Lung Water Changes After Thermal Burns An Observational Study ALFRED MORGAN, M.D., DAVID KNIGHT, B.A., NICHOLAS O'CONNOR, M.D.
From the Department of Surgery of Harvard Medical School at the Peter Bent Brigham Hospital, Boston, Massachusetts
Pulmonary extravascular water has been measured as lung thermal volume (LTV) in a group of nine burned patients. Transducer-detectable indicators were used to permit frequent repetition and quick results. Concurrent recordings were made of cardiac output, pulmonary capillary wedge pressure and the usual hemodynamic variables. Moderate elevation of LTV was seen in all, reaching a maximum value before peripheral edema formation was complete. Left heart fiUling pressures were low as was plasma albumin concentration. Clinical pulmonary edema occurred in one patient treated mostly with crystaUloid solution. In several, a secondary peak coincided with edema mobilization.
in patients with thermal burns; in one large series 25% developed a pulmonary complication. "I The cause is often uncertain. Lung damage can be a part of the original injury when caused by toxic inhalation, associated injury, or less certainly, circulating burn toxins. It can be the result of treatment when osmotic and circulatory changes follow fluid resuscitation. Later, respiratory failure can be associated with infection, ventilatory assistance, and the poorly defined syndrome of multiple system failure. Histopathologic information about pulmonary injury in burns comes mostly from autopsy material which shows end-stage changes.6 Earlier changes are only detectable by functional testing, auscultation and x-ray; all relatively insensitive measures. Pulmonary extravascular water (PEVW) must be increased three to five fold to be clinically recognizable.5 PEVW can be measured directly in vivo. Chinard3 described a technique in which two indicators are injected in or near the right atrium and their dilution curves measured in arterial blood. The indicators are chosen so that P ULMONARY INJURY IS FREQUENT
one equilibrates with extravascular fluid and the other remains intravascular. Two central volumes can be calculated from the curves; one includes PEVW and the other does not, so that PEVW is approximated by their difference. The method, as originally described, is cumbersome. Measurements cannot be repeated frequently and results are not immediately available. An adaptation has been developed for clinical studies in which the two indicators are detected by transducers on an arterial monitoring catheter.2 The intravascular indicator is hypertonic saline solution which causes a change in blood conductivity; the extravascular one is a temperature pulse. Central injection of a bolus of iced saline yields information that allows calculation of PEVW. Whatever indicators are used, the method is perfusion dependent, so lung water measurements made with it can be compared only when cardiac output is measured simultaneously. There is another potential source of error. A thermal indicator may not exchange with the same compartment, or to the same degree, as the tritiated water used in the Chinard technique. For this reason, the measurement's result has been called lung thermal volume (LTV). LTV, measured with the instream arterial catheter has been compared with weighed lung water.2 Their correspondence is fair. The equation of the regression line relating LTV and weighted lung water (WLW) is LTV (ml/kg) = (0.73) WLW + 5.35 (r = 0.99). This method does make sequential measurement of LTV possible and was used to examine the natural history of pulmonary water changes with burn injury and its treatment. This report presents results from nine
Address correspondence to: Alfred Morgan, M.D., 721 Huntington Ave., Boston, Massachusetts 02115. Supported by Public Health Service Grants 5 ROI HS 01472 and 1 ROI MB 00128. Submitted for publication: July 19, 1977. 0003-4932-78-0300-0288-0075 © J. B. Lippincott Company
288
Vol. 187.o No. 3
LUNG WATER CHANGES
patients. The group is small because interpretation of LTV changes requires information about pulmonary capillary wedge pressure. All of the patients studied had Swan-Ganz catheters in the pulmonary artery. It was thought that the clinical advantage was worth the risk until the frequency of endocarditis associated with use of these catheters in burned patients was appreciated and indications for their use changed.4 Methods Nine patients with major thermal burns (20-80% body surface area) were studied. As soon as was practical after admission, urinary, central venous, Swan-Ganz and peripheral arterial catheters were inserted. The arterial monitoring-catheter carried a thermistor and conductivity cell. The usual clinical record of pressures, intake, and outputs were kept using a Hewlett-Packard 3500A computer-based ICU information system. As soon as possible after initiation of acute-phase therapy LTV measurement was begun and repeated at least twice daily and more frequently if there were changes in the patient's respiratory status. Patients The characteristics of the patient group are summarized in Table 1. None had a past medical history of heart or lung disease. The likelihood of inhalation injury, considered at least possible for all patients, was judged probable if two or more of the following were present: occurrence of injury in a closed space, facial burns, soot in sputum, or elevated admission carboxyhemoglobin. A pulmonary complication was defined as tracheal intubation, for more than 48 hours, for indications other than upper airway obstruction.
Therapy Except for one patient (Case 1) transferred about a day postburn, primary fluid therapy given during the study followed standard practices for the institution.8 The first estimate of plasma requirement was 10% of body weight. Sodium containing solutions were given to replace known losses. The initial budget was modified, hour by hour, according to observed urine volume, hematocrit, serum sodium and central pressure. Lung thermal volume measurement Instead of the single-lumen peripheral arterial catheter ordinarily used for pressure measurement and arterial blood sampling, a double-lumen five French catheter placed in the radial artery by direct cutdown
289 TABLE 1. Patient Characteristics
PulPatient
Age
Sex
Percent Burn
1 2 3 4 5 6 7 8 9
46 51 24 63 47 50 30 48 20
M M M M M F M M M
75 80 20 60 60 40 60 70 80
Inhalation Injury
monary Complication
Outcome
Possible Probable Possible Possible Possible Probable Possible Probable Probable
Yes Yes No Yes No Yes No Yes Yes
Lived Died Lived Died Lived Lived Died Died Lived
and advanced until a phasic conductivity flow signal was obtained. The second lumen carried leads to a thermistor bead and platinum ring conductivity electrodes at the tip of the catheter. The arterial thermistor, and the thermistor at the tip of the Swan-Ganz pulmonary artery catheter were connected to Hewlett Packard conductivity bridges and from them to both an analogue data tape recorder and the analogue-digital converter of the ICU computer system. Leads from the arterial conductivity electrodes were connected to a low leakage impedance bridge, made for the purpose, which has been described elsewhere.10 Each LTV measurement was made, in triplicate, by central injection of a bolus of 5, 10, or 15 ml of 3% saline solution at 0°. The volume required varied with the patient's body size and cardiac output. Injections were made into the central venous line or the right atrial injection port of the Swan-Ganz cardiac output catheter. The recorded analogue signals were used to compute cardiac output from pulmonary artery and peripheral artery temperature curves. LTV was derived from thermal and conductivity signals using techniques, assumptions and approximations described elsewhere.2 Results
LTV measurements are summarized in Figure 1. The points are averages of three or more measurements made in rapid sequence. Standard deviation brackets have been omitted for clarity; SE for all observations averaged 7.7% of the respective means. Both the starting time and duration of each series of measurements were influenced by clinical considerations, but in spite of varying observational times several characteristics of the data can be seen. Most of the values lie somewhere between normal and the range of clinical pulmonary edema. Staub3 synthesized data available for normal human lungs. Average total wet lung weight was 672 g, extravascular water content 383 g. In clinical pulmonary edema, extra-
290
MORGAN, KNIGHT AND O'CONNOR 1200
Ann.
Surg. a March
1978
r
1000 k
Goo F
LTV
FIG. 1. Each point is the average of 3-5 measurements in rapid sequence. Values are total LTV, not
ml
600 I-
normalized to a body size parameter; data from case 1 are off the scale and are shown separately in
Figure 4.
200 -
oL 0
6
12
16
24
30
36
40
48
POST BURN HOUR vascular water is at least 1000 ml. Several curves have their minimum value at 24-36 hours, the time of maximum peripheral burn edema as measured by weight gain. Pulmonary capillary wedge pressure during acute phase therapy never exceeded 10 mm Hg in any patient. None received steroids of bronchodilators. Results for individual patients have to be interpreted in light of their fluid therapy and other cardiovascular and pulmonary variables. Two were of special interest. Case Reports Case 1. Acute phase therapy with crystalloid solution. Patient I was burned by clothing ignition after throwing gasoline on an outdoor fire. Although there was some facial burn and the COHb level was not measured, the likelihood of inhalation injury was estimated only as "possible" in Table 1 because of the outdoor circumstances and absence of physical signs. He was anuric on arrival at another hospital where he was vigorously resuscitated. Details of his therapy are shown in Figure 2. A large volume of lactated Ringer's solution was required to restore urine volume and maintain hemodynamic stability but did so successfully and he was transferred to our hospital 46 hours after injury. Edema mobilization began almost immediately and led to a hypertonicity syndrome. Plasma sodium peaked at 154 mEq/L (Fig. 3). Paradoxically low sodium excretion was associated with an extraordinarily high plasma renin level: 22.3 ng/mllhr (14). Pulmonary capillary wedge pressure was maintained at 12 cm H20 or below but auscultatory and radiographic signs of pulmonary edema appeared and were treated with positive end expiratory pressure ventilation. LTV measurements were made during this phase of treatment. The initial measurement, 3000 ml, was in the clinical pulmonary edema
range, and associated with moderate bilateral hilar pulmonary infiltrates and increased A-a gradient (arterial Po2 280 mm Hg with 100% oxygen inspired). LTV fell with institution of IPPB, and fell further with PEEP (Fig. 4). When PEEP was discontinued, LTV more than doubled, rising from 600-1400 ml. Concurrent measurements of cardiac output showed little change. The patient was extubated three days later, grafted in several stages and
discharged.
Comment
This patient's pulmonary edema occurred with normal pulmonary capillary wedge and mean pulmonary artery pressures. Plasma total protein concentration was low (3.6 g%), and plasma osmotic pressure could be presumed to have been low also. Rising serum sodium, with body weight falling and urinary sodium excretion inhibited suggests that as the large volume of crystalloid initially required for resuscitation returned to the circulation volume overload was avoided by extrarenal losses, mostly evaporative, but water nevertheless moved into the lungs because of dilutional effects on plasma oncotic pressure. The unusually high renin levels may be related to the episode of oliguric hypovolemia early in the course. The effect of positive pressure on pulmonary edema varies with the hemodynamic setting but the usual effect is to decrease pulmonary water. When PEEP was discontinued after 18 hours there was a
291
LUNG WATER CHANGES
Vol. 187 9 No. 3
large (60%) step increase in LTV without corresponding change in cardiac output. Observations in this patient suggest, in spite of the favorable outcome, that the hazards of the edema mobilization phase of burn therapy may be increased by acute phase treatment based entirely on crystalloid fluids. Case 2. Acute therapy emphasizing plasma with secondary overload: A 51-year-old man fell asleep while smoking in an upholstered chair. The burn area was estimated to be 80% of body surface, mostly full thickness, and involved the perineum, both legs, trunk, arms and face. Inhalation injury was considered probable because of the burn circumstances, facial and intraoral burns, and soot in the sputum. On admission the left foot was pulseless and ischemic. Escharotomy did not improve its appearance; he was taken to the operating room for a three-compartment fasciotomy. Wet ischemic gangrene of the foot and lower leg followed and a guillotine amputation above the knee was done 10 days later. Early fluid therapy included substantial volumes of Plasmanate (117 ml per per cent burn) and crystalloid solutions (132 ml per
PEEP
I///z
*OF Nap
MEq/L
MO I
HCT
201 PLASMA ml 5% DEXTROSE ml
HOURLY
5loo
or-mOo
Units Whole Blood ~~~~~~2 X
_
I
200 [
URINE VOLUME ml
B WI
F,ol[.
kg
UN.
12r-
a
RINGER'S LACTATE L
PLASMA
RENIN ng /ml / hr
*
0r
F0
5Y.
I
I1 1
1
1
1
Furosemide 40 mg IV HOURLY URINE VOLUME 2001ml
45, 35
1526 83
11
111814 27
4
38 A
5
6
POSTBURN DAYS
Transferred to PBBH
I
DEXTROSE L
30
22 3 2
vAlF
l
4.
40
MEq/L
_i
f
750
Mi~4 I
1II°°
-
FIG. 3. Case 1. Partial control of hypertonicity syndrome by diuresis and salt restriction. Peak serum sodium 154 mEq/L. per cent burn) given in the first 48 hours. Figure 5 outlines his course during resuscitation. Urine output was well maintained. Body weight peaked on the sixth postburn day but there was no well marked diuretic phase after it as evidenced by the continuously positive input-output difference. Nevertheless, insensible losses permitted negative daily fluid balance as great as 3.7 L, reflected by body weight changes after day 5. Circulatory overload was avoided (pulmonary artery wedge pressure never exceeding 10 mm Hg) by restricting intake but at the cost of mild hypernatremia. On the sixth day the patient became fatigued, obtunded, and required ventilatory assistance. He died of sepsis on the thirtieth postburn day. LTV measurement began 19 hours after injury. The first measurements were elevated, although below the range of clinical pulmonary edema. As acute phase therapy proceeded LTV fell steadily to a value in the normal range at the time peripheral burn edema was maximum. There were variations in cardiac output, but no corresponding trend. Another series of observations were made during the mild hypertonicity state that occurred during edema mobilization, and a secondary peak in LTV recorded. Plasma albumin concentration at this time was 2.2 g%.
0
Comment
B Wt
kg
96 0
I
I
~
2
POSTBURN DAYS FIG. 2. Case 1. Fluid therapy before transfer.
Interstitial fluid movements in the periphery and in the lungs are subject to different forces, and here showed completely opposite trends. The initial high value of LTV is presumed to be the result of alveolo-capillary damage from inhaled or burn-
Ann. Surg.
MORGAN, KNIGHT AND O'CONNOR
292 40
PA
mmHg 2to _
LTV ml
o
I
I
I
'I
March 1978
ideally, be unchanged but therapy introduces the possibility of increased lung water by two mechanisms: circulatory overload and decreased plasma oncotic pressure. The water content of the lung is determined not only by pressures across the capillary membrane and lymphatic drainage but also by membrane properties which may be changed by heat or toxins. It is generally agreed that heat effects are limited to the upper airway unless superheated steam is inhaled. Steam causes a rapid increase in water content; in an experimental animal model it doubles in four hours.7 Toxic products of combustion may not work quite so fast; there is a recognized latent
PEEP 7cm,50% IPPB 50%
PAW mm Hg
o
I
21W000-
period. 12
J
,i T
_b
600
l
The idea that burn injury is more than a traumatic third space complicated by sepsis persists.' The possibility that pulmonary damage is caused by a burn toxin is speculative but would help explain the very early increases in LTV that were observed. With or without a toxic component it appears that a moderate increase in pulmonary extravascular water is common in burned patients and universal in the group
I______________ ~~~~~~~~~~~~~~~~~~~~~~~~~~~ Pa02
Fio
--
100 %
J
1>
200 _
1
/1
1
/
20 [ CO 1/rnin
I
2
4
POSTBURN DAYS FIG. 4. Case 1. First LTV measured exceeded 3000 pressure 10 mm Hg or less. LTV fell with PEEP, with little change in CO when IPPB was resumed.
5
+Z
IZ S
LTV
WI) ml., wedge rose again
generated toxins. In spite of the plasma-rich fluid therapy given during the development of burn edema, net water movement was away from the interstitium into the circulation. The potential effect of colloidal solutions, holding water in the pulmonary extracellular fluid space, did not occur. There was a secondary increase in LTV associated with dilutional hypoproteinemia during edema mobilization: mild, low pressure pulmonary edema. It occurred in the same setting and at about the same time in several other patients and appears to be a frequent part of the sequence of fluid shifts in burn injury and therapy. Discussion Reasons can be found to predict both an increase and a decrease in lung water after a cutaneous burn. Without treatment reduced plasma volume would be expected to be partially repleted by extracellular fluid, including that of the lung, and this in fact occurs. After a 30% scald burn rats show a progressive decrease in weighed lung water.9 With the plasma volume supported by fluid therapy lung water might,
Co ()
5
j
I
FA(
1
(mmNO 0o
I
I
\-
I
--II
-~~~~~~~~~~~~~~~
No
I140
13F
I
J
I
1--
uRV* OUTPUT
IW/6hi)
INPUT OUTPUT DIFFERENCE
I
1
I1 1 [
0
Wt (kg)
I q
0
1
Xm 2
3 qmm 0 Ss i [g
3
qE
gm2
4
7
9
POST-SUL'N DAY
FIG. 5. Case. 2. LTV maximum on admission, minimum on third post-burn day. A secondary increase occurred with diuresis on days 8 and 9.
Vol. 187 . No. 3
LUNG WATER CHANGES
studied. It appears very early in the course of the injury, perhaps but not necessarily in association with toxic inhalation. It is not high-pressure pulmonary edema but associated with dilutional hypoproteinemia. It appears early and subsides early to a minimum value at the time peripheral burn edema is maximum. A secondary increase may be associated with burn edema mobilization. References 1. Allgoewer, M., Staedler, K. and Schoenenberger, G. A.: Burn Sepsis and Burn Toxin. Ann. R. Coll. Surg., 55:226 (1974). 2. Anderson, W. P., Dunegan, L. J., Knight, D. C., et al.: Rapid Estimation of Pulmonary Extravascular Water with an Instream Catheter. J. Appl. Physiol., 39:843 (1975). 3. Chinard, F. P., Enns, T. and Nolan, M. F.: Indicatordilution Studies with "Diffusable" Indicators. Circ. Res., 10: 473 (1962). 4. Ehrie, M., O'Connor, N., Morgan, A. and Moore, F. D.: Endocarditis with the Indwelling Balloon-tipped Pulmonary Artery Catheter in Burned Patients. J. Trauma (In press).
293
5. Fishman, A. P.: Pulmonary Edema. The Water Exchanging Function of the Lung. Circulation, 46:390 (1972). 6. Foley, C. D., Moncrief, J. A. and Mason, A. D., Jr.: Pathology of the Lung in Fatally Burned Patients. Ann. Surg., 167:251 (1968). 7. Gump, F. E., Zikria, B. A. and Mashima, Y.: The Effect of Interstitial Edema on Pulmonary Function in the Dog. J. Trauma, 12:764 (1972). 8. Moore, F. D.: The Body-weight Burn Budget. Basic Fluid Therapy for the Early Burn. Surg. Clin. North Am., 50:1249 (1970). 9. Morgan, A.: Data in Preparation for Publication. 10. Morgan, A., Collins, J. J., Jr. and Griswold, A. B.: A System for Measurement of Pulmonary Extravascular Water in the I.C.U. in Computers in Cardiology, Institute of Electrical and Electronic engineers, Long Beach, 1975. 11. Pruitt, B. A., Jr., Flemma, R. J., Divincenti, F. C., et al.: Pulmonary Complications in Burn Patients. J. Thorac. Cardiovasc. Surg., 59:7 (1970). 12. Spencer, H.: Pathology of the Lung. Oxford, Pergamon Press, Inc. 1968, p. 675. 13. Staub, N. C.: Pulmonary Edema. Physiol. Rev., 54:678 (1974). 14. Assays by courtesy of Dr. C. Barger.
From the Department of Surgery of Harvard Medical School at the Peter Bent Brigham Hospital, Boston, Massachusetts
Pulmonary extravascular water has been measured as lung thermal volume (LTV) in a group of nine burned patients. Transducer-detectable indicators were used to permit frequent repetition and quick results. Concurrent recordings were made of cardiac output, pulmonary capillary wedge pressure and the usual hemodynamic variables. Moderate elevation of LTV was seen in all, reaching a maximum value before peripheral edema formation was complete. Left heart fiUling pressures were low as was plasma albumin concentration. Clinical pulmonary edema occurred in one patient treated mostly with crystaUloid solution. In several, a secondary peak coincided with edema mobilization.
in patients with thermal burns; in one large series 25% developed a pulmonary complication. "I The cause is often uncertain. Lung damage can be a part of the original injury when caused by toxic inhalation, associated injury, or less certainly, circulating burn toxins. It can be the result of treatment when osmotic and circulatory changes follow fluid resuscitation. Later, respiratory failure can be associated with infection, ventilatory assistance, and the poorly defined syndrome of multiple system failure. Histopathologic information about pulmonary injury in burns comes mostly from autopsy material which shows end-stage changes.6 Earlier changes are only detectable by functional testing, auscultation and x-ray; all relatively insensitive measures. Pulmonary extravascular water (PEVW) must be increased three to five fold to be clinically recognizable.5 PEVW can be measured directly in vivo. Chinard3 described a technique in which two indicators are injected in or near the right atrium and their dilution curves measured in arterial blood. The indicators are chosen so that P ULMONARY INJURY IS FREQUENT
one equilibrates with extravascular fluid and the other remains intravascular. Two central volumes can be calculated from the curves; one includes PEVW and the other does not, so that PEVW is approximated by their difference. The method, as originally described, is cumbersome. Measurements cannot be repeated frequently and results are not immediately available. An adaptation has been developed for clinical studies in which the two indicators are detected by transducers on an arterial monitoring catheter.2 The intravascular indicator is hypertonic saline solution which causes a change in blood conductivity; the extravascular one is a temperature pulse. Central injection of a bolus of iced saline yields information that allows calculation of PEVW. Whatever indicators are used, the method is perfusion dependent, so lung water measurements made with it can be compared only when cardiac output is measured simultaneously. There is another potential source of error. A thermal indicator may not exchange with the same compartment, or to the same degree, as the tritiated water used in the Chinard technique. For this reason, the measurement's result has been called lung thermal volume (LTV). LTV, measured with the instream arterial catheter has been compared with weighed lung water.2 Their correspondence is fair. The equation of the regression line relating LTV and weighted lung water (WLW) is LTV (ml/kg) = (0.73) WLW + 5.35 (r = 0.99). This method does make sequential measurement of LTV possible and was used to examine the natural history of pulmonary water changes with burn injury and its treatment. This report presents results from nine
Address correspondence to: Alfred Morgan, M.D., 721 Huntington Ave., Boston, Massachusetts 02115. Supported by Public Health Service Grants 5 ROI HS 01472 and 1 ROI MB 00128. Submitted for publication: July 19, 1977. 0003-4932-78-0300-0288-0075 © J. B. Lippincott Company
288
Vol. 187.o No. 3
LUNG WATER CHANGES
patients. The group is small because interpretation of LTV changes requires information about pulmonary capillary wedge pressure. All of the patients studied had Swan-Ganz catheters in the pulmonary artery. It was thought that the clinical advantage was worth the risk until the frequency of endocarditis associated with use of these catheters in burned patients was appreciated and indications for their use changed.4 Methods Nine patients with major thermal burns (20-80% body surface area) were studied. As soon as was practical after admission, urinary, central venous, Swan-Ganz and peripheral arterial catheters were inserted. The arterial monitoring-catheter carried a thermistor and conductivity cell. The usual clinical record of pressures, intake, and outputs were kept using a Hewlett-Packard 3500A computer-based ICU information system. As soon as possible after initiation of acute-phase therapy LTV measurement was begun and repeated at least twice daily and more frequently if there were changes in the patient's respiratory status. Patients The characteristics of the patient group are summarized in Table 1. None had a past medical history of heart or lung disease. The likelihood of inhalation injury, considered at least possible for all patients, was judged probable if two or more of the following were present: occurrence of injury in a closed space, facial burns, soot in sputum, or elevated admission carboxyhemoglobin. A pulmonary complication was defined as tracheal intubation, for more than 48 hours, for indications other than upper airway obstruction.
Therapy Except for one patient (Case 1) transferred about a day postburn, primary fluid therapy given during the study followed standard practices for the institution.8 The first estimate of plasma requirement was 10% of body weight. Sodium containing solutions were given to replace known losses. The initial budget was modified, hour by hour, according to observed urine volume, hematocrit, serum sodium and central pressure. Lung thermal volume measurement Instead of the single-lumen peripheral arterial catheter ordinarily used for pressure measurement and arterial blood sampling, a double-lumen five French catheter placed in the radial artery by direct cutdown
289 TABLE 1. Patient Characteristics
PulPatient
Age
Sex
Percent Burn
1 2 3 4 5 6 7 8 9
46 51 24 63 47 50 30 48 20
M M M M M F M M M
75 80 20 60 60 40 60 70 80
Inhalation Injury
monary Complication
Outcome
Possible Probable Possible Possible Possible Probable Possible Probable Probable
Yes Yes No Yes No Yes No Yes Yes
Lived Died Lived Died Lived Lived Died Died Lived
and advanced until a phasic conductivity flow signal was obtained. The second lumen carried leads to a thermistor bead and platinum ring conductivity electrodes at the tip of the catheter. The arterial thermistor, and the thermistor at the tip of the Swan-Ganz pulmonary artery catheter were connected to Hewlett Packard conductivity bridges and from them to both an analogue data tape recorder and the analogue-digital converter of the ICU computer system. Leads from the arterial conductivity electrodes were connected to a low leakage impedance bridge, made for the purpose, which has been described elsewhere.10 Each LTV measurement was made, in triplicate, by central injection of a bolus of 5, 10, or 15 ml of 3% saline solution at 0°. The volume required varied with the patient's body size and cardiac output. Injections were made into the central venous line or the right atrial injection port of the Swan-Ganz cardiac output catheter. The recorded analogue signals were used to compute cardiac output from pulmonary artery and peripheral artery temperature curves. LTV was derived from thermal and conductivity signals using techniques, assumptions and approximations described elsewhere.2 Results
LTV measurements are summarized in Figure 1. The points are averages of three or more measurements made in rapid sequence. Standard deviation brackets have been omitted for clarity; SE for all observations averaged 7.7% of the respective means. Both the starting time and duration of each series of measurements were influenced by clinical considerations, but in spite of varying observational times several characteristics of the data can be seen. Most of the values lie somewhere between normal and the range of clinical pulmonary edema. Staub3 synthesized data available for normal human lungs. Average total wet lung weight was 672 g, extravascular water content 383 g. In clinical pulmonary edema, extra-
290
MORGAN, KNIGHT AND O'CONNOR 1200
Ann.
Surg. a March
1978
r
1000 k
Goo F
LTV
FIG. 1. Each point is the average of 3-5 measurements in rapid sequence. Values are total LTV, not
ml
600 I-
normalized to a body size parameter; data from case 1 are off the scale and are shown separately in
Figure 4.
200 -
oL 0
6
12
16
24
30
36
40
48
POST BURN HOUR vascular water is at least 1000 ml. Several curves have their minimum value at 24-36 hours, the time of maximum peripheral burn edema as measured by weight gain. Pulmonary capillary wedge pressure during acute phase therapy never exceeded 10 mm Hg in any patient. None received steroids of bronchodilators. Results for individual patients have to be interpreted in light of their fluid therapy and other cardiovascular and pulmonary variables. Two were of special interest. Case Reports Case 1. Acute phase therapy with crystalloid solution. Patient I was burned by clothing ignition after throwing gasoline on an outdoor fire. Although there was some facial burn and the COHb level was not measured, the likelihood of inhalation injury was estimated only as "possible" in Table 1 because of the outdoor circumstances and absence of physical signs. He was anuric on arrival at another hospital where he was vigorously resuscitated. Details of his therapy are shown in Figure 2. A large volume of lactated Ringer's solution was required to restore urine volume and maintain hemodynamic stability but did so successfully and he was transferred to our hospital 46 hours after injury. Edema mobilization began almost immediately and led to a hypertonicity syndrome. Plasma sodium peaked at 154 mEq/L (Fig. 3). Paradoxically low sodium excretion was associated with an extraordinarily high plasma renin level: 22.3 ng/mllhr (14). Pulmonary capillary wedge pressure was maintained at 12 cm H20 or below but auscultatory and radiographic signs of pulmonary edema appeared and were treated with positive end expiratory pressure ventilation. LTV measurements were made during this phase of treatment. The initial measurement, 3000 ml, was in the clinical pulmonary edema
range, and associated with moderate bilateral hilar pulmonary infiltrates and increased A-a gradient (arterial Po2 280 mm Hg with 100% oxygen inspired). LTV fell with institution of IPPB, and fell further with PEEP (Fig. 4). When PEEP was discontinued, LTV more than doubled, rising from 600-1400 ml. Concurrent measurements of cardiac output showed little change. The patient was extubated three days later, grafted in several stages and
discharged.
Comment
This patient's pulmonary edema occurred with normal pulmonary capillary wedge and mean pulmonary artery pressures. Plasma total protein concentration was low (3.6 g%), and plasma osmotic pressure could be presumed to have been low also. Rising serum sodium, with body weight falling and urinary sodium excretion inhibited suggests that as the large volume of crystalloid initially required for resuscitation returned to the circulation volume overload was avoided by extrarenal losses, mostly evaporative, but water nevertheless moved into the lungs because of dilutional effects on plasma oncotic pressure. The unusually high renin levels may be related to the episode of oliguric hypovolemia early in the course. The effect of positive pressure on pulmonary edema varies with the hemodynamic setting but the usual effect is to decrease pulmonary water. When PEEP was discontinued after 18 hours there was a
291
LUNG WATER CHANGES
Vol. 187 9 No. 3
large (60%) step increase in LTV without corresponding change in cardiac output. Observations in this patient suggest, in spite of the favorable outcome, that the hazards of the edema mobilization phase of burn therapy may be increased by acute phase treatment based entirely on crystalloid fluids. Case 2. Acute therapy emphasizing plasma with secondary overload: A 51-year-old man fell asleep while smoking in an upholstered chair. The burn area was estimated to be 80% of body surface, mostly full thickness, and involved the perineum, both legs, trunk, arms and face. Inhalation injury was considered probable because of the burn circumstances, facial and intraoral burns, and soot in the sputum. On admission the left foot was pulseless and ischemic. Escharotomy did not improve its appearance; he was taken to the operating room for a three-compartment fasciotomy. Wet ischemic gangrene of the foot and lower leg followed and a guillotine amputation above the knee was done 10 days later. Early fluid therapy included substantial volumes of Plasmanate (117 ml per per cent burn) and crystalloid solutions (132 ml per
PEEP
I///z
*OF Nap
MEq/L
MO I
HCT
201 PLASMA ml 5% DEXTROSE ml
HOURLY
5loo
or-mOo
Units Whole Blood ~~~~~~2 X
_
I
200 [
URINE VOLUME ml
B WI
F,ol[.
kg
UN.
12r-
a
RINGER'S LACTATE L
PLASMA
RENIN ng /ml / hr
*
0r
F0
5Y.
I
I1 1
1
1
1
Furosemide 40 mg IV HOURLY URINE VOLUME 2001ml
45, 35
1526 83
11
111814 27
4
38 A
5
6
POSTBURN DAYS
Transferred to PBBH
I
DEXTROSE L
30
22 3 2
vAlF
l
4.
40
MEq/L
_i
f
750
Mi~4 I
1II°°
-
FIG. 3. Case 1. Partial control of hypertonicity syndrome by diuresis and salt restriction. Peak serum sodium 154 mEq/L. per cent burn) given in the first 48 hours. Figure 5 outlines his course during resuscitation. Urine output was well maintained. Body weight peaked on the sixth postburn day but there was no well marked diuretic phase after it as evidenced by the continuously positive input-output difference. Nevertheless, insensible losses permitted negative daily fluid balance as great as 3.7 L, reflected by body weight changes after day 5. Circulatory overload was avoided (pulmonary artery wedge pressure never exceeding 10 mm Hg) by restricting intake but at the cost of mild hypernatremia. On the sixth day the patient became fatigued, obtunded, and required ventilatory assistance. He died of sepsis on the thirtieth postburn day. LTV measurement began 19 hours after injury. The first measurements were elevated, although below the range of clinical pulmonary edema. As acute phase therapy proceeded LTV fell steadily to a value in the normal range at the time peripheral burn edema was maximum. There were variations in cardiac output, but no corresponding trend. Another series of observations were made during the mild hypertonicity state that occurred during edema mobilization, and a secondary peak in LTV recorded. Plasma albumin concentration at this time was 2.2 g%.
0
Comment
B Wt
kg
96 0
I
I
~
2
POSTBURN DAYS FIG. 2. Case 1. Fluid therapy before transfer.
Interstitial fluid movements in the periphery and in the lungs are subject to different forces, and here showed completely opposite trends. The initial high value of LTV is presumed to be the result of alveolo-capillary damage from inhaled or burn-
Ann. Surg.
MORGAN, KNIGHT AND O'CONNOR
292 40
PA
mmHg 2to _
LTV ml
o
I
I
I
'I
March 1978
ideally, be unchanged but therapy introduces the possibility of increased lung water by two mechanisms: circulatory overload and decreased plasma oncotic pressure. The water content of the lung is determined not only by pressures across the capillary membrane and lymphatic drainage but also by membrane properties which may be changed by heat or toxins. It is generally agreed that heat effects are limited to the upper airway unless superheated steam is inhaled. Steam causes a rapid increase in water content; in an experimental animal model it doubles in four hours.7 Toxic products of combustion may not work quite so fast; there is a recognized latent
PEEP 7cm,50% IPPB 50%
PAW mm Hg
o
I
21W000-
period. 12
J
,i T
_b
600
l
The idea that burn injury is more than a traumatic third space complicated by sepsis persists.' The possibility that pulmonary damage is caused by a burn toxin is speculative but would help explain the very early increases in LTV that were observed. With or without a toxic component it appears that a moderate increase in pulmonary extravascular water is common in burned patients and universal in the group
I______________ ~~~~~~~~~~~~~~~~~~~~~~~~~~~ Pa02
Fio
--
100 %
J
1>
200 _
1
/1
1
/
20 [ CO 1/rnin
I
2
4
POSTBURN DAYS FIG. 4. Case 1. First LTV measured exceeded 3000 pressure 10 mm Hg or less. LTV fell with PEEP, with little change in CO when IPPB was resumed.
5
+Z
IZ S
LTV
WI) ml., wedge rose again
generated toxins. In spite of the plasma-rich fluid therapy given during the development of burn edema, net water movement was away from the interstitium into the circulation. The potential effect of colloidal solutions, holding water in the pulmonary extracellular fluid space, did not occur. There was a secondary increase in LTV associated with dilutional hypoproteinemia during edema mobilization: mild, low pressure pulmonary edema. It occurred in the same setting and at about the same time in several other patients and appears to be a frequent part of the sequence of fluid shifts in burn injury and therapy. Discussion Reasons can be found to predict both an increase and a decrease in lung water after a cutaneous burn. Without treatment reduced plasma volume would be expected to be partially repleted by extracellular fluid, including that of the lung, and this in fact occurs. After a 30% scald burn rats show a progressive decrease in weighed lung water.9 With the plasma volume supported by fluid therapy lung water might,
Co ()
5
j
I
FA(
1
(mmNO 0o
I
I
\-
I
--II
-~~~~~~~~~~~~~~~
No
I140
13F
I
J
I
1--
uRV* OUTPUT
IW/6hi)
INPUT OUTPUT DIFFERENCE
I
1
I1 1 [
0
Wt (kg)
I q
0
1
Xm 2
3 qmm 0 Ss i [g
3
qE
gm2
4
7
9
POST-SUL'N DAY
FIG. 5. Case. 2. LTV maximum on admission, minimum on third post-burn day. A secondary increase occurred with diuresis on days 8 and 9.
Vol. 187 . No. 3
LUNG WATER CHANGES
studied. It appears very early in the course of the injury, perhaps but not necessarily in association with toxic inhalation. It is not high-pressure pulmonary edema but associated with dilutional hypoproteinemia. It appears early and subsides early to a minimum value at the time peripheral burn edema is maximum. A secondary increase may be associated with burn edema mobilization. References 1. Allgoewer, M., Staedler, K. and Schoenenberger, G. A.: Burn Sepsis and Burn Toxin. Ann. R. Coll. Surg., 55:226 (1974). 2. Anderson, W. P., Dunegan, L. J., Knight, D. C., et al.: Rapid Estimation of Pulmonary Extravascular Water with an Instream Catheter. J. Appl. Physiol., 39:843 (1975). 3. Chinard, F. P., Enns, T. and Nolan, M. F.: Indicatordilution Studies with "Diffusable" Indicators. Circ. Res., 10: 473 (1962). 4. Ehrie, M., O'Connor, N., Morgan, A. and Moore, F. D.: Endocarditis with the Indwelling Balloon-tipped Pulmonary Artery Catheter in Burned Patients. J. Trauma (In press).
293
5. Fishman, A. P.: Pulmonary Edema. The Water Exchanging Function of the Lung. Circulation, 46:390 (1972). 6. Foley, C. D., Moncrief, J. A. and Mason, A. D., Jr.: Pathology of the Lung in Fatally Burned Patients. Ann. Surg., 167:251 (1968). 7. Gump, F. E., Zikria, B. A. and Mashima, Y.: The Effect of Interstitial Edema on Pulmonary Function in the Dog. J. Trauma, 12:764 (1972). 8. Moore, F. D.: The Body-weight Burn Budget. Basic Fluid Therapy for the Early Burn. Surg. Clin. North Am., 50:1249 (1970). 9. Morgan, A.: Data in Preparation for Publication. 10. Morgan, A., Collins, J. J., Jr. and Griswold, A. B.: A System for Measurement of Pulmonary Extravascular Water in the I.C.U. in Computers in Cardiology, Institute of Electrical and Electronic engineers, Long Beach, 1975. 11. Pruitt, B. A., Jr., Flemma, R. J., Divincenti, F. C., et al.: Pulmonary Complications in Burn Patients. J. Thorac. Cardiovasc. Surg., 59:7 (1970). 12. Spencer, H.: Pathology of the Lung. Oxford, Pergamon Press, Inc. 1968, p. 675. 13. Staub, N. C.: Pulmonary Edema. Physiol. Rev., 54:678 (1974). 14. Assays by courtesy of Dr. C. Barger.
