|Year : 2022 | Volume
| Issue : 2 | Page : 64-68
Neonatal hypernatremic dehydration
Mohd Ashraf1, Umer Amin Qureshi2, Nucksheeba Aziz Bhat2
1 Department of Pediatric Nephrology, Government Medical College, Srinagar, India
2 Department of Pediatrics, Government Medical College, Srinagar, India
|Date of Submission||18-Mar-2022|
|Date of Decision||07-Jun-2022|
|Date of Acceptance||26-Sep-2022|
|Date of Web Publication||31-Dec-2022|
Department of Pediatric Nephrology, Government Medical College, Srinagar, Jammu and Kashmir
Source of Support: None, Conflict of Interest: None
Hypernatremic dehydration is a medical emergency which adversely affects central nervous system and kidneys, resulting in high mortality and morbidity, especially in neonates. Neonates are typically affected within the first 2 weeks of life, with those born in hot summers to primigravida mothers with insufficient lactation being particularly prone. Clinical features are usually nonspecific, including weight loss, hyperthermia, irritability, lethargy, hyperbilirubinemia, poor oral intake, oliguria, seizures, and/or shock. Restoration of vascular volume by administering 10–20 ml/kg of isotonic intravenous fluid is essential in the presence of circulatory collapse, followed by controlled slow rehydration to prevent rapid changes in serum sodium (Na). The outcome of hypernatremia in neonates largely depends on its severity, the timeliness of intervention, and the rate of fall of serum Na during the management process, for which qualitative standards are lacking. This review aims to help pediatric nephrologists, neonatologists, other clinicians, and postgraduate scholars to recognize, understand, and treat neonatal hypernatremic dehydration in lucid manner based on available evidence.
Keywords: Acute kidney injury, dehydration, newborn, sodium
|How to cite this article:|
Ashraf M, Qureshi UA, Bhat NA. Neonatal hypernatremic dehydration. Asian J Pediatr Nephrol 2022;5:64-8
| Introduction|| |
Dehydration, or loss of body water, may follow decreased intake, increased output, or increased utilization of water to meet the body demands. Neonates, infants, and young children are predisposed to rapid and severe dehydration because of greater body surface area to weight ratio. Based on serum sodium (Na), the state of dehydration is categorized as hyponatremic, isonatremic, or hypernatremic. Normal serum Na levels are maintained between 135 and 145 mEq/L: a level <135 mEq/L is termed hyponatremia, while serum levels >145 mEq/L indicate hypernatremia. Hypernatremic dehydration, i.e., dehydration accompanied by serum Na >145 mEq/L, indicates a hyperosmolar state caused by a deficiency of water relative to Na. However, total body Na may be high, normal, or low.
The incidence of hypernatremic dehydration appears to be rising. Its incidence among breastfed infants is 1.8% in the West, and 3.1% in Asia. Hypernatremic dehydration in neonates implies a relatively common but salvageable entity, which carries a huge potential for morbidity and mortality in the form of seizures, cerebral thrombosis, hemorrhage, and acute kidney injury (AKI).
| Pathophysiology|| |
The serum level of Na is tightly controlled within a narrow range despite wide variations in Na and water intake. The physiological concept for the osmoregulatory system is based on body fluid, particularly the volume occupied by the arterial tree of the circulatory system (effective osmolality). The tonicity of body fluid represents the osmotic pressure generated by solutes which cannot cross the cell membranes passively, and determines water movements across the membranes. Salts of Na, such as Na chloride and Na bicarbonate, are the primary solutes involved in plasma tonicity. Various solutes, such as urea and glucose, which are included in estimates of plasma osmolality, do not change the plasma tonicity since they cross cell membranes. Hypernatremic dehydration results from either loss of water in excess of Na, and/or gain of Na in excess of water. The causes of hypernatremic dehydration are detailed in [Table 1]. Based on serum Na levels, hypernatremia is classified as mild (serum Na 146–149 mEq/L), moderate (Na 150–169 mEq/L), and severe (Na >170 mEq/L).
Neonatal hypernatremic dehydration in majority of situations is due to unsuccessful feeding. Basic mechanisms for hypernatremic dehydration are as follows:
Inadequate water intake
Breast milk, which is advocated as the best feed for neonates given every 2–3 hourly to all-term and near-term neonates, contains 87% water. Total daily milk intake by an infant depends on the frequency and duration of feeds, unimpeded initiation of lactation, sustained ongoing milk synthesis, and effective milk removal. Failure of any one or more of these can lead to neonatal hypernatremic dehydration. Early discharge without proper breastfeeding counseling is a major cause of neonatal hypernatremic dehydration.
Excessive water loss
This could be insensible, gastrointestinal, or renal losses. Urinary loss is attributed to immaturity and smaller size of nephrons at birth, with consequent low glomerular filtration rate (GFR). GFR smoothly increases in the 1st week from birth, and continues to improve till the child's second birthday., As compared to adults, who can concentrate urine up to 1200 mOsm/L, preterm and term neonates can concentrate urine only up to 550 mOsm/L and 700 mOsm/L, respectively. The effects of renin–angiotensin–aldosterone system and arginine vasopressin are limited due to renal immaturity, which predisposes newborns at risk of volume depletion in situations of high solute load and/or low breast milk intake, as the urinary concentrating ability is limited.
Intake of Na in large quantities, whether orally or parenterally, or uncommonly, mineralocorticoid excess, can cause neonatal hypernatremic dehydration.
| Clinical Presentation|| |
Usual clinical presentations of neonatal hypernatremic dehydration are failure to gain weight, fever, and decreased urine output. In a landmark study of 70 term and near-term hypernatremic neonates, common clinical presentations were fever, lethargy, decrease in weight gain, hyperbilirubinemia, apnea, bradycardia, and intracranial hemorrhage.
| Diagnosis|| |
Careful history and meticulous clinical examination are helpful in enabling the diagnosis of hypernatremic dehydration. Weight loss of 7% or more during the 1st week of life warrants an evaluation of the clinical status. A proportion of neonates may be hyperthermic and lethargic, a few are alert but hungry and dehydrated, while others may present with jaundice and seizures. In moderate-to-severe hypernatremic dehydration, fever, tachycardia, poor perfusion, and hypotension are well documented; however, skin turgor appears deceptively normal due to maintained intravascular volume at initial stages of illness. Skin appears thick and doughy and may even feel moist due to perspiration, while mucous membranes are dry. Laboratory tests such as complete blood counts, C-reactive protein, blood sugar, blood or serum levels of urea, creatinine, Na, potassium, calcium, phosphorus and osmolality; urinalysis, urine osmolality, spot urine Na, calcium and creatinine; ultrasonography of cranium and abdomen (kidney, ureter, and bladder), are usually performed to reach the diagnosis.
Most often, the weight loss in hypernatremic dehydration can either be explained by the inadequate volume of intake, caused by insufficient lactation or wrong technique of breastfeeding. However, one important differential diagnosis with similar clinical presentation is diabetes insipidus (DI), which can be ruled out by noting urine output of ≥1 mL/kg/hour in a setting of severe dehydration. However, it is noteworthy that central DI can also follow hypernatremic dehydration as a complication of intracranial hemorrhage, cerebral infarct, disseminated intravascular coagulation (DIC), or central venous thrombosis.,,
Another important but much rarer condition is neonatal severe primary hyperparathyroidism, an entity with disturbed calcium homeostasis, which has similar clinical manifestations such as polyuria, dehydration, gastrointestinal dysmotility, poor feeding, respiratory distress, and failure to thrive. However, blood and urine chemistry of calcium, phosphorus, and parathyroid levels will clinch the diagnosis.
| Complications|| |
Major complications of hypernatremic dehydration are seizures, cerebral dysfunction, intracranial hemorrhage, AKI, DIC, shock, and death., As such, brain is the most vulnerable organ in hypernatremic neonates. With the rise of plasma Na, intracellular water moves to extracellular space, causing brain cells to shrink by as much as 10%–15%, depending on the degree of hypernatremia, which leads to rupture of bridging vessels. This results in subarachnoid and parenchymal hemorrhages and thrombosis. As a defense mechanism, over a period of several hours to few days, the brain cells respond to the hypernatremic state by generating intracellular solutes known as “idiogenic osmoles,” including glutamine, taurine, myo-inositol, and glycerophosphorylcholine. In such a situation, rapid rehydration with relatively hypotonic intravenous fluids (IVFs) results in movement of water into cerebral cells, leading to rebound cerebral edema because of the brain cells' inability to remove the idiogenic osmoles. Seizures, cerebral dysfunction, cognitive decline, and spastic paralysis have been reported under such circumstances. About 50% of patients develop neurological sequelae that present as seizures and/or impairment of consciousness.
While AKI is one of the most common complications of hypernatremic dehydration, it has attracted lesser attention, possibly due to less overt symptoms and signs compared to neurological injury. Besides the established risk factors of neonatal AKI, such as low birth weight, prematurity, perinatal asphyxia, and postcardiac surgery, severe form of hypernatremic dehydration is an important but less reported cause of neonatal AKI., The exact incidence of AKI secondary to hypernatremic dehydration is difficult to estimate. A study from Turkey reported that 84 out of 85 patients had AKI, while another study by Chouchane et al. reported that 76.2% of patients developed AKI while in hospital.
Other complications of hypernatremic dehydration include facial palsy, apnea or bradycardia, seizures, hypertension, DIC, iliac artery thrombus, “slowing” on electroencephalography, and multiple cerebral infarctions.
| Treatment|| |
Treatment of hypernatremic dehydration is based on the cause, assessment of intravascular volume, free water replacement, and provision of maintenance and ongoing losses [Textbox 2]. Although there are no guidelines regarding best practices for the management of hypernatremic dehydration, the current evidence is based on the principle of a very slow rehydration in all cases where the cause and duration is unknown. An attempt to reverse the high Na concentration quickly can cause brain edema, seizures, and death.
The speed of hypernatremia reversal depends on the rate of its development. Except in the cases of acute massive Na overload, the goal should be to drop the serum Na concentration at a rate no >0.5–0.6 mEq/L/hour. This approach provides a reasonable chance that the serum Na concentration will gradually decrease to the normal range over a period of 2 days or longer. Milder forms of hypernatremia can be managed by appropriate breastfeeding or oral nasogastric feeding while monitoring serum Na. Healthy neonates can be rehydrated at a rate of 100 ml/kg/day using expressed breast milk or artificial feeds, or a combination of both. If the neonate is unwell, IVF is the therapy of choice. Any neonate with moderate-to-severe hypernatremic dehydration would need the steps outlined in [Textbox 1], and its management is described in [Table 2].
|Table 2: Management of neonatal hypernatremic dehydration for the case scenario described in Textbox 1, using principles enunciated in Textbox 2^|
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| Management of Acute Kidney Injury in Hypernatremic Dehydration|| |
Impaired kidney function is initially managed by controlled restoration of fluid and electrolyte balance, discontinuing potassium and nephrotoxic medications, correcting hyperkalemia (K+>7.0 mmol/L) expeditiously but cautiously, and by reversing acidosis slowly. Failure of these measures often necessitates kidney replacement therapy (KRT). Modalities for KRT that can be offered to neonates include peritoneal dialysis, intermittent hemodialysis (HD), and continuous renal replacement therapy. The choice of the modality of KRT depends on availability of facility, the experience, and indications and contraindications. Traditionally and most commonly, acute peritoneal dialysis is used for neonates, because it is less technical, readily available, and cost-efficient. Acute peritoneal dialysis has been shown to be effective in managing neonatal AKI in both premature and mature newborns. However, care must be taken to ensure that the dialysate fluid has a Na concentration within 10–15 mEq/L of the serum Na, to achieve a slow and adequate rate of Na fall. HD has been the preferred modality in older children, and in patients with salt poisoning.
| Conclusion|| |
Neonatal hypernatremic dehydration is a serious, potentially life-threatening disorder with high rates of mortality and morbidity. Till robust prospective studies and randomized controlled trails can provide evidence base for clinical practice guidelines, slow and calibrated Na correction appears to be the most appropriate basic principle to follow when managing patients with hypernatremic dehydration. This is necessary to prevent water intoxication and neurological and renal sequelae. In general, early diagnosis and prompt management of this clinical entity can be performed by monitoring weight change, urinary frequency, and status of hydration during the first 3 weeks of life. Breastfeeding counseling is very important, particularly in resource-limited countries and hot weather.
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Conflicts of interest
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[Table 1], [Table 2]