at home on the following day. Orthodontic devices included a band on each upper first
Parotitis During Orthodontic Treatment
Children have come to our office with an illness that we have nicknamed "orthodontic parotitis." It is an atypical parotitis associated with signs of irritation of the outlet of the parotid duct in the presence of a bracket projecting laterally toward the duct from a band around an upper molar tooth. Only five cases have appeared in six years of pediatric practice, and two of them have provided an opportunity for fuller observation, including virus isolation and serologic studies done by the Viral and Rickettsial Disease Laboratory of the California Department of Health, courtesy of Edwin H. Lennette, MD, PhD.
Report of Cases.\p=m-\Case1.\p=m-\A12-year-old boy with Down syndrome had received or-
thodontic treatment for five years. He had been inoculated with mumps vaccine 20 months before this episode and was exposed to mumps three weeks before. He suddenly developed swelling below the left ear and worsening of his chronic rhinitis. Examination on the day of onset showed typical tender swelling of the left parotid gland, with overlying edema of subcutane¬ ous tissue and enlargement of nearby lymph nodes. There were arches on the up¬ per teeth attached to metal brackets on bands around the upper first molars. Where the bracket made contact with the buccal mucosa on the left side, the mem¬ brane was very erythematous and covered with white material that hid the opening of the parotid duct. The right duct outlet and surrounding mucosa were reddened also. The child's general health seemed good, and he had no fever. Treatment con¬ sisted of partial rest and removal of the bands four days after onset. Parotid swell¬ ing subsided in less than ten days, buccal irritation improved, but some mucosal ery¬ thema could be seen a month later. At the beginning of the illness, two culture speci¬ mens were obtained from the white-coated area while attempting to express fluid from the duct. Cultures yielded strepto¬ cocci but no Candida. Herpes simplex virus was recovered in cell cultures of hu¬ man fetal lung (HFL) cells; mumps virus was not found. Acute and convalescent sera showed a stationary complement-fix¬ ing (CF) antibody titer of 1:64 to herpes simplex virus but no significant CF anti¬ body (< 1:8) to mumps virus. Case 2.-A 12-year-old girl had had mumps four years earlier, diagnosed by a pediatrician. Three months before this attack she began treatment to improve alignment of her crowded teeth. The pres¬ ent illness began abruptly with swelling of the left parotid gland. She was examined
molar tooth, from which a bracket pro¬ jected laterally toward Stensen duct. The left parotid gland was swollen and tender, the overlying subcutaneous tissue was puffy and soft, and several neighboring lymph nodes were enlarged. The opening of the left parotid duct was red and swol¬ len. The tonsils were also reddened, but
there was no fever. She was treated with rest and soft diet. On the third day, she lost hearing in her left ear. Blood obtained at this time showed no CF antibody to mumps virus. Clear fluid was expressed from Stensen duct, and a culture taken by swab yielded Haemophilus (species unde¬ termined), while a swab of the surface of the tonsils yielded mumps virus in HFL cell cultures. Further treatment consisted of repositioning of the bands on the fourth day and administering tetracycline. Swell¬ ing of the gland, surrounding tissues, and duct outlet continued to increase, and there was slight swelling of the right parotid gland. On the fourth day, there was a sud¬ den return of hearing. After the fifth day, all signs of illness subsided slowly. On the 21st day she had no residua except swell¬ ing of the outlet of the left parotid duct. At this time the titer of mumps CF antibody was 1:64, confirming the diagnosis of mumps. The atypical features were the well-documented previous attack and the persistent swelling of the opening of Sten¬ sen duct.
Comment.—These two presenta¬ tions suggest that orthodontic appli¬ ances can precipitate parotitis and that the explanation may be more complex than we have supposed. The acute episodes in children resemble the chronic or recurrent disease of adults described by Furstenberg and Blatt.1 They suggest that adjusting and sucking motions damage the duct outlet, while our suspicion was di¬ rected more toward irritation by the bracket or the arch wire protruding posteriorly from it. However, when only a few cases are available, no con¬ clusions can be drawn, and any causal connection between the inflammation of the parotid gland and the presence of bands and arches in the mouth is conjectural. Have other pediatricians seen similar cases? GRANGE S. COFFIN, MD Department of Pediatrics University of California School of Medicine 2915 Telegraph Ave Berkeley, CA 94705
1. Furstenberg AC, Blatt IM: Intermittent parotid swelling due to ill-fitting dentures. Laryngoscope 68:1165-1181,1958.
Complications of Ventilator Therapy in Respiratory Distress Syndrome Sir.\p=m-\Arecent article by Kirket al, which appeared in the October issue of the Journal (128:496, 1974), reports a high incidence of pulmonary air leaks in patients with respiratory distress syndrome who were treated with assisted ventilation by means of a volume-controlled ventilator. The figures included in the article consisted of reproductions of the chest roentgenograms of several patients. The endotracheal tubes in some of them seem to be at or beyond the carina. If an endotracheal tube inadvertently slips down into one bronchus, then the hazard exists of introducing the entire volume of air into one lung when using a volume\x=req-\ cycled ventilator and of producing atelectasis on the opposite side. This could potentially produce a pulmonary air leak that may be prevented by keeping the tip of the endotracheal tube at least 2 cm above the carina. RICHARD E. KRAVATH, MD Department of Pediatrics Montefiore Hospital and Medical Center 111 E 210th St Bronx, NY 10467
patrick
Epidemiological Aspects of Neonatal Necrotizing Enterocolitis Sir.\p=m-\Iwas
little disturbed by a interesting article by Virnig and Reynolds, which appeared in the August issue of the Journal (128:186, 1974). In "Materials and Methods," the authors stated that "Blood specimens for culture were oba
sentence in the
tained from either umbilical vessel catheters immediately after insertion, or from peripheral vessels." With this method, "Blood cultures of samples from nine of the 20 babies in whom they were performed were positive. ." As the umbilicus is heavily contaminated and not easily sterilized, umbilical catheters are regularly contaminated during their insertion. Krauss et al1 and Balactas et al2 reported a high incidence of contaminated umbilical catheters (57% and 52%, respectively). In a recent study,3 we found that 47 out of 75 catheters (63%) inserted aseptically following a very careful cleansing procedure were contaminated. It is
Downloaded From: http://archpedi.jamanetwork.com/ by a University of Michigan User on 06/16/2015
.
.
surprising, therefore, that blood cultures obtained via umbilical catheters are positive even in the absence of septicemia. Lipsitz and Cornet4 re¬ ported that 45% of the blood samples drawn through the umbilical cathe¬ ters were contaminated. Similarly, high rates (47%) were also obtained by Nelson and associates.5 In our own study,3 while blood cultures taken from 74 infants prior to catheter¬ ization from a peripheral vein were all negative, bacteria were isolated from 31 out of 69 (45%) blood speci¬ mens drawn via the umbilical cathe¬ ter immediately after the insertion. I, therefore, strongly believe that blood cultures obtained in this way are of no value for establishing a diagnosis of septicemia. Thus, the nine positive blood cultures reported by Virnig and Reynolds may be falsely high. DIMITRIS ANAGNOSTAKIS, MD First Department of Pediatrics Athens University "St. Sophie's" Children's Hospital Athens, 608, Greece not
1. Krauss KN, Albert RF, Kannan MM: Contamination of umbilical catheters in the newborn infant. J Pediatr 77:965-969,
1970. 2. Balactas RC, Bell CE, Edwards LD, et al: Risk of local and systemic infection associated with umbilical vein catheterization: A prospective study in 86 newborn patients. Pediatrics 48:359-367, 1971. 3. Anagnostakis D, Camba A, Arseni A, et al: Risk of infection associated with umbilical catheterization: A prospective study. 4th European Congress of Perinatal Medicine, abstract IV-2/25. Prague, Aug 28-31, 1974. 4. Lipsitz PJ, Cornet JM: Blood cultures from the umbilical vein in the newborn infant. Pediatrics 26:657-660, 1960. 5. Nelson JD, Richardson J, Sheldon S: The significance of bacteremia with exchange transfusion. J Pediatr 66:291-299, 1965.
Neonatal Hematuria
Sir.\p=m-\Iam writing in reference to the article by Emanuel and Aronson, which appeared in the August issue of the Journal (128:204,1974). Six of the seven patients referred to with hematuria and renal vein thrombosis were treated with nephrectomy. The series includes a review from 1950 to 1967 and does not conform to the present philosophy of care of patients with renal vein thrombosis. Subsequent to this time period, a nonsurgical approach to renal vein thrombosis has been followed\p=m-\theresults being as satisfactory as those reported with
nephrectomy in terms of survival and
satisfactory
more
in terms of renal
function.1
Controversy may still exist regarding the treatment of patients with bilateral renal vein thrombosis; however, it is my impression that these patients, too, do better without the benefit of surgical intervention. A. BARRY BELMAN, MD Department of Urology Children's Memorial Hospital 2300 Children's Plaza Chicago, IL 60614
1. Belman et al:
AB, Susmano DF, Burden JJ,
Nonoperative treatment of unilateral
renal vein thrombosis in the newborn. JAMA 211:1165-1168, 1970.
Riboflavin and Creatinine Excretion in Children Treated With Anticonvulsant Drugs
Urinary
Sir.\p=m-\Hillet al in their article on infants exposed in utero to anticonvulsant drugs, which appeared in the May issue of the Journal (127:645, 1974), mentioned folic acid deficiency states and altered calcium metabolism occurring among subjects who have been taking diphenylhydantoin. Other deficiency states may also occur. We conducted a pilot study of riboflavin status of eight children under 10 years of age who were being followed up at the Seizure Clinic, Childrens Hospital of Los Angeles, while being given anticonvulsant
drugs (diphenylhydantoin [Dilantin] sodium plus another drug). We found, using the method of Slater and Morell,1 that they had significantly lower 24-hour urinary riboflavin ex-
cretion (0.28 mg \m=+-\0.17;range, 0.056 to 0.45 mg), than 28 normal children in the same age range (0.55 mg \m=+-\0.28; range, 0.13 to 1.37 mg) (J. S. Lewis, unpublished data). A urinary excretion of less than 20% of riboflavin intake is an indication that intake was insufficient.2 Diphenylhydantoin-treated children (No. 5) with a mean intake of 1.05 mg of ri¬ boflavin had a mean excretion of 14% ± 9% of intake, while normals (No. 6) with a mean intake of 1.39 mg had a mean excretion of 39% ± 13%. Horwitt et al state that ribofla¬ vin excretions of less than 0.1 mg per day are indicative of insufficient in¬ take in adults.1 Two drug-treated children but none of the 28 normals =
=
Downloaded From: http://archpedi.jamanetwork.com/ by a University of Michigan User on 06/16/2015
had riboflavin excretions below 0.1 mg. Yunis et al described a case of erythroid aplasia due to diphenylhydantoin drug therapy that was reversed by concomitant administration of ri¬ boflavin.4 We also found that four of the eight treated children had extremely low creatinine excretions, less than 50% of published norms for their height5 and lower than any of the cre¬ atinine height indexes found for 28 normal children (J. S. Lewis, unpub¬ lished data), although their relative weight was normal. Creatinine excre¬ tion is related to muscle mass. These data suggest that these children might have less muscle mass, al¬ though they may mean only that the children's creatinine excretions were low that particular day." We are continuing this study of ri¬ boflavin and creatinine excretion of diphenylhydantoin-treated children to see if a larger sample will substan¬ tiate these findings. This investigation was supported in part by Maternal Child Health grant 45-2220, project
914.
JANE S. LEWIS, DPH Home Economics Department California State University at Los Angeles Los Angeles, CA 90032
MARION T. BAER, MSNS University Affiliated Training
Program Hospital of
Childrens
MARGARET A. Tualatin, Ore
Los
Angeles
LAUFER, MA
1. Slater EC, Morell DB: A modification of the fluorometric method of determining riboflavin in biological materials. Biochem J 40:644-652, 1946. 2. Pearson WN: Biochemical appraisal of nutritional status in man. Am J Clin Nutr 11:462-476, 1962. 3. Horwitt MK, Harvey CC, Hills OW, et al: Correlation of urinary excretion of riboflavin with dietary intake and symptoms of ariboflavinosis. J Nutr 41:247-264,1950. 4. Yunis AA, Arimura GK, Lutcher CL, et al: Biochemical lesion in dilantin-induced erythroid aplasia, abstracted. J Clin Invest 44:1114-1115, 1965. 5. Viteri FD, Alvarado J: The creatinine height index: Its use in the estimation of the degree of protein depletion and repletion in protein calorie malnourished children. Pediatrics 46:696-705, 1970. 6. Ritchey SJ, Derise NL, Abernathy RP, et al: Variability of creatinine excretion in preadolescent girls consuming a wide range of dietary nitrogen. Am J Clin Nutr 26:690-695, 1973.
Parotitis During Orthodontic Treatment
Children have come to our office with an illness that we have nicknamed "orthodontic parotitis." It is an atypical parotitis associated with signs of irritation of the outlet of the parotid duct in the presence of a bracket projecting laterally toward the duct from a band around an upper molar tooth. Only five cases have appeared in six years of pediatric practice, and two of them have provided an opportunity for fuller observation, including virus isolation and serologic studies done by the Viral and Rickettsial Disease Laboratory of the California Department of Health, courtesy of Edwin H. Lennette, MD, PhD.
Report of Cases.\p=m-\Case1.\p=m-\A12-year-old boy with Down syndrome had received or-
thodontic treatment for five years. He had been inoculated with mumps vaccine 20 months before this episode and was exposed to mumps three weeks before. He suddenly developed swelling below the left ear and worsening of his chronic rhinitis. Examination on the day of onset showed typical tender swelling of the left parotid gland, with overlying edema of subcutane¬ ous tissue and enlargement of nearby lymph nodes. There were arches on the up¬ per teeth attached to metal brackets on bands around the upper first molars. Where the bracket made contact with the buccal mucosa on the left side, the mem¬ brane was very erythematous and covered with white material that hid the opening of the parotid duct. The right duct outlet and surrounding mucosa were reddened also. The child's general health seemed good, and he had no fever. Treatment con¬ sisted of partial rest and removal of the bands four days after onset. Parotid swell¬ ing subsided in less than ten days, buccal irritation improved, but some mucosal ery¬ thema could be seen a month later. At the beginning of the illness, two culture speci¬ mens were obtained from the white-coated area while attempting to express fluid from the duct. Cultures yielded strepto¬ cocci but no Candida. Herpes simplex virus was recovered in cell cultures of hu¬ man fetal lung (HFL) cells; mumps virus was not found. Acute and convalescent sera showed a stationary complement-fix¬ ing (CF) antibody titer of 1:64 to herpes simplex virus but no significant CF anti¬ body (< 1:8) to mumps virus. Case 2.-A 12-year-old girl had had mumps four years earlier, diagnosed by a pediatrician. Three months before this attack she began treatment to improve alignment of her crowded teeth. The pres¬ ent illness began abruptly with swelling of the left parotid gland. She was examined
molar tooth, from which a bracket pro¬ jected laterally toward Stensen duct. The left parotid gland was swollen and tender, the overlying subcutaneous tissue was puffy and soft, and several neighboring lymph nodes were enlarged. The opening of the left parotid duct was red and swol¬ len. The tonsils were also reddened, but
there was no fever. She was treated with rest and soft diet. On the third day, she lost hearing in her left ear. Blood obtained at this time showed no CF antibody to mumps virus. Clear fluid was expressed from Stensen duct, and a culture taken by swab yielded Haemophilus (species unde¬ termined), while a swab of the surface of the tonsils yielded mumps virus in HFL cell cultures. Further treatment consisted of repositioning of the bands on the fourth day and administering tetracycline. Swell¬ ing of the gland, surrounding tissues, and duct outlet continued to increase, and there was slight swelling of the right parotid gland. On the fourth day, there was a sud¬ den return of hearing. After the fifth day, all signs of illness subsided slowly. On the 21st day she had no residua except swell¬ ing of the outlet of the left parotid duct. At this time the titer of mumps CF antibody was 1:64, confirming the diagnosis of mumps. The atypical features were the well-documented previous attack and the persistent swelling of the opening of Sten¬ sen duct.
Comment.—These two presenta¬ tions suggest that orthodontic appli¬ ances can precipitate parotitis and that the explanation may be more complex than we have supposed. The acute episodes in children resemble the chronic or recurrent disease of adults described by Furstenberg and Blatt.1 They suggest that adjusting and sucking motions damage the duct outlet, while our suspicion was di¬ rected more toward irritation by the bracket or the arch wire protruding posteriorly from it. However, when only a few cases are available, no con¬ clusions can be drawn, and any causal connection between the inflammation of the parotid gland and the presence of bands and arches in the mouth is conjectural. Have other pediatricians seen similar cases? GRANGE S. COFFIN, MD Department of Pediatrics University of California School of Medicine 2915 Telegraph Ave Berkeley, CA 94705
1. Furstenberg AC, Blatt IM: Intermittent parotid swelling due to ill-fitting dentures. Laryngoscope 68:1165-1181,1958.
Complications of Ventilator Therapy in Respiratory Distress Syndrome Sir.\p=m-\Arecent article by Kirket al, which appeared in the October issue of the Journal (128:496, 1974), reports a high incidence of pulmonary air leaks in patients with respiratory distress syndrome who were treated with assisted ventilation by means of a volume-controlled ventilator. The figures included in the article consisted of reproductions of the chest roentgenograms of several patients. The endotracheal tubes in some of them seem to be at or beyond the carina. If an endotracheal tube inadvertently slips down into one bronchus, then the hazard exists of introducing the entire volume of air into one lung when using a volume\x=req-\ cycled ventilator and of producing atelectasis on the opposite side. This could potentially produce a pulmonary air leak that may be prevented by keeping the tip of the endotracheal tube at least 2 cm above the carina. RICHARD E. KRAVATH, MD Department of Pediatrics Montefiore Hospital and Medical Center 111 E 210th St Bronx, NY 10467
patrick
Epidemiological Aspects of Neonatal Necrotizing Enterocolitis Sir.\p=m-\Iwas
little disturbed by a interesting article by Virnig and Reynolds, which appeared in the August issue of the Journal (128:186, 1974). In "Materials and Methods," the authors stated that "Blood specimens for culture were oba
sentence in the
tained from either umbilical vessel catheters immediately after insertion, or from peripheral vessels." With this method, "Blood cultures of samples from nine of the 20 babies in whom they were performed were positive. ." As the umbilicus is heavily contaminated and not easily sterilized, umbilical catheters are regularly contaminated during their insertion. Krauss et al1 and Balactas et al2 reported a high incidence of contaminated umbilical catheters (57% and 52%, respectively). In a recent study,3 we found that 47 out of 75 catheters (63%) inserted aseptically following a very careful cleansing procedure were contaminated. It is
Downloaded From: http://archpedi.jamanetwork.com/ by a University of Michigan User on 06/16/2015
.
.
surprising, therefore, that blood cultures obtained via umbilical catheters are positive even in the absence of septicemia. Lipsitz and Cornet4 re¬ ported that 45% of the blood samples drawn through the umbilical cathe¬ ters were contaminated. Similarly, high rates (47%) were also obtained by Nelson and associates.5 In our own study,3 while blood cultures taken from 74 infants prior to catheter¬ ization from a peripheral vein were all negative, bacteria were isolated from 31 out of 69 (45%) blood speci¬ mens drawn via the umbilical cathe¬ ter immediately after the insertion. I, therefore, strongly believe that blood cultures obtained in this way are of no value for establishing a diagnosis of septicemia. Thus, the nine positive blood cultures reported by Virnig and Reynolds may be falsely high. DIMITRIS ANAGNOSTAKIS, MD First Department of Pediatrics Athens University "St. Sophie's" Children's Hospital Athens, 608, Greece not
1. Krauss KN, Albert RF, Kannan MM: Contamination of umbilical catheters in the newborn infant. J Pediatr 77:965-969,
1970. 2. Balactas RC, Bell CE, Edwards LD, et al: Risk of local and systemic infection associated with umbilical vein catheterization: A prospective study in 86 newborn patients. Pediatrics 48:359-367, 1971. 3. Anagnostakis D, Camba A, Arseni A, et al: Risk of infection associated with umbilical catheterization: A prospective study. 4th European Congress of Perinatal Medicine, abstract IV-2/25. Prague, Aug 28-31, 1974. 4. Lipsitz PJ, Cornet JM: Blood cultures from the umbilical vein in the newborn infant. Pediatrics 26:657-660, 1960. 5. Nelson JD, Richardson J, Sheldon S: The significance of bacteremia with exchange transfusion. J Pediatr 66:291-299, 1965.
Neonatal Hematuria
Sir.\p=m-\Iam writing in reference to the article by Emanuel and Aronson, which appeared in the August issue of the Journal (128:204,1974). Six of the seven patients referred to with hematuria and renal vein thrombosis were treated with nephrectomy. The series includes a review from 1950 to 1967 and does not conform to the present philosophy of care of patients with renal vein thrombosis. Subsequent to this time period, a nonsurgical approach to renal vein thrombosis has been followed\p=m-\theresults being as satisfactory as those reported with
nephrectomy in terms of survival and
satisfactory
more
in terms of renal
function.1
Controversy may still exist regarding the treatment of patients with bilateral renal vein thrombosis; however, it is my impression that these patients, too, do better without the benefit of surgical intervention. A. BARRY BELMAN, MD Department of Urology Children's Memorial Hospital 2300 Children's Plaza Chicago, IL 60614
1. Belman et al:
AB, Susmano DF, Burden JJ,
Nonoperative treatment of unilateral
renal vein thrombosis in the newborn. JAMA 211:1165-1168, 1970.
Riboflavin and Creatinine Excretion in Children Treated With Anticonvulsant Drugs
Urinary
Sir.\p=m-\Hillet al in their article on infants exposed in utero to anticonvulsant drugs, which appeared in the May issue of the Journal (127:645, 1974), mentioned folic acid deficiency states and altered calcium metabolism occurring among subjects who have been taking diphenylhydantoin. Other deficiency states may also occur. We conducted a pilot study of riboflavin status of eight children under 10 years of age who were being followed up at the Seizure Clinic, Childrens Hospital of Los Angeles, while being given anticonvulsant
drugs (diphenylhydantoin [Dilantin] sodium plus another drug). We found, using the method of Slater and Morell,1 that they had significantly lower 24-hour urinary riboflavin ex-
cretion (0.28 mg \m=+-\0.17;range, 0.056 to 0.45 mg), than 28 normal children in the same age range (0.55 mg \m=+-\0.28; range, 0.13 to 1.37 mg) (J. S. Lewis, unpublished data). A urinary excretion of less than 20% of riboflavin intake is an indication that intake was insufficient.2 Diphenylhydantoin-treated children (No. 5) with a mean intake of 1.05 mg of ri¬ boflavin had a mean excretion of 14% ± 9% of intake, while normals (No. 6) with a mean intake of 1.39 mg had a mean excretion of 39% ± 13%. Horwitt et al state that ribofla¬ vin excretions of less than 0.1 mg per day are indicative of insufficient in¬ take in adults.1 Two drug-treated children but none of the 28 normals =
=
Downloaded From: http://archpedi.jamanetwork.com/ by a University of Michigan User on 06/16/2015
had riboflavin excretions below 0.1 mg. Yunis et al described a case of erythroid aplasia due to diphenylhydantoin drug therapy that was reversed by concomitant administration of ri¬ boflavin.4 We also found that four of the eight treated children had extremely low creatinine excretions, less than 50% of published norms for their height5 and lower than any of the cre¬ atinine height indexes found for 28 normal children (J. S. Lewis, unpub¬ lished data), although their relative weight was normal. Creatinine excre¬ tion is related to muscle mass. These data suggest that these children might have less muscle mass, al¬ though they may mean only that the children's creatinine excretions were low that particular day." We are continuing this study of ri¬ boflavin and creatinine excretion of diphenylhydantoin-treated children to see if a larger sample will substan¬ tiate these findings. This investigation was supported in part by Maternal Child Health grant 45-2220, project
914.
JANE S. LEWIS, DPH Home Economics Department California State University at Los Angeles Los Angeles, CA 90032
MARION T. BAER, MSNS University Affiliated Training
Program Hospital of
Childrens
MARGARET A. Tualatin, Ore
Los
Angeles
LAUFER, MA
1. Slater EC, Morell DB: A modification of the fluorometric method of determining riboflavin in biological materials. Biochem J 40:644-652, 1946. 2. Pearson WN: Biochemical appraisal of nutritional status in man. Am J Clin Nutr 11:462-476, 1962. 3. Horwitt MK, Harvey CC, Hills OW, et al: Correlation of urinary excretion of riboflavin with dietary intake and symptoms of ariboflavinosis. J Nutr 41:247-264,1950. 4. Yunis AA, Arimura GK, Lutcher CL, et al: Biochemical lesion in dilantin-induced erythroid aplasia, abstracted. J Clin Invest 44:1114-1115, 1965. 5. Viteri FD, Alvarado J: The creatinine height index: Its use in the estimation of the degree of protein depletion and repletion in protein calorie malnourished children. Pediatrics 46:696-705, 1970. 6. Ritchey SJ, Derise NL, Abernathy RP, et al: Variability of creatinine excretion in preadolescent girls consuming a wide range of dietary nitrogen. Am J Clin Nutr 26:690-695, 1973.
