Presentation on theme: "Hyponatremia in neonatology Kirsten L Brunsvig 03.05.10."— Presentation transcript:
Hyponatremia in neonatology Kirsten L Brunsvig
Sodium Dominating cation in the ECF Princible determinant for extracellular osmolality –Necessary for the maintenance of intravascular volume. Unique among electrolytes because water balance, not sodium balance, usually determines its concentration.
Total body water Distribution of body water –Extracellular fluid Intravascular Interstitial –Intracellular fluid 40 SA –Total body water = 75% of body weight –ECF = 45 % of total body water 27 SA –Totale body water = 80% of body weight –ECF = 70% of total body water
Water loss Preterm infants have greater weight loss (10- 15% vs 5%), associated with increased diuresis, comparet to term infants. Water loss: –Kidneys –Skin Large insensible water loss, especially in the ELBW infants with very thin skin –Lungs Decreases with increasing GA, but less important than skin water loss. –Other (stoll, gastric drainage, thoracostomy)
[Na] regulation [Na] thirst and ADH water intake/retention and normalization of [Na] [Na] decreased ADH water loss and normalization of [Na] However, volume depletion takes presendence over osmolality and causes increase in ADH even if the patient has hyponatremia. Also, excretion of Na in the kidneys is not regulated by osmolality, but plasma volume and a variety of regulatory systems.
Mechanism of hyponatremia Dilutional (most common in the neonate) Excessive Na+ loss Na+ deficiency
Differential diagnoses Volume overload –Too much volume given –Congestive heart failure –Renal/liver failure –Paralysis with fluid retention –Diluted formulas
Differential diagnosis Increased Na+ loss –VLBW: renal tubular Na+ losses high –Salt-losing nephropathies –GI-losses –Skin losses –3rd space (e.g. NEC) –Adrenal insufficiency Mineralocorticoid deficiency => Na, K, metabolic acidosis and shock
Differential diagnosis Inadequate Na+ intake –Normal: 2-4mmol/kg/j Drug induced –Diuretics –Indomethacine can lead to H2O retention –Opiates, carbamazepine, barbiturates can cause SIADH –Mannitol/hypertonic glucose can cause hyperosmolarity with salt wasting.
Differential diagnosis SIADH = syndrome of inappropriate ADH secretion –CNS disorders (IVH, hydrocephalus, asphyxia, meningitis) –Lung diseases –Critically ill preterm and term neonates
Patient with hyponatremia Important questions –Seizures? (<120mmol/l) –urgency! –How much Na and free water is the patient receiving? –Weight gain or weight loss? –Urine output? –Renal salt-wasting medication?
Clinical examination Complete examination Seizures? Oedema? Decreased skin turgor/ dry mucous membranes as signs of dehydration? Weight gain/loss Fluid intake/output over 24hours
Further tests S-Na, S-Osmolality U-Na, U-osmolality, U-specific gravity S-electrolytes, S-creatinin, S-total protein to evalue renal function
Treatment Seizures: emergency –NaCl 3% –Total body Na-deficit/2 over hours Rapid corrections may result in brain damage. [Na] deficit x weight (kg) x 0.6 Total body water = 60-75% of weight Usually use 60% to minimize the likelihood of overly rapid correction [Na] deficit = [Na] desired – [Na] patient
Treatment Volume overload –Fluid restriction usually by 20ml/kg/d –S-NA every 6-8h –Treat underlying cause Inadequate intake of Na –2-4 mmol/kg/d, increased in premature Increased Na-losses –Treat underlying cause –Increase Na-intake
Treatment Drug induced (e.g. Furosemid) –Increase intake may be required –Indomethacin Treated with fluid restriction SIADH –Restrict fluids, –Furosemide can be tried.
Long term prognosis Hyponatremia has been associated with adverse neurological developmental outcomes. –Increased risk of cerebral palsy –Increased risk of hearing loss Large variations in Na have also been found associated with impaired functional outcomes at 2 years.