Hyponatremia & Hypernatremia Year 2 PDF

RCSI Royal College of Surgeons in Ireland Coláiste Ríoga na Máinleá in Éirinn Hyponatraemia - Hypernatraemia Department of Medicine Dr. Shohdan Mohamed Osman Clinical Lecturer and Nephrologist LEARNING OUTCOMES 1. Define hyponatraemia and hypernatraemia 2. Explain the pathophysiology of hyponatra...

RCSI Royal College of Surgeons in Ireland Coláiste Ríoga na Máinleá in Éirinn Hyponatraemia - Hypernatraemia Department of Medicine Dr. Shohdan Mohamed Osman Clinical Lecturer and Nephrologist LEARNING OUTCOMES 1. Define hyponatraemia and hypernatraemia 2. Explain the pathophysiology of hyponatraemia and hypernatraemia 3. List the cardinal signs and symptoms of hyponatraemia and hypernatraemia 4. Explain how each sign and symptom is caused in hyponatraemia and hypernatraemia 5. Develop a differential diagnosis for hyponatraemia and hypernatraemia 6. Outline the overarching principles of investigation and management for hyponatraemia / hypernatraemia DEFINITIONS Hyponatraemia is defined as a serum sodium (Na+) concentration of < 135 mmol/L Hypernatraemia is defined as a serum sodium (Na+) concentration of > 145 mmol/L Osmolality is defined as the concentration of a solution expressed as the total number of solute particles per kilogram Osmolarity is defined as the concentration of a solution expressed as the total number of solute particles per litre – Osmolarity formula = 2(Na+) + 2(K+) + Glucose + Urea ROLE OF SODIUM IN THE BODY Sodium is a key determinant of osmolality and fluid balance Although the serum sodium is abnormal in hypo/hypernatremia, these conditions primarily indicate an abnormality with of water balance. This may or may not be accompanied by changes in sodium balance Hyponatremia = too much water / Hypernatremia = too little water Both of these conditions can manifest at any level of total body sodium TOTAL BODY WATER (TBW) TBW consists of two main compartments: extracellular fluid (ECF) and intracellular fluid (ICF), separated by cell membranes.​ ECF TOTAL BODY WATER (TBW) TBW consists of two main compartments: extracellular fluid (ECF) and intracellular fluid (ICF), separated by cell membranes. Cell membranes allow the passage of water but not electrolytes, maintaining different solute compositions Extracellular Fluid (ECF) In normal adults, ECF volume is approximately 33-40% of TBW. ECF volume determined by sodium and water content in ECF. Rest of TBW (67%) is in cells. Regulation of ECF volume: Mediated by urinary sodium excretion. Controlled by renin-angiotensin-aldosterone and sympathetic systems for sodium retention. Natriuretic peptides promote sodium excretion. TOTAL BODY WATER (TBW) Total Body Water (60% of weight in men, 50% in women) 2/3 Intracellular fluid (ICF) 1/3 Extracellular fluid (ECF) ¼ Intravascular Fluid ¾ Interstitial Fluid  TOTAL BODY WATER (TBW) - E.G.- 80 KG MALE Total Body Water (60% of weight in men, 50% in women) 48 L 2/3 Intracellular fluid (ICF) 1/3 Extracellular fluid (ECF) 32.2 L 15.8 L ¼ Intravascular Fluid ¾ Interstitial Fluid 3.95 L 11.85 L  PLASMA OSMOLALITY Plasma osmolality is a measure of solute concentration Determined by the ratio of plasma solutes to plasma water Primarily influenced by sodium salts, with contributions from potassium, calcium, glucose, and urea Normal Plasma Osmolality (Posm): 275-290 mosmol/kg Equation for estimating Posm: Posm = 2 x [Na] + [Glucose] + [Urea] Glucose and urea have a significant impact when markedly elevated (e.g., uncontrolled diabetes or reduced kidney function) Osmolality Across Membranes: Plasma and ECF osmolality are similar to intracellular osmolality due to water permeability of cell membranes. ECF ICF ICF ECF ROLE OF SODIUM IN THE BODY Extreme variation in osmolarity causes cells to shrink or swell, damaging or destroying cellular structure. The overall mass of Na+ is under aldosterone regulation (manipulates Na+ retention in the kidney), whereas the Na+ concentration in plasma is under antidiuretic hormone (ADH) regulation (manipulates H20 retention in the kidney). Thus, low Na+ concentrations do not necessarily mean that total Na+ mass is low. In chronic heart failure, osmolarity can be low, yet Na+ mass can be high because of both excess water and Na+ in the ECF, with greater increases in total body water than in Na+ mass.  Key concept: Body osmolality and fluid volume are regulated by different mechanisms Osmoreceptors in hypothalamus detect rises in PATHOPHYSIOLOGY osmolality and release ADH Baroreceptors: assess vascular fullness or total body water Osmoreceptors and baroreceptors in a tug of war Water content controlled by: INTAKE: Thirst (Consumption of H20/sodium is regulated by CNS stimulation of thirst and salt craving), begins at a plasma osm of ~285mOsm/kg OUTPUT: Kidneys, excretion is regulated hormonally at the kidney. Antidiuretic hormone(ADH)/Arginine Vasopressin (AVP)- key player, directly controls water excretion by the kidneys. Secreted from posterior pituitary. ADH binds to V2 receptors in the kidney and stimulates insertion of aquaporins into the cell membrane of collecting ducts, increases water reabsorption, and concentrates excreted urine. Other factors influencing ADH release: Angiotensin II (stimulates) Natriuretics (inhibits) Ethanol (inhibits)- excessive diuresis- why we want salty food when drunk HYPONATRAEMIA SYMPTOMS AND SIGNS – HYPO NATRAEMIA Acute Hyponatremia Symptoms: Nausea, malaise, headache, lethargy, obtundation, seizures, coma, and respiratory arrest in severe cases. Chronic Hyponatremia Symptoms: Fatigue, nausea, dizziness, gait disturbances, forgetfulness, confusion, lethargy, and muscle cramps. Signs of Hyponatremia: May include altered mental status, hypothermia, hyperreflexia, and signs of brain herniation in severe cases. Neurological signs and symptoms due to osmotic injury to neurons: Confusion, lethargy, headaches, coma, seizures Influence of Cause and Volume Status: The specific symptoms and signs depend on the underlying cause (water retention, solute loss) and the patient's volume status. SIGNS AND SYMPTOMS DUE TO - HYPOVOLAEMIA Can cause: Dry mucous membranes Reduced skin turgor Hypotension Orthostatic hypotension Reduced urine output Concentrated urine SIGNS AND SYMPTOMS DUE TO - HYPERVOLAEMIA Can cause: – Ascites / Anasarca. – Peripheral / leg oedema. – Puffy facial features (nephrotic syndrome). – Raised JVP. – S3 heart sound. – Bi-basal crackles on lung auscultation due to peripheral oedema. – Breathlessness SIADH: SYNDROME OF Na INAPPROPRIATE ADH Osmoreceptors Detect Na+ Levels: Special sensors in the hypothalamus (osmorceptors) detect changes in sodium levels (osmolality). ADH Release: When sodium levels are high or blood volume is low, these sensors signal the release of Antidiuretic Hormone (ADH) from the posterior pituitary gland. Causes of Low Blood Volume: Low blood volume can result from actual fluid loss (e.g., dehydration) or apparent loss (e.g., congestive heart failure, which reduces blood vessel pressure). This activated barorceptors which then stimulate the release of ADH ADH Promotes Water Retention: ADH causes the kidneys reabsorb water, reducing urine output. Result: This excess water retention dilutes the concentration of sodium in the blood, leading to hyponatremia.  SIADH: SYNDROME OF INAPPROPRIATE ADH Definition: Disorder of impaired water excretion caused by excess of antidiuretic hormone (ADH), characterised by a euvolaemic hypotonic hyponatraemia. Pathophysiology: ADH secretion leads to concentrated urine and reduced urine volume. In SIADH, water ingestion does not adequately suppress ADH, leading to continued water retention, which dilutes plasma sodium concentration. CNS insult Malignancies Drugs Hypothyroidism Stroke, haemorrhage, Ectopic ADH Thiazide diuretics, pituitary pathology, production by SSRIs. trauma, infection tumour, small cell Carbamazepine,, lung cancer classically ciprofloxacin **Need to out rule adrenal insufficiency and hypothyroidism to make this diagnosis SIADH: SYNDROME OF INAPPROPRIATE ADH Clinical Presentation: SIADH should be suspected in patients with hyponatremia, hypoosmolality, and urine osmolality above 100 mosmol/kg. Management Overview: The primary approach includes fluid restriction and addressing the underlying cause. LESS COMMON CAUSES OF HYPONAETREMIA Beer potomania Tea and toast syndrome Primary (pyschogenic) polydipsia Excessive beer Low solute diet common to Abnormal thirst leading to drinking elderly people who are unable excessive intake of water, often Beer contains a low to cook for themselves and seen in psychiatric disorders solute intake depend on tea and toast Drinking more water daily than Solutes are required Solutes are required to facilitate kidney can manage to excrete to facilitate free water free water excretion excretion DIFFERENTIAL – HYPO NATRAEMIA Differential really depends on classifying your patient’s osmolarity and fluid status first. INVESTIGATIONS – HYPO NATRAEMIA Assess the degree of hyponatraemia in the serum INVESTIGATIONS – HYPO NATRAEMIA Assess the degree of hyponatraemia in the serum Assess for symptoms INVESTIGATIONS – HYPO NATRAEMIA Assess the degree of hyponatraemia in the serum Assess for symptoms Emergency treatment required  TRUE hyponatraemia HYPOTONIC HYPONATRAEMIA: TREATMENT Treat the underlying cause​ Other considerations with endocrine guidance: Slow sodium​ tablets Vaptans: vasopressin receptor antagonists INVESTIGATIONS – HYPO NATRAEMIA Initial Laboratory Tests: Include serum glucose, creatinine, potassium, bicarbonate, and a basic metabolic panel. Assess Serum Osmolality: To differentiate between hypotonic, isotonic, and hypertonic hyponatremia. Urine Osmolality and Sodium: Helps to determine the cause of hyponatremia. Additional Tests: May include complete blood count, liver function tests, serum calcium. Consideration of Clinical Context: History and physical examination guide further diagnostic approach. Other Factors: Evaluate the effect of medications, recent surgery, and other clinical conditions. INVESTIGATIONS – HYPO NATRAEMIA Blood tests (ordered based on suspected aetiology and fluid status of patient) – Serum cortisol (low cortisol indicates adrenal insufficiency). – Serum glucose (diabetes). – Thyroid hormone levels (part of the exclusion criteria for SIADH). – Liver enzymes / Albumin / BNP / Creatinine – Assess for liver, heart or renal failure. – Pituitary hormone screen – help rule out cranial DI or a space- occupying lesion. – CT Thorax/Abdomen and Pelvis – to rule out malignancies associated with SIADH. SEVERE HYPONATRAEMIA Life threatening emergency Cerebral oedema leading to fatal herniation >48 hours: chronic 600 Cranial Diabetes High 800 Insipidus (AVP-D) dilute) Nephrogenic High