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Similar to 20221030 Hyponatremia.pptx
20221030 Hyponatremia.pptx
- 1. Journal reading 報告人: 住院醫師蔡丞峻 Date:2022/10/30
- 3. • defined asa serum sodium level of less than 135mEq/L • Approximately 20% of people who are older than 65 years of age have hyponatremia as well as 35%of patients who are hospitalized,30% of patients with heart failure, and 50% of patients with cancer or cirrhosis. Introduction
- 4. • English-language studiesof pathogenesis, clinical presentation, diagnosis, and management of adult hyponatremia published between January 2010 and December 2021 • 224 publications identified during the search, 77 were included and consisted of 33 clinical trials, 14 systematic reviews,26 reviews, 1meta-analysis, and 3 clinical practice guidelines. Methods
- 5. • Osmolality – isa measurement of the number of particles in a solution. • Tonicity (Effective Osmolality) – refers to how much the particles in a solution pull water across a semi- permeable biological membrane. This depends on the number of effective osmoles in the solution. Pathogenesis
- 6. • Most commonly,hyponatremia is associated with low osmolality and tonicity (<270 mOsm/kg) because levels of glucose and urea are normal. • Water homeostasis depends on receptors residing along the anterior wall of the brain’s third ventricle that respond to serum tonicity and angiotensin II by regulating water intake (thirst) and water excretion (release of vasopressin) Pathogenesis
- 7. • Manifestations ofhyponatremia depend on the rapidity of development, duration, and severity • Symptoms of hyponatremia range from mild and nonspecific(weakness, nausea, headache) to severe and life- threatening (vomiting, somnolence, seizures, cardiorespiratory distress) • Symptoms are more common in patients with acute hyponatremia (developing within <48 hours) than in those with chronic hyponatremia (developing over >48 hours) because of brain volume adaptation Symptoms of Hyponatremia
- 8. • Brain volumeadaptation – a process that corrects hypotonicity-induced brain swelling – brain swelling from hypotonicity induced water entry into brain cells causes intracranial hypertension – Prompt electrolyte and water loss from brain cells occurs (known as rapid adaptation to hypotonic water entry) – Brain volume normalization is completed within approximately 2 days through the loss of organic osmolytes (eg, myoinositol, glutamate) and water from brain cells (slow adaptation) Symptoms of Hyponatremia
- 9. • Brain volumeadaptation –Brain volume adaptation to hyponatremia increases the risk of osmotic demyelination –Osmotic demyelination syndrome (ODS) • Depletion of organic osmolytes predisposes individuals to astrocyte injury, disruption of the blood-brain barrier, and myelinolysis • overly rapid correction of the serum sodium level by greater than 12mEq/L, but rarely after correction by 10mEq/L or less • can be temporary, permanent,or progressive;and parkinsonism, locked-in syndrome, quadriparesis, and death. Symptoms of Hyponatremia
- 10. • Hypotonic hyponatremiacan be diagnosed after excluding hyperglycemia and other causes of non-hypotonic hyponatremia • History – an acute or chronic illness, medication use, alcohol and illicit drug misuse, and recent surgery. – fluid intake and loss, changes in body weight, and past episodes of hyponatremia Diagnosing Hyponatremia
- 11. • Physical Examination –facilitates the classification of hypovolemic, euvolemic, or hypervolemic hyponatremia • Lab – Sodium level in urine and the urine osmolality or urine specific gravity Diagnosing Hyponatremia
- 13. • Syndrome ofinappropriate antidiuresis (SIAD) – defined by clinical euvolemic hyponatremia; inappropriately concentrated urine (osmolality>100 mOsm/kg and urine specific gravity >1.003); high urine sodium level (>30mEq/L); and absence of thyroid, adrenal, or kidney dysfunction – hyponatremia without hypovolemia • the etiology was approximately equally divided between patients with hypervolemic hyponatremia(51% for heart failure and 42%for cirrhosis) and patients with euvolemic hyponatremia (95%for SIAD) • Antidepressants are the most commonly implicated drugs in patients with SIAD. Selective serotonin reuptake inhibitors induce SIAD in up to 32%of patient. Thiazides induce hyponatremia in up to 30% of patients. Diagnosing Hyponatremia
- 14. • Presence ofsymptoms determines the intensity of treatment • Emergency Treatment – Patients with severe manifestations(somnolence, seizures, cardiorespiratory distress) and those with moderately severe symptoms (vomiting, confusion) – Immediate treatment may include airway intubation, supplemental oxygen, ventilatory support, or anticonvulsant therapy. Admission to an intensive care unit may be necessary for monitoring of vital signs, central nervous system status, urine output, and fluid administration. – Current guidelines recommend correction of the serum sodium level by 4mEq/L to 6mEq/L within 1 to 2 hours, which can reverse hyponatremic encephalopathy – 100-mL or150-mL dose of 3% sodium chloride, administered over 10minutes or 20minutes and repeated 2 to 3 times Treatment
- 15. • Emergency Treatment –the serum sodium level should not be increased by more than 10 mEq/L within the first 24 hours and by 18 mEq/L within the first 48 hours – In patients at high risk of osmotic demyelination, the serum sodium level should not be increased by more than 8mEq/L within any 24-hour period Treatment
- 16. • Emergency Treatment –bolus infusion of 3% sodium chloride vs conventional treatments consisting of continuous infusion of 3% sodium chloride • Osmotic demyelination did not occur in any of the 3 studies. • In summary, bolus infusion attained the target change in serum sodium level faster, but was associated with higher rates of overly rapid correction and need for relowering therapy for serum sodium level – To counter risk of overly rapid correction, desmopressin can be used, anticipating water diuresis or in response to water diuresis – the recommended dose is 2 μg to 4 μg parenterally every 6 hours to 8 hours. – If signs of osmotic demyelination appear, immediate relowering of the serum sodium level should be pursued – completing emergency treatment of hyponatremia, the underlying cause of hyponatremia should be addressed. Treatment
- 17. • Non-Emergency Treatment –Regardless of the cause and symptoms, patients with a serum sodium level of less than 120 mEq/L require hospitalization and close monitoring of the serum sodium level during treatment, initially at least every 8 hours. – Patients with mild or moderate hyponatremia and only mild symptoms can be treated as outpatients unless the underlying cause requires hospitalization Treatment
- 18. • Hypovolemic Hyponatremia –Isotonic saline or other crystalloid solution is used for parenteral volume repletion. Sodium-rich broth and sodium chloride tablets can be used for oral treatment. – Uncertainty about the presence of hypovolemic hyponatremia can be addressed by infusing 1 L to 2 L of saline and assessing urine flow and the serum sodium level – In patients with thiazide-induced hyponatremia, drug replacement with loop diuretics (rarely associated with hyponatremia)may be required. Treatment
- 19. • Euvolemic Hyponatremia –most common causes of SIAD are malignancies, central nervous system disorders, and medications – Therapeutic measures for SIAD include fluid restriction, increased solute intake (sodium chloride, protein, urea), and vaptans; isotonic saline worsens the serum sodium level and is not indicated – The sum of urine sodium and potassium levels divided by the serum sodium level can guide stringency of fluid restriction. A ratio of less than 1 calls for mild fluid restriction (<1.5 L/d), whereas higher ratios require severe fluid restriction (<1 L/d). Treatment
- 20. • Euvolemic Hyponatremia –Oral or enteral urea therapy (15-60g/d) increases the serum sodium level by promoting water diuresis – Urea therapy can be substituted for sodium chloride tablets and furosemide or vaptans – Vaptans (vasopressin receptor antagonists) block the vasopressin receptor 2 located in the collecting duct and promote water diuresis – Long treatment is not recommended because of interactions with drugs also metabolized by the CYP3A4 hepatic isoenzyme Treatment
- 21. • Hypervolemic Hyponatremia –Fluid restriction, loop diuretics, and potassium repletion are treatments for patients with cirrhosis and mild hyponatremia and also in patient with heart failure – Heart failure requires additional adjustment of medications to attain optimal hemodynamics. – Advanced liver disease is associated with more severe hyponatremia and with hypotension and oliguria, diuretics and antihypertensives should be with drawn; potassium levels should be increased; and midodrine, albumin, hypertonic saline, Treatment
- 22.
Editor's Notes
- #6 For example: Sodium is an effective osmole, because it cannot cross the semi-permeable membrane. Therefore, sodium will tend to pull water across the membrane. If you bolus a patient with concentrated sodium solutions, this affects the volume of fluid in their cells.
- #7 For example: Sodium is an effective osmole, because it cannot cross the semi-permeable membrane. Therefore, sodium will tend to pull water across the membrane. If you bolus a patient with concentrated sodium solutions, this affects the volume of fluid in their cells.
- #8 acute hyponatremia (developingin <48 hours) than in those with chronic hyponatremia (developingover >48 hours) because of brain volume adaptation
- #9 acute hyponatremia (developingin <48 hours) than in those with chronic hyponatremia (developingover >48 hours) because of brain volume adaptation
- #10 因此橋腦中央髓鞘溶解症(CENTRAL PONTINE MYELINOLYSIS-CPM)逐漸被滲透壓性去髓鞘症候群(Osmotic demyelination syndrome-ODS
- #11 Hyperglycemia Contrast Mannitol => SOsm
- #12 Hyperglycemia Contrast Mannitol => SOsm
- #14 Hyperglycemia Contrast Mannitol => SOsm
- #17 dysarthria, dysphagia, tetraparesis, behavioral disturbances, lethargy, confusion, disorientation, and coma
- #19 Thiazide diuretics are more likely to cause hyponatremia because their major effect is in the distal tubule, the major diluting site of the kidney. In contrast, the main effect of loop diuretics is in the ascending limb of the loop of Henle, which is a less important diluting site with less effect on maximum dilution
- #20 Thiazide diuretics are more likely to cause hyponatremia because their major effect is in the distal tubule, the major diluting site of the kidney. In contrast, the main effect of loop diuretics is in the ascending limb of the loop of Henle, which is a less important diluting site with less effect on maximum dilution
- #21 Thiazide diuretics are more likely to cause hyponatremia because their major effect is in the distal tubule, the major diluting site of the kidney. In contrast, the main effect of loop diuretics is in the ascending limb of the loop of Henle, which is a less important diluting site with less effect on maximum dilution
- #22 Thiazide diuretics are more likely to cause hyponatremia because their major effect is in the distal tubule, the major diluting site of the kidney. In contrast, the main effect of loop diuretics is in the ascending limb of the loop of Henle, which is a less important diluting site with less effect on maximum dilution