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Cerebral resuscitation therapy in pediatric near-drowning
Volume 106 Number 4
Clinical and laboratory observations
6 15
Cerebral resuscitation therapy in pediatric near-drowning Timothy C. Frewen, M.D., Washington O. Sumabat, M.D., Victor K. Han, M.D., A. Loren Amacher, M.D., Rolando F. Del Maestro, M.D., and William J. Sibbald, M.D, London, Ontario, Canada
N EAR- OROWN ING is a major cause of neurologic morbidity and mortality in children. ~'~ Some investigators believe this morbidity and mortality is related to uncontrolled rises in intracranial pressure and concomitant derangement in cerebral blood flow and metabolism? Control of ICP and reduction of cerebral metabolic demands has therefore been the goal of therapeutic efforts to reduce the morbidity and mortality seen in near-drowning. However, because the therapies necessary to achieve these goals remain unproved and carry significant morbidity, many authors have thought that they should be reserved for severely comatose children.4 Our group investigated all severely comatose near-drowned children for ICP as defined by Orlowski score and, more recently, Glasgow coma Scale, and administered treatment according to a protocol including hyperventilation and dexamethasone in an effort to control ICP and maintain cerebral perfusion. Our results with this regimen are presented.
METHODS All near-drowning victims in the pediatric age group admitted to the Critical Care Unit at Victoria Hospital from July 1978 to December 1983 were given treatment according to a protocol defined below. The severity of the drowning episode was scored according to the system proposed by Orlowski, and after January 1981, modified GCS score 4 was also assigned to each patient on entry into therapy. The Orlowski system assigns one point for each of five unfavorable prognostic factors, including age <3 years, estimated maximum submersion time >5 minutes, no attempt at resuscitation for at least 10 minutes after the rescue, pupils fixed and dilated on From the Department of Pediatrics and Neurosurgery, Critical Care Trauma Unit, Victoria Hospital. Supported by John Labatt Ltd. and the Corporation of War Memorial Children's Hospital. Submitted for publication June 18, 1984; accepted Oct. 5, 1984. Reprint requests: Timothy C. Frewen, M.D., Department of Pediatrics, Victoria Hospital, 375 South St., London, Ontario, Canada N6A 4G5.
admission to the Emergency Department, and initial arterial blood gas pI-I <7.1. Thirteen children with a score of <2 constituted group 1, and were given fluids intravenously at three fourths the maintenance dose and observed. Seizures were treated with diazepam and a single dose of 7 mg/kg phenobarbital. Neurologic examination and blood gas values were followed serially, along with urine output. No invasive monitoring was used in this group. Fifteen children with an Orlowski score >~2 constituted group 2, and their intracranial, systemic arterial, and pulmonary artery pressures were monitored continuously; ICP monitoring was maintained for a minimum of 3 days in these patients or until the baseline ICP was <20 torr without hyperventilation therapy. We endeavored to keep the baseline ICP <20 torr and the cerebral perfusion pressure >50 torr. s Therapies used to achieve these goals
See related article, p. 603. CRT GCS 1CP
Cerebral resuscitation therapy GlasgowComa Scale lntracranial pressure
included controlled hyperventilation facilitated by neuromuscular blockade with pancuronium, by which the Paco2 was kept between 24 and 26 torr, and dexamethasone in a dose of 1 to 3 mg/kg/day for 48 hours, then tapered. Intermittent doses of mannitol and thiopental were also given in response to elevations in ICP. Rectal temperature was reduced to 31.5 ~ to 34 ~ C in three severely comatose children in whom ICP remained between 20 and 25 torr despite the above therapy for up to 1 hour, although crebral perfusion pressure remained >50 tort throughout. Patient outcome, based on a minimum follow-up period of 6 months, was categorized as (1) good recovery, with a normal findings on',neurologic examination; (2) impaired, with abnormal neurologic findings including mental retardation; and (3) death. All charts of severely comatose children were reviewed
6 16
Clinical and laboratory observations
The Journal of Pediatrics April 1985
Table. GCS and Orlowski score, and outcome in 12 patients
12 GCS Orlowski score Outcome
3 4 D
3 2 D
3 4 D
3 3 ND
3 4 ND
3 3 GR
15 0 GR
J5 0 GR
13 1 GR
9 1 GR
9 1 GR
9 0 GR
GR, good recovery;ND, neurologicdamage; D, dead.
for complications during therapy, and the cause of death was determined from the clinical record and autopsy report if available. Autopsy reports were also reviewed for the presence or absence of cerebral anoxia and brain herniation syndromes. Complications during therapy included ventriculitis, pneumonia, or significant bacteremia. Pneumonia was defined on the basis of roentgenographic findings consistent with this diagnosis in the presence of clear lungs on admission. Patient outcome in group 1 was compared by chi-square analysis with outcome in group 2. Correlation coefficient was computed to determine the relationship between Orlowski score and initial GCS for 12 patients seen after 1981. The Fisher exact test was used to determine significant differences between the groups in the incidence of pneumonia. RESULTS Outcome. All 13 patients in group 1 survived, with normal neurologic findings on discharge. Of the 15 children in group 2, two recovered, with normal neurologic findings on discharge; eight died; and five others survived, but four of these had severe neurologic damage and are totally dependent on others for activities of daily living, and the fifth child is mild to moderately retarded in terms of intellectual functioning. In all patients who died, ICP was <20 torr during CRT. The outcome in patients in group 1 was significantly different from that in group 2 (X2 = 21.03, P < 0.001). Twelve patients after 1981 were assigned both GCS and Orlowski scores (Table). A strong negative correlation (r = -0.92) existed between initial scores on both tests, so that an Orlowski score ~ 2 was associated with a low GCS score. Cause of death. A cerebral cause for death, defined as the presence of clinical brain death, coroborrated by either an isoelectric EEG or radionucleotide study6 showing no cerebral blood flow, was present in all eight children who died. Autopsies carried out in six of the eight confirmed this clinical impression, with brain histopathology demonstrating severe anoxia and edema. Only one patient had
uncal herniation in addition to severe anoxic change and edema. Complications. Complications during treatment includes Staphylococcus epidermidis ventriculitis in one patient and pneumonia in four others. The ventriculitis, probably attributable to the placement of an intraventricular cannula, was treated successfully by removal of the catheter and intravenous administration of antibiotics. Four patients in group 2 developed pneumonia, compared with none of 13 patients in group 1 (Fisher exact test, one tailed, P = 0.07). In addition, one had a positive blood culture for Staphylococcus aureus. Two of the four patients with pneumonia died, and in both, autopsies demonstrated changes consistent with brain death and bronchopneumonia, and one also had findings of adult respiratory distress syndrome. DISCUSSION Our experience suggests that OrIowski score and GCS score correlate well with each other and are useful guides to survival and possibly the need for cerebral resuscitation therapy. This finding is in agreement with those of other authors.4.7.8 In one patient an Orlowski score of 2 was assigned, but CRT was offered because of an inability to estimate in an unobserved submersion both the duration of the incident and the promptness of resuscitative effort. However, because the child arrived in the emergency room with asystole and fixed, dilated pupils, and had severe systemic acidosis, vigorous brain resuscitation therapy was offered. In the face of equal predictive ability of both GCS and Orlowski score, we favor GCS as a prognostic marker of outcome, because documentation of these events can be difficult and historical reporting unreliable. However, our results also illustrate the need for further prospective study of near-drowned children and the mechanism of their brain injury, because two patients survived with normal neurologic findings despite their initial Orlowski scores and the presence of severe coma. Their recovery was especially remarkable in that both of these patients had asystole with fixed, dilated pupils on arrival in the emergency room and were not immersed in severely cold water, and justifies an aggressive approaeb to resuscitation of all near-drowned victims.
Volume 106 Number 4
Our experience also indicates that C R T , at least as defined by our protocol, is not effective in completely eliminating morbidity or mortality in severely comatose patients, and may be itself associated with an increased incidence of pneumonia? Certainly, inasmuch as all children not severely comatose survived with normal neurologic findings without this therapy, a conservative approach to the care of these children is justified. 4 Whether C R T altered outcome in the 15 severely comatose drowned children cannot be answered by our study, because entry to the treatment protocol was not randomized. A multicenter, randomized trial of C R T would be a useful endeavor in view of the continued controversy regarding the efficacy of these therapies, the potential morbidity of the therapies themselves, and the severity and extent of the problems related to drowning. Finally, the outcome in our patients, like that reported by previous authors, demonstrates that control of intracranial pressure does not necessarily mean the absence of damage to the central nervous system?. 5.9 Only two of the 15 severely comatose children survived with normal neurologic findings, and five others survived with abnormal findings, four of these in a completely vegetative state a minimum of 6 months later. Although it is possible that ICP monitoring was not carried out long enough and that elevations in ICP occurred after monitoring was discontinued, this explanation appears unlikely inasmuch as therapy was withdrawn for 12 to 24 hours before disconnecting the ICP monitor. In addition, autopsy findings did not suggest brain herniation as a common or significant finding in children who died. The occurrence of brain death or severe brain injury
Clinical and laboratory observations
6 17
in drowning despite control of ICP suggests then the mechanism of these untoward events is not necessarily related to changes in pressure, but may be determined by the duration of the complete cerebral ischemic insult and subsequent changes in cerebral metabolism or cerebral blood flow after brain reperfusion. Further study of these variables may be important in sorting out these hypotheses. We thank Dr. George Wells of the Department of Statistics, University of Western Ontario; and Hazel Wilson for secretarial assistance.
REFERENCES 1. Petersen B: Morbidity of childhood near-drowning. Pediatrics 59:364, 1977. 2. Schuman SH, Rowe JR, Glazer HM, et al: The ieeburg phenomenon of near-drowning. Crit Care Med 4:127, 1976 3. Dean JM, McComb JG: lntracranial pressure monitoring in severe pediatric near-drowning. Neurosurgery 9:627, 1981. 4. Dean JM, Kaufman ND: Prognostic indicators in pediatric near-drowning: The Glasgow Coma Scale. Crit Care Med 9:536-539, 1981. 5. Nussbaum E, Galant S: Intracranial pressure monitoring as a guide to prognosis in the nearly drowned, severely comatose child. J PEDIATn 102:215, 1983. 6. Nagle CE: Use of immediate static scans in combination with radlonuclide cerebral angiography as a confirmatory test in the diagnosis of brain death. Clin Nucl Med 5:152, 1980. 7. Orlowski JP: Prognostic factors in pediatric cases of drowning and near-drowning. Crit Care Med 6:94, 1978. 8. Orlowski JP: Prognostic factors in pediatric cases of drowning and near-drowning. JACEP 8:176, 1979. 9. Oakes DD, Sherck JP, Maloney JR, Charters AC: Prognosis and management of victims of near-drowning. J Trauma 22:544, I982.
Tenosynovitis of the superior oblique muscle (Brown syndrome) associated with juvenile rheumatoid arthritis Chaim M. Roifman, M.D., Sasson Lavi, M.D., Anthony T. Moore, M.D., Donald J. Morin, M.D., Leonard D. Stein, M.D., and Erwin W. Gelfand, M.D. Toronto, Ontario, Canada
From the Divisions of Immunology and Rheumatology, and Ophthalmology, The Hospital for Sick Children. Submitted for publication July 19, 1984; accepted Sel~t. 7, 1984. Reprint requests: Erwin W. Gelfand, M.D., Research Institute, The Hospital for Sick Children, 555 University Ave., Toronto, Ontario, Canada M5G IX8.
BR O w N ~first described a syndrome characterized by diplopia during upward'~aze, particularly during adduction. Originally thought to represent congenital paralysis of the inferior oblique muscle, the syndrome actually reflects a mechanical obstruction to movement of the superior oblique tendon as it passes through the trochlea?
Clinical and laboratory observations
6 15
Cerebral resuscitation therapy in pediatric near-drowning Timothy C. Frewen, M.D., Washington O. Sumabat, M.D., Victor K. Han, M.D., A. Loren Amacher, M.D., Rolando F. Del Maestro, M.D., and William J. Sibbald, M.D, London, Ontario, Canada
N EAR- OROWN ING is a major cause of neurologic morbidity and mortality in children. ~'~ Some investigators believe this morbidity and mortality is related to uncontrolled rises in intracranial pressure and concomitant derangement in cerebral blood flow and metabolism? Control of ICP and reduction of cerebral metabolic demands has therefore been the goal of therapeutic efforts to reduce the morbidity and mortality seen in near-drowning. However, because the therapies necessary to achieve these goals remain unproved and carry significant morbidity, many authors have thought that they should be reserved for severely comatose children.4 Our group investigated all severely comatose near-drowned children for ICP as defined by Orlowski score and, more recently, Glasgow coma Scale, and administered treatment according to a protocol including hyperventilation and dexamethasone in an effort to control ICP and maintain cerebral perfusion. Our results with this regimen are presented.
METHODS All near-drowning victims in the pediatric age group admitted to the Critical Care Unit at Victoria Hospital from July 1978 to December 1983 were given treatment according to a protocol defined below. The severity of the drowning episode was scored according to the system proposed by Orlowski, and after January 1981, modified GCS score 4 was also assigned to each patient on entry into therapy. The Orlowski system assigns one point for each of five unfavorable prognostic factors, including age <3 years, estimated maximum submersion time >5 minutes, no attempt at resuscitation for at least 10 minutes after the rescue, pupils fixed and dilated on From the Department of Pediatrics and Neurosurgery, Critical Care Trauma Unit, Victoria Hospital. Supported by John Labatt Ltd. and the Corporation of War Memorial Children's Hospital. Submitted for publication June 18, 1984; accepted Oct. 5, 1984. Reprint requests: Timothy C. Frewen, M.D., Department of Pediatrics, Victoria Hospital, 375 South St., London, Ontario, Canada N6A 4G5.
admission to the Emergency Department, and initial arterial blood gas pI-I <7.1. Thirteen children with a score of <2 constituted group 1, and were given fluids intravenously at three fourths the maintenance dose and observed. Seizures were treated with diazepam and a single dose of 7 mg/kg phenobarbital. Neurologic examination and blood gas values were followed serially, along with urine output. No invasive monitoring was used in this group. Fifteen children with an Orlowski score >~2 constituted group 2, and their intracranial, systemic arterial, and pulmonary artery pressures were monitored continuously; ICP monitoring was maintained for a minimum of 3 days in these patients or until the baseline ICP was <20 torr without hyperventilation therapy. We endeavored to keep the baseline ICP <20 torr and the cerebral perfusion pressure >50 torr. s Therapies used to achieve these goals
See related article, p. 603. CRT GCS 1CP
Cerebral resuscitation therapy GlasgowComa Scale lntracranial pressure
included controlled hyperventilation facilitated by neuromuscular blockade with pancuronium, by which the Paco2 was kept between 24 and 26 torr, and dexamethasone in a dose of 1 to 3 mg/kg/day for 48 hours, then tapered. Intermittent doses of mannitol and thiopental were also given in response to elevations in ICP. Rectal temperature was reduced to 31.5 ~ to 34 ~ C in three severely comatose children in whom ICP remained between 20 and 25 torr despite the above therapy for up to 1 hour, although crebral perfusion pressure remained >50 tort throughout. Patient outcome, based on a minimum follow-up period of 6 months, was categorized as (1) good recovery, with a normal findings on',neurologic examination; (2) impaired, with abnormal neurologic findings including mental retardation; and (3) death. All charts of severely comatose children were reviewed
6 16
Clinical and laboratory observations
The Journal of Pediatrics April 1985
Table. GCS and Orlowski score, and outcome in 12 patients
12 GCS Orlowski score Outcome
3 4 D
3 2 D
3 4 D
3 3 ND
3 4 ND
3 3 GR
15 0 GR
J5 0 GR
13 1 GR
9 1 GR
9 1 GR
9 0 GR
GR, good recovery;ND, neurologicdamage; D, dead.
for complications during therapy, and the cause of death was determined from the clinical record and autopsy report if available. Autopsy reports were also reviewed for the presence or absence of cerebral anoxia and brain herniation syndromes. Complications during therapy included ventriculitis, pneumonia, or significant bacteremia. Pneumonia was defined on the basis of roentgenographic findings consistent with this diagnosis in the presence of clear lungs on admission. Patient outcome in group 1 was compared by chi-square analysis with outcome in group 2. Correlation coefficient was computed to determine the relationship between Orlowski score and initial GCS for 12 patients seen after 1981. The Fisher exact test was used to determine significant differences between the groups in the incidence of pneumonia. RESULTS Outcome. All 13 patients in group 1 survived, with normal neurologic findings on discharge. Of the 15 children in group 2, two recovered, with normal neurologic findings on discharge; eight died; and five others survived, but four of these had severe neurologic damage and are totally dependent on others for activities of daily living, and the fifth child is mild to moderately retarded in terms of intellectual functioning. In all patients who died, ICP was <20 torr during CRT. The outcome in patients in group 1 was significantly different from that in group 2 (X2 = 21.03, P < 0.001). Twelve patients after 1981 were assigned both GCS and Orlowski scores (Table). A strong negative correlation (r = -0.92) existed between initial scores on both tests, so that an Orlowski score ~ 2 was associated with a low GCS score. Cause of death. A cerebral cause for death, defined as the presence of clinical brain death, coroborrated by either an isoelectric EEG or radionucleotide study6 showing no cerebral blood flow, was present in all eight children who died. Autopsies carried out in six of the eight confirmed this clinical impression, with brain histopathology demonstrating severe anoxia and edema. Only one patient had
uncal herniation in addition to severe anoxic change and edema. Complications. Complications during treatment includes Staphylococcus epidermidis ventriculitis in one patient and pneumonia in four others. The ventriculitis, probably attributable to the placement of an intraventricular cannula, was treated successfully by removal of the catheter and intravenous administration of antibiotics. Four patients in group 2 developed pneumonia, compared with none of 13 patients in group 1 (Fisher exact test, one tailed, P = 0.07). In addition, one had a positive blood culture for Staphylococcus aureus. Two of the four patients with pneumonia died, and in both, autopsies demonstrated changes consistent with brain death and bronchopneumonia, and one also had findings of adult respiratory distress syndrome. DISCUSSION Our experience suggests that OrIowski score and GCS score correlate well with each other and are useful guides to survival and possibly the need for cerebral resuscitation therapy. This finding is in agreement with those of other authors.4.7.8 In one patient an Orlowski score of 2 was assigned, but CRT was offered because of an inability to estimate in an unobserved submersion both the duration of the incident and the promptness of resuscitative effort. However, because the child arrived in the emergency room with asystole and fixed, dilated pupils, and had severe systemic acidosis, vigorous brain resuscitation therapy was offered. In the face of equal predictive ability of both GCS and Orlowski score, we favor GCS as a prognostic marker of outcome, because documentation of these events can be difficult and historical reporting unreliable. However, our results also illustrate the need for further prospective study of near-drowned children and the mechanism of their brain injury, because two patients survived with normal neurologic findings despite their initial Orlowski scores and the presence of severe coma. Their recovery was especially remarkable in that both of these patients had asystole with fixed, dilated pupils on arrival in the emergency room and were not immersed in severely cold water, and justifies an aggressive approaeb to resuscitation of all near-drowned victims.
Volume 106 Number 4
Our experience also indicates that C R T , at least as defined by our protocol, is not effective in completely eliminating morbidity or mortality in severely comatose patients, and may be itself associated with an increased incidence of pneumonia? Certainly, inasmuch as all children not severely comatose survived with normal neurologic findings without this therapy, a conservative approach to the care of these children is justified. 4 Whether C R T altered outcome in the 15 severely comatose drowned children cannot be answered by our study, because entry to the treatment protocol was not randomized. A multicenter, randomized trial of C R T would be a useful endeavor in view of the continued controversy regarding the efficacy of these therapies, the potential morbidity of the therapies themselves, and the severity and extent of the problems related to drowning. Finally, the outcome in our patients, like that reported by previous authors, demonstrates that control of intracranial pressure does not necessarily mean the absence of damage to the central nervous system?. 5.9 Only two of the 15 severely comatose children survived with normal neurologic findings, and five others survived with abnormal findings, four of these in a completely vegetative state a minimum of 6 months later. Although it is possible that ICP monitoring was not carried out long enough and that elevations in ICP occurred after monitoring was discontinued, this explanation appears unlikely inasmuch as therapy was withdrawn for 12 to 24 hours before disconnecting the ICP monitor. In addition, autopsy findings did not suggest brain herniation as a common or significant finding in children who died. The occurrence of brain death or severe brain injury
Clinical and laboratory observations
6 17
in drowning despite control of ICP suggests then the mechanism of these untoward events is not necessarily related to changes in pressure, but may be determined by the duration of the complete cerebral ischemic insult and subsequent changes in cerebral metabolism or cerebral blood flow after brain reperfusion. Further study of these variables may be important in sorting out these hypotheses. We thank Dr. George Wells of the Department of Statistics, University of Western Ontario; and Hazel Wilson for secretarial assistance.
REFERENCES 1. Petersen B: Morbidity of childhood near-drowning. Pediatrics 59:364, 1977. 2. Schuman SH, Rowe JR, Glazer HM, et al: The ieeburg phenomenon of near-drowning. Crit Care Med 4:127, 1976 3. Dean JM, McComb JG: lntracranial pressure monitoring in severe pediatric near-drowning. Neurosurgery 9:627, 1981. 4. Dean JM, Kaufman ND: Prognostic indicators in pediatric near-drowning: The Glasgow Coma Scale. Crit Care Med 9:536-539, 1981. 5. Nussbaum E, Galant S: Intracranial pressure monitoring as a guide to prognosis in the nearly drowned, severely comatose child. J PEDIATn 102:215, 1983. 6. Nagle CE: Use of immediate static scans in combination with radlonuclide cerebral angiography as a confirmatory test in the diagnosis of brain death. Clin Nucl Med 5:152, 1980. 7. Orlowski JP: Prognostic factors in pediatric cases of drowning and near-drowning. Crit Care Med 6:94, 1978. 8. Orlowski JP: Prognostic factors in pediatric cases of drowning and near-drowning. JACEP 8:176, 1979. 9. Oakes DD, Sherck JP, Maloney JR, Charters AC: Prognosis and management of victims of near-drowning. J Trauma 22:544, I982.
Tenosynovitis of the superior oblique muscle (Brown syndrome) associated with juvenile rheumatoid arthritis Chaim M. Roifman, M.D., Sasson Lavi, M.D., Anthony T. Moore, M.D., Donald J. Morin, M.D., Leonard D. Stein, M.D., and Erwin W. Gelfand, M.D. Toronto, Ontario, Canada
From the Divisions of Immunology and Rheumatology, and Ophthalmology, The Hospital for Sick Children. Submitted for publication July 19, 1984; accepted Sel~t. 7, 1984. Reprint requests: Erwin W. Gelfand, M.D., Research Institute, The Hospital for Sick Children, 555 University Ave., Toronto, Ontario, Canada M5G IX8.
BR O w N ~first described a syndrome characterized by diplopia during upward'~aze, particularly during adduction. Originally thought to represent congenital paralysis of the inferior oblique muscle, the syndrome actually reflects a mechanical obstruction to movement of the superior oblique tendon as it passes through the trochlea?