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Hypo &hpernatrimia


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Hype and hyper Natrimia

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Hypo &hpernatrimia

  1. 1. Dr. Saroj K. Suwal MO, Oncosurgery Department, Bhaktapur Cancer Hospital
  2. 2. Na + (Sodium)  90 % of total ECF cations, Low in ICF  Normal range : 135 -145 mEq / L  Pairs with Cl- , HCO3 - to neutralize charge  Most important ion in regulating water balance  Important in nerve and muscle function
  3. 3. Hyponatremia  Defined as sodium concentration < 135 mEq/L  Generally considered with disorder of water as opposed to disorder of salt  Results from increased water retention
  4. 4. Types of Hyponatremia depletional and dilutional  Depletional Hyponatremia Na+ loss:  diuretics, chronic vomiting  Chronic diarrhea  Decreased aldosterone  Decreased Na+ intake 4
  5. 5.  Dilutional Hyponatremia:  Renal dysfunction with ↑ intake of hypotonic fluids  Excessive sweating→ increased thirst → intake of excessive amounts of pure water  Syndrome of Inappropriate ADH (SIADH) or oliguric renal failure, severe congestive heart failure, cirrhosis all lead to:  Impaired renal excretion of water Hyperglycemia – pulls interacellular water to ECF translocation of water lowers sodium (also called translocational hyponatrimia)-  serum sodium concerntraion falls 2mEq/L for every 100mg/dl when glucose concerntration is between 200 to 400 mg/dl  Falls to 4mEq/L when greater than 400mg/dl of Glucose 5
  6. 6. Cause Hyponatremia can be classified based on  volume status,  Serum /Plasma Osmolality  ADH level inappropireatly suppressed or appropriately elevated
  7. 7. Hypovolemic, Euvolemic or Hypervolemic
  8. 8. Volume status helps predict cause  Hypovolemia  True Volume Depletion  Adrenal insufficiency  Thiazide overdose  Exercised induced Hyponatremia  Euvolemia  SIADH  Primary Polydipsia  Hypervolemia  Cirrhosis and CHF
  9. 9. Isotonic(280-295mosm/kg),Hypotonic and Hypertonic Hyponatremia
  10. 10. ADH-Antidiuretic Hormone  Release by the postrior pitutary  Function :is water retension, Raise BP by peripheral vasoconstrictions  Vasopressin has two effects 1. increased urine osmolarity (increased concentration) and decreased water excretion. These are:  Increasing the water permeability of distal tubule and collecting duct cells in the kidney, thus allowing water reabsorption and excretion of more concentrated urine, i.e., antidiuresis  Increasing permeability of the inner medullary portion of the collecting duct to urea which facilitates its reabsorption into the medullary interstitiumm as it travels down the concentration gradient created by removing water from the connecting tubule, cortical collecting duct, and outer medullary collecting duct
  11. 11. ADH inappropriately elevated or appropriately suppressed
  12. 12. ADH suppression  Conditions which ADH is suppressed  Primary Polydipsia or psychogenic Polydipsia (associated with a patient's increasing fluid intake due to the sensation of having a dry mouth ,generally >10L/day, )  Low dietary solute intake or “Beer Potomania”  Advanced Renal Failure
  13. 13. ADH elevation  Conditions which ADH is elevated  Volume Depletion  True volume depletion (i.e. bleeding)  Effective circulating volume depletion (i.e. heart failure and cirrhosis)  Exercised induced Hyponatremia  Thiazide Diuretics  Adrenal insufficiency  SIADH
  14. 14. Causes  Psuedohyponatremia –, Serum Sodium Level falsely depressed due to Hyper lipidemia or protein level (multiple myeloma). In this Serum Osmolality is Normal as protien and lipid doesn’t alter serum osmolatiyalso called isotonic hyponatrimia  High blood sugar (esp. DKA) Hypertonic hypernatrimia
  15. 15. Symptoms of Hyponatremia  Neurological symptoms  Lethargy, headache, confusion, apprehension, depressed reflexes, seizures and coma Muscle symptoms  Cramps, weakness, fatigue  Gastrointestinal symptoms  Nausea, vomiting, abdominal cramps, and diarrhea
  16. 16. Workups For Hyponatremia  3 mandatory lab tests  Serum Osmolality- solute concerntration  Urine Osmolality  Urine Sodium Concentration
  17. 17. Interpretations :  Serum Osmolality  Can differentiate between true Hyponatremia, pseudohyponatremia and hypertonic Hyponatremia  Urine Osmolality  Can differentiate between primary Polydipsia and impaired free water excretion  Urine Sodium concentration  Can differentiate between Hypovolemia Hyponatremia and SIADH
  18. 18. Conditions that increased osmolality3 Serum Urine •Dehydration/sepsis/fever/sweating/bur ns •Diabetes mellitus (hyperglycemia) •Diabetes insipidus •Uremia •Hyponatremia •Ethanol, methanol, or ethylene glycol ingestion •Mannitol therapy •Dehydration •Syndrome Inappropriate ADH secretion (SIADH) •Adrenal insufficiency •Glycosuria •Hyponatremia •High protein diet Conditions that decrease Osmolality Serum Urine •Excess hydration •Hyponatremia •Syndrome Inappropriate ADH secretion (SIADH) •Diabetes insipidus •Excess fluid intake •Acute renal insufficiency •Glomerulonephritis
  19. 19. Additional Tests TSH, (Hypothyroidism or Adrenal insufficiency) Albumin, triglycerides and SPEP –serum protein electrophoresis (pseudohyponatremia, cirrhosis, MM Cortisol – low in adrenal insufficiency, though may be inappropriately normal in infection/stressful state, therefore should get Corti-Stim test to confirm Head CT and Chest Xray – may see evidence of cerebral salt wasting or small cell carcinoma which can both cause Hyponatremia )
  20. 20. not so common test  Iatrogenic infusion of hypotonic fluids (“Surgeon sign”)  Ecstasy use – increased water intake with inappropriate ADH secretion  Underlying infections  Test for SIADH  Reset Osmostat – Occurs in elderly and pregnancy where regulated sodium set point is lowered
  21. 21. SIADH: concept to understand  Caused by various etiologies  CNS disease – tumor, infection, CVA, SAH,GBS,Meningitis,  Pulmonary disease – TB, Bacterial pneumonia, Aspergilosis, Bronchiaectiasis, Neoplasm,positive pressure ventilation  Cancer – Lung ca, pancreas ca, thymoma, ovary ca, lymphoma, adenocarcinoma of colon, Prostatic ca.Renal Cell ca,Osteosarcoma ,Lymphoma, Leukemia  Drugs – NSAIDs, SSRIs, diuretics, TCAs, Antineopalastic(cyclophosphomide, vincristine, Carbamazapine,),Neuroleptics-haloperidol, thiothixene, thioridazine  Postoperative,Pain,Stress, AIDS, Pregnancy(Physiologic), Hypokalemia
  22. 22. Diagonositc criteria for SIADH  Clinicaly –Euvolemia, Hypotonic Hyponatremia  Normal hepatic, renal and cardiac function  Normal thyroid and adrenal function  plasma sodium concentration <135 mmol/l  plasma Osmolality <280 mOsmol/kg  urine Osmolality > 100 mOsmol/kg  urinary sodium concentration >30mmol/L  no diuretic use (recent or past) The following investigations could be carried out in SIADH  urea and electrolytes  plasma and urine Osmolality  urinary sodium  thyroid function tests short , corti-stim test  chest and skull radiographs may be useful in excluding other causes of SIADH.
  23. 23. Treatment :Hyponatremia  Patients with serum sodium above 120 are generally asymptomatic  Symptoms tend to occur at serum sodium levels lower than 120 or when a rapid decline in sodium levels occur  Patients can have mild symptoms at sodium concentrations of 110-115 mEq/L when this level is reached gradually. nausea and malaise (earliest) or headache and lethargy as mild symptoms
  24. 24. With No severe symptoms & fluid restriction started, next step is to assess volume status to help determine cause  Hypovolemic – urine output, dry mucous membranes, sunken eyes  Euvolemic – normal appearing  Hypervolemic – Edema, past medical history, Jaundice (cirrhosis), (CHF)
  25. 25. What if little to no symptoms are present?  Oral fluid restriction is the first step  No more than 1500 mL per day (NOTE: This only pertains to oral fluid, isotonic IV fluids do not count towards fluid intake )  If volume depletion is present, isotonic (0.9%) saline can be given intravenously  Careful monitoring should be used whether symptoms are present or not  Other non pharmacological practices:Salt added diet,ORS,Salt Capsule – salt powder inside b-complex capsule layer
  26. 26. When Severe symptoms(coma, seizures present starting bolus of 100 ml of 3% hypertonic saline which generally raise serum sodium level by 2-3 mEq/L (moniter serum sodium –2 hrly in ICU setup or 4-6 hrly as per need)  Goals for correction:  1.5 to 2 mEq/L per hour for first 3-4 hours until symptoms resolve  Increase by no more than 10 mEq/L in first 24 hrs  Inscrease by no more than 18 meq/L in first 48 hrs (half correction approach after serum sodium =>120
  27. 27. How much sodium does the patient need? Sodium deficit = Total body water x (desired Na – actual Na) Total body water is estimated as lean body weight x 0.5 for women or 0.6 for men
  28. 28. Case example:  A 60 kg woman with sodium level of 116mEq/L. How much sodium will bring him up to 124 in the next 24 hours?  Sodium Deficit(Needed) = 0.5 x 60 x (124-116) = 240 mEq  The patient needs 240 mEq in next 24 hours
  29. 29. Na Concerntration in IV Fluid Nacl 0.9%  154mEq/L Ringer lactate130 mEq/L 3 % Nacl513 mEq/L 5% Albumin130-160 mEq/L Hestarch 154 mEq/L Dextran154 mEq/L
  30. 30. What if the sodium increases too fast?  Central Pontine Myelinolysis which is a form of osmotic demyelination  Symptoms generally occur 2-6 days after elevation of sodium and usually either irreversible or only partially reversible  Symptoms include: dysarthria, dysphagia, paraparesis, quadriparesis, lethargy, coma or even seizures
  31. 31. Risk Factors for Demyelination  Rate of correction over 24 hours more important than rate of correction in any one particular hour  More common if sodium increases by more than 20 mEq/L in 24 hours  Very uncommon if sodium increases by 12 mEq/L or less in 24 hours  CT but preferably MRI to diagnose demyelination if suspected, though imaging studies may not be positive for up to 4 weeks after initial correction
  32. 32. Summary of Hyponatremia  Hyponatremia has variety of causes  Treatment is based on symptoms  Severe symptoms = Hypertonic Saline  Mild or no symptoms = Fluid restriction  Overcorrection, more than 12 mEq increase in 24 hours must be avoided with monitoring  Serum Osmolality, Urine Osmolality and Urine sodium concentration are initial tests to order
  33. 33. Hypernatremia Serum Na >145 mEq/L [deficit of (TBW) relative to Na]  Incidence >1% in hospitalized patients.  Can have normal,hypo and hyperosmolality  Generally hypovolumic due to free water loss , also hypervolumic is seen as itragenic treatment with free accesses of water in hospitals
  34. 34. Causes  Insensible and sweat losses  GI losses  Diabetes Insipidus (both central and nephrogenic)  Osmotic Diuresis – DKA  Hypothalamic lesions which affect thirst function – Causes include tumors, granulomatous diseases or vascular disease  Sodium Overload – Infusion of Hypertonic sodium bicarbonate for metabolic acidosis
  35. 35. Symptoms of Hypernatremia  Initial symptoms include lethargy, weakness and irritability Can progress to twitching, seizures,or coma  Resulting decrease in brain volume can lead to rupture of cerebral veins leading to hemorrhage  Severe symptoms usually occur with rapid increase to sodium concentration of 158 mEq or more.. (hyperthermia, delirium , sizure and coma)  Sodium concentration greater than 180 mEq are associated with high mortality
  36. 36. Lab findings  Urine Osmolaity >400 mosm/kg  Renal losssevere hyperglacemiatranslocatinal hyponatrimia progressive volume depletion from glucosuria lead to Hypernatrimia  Non Rneal LossFluid Loss from excessive sweating, respirator tract or bowel movements. Lactulose cause osmotic diarrohea with loss of free water Urine Osmolaity <250 msom/kg  Hypernatrimia with dilue urine is charactersitc of DI.  Central DI results from Inadequate ADH release  Nephrogenic DI results from renal insensitivity to ADH
  37. 37.  If urine Osmolality is lower than serum Osmolality then DI is present  Administration of DDAVP(desmopressin) will differentiate  Urine Osmolality will increase in central DI, no response in nephrogenic DI DDAVGreatly enhanced ADH activity. Less vasopressor activity. Longer DOA. (Synthetic analog of vasopressin- posterior pituitary hormone).
  38. 38. Treatment of Hypernatremia  First, calculate water deficit  Water deficit = CBW x ((plasma Na/desired Na level)- 1)  CBW = current body water assumed to be 50% of body weight in men and 40% in women
  39. 39. •60 kg woman with 168 mEq/L •How much water will it take to reduce her sodium to 140 mEq/L sample calculation: Water deficit = 0.4 x 60 ([168/140]-1) = 4.8 L
  40. 40. Calculation continued But how fast should I correct it?  Same as Hyponatremia, sodium should not be lowered by more than 12 mEq/L in 24 hours  Overcorrection can lead to cerebral edema which can lead to encephalopathy, seizures or death  So what does that mean for our patient?  The 4.8 L which will lower the sodium level by 28 should be given over 56-60 hours, or at a rate of 75-80 mL/hr  Typical fluids given in form of D5 water
  41. 41. Summary of Hyponatremia  Loss of thirst usually has to occur to produce hypernatremia  Rate of correction same as Hyponatremia  D5 water infusion is typically used to lower sodium level  Same diagnostic labs used: Serum Osmolality, Urine Osmolality and Urine sodium  Beware of overcorrection as cerebral edema may develop
  42. 42. Thank you .