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Careful Sodium Correction and Osmotic Demylination Syndrome

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Patients who present with symptomatic hyponatremia (usually the Na+ is lower than 120mmol/L) should be treated with hypertonic saline (HTS) and then fluid restricted. The goal of HTS therapy is to reverse the symptoms and raise the plasma Na+ by 5mmol per liter. What then? It depends on the circumstance – acute or chronic, high risk or low risk. This tutorial addresses the issue of rate of correction of plasma sodium, explains why you need to modify that rate in high risk patients (very low sodium, alcoholics, the malnourished, those with liver disease and profound hypokalemia). The reason why you need to be careful is because of concerns regarding the development of Central Pontine Myelinolysis – usually known now as Osmotic Demyelination Syndrome.

I wish to acknowledge the help of my colleagues Dr Bairbre McNicholas, Dr Peter Moran, Prof. John Bates, Dr Leo Kevin and Ms Aoife Boyle for clarifying my thoughts on this topic.

Click on this link for the 2014 European Guidelines (and a good review of the topic).

The Syndrome of Antidiuresis (SIADH)

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This tutorial is about the Syndrome of Inappropriate Diuresis. SIAD also known as SIADH is a form of hypotonic hyponatremia associated with iso- or hypervolemia, high urinary osmolality and high urinary sodium. Traditionally this is associated with high levels of circulating vasopressin (antidiuretic hormone – ADH), that may be associated with sepsis, acute critical illness, pneumonia or mechanical ventilation. However, SIAD is also associated with a variety of brain injuries, drugs (SSRIs and anticonvulsants) and a variety of cancers.

Treatment of symptomatic SIAD is with hypertonic saline (150ml of 3% over 20 minutes). Chronic or asymptomatic SIAD is treated with fluid restriction (determined by the Furst equation uNa + uK/pNa – if the result is less than1 the patient is suitable for fluid restriction).

Alternative inexpensive therapies include Urea (30 to 60mg per day), salt tablets plus frusemide or demeclocycline.

Vaptan agents, the block the V2 receptors, appear to be effective for long term therapy. Tolvaptan is available commercially but quite expensive for the majority of patients.

Cerebral salt wasting is associated with subarachnoid hemorrhage. It shares the same blood and urinary profile as SIAD(H) but is associated with hypovolemia. The disorder is self limiting and is treated with isotonic fluids.

Mechanisms of Hypoxemia – Part 1

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If you treat patient with hypoxic respiratory failure you really need to understand what is going on in their lungs. These two tutorials look at diseases of the lung parenchyma and how blood flow and gas flow interact. The first tutorial focuses on alveolar oxygen content and how it is impacted by disease. I explain the concept of airway closure (which will will revisit in detail several times during this series), stale alveolar gas, the various causes of atelectasis and the six S approach to figuring out what is going on in the airways (Slimy, Soggy, Sticky, Stiff, Squished, Shunty).

Identifying and Quantifying Hypoxemia

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The next part of the course is all about hypoxic respiratory failure. To treat hypoxemia you must understand it. The purpose of this sequence of tutorials is to lead up to discussions on CPAP and PEEP and provide a platform for understanding Pressure Controlled Modes of Ventilation. The first tutorial looks at oxyhemoglobin saturation, why the oxyhemoglobin dissociation curve is essential knowledge for the practicing clinician, how pulse oximeters work and how to quantify hypoxemia (A-aO2 gradient and PaO2/FiO2 ratio).