A 10 year-old boy with a history of enuresis was BIBA to the ED after a first episode generalized tonic-clonic convulsion. He seemed tired in the morning but still attended his inter-school sports competition. While getting ready to compete he collapsed and had a self-limiting seizure (5 minutes duration).
He was afebrile and had GCS 13 (E3 V4 M6) (fluctuating) for about 4 hours without improvement. Pupils were equal and reactive and he had no focal neurological deficits. He vomited 5 times during this time but was clinically euvolemic. His CT head was normal.
He had the following laboratory test results:
PH 7.37
PCO2 42
HCO3 24
Cl 96
Na 124
K 4.1
Glucose 7.1
Lactate 2.7
Answers: 1.
Moderate Hyponatremia (124 mmol/L)
Borderline low chloride — chloride may be lost due to vomiting.
Mildly increased lactate — hyperlactemia is typically found following a seizure, in this case it may actually be normalizing after the first seizure
Mildly increased glucose — glucose is commonly elevated after a brief seizure, or in the early stages of status, due to a catecholamine-mediated ‘stress response’.
Symptoms of hyponatremia do not necessarily correlate well with the degree of hyponatremia. Expected symptoms are typically:
- <125-130 mmol/L – nausea and malaise
- <115-120 mmol/L – headache, lethargy, obtundation, seizures, coma, respiratory arrest, noncardiogenic pulmonary edema.
However, significant symptoms may be found at higher levels depending on the ‘starting concentration’ and the rate of decrease. For instance, worse symptoms are more likely if sodium rapidly drops from 140 mmol/L to 125 mmol/L than if there is a slow decrease from 130 mmol/L to 115 mmol/L.
2.
Serum cortisol 1100 NM (60-420)
TFTs were normal
Osmolality plasma 265 mmol/kg L (275-295)
Spot urine sodium 209 mM
Spot urine osmolality 681 mmol/kg (50-1200)
These results are consistent with the syndrome of inappropriate anti-diuretic hormone secretion (SIADH).
Features of SIADH include:
- Low plasma osmolality
- urine osmolality > plasma osmolality (usually >300-400 mosmol/kg)
- Urine sodium concentration usually >40 meq/L
- Normal acid-base and potassium balance
- Normal renal, liver, adrenal and thyroid function
- Diuretics are not in use
- improves with water restriction
3. The child had started using a nightly nasal spray of desmopressin to treat his enuresis about 4 days prior to his ED presentation. This exogenously administered analogue of ADH resulted in hyponatremia mimicking SIADH, probably exacerbated by increased water intake prior to his sports competition.
Over the next 12-24 hours he had a large diuresis and his laboratory values all normalized. He remained well at discharge.
Correction of symptomatic hyponatremia :
There may be a reluctance to administer hypertonic saline due to the fear of the dreaded complication of cerebral pontine myelinolysis (perhaps better called osmotic demyelination syndrome – more than the pons may be involved). This complication may occur with the excessive correction of hyponatremia in patients that have chronic severe hyponatremia (e.g. Na 110-115 for at least 2 days).
Chronicity is important because the brain adapts to hyponatremia by extruding intracellular osmolytes to guard against cerebral edema. The adaptation process occurs over about 2 days, and until it occurs correcting hyponatremia is safe.
In acute symptomatic hyponatremia the risk of osmotic demyelination syndrome from rapid correction of hyponatremia is minimal.
Hyper tonic saline should be administered to patients with significant symptoms (e.g. altered mental state, seizures, coma, noncardiogenic pulmonary edema) of hyponatremia, regardless of the sodium level. Usually the aim is to increase the sodium by 1-1.5 mmol/h for 2 or 3 hours, and a small rise can markedly improve symptoms.
Formula to figure how much hypertonic saline to give = 3 ml per Kg of ” X percentage saline” will increase Na by X.