HYPERNATRAEMIC DEHYDRATION - keywords
hypernatremic dehydration
Del Castillo-Hegyi C, Achilles J, Segrave-Daly BJ, Hafken L. Fatal Hypernatremic Dehydration in a Term Exclusively Breastfed Newborn. Children (Basel). 2022 Sep 13;9(9):1379.
Duran R, Aladağ N, Vatansever U, Temízöz O, Gençhallaç H, Acunaş B. Cranial MR venography findings of severe hypernatremic dehydration in association with cerebral venous thrombosis in the neonatal period. Pediatr Hematol Oncol. 2007 Jul-Aug;24(5):387-91.
Han BK, Lee M, Yoon HK. Cranial ultrasound and CT findings in infants with hypernatremic dehydration. Pediatr Radiol. 1997 Sep;27(9):739-42. doi: 10.1007/s002470050214. PMID: 9285735.
Meena A, Singh A, Goyal VK, Gupta N, Payal V, Chaturvedi K. Brain Injury Patterns in Neonates With Hypernatremic Dehydration: Single Center Experience. Indian Pediatr. 2021 Oct 15;58(10):947-950.
Musapasaoglu H, Agildere AM, Teksam M, Tarcan A, Gurakan B. Hypernatraemic dehydration in a neonate: brain MRI findings. Br J Radiol. 2008 Feb;81(962):e57-60.
Ozer PA, Kabatas EU, Kurtul BE, Dilli D, Zenciroglu A, Okumus N. A Rare Cause of Retinal Artery Occlusion in Severe Hypernatremic Dehydration in Newborns. Ophthalmic Surg Lasers Imaging Retina. 2016 May 1;47(5):482-5.
Righini A, Ramenghi L, Zirpoli S, Mosca F, Triulzi F. Brain apparent diffusion coefficient decrease during correction of severe hypernatremic dehydration. AJNR Am J Neuroradiol. 2005 Aug;26(7):1690-4.
Rosenbloom AL. Permanent brain damage from hypernatremic dehydration in breastfed infants: patient reports. Clin Pediatr (Phila). 2004 Nov-Dec;43(9):855-7.
Unal S, Arhan E, Kara N, Uncu N, Aliefendioğlu D. Breast-feeding-associated hypernatremia: retrospective analysis of 169 term newborns. Pediatr Int. 2008 Feb;50(1):29-34.
van Amerongen RH, Moretta AC, Gaeta TJ. Severe hypernatremic dehydration and death in a breast-fed infant. Pediatr Emerg Care. 2001 Jun;17(3):175-80.
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references to hypernatremic dehydration in the newborn
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hypernatremic dehydration in the newborn
Neonatal hypernatremic dehydration (NHD) is a potentially lethal condition in neonates defined as a serum sodium of >145 mEq/L. It is often associated with inadequate feeding in exclusively breastfed infants in the first days to weeks after delivery. Serum sodium levels between 145 and 149 mEq/L are considered mild; 150–160 mEq/L moderate and above 160 mEq/L severe hypernatremia. Imaging evidence of brain injury was reported in infants developing moderate or severe hypernatremia: multifocal haemorrhage and edema, sinus thrombosis, subdural haemorrhage. Other consequences are: acute kidney injury, hepatic injury, peripheral venous and arterial thrombosis (e.g. retinal artery occlusion Ozer et al. 2016), disseminated intravascular coagulation and death. Hypernatremic dehydration in term newborns increased in incidence following efforts to promote exclusive breastfeeding before hospital discharge. Fatal case histories demonstrated pitfalls of current perceptions of normal vs. abnormal newborn feeding behavior, weight loss and clinical thresholds believed to be safe for neonates.
- Han et al. 1997 presented two newborn infants with hypernatremic dehydration with central nervous system (CNS) involvement. Both suffered multifocal areas of haemorrhagic infarction.
- Righini et al. 2005: hypernatremic dehydration presenting in the late neonatal period; MRI scan at 2 days after admission, during slow rehydration, demonstrated brain swelling (e.g. splenium and PLIC) plus low ADC values (cytotoxic oedema) in thalamus and PLIC. These changes reversed without infarction. The authors concluded that even careful rehydration leads to neuronal (and axonal, myelinic and glial) swelling due to slow decrease of intracellular increased osmolality built up during the slow phase of dehydration.
- Duran et al. 2007 reported cranial MR venography findings suggestive of thombosis of a newborn infant with severe hypernatremic dehydration.
- Unal et al. 2008 retrospectively studied 169 hypernatremic infants (among 4136 hospitalized term neonates): mean gestational age, 39.1 weeks (37-42 weeks); birthweight, 3352 g (2200-4500 g); weight loss, 15.9% (5.4-32.7%). Major presenting symptoms were neonatal jaundice (47.3%) and poor sucking (29.6%). The median sodium; blood urea nitrogen (BUN); and creatinine levels on admission were 155 mmol/L (150-194 mmol/L), 35 mg/dL (7-253 mg/dL), and 0.9 mg/dL (0.2-10 mg/dL), respectively. Major complications were: acute renal failure 82.8%; elevated liver enzymes 20.7%; disseminated intravascular coagulation 6.5%; brain edema 5.2%; intracranial haemorrhage 3.6%; cavernous sinus thrombosis 1.2%; bilateral iliac artery thrombosis 0.6%. Ten patients (5.9%) developed seizures within the first 24 h of rehydration therapy with a mean serum sodium drop of 11.9 mmol/L per day (4-19 mmol/L per day). Two patients (1.2%) died.
- Meena et al. 2021 prospectively enrolled 100 consecutive neonates admitted with hypernatremic dehydration, of which 93 underwent MRI. Lesions were found in 42 (45.2%) babies. Edema was the most common finding in 37 (39.8%), followed by hemorrhage in 13 (13.9%) and thrombosis in 6 (6.4%). Edema predominantly affected juxtacortical/subcortical white matter followed by periventricular white matter and centrum semiovale, posterior part of internal capsule, and basal ganglia/thalamus. Occipital horns were the main sites of haemorrhage. Thrombotic lesions predominantly involved sagittal, straight and transverse sinuses. Among combination of lesions, edema was associated with thrombosis in 4 (4.3%) babies, with haemorrhage in 7 (7.5%) babies, and with both thrombosis and haemorrhage in 2 (2.15%) babies. Brain lesions were observed only in the severe hypernatremia group.
- Musapasaoglu et al. 2008 described linear haemorrhages at the grey-white matter junction, helpful for ruling out other conditions.
Han et al. 1997: multifocal haemorrhage
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Musapasaogly et al. 2008: linear subcortical changes
Righini et al. 2005: high DWI intensity values (cytotoxic oedema) in thalamus and PLIC
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