- Email: [email protected]
Continuous measurement of oxygen saturation in sick newborn infants
1016
Brief clinical and laboratory observations
metabolism, which ultimately impairs adenosine triphosphate production. Without this trophic source the muscle degenerates. This could be the mechanism for rhabdomyolysis in primary anoxic damage to muscle, as well as in the hereditary muscle enzyme deficiencies of muscle phosphorylase and muscle phosphofructokinase. Direct muscle trauma leads to the appearance of myoglobinuria, with or without renal damage.' Our patient was not subjected to unusual birth trauma, but the degree of muscle injury incurred during an unimpeded, spontaneous delivery through an adequate pelvis has never been quantified. CPK values for large populations of vaginally delivered term infants are not available. In a large review of myoglobinuria in childhood, not one example of neonatal renal failure is cited." Savage et alB searched the literature for 'Type II'ATN, of nontraumatic etiology; of 23 patients cited, the youngest was 9 months of age at the onset. Of interest was the association in one 14·month-old child of underlying E. coli sepsis, the same organism as in our patient. Of reported infectious causes, viral influenza is the only heretofore frequently cited agent known to cause rhabdomyolysis with subsequent myoglobinuria." 10 Cifuentes" cites two patients with postviral myoglobinuria progressing to complete anuria, but the youngest in this series was 8 years of age. Birth trauma, anoxia, or sepsis, or combinations there-
The Journal of Pediatrics December 1978
of, may have acted to precipitate the rhabdomyolysis and subsequent renal failure in our patient. There was no evidence for any of the other well-recognized causes of myoglobinuria, such as hypothermia, hyperthermia, hypokalemia, myositis, myopathy, enzyme deficiency exogenous toxin, or drugs. REFERENCES 1. Grossman RA, Hamilton RW, Morse BM, et al: Nontraumatic rhabdomyolysis and acute renal failure, N Engl J
Med 291:807. 1974. 2. Cifuentes E: Myoglobinuria and acute renal failure in children, Clin Pcdiatr 15:63, 1976. 3. Robotham JL, and Haddow JE: Rhabdamyolysis and myoglobinuria in childhood, Pediatr Clin North Am 23:279. 1976. 4. Rowland LP, and Penn AS: Myoglobinuria, Med Clin North Am 56:1233.1972. 5. Jain R: Acute renal failure in the neonate, Pcdiatr Clin North Am 24:605, 1977. 6. Aschinberg LC, Petros MZ, et al: Acute renal failure in the newborn, Crit Care Med 5:36, 1977. 7. BywatersEOI, and Beall D: Crush injuries with impairment of renal function, Br Med J 1:427, 1941. 8. Savage DCL, Forbes M, and Pearce GW: Idiopathic rhabdomyolysis, Arch Dis Child 46:594, 1971. 9. Minow RA, Gorbaeh S, et al: Myoglobinuria associated with influenza illness, Ann Intern Med 80:359, 1974. 10. Simon NM, Rovner RN, and Berlin BS: Acute myoglobinuria associated with Type A2 Influenza, JAMA 212: 1704, 1970.
Continuous measurement of oxygen saturation newborn infants
In
sick
Andrew R. Wilkinson, M.B., CIt.B., M.R.C.P.,* Roderic H. Phibbs, M.D.,"'* and George A. Gregory, M.D., San Francisco, Calif .
A NEW UMBILICAL arterial catheter oximeter (Oximetrix, Inc., Mt, View, Calif.) has made it possible to measure the oxygen saturation of hemoglobin continuously in the arterial blood of new bam infants. We have evaluated the From the Departments of Pediatrics. Anesthesia and the Cardiovascular Research Institute, University of California. Supported in part by United States Public Health Service Pulmonary SCOR Grants HL 14 201, HL 19 185. 'Supported by a Francis S. North Foundation Senior Fellowhip and a Fulbright-Hays Scholarship. ••Reprint address: Department of Pediatrics, Universuy of
California-S.F., San Prancisco, CA 94143.
performance of this instrument in 34 sick newborn infants and report our findings. Abbreviations used Sao..: saturation of arterial blood hemoglobin with oxygen Pao:: partial pressure of oxygen in arterial blood Pac;,: partial pressure carbon dioxide in arterial blood pH.: pH of arterial blood
THE OXIMETER SYST EM The system comprises a catheter which contains fiberoptics, an optical module, and a processor unit with controls and displays. The catheter is 4 Fr gauge polyurethane dual-lumen tubing. One lumen is for infusing
0022-3476/78/121016+04$00.40/0
e 1978 The
C. V.
Mosby Co.
Brief clinicaland laboratory observations
Volume 93
tOt7
Number 6
100
SaO, (")
CATHETER OXIMETER 50
N=139 r = 0.976
S.D. = 2.46
SaO, (")
CUVETIE OXIMETER Figure. Correlation between Sao" from the catheter oximeter at the time of blood sampling and Sao" of the sampled blood measured in a cuvette oximeter. -
fluids, blood sampling, and pressure measurements. The other lumen contains two plastic optical fibers and a radio-opaque filament which enables localization of the catheter on a roentgenogram. The proximal end of the optical fibers connect to the optical module which contains diodes that emit three wavelengths of red and near-infrared light (range 600 to 1,000 nm). Each wavelength of light is pulsed in sequence at 1 msec intervals through one optical fiber to the blood. The light reflected by the blood is transmitted along the second optical fiber to a light detector. The processor samples this signal and, from the intensities of the three wavelengths of reflected light, computes and displays the average Sao, for the preceding 5 seconds. This average is updated every second. The Sao, is also continuously recorded by a two-speed recorder. Audible and visible alarms are triggered when oxygen saturation exceeds either low or high limits that can be selected by the operator. The instrument also has an "artifact condition" alarm which is triggered when the intensity or character of the reflected light differs from that expected from flowing blood. This occurs during insertion of the catheter before the tip reaches flowing blood or if the tip
impinges on a vessel wall instead of lying in the bloodstream. The alarm is also triggered if the catheter is disconnected from the optical module or if the fiberoptics are damaged, resulting in "cross talk" between them. This alarm would also show if a clot forms on the catheter tip and covers the optics. The catheters are disposable after single use. They are packed and sterilized in a plastic tray with the tip positioned against a standard reflection surface contained in a 1 X 2 X 3 em plastic block. To calibrate the system, the catheter package is opened and the fiberoptics are connected to the optical module. An inner plastic cover keeps the rest of the catheter sterile. With the tip of the catheter against the reflecting surface, the oximeter measures the light intensity, and analog circuits complete a calibra tion process. This takes less than 30 seconds and the catheter is then ready for use. The system can also be calibrated in vivo after the catheter has been passed into the descending aorta. This is done by measuring Sao' in a cuvette oximeter on a sample of blood drawn through the sampling lumen, and correcting the system for the difference between the cuvette measurement and the Sao, displayed by the system at the time of sampling.
1018
Brief clinical and laboratory observations
The sampling lumen of the ca theter has an internal diameter of 0.024 inch and a lumen volum e of 0.1 5 ml (for comparison standard 3.5F and SF Argyle [Argyle umbilical artery ca theter, ALOE Medical Co., St. Louis] catheters are 0.16 ml and 0.20 rnl, respectively). The catheter when connected to a pressure transducer (Sta th am P35D series) has a frequency response flat to 9 Hertz at 37°C (comp ared to Argyle 3.SF = 9 Hz , SF = 8 Hz) as determined by a square wave pressure change.
PATIENTS We placed 35 catheters in 34 newborn infants (birth weights from 1.05 to 3.3 kg-mean 1.84), who required an indwelling arterial line for clinical management of cardiorespiratory distress. We obtained consent from the parents to use this catheter instead of the standard polyvinyl chloride umbilical artery catheter (Argyle, ALOE Medical Co.). METHODS We have described the technique used for catheterization of umbilical ar teries'; when the catheter is in place, we attach it to a pressure transducer to record and measure mean and phasic aortic pressures.' Before insertion we calibrated the oxi meter as described above and did not recalibrate while the catheter was in place in order to evaluate its stability. We took a total of 139 blood samples (1.0 ml) and noted the Sao, reading at the time of sampling. We measured Sao, in a cuvette oximeter (IL No . 182, Instrumentation Laboratory, Inc., Lexington, Mass.), corrected for carboxyhemoglobin concentration, and then compared it with the in vivo results. We measured Pao" Paeo" pHa, and hematocrit on each specimen, and noted the bilirubin concentration if it was measured within two hours. We also noted the mean and phasic blood pressure, and examined pressure wave form for presence of a dicrotic notch ( which we accepted as an adequate tracing without significan t damping).
RESULTS Accuracy. The Figure shows the regression analysis of the 139 paired measurements. Accuracy was not affected by presence of bilirubin to a level of 18 mgtdl, variation in hem atocrit from 19 to 66%, hemoglobin F from < 5 to > 90%, change in pHafrom 7.01 to 7.59, or Paco, from 17 to 81 torr. Continuous infusion of fluid through the sampling lumen or stopping the in fusion did not affect the Sao' value . There was minimal loss of accuracy with the time catheter in place, if the instrument was not recalibrated in vivo. The average time for a 1% loss of accuracy was S4 hours. Peformance and complications. The catheters were in
Tile Journal of Pediatrics December 1978
place from 50 minutes to 20 days (average 87 hours). We performed one or more exchange transfusions (maximum 6) through 13 catheters. In all 35 patients the oximeter system functioned well up to the time of removal of the catheter; no evidence of blood clot was found . In 24 of these , the catheter was removed when it was no longer needed for patient care ; in these, blood sampling and pressure measurements were also satisfactory up to the time of removal. In two others, we removed catheters at 52 and 160 hours, respectively, because of cyanosis or blanching of one or bo th feet; in both, the feet returned to normal appearance. In four patients, the catheter was removed between 55 and 180 hours after insertion because of difficulty in sampling blood. We found no clots and there were no subsequent signs of thrombosis in the infants. Two attempts to insert a catheter were unsuccessful ; efforts to pass a conventional catheter also failed . In one of these, multiple attempts to insert an umbilical catheter had been made before transfer to our hospital. W e determined later that there was a perforation of on umbilical artery; it was imp ossible to tell which catheter cau sed this.
DISCUSSION Fibero ptic catheter oximeters have been developed and used during cardiac ca th eteriza tion in adult patients."' " Catheters used by previous investigators have been either too large or too stiff to be passed through the umbilical artery of a newborn infant. The system described is the first to use polyurethane double-lumen tubing and plastic fiberoptics. The catheter is flexible and does not appear more prone to the usual complications of umbilical arterial catheterization than does the standard catheter. Blanching or cyanosis of a foot or difficulty in sampling are common problems of catheters left in place two to seven days" ';.;; we remove them when such an incident occurs . Recently Clark and lung; reported that perforation of the umbilical artery is a comm on complication of repeated unsuccessful attempts to catheterize the vessel. Because a tight suture may damage the fiberoptics, the catheter must be secured using a " tape bridge" to prevent the catheter slipping out of the descending aorta. The system allows early detection of changes in Sao " reflecting oxygen content mo re accurately than Pao , over the steep part of the oxygen dissociation curve . Because the instrument is calibrated before insertion of the catheter, it is available for use immediately during the resuscitation of a severely asphyxi ated infant. The system does not replace measurements of blood gas tensions and pH, but they are requ ired less frequently. Since we completed this study we have substantially reduced the number of blood samples removed and the
Brief clinical and laboratory observations
Volume 93 Number 6
need for transfusion. Low levels of Sao. indicate that changes in oxygen or ventilation therapy are necessary and we use the oximeter as a guide to effect these changes. After an adequate improvement in Sao., we check blood gas tensions and pH. We adjust inspired oxygen and ventilatory support to keep Sao. at approximately 90%, and when above 96% we measure Pao•. We have shown that if Sao. is 96% or less, the chance of the Pao. exceeding 100 torr is less than 5%." In the majority of infants who are sick enough to need an arterial catheter, the Sao. fluctuates between 85 and 95% when they are in a stable condition. We are grateful to the staff of the Intensive Care Nursery of H.C. Moffitt Hospital and the staff of the Clinical Physiology Services Laboratory of the Cardiovascular Research Institute for thier help in carrying out this study.
1019
2. Kitterman lA, Phibbs RH, and Tooley WH: Aortic blood pressure in normal newborn infants during the first 12hours of life, Pediatrics 44:959, 1969. 3. Polanyi ML, and Hihir RM: In vivo oximeter with fast dynamic response, Rev Sci Instrum 33:1050, 1962. 4. Ensen Y, Briscoe WA, Polanyi ML, and Cournand A: In vivo studies with an intravascular and intracardiac reflection oximeter, J Appl Physiol 17:552, 1962. 5. Symansky MR, and Fox HA: Umbilical vessel catheterization: Indications, management, and evaluation of the technique, J PEDIATR 80:820, 1972. 6. Cochran WD, Davis HT, and Smith CA: Advantages and complications of umbilical artery catheterization in the newborn, Pediatrics 42:769, 1968. 7. Clark 1M, and Jung AL: Umbilical artery catheterization by a cutdown procedure, Pediatrics 59:1036, 1977. 8. Wilkinson AR, Phibbs RH, and Gregory GA: In vivo oxygen dissociation curves in transfused and untransfused newborn infants, Clin Res 26:202A, 1978 (abstr),
REFERENCES l.
Kitterman JA, Phibbs RH, and Tooley WH: Catheterization of umbilical vessels in newborn infants, Pediatr Clin North Am 17:895, 1970.
Neonatal lead intoxication in a prenatally exposed infant Nalini Singh, M.B., B.S., Carol M. Donovan, M.A., R.P.T., and James B. Hanshaw, M.D., Worcester, Mass.
LEAD POISONING is a significant problem among infants and children in contact with lead-based paint. The transfer of lead across the human placenta and its potential threat to the conceptus have been recognized since the early part of this century. The effects oflead are dose related; the mother in this report had far less plumbism than those reports of many years ago, which were clearly' associated with severe fetal damage. It is known that lead can be transferred from the placenta to the fetus at different stages of gestation, I. , and lead has been found in the cord blood of newborn infants delivered in Boston- and New York City' in concentrations ranging from 10 to 30 ug/dl. The following report represents the first example of a liveborn infant with biochemical evidence of lead intoxication due to prenatal exposure to lead.
CASE REPORT A 3,200 gm white girl was born after 40 weeks gestation to a 20-year-old" mother who, with her husband, had removed paint From the Department of Pediatrics, University of Massachusetts Medical School.
0022-3476/781121019+03$00.30/0
from her house with a torch and sandpaper during the third trimester. Six weeks prior to the delivery the father presented in an emergencyroom after two episodes of epigastric pain. Lead lines on the lower gum were seen, and the blood revealed a lead level of 115 flg/dl, hemoglobin 12.5 gm/dl, hematocrit 35.8%, and basophilic stippling of 5.8% of the red blood cells. The urine revealed a coproporphyrin level of 332 flg/l with a deita aminolevulinic acid level of 57 mg/l. He was treated with calcium EDTA and was discharged with a blood level of 57 flg/dl. Subsequently the mother was evaluated for lead poisoning (Table I); it is evident that she had lead intoxication. Twenty days before delivery amniotic fluid obtained by amniocentesis, showed levels of lead and erythrocyte protoporphyrin less than 2flg/dl. Abdominal ultrasound performed the same day showed a biparietal diameter of 9.5 em, corresponding to a pregnancy of 37.5 weeks' gestation. The two siblings, 21h years and 20 months old, were also found to have lead intoxication. The infant was delivered by spontaneous vaginal delivery with Apgar scores of 9 at one minute and 10 at five minutes, respectively. The length was 49.5 em; head circumference 33 em. At birth, physical and neurologic examination, radiographs of the long bones, chest, and abdomen, and the electroencephalogram
Brief clinical and laboratory observations
metabolism, which ultimately impairs adenosine triphosphate production. Without this trophic source the muscle degenerates. This could be the mechanism for rhabdomyolysis in primary anoxic damage to muscle, as well as in the hereditary muscle enzyme deficiencies of muscle phosphorylase and muscle phosphofructokinase. Direct muscle trauma leads to the appearance of myoglobinuria, with or without renal damage.' Our patient was not subjected to unusual birth trauma, but the degree of muscle injury incurred during an unimpeded, spontaneous delivery through an adequate pelvis has never been quantified. CPK values for large populations of vaginally delivered term infants are not available. In a large review of myoglobinuria in childhood, not one example of neonatal renal failure is cited." Savage et alB searched the literature for 'Type II'ATN, of nontraumatic etiology; of 23 patients cited, the youngest was 9 months of age at the onset. Of interest was the association in one 14·month-old child of underlying E. coli sepsis, the same organism as in our patient. Of reported infectious causes, viral influenza is the only heretofore frequently cited agent known to cause rhabdomyolysis with subsequent myoglobinuria." 10 Cifuentes" cites two patients with postviral myoglobinuria progressing to complete anuria, but the youngest in this series was 8 years of age. Birth trauma, anoxia, or sepsis, or combinations there-
The Journal of Pediatrics December 1978
of, may have acted to precipitate the rhabdomyolysis and subsequent renal failure in our patient. There was no evidence for any of the other well-recognized causes of myoglobinuria, such as hypothermia, hyperthermia, hypokalemia, myositis, myopathy, enzyme deficiency exogenous toxin, or drugs. REFERENCES 1. Grossman RA, Hamilton RW, Morse BM, et al: Nontraumatic rhabdomyolysis and acute renal failure, N Engl J
Med 291:807. 1974. 2. Cifuentes E: Myoglobinuria and acute renal failure in children, Clin Pcdiatr 15:63, 1976. 3. Robotham JL, and Haddow JE: Rhabdamyolysis and myoglobinuria in childhood, Pediatr Clin North Am 23:279. 1976. 4. Rowland LP, and Penn AS: Myoglobinuria, Med Clin North Am 56:1233.1972. 5. Jain R: Acute renal failure in the neonate, Pcdiatr Clin North Am 24:605, 1977. 6. Aschinberg LC, Petros MZ, et al: Acute renal failure in the newborn, Crit Care Med 5:36, 1977. 7. BywatersEOI, and Beall D: Crush injuries with impairment of renal function, Br Med J 1:427, 1941. 8. Savage DCL, Forbes M, and Pearce GW: Idiopathic rhabdomyolysis, Arch Dis Child 46:594, 1971. 9. Minow RA, Gorbaeh S, et al: Myoglobinuria associated with influenza illness, Ann Intern Med 80:359, 1974. 10. Simon NM, Rovner RN, and Berlin BS: Acute myoglobinuria associated with Type A2 Influenza, JAMA 212: 1704, 1970.
Continuous measurement of oxygen saturation newborn infants
In
sick
Andrew R. Wilkinson, M.B., CIt.B., M.R.C.P.,* Roderic H. Phibbs, M.D.,"'* and George A. Gregory, M.D., San Francisco, Calif .
A NEW UMBILICAL arterial catheter oximeter (Oximetrix, Inc., Mt, View, Calif.) has made it possible to measure the oxygen saturation of hemoglobin continuously in the arterial blood of new bam infants. We have evaluated the From the Departments of Pediatrics. Anesthesia and the Cardiovascular Research Institute, University of California. Supported in part by United States Public Health Service Pulmonary SCOR Grants HL 14 201, HL 19 185. 'Supported by a Francis S. North Foundation Senior Fellowhip and a Fulbright-Hays Scholarship. ••Reprint address: Department of Pediatrics, Universuy of
California-S.F., San Prancisco, CA 94143.
performance of this instrument in 34 sick newborn infants and report our findings. Abbreviations used Sao..: saturation of arterial blood hemoglobin with oxygen Pao:: partial pressure of oxygen in arterial blood Pac;,: partial pressure carbon dioxide in arterial blood pH.: pH of arterial blood
THE OXIMETER SYST EM The system comprises a catheter which contains fiberoptics, an optical module, and a processor unit with controls and displays. The catheter is 4 Fr gauge polyurethane dual-lumen tubing. One lumen is for infusing
0022-3476/78/121016+04$00.40/0
e 1978 The
C. V.
Mosby Co.
Brief clinicaland laboratory observations
Volume 93
tOt7
Number 6
100
SaO, (")
CATHETER OXIMETER 50
N=139 r = 0.976
S.D. = 2.46
SaO, (")
CUVETIE OXIMETER Figure. Correlation between Sao" from the catheter oximeter at the time of blood sampling and Sao" of the sampled blood measured in a cuvette oximeter. -
fluids, blood sampling, and pressure measurements. The other lumen contains two plastic optical fibers and a radio-opaque filament which enables localization of the catheter on a roentgenogram. The proximal end of the optical fibers connect to the optical module which contains diodes that emit three wavelengths of red and near-infrared light (range 600 to 1,000 nm). Each wavelength of light is pulsed in sequence at 1 msec intervals through one optical fiber to the blood. The light reflected by the blood is transmitted along the second optical fiber to a light detector. The processor samples this signal and, from the intensities of the three wavelengths of reflected light, computes and displays the average Sao, for the preceding 5 seconds. This average is updated every second. The Sao, is also continuously recorded by a two-speed recorder. Audible and visible alarms are triggered when oxygen saturation exceeds either low or high limits that can be selected by the operator. The instrument also has an "artifact condition" alarm which is triggered when the intensity or character of the reflected light differs from that expected from flowing blood. This occurs during insertion of the catheter before the tip reaches flowing blood or if the tip
impinges on a vessel wall instead of lying in the bloodstream. The alarm is also triggered if the catheter is disconnected from the optical module or if the fiberoptics are damaged, resulting in "cross talk" between them. This alarm would also show if a clot forms on the catheter tip and covers the optics. The catheters are disposable after single use. They are packed and sterilized in a plastic tray with the tip positioned against a standard reflection surface contained in a 1 X 2 X 3 em plastic block. To calibrate the system, the catheter package is opened and the fiberoptics are connected to the optical module. An inner plastic cover keeps the rest of the catheter sterile. With the tip of the catheter against the reflecting surface, the oximeter measures the light intensity, and analog circuits complete a calibra tion process. This takes less than 30 seconds and the catheter is then ready for use. The system can also be calibrated in vivo after the catheter has been passed into the descending aorta. This is done by measuring Sao' in a cuvette oximeter on a sample of blood drawn through the sampling lumen, and correcting the system for the difference between the cuvette measurement and the Sao, displayed by the system at the time of sampling.
1018
Brief clinical and laboratory observations
The sampling lumen of the ca theter has an internal diameter of 0.024 inch and a lumen volum e of 0.1 5 ml (for comparison standard 3.5F and SF Argyle [Argyle umbilical artery ca theter, ALOE Medical Co., St. Louis] catheters are 0.16 ml and 0.20 rnl, respectively). The catheter when connected to a pressure transducer (Sta th am P35D series) has a frequency response flat to 9 Hertz at 37°C (comp ared to Argyle 3.SF = 9 Hz , SF = 8 Hz) as determined by a square wave pressure change.
PATIENTS We placed 35 catheters in 34 newborn infants (birth weights from 1.05 to 3.3 kg-mean 1.84), who required an indwelling arterial line for clinical management of cardiorespiratory distress. We obtained consent from the parents to use this catheter instead of the standard polyvinyl chloride umbilical artery catheter (Argyle, ALOE Medical Co.). METHODS We have described the technique used for catheterization of umbilical ar teries'; when the catheter is in place, we attach it to a pressure transducer to record and measure mean and phasic aortic pressures.' Before insertion we calibrated the oxi meter as described above and did not recalibrate while the catheter was in place in order to evaluate its stability. We took a total of 139 blood samples (1.0 ml) and noted the Sao, reading at the time of sampling. We measured Sao, in a cuvette oximeter (IL No . 182, Instrumentation Laboratory, Inc., Lexington, Mass.), corrected for carboxyhemoglobin concentration, and then compared it with the in vivo results. We measured Pao" Paeo" pHa, and hematocrit on each specimen, and noted the bilirubin concentration if it was measured within two hours. We also noted the mean and phasic blood pressure, and examined pressure wave form for presence of a dicrotic notch ( which we accepted as an adequate tracing without significan t damping).
RESULTS Accuracy. The Figure shows the regression analysis of the 139 paired measurements. Accuracy was not affected by presence of bilirubin to a level of 18 mgtdl, variation in hem atocrit from 19 to 66%, hemoglobin F from < 5 to > 90%, change in pHafrom 7.01 to 7.59, or Paco, from 17 to 81 torr. Continuous infusion of fluid through the sampling lumen or stopping the in fusion did not affect the Sao' value . There was minimal loss of accuracy with the time catheter in place, if the instrument was not recalibrated in vivo. The average time for a 1% loss of accuracy was S4 hours. Peformance and complications. The catheters were in
Tile Journal of Pediatrics December 1978
place from 50 minutes to 20 days (average 87 hours). We performed one or more exchange transfusions (maximum 6) through 13 catheters. In all 35 patients the oximeter system functioned well up to the time of removal of the catheter; no evidence of blood clot was found . In 24 of these , the catheter was removed when it was no longer needed for patient care ; in these, blood sampling and pressure measurements were also satisfactory up to the time of removal. In two others, we removed catheters at 52 and 160 hours, respectively, because of cyanosis or blanching of one or bo th feet; in both, the feet returned to normal appearance. In four patients, the catheter was removed between 55 and 180 hours after insertion because of difficulty in sampling blood. We found no clots and there were no subsequent signs of thrombosis in the infants. Two attempts to insert a catheter were unsuccessful ; efforts to pass a conventional catheter also failed . In one of these, multiple attempts to insert an umbilical catheter had been made before transfer to our hospital. W e determined later that there was a perforation of on umbilical artery; it was imp ossible to tell which catheter cau sed this.
DISCUSSION Fibero ptic catheter oximeters have been developed and used during cardiac ca th eteriza tion in adult patients."' " Catheters used by previous investigators have been either too large or too stiff to be passed through the umbilical artery of a newborn infant. The system described is the first to use polyurethane double-lumen tubing and plastic fiberoptics. The catheter is flexible and does not appear more prone to the usual complications of umbilical arterial catheterization than does the standard catheter. Blanching or cyanosis of a foot or difficulty in sampling are common problems of catheters left in place two to seven days" ';.;; we remove them when such an incident occurs . Recently Clark and lung; reported that perforation of the umbilical artery is a comm on complication of repeated unsuccessful attempts to catheterize the vessel. Because a tight suture may damage the fiberoptics, the catheter must be secured using a " tape bridge" to prevent the catheter slipping out of the descending aorta. The system allows early detection of changes in Sao " reflecting oxygen content mo re accurately than Pao , over the steep part of the oxygen dissociation curve . Because the instrument is calibrated before insertion of the catheter, it is available for use immediately during the resuscitation of a severely asphyxi ated infant. The system does not replace measurements of blood gas tensions and pH, but they are requ ired less frequently. Since we completed this study we have substantially reduced the number of blood samples removed and the
Brief clinical and laboratory observations
Volume 93 Number 6
need for transfusion. Low levels of Sao. indicate that changes in oxygen or ventilation therapy are necessary and we use the oximeter as a guide to effect these changes. After an adequate improvement in Sao., we check blood gas tensions and pH. We adjust inspired oxygen and ventilatory support to keep Sao. at approximately 90%, and when above 96% we measure Pao•. We have shown that if Sao. is 96% or less, the chance of the Pao. exceeding 100 torr is less than 5%." In the majority of infants who are sick enough to need an arterial catheter, the Sao. fluctuates between 85 and 95% when they are in a stable condition. We are grateful to the staff of the Intensive Care Nursery of H.C. Moffitt Hospital and the staff of the Clinical Physiology Services Laboratory of the Cardiovascular Research Institute for thier help in carrying out this study.
1019
2. Kitterman lA, Phibbs RH, and Tooley WH: Aortic blood pressure in normal newborn infants during the first 12hours of life, Pediatrics 44:959, 1969. 3. Polanyi ML, and Hihir RM: In vivo oximeter with fast dynamic response, Rev Sci Instrum 33:1050, 1962. 4. Ensen Y, Briscoe WA, Polanyi ML, and Cournand A: In vivo studies with an intravascular and intracardiac reflection oximeter, J Appl Physiol 17:552, 1962. 5. Symansky MR, and Fox HA: Umbilical vessel catheterization: Indications, management, and evaluation of the technique, J PEDIATR 80:820, 1972. 6. Cochran WD, Davis HT, and Smith CA: Advantages and complications of umbilical artery catheterization in the newborn, Pediatrics 42:769, 1968. 7. Clark 1M, and Jung AL: Umbilical artery catheterization by a cutdown procedure, Pediatrics 59:1036, 1977. 8. Wilkinson AR, Phibbs RH, and Gregory GA: In vivo oxygen dissociation curves in transfused and untransfused newborn infants, Clin Res 26:202A, 1978 (abstr),
REFERENCES l.
Kitterman JA, Phibbs RH, and Tooley WH: Catheterization of umbilical vessels in newborn infants, Pediatr Clin North Am 17:895, 1970.
Neonatal lead intoxication in a prenatally exposed infant Nalini Singh, M.B., B.S., Carol M. Donovan, M.A., R.P.T., and James B. Hanshaw, M.D., Worcester, Mass.
LEAD POISONING is a significant problem among infants and children in contact with lead-based paint. The transfer of lead across the human placenta and its potential threat to the conceptus have been recognized since the early part of this century. The effects oflead are dose related; the mother in this report had far less plumbism than those reports of many years ago, which were clearly' associated with severe fetal damage. It is known that lead can be transferred from the placenta to the fetus at different stages of gestation, I. , and lead has been found in the cord blood of newborn infants delivered in Boston- and New York City' in concentrations ranging from 10 to 30 ug/dl. The following report represents the first example of a liveborn infant with biochemical evidence of lead intoxication due to prenatal exposure to lead.
CASE REPORT A 3,200 gm white girl was born after 40 weeks gestation to a 20-year-old" mother who, with her husband, had removed paint From the Department of Pediatrics, University of Massachusetts Medical School.
0022-3476/781121019+03$00.30/0
from her house with a torch and sandpaper during the third trimester. Six weeks prior to the delivery the father presented in an emergencyroom after two episodes of epigastric pain. Lead lines on the lower gum were seen, and the blood revealed a lead level of 115 flg/dl, hemoglobin 12.5 gm/dl, hematocrit 35.8%, and basophilic stippling of 5.8% of the red blood cells. The urine revealed a coproporphyrin level of 332 flg/l with a deita aminolevulinic acid level of 57 mg/l. He was treated with calcium EDTA and was discharged with a blood level of 57 flg/dl. Subsequently the mother was evaluated for lead poisoning (Table I); it is evident that she had lead intoxication. Twenty days before delivery amniotic fluid obtained by amniocentesis, showed levels of lead and erythrocyte protoporphyrin less than 2flg/dl. Abdominal ultrasound performed the same day showed a biparietal diameter of 9.5 em, corresponding to a pregnancy of 37.5 weeks' gestation. The two siblings, 21h years and 20 months old, were also found to have lead intoxication. The infant was delivered by spontaneous vaginal delivery with Apgar scores of 9 at one minute and 10 at five minutes, respectively. The length was 49.5 em; head circumference 33 em. At birth, physical and neurologic examination, radiographs of the long bones, chest, and abdomen, and the electroencephalogram