A child, seizures and sodium
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A child, seizures and sodium

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A case of seizures in a child, with many questions and a few answers...

A case of seizures in a child, with many questions and a few answers...

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  • 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.

A child, seizures and sodium A child, seizures and sodium Presentation Transcript

  • A case, many questions, and hopefully a few answers…
    Chris NicksonEmergency Registrar, PMH19 August 2010
  • 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)
  • 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)
  • Lab results
    UECNa 125K 4.1Urea 3.7    Cr 49
    FBC normal
    LFTs normal
    VBGpH7.37 PCO2 42   HCO3 24    Cl 96    glc 7.2   lac 1.9
  • Question -Is the sodium of 125 mmol/L likely to be significant?
  • Symptoms of hyponatremia
    UpToDate says typical symptoms of hyponatremia are:<125-130 mmol/L – nausea malaise
    <115-120 mmol/L – headachelethargyobtundationseizurescomarespiratory arrest noncardiogenic pulmonary edema
  • But…
    Symptoms correlate poorly with degree of hyponatremia
    May vary depending on: starting sodium concentration rate of decrease
  • For instance…
    A RAPID drop in Na of 140 to 125SYMPTOMS
    A SLOW drop in Na of 130 to 115NO SYMPTOMS
  • Question –How can we find out if the Na 125 mmol/L is important in this case?
  • 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
  • Question -Was it safe to give hypertonic sodium?
  • What we fear…Fleming JD, Babu S. N Engl J Med 2008; 359:e29
  • 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
  • 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
  • Question -How rapidly should hyponatremia be corrected?
  • 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
  • More Lab tests…
    Serum cortisol 1100 nM (60-420)TFTs normalOsmolality plasma 265 mmol/kg L (275-295)Spot urine sodium 209 mMSpot urine osmolality 681 mmol/kg (50-1200)
  • Question -What do these results suggest?
  • 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
  • Question -How does ADH cause hyponatremia?
  • 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
  • Question -But SIADH is not a diagnosis…What is the cause?
  • 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
  • In fact, the patient has none of these!Question -What can mimic SIADH?
  • SIADH mimics
    Hereditary vasopressin receptor abnormalities (‘nephrogenic SIADH’)
    Cerebral salt wasting
    Exogenously administered vasopressin agonists
    Vasopressin
    Desmopressin
    Oxytocin
  • The Answer…Remember the history of enuresis?
  • 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
  • Question -Is hyponatremia a serious risk when treating enuresis with desmopressin?
  • 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)
  • THE ENDhttp://lifeinthefastlane.com