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IRRITABLE HIPS: RELATIONSHIP WITH TRAUMA
220 IRRITABLE HIPS: RELATIONSHIP WITH TRAUMA
Six,-The irritable hip syndrome is common in childhood, and in Glamorgan accounts for 2 -5% of the admissions to the paediatric ward servicing the accident and emergency department. South
Surprisingly little is understood about the cause of this syndrome. Hardinge’s 19701 review revealed no connection with infections or allergic disease but he did note a "loose similarity" between the monthly incidence of tibial fractures and irritable hips, and trauma is still often referred to as a possible cause. Since the incidence of children’s trauma varies significantly with the seasons, it should follow, if there is a causal relation between and irritable hips, that the seasonal incidence of irritable hips should show a similar pattern. The only paper on this seasonal variation involved small numbers, and was from Australia.2 We have looked at this question by retrospectively identifying cases of the irritable hip syndrome admitted to the children’s ward servicing the accident and emergency department. As a comparative measure of the incidence of trauma in the childhood population, we also identified children with head injuries or fractures admitted to the same ward over the same period. Since this accident and emergency department was the only one covering that district, this was an accurate reflection of the children’s injuries in that period. The total number of cases of irritable hips was still small when analysed on a monthly basis, so we identified other cases from the whole of Wales over the same period, using Hospital Activity Analysis data, with the diagnostic code 7873 (ICD 1977-78) or 7194 (ICD 1979-83)-transient synovitis of the hip, irritable hip, or3 "observation hip". The results were analysed by the Hewitt test,3 and by a partitioned chi-square analysis. Over the six years studied, there were 2541 admissions with head injuries, 1208 admissions with fractures, and 238 admissions with irritable hips to the children’s ward. The admissions for head injuries and fractures demonstrated a clear seasonal pattern. The admissions for irritable hip peaked around September, but the pattern was not sufficiently clear cut to reach significance (rank trauma
52, p>0 05). Hospital Activity Analysis identified a further 1340 children with the appropriate diagnostic coding. Again there was no significant seasonal variation (peak June, rank sum=49, p>0’05) (figure). A chi-square statistic (55 degrees of freedom) was calculated to express clustering of cases by month over and above differences sum =
between years and differences between months of the year. This did not reach significance. All children with irritable hips may not be admitted to hospital and HAA data may not be complete; also, some children with irritable hips will subsequently present with Perthes’ disease or coxa magna.3-5 Nevertheless, we feel that the data obtained probably do accurately reflect the pattern of the disease in the community. Whereas a clear seasonal pattern was demonstrated for children’s injuries, this was not so for irritable hips. It is apparent, therefore, that we should discount trauma as a possible aetiology, and concentrate our search on other factors. Illingworth’s study6 demonstrated a high incidence of recurrent symptoms, which suggests that individual constitutional factors may have an important role, and it may well be that it would be profitable to study these individuals more closely.
C. P. Q. SAINSBURY R. G. NEWCOMBE A. ESSEX-CATER
Department of Child Health, University of Wales College of Medicine, Cardiff CF4 4XN
1.
Hardinge K. The etiology of transient synovitis in childhood. J Bone Joint Surg 1970;
52: 100-07. 2. Sharwood F. The irritable hip syndrome
in
children.
Long term follow up. Acta Orthop
Scand 1981; 52: 633-38. 3. Hewitt D, Milner J, Csima A, Pakula A. On Edwards’ criterion of seasonality and a nonparametric alternative. Br J Prev Soc Med 1971; 25: 174-76. 4. Jacobs BW. Synovitis of the hip in children and its significance. Paediatrics 1971; 47: 558-66. 5. Adams JA. Transient synovitis of the hip joint in children. J Bone Joint Surg 1963; 45B: 471-76. 6. Illingworth CM Recurrences oftransient synovitis ofthe hip. Arch Dis Child 1983; 58: 620-23.
CEREBRAL OEDEMA IN DIABETIC KETOACIDOSIS: DO WE USE TOO MUCH INSULIN?
SIR,-Subclinical brain swelling during treatment of diabetic ketoacidosis is quite a common finding in children but clinically apparent cerebral oedema is exceptional in adults. However, rapidly fatal cerebral oedema may occur in adult diabetics despite hypernatraemia, low insulin infusion rates, slow fluid administration, and no bicarbonate infusion. A 20-year-old woman was admitted with diabetic ketoacidosis and treatment began at 1130 hours. By 1620 only 1200 ml 2-5% dextrose, 2 g potassium chloride, and 24 units of ordinary insulin had been given, by constant infusion. The patient remained fully conscious and did not complain of a headache. However, at 1620 hours she collapsed with respiratory arrest, a brain scan revealing narrowing of the ventricles compatible with acute brain oedema. 20 min later clinical examination was compatible with brain death which was confirmed by electroencephalography. The CSF was normal except for a slightly raised protein (70 mg/dl). This patient died suddenly with brain oedema after 5 h of treatment for diabetic ketoacidosis. Except for a fall in blood glucose, none of the aetiological factors discussed by Krane and colleagues was present. Moreover, the corrected2 plasma sodium remained high (table). LABORATORY DATA BEFORE AND AFTER INSULIN THERAPY
*Derived from Katz’ formula.2
This complication, though rare, is unpredictable and nearly always fatal; it happened even though the insulin infusion rate was half that usually recommended.3 5 U/h has proved satisfactory in our experience; slower insulin infusion rates (25 U/h) are sometimes
ineffective.4 What is the ideal insulin schedule to resolve the ketoacidosis in a reasonable time but without the risk of cerebral oedema? M. GARRE Intensive Care Unit,
Hôpital Morvan, 29200 Brest, France
J. M. BOLES B. GARO D. MABIN
1. Krane
EJ, Rockoff MA, Wallman JK, Wolfsdorf JJ. Subclinical brain swelling in children during treatment of diabetic ketoacidosis. N Engl J Med 1985; 312: 1147-51. 2. Katz MA. Hyperglycemia-induced hyponatremia: Calculation of expected serum sodium depression. N Engl J Med 1973; 131: 843-44. 3. Foster DW, McGarry JD. The metabolic derangements and treatment of diabetic ketoacidosis. N Engl J Med 1983; 309: 159-69. 4. Piters KM, Kumar D, Pei E, Bessman AN. Comparison of continuous and intermittent intravenous insulin therapies for diabetic ketoacidosis. Diabetologia 1977; 13: 317-21.
MYOGLOBIN TO PREDICT MYOCARDIAL INFARCTION DURING HEART SURGERY
SIR,-Myoglobin has been reported to be an earlier and more valuable indicator of myocardial infarct than measurement of creatine phosphokinase MB activity (CKIMB). 1,2 We wondered if measurement of myoglobin during cardiac surgery might reflect peroperative myocardial ischaemia more precisely than ECG findings or CK-MB. Blood was collected from twenty patients aged 5 lt 14 years from an arm vein immediately after anaesthesia, at the start of cardiopulmonary bypass, during cardiac arrest, and 2, 4, 6, 8, 10, 14, 24, and 48 h after restoration of coronary flow. During cardiac arrest blood samples were also collected from the coronary sinus. Myoglobin levels were measured by a latex agglutination test. Fifteen patients had an uncomplicated postoperative outcome. The other five had a perioperative myocardial infarction, as
Six,-The irritable hip syndrome is common in childhood, and in Glamorgan accounts for 2 -5% of the admissions to the paediatric ward servicing the accident and emergency department. South
Surprisingly little is understood about the cause of this syndrome. Hardinge’s 19701 review revealed no connection with infections or allergic disease but he did note a "loose similarity" between the monthly incidence of tibial fractures and irritable hips, and trauma is still often referred to as a possible cause. Since the incidence of children’s trauma varies significantly with the seasons, it should follow, if there is a causal relation between and irritable hips, that the seasonal incidence of irritable hips should show a similar pattern. The only paper on this seasonal variation involved small numbers, and was from Australia.2 We have looked at this question by retrospectively identifying cases of the irritable hip syndrome admitted to the children’s ward servicing the accident and emergency department. As a comparative measure of the incidence of trauma in the childhood population, we also identified children with head injuries or fractures admitted to the same ward over the same period. Since this accident and emergency department was the only one covering that district, this was an accurate reflection of the children’s injuries in that period. The total number of cases of irritable hips was still small when analysed on a monthly basis, so we identified other cases from the whole of Wales over the same period, using Hospital Activity Analysis data, with the diagnostic code 7873 (ICD 1977-78) or 7194 (ICD 1979-83)-transient synovitis of the hip, irritable hip, or3 "observation hip". The results were analysed by the Hewitt test,3 and by a partitioned chi-square analysis. Over the six years studied, there were 2541 admissions with head injuries, 1208 admissions with fractures, and 238 admissions with irritable hips to the children’s ward. The admissions for head injuries and fractures demonstrated a clear seasonal pattern. The admissions for irritable hip peaked around September, but the pattern was not sufficiently clear cut to reach significance (rank trauma
52, p>0 05). Hospital Activity Analysis identified a further 1340 children with the appropriate diagnostic coding. Again there was no significant seasonal variation (peak June, rank sum=49, p>0’05) (figure). A chi-square statistic (55 degrees of freedom) was calculated to express clustering of cases by month over and above differences sum =
between years and differences between months of the year. This did not reach significance. All children with irritable hips may not be admitted to hospital and HAA data may not be complete; also, some children with irritable hips will subsequently present with Perthes’ disease or coxa magna.3-5 Nevertheless, we feel that the data obtained probably do accurately reflect the pattern of the disease in the community. Whereas a clear seasonal pattern was demonstrated for children’s injuries, this was not so for irritable hips. It is apparent, therefore, that we should discount trauma as a possible aetiology, and concentrate our search on other factors. Illingworth’s study6 demonstrated a high incidence of recurrent symptoms, which suggests that individual constitutional factors may have an important role, and it may well be that it would be profitable to study these individuals more closely.
C. P. Q. SAINSBURY R. G. NEWCOMBE A. ESSEX-CATER
Department of Child Health, University of Wales College of Medicine, Cardiff CF4 4XN
1.
Hardinge K. The etiology of transient synovitis in childhood. J Bone Joint Surg 1970;
52: 100-07. 2. Sharwood F. The irritable hip syndrome
in
children.
Long term follow up. Acta Orthop
Scand 1981; 52: 633-38. 3. Hewitt D, Milner J, Csima A, Pakula A. On Edwards’ criterion of seasonality and a nonparametric alternative. Br J Prev Soc Med 1971; 25: 174-76. 4. Jacobs BW. Synovitis of the hip in children and its significance. Paediatrics 1971; 47: 558-66. 5. Adams JA. Transient synovitis of the hip joint in children. J Bone Joint Surg 1963; 45B: 471-76. 6. Illingworth CM Recurrences oftransient synovitis ofthe hip. Arch Dis Child 1983; 58: 620-23.
CEREBRAL OEDEMA IN DIABETIC KETOACIDOSIS: DO WE USE TOO MUCH INSULIN?
SIR,-Subclinical brain swelling during treatment of diabetic ketoacidosis is quite a common finding in children but clinically apparent cerebral oedema is exceptional in adults. However, rapidly fatal cerebral oedema may occur in adult diabetics despite hypernatraemia, low insulin infusion rates, slow fluid administration, and no bicarbonate infusion. A 20-year-old woman was admitted with diabetic ketoacidosis and treatment began at 1130 hours. By 1620 only 1200 ml 2-5% dextrose, 2 g potassium chloride, and 24 units of ordinary insulin had been given, by constant infusion. The patient remained fully conscious and did not complain of a headache. However, at 1620 hours she collapsed with respiratory arrest, a brain scan revealing narrowing of the ventricles compatible with acute brain oedema. 20 min later clinical examination was compatible with brain death which was confirmed by electroencephalography. The CSF was normal except for a slightly raised protein (70 mg/dl). This patient died suddenly with brain oedema after 5 h of treatment for diabetic ketoacidosis. Except for a fall in blood glucose, none of the aetiological factors discussed by Krane and colleagues was present. Moreover, the corrected2 plasma sodium remained high (table). LABORATORY DATA BEFORE AND AFTER INSULIN THERAPY
*Derived from Katz’ formula.2
This complication, though rare, is unpredictable and nearly always fatal; it happened even though the insulin infusion rate was half that usually recommended.3 5 U/h has proved satisfactory in our experience; slower insulin infusion rates (25 U/h) are sometimes
ineffective.4 What is the ideal insulin schedule to resolve the ketoacidosis in a reasonable time but without the risk of cerebral oedema? M. GARRE Intensive Care Unit,
Hôpital Morvan, 29200 Brest, France
J. M. BOLES B. GARO D. MABIN
1. Krane
EJ, Rockoff MA, Wallman JK, Wolfsdorf JJ. Subclinical brain swelling in children during treatment of diabetic ketoacidosis. N Engl J Med 1985; 312: 1147-51. 2. Katz MA. Hyperglycemia-induced hyponatremia: Calculation of expected serum sodium depression. N Engl J Med 1973; 131: 843-44. 3. Foster DW, McGarry JD. The metabolic derangements and treatment of diabetic ketoacidosis. N Engl J Med 1983; 309: 159-69. 4. Piters KM, Kumar D, Pei E, Bessman AN. Comparison of continuous and intermittent intravenous insulin therapies for diabetic ketoacidosis. Diabetologia 1977; 13: 317-21.
MYOGLOBIN TO PREDICT MYOCARDIAL INFARCTION DURING HEART SURGERY
SIR,-Myoglobin has been reported to be an earlier and more valuable indicator of myocardial infarct than measurement of creatine phosphokinase MB activity (CKIMB). 1,2 We wondered if measurement of myoglobin during cardiac surgery might reflect peroperative myocardial ischaemia more precisely than ECG findings or CK-MB. Blood was collected from twenty patients aged 5 lt 14 years from an arm vein immediately after anaesthesia, at the start of cardiopulmonary bypass, during cardiac arrest, and 2, 4, 6, 8, 10, 14, 24, and 48 h after restoration of coronary flow. During cardiac arrest blood samples were also collected from the coronary sinus. Myoglobin levels were measured by a latex agglutination test. Fifteen patients had an uncomplicated postoperative outcome. The other five had a perioperative myocardial infarction, as