Brief clinical and laboratory observations
VO/I/me 93 Number 6
1015
Brief clinical and laboratory observations Myoglobinuria renal failure in a newborn infant A. J. Hartel, M.D., J. Eichner, M.D.,· J. Haling, M.D., and M. L. Wilson, B.S., Seattle. Wash. and Great Falls. Mom.
IN A RECENT REVIEW of acute renal failure in the general population, acute tubular necrosis due to myoglobinuria accounted for 5% of all cases over a three-year period.' RhabdomyoIysis and subsequent myoglobinuria have not been reported in the neonate."! This report describes myoglobinuric renal failure appearing on the first day of life in an infant with anoxia and sepsis. CASE REPORT Patient CP, was born at term to a gravida 2, para O. abortus J white 25-year-old woman following a pregnancy uncomplicated by prenatal hemorrhage, infection, immunizations, or drugs. Labor was uneventful, but the infant was thickly covered with meconium at the time of delivery. Initial direct examination of the vocal cords revealed meconium staining. One- and fiveminute Apgar scores were 5 and 7, respectively. Although he was resuscitated immediately with thorough suctionlng and postural drainage, he gradually developed respiratory distress and required increasing concentrations of environmental oxygen, then continuous positive airway pressure via nasal prongs, and finally endotracheal intubation for persistent anoxia and acidosis. Despite vigorous therapy with sodium bicarbonate, arterial pH values remained in the 7.0 to 7.1 range and arterial oxygen tension remained in the 30 to 40 torr range. Because of persistent anoxia and acidosis, the child was transferred to the Montana Deaconess Medical Center in Great Falls at 12 hours of age. The infant was initially started on the IMV-Bird respirator with rapid improvement of his arterial oxygen tension. Initial chest radiograph revealed bilateral infiltrates. The infant had been oliguric since birth. Initial studies revealed that the blood urea nitrogen was 19 mg/dl and the creatinine concentration was 3.1 mg/dl. Urinalysis showed a 4+ orthotoluidene reaction for blood. but high-power microscopic examination of the spun sediment revealed only 0 to 3 red blood cells and numerous dark pigmented casts; white blood cells and bacteria were absent.
From the Department of Pediatrics, University of Washing/on School Of Medicine, and Department of Pediatrics, Montana Deaconess Medical Center. • Reprint address: Pediatric Department, Children's Orthopedic Hospital & Medical Cell Tel'. 4800 Sandpoint Way. N.E., POB#C5371. Seattle. IVA 98105.
0022-34761781121016+02$00.20/0 ID 1978 The C. V. Mosby Co.
Serum CPK activity was 2,500 IU (normal = 0 to 83 IU); isoenzyme fractionation was not available. Urine electrophoresis was positive for myoglobin. Therapy for the renal failure consisted solely of mannitol osmotic diuresis. Renal function improved, with creatinine concentration and CPK level on the fifth day being 1.0 mg/dl and 150 IV, respectively. During recovery he had a typical diuretic phase with transient polyuria and increased urine sodium concentration. Serum calcium values remained normal at all times.
See related article, p. 970 Abbreviation used CPK: creatinine phosphokinase Blood and endotracheal cultures grew out abundant Escherichia coli. He was treated intravenously with ampicillin and kanamycin at daily dosages of ISO and 15mg/kg, respectively. By the sixth day urine volume had become normal and urinalysis revealed no pigment. He remained afebrile and his chest radiograph cleared. Antibiotic therapy was discontinued on the tenth day. He was discharged on the twelth day.
DISCUSSION Recent reviews of acute renal failure in the newborn infant fail to cite examples of myoglobinuric renal failures." B However, since myoglobin screening is rarely included in the evaluation of neonatal renal failure, neonatal myoglobinuria may be more common than past experience would indicate. Most reviews of myoglobinuria include conditions which predispose to muscle breakdown, with eventual appearance of myoglobin pigment in the blood and then in the urine. Though the mechanism is still unclear, there is little doubt that this pigment is itself toxic to the kidneys, causing a spectrum of disease from minimal tubular damage to one of fulminant severe acute tubular necrosis. Rowland and Penrr' suggest that the final common pathway of myofibril dissolution is a block in glycogen
Vol. 93, No.6, pp. 1015-1016
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.
VO/I/me 93 Number 6
1015
Brief clinical and laboratory observations Myoglobinuria renal failure in a newborn infant A. J. Hartel, M.D., J. Eichner, M.D.,· J. Haling, M.D., and M. L. Wilson, B.S., Seattle. Wash. and Great Falls. Mom.
IN A RECENT REVIEW of acute renal failure in the general population, acute tubular necrosis due to myoglobinuria accounted for 5% of all cases over a three-year period.' RhabdomyoIysis and subsequent myoglobinuria have not been reported in the neonate."! This report describes myoglobinuric renal failure appearing on the first day of life in an infant with anoxia and sepsis. CASE REPORT Patient CP, was born at term to a gravida 2, para O. abortus J white 25-year-old woman following a pregnancy uncomplicated by prenatal hemorrhage, infection, immunizations, or drugs. Labor was uneventful, but the infant was thickly covered with meconium at the time of delivery. Initial direct examination of the vocal cords revealed meconium staining. One- and fiveminute Apgar scores were 5 and 7, respectively. Although he was resuscitated immediately with thorough suctionlng and postural drainage, he gradually developed respiratory distress and required increasing concentrations of environmental oxygen, then continuous positive airway pressure via nasal prongs, and finally endotracheal intubation for persistent anoxia and acidosis. Despite vigorous therapy with sodium bicarbonate, arterial pH values remained in the 7.0 to 7.1 range and arterial oxygen tension remained in the 30 to 40 torr range. Because of persistent anoxia and acidosis, the child was transferred to the Montana Deaconess Medical Center in Great Falls at 12 hours of age. The infant was initially started on the IMV-Bird respirator with rapid improvement of his arterial oxygen tension. Initial chest radiograph revealed bilateral infiltrates. The infant had been oliguric since birth. Initial studies revealed that the blood urea nitrogen was 19 mg/dl and the creatinine concentration was 3.1 mg/dl. Urinalysis showed a 4+ orthotoluidene reaction for blood. but high-power microscopic examination of the spun sediment revealed only 0 to 3 red blood cells and numerous dark pigmented casts; white blood cells and bacteria were absent.
From the Department of Pediatrics, University of Washing/on School Of Medicine, and Department of Pediatrics, Montana Deaconess Medical Center. • Reprint address: Pediatric Department, Children's Orthopedic Hospital & Medical Cell Tel'. 4800 Sandpoint Way. N.E., POB#C5371. Seattle. IVA 98105.
0022-34761781121016+02$00.20/0 ID 1978 The C. V. Mosby Co.
Serum CPK activity was 2,500 IU (normal = 0 to 83 IU); isoenzyme fractionation was not available. Urine electrophoresis was positive for myoglobin. Therapy for the renal failure consisted solely of mannitol osmotic diuresis. Renal function improved, with creatinine concentration and CPK level on the fifth day being 1.0 mg/dl and 150 IV, respectively. During recovery he had a typical diuretic phase with transient polyuria and increased urine sodium concentration. Serum calcium values remained normal at all times.
See related article, p. 970 Abbreviation used CPK: creatinine phosphokinase Blood and endotracheal cultures grew out abundant Escherichia coli. He was treated intravenously with ampicillin and kanamycin at daily dosages of ISO and 15mg/kg, respectively. By the sixth day urine volume had become normal and urinalysis revealed no pigment. He remained afebrile and his chest radiograph cleared. Antibiotic therapy was discontinued on the tenth day. He was discharged on the twelth day.
DISCUSSION Recent reviews of acute renal failure in the newborn infant fail to cite examples of myoglobinuric renal failures." B However, since myoglobin screening is rarely included in the evaluation of neonatal renal failure, neonatal myoglobinuria may be more common than past experience would indicate. Most reviews of myoglobinuria include conditions which predispose to muscle breakdown, with eventual appearance of myoglobin pigment in the blood and then in the urine. Though the mechanism is still unclear, there is little doubt that this pigment is itself toxic to the kidneys, causing a spectrum of disease from minimal tubular damage to one of fulminant severe acute tubular necrosis. Rowland and Penrr' suggest that the final common pathway of myofibril dissolution is a block in glycogen
Vol. 93, No.6, pp. 1015-1016
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.
