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A child, seizures and sodium
1. A case, many questions, and hopefully a few answers… Chris NicksonEmergency Registrar, PMH19 August 2010
2. The Case 10 year-old boy, previously well except for a history of enuresis BIBA after a first episode generalized tonic-clonic convulsion tired in the morning but still went to school sports competition While getting ready to compete he collapsed and had a self-limiting seizure (5 min)
3. In the ED Afebrile GCS 13 (E3 V4 M6) (fluctuating) for about 4 hours without improvement PERL, no focal neurological deficits vomited x5, but clinically euvolemic CT head was normal After the scan he had another self-limiting seizure (2 min)
7. But… Symptoms correlate poorly with degree of hyponatremia May vary depending on: starting sodium concentration rate of decrease
8. For instance… A RAPID drop in Na of 140 to 125SYMPTOMS A SLOW drop in Na of 130 to 115NO SYMPTOMS
9. Question –How can we find out if the Na 125 mmol/L is important in this case?
10. Fix it and see what happens! 3mL/kg of 3% saline over 30 minutes Immediately following this infusion he was alert with a GCS 15 and had no further vomiting His only complaint was a mild headache that improved after paracetamol
13. Weighing the risks Most likely acute hyponatremia The brain adapts extrudes intracellular osmolytes to guard against cerebral edema Occurs over about 2 days Risk of osmotic demyelination syndrome is minimal until adaptation occurs
14. Weighing the risks Give hypertonic saline to patients with significant symptoms of hyponatremiaregardless of how low the sodium is AMS Seizures Coma Noncardiogenic pulmonary edema
16. Rate of correction Aim to increase sodium by1-1.5 mmol/h for 2 or 3 hours a small rise can markedly improve symptoms Sodium should not be increased by more than:12mmol/Lover 24h18 mmol/L over 48hLower rates are advised for high risk patients
19. Syndrome of Inappropriate ADH Secretion Low plasma osmolality urine osmolality > plasma osmolality(usually >300-400 mosmol/kg) Urine sodium usually >40 meq/L Normal acid-base and potassium balance Normal renal, liver, adrenal & thyroid function Diuretics are not in use improves with water restriction
21. ADH (aka vasopressin) action promotes water reabsorption from the collecting ducts of the kidney activates the vasopressin V2 receptor aquaporin-2 water channels translocatefrom intracellular sites to the luminal membranes of the principal cells end result is concentrated ‘water-poor’ urine and dilute ‘water-rich’ blood
23. Causes of SIADH CNS disorders Pulmonary disorders Ectopic ADH secretion by a tumour –lung cancers (especially small cell lung cancers), others less common Major surgery Many drugs
24. In fact, the patient has none of these!Question -What can mimic SIADH?
27. They all lived happily ever after… A nightly nasal spray of desmopressin was started 4 daysprior for nocturnal enuresis His parents encouraged him to ‘drink lots of water’ before competing Over the next 12-24 hours he had a large diuresis, his laboratory values all normalized and he remained well
29. Robson WL et al. The comparative safety of oral versus intranasal desmopressin for the treatment of children with nocturnal enuresis.J Urol. 2007 Jul;178(1):24-30. Hyponatremia resulting from treatment of enuresis with desmopressin No reports in 21 clinical trials 48 case reports (all nasal route) Post-marketing safety data: 145 nasal, 6 oral cases Risk factors High fluid intake, age <6 years, high dose, other medications (e.g. anticholinergics)
A 26-year-old man with a history of chronic alcohol abuse presented with dysarthria, lethargy, and horizontal nystagmus. Results of a clinical examination and blood tests were otherwise normal, including a serum sodium level of 137 mmol per liter and serum osmolality of 287 mOsm per kilogram. Over the next 5 days, spastic quadriparesis and pseudobulbar palsy developed. Magnetic resonance imaging of the brain revealed central pontine myelinolysis with a well-defined lesion in the pons of low T1-signal intensity (Panel A, arrow) and high T2-signal intensity (Panel B, arrow). There was sparing of the ventral lateral and cortical spinal tracts and no space-occupying effect or distortion of the adjacent fourth ventricle. Central pontine myelinolysis is a noninflammatory, demyelinating condition commonly associated with the rapid correction of hyponatremia. However, it was originally described in those with chronic alcoholism and in malnourished persons. There is no specific treatment for central pontine myelinolysis, and this patient had no clinical improvement 6 months later.
Hereditary vasopressin receptor abnormalities (‘nephrogenic SIADH’)Cerebral salt wasting (classically in neurological disorders such as subarachnoid haemorhage – it resembles SIADH but the patient is hypovolemic and is responsive to normal saline rather than water restriction)Exogenously administered vasopressin agonists such as vasopressin, desmopressin and oxytocin.
Any CNS disorder –stroke, hemorrhage, infection, trauma, and psychosisPulmonary disorders –lung cancer, pneumonia, bronchiolitis, pneumothorax, asthma, etc.Ectopic ADH secretion by a tumour –lung cancers (especially small cell lung cancers), and less commonly:cancer of the duodenum or pancreas, head and neck cancer, and olfactory neuroblastomasMajor surgery –especially thoracic or abdominal.Drugs –many drugs, including:SSRIs, ecstasy, antipsychotics like haloperidol, antiepileptics (e.g. valproate and carbamazepine), MAOIs, NSAIDs, opiates, chemotherapy (e.g. cyclophosphamide, vincristine), amiodarone, bromcriptine, ciprofloxacin…
Hereditary vasopressin receptor abnormalities (‘nephrogenic SIADH’)Cerebral salt wasting (classically in neurological disorders such as subarachnoid haemorhage – it resembles SIADH but the patient is hypovolemic and is responsive to normal saline rather than water restriction)Exogenously administered vasopressin agonists such as vasopressin, desmopressin and oxytocin.
Hereditary vasopressin receptor abnormalities (‘nephrogenic SIADH’)Cerebral salt wasting (classically in neurological disorders such as subarachnoid haemorhage – it resembles SIADH but the patient is hypovolemic and is responsive to normal saline rather than water restriction)Exogenously administered vasopressin agonists such as vasopressin, desmopressin and oxytocin.
Hereditary vasopressin receptor abnormalities (‘nephrogenic SIADH’)Cerebral salt wasting (classically in neurological disorders such as subarachnoid haemorhage – it resembles SIADH but the patient is hypovolemic and is responsive to normal saline rather than water restriction)Exogenously administered vasopressin agonists such as vasopressin, desmopressin and oxytocin.
