ELECTRONIC ARTICLE |


* Department of Neonatology, University of Crete, Crete, Greece
Department of Orthopedics, University of Crete, Crete, Greece
| ABSTRACT |
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We report the case of a full-term infant of an insulin-dependent diabetic mother with poor blood glucose control who developed a left peroneal nerve palsy after ischemic necrosis of the gluteal region after umbilical artery catheterization. The infant was born weighing 5050 g. The mother of the infant had preexisting diabetes mellitus that was treated with insulin from the age of 14 years. The metabolic control of the mother had been unstable both before and during the pregnancy.
The neonate developed respiratory distress syndrome soon after birth and was immediately transferred to the neonatal intensive care unit. Mechanical ventilation via endotracheal tube was quickly considered necessary after rapid pulmonary deterioration. Her blood glucose levels were 13 mg/dL. A 3.5-gauge umbilical cathether was inserted into the left umbilical artery for blood sampling without difficulty when the infant required 100% oxygen to maintain satisfactory arterial oxygen pressure. Femoral pulses and circulation in the lower limbs were normal immediately before and after catheterization. A radiograph, which was taken immediately, showed the tip of the catheter to be at a level between the fourth and fifth sacral vertebrae. The catheter was removed immediately. Circulation and femoral pulses were normal and no blanching of the skin was observed. Another catheter was repositioned and the tip was confirmed radiologically to be in the thoracic aorta between the sixth and seventh thoracic vertebrae. The catheter was continuously flushed with heparinized solution. Three days after umbilical arterial catheterization, bruising was observed over the left gluteal region. The catheter was immediately removed despite its correct position. Over the next few days, the bruised skin and underlying tissues became necrotic. The area affected was 3 x 4 cm in diameter, with central necrosis surrounded by a rim of dark, red skin, which, in turn, was sharply demarcated from normal skin by a narrow, pale zone. Surgical excision of the gluteal necrosis was performed, but a deep ulcer 3 cm in diameter was left. The gluteal ulcer required 1 month to heal completely with extensive scar tissue formation. Throughout this period, the infant showed active movements in all of her limbs. At 4 weeks of age deterioration of all movement below the left knee with a dropping foot was observed. Severe peroneal nerve palsy was confirmed through nerve conduction studies, and there was electromyographic evidence of degeneration of the muscles supplied by the peroneal branch of the sciatic nerve. A Doppler study, which was also conducted, revealed no vascular damage. Treatment with physiotherapy and night-splinting of the left ankle was instituted. Repeated examination and nerve conduction tests at 3 months showed slow improvement with the left peroneal nerve remaining nonexcitable. At the time of this writing, the infant is 6 months old, and muscular strength below the left knee is still weak and atrophic changes in the form of muscle-wasting are already present. The rest of her motor development is normal.
In our case, gangrene of the buttocks and sciatic nerve palsy followed displacement of the tip of the catheter into the inferior gluteal artery, a main branch of the internal iliac artery supplying the gluteus maximus, the overlying skin, and the sciatic nerve. The gangrenous changes were probably caused by vascular occlusion resulting from catheter-induced vasospasm of the inferior gluteal artery. Sciatic nerve palsy associated with umbilical artery catheterterization has been postulated to be caused by vascular occlusion of the inferior gluteal artery. Infants of diabetic mothers may exhibit changes in coagulation factors and be at increased risk of thrombotic complications in utero and postnatally. In addition, maternal diabetes mellitus is associated with an increased incidence of congenital abnormalities, the incidence of which is 3 to 5 times higher than that among nondiabetic mothers. Although no particular or specific abnormalities have been associated with maternal disabilities, abnormalities of the cardiovascular system, including the development of umbilical vessels, frequently occur.
This complication of umbilical artery catheterization has not been widely reported. We describe the first case that refers to gluteal gangrene and peroneal nerve palsy after umbilical artery catheterization of a newborn infant of a diabetic mother with poor blood glucose control. It should be noted that there were no contributing factors except that of the displacement of the catheter into the inferior gluteal artery. We speculate that the displacement of the tip of the catheter, with no difficulty in the present case, was associated with the maldevelopment of normal branching patterns of arteries after exposure of the fetus to hyperglycemia.
In conclusion, umbilical artery catheterization is possibly associated with vascular occlusion, particularly in infants of diabetic mothers. Frequent inspection after the procedure has been performed is of the utmost importance especially in these neonates who often suffer from cardiopulmonary disease and require catheterization of their umbilical artery.
Key Words: newborn umbilical artery catheterization peroneal nerve palsy diabetes mellitus
| INTRODUCTION |
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We present the case of peroneal nerve palsy as a complication of umbilical artery catheterization in a full-term newborn infant of a mother with insulin-dependent diabetes and poor blood glucose control.
| CASE REPORT |
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The neonate developed respiratory distress syndrome soon after birth and was immediately transferred to the neonatal intensive care unit. Mechanical ventilation via endotracheal tube was quickly considered necessary after rapid pulmonary deterioration, and pulmonary surfactant was administered. A 3.5-gauge umbilical catheter was inserted into the left umbilical artery for blood sampling without difficulty when the infant required 100% oxygen to maintain satisfactory arterial oxygen pressure. Femoral pulses and circulation in the lower limbs both were normal immediately before and after catheterization. A radiograph, which was performed immediately, showed the tip of the catheter to be at a level between the fourth and fifth sacral vertebrae (Fig 1). The catheter was removed immediately. Circulation and the femoral pulses were normal, and no blanching of the skin was observed. Another catheter was repositioned, and the tip was confirmed radiologically to be in the thoracic aorta between the sixth and seventh thoracic vertebrae (Fig 2). The catheter was continuously flushed with heparinized solution. Laboratory evaluation revealed a peripheral white blood cell count of 12.9 x 109/L, with 33% neutrophils, 39% lymphocytes, 16% monocytes, 8% eosinophils, and 4% basophils. Blood hemoglobin was 17.4 g/dL, Ht was 51.4%, and platelet count was 250 000/mm3. Blood glucose levels were 13 mg/dL. Blood, cerebrospinal fluid, and tracheal aspirate cultures did not grow any organisms. Antibiotic treatment with intravenous vancomycin and gentamicin was started.
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| DISCUSSION |
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Infants of mothers with diabetes may exhibit changes in coagulation factors and be at increased risk of thrombotic complications in utero and postnatally.4 In addition, maternal diabetes mellitus is associated with an increased incidence of congenital abnormalities, which is 3 to 5 times higher than that among mothers without diabetes.5,6 Although no particular or specific abnormalities have been associated with maternal diabetes, abnormalities of the cardiovascular system, including the development of umbilical vessels, frequently occur.5
A number of causative factors have been proposed to explain the increased rate of congenital anomalies in infants of mothers with diabetes. These factors include genetic influences, teratogenic agents, maternal vascular disease, and metabolic effects of maternal diabetes.7 The basic pathogenesis is believed to be fetal hyperinsulinemia.5 The frequency of congenital abnormality is significantly increased in the newborns of mothers with poor metabolic control antepartum, as in the present case. Accordingly, it is essential in both gestational and preexisting diabetes to achieve the level of sustained glycemic control necessary to prevent congenital malformations before and after conception.6
In our case, gangrene of the buttock and sciatic nerve palsy followed displacement of the tip of the catheter into the inferior gluteal artery, a main branch of the internal iliac artery that supplies the gluteus maximus, the overlying skin, and the sciatic nerve (Figs 5 and 6). The gangrenous changes were probably caused by vascular occlusion resulting from catheter-induced vasospasm of the inferior gluteal artery. Sciatic nerve palsy associated with umbilical arterial catheterization has been postulated to be caused by vascular occlusion of the inferior gluteal artery.3,8
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This complication of umbilical artery catheterization has not been widely reported. Our case is the first in the literature that refers to gluteal gangrene and peroneal nerve palsy after umbilical artery catheterization of a newborn infant of a mother with diabetes and poor blood glucose control.
Purohit et al3 reported the case of a neonate who developed similar complications after umbilical artery catheterization. The clinical features of the neonate described by them suggests the infant of a mother with diabetes. However, the cause of the complication in their case was multifactorial, being related to the displacement of the catheter tip; the duration of the malplacement, which might have been as long as 30 hours; the occurrence of hypotension; and the infusion of hypertonic glucose and multiple medications via the umbilical catheter.
In contrast, in our case, the duration of the malposition of the tip of the catheter was only approximately 40 minutes, and no drugs or other hypertonic solutions were administered intraumbilically. It should be noted that there were no other contributing factors except that of the displacement of the catheter into the inferior gluteal artery. We speculate that the displacement of the tip of the catheter, with no difficulty in the present case, was associated with the maldevelopment of normal branching patterns of arteries after exposure of the fetus to hyperglycemia.5
| CONCLUSION |
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| FOOTNOTES |
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Reprint requests to (C.G.) 37 Atlantithos St, 71305 Heraklion, Crete, Greece. E-mail: aligisak{at}med.uoc.gr
| REFERENCES |
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N. Bednarek, P. Morville, G. Delebarre, A. Akhavi, and C. Sommer Necrotic Skin Lesions and Cerebral Infarction in the Newborn: Two Case Reports J Child Neurol, March 1, 2007; 22(3): 354 - 357. [Abstract] [PDF] |
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