coast Surgical Association, Yosemite National Park, California, February 19-22, 1979.

8

nally, the routine use of these filters may be associated with significant disadvantages including removal of platelets from fresh whole blood [18], additional expense, and reduced speed of transfusion. To evaluate the pulmonary effects of microaggregate infusion, this study prospectively examined the pulmonary function of patients who received large amounts of blood after trauma or other causes of massive bleeding. To obtain a wide range of microaggregate infusion, the patients were classified into two groups. One group received blood through both standard and 40 P filters, whereas the other group received blood through a standard filter only. Material and Methods

This study was conducted in a trauma and burn referral center admitting approximately 3,000 injured patients annually. Three hundred of these patients are admitted to the Trauma Intensive Care Unit. The trauma service consists of two surgical ternate days.

teams

admitting

patients

on al-

From February 1977to June 1978, all adult patients who were admitted because of trauma or massive bleeding and who had (1) a systolic blood pressure of less than 80 mm Hg, (2) a pelvic fracture with displaced fragments, or (3) massive soft tissue trauma were evaluated for inclusion in this study. Patients anticipated to require more than 10 units of blood during their immediate hospital course were included. Patients with known pulmonary, hepatic, or hematologic disease were excluded.

The American Journal of Surgery

Transfusion

This process resulted in the selection of 27 patients ranging in age from 18 to 80 years (mean 42.6) who were included in the study and then assigned to one of two groups depending on the date of their admission to the trauma service. Group I consisted of 13 patients who received an average of 26.1 units of blood through a 40 /.L(Pall Ultipor@) filter as well as a standard blood transfusion filter (160 to 265 p Cutter Saftifilterm). Group II consisted of 14 patients who received an average of 39.9 units of blood, filtered only by the standard filter. Clinical summaries are presented in Table I. Patients who died within the first 24 hours of hospitalization were excluded; two study patients died at 48 hours.

TABLE i

Patient No.

Filtration

and Pulmonary

Function

The remaining study patients survived at least 3 days after transfusion and had the following respiratory variables recorded for the first 72 hours after transfusion or longer if the patient’s clinical condition warranted it: arterial blood gases (ABG), respiratory rate, percentage of oxygen in the inspired gas (FIOz), ratio of arterial Pa02 to FIOs (P/F), effective static compliance (C), dead space to tidal volume ratio (Vn/V,r), and level of positive end expiratory pressure (PEEP) required. Shunt fractions were measured in the patients with Swan-Ganz pulmonary artery catheters in place. Daily chest X-ray films were taken while patients were in the Trauma Intensive Care Unit, and sputum cultures were taken every other day. The consis-

Clinical History Lowest Systolic BP During Resuscitation (mm Hg)

F/UF

Age (yr) Sex

F

47 M

0

2

F

40 M

60

3 4 5

UF UF F

27 M 21 M 23 M

0 0 70

6 7

UF F

22 F 29 M

280 0

8

F

59 F

0

9 10 11

UF UF F

74 M 52 F 30 M

0 0 0

12 13 14 15

F F F UF

70 71 21 72

F M M M

180 280 60

16

UF

21 F

0

17 18

UF F

18M 27 M

280 0

19

F

27 M

30

20 21

UF F

47 F 47 M

180 0

22 23 24

F UF UF

64 M 80 M 23 M

60 0 0

25 26

UF UF

38 M 24 F

0 60

27

UF

79 M

70

0

Diagnosis and Complications MVA; laceration of R atrium and thoracic aorta; cardiac arrest in OR; ARDS; culture neg sepsis Stab to L chest and L abdomen: laceration of lower lobe of L lung MVA; basilar skull fx; multiple rib and long bone fx’s MVA; fx of spleen; L pneumothorax; R temporal skull fx MVA; ruptured diaphragm, spleen, stomach, and bladder; multiple rib fx’s with flail chest; Pseudomonas sepsis MVA; multiple long bone and pelvic fx’s Crush injury to chest; avulsion of innominate a. cardiac contusion: wrist fx MVA; multiple skull fx’s; L subdural hematoma; pelvic, long bone, and facial fx’s Ruptured AAA; Pseudomonas sepsis; MOF; ARDS MVA; skull, pelvic, and long bone fx’s; liver fracture; ARDS Stab wound of abdomen; lacerations of R common iliac a, small bowel, and liver; ARDS Ruptured AAA; intraop anterior MI, postop CHF GSW to pelvis; bladder perforation; L acetabular fx MVA; basilar skull, pelvic, long bone, and splenic fx’s MVA: ruptured spleen and kidney; L 1st rib fx; L flail chest; L pneumothorax; multiple long bone fx’s; Bacillus fragilis sepsis; ARDS MVA; hepatic, basilar skull, pelvic, multiple rib, and long bone fx’s; Enterococcus sepsis MVA, hepatic and splenic laceration; long bone fx’s Stab wound of abdomen and L groin; lacerated liver, spleen, stomach, diaphragm, and femoral a and v GSW to abdomen; injury of IVC, small bowel, and R common iliac artery GI hemorrhage; Escherichia coli sepsis; ARDS Beating; bilateral rib fx’s with flail chest; liver and mesenteric lacerations; ARDS Ruptured AAA; intraop MI; ARF Ruptured AAA; ? acute MI MVA; transected thoracic aorta; L hemothorax; pelvic and long bone fx’s; traumatic pancreatitis; brainstem contusion; culture neg for sepsis GSW to R chest: laceration of R diaphragm and R lobe of liver MVA; pelvic and long bone fx’s; ruptured bladder: ? cardiac contusion Ruptured AAA; cardiac arrest during resuscitation; ARDS

a = artery; AAA = abdominal aortic aneurysm; ARDS = adult respiratory distress syndrome; ARF = acute renal failure; BP = blood pressure; CHF = congestive heart failure; F = filtered; fx = fracture; GSW = gunshot wound: IVC = inferior vena cava; L = left: Ml = myocardial infarction; MOF = multiple organ failure; MVA = motor vehicle accident; neg = negative; R = right; UF = unfiltered: v = vein.

Volume 138, July 1979

9

Durtschi

et al

420

rs = .3 I p z.002

h 300-

l

-8 .

TABLE II

OXYGENATION VS NUMBER OF MICROAGGREGATES



Transfusion Volume

r* = 0.039 p = 0.446

r* = 0.28 p = 0.009

r* = 0.26 p = 0.012

r* = 0.22 p = 0.021

C

r* = 0.012 p = 0.704

r* = 0.34 p = 0.007

r* = 0.16 p = 0.081

r* = 0.14 p = 0.102

P/F

r* = 0.043 p = 0.366

r* = 0.36 p = 0.001

r* = 0.31 p = 0.002

r* = 0.21 p = 0.015

Transfusion volume

r* = 0.068 p = 0.253

.

Oibd

300 Number

“DEAD SPACE” VS NUMBER OF MICROAGGREGATES

.85

340

(x IO’)

Microaggregate Number Size

AIS Value

l

V&VT

A

Coefficient of Determination and Statistical Significance

AIS = Abbreviated Injury Scale; C = effective static compliance; P/F = ratio of arterial P,02 to F102; Vo/Vr = dead space to tidal volume ratio.

.

1

Results .

l

IiDeod spoce’15 5 (v,/vT) l

,45)2y

.31j

,I.-

0

,

1

,

,

,

,

loo

,

,

,

,

3ocl 340

200 Number

(x IO’

, g’-;:,

1

Figure 1. A, P/F (oxygenation) versus number of microaggregates (X IO’). 6, Vo/VT (dead space) versus number of microaggregafes ( X 10 ’ ) .

tently lowest P/F ratio, the lowest C value, and the highest Vo/Vr ratio of each patient for the first 12 hours after transfusion were selected for analysis. Patients were judged to have the adult respiratory distress syndrome (ARDS) by their attending physician using the following criteria: (1) inadequate oxygenation, that is, a P/F ratio less than or equal to 200; (2) the need for mechanical ventilation for 48 hours or longer after injury, a surgical procedure or both; (3) a chest X-ray film compatible with a diagnosis of ARDS; and (4) the absence of other known pulmonary pathophysiologic conditions such

as cardiogenic pulmonary edema, pulmonary embolism, pneumonia, and pneumothorax. The relative magnitude of each patient’s thoracic, abdominal, orthopedic, and soft tissue injuries was assigned a numeric value from the Abbreviated Injury Scale (AIS) of Baker et al [19]. The total number and size distribution (M2) of the microaggregates given each patient during transfusion was calculated by multiplying the number of units of blood received by the number and size distribution of the microaggregates present in a standard blood sample of that age, as determined with an optic measurement technique for microaggregate sizing and counting developed by one of us (LR) [20,21].

10

I. The effect of the dose of administered microaggregates on pulmonary function was analyzed in all patients. There was a positive correlation between the number and size of microaggregates infused during massive transfusion and the subsequent abnormality in pulmonary function as measured by the P/F ratio (oxygenation) and VD/VT ratio (dead space) (Figure 1, A and B). There was no correlation between compliance and the number and size of microaggregates (Table II). Furthermore, when considering patients with ARDS (no. = 8) versus those without ARDS (no. = 19), it was apparent that patients with ARDS received a larger volume of transfusion (p = 0.054), a larger number of microaggregates (p = 0.059), as well as larger sized microaggregates (p = 0.070). Even though the difference between these two groups did not quite attain statistical significance, a correlation between the volume of transfusion and the number and size of microaggregates with subsequent development of ARDS is suggested. In contrast, there was no significant correlation between the severity of injury (AIS scores) and the volume of blood transfused on the 1st hospital day. Similarly, there was no significant correlation between AIS scores and pulmonary dysfunction (VD/VT ratio, P/F ratio, and C value) (Table II). II. The groups established to vary the dose of microaggregates infused were then analyzed separately. The following variables of Groups I (filtered) and II (unfiltered) were compared: the number and size of transfused microaggregates, mortality, incidence of ARDS, AIS score, transfusion volume, and mean pulmonary variables (P/F ratio, VDIVT ratio, and C value): The results of the comparison of these two groups are shown in Table III.

The American Journal of Surgery

Transfusion Filtration and Pulmonary Function

TABLE III

TABLE IV

Comparison of Filtered and Unfiltered Groups Group I (Filtered)

Data Number

Group II (Unfiltered)

Group I (Filtered) p Value

13

14

42.6 21-71

42.7 18-80

26.1 f 4.8’ 18.8 f 3.0 25.3 f 1.4

39.9 f 9.8 26.6 f 5.1 27.1 f 4.9

0.223 0.20 0.725

43.9 f 15.9 35.4 f 9.7

98.6 f 76.8 f

0.136 0.179

Age W Mean Range Mean transfusions Total Day 1 AIS value Microaggregates No. (mean) X lo7 M2 (mean) X log Injury Gastrointestinal hemorrhage Stab wound Gunshot wound Ruptured abdominal aortic aneurysm Blunt trauma

0

.

31.2 27.8

Results in Filtered and Unfiltered Groups

Mortality ARDS Mean P/F Mean VolVT Mean C

o/13 3113 213 f 68.70 0.46 f .05 30 f 2.79

0 1 3

6

9

* Standard error of the mean

5114 5/14 199 f 104.80’ 0.55 f 0.40 27 f 3.60

Volume

138, July 1979

p Value 0.025 0.385 0.682 0.126 0.478

iRAN!,FUSION

INJURY i. Endogenous Microaggregates

Ex0genO"IlniCrOaggPecates +--Filtration

11 LUNG

Release of VasoActive Substances

1

-MICROVASCULAR

OCCLUSION

I

Patients in Group II (unfiltered blood) received more blood, and because the micropore filter removed some microaggregates, they received both a larger number and larger sized microaggregates than did patients in Group I (filtered blood). However, this difference was not statistically significant. Mortality and incidence of ARDS in the two groups are seen in Table IV. No patients in Group I (filtered blood) died, but 5 of 14 in Group II died (p = 0.025). Although four of five patients who died had ARDS during their hospital courses, it was the cause of death in only one patient. The cause of death in the other four patients was sepsis with pneumonia in two and renal failure in two. In 3 of 13 patients who received filtered blood and in 5 of 14 who received unfiltered blood, clinical ARDS developed. The mean pulmonary function variables (P/F, VDIVT, and C) of each group are compared in Table IV; there was no statistically significant difference between the two groups in any of the three variables examined. To evaluate other possible etiologic factors of pulmonary dysfunction, patients with a clinical diagnosis of ARDS were compared to those without ARDS. Of the eight patients with ARDS, six were diagnosed as having the respiratory distress syndrome within 72 hours of transfusion whereas in the remaining two patients ARDS developed at 96 and 120 hours, respectively. There was no difference between patients with and those without ARDS in the incidence of bone fracture (p = 0.292), chest trauma (p = 0.484), or overall injury score (p = 0.35). Four of

--

ARDS = adult respiratory distress syndrome: C = effective static compliance; P/F = ratio of arterial P,Op to F102; Vo/VT = dead space to tidal volume ratio. * Standard error of the mean.

1

3 2 2

Group II (Unfiltered)

In viva

---+

aggregation

I Flow redistribution in pulmonary vasculature Post-obstruction venular dilatation intravascular pressures C "leakage" ? microinfarction

t

I & Intra-alveolar flooding Interstitial edema Shunting

s

I

&

ARDS tQs/Qt; rFRC; +C; rPaOp; ;.VD,lV,

Figure 2. Hypothesized development of adult respiratory distress syndrome from microaggregates.

8 patients with ARDS also had sepsis whereas only 3 of 19 patients without ARDS had sepsis; the difference between the two did not quite reach statistical significance (p = 0.088). The mean age of the patients with ARDS (56.0 years) was significantly higher than that of those without ARDS (37.1 years) (p = 0.31). Comments

Figure 2 outlines the hypothesized development of clinical ARDS from massive pulmonary microembolism. This study of 27 patients requiring large amounts of blood secondary to trauma or hemorrhage was designed to give information on the role of microembolism from massive blood transfusion in the development of ARDS. We hoped to vary the dose of microaggregates by employing a micropore filter in random patients.

11

Durtschi et al

The correlation between pulmonary dysfunction and large volumes of transfusion found in our patients has previously been noted [7,8] by some investigators but has not universally been accepted [IO]. One explanation for our observed correlation between transfusion and pulmonary dysfunction is that the need for transfusion of large volumes of blood reflects the severity of injury, and that the severity of injury may be more directly related to the development of pulmonary dysfunction than the transfusion itself. However, we did not find that the most severely injured patients (those with high AIS scores) necessarily received the largest initial transfusions or that they had the most severely deranged lung function. We therefore examined other factors throught to be associated with pulmonary dysfunction and ARDS such as sepsis, direct chest trauma, and bone fracture (with presumed fat embolism). A comparison of the incidence of bone fracture and chest trauma in those with versus those without ARDS revealed no statistically significant difference between the two. Even though the difference in the incidence of sepsis did not quite attain statistical significance, the large observed difference between the two groups suggests that sepsis was an operative factor in the development of ARDS in our patients. Certainly, many previous reports verify that sepsis is associated with ARDS [1,22,23]. To determine whether a true cause-and-effect relation between microaggregates and pulmonary dysfunction existed in our patients, we attempted to reduce the number and size of microaggregates given to one group of patients by micropore filtration during transfusion. The Ultipor 40 p filter was chosen because of its widespread clinical acceptance and a previous report in the literature suggesting that it was clinically useful [ 151. We then compared the mean P/F ratios (oxygenation), V&‘T ratios (dead space), and C values (compliance) as well as the incidence of ARDS in Group I (filtered blood) and Group II (unfiltered blood) patients. If micropore filtration, commonly used at present, is of value, its value lies in the prevention of microembolism by removal of the microaggregates present in stored blood. By eliminating their infusion into the pulmonary vasculature, the chain of events that results from microvascular occlusion is averted. Therefore, the use of micropore filters might be expected either to decrease the incidence of ARDS or prevent deterioration of pulmonary variables. Our comparison of two groups of patients failed to reveal a significant difference in either the degree of pulmonary abnormality or the development of clinically 12

recognizable ARDS. Other workers have also failed to demonstrate the efficacy of this filter in clinical use

[171. Further analysis revealed that the two groups did not receive significantly different numbers of microaggregates. We therefore subjected the micropore filter used in this study to an in vitro analysis of its filtration efficiency by means of the optic scattering technique previously noted. The filter was able to remove only 12 per cent of microaggregates contained in the 1st unit of blood passed through it, and by the 10th unit was releasing more microaggregates into the transfusion line than were being introduced into it via the stored blood [21]. Our inability to show that the severity of injury correlates with either initial transfusion volume or pulmonary dysfunction reflects the selection process employed to enroll patients into this study. Because of the entry requirement of an anticipated immediate transfusion of 10 units of blood, only patients at the extreme end of the injury spectrum were selected. The observation that there was no statistically significant difference between the number of microaggregates given each of the two subgroups may be explained on two different bases. First, the 27 patients used in this study might not have been a large enough number to attain true statistical significance. However, statistical analysis confirms the adequacy of the group size. Second, it might be postulated that inadequate removal of microaggregates by the filter employed could account for failure to create two distinct groups. In fact, we found that the filter used under the conditions of this study did allow most microaggregates to pass into the recipients during transfusion. Further studies of this problem are needed. The use of a more effective filter may allow a true division of massively transfused patients into low and high microaggregate recipient groups. Randomization, difficult under the urgent and sometimes hectic conditions surrounding the admission of patients with trauma, must be improved as evidenced by the difference (although not statistically significant) in transfusion volume received by our two groups. Finally, a difference between patients receiving filtered and those receiving unfiltered blood may exist undetected, and more sensitive methods of detecting subtle differences in pulmonary function may be valuable. Summary

1. This study demonstrates a positive correlation between the number and size of infused microaggregates and the subsequent abnormality in pulThe American Journal of Surgery

Transfusion Filtration and Pulmonary Function

monary function as measured by oxygenation and dead space. 2. No such correlation between the severity of injury and the altered pulmonary function or transfusion volume was demonstrated. 3. We were unable to demonstrate an advantage to the use of a 40 p micropore filter in preventing the adult respiratory distress syndrome (ARDS) or in improving pulmonary function in our patients. 4. One explanation for the failure to demonstrate such an advantage is the low efficiency of the filter used.

References 1. Blaisdell FW, Lewis FE: Respiratory Distress Syndrome of Shock and Trauma, chap 3, 5. Philadelphia, WB Saunders, 1977. 2. Barrett J, Dhurandhar HN, Miller E, Litwin MS: A comparison in vivo of Dacron wool (Swank) and polyester mesh (Pall) micropore blood transfusion filters in the prevention of pulmonary microembolism associated with massive transfusion. Ann Surg 182: 690, 1975. 3. Barrett J, Dawidson I, Dhurandhar HN, Miller E, Litwin MS: Pulmonary microembolism associated with massive transfusion: the basic pathophysiology of its pulmonary effects. Ann Surg 182: 56, 1975. 4. Dawidson I, Barrett JA, Miller E, Litwin MS: Pulmonary microembolism associated with massive transfusion: physiologic effects and comparison in vivo of standard and Dacron wool (Swank) blood transfusion filters in its prevention. Ann Surg 181: 51, 1975. 5. Lim RC, Blaisdell FW, Choy SH, et al: Massive pulmonary microembolism in regional shock. Surg Forum 1966: 13, 1967. 6. Connell RS, Swank RL: Pulmonary fine structure after hemorrhagic shock and transfusion of aging blood. Basel, New York, S. Karger, Symposia of the 6th European Conference on Microcirculation, p 49, 1970. 7. Mosely RE, Doty D: Death associated with multiple pulmonary emboli soon after battle injury. Ann Surg 17 1: 336, 1970. 8. McNamara JJ, Molot MD, Stremple JF: Screen filtration pressure in combat casualties. Ann Surg 172: 334, 1970. 9. Swank RL: Alteration of blood on storage: measurement of adhesiveness of “aging” platelets and leukocytes and their removal by filtration. N EnglJ Med 265: 728, 1961. 10. Collins JA, James PM, Bredenberg CE, et al.: The relationship between transfusion and hypoxia in combat casualties. Ann Surg 188: 513, 1978. 11. Geelhoed GW, Bennett SH: “Shock lung” resulting from perfusion of canine lungs with stored bank blood. Am Surg 41: 671, 1975. 12. Swank RL, Connell RS, Webb MC: Dacron wool filtration and hypotensive shock: an electron microscopical study. Ann Surg 179: 427, 1974. 13. Connell RS, Swank RL: Pulmonary microembolism after blood transfusion: an electron microscopic study. Ann Surg 177: 40, 1973. 14. Barrett J, Takir AH, Litwin MS: Increased pulmonary arteriovenous shunting in humans following blood transfusion. Arch Surg 113: 947, 1978. 15. Reul GJ, Greenberg SD, Lefrak EA, et al.: Prevention of posttraumatic pulmonary insufficiency. Arch Surg 106: 386, 1973. 16. Reul JG, Beall AC, Greenberg SD: Protection of the pulmonary microvasculature by fine screen blood filtration. Chest 66: 4, 1974. 17. Virgilio RW, Rice CL, Smith DE, et al.: Blood filters and postoperative pulmonary dysfunction. Surg Gynecol Obstet, in

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press 18. Gervin AS, Limbird TJ, Puckett CL, et al: Ultrapore hemofiltration. Arch Surg 106: 333, 1973. 19. Baker SP, O’Neill B, Haddon W. et al: The injure severity score: a method for describing patients with &ul$ple injuiies and evaluating emergency care. J Trauma 14: 187, 1974. 20. Reynolds L, Simon T: Optical scattering size distribution measurements correlated with screen filtration pressure. Bethesda, Maryland, Alliance for Engineering in .Medicine and Biology, Proceedings of the 31st Annual Conference on Engineering and Biology, p 303, 1978. 21. Reynolds L, Simon T: Size distribution measurements of microaggregates in stored whole blood. Transfusion, submitted for publication. 22. Horovitz JH, Carrico CJ, Shires GT: Pulmonary response to major injury. Arch Surg 108: 349. 1974. 23. Shires GT, Carrico CJ, Canizaro PC: Pulmonary responses. Shock, chap 4. Philadelphia, WB Saunders, 1973.

Discussion F. William Blaisdell (Sacramento, CA): Since 1961 when Swank emphasized the importance of “sludge” in banked blood and introduced the concept of micropore filtration, there has been considerable controversy regarding the benefit of t,hese filters. I have been a principal proponent of the thromboembolic etiology of the respiratory distress syndrome and therefore have accepted the rationale for the use of these filters. Nonetheless, the filters have not made much difference in preventing this syndrome. I believe the reason for this must relate to the fact that shock and soft tissue injury generate far more intrinsic “sludge” than can be extrinsically administered through transfusion. It is probable that a slowdown of the circulation, or shock, is the important variable that renders the patient vulnerable to these microemboli and that a normal or hyperdynamic circulation results in prompt clearance of particulate matter from the circulation. Therefore it is possible to speculate that the patients with the greatest transfusion requirement had hemorrhage that was difficult to control and therefore had the most prolonged shock. Does Dr. Carrico have any information on this point? The most significant part of this paper, however, is the observation that the filter removed only 12 per cent of the “sludge” from the first unit of transfused blood and actually added aggregates to the later units. I believe this observation is unique and explains the controversy regarding filters. I conclude by asking Dr. Carrico to comment in more detail on this study. What was the rate and perfusion pressure used to study the Pall filter? Have you studied other filters such as the Dacron Wool (Swank) to find out if the problem is similar? William W. Krippaehne (Portland, OR): The micropore filter has never made much sense. It converts large emboli of bank blood into smaller and more numerous emboli. There appears to be sufficient experimental and clinical evidence today to suggest that the sticky platelets and their aggregates are best removed by surface area filters rather than micropore filtration. The data, including the recent papers from Tulane, support this viewpoint. I believe the use of componentized blood pr0duct.s that are now available in most metropolitan institutions reduce 13

Durtschi et al

the risk. The use of fresh frozen plasma, packed red cells, or washed red cells reduces the volume of platelet aggregates infused. Crystalloid use also totally removes the infused aggregates. As we have moved from whole bank blood to alternatives or have used surface area filters, we are seeing less of the acute respiratory distress syndrome that was so common several years ago. Richard M. Peters (San Diego, CA): I would like to confirm the results of Dr. Carrico and his group. Dr. Virgilio at the Navy Trauma Research Center and his group in San Diego tested a group of patients using filters in a similar manner and obtained essentially the same results, although they did not perform an elegant study of the filter. One question that concerns me is whether the tests we are using are the most appropriate for the problem that we are looking at. Dr. Carrico reported an increase in dead space and in the ratio of arterial POs to FIOs, both of which would increase if cardiac output was decreased in his sicker patients. We find the penetrance of this disease to be very small, and thus the two types of filters may differ little, which may be the basic problem. We must determine whether a more sensitive test of early ARDS is essential, such as the one that Dr. Blaisdell’s group has worked out of lung water. C. J. Carrico (closing): In response to Dr. Blaisdell’s questions, we did try (as best as one can clinically) to evaluate the intensity and duration of shock in the two groups of patients. The time the patients were in shock, as defined by pressures less than 90, no urinary output, and so forth, was the same in both groups. To answer the questions regarding flow rates and types of filters, I refer to data we obtained by passing samples of stored blood through various filt,ers at a rate roughly equivalent to a unit of blood every 5 minutes. The number and size of particles emerging from the filter were counted using Dr. Reynold’s method. Although we are hesitant to make major conclusions based on these data yet, they certainly suggest that the filter that we use, the Pall filter, is quite inefficient. The Dacron wool filters, on the other hand, are very efficient, but the problem with them is that very high pressures are necessary to get decent flow rates,

14

and the filters end up not being used when you need them the most because you cannot obtain the flow rates clinically. One filter looked quite attractive initially and allowed very good flow rates. However, after 5 units this filter begins to put out new particles in and of itself. Now we have a way to test these filters, but that may not have anything to do with what happens in the patient. That is basically the answer to Dr. Blaisdell’s question regarding the Pall, Fenwall, and Dacron wool filters. Dr. Krippaehne mentioned the surface filtration with Dacron wool. Again, we certainly agree that it is efficient, but it is very difficult to use clinically because of rate limitation. By using component therapy, can we limit the number of microaggregates that people get? The common types of blood that one could consider using, such as packed red cells, have at least as many if not more microaggregates than modified whole blood. The only types that have lower microaggregates, at least by this technique, are plateletpoor or white cell-depleted blood. We certainly agree that if we could obtain better product, we would reduce the number of microaggregates, but to do that, it looks like we will have to use either platelet-poor or white cell-depleted transfusions. We are aware of Dick Virgilio’s work, which was one of the factors that led to our study. Dr. Peters raises another significant question, and that is whether the tests are appropriate and sensitive enough. As he points out, a difference in cardiac output could have accounted for the difference we observed. In all patients who had a Swan-Ganz catheter, we measured cardiac output and shunt fraction. The cardiac outputs in the two groups did not differ. The shunt fractions that were measured showed the same trends as the grosser measures of pulmonary function. Thus in this particular instance, at least, we think that what the data suggested is valid. The idea of measuring more sensitive or more appropriate pulmonary functions is appealing. To try to do this, we are performing a prospective study in patients undergoing surgical excision of burns. We are using the multiple inert gas elimination technique, which ought to show much smaller changes in gas exchanges and lung water, and we are using a better filter.

The American Journal of Surgery

Effect of micropore filtration on pulmonary function after massive transfusion.

SCIENTIFIC PAPERS Effect of Micropore Filtration on Pulmonary Function After Massive Transfusion M. B. Durtschi, MD, Seattle, Washington C. E. Maisc...
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