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Acute fluid volume requirements in infants with anterior abdominal wall defects
Acute Fluid Volume Requirementsin Infants withAnterior Abdominal Wall Defects By Arvin I. Philippart, Timothy G. Canty, and Robert M. Filler
T
HE SURVIVAL OF INFANTS with severe anterior abdominal wall defects has improved markedly since introduction of the use of prosthetic materials by Schuster’ and the advent of intravenous hyperalimentation.2 However, a significant morbidity remains; and our recent experience suggests that some of this results from difficulties in assessing fluid-volume deficits during early therapy. The limitations in the use of vital signs and present monitoring techniques in assessing fluid administration in infants are widely recognized. Recent studies have established the value of continuous measurement of muscle surface pH as a monitor of vital physiologic functions3 Since muscle pH is an index of tissue perfusion, this technique appeared especially applicable for assessing volume deficits in sick newborns with anterior abdominal wall defects. Muscle pH was a useful guide to fluid therapy in these neonates. MATERIALS AND METHODS Six newborns with gastroschisis and/or omphalocele were studied. A sterile combination glass pH electrode (Coming Glass, Medford, Mass.) was inserted on the surface of the vastus Iateralis muscle under the fascia lata by methods previously described.3 Continuous pH recordings were obtained from an expanded-scale battery pH meter (Orion Research, Cambridge, Mass.). In five cases the pH probe was inserted prior to the initial staged closure of the defect. In the sixth (case 1) the probe was placed at the completion of the operation. At the time of the first muscle pH recording, all infants were found to have low core temperature (86’F-97”F) and severe muscle acidosis (pH 6.8-7.0). Routine vital signs were monitored, as was continuous-core temperature. Arterial and/or venous blbod gases and acid-base status were obtained from indwelling catheters as indicated by change in clinical status or muscle pH. Central venous pressures and blood lactates also were ascertained in selected patients. Initial therapy in all infants consisted of correction of hypothermia, administration of fluid, and closure of the defect. The standard intravenous solution administered was 5% dextrose in one-fourth normal saline (35 meq Na/liter) with 2 g albumin/100 ml. Blood was transfused as indicated by falling hematocrit or operative blood loss. Fluid replacement was assessed by changes in muscle pH after correction of hypothermia. Fluid was given as long as muscle pH was below 7.30 and responded to fluid administraFrom the Departments of Surgery, Children‘s Hospital Medical Center, and Harvard Medical School, Boston, Mass. Supported in part by a granf from the Charles A. King Trust. Presented at the Third Annual Meeting of the American Pediatric Surgical Association, Hot Springs, Va., April 13-15, 1972. Arvin I. Philippart, M.D.: Chief Resident in Surgery, Children’s Hospital Medical Center, Boston, Mass. Timothy G. Canty, M.D.: Senior Resident in Surgery, Children’s Hospital MedicaZ Center, Boston, Mass. Robert M. Filler, M.D.: Chief of Clinical Surgery, Children’s Hospital Medical Center, and Associate Professor of Surgery at Children’s Hospital Medical Center, Harvard Medical School, Boston, Mass. Joufnef of Pediatric Surgery, Vol. 7, No. 5 (October-November),
1972
553
554
PHILIPPART, CANTY, AND FILLER
tion. When muscle pH reached the normal range (7.30), replacement was considered adequate. In three infants muscle pH plateaued in the acidotic range (below 7.3Q), and the volume necessary to reach that plateau was considered adequate replacement. In these cases blood pH was correspondingly low because of a respiratory or metabolic acidosis. Further assessment of fluid therapy by muscle pH monitoring was possible only after the other causes of acidosis were corrected. During the remaining 24 hr of the first day, fluids were administered at the rate of 3-g mll’kglhr. This rate was continued as long as muscle pH remained in the normal range (above 7.30).
RESULTS
Case 1 (Fig. 1) demonstrated the need for study of volume deficits in children with these defects. Despite the ad@nistration of 34 ml/kg during surgery, postoperative muscle pH suggested that the volume administered had been inadequate. This infant required an additional 20 ml/kg to establish adequate tissue perfusion as judged by muscle PH. C.R.Z.Skg
GASTROSCHISIS
-4
_ ____--Venous-
210
v
,A_+____--+---
Muscle
-
4-
7.00 ad 6.90
96’
/4fU-lOlV
20
cdkghr
F
,. _
0
I
IIll 0
2
4
I 6
I
I
I
I 10
III
III 12
14
16
Fig. 1. Muscle pH and fluid replacement in 2.5kg neonate (Case 1) with gastroschisis and aspiration pneumonia. Patient received 34 . ml/kg of fluid . during operation. Muscle probe placed 4 hr after surgery revealed unexpected decrease in muscle perfusion (muscle pH 6.93, blood pH 7.28). Perfusion defect was partially corrected by infusion of 20 ml/kg over 2 hr. Muscle pH plateaued in acidotio range (7.24), and rose to 7.30 after correction of recurrent hypothermia (Se.S’F) as well as fluid administration.
AFjTERlOR ABDOMINAL WALL DEFECTS
555
Case 3 (Fig. 2) illustrates how muscle pH data were used to determine volume requirements. Warming from core temperature of 9S’F to 99°F elevated muscle pH from 6.8 to 7.04 before the infusion of fluid was started. Since blood pH was normal, the muscle pH of 7.04 was not due to respiratory or metabolic acidosis and represented inadequate muscle perfusion. Fluid was infused until the muscle pH rose to 7.30. The volume required to produce this correction was 17 ml/kg given over a 45-min period as noted in Table 1. At the end of 24 hr vital signs, urine output, blood and muscle pH, and blood lactates were normal. The volumes required to produce normal tissue perfusion in this series of infants are presented in Table 1. In cases 2, 3, and 5, 17-27 ml of fluid were required during the first 45-90 min of therapy. Much larger volumes were J B I5 kg GASTROSCHISIS r
I
OPERATION 7.50
1
,o_
Fig. 2. Muscle pH and fluid replacement in l&kg neonate (case 3) with gastroschisis. Muscle probe placed prior to warming and primary closure of defect. Muscle pH rose (6.8 to 7.04) with warming before administration of fluid. Residual perfusion defect (muscle pH 7.04, blood pH 7.40) was corrected by administration of 17 ml/kg of fluid in 45 min. Recurrent muscle acidosis at hour 2 led to blood-gas determinations revealing unsuspected respiratory acidosis (pCO2 59). Blood lactate rise to 27 mg/lOO ml at 1 hr and 29 mg/lOO ml at 3 hr reflected “washout” from muscle and explained the low blood pH (7.22) at hour 3 with stibsequent slow rise.
556
PHILIPPART, CANTY, AND FILLER Table 1. initial Fluid Volumes To Achieve Normal Muscle pH VolumeInfused Case
(ml/kg)
Duration of Infusion (min)
1 2 3 4 5 6
54 20 17 63 27 60
120 90 45 90 45 45
needed in cases ~4, and 6. Cases 2,3, and 5 were children with uncomplicated abdominal wall defects. Case 1 was an infant with gastroschisis who had a temperature of 86’ and massive bilateral aspiration pneumonia at admission. Case 4, a S.&kg infant with ruptured omphalocele, lost excessive volumes of blood and fluid during dissection for associated small-bowel atresia. Case 6, a l.bkg moribund infant with ruptured omphalocele, had received no supportive therapy until arrival at our hospital at 12 hr of age. Total volume infused (acute plus maintenance) and urine outputs during the first 24 hr of treatment are shown in Table 2. In those patients with uncomplicated defects, 82-140 ml/kg were administered during this first day of therapy. Cases 4 and 6 continued to require extraordinary volumes postoperatively. Case 4 had persistent fluid losses from his wound. Case 6 received an excessive fluid load and intravenous diuretics in an attempt to reverse acute renal failure. DISCUSSION
Muscle surface pH integrates many variables; it reflects both respiratory and metabolic acid-base status as well as peripheral tissue perfusion. Proper evaluation of abnormal muscle pH requires knowledge of blood pH and pCOz. A very low muscle pH with a corresponding normal blood pH and normal vital signs were noted initially in all infants. Although low muscle pH may reflect respiratory or metabolic acidosis, when blood pH is normal muscle acidosis indicates poor tissue perfusion.3 Usual causes of inadequate peripheral perfusion are decreased cardiac output, decreased blood volume, vasoconstriction, and local interruption of blood supply. In the infants studied, local blood supply was intact and cardiac func-
Table 2. Twenty-four-Hour Fluid Therapy and Urine Output Case 1
2 3 4 5 6
Volume Infused (ml/kg)
92 82 140 280 140 312
Urine Output (ml/kg@4 hr)
3.5 10 10 9 14 5
ANTERIOR ABDOMINAL WALL DEFECTS
557
tion was clinically normal. Vasoconstriction secondary to hypothermia was partially responsible for the initial muscle acidosis. After hypothermia was corrected, the persistent muscle acidosis in the face of normal blood pH reflected decreased blood volume and need for replacement. The rise of muscle pH in response to volume administration supported this thesis. The lactate “washout” effect noted in case 3 (Fig. 2) also indicates improved muscle perfusion in response to fluid administration. In all infants a volume equal to or greater than 25% of estimated blood volume was infused during surgery, suggesting that infants with these anomalies rapidly lose the usual excess of extracellular fluid found in the normal newborn. The variability of fluid demands was notable, with even larger volumes required in infants with superimposed complications. Clinical evaluation and urine outputs that ranged from 3.5 to 14 ml/kg/24 hr suggested that volumes infused during therapy were not excessive. Although muscle pH has been extremely useful in managing these newborns, certain precautions must be observed when using this technique. Fluid should be administered only as long as muscle pH continues to rise. Maintenance fluids are given after pH is in the normal range. When muscle pH plateaus in the acidotic range, infusions should be decreased and a search for respiratory or metabolic acidosis, decreased cardiac function, or recurrent hypothermia instituted. These other causes of muscle acidosis can be detected by clinical evaluation, blood-gas determinations, and temperature monitoring. In two infants low muscle pH was the first warning of inadequate ventilation during surgery (Fig. 2). SUMMARY
Fluid was administered to infants with severe anterior abdominal defects to correct a perfusion deficit detected by muscle surface pH monitoring and not recognized by conventional means of monitoring. Immediate fluid need ranged from 17 to 80 ml/kg. Even in uncomplicated cases these needs were equivalent to or greater than 25% of estimated blood volume. Accurate replacement of volume deficits that appear to be aided by muscle pH monitoring will obviate much of the uncertainty in the care of these infants. ACKNOWLEDGMENT The authors express their gratitude to Doris Fina, R.N., and Honorina M. Espinosa, M.D., for their assistance in this study. REFERENCES 1. Schuster, S. R.: A new method for the staged repair of large omphaloceles. Surg. Gynec. Obstet. 125:837, 1967. 2. Filler, R. M., Eraklis, A. J., Das, J. B., and Schuster, S. R.: Total intravenous nutrition: An adjunct to the management of infants with ruptured omphalocele. Amer. J.
Surg. 121:454,1971. 3. -, Das, J. B., and Espinosa, H. M.: Clinical experience with continuous muscle pH monitoring as an index of tissue perfusion and oxygenation and acid base status. Surgery. In press.
558
PHILIPPART, CANTY, AND FILLER
Discussion Dr. R. 7. Touloukian (New Haoen): I am a little concerned about the relative importance of rewarming hypothermic patients compared with fluid replacement in correction of muscle pH. In the patients with severe hypothermia, what happens to their muscle pH after correction of their hypothermia and before additional fluids are infused? Dr. Guttenberger (Pittsburgh): We have studied 12 children this past year with omphaloceles and measured their total serum protein. The five who had covered sacs had normal levels. However, the seven with ruptured sacs had very low total serum proteins. Their albumin was 60% normal and their immunoglobulin G ranged from 7% to 50% normal. Therefore, we would recommend giving these children not only albumin, but also gamma globulin. Dr. E. W. Fonkalsrud (Los Angeles): I am concerned about the suggestion that muscle pH actually measures blood volume, suggesting that fluid replacement may be monitored by muscle pH changes, The patients presented most likely are fluid-depleted because of “third-space” fluid loss from prolonged exposure of the gut. Have you measured central venous pressures or other parameters together with muscle pH that might give YOU an idea of accurate fluid volume replacement? Dr. M. M. Woolley (Los Angeles): We feel that maintenance fluids for newborns should be calculated at approximately 750-1500 cc/sq m. Assuming that your neonates had a body surface area of 0.2 sq m, I am wondering whether the volumes of fluid used in the patients reported should be considered “therapeutic” or just in the realm of “maintenance.” Dr. D. M. Hays (Los Angeles): In those cases in which the serum pH and the muscle pH were different, do you have any serum lactic acid determinations? Would not serum lactate reflect the same factors that produce this difference? Dr. Philippart: I am not particularly surprised by this flurry of discussions. I think Dr. Touloukian’s question about the effects of both hypothermia and diminished volume on peripheral resistance is appropriate. Both hypothermia and decreased volume do change peripheral resistance. Because of the time limitation, I did not present those patients in whom we separated the effects of volume and of temperature on the pH curve. These effects can be separated. We agree with Dr. Guttenberger’s proposition and have done that for some time. In answer to Dr. Fonkalsrud, we did not intend to imply that we were measuring blood volume with muscle pH. What we are measuring is end-organ performance, and I think we have demonstrated that the infusion of volume will improve this performance.‘Bloodvolume measurements by available techniques are inaccurate in these patients for many reasons, not the least of which is the nature of the anomaly that included them in this study. Central venous pressure monitoring, as well as arterial monitoring, was used in various combinations in these patients. We rely more on pH monitoring because of the inaccuracies in measuring central venous pressure. If the CVP is low, it is helpful. If elevated it may be misleading because of the stress response, coexistent congenital heart disease, or the normally elevated pulmonary vascular resistance in the newborn. I think that Dr. Woolley is aware of our concepts of postoperative fluid management. Certainly, many of us have been brought up to think that one had to restrict infants in the early newborn period, I would agree that what we have demonstrated is the need for full maintenance replacement. In other words, the usual excess of extracellular fluid that we all attribute to the newborn is in essence unavailable to these children, and thus they require maintenance replacement. Bicarbonate is used when there is a metabolic acidosis that is coincident with the low muscle pH. In answer to Dr. Hays, we do have lactate data and, in fact, the lactates do rise. They are initially mildly elevated, demonstrating the diminished peripheral perfusion. With the establishment of proper perfusion, the lactates rise in what we refer to as the lactate “washout effect.” They subsequently subside to normal levels. If systemic acidosis is marked at the time of the peak of the lactate washout, bicarbonate is appropriate.
T
HE SURVIVAL OF INFANTS with severe anterior abdominal wall defects has improved markedly since introduction of the use of prosthetic materials by Schuster’ and the advent of intravenous hyperalimentation.2 However, a significant morbidity remains; and our recent experience suggests that some of this results from difficulties in assessing fluid-volume deficits during early therapy. The limitations in the use of vital signs and present monitoring techniques in assessing fluid administration in infants are widely recognized. Recent studies have established the value of continuous measurement of muscle surface pH as a monitor of vital physiologic functions3 Since muscle pH is an index of tissue perfusion, this technique appeared especially applicable for assessing volume deficits in sick newborns with anterior abdominal wall defects. Muscle pH was a useful guide to fluid therapy in these neonates. MATERIALS AND METHODS Six newborns with gastroschisis and/or omphalocele were studied. A sterile combination glass pH electrode (Coming Glass, Medford, Mass.) was inserted on the surface of the vastus Iateralis muscle under the fascia lata by methods previously described.3 Continuous pH recordings were obtained from an expanded-scale battery pH meter (Orion Research, Cambridge, Mass.). In five cases the pH probe was inserted prior to the initial staged closure of the defect. In the sixth (case 1) the probe was placed at the completion of the operation. At the time of the first muscle pH recording, all infants were found to have low core temperature (86’F-97”F) and severe muscle acidosis (pH 6.8-7.0). Routine vital signs were monitored, as was continuous-core temperature. Arterial and/or venous blbod gases and acid-base status were obtained from indwelling catheters as indicated by change in clinical status or muscle pH. Central venous pressures and blood lactates also were ascertained in selected patients. Initial therapy in all infants consisted of correction of hypothermia, administration of fluid, and closure of the defect. The standard intravenous solution administered was 5% dextrose in one-fourth normal saline (35 meq Na/liter) with 2 g albumin/100 ml. Blood was transfused as indicated by falling hematocrit or operative blood loss. Fluid replacement was assessed by changes in muscle pH after correction of hypothermia. Fluid was given as long as muscle pH was below 7.30 and responded to fluid administraFrom the Departments of Surgery, Children‘s Hospital Medical Center, and Harvard Medical School, Boston, Mass. Supported in part by a granf from the Charles A. King Trust. Presented at the Third Annual Meeting of the American Pediatric Surgical Association, Hot Springs, Va., April 13-15, 1972. Arvin I. Philippart, M.D.: Chief Resident in Surgery, Children’s Hospital Medical Center, Boston, Mass. Timothy G. Canty, M.D.: Senior Resident in Surgery, Children’s Hospital MedicaZ Center, Boston, Mass. Robert M. Filler, M.D.: Chief of Clinical Surgery, Children’s Hospital Medical Center, and Associate Professor of Surgery at Children’s Hospital Medical Center, Harvard Medical School, Boston, Mass. Joufnef of Pediatric Surgery, Vol. 7, No. 5 (October-November),
1972
553
554
PHILIPPART, CANTY, AND FILLER
tion. When muscle pH reached the normal range (7.30), replacement was considered adequate. In three infants muscle pH plateaued in the acidotic range (below 7.3Q), and the volume necessary to reach that plateau was considered adequate replacement. In these cases blood pH was correspondingly low because of a respiratory or metabolic acidosis. Further assessment of fluid therapy by muscle pH monitoring was possible only after the other causes of acidosis were corrected. During the remaining 24 hr of the first day, fluids were administered at the rate of 3-g mll’kglhr. This rate was continued as long as muscle pH remained in the normal range (above 7.30).
RESULTS
Case 1 (Fig. 1) demonstrated the need for study of volume deficits in children with these defects. Despite the ad@nistration of 34 ml/kg during surgery, postoperative muscle pH suggested that the volume administered had been inadequate. This infant required an additional 20 ml/kg to establish adequate tissue perfusion as judged by muscle PH. C.R.Z.Skg
GASTROSCHISIS
-4
_ ____--Venous-
210
v
,A_+____--+---
Muscle
-
4-
7.00 ad 6.90
96’
/4fU-lOlV
20
cdkghr
F
,. _
0
I
IIll 0
2
4
I 6
I
I
I
I 10
III
III 12
14
16
Fig. 1. Muscle pH and fluid replacement in 2.5kg neonate (Case 1) with gastroschisis and aspiration pneumonia. Patient received 34 . ml/kg of fluid . during operation. Muscle probe placed 4 hr after surgery revealed unexpected decrease in muscle perfusion (muscle pH 6.93, blood pH 7.28). Perfusion defect was partially corrected by infusion of 20 ml/kg over 2 hr. Muscle pH plateaued in acidotio range (7.24), and rose to 7.30 after correction of recurrent hypothermia (Se.S’F) as well as fluid administration.
AFjTERlOR ABDOMINAL WALL DEFECTS
555
Case 3 (Fig. 2) illustrates how muscle pH data were used to determine volume requirements. Warming from core temperature of 9S’F to 99°F elevated muscle pH from 6.8 to 7.04 before the infusion of fluid was started. Since blood pH was normal, the muscle pH of 7.04 was not due to respiratory or metabolic acidosis and represented inadequate muscle perfusion. Fluid was infused until the muscle pH rose to 7.30. The volume required to produce this correction was 17 ml/kg given over a 45-min period as noted in Table 1. At the end of 24 hr vital signs, urine output, blood and muscle pH, and blood lactates were normal. The volumes required to produce normal tissue perfusion in this series of infants are presented in Table 1. In cases 2, 3, and 5, 17-27 ml of fluid were required during the first 45-90 min of therapy. Much larger volumes were J B I5 kg GASTROSCHISIS r
I
OPERATION 7.50
1
,o_
Fig. 2. Muscle pH and fluid replacement in l&kg neonate (case 3) with gastroschisis. Muscle probe placed prior to warming and primary closure of defect. Muscle pH rose (6.8 to 7.04) with warming before administration of fluid. Residual perfusion defect (muscle pH 7.04, blood pH 7.40) was corrected by administration of 17 ml/kg of fluid in 45 min. Recurrent muscle acidosis at hour 2 led to blood-gas determinations revealing unsuspected respiratory acidosis (pCO2 59). Blood lactate rise to 27 mg/lOO ml at 1 hr and 29 mg/lOO ml at 3 hr reflected “washout” from muscle and explained the low blood pH (7.22) at hour 3 with stibsequent slow rise.
556
PHILIPPART, CANTY, AND FILLER Table 1. initial Fluid Volumes To Achieve Normal Muscle pH VolumeInfused Case
(ml/kg)
Duration of Infusion (min)
1 2 3 4 5 6
54 20 17 63 27 60
120 90 45 90 45 45
needed in cases ~4, and 6. Cases 2,3, and 5 were children with uncomplicated abdominal wall defects. Case 1 was an infant with gastroschisis who had a temperature of 86’ and massive bilateral aspiration pneumonia at admission. Case 4, a S.&kg infant with ruptured omphalocele, lost excessive volumes of blood and fluid during dissection for associated small-bowel atresia. Case 6, a l.bkg moribund infant with ruptured omphalocele, had received no supportive therapy until arrival at our hospital at 12 hr of age. Total volume infused (acute plus maintenance) and urine outputs during the first 24 hr of treatment are shown in Table 2. In those patients with uncomplicated defects, 82-140 ml/kg were administered during this first day of therapy. Cases 4 and 6 continued to require extraordinary volumes postoperatively. Case 4 had persistent fluid losses from his wound. Case 6 received an excessive fluid load and intravenous diuretics in an attempt to reverse acute renal failure. DISCUSSION
Muscle surface pH integrates many variables; it reflects both respiratory and metabolic acid-base status as well as peripheral tissue perfusion. Proper evaluation of abnormal muscle pH requires knowledge of blood pH and pCOz. A very low muscle pH with a corresponding normal blood pH and normal vital signs were noted initially in all infants. Although low muscle pH may reflect respiratory or metabolic acidosis, when blood pH is normal muscle acidosis indicates poor tissue perfusion.3 Usual causes of inadequate peripheral perfusion are decreased cardiac output, decreased blood volume, vasoconstriction, and local interruption of blood supply. In the infants studied, local blood supply was intact and cardiac func-
Table 2. Twenty-four-Hour Fluid Therapy and Urine Output Case 1
2 3 4 5 6
Volume Infused (ml/kg)
92 82 140 280 140 312
Urine Output (ml/kg@4 hr)
3.5 10 10 9 14 5
ANTERIOR ABDOMINAL WALL DEFECTS
557
tion was clinically normal. Vasoconstriction secondary to hypothermia was partially responsible for the initial muscle acidosis. After hypothermia was corrected, the persistent muscle acidosis in the face of normal blood pH reflected decreased blood volume and need for replacement. The rise of muscle pH in response to volume administration supported this thesis. The lactate “washout” effect noted in case 3 (Fig. 2) also indicates improved muscle perfusion in response to fluid administration. In all infants a volume equal to or greater than 25% of estimated blood volume was infused during surgery, suggesting that infants with these anomalies rapidly lose the usual excess of extracellular fluid found in the normal newborn. The variability of fluid demands was notable, with even larger volumes required in infants with superimposed complications. Clinical evaluation and urine outputs that ranged from 3.5 to 14 ml/kg/24 hr suggested that volumes infused during therapy were not excessive. Although muscle pH has been extremely useful in managing these newborns, certain precautions must be observed when using this technique. Fluid should be administered only as long as muscle pH continues to rise. Maintenance fluids are given after pH is in the normal range. When muscle pH plateaus in the acidotic range, infusions should be decreased and a search for respiratory or metabolic acidosis, decreased cardiac function, or recurrent hypothermia instituted. These other causes of muscle acidosis can be detected by clinical evaluation, blood-gas determinations, and temperature monitoring. In two infants low muscle pH was the first warning of inadequate ventilation during surgery (Fig. 2). SUMMARY
Fluid was administered to infants with severe anterior abdominal defects to correct a perfusion deficit detected by muscle surface pH monitoring and not recognized by conventional means of monitoring. Immediate fluid need ranged from 17 to 80 ml/kg. Even in uncomplicated cases these needs were equivalent to or greater than 25% of estimated blood volume. Accurate replacement of volume deficits that appear to be aided by muscle pH monitoring will obviate much of the uncertainty in the care of these infants. ACKNOWLEDGMENT The authors express their gratitude to Doris Fina, R.N., and Honorina M. Espinosa, M.D., for their assistance in this study. REFERENCES 1. Schuster, S. R.: A new method for the staged repair of large omphaloceles. Surg. Gynec. Obstet. 125:837, 1967. 2. Filler, R. M., Eraklis, A. J., Das, J. B., and Schuster, S. R.: Total intravenous nutrition: An adjunct to the management of infants with ruptured omphalocele. Amer. J.
Surg. 121:454,1971. 3. -, Das, J. B., and Espinosa, H. M.: Clinical experience with continuous muscle pH monitoring as an index of tissue perfusion and oxygenation and acid base status. Surgery. In press.
558
PHILIPPART, CANTY, AND FILLER
Discussion Dr. R. 7. Touloukian (New Haoen): I am a little concerned about the relative importance of rewarming hypothermic patients compared with fluid replacement in correction of muscle pH. In the patients with severe hypothermia, what happens to their muscle pH after correction of their hypothermia and before additional fluids are infused? Dr. Guttenberger (Pittsburgh): We have studied 12 children this past year with omphaloceles and measured their total serum protein. The five who had covered sacs had normal levels. However, the seven with ruptured sacs had very low total serum proteins. Their albumin was 60% normal and their immunoglobulin G ranged from 7% to 50% normal. Therefore, we would recommend giving these children not only albumin, but also gamma globulin. Dr. E. W. Fonkalsrud (Los Angeles): I am concerned about the suggestion that muscle pH actually measures blood volume, suggesting that fluid replacement may be monitored by muscle pH changes, The patients presented most likely are fluid-depleted because of “third-space” fluid loss from prolonged exposure of the gut. Have you measured central venous pressures or other parameters together with muscle pH that might give YOU an idea of accurate fluid volume replacement? Dr. M. M. Woolley (Los Angeles): We feel that maintenance fluids for newborns should be calculated at approximately 750-1500 cc/sq m. Assuming that your neonates had a body surface area of 0.2 sq m, I am wondering whether the volumes of fluid used in the patients reported should be considered “therapeutic” or just in the realm of “maintenance.” Dr. D. M. Hays (Los Angeles): In those cases in which the serum pH and the muscle pH were different, do you have any serum lactic acid determinations? Would not serum lactate reflect the same factors that produce this difference? Dr. Philippart: I am not particularly surprised by this flurry of discussions. I think Dr. Touloukian’s question about the effects of both hypothermia and diminished volume on peripheral resistance is appropriate. Both hypothermia and decreased volume do change peripheral resistance. Because of the time limitation, I did not present those patients in whom we separated the effects of volume and of temperature on the pH curve. These effects can be separated. We agree with Dr. Guttenberger’s proposition and have done that for some time. In answer to Dr. Fonkalsrud, we did not intend to imply that we were measuring blood volume with muscle pH. What we are measuring is end-organ performance, and I think we have demonstrated that the infusion of volume will improve this performance.‘Bloodvolume measurements by available techniques are inaccurate in these patients for many reasons, not the least of which is the nature of the anomaly that included them in this study. Central venous pressure monitoring, as well as arterial monitoring, was used in various combinations in these patients. We rely more on pH monitoring because of the inaccuracies in measuring central venous pressure. If the CVP is low, it is helpful. If elevated it may be misleading because of the stress response, coexistent congenital heart disease, or the normally elevated pulmonary vascular resistance in the newborn. I think that Dr. Woolley is aware of our concepts of postoperative fluid management. Certainly, many of us have been brought up to think that one had to restrict infants in the early newborn period, I would agree that what we have demonstrated is the need for full maintenance replacement. In other words, the usual excess of extracellular fluid that we all attribute to the newborn is in essence unavailable to these children, and thus they require maintenance replacement. Bicarbonate is used when there is a metabolic acidosis that is coincident with the low muscle pH. In answer to Dr. Hays, we do have lactate data and, in fact, the lactates do rise. They are initially mildly elevated, demonstrating the diminished peripheral perfusion. With the establishment of proper perfusion, the lactates rise in what we refer to as the lactate “washout effect.” They subsequently subside to normal levels. If systemic acidosis is marked at the time of the peak of the lactate washout, bicarbonate is appropriate.