Pediatr Radiol (2000) 30: 323±325 Ó Springer-Verlag 2000

AysËe Korkmaz SËule YigÆit Murat Fõrat Olcay Oran

Received: 29 April 1999 Accepted: 15 November 1999 A. Korkmaz ´ SË. YigÆit ´ O. Oran Neonatology Unit, IÇhsan DogÆramacõ Children's Hospital, University of Hacettepe, Ankara, Turkey

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A. Korkmaz ( ) Kõbrõs Sk. No: 1/18, TR-06 690 Güvenevler, Ankara, Turkey M. Fõrat Department of Radiology, University of Hacettepe, Ankara, Turkey

Cranial MRI in neonatal hypernatraemic dehydration

Abstract Severe neonatal hypernatraemia is a life-threatening electrolyte disorder because of its neurological complications. These are brain oedema, intracranial haemorrhages, haemorrhagic infarcts and thromboses. There are few reports concerning the radiological findings in the central nervous system in severe neonatal hypernatraemia. Cranial MRI findings in hypernatraemia have been reported in an older child, but have not been described in newborn in-

fants. We report the cranial MRI findings in a newborn infant with acute renal failure and severe hypernatraemia.

Introduction

Case report

Hypernatraemia in the neonatal period is an important electrolyte disorder that has serious deleterious effects on the central nervous system (CNS). Newborn infants are susceptible to hypernatraemia due to increased insensible water loss as a consequence of relatively large body surface area and inefficient renal conservation of water due to renal immaturity. Neonatal hypernatraemia has a wide spectrum of neurological signs and symptoms according to the serum sodium level and vary from mild lethargy to deep coma [1]. The medical literature contains only a few reports of the radiological findings in the CNS in neonatal hypernatraemia [2, 3]. Transient thalamic changes on MRI in a 7-month-old infant with severe hypernatraemia have been reported [4]. To our knowledge, the cranial MRI findings in neonatal hypernatraemia have not been previously reported. We present a newborn infant with acute renal failure and severe hypernatraemic dehydration.

A 15-day-old girl was admitted to the Neonatal Intensive Care Unit because of lethargy, poor feeding, anuria and convulsions. She had been born by caesarean section to a 26-year-old woman at 38 weeks' gestation after an uncomplicated pregnancy. Birth weight was 3,100 g. Although maternal lactation was inadequate, she was only breast fed. After the tenth day of life she developed lethargy, poor feeding and could be breast fed only once a day. She was brought to hospital after developing anuria and convulsions. Physical examination revealed a lethargic infant weighing 2,100 g, with signs of severe dehydration and hypovolaemic shock and having focal convulsions of her left arm and leg. Serum electrolyte concentrations were sodium 185 mEq/l, potassium 6.3 mEq/l, chloride 148 mEq/l, BUN 188 mg/dl, creatinine 2.7 mg/dl, uric acid 22 mg/dl, calcium 11.1 mg/dl and phosphorus 5.3 mg/dl. Arterial blood gas analysis showed pH 7.0, HCO3 12 mEq/l, BE ±15, p02 85 mm Hg, pCO2 45 mm Hg. Renal failure index and fractional Na excretion were 2.5 and 2.6, respectively. Breast milk sodium concentration was normal. Abdominal US showed bilateral diffusely increased renal parenchymal echogenicity, suggestive of acute renal injury. She was treated for severe dehydration and acute renal failure with appropriate intravenous fluid and electrolyte therapy. She was given phenobarbital and phenytoin for her convulsions. After

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Fig. 1 Sagittal T1-W image (TR/TE 600/15) shows superior sagittal sinus thrombosis (straight arrows) and a parieto-occipital haemorrhagic infarct (curved arrow) Fig. 2 Coronal T1-W image (TR/TE 600/15) reveals multifocal hyperintense areas corresponding to haemorrhagic venous infarcts (small arrows). Bold arrow: right lateral sinus thrombosis Fig. 3 Axial T2-W image (TR/TE 3500/150) shows hypointense cortical lesions corresponding to early subacute haemorrhagic infarcts (bold arrows). Small arrows: oedema

16 h of treatment, she began to pass urine and at the end of 3 days the serum sodium, BUN, creatinine and uric acid concentrations returned to normal. On the third day of admission, cranial US showed multiple foci of increased echoes in the brain. On the fifth day of admission cranial MRI revealed multiple cortical and subcortical lesions (hyperintense on T1-weighted [T1-W] and hypointense on T2-weighted [T2-W] images) in the right temporal and parieto-occipital lobes which were compatible with early subacute venous haemorrhagic infarcts (Figs. 1±3). T2-W images revealed hyperintense oedema surrounding the cortical and subcortical lesions (Fig. 3). There was also hyperintense signal on T1-W and T2-W images in the right transverse and sagittal sinuses indicative of thrombosis. There was no subdural haematoma. After 15 days the infant was discharged from hospital with only mildly increased tone and deep tendon reflexes on the left side of the body. She was continued on phenobarbital for the next few months and kept under neurological follow-up.

Discussion Hypernatraemia is defined as serum sodium concentration of 150 mEq/l or greater. Under normal conditions, serum sodium concentration is tightly regulated between 135 and 145 mEq/l. Clinical consequences are often severe when the sodium concentration increases above 160 mEq/l.

3 Hypernatraemia can be the result of pure sodium excess (rare), of water deficit, or of water deficit coupled with a lesser degree of sodium deficit such as occurs with abnormal hypotonic fluid losses, e. g. diarrhoea. Newborn infants are more susceptible to hypernatraemia due to relatively large evaporative water losses per kilogram of body weight and the inefficiency of renal conservation of water due to renal immaturity [1, 2]. One of the most important causes of hypernatraemia in breast-fed newborn infants is maternal lactation failure. It has been reported that there is a statistically significant annual increase in the number of infants admitted with breast-feeding malnutrition and hypernatraemia [5]. In our case, severe dehydration and hypernatraemia were secondary to maternal lactation failure, poor fluid intake and increased insensible water loss. There are several reports concerning the pathogenesis and pathology of CNS findings in hypernatraemia. A common intracranial pathological finding is diffuse haemorrhagic encephalopathy. Brain haemorrhage, either massive haemorrhage or multiple small haemorrhages and thromboses, may occur when hypernatraemia causes cellular dehydration with resultant brain shrinkage and tearing of cerebral vessels [1, 6]. Hypernatraemia can cause acute CNS dysfunction and even lead to permanent CNS sequelae. Acute symptomatology is seen in most infants and children with a serum sodium concentration of over 158 mEq/l and symptoms correlate with the height of serum sodium concentration. Disturbance of consciousness, lethargy, irritability, tremors, increased deep tendon reflexes, increased muscle tone and seizures are the most frequent neurological findings. The overall mortality of hypernatraemia is about 10 % [1, 7]. Correction of hypernatraemia can also be complicated by CNS injury. Rapid correction of hypernatraemia may result in central pontine myelinolysis and perma-

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nent neurological damage. It has been suggested that the decrease in plasma sodium should not exceed 0.5 mEq/l/h or 48±72 h [8]. In our case plasma sodium concentration was corrected in 72 h. The radiological diagnosis of neonatal cerebral venous thrombosis (CVT) can be made by transcranial Doppler US (TCD) studies easily, noninvasively and accurately. Serial TCD allows monitoring of venous haemodynamics and collateral pathways. However, normal venous velocities in serial measurements do not exclude a diagnosis of CVT [9]. Cranial CT may fail to demonstrate all the thrombotic regions. Conventional T1-W and T2-W MR images often indicate more extensive thromboses than were suggested by cranial CT [10]. MRI is superior to other modalities for the diagnosis of CVT, and MR angiography is an alternative means for monitoring the evolution of CVT and the efficacy of therapeutic intervention [11]. There are few reports of the radiological findings in the CNS in neonatal hypernatraemia. Cranial US and CT have been reviewed [2, 3]. In these reports, cranial US showed diffuse increased brain parenchymal echogenicity, obliterated sulci and fissures and compressed lateral ventricles consistent with generalised cerebral

oedema. Cranial CT showed areas of encephalomalacia and bilateral multifocal haemorrhagic lesions. Hilliard et al. [12] reported sagittal sinus thrombosis in hypernatraemic dehydration. Hartfield et al. [4] reported transient thalamic signal changes in a 7-month-old male infant with severe hypernatraemia that resolved on follow-up study and correlated with complete clinical recovery. The cranial MRI findings in severe neonatal hypernatraemia have not been reported previously. The cranial MRI of our patient revealed multiple cortical and subcortical lesions on right temporal and parieto-occipital lobes on T1-W and T2-W images, which were compatible with early subacute haemorrhagic infarcts. There was also right transverse and sagittal sinus thromboses. In conclusion, neonatal hypernatraemia is a serious electrolyte disorder that may cause CNS injury as a result of intracranial haemorrhages, infarcts and thromboses. It should be included in the differential diagnosis of neonatal intracranial haemorrhages and CVT. Cranial US or TCD US should be performed as an initial screening procedure. MRI is recommended for detailed radiological examination and for follow-up.

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