Maternal Over-Hydration in Labor can Cause Dilutional Hyponatremia in Neonates
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COMMENTARY Maternal Over-Hydration in Labor can Cause Dilutional Hyponatremia in Neonates Siba Prosad Paul & Snehalata Basude & Adam Paul Smith-Collins Received: 27 July 2013 /Accepted: 21 October 2013 # Dr. K C Chaudhuri Foundation 2013 A term baby was born by semi-elective cesarean section for maternal prolonged rupture of membranes and non- progression of labor. His mother had received 2 L of intravenous fluids prior to delivery. The baby was well at birth and establishing breast feeds. He underwent blood investigations for risk of sepsis and intravenous antibiotics were started. At 4 h of age, the baby developed brief (<2 min) seizures, and was admitted to the neonatal unit. Cerebral function monitoring did not reveal any abnormality. Blood glucose was normal, while the blood investigations conducted previously, revealed serum sodium of 124 mmol/L (normal range 135–145 mmol/L), with other electrolytes and inflammatory markers being normal. He was successfully treated with a bolus of 3 % sodium chloride and no further seizures were noted. Further history revealed that his mother had ingested 2.5 L of water during the 8 h prior to delivery, which had not been recorded in obstetric charts. A diagnosis of dilutional hyponatremia secondary to maternal over- hydration was made. Pediatricians should consider potential mechanisms and differential diagnoses in newborn babies presenting with hyponatremia within the first 24 h of life. Most cases in neonates will be of dilutional hyponatremia, with imbalance between fluid intake and urine output, and low levels of urine sodium. Oliguria with a risk of dilutional hyponatremia can occur in the syndrome of inappropriate antidiuretic hormone secretion (SIADH) which is typically associated with infection e.g., congenital pneumonia, in birth asphyxia (with hypoxic renal injury) and in preterm infants who have impaired ability to concentrate urine [1–4]. Dilutional hyponatremia with apparently normal urine output occurs with excess administration of hypotonic fluids to an infant (as revealed by assessing fluid balance, input/output charts and weight). Situations where that administration has occurred in utero as a result of maternal over-hydration, it may not be evident immediately [3]. It is worth noting that these conditions may co-exist, such as an infant with disrupted tubular function due to birth asphyxia will be more vulnerable to incautious intravenous fluid management. Non-dilutional hyponatremia is most typically associated with renal salt-wasting, for example in congenital adrenal hyperplasia (CAH). The source of sodium loss can be confirmed by an inappropriately high urinary sodium in the presence of low serum sodium, and other clinical and biochemical abnormalities may be evident (e.g., hyperkalemia, poor glycemic control and ambiguous genitalia in CAH). There are multiple reports of dilutional hyponatremia in infants due to maternal water intoxication [5]. It occurs due to excess transfer of free water across the placenta following excessive administration of fluids to the mother in labor [4, 5]. Pregnant women have lower serum sodium (by ~3–5 mmol/L) than non-pregnant women, while the sodium concentration in the fetus is about 3 mmol/L lower than that of the mother [5]. Thus, maternal hyponatremia (due to iatrogenic fluid overload and/or drinking hypotonic fluids), results in the fetus becoming hyponatremic [3]. Anti-diuretic hormone (ADH) levels in the fetus rise before the onset of labor and remain elevated. High ADH and limited renal capacity in neonates makes them vulnerable to water overload causing hyponatremia [5]. S. P. Paul (*) Department of Pediatric Gastroenterology, Bristol Royal Hospital for Children, Paul O’Gorman Building, Upper Maudlin Street, Bristol BS2 8BJ, UK e-mail: [email protected] S. Basude Department of Obstetrics and Gynecology, St Michael’ s Hospital, Bristol, UK A. P. Smith-Collins Department of Neonatology, St Michael’ s Hospital, Bristol and School of Clinical Sciences, University of Bristol, Bristol, UK Indian J Pediatr DOI 10.1007/s12098-013-1282-6
Transcript of Maternal Over-Hydration in Labor can Cause Dilutional Hyponatremia in Neonates
COMMENTARY
Maternal Over-Hydration in Labor can Cause DilutionalHyponatremia in Neonates
Siba Prosad Paul & Snehalata Basude &
Adam Paul Smith-Collins
Received: 27 July 2013 /Accepted: 21 October 2013# Dr. K C Chaudhuri Foundation 2013
A term baby was born by semi-elective cesarean section formaternal prolonged rupture of membranes and non-progression of labor. His mother had received 2 L ofintravenous fluids prior to delivery. The baby was well at birthand establishing breast feeds. He underwent bloodinvestigations for risk of sepsis and intravenous antibioticswere started. At 4 h of age, the baby developed brief (<2 min)seizures, and was admitted to the neonatal unit. Cerebralfunction monitoring did not reveal any abnormality. Bloodglucose was normal, while the blood investigations conductedpreviously, revealed serum sodium of 124 mmol/L (normalrange 135–145 mmol/L), with other electrolytes andinflammatory markers being normal. He was successfullytreated with a bolus of 3 % sodium chloride and no furtherseizures were noted. Further history revealed that his motherhad ingested 2.5 L of water during the 8 h prior to delivery,which had not been recorded in obstetric charts. A diagnosisof dilutional hyponatremia secondary to maternal over-hydration was made.
Pediatricians should consider potential mechanisms anddifferential diagnoses in newborn babies presenting withhyponatremia within the first 24 h of life.Most cases in neonateswill be of dilutional hyponatremia, with imbalance between
fluid intake and urine output, and low levels of urine sodium.Oliguria with a risk of dilutional hyponatremia can occur in thesyndrome of inappropriate antidiuretic hormone secretion(SIADH) which is typically associated with infection e.g.,congenital pneumonia, in birth asphyxia (with hypoxic renalinjury) and in preterm infants who have impaired ability toconcentrate urine [1–4].
Dilutional hyponatremia with apparently normal urineoutput occurs with excess administration of hypotonic fluidsto an infant (as revealed by assessing fluid balance, input/outputcharts and weight). Situations where that administration hasoccurred in utero as a result of maternal over-hydration, itmay not be evident immediately [3]. It is worth noting thatthese conditions may co-exist, such as an infant with disruptedtubular function due to birth asphyxia will be more vulnerableto incautious intravenous fluid management.
Non-dilutional hyponatremia is most typically associatedwith renal salt-wasting, for example in congenital adrenalhyperplasia (CAH). The source of sodium loss can beconfirmed by an inappropriately high urinary sodium in thepresence of low serum sodium, and other clinical andbiochemical abnormalities may be evident (e.g., hyperkalemia,poor glycemic control and ambiguous genitalia in CAH).
There are multiple reports of dilutional hyponatremia ininfants due to maternal water intoxication [5]. It occurs due toexcess transfer of free water across the placenta followingexcessive administration of fluids to the mother in labor [4, 5].Pregnant women have lower serum sodium (by ~3–5 mmol/L)than non-pregnant women, while the sodium concentration inthe fetus is about 3 mmol/L lower than that of the mother [5].Thus, maternal hyponatremia (due to iatrogenic fluid overloadand/or drinking hypotonic fluids), results in the fetus becominghyponatremic [3]. Anti-diuretic hormone (ADH) levels in thefetus rise before the onset of labor and remain elevated. HighADH and limited renal capacity in neonates makes themvulnerable to water overload causing hyponatremia [5].
S. P. Paul (*)Department of Pediatric Gastroenterology, Bristol Royal Hospital forChildren, Paul O’Gorman Building, Upper Maudlin Street,Bristol BS2 8BJ, UKe-mail: [email protected]
S. BasudeDepartment of Obstetrics and Gynecology, St Michael’s Hospital,Bristol, UK
A. P. Smith-CollinsDepartment of Neonatology, St Michael’s Hospital, Bristol andSchool of Clinical Sciences, University of Bristol, Bristol, UK
Indian J PediatrDOI 10.1007/s12098-013-1282-6
Mild cases of neonatal hyponatremia may have no clinicalmanifestations. Symptomatic cases can present with crying,cyanotic spells, tachypnea, feeding difficulties and excessiveweight loss [3, 5–7]. Severe cases can present with cerebralirritability, lethargy, recurrent apneas, seizures, and coma [5, 7].Many of these symptoms are non-specific and may promptinvestigations for sepsis, other biochemical or metabolicconditions, maternal drug withdrawal or non-accidental injury[2, 3].
Diagnosis of dilutional hyponatremia should become evidentfrom a focused history, including reviewing maternal oral andintravenous fluid intake and output during labor. Whilstintravenous fluids are normally meticulously documented inmaternal notes, this may not be true of oral fluids ingested bya mother in labor [3]. Oral fluids do contribute to overall fluidbalance and risk of hyponatremia, as highlighted by Moen et al[8]. Diagnosis is made by confirmation of (low) serum sodiumof <130 mmol/L in the neonate, appropriately low urine sodiumand adequate urine output, in conjunction with maternal history.Any neonate with seizures should also have blood glucose,serum calcium and potassium levels assessed as a minimum. Ifthe serum sodium level is persistently low even after first 24 h oflife, it is unlikely to be pure maternal over-hydration and otherdifferential diagnoses should be considered.
Infants with established dilutional hyponatremia should bemanaged in a neonatal unit. Mild to moderate cases withoutcerebral symptoms can be managed with fluid restriction,although breastfed babies may feed on demand [3]. Whereintravenous fluids are required, relatively concentratedglucose solutions may allow adequate fluid restriction. Abolus of 4–6 mL/kg of 3 % NaCl may be useful where theneonate shows cerebral signs, has seizures or serum sodiumlevel is <120 mmol/L [5], followed by close monitoring ofserum sodium levels every 4–6 hourly until normalized.
This discussion would remain incomplete withouthighlighting the dangers that mothersmay face due to peripartumdilutional hyponatremia. In modern obstetric practice,women in labor are encouraged to drink fluids, often water,which may not get documented in nursing / midwiferyrecords [3, 7, 9]. A study of 287 Swedish women in labor atterm found that 61 women (26 %) were hyponatremic(sodium <130 mmol/L) [8]. Sixteen of those 61 women hadreceived >2.5 L of fluid in labor, with 2/3rd of that fluidingested orally. The same study highlighted that total fluidintake of over 2.5 L during labor was associated with anincreased risk of maternal hyponatremia, which influencesuterine contractility, and may be life-threatening [8]. Casestudies have reported excessive fluid intake causingeclampsia-like presentations (confusion, visual disturbances,reduced consciousness and seizures) during labor without aprevious history of hypertension, proteinuria or other pre-eclamptic features [7, 10, 11]. Low-dose epidural regimensused in modern obstetric practice do not necessitate the use of
high volume of intravenous fluids to preserve blood pressure,and fluid management should be judged on an individual basisand given orally where feasible; this would lower the risk ofinadvertent dilutional hyponatremiawith epidural anesthesia [8].
Dilutional hyponatremia is avoidable in most cases bycareful monitoring and meticulous documentation of total fluidintake and output during labor. The Royal College ofObstetricians and Gynecologists, UK in a press releasepublished in 2009 have commented that “researchers warn thatas water load tolerance falls during labor, and increased fluidvolumes can cause hyponatremia, women should not beallowed to drink excessively during labor”.Moen et al. suggestsan input of 300 mL/h or more in labor is associated with risk ofmoderate hyponatremia in mothers [8]. Neonatal teams shouldbemade aware of the risk of dilutional hyponatremia inmotherswhere excessive (oral / intravenous) fluids are administered. Anunexpectedly low sodium level in the neonate soon after birthshould raise suspicion about dilutional hyponatremia secondaryto maternal over-hydration in labor. Increased awareness of thiscondition is associated with an improved outcome andminimizing unnecessary interventions.
Conflict of Interest None.
Role of Funding Source None.
References
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