Hyponatremia is excess of water relative to sodium and almost always due to increased ADH.
- SIADH: inappropriate increase (Conrad: any lung, brain, drugs and cancer)
- SADH: appropriate increase such as in hypovolemia or hypervolemia with decreased effective arterial volume
Evaluation of hyponatremia begins with the following laboratory datas
- Plasma osmolality: to determine if the patient really has hyponatremia
- Pseudohyponatremia: will be high in patients with osmotic substances that draw water to dilute the concentration of sodium
- Urine osmolality: useful in limited circumstances -> Uosm will be < 100
- malnutrition(decrease solute intake)
- primary polydipsia(increase water intake)
- Urinary sodium: used to determine the kidney’s concentrating capabilities(basically how the body is responding to this state, or did it cause it)
- Normally should be low < 20
Continue reading “Hyponatremia: Primary polydipsia”
Symptoms and signs:
- GI: abdominal pain, constipation, anorexia, lead lines on gum(Burton’s lines)
- Neurological : headache, neurocognitive deficits(forgetfullness, encephalopathy, behavior problems, language regression; childrens especially susceptible due to incomplete BBB maturation), motor/sensory peripheral neuropathies(stocking-glove pattern ddx with GBS, DM… etc, extensor weakness)
- Hematologic:al microcytic anemia(99% bound to erythrocytes and can disrupt heme synthesis)
- Nonspecific signs: fatigue, irritability, insomnia,
- Chronic s/s: hypertension, nephropathy
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Pathogenesis: Increased NO generation in splanchnic circulation secondary to portal HTN. This causes systemic vasodilation, which reduces PVR and BP, causing renal hypoperfusion. In turn, compensatory mechanisms such as RAAS, SANS and ADH increase water and sodium retention worsen volume overload.
Risk factor: Severe cirrhosis with portal HTN and edema
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Anaphylactic: Rapid onset(seconds to minutes) of shock, respiratory distress(difficulty breathing with wheezing or bronchospasm), angioedema, urticaria and hypotension. Occurs in those that are IgA deficient, due to the production of anti-IgA IgG Abs.
Treatment: Stop transfusion, antihistamines, steroids and IM epi. +/- hemodynamic support with vasopressor and MV.
Prevention: Future transfusion with IgA-deficient plasma and washed red cell products.
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