Hyponatremia and hypernatremia


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Hyponatremia and hypernatremia

  1. 1. Presented by: Dr Vineet ChowdharyModerator: Dr Chandrashekar Chatterji
  2. 2.  Sodium is the most prevalent cation in the extracellular fluid (ECF),with a normal level of around 135- 145mmol/L & intracellularconcentration of around 10mmol/L Total body Sodium is about 5000 mEq in a normal adult person Responsible for 90% of total osmolality of ECF Daily requirement of sodium is about 100 mEq or 6gm Major function of sodium is to maintain ECF volume and thereforeblood pressure In normal individuals, the kidney strives to achieve Na+ balance – thatis, to have Na+ excretion equal to Na+ ingestion. The long-term controlof blood pressure is achieved by the excretion or retention of Na+ (andhence plasma volume) in the kidney
  3. 3. Hormones increasing sodium reabsorption:Renin: - Released from the juxtaglomerular apparatus of the kidney - Release is stimulated by: raised sympathetic tone, falling plasma volume, andcertain prostaglandins, such as PGE2 - No direct effects promoting Na+ retention, it controls the renin-angiotensin-aldosterone axisAngiotensin II: - Levels rise as result of renin release - In turn, it stimulates the release of aldosterone - Also increases tone in the efferent glomerular arteriole. The net effect is toenhance Na+ reabsorption from the proximal tubule.Aldosterone: - Steroid hormone released from the adrenal cortex - End product of the renin-angiotensin-aldosterone system - Acts on the distal tubule and collecting duct to increase Na+ and waterreabsorption (proportionately more Na+ than water)
  4. 4. Arginine vasopressin(AVP), AKA anti-diuretichormone (ADH): -ADH is produced in neuron cellbodies in supraoptic andparaventricular nuclei of theHypothalamus, and stored inposterior pituitary. - passive absorption of water fromthe collectingducts, concentrating the urine - Causes a small degree ofNa+ reabsorption, but theretention of water isproportionately much greater·
  5. 5. Hormones increasingsodium excretion:Atrial NatriureticPeptide (ANP): - A small peptideproduced from the atrialwall as a result of atrialstretching due tohypervolaemia - Acts to increase Na(and hence water)excretion by increasingGFR and blocking Nareabsorption in theproximal collecting duct Other factors secreted bythe hypothalamus,termed brain natriureticpeptides (BNP), mayhave similar roles.
  6. 6.  Types and distribution Include guanylin, uroguanylin, lymphoguanylinand exogenous peptide toxin produced byenteric bacteria Function In gastrointestinal tract, stimulate epithelialsecretion of Cl- and HCO-, causing enhancedsecretion of fluid and electrolyte into theintestinal lumen. in kidney, increase excretion of Na+, Cl-, K+ andwater
  7. 7. Serum sodium concentration regulation Stimulation of thirst Secretion of ADH Feedbackmechanism of Renin- Angiotensin -Aldosterone Renal handlingof filtered sodium Stimulation of thirst :(a) Increase in osmolality is the main drivingforce which is sufficient if it increases by 2-3 %. (b) A decrease inblood pressure or volume by 10-15 % Thirst centre is located in the anterolateral centre of the Hypothalamus Secretion of ADH is triggered by increase in osmolality by approx 1%or the vol. or pressure of the vascular sytem. This increases the passiveabsorption of water and urea concentrating the urine. Renin- Angoitensin- Aldosterone axis acts to cause retention ofsodium in the event of decreased osmolarity
  8. 8.  Definition: Hyponatremia is defined as a plasma Na+concentration <135 mEq/L It is due to a relative excess of water in relation to sodium. It can result from excessive loss of sodium from excessivesweating, vomiting, diarrhoea, burns, and diuretics. It is a very common disorder, occurring in up to 22% ofhospitalized patients. Result of an increase in circulating AVP and/or increasedrenal sensitivity to AVP, combined with any intake of freewater; a notable exception is hyponatremia due to lowsolute intake.
  9. 9.  Patients’ intravascular volume status must beevaluated to understand further the underlyingproblem leading to abnormalities in sodiumphysiology. Hyponatremia thus is subdivided diagnostically intothree groups, depending on clinical history andvolume status: hypovolemic, euvolemic, andhypervolemic
  10. 10. I- Hypo-osmolar hyponatremia (true hyponatremia) Hypovolemic Hyponatremia Euvolemic Hyponatremia Hypervolemic HyponatremiaII- Pseudo hyponatremia Normal Osmolality High Osmolality
  11. 11.  Patient dehydrated; reduction in total body sodium exceedsreduction in total body water NON RENAL LOSSES ( Urinary Sodium excretion < 20mEq/L)- Vomiting, Diarrhea, Third space losses, Pancreatitis,Burns RENAL LOSSES (Urinary Sodium excretion > 20 mEq/L)-The renal causes of hypovolemic hyponatremia share aninappropriate loss of Na+-Cl– in the urine, leading to volumedepletion and an increase in circulating AVP. Causes includereflux nephropathy recovery phase of acute tubular necrosis,diuretics ,mineralocorticoid deficiency, osmotic diuresis,ketonuria
  12. 12.  “Cerebral salt wasting" : rare cause of hypovolemichyponatremia, and inappropriate natriuresis in associationwith intracranial disease Associated disorders include subarachnoid hemorrhage,traumatic brain injury, craniotomy, encephalitis, andmeningitis. Cerebral salt wasting typically responds to aggressive Na+-Cl– repletion.
  13. 13.  Patient has a normal store of sodium but an excess of totalbody water The most common form seen in hospitalized patients. Themost common cause is the inappropriate administration ofhypotonic fluid The syndrome of inappropriate antidiuresis is the mostcommon cause of euvolemic hyponatremia Other causes include glucocorticoid therapy, stress, drugs ,hypothyroidism.
  14. 14.  Most common cause of euvolemic hyponatremia The osmotic threshold and osmotic response curves forsensation of thirst are shifted downward High levels of ADH are secreted intermittently at an abnormallylow threshold or continuously despite low osmolality. The presence of hyponatremia plus a urine osmolality higherthan maximal dilution confirms the diagnosis. Urinary sodium concentration usually exceeds 30 mEq/L The fractional excretion of sodium is greater than 1%. Patients with SIADH exhibit a characteristic response to waterrestriction; a 2- to 3-kg weight loss is accompanied by correctionof hyponatremia and cessation of salt wasting over 2 to 3 days
  15. 15.  Increase in total body water exceeds increase in total bodysodium. Patients are edematous. RENAL CAUSES(urinary sodium > 20mEq/L): Acute or Chronicrenal failure NON RENAL CAUSES: CHF, Cirrhosis, nephrotic syndrome
  16. 16. Normal Osmolarity - Due to a measurement error which can result when the solid phase ofplasma (that due to lipid and protein) is increased - Typically caused by hypertriglyceridaemia or paraproteinaemia.High Osmolarity: Translocational hyponatraemia - Occurs when an osmotically active solute that cannot cross the cellmembrane is present in the plasma. -In the case of the insulinopaenic diabetic patient, glucose cannot entercells and hence water is displaced across the cell membrane,dehydrating the cells and “diluting” the sodium in the serum. - This is also the cause of hyponatraemia seen in the TURP syndrome,in which glycine is inadvertently infused to the same effect.
  17. 17.  Severity of symptoms depends upon the severity ofhyponatremia and the rate at which the sodiumconcentration is lowered. Acute – develops in 48 hours or less. Subjected tomore severe degrees of cerebral edema Chronic- develops over 48 hours and brain edema isless and is well tolerated. The signs and symptoms are due to increase in volumeof ICF and increase in volume of brain cells ratherthan decrease in serum sodium.
  18. 18. SIGNS AND SYMPTOMS OF HYPONATREMIACentral Nervous System Mild – Apathy ,Headache, Lethargy Moderate- Disorientation, Psychosis, Agitation, AtaxiaConfusion Severe-Stupor, Coma, Pseudobulbar palsyTentorial herniation , Cheyne-Stokes respiration, DeathGastrointestinal System Anorexia, Nausea ,VomitingMusculoskeletal System Cramps Diminished deep tendon reflexes
  19. 19.  History and physical examination- to identify hypovolemichyponatremia (diarrhoea, vomitting, burns) Radiologic imaging - to assess whether patients have a pulmonary orCNS cause for hyponatremia. CT scanning of the thorax should beconsidered in patients at high risk small cell carcinoma Laboratory tests- Provide important initial clue in the differentialdiagnosis1. Plasma Osmolality2. Urine Osmolality3. Urine Sodium concentration4. Uric acid level5. Serum potassium6. Serum glucose
  20. 20. Plasma Osmolality- Normal plasma osmolality is 275-290mEq/l. >290 mEq/L- hyperglycemia or administration of mannitol 275-290 mEq/L- Hyperlipidemia or hyperproteinemia <275 mEq/L- Evaluate volume status1. Increased Volume- CHF, Cirrhosis, Nephrotic syndrome2. Euvolemic- SIADH, Hypothyroidism, psychogenic polydipsia3. Decreased Volume- GI and 3rd space loss, renal losses Urine Osmolality- Normal value is > 100 mosmol/kg Normal to high: Hyperlipidemia, hyperproteinemia, hyperglycemia,SIADH < 100 mosmol/kg Hypo-osmolar hyponatremia -Excessive sweating,Burns,Vomiting, Diarrhea , Urinary loss
  21. 21.  Urine Sodium >20 mEq/LSIADH, diuretics <20 mEq/Lcirrhosis, nephrosis, congestive heart failure, GI loss, skin,3rd spacing, psychogenic polydipsia Uric Acid Level< 4 mg/dl consider SIADH FeNa(Fractional Excretion of Sodium) Help to determine pre-renal from renal causes Serum glucose -also should be measured; plasma Na+concentration falls by 1.6 to 2.4 mM for every 100-mg/dL increasein glucose due to glucose-induced water efflux from cells; this"true" hyponatremia resolves after correction of hyperglycemia Serum Potassium: Hyperkalemia- Renal insufficiency orAdrenal insufficiency with hypoaldosteronismHypokalemia- with metabolic acidosis suggests vomiting ordiuretic therapy
  22. 22.  Treatment needs to be individualized considering etiology, rate ofdevelopment, severity and clinical signs and symptoms Hyponatremia which developed quickly needs to be treated fastwhereas slow developing hyponatremia should be corrected slowlyGOALS of THERAPY:1. To raise the plasma sodium concentration at a slow rate2. To replace sodium or potassium deficit or both3. To correct underlying etiologyBASIC PRINCIPLES OF CORRECTION: Rapid correction is indicated in acute (<48hours) symptomatic orsevere hyponatremia.(serum Na <120 mEq/L) In chronic cases patients are at little risk, however rapid correction canlead to demylination. Use slower acting therapies like water restriction
  23. 23. Treatment of acute symptomatic hyponatremia Hypertonic 3% saline (513 mM) to acutely increase plasma Na+concentration by 1–2 mM/h to a total of 4–6 mM; alleviate severeacute symptoms, after which corrective guidelines for "chronic"hyponatremia are appropriate The increase in plasma Na+ concentration can be highlyunpredictable during treatment ,plasma Na+ concentrationshould be monitored every 2–4 h during treatment Vasopressin antagonists do not have an approved role in themanagement of acute hyponatremia.Treatment of chronic hyponatremia Rate of correction should be comparatively slow <8–10 mM in the first 24 h and <18 mM in the first 48 h to avoidODS
  24. 24.  Hypovolemic hyponatremia will respond to intravenoushydration with isotonic normal saline, with a rapidreduction in circulating AVP and a brisk water diuresis.Diuretics induced hyponatremia is treated with saline andpotassium supplementation Hypervolemic hyponatremia responds to no salt, waterrestriction(intake< urine output), and loop diuretics Euvolemic hyponatremia will respond to successfultreatment of the underlying cause, with an increase inplasma Na+ concentration Regardless of the initial rate of correction, chosen acutetreatment is stopped once1. patient’s symptoms are abolished2. A safe plasma sodium (120-125 mEq/L) is achieved
  25. 25. SPECIFIC THERAPY: 1. Removal of responsible drugs- diuretics, chlorproamide etc 2. Management of physical stress or post operative pain 3. Specific treatment of underlying cause 4. Vasopressin antagonists (vaptans) are highly effective intreating SIAD and hypervolemic hyponatremia, reliablyincreasing plasma Na+ concentration as a result of their aquareticeffects (augmentation of free-water clearance). Most of theseagents specifically antagonize theV2 vasopressin receptorTO CALCULATE NEED OF REPLACEMENT SODIUMCONTAINING FLUID: 0.9% saline (154mEq/L) and 3% NaCl- hypertonic saline (513mEq/L) are the only two routinely used I.V. fluids . However0.9% NS is not used to correct hyponatremia in SIADH
  26. 26.  estimate SNa change on the basis of the amount of Na inthe infusate ΔSNa = {[Na + K]inf − SNa} ÷ (TBW + 1) ΔSNa is a change in SNa [Na + K]inf is infusate Na and K concentration in 1 liter ofsolution Total Body Water= 0.6* B.W(kg) in children and nonelderly man=0.5*B.W.(kg) in nonelderly woman andelderly man=0.45*B.W.(kg) in elderly women
  27. 27.  Asymptomatic or Chronic SIADH response to isotonic saline is different in the SIADH In hypovolemia both the sodium and water are retained Sodium handling is intact in SIADH Administered sodium will be excreted in the urine, whilesome of the water may be retained possibly worsening thehyponatremia Water restriction0.5-1 liter/day Salt tablets Demeclocycline Inhibits the effects of ADH Onset of action may require up to one week
  28. 28.  Hypernatremia is defined as an increase in the plasma Na+concentration to >145 mM. Considerably less common thanhyponatremia, hypernatremia nonetheless is associatedwith mortality rates as high as 40–60%.Hypernatremia iscaused by a relative deficit of water in relation to sodiumwhich can result from Net water loss: accounts for majority of cases pure water loss hypotonic fluid loss Hypertonic gain results from iatrogenic sodium loading
  29. 29. Net water lossPure water loss•Unreplaced insensible losses (dermal and respiratory)•Hypodipsia•Neurogenic diabetes insipidus Post-traumatic tumors, cysts, histiocytosis, tuberculosis, sarcoidosis Idiopathic aneurysms, meningitis, encephalitis, Guillain-Barresyndrome Congenital nephrogenic diabetes insipidus Acquired nephrogenic diabetes insipidus Renal disease (e.g. medullary cystic disease) Hypercalcemia or hypokalemia Drugs (lithium, methoxyflurane, amphotericin B, vasopressinV2-receptor antagonists)
  30. 30.  Hypotonic fluid loss• Renal causesLoop diureticsOsmotic diuresis (glucose, urea, mannitol)Post obstructive diuresisPolyuric phase of acute tubular necrosis• Gastrointestinal causesVomitingNasogastric drainageEntero cutaneous fistulaDiarrheaUse of osmotic cathartic agents (e.g., lactulose)• Cutaneous causesBurnsExcessive sweating
  31. 31. Hypertonic sodium gainHypertonic sodium bicarbonate infusionIngestion of sodium chlorideIngestion of sea waterHypertonic sodium chloride infusionPrimary hyper-aldosteronismCushing’s syndrome
  32. 32.  The symptoms of hypernatremia are predominantlyneurologic. Altered mental status is the most common manifestation,ranging from mild confusion and lethargy to deep coma. The sudden shrinkage of brain cells in acute hypernatremiamay lead to parenchymal or subarachnoid haemorrhagesand/or subdural hematomas; however, these vascularcomplications are encountered primarily in paediatric andneonatal patients Osmotic damage to muscle membranes also can lead tohypernatremic rhabdomyolysis
  33. 33. HISTORY AND PHYSICAL EXAMINATION: The history should focus on the presence or absence of thirst, polyuria,and/or an extrarenal source for water loss, such as diarrhoea The physical examination should include a detailed neurologic examand an assessment of the ECFV; patients may be hypovolemic, withreduced JVP and orthostasis Accurate documentation of daily fluid intake and daily urine outputLAB INVESTIGATIONS: Measurement of serum and urine osmolality in addition to urineelectrolytes- The appropriate response to hypernatremia and a serum osmolality>295 mosmol/kg is an increase in circulating AVP and the excretion oflow volumes (<500 mL/d) of maximally concentrated urine, i.e., urinewith osmolality >800 mosmol/kg
  34. 34.  Diabetes insipidus may result from a deficiency of ADH(vasopressin) or inability of the kidney to produce ahypertonic medullary interstitium Diabetes insipidus is characterized by production of a largevolume of dilute urine. Deficiency of vasopressin is known as central diabetesinsipidus .Vasopressin deficiency is seen after pituitarysurgery, basal skull fracture, and severe head injury. Nephrogenic diabetes insipidus is defined as renal tubulecell insensitivity to the effects of vasopressin. In patients with DI a significant amount of body water islost in a short period, which can cause profoundhypovolemia
  35. 35.  Patients with continued urine output of more than 100mL/hr who develop hypernatremia should be evaluated fordiabetes insipidus by determining the osmolalities ofurine and serum. If the urine osmolality is less than 300 mOsm/L, andserum sodium exceeds 150 mEq/L, the diagnosis of diabetesinsipidus is likely. Patients with central DI should respond to theadministration of intravenous, intranasal, or oralDesmopressin. Patients with NDI due to lithium may reduce their polyuriawith amiloride (2.5–10 mg/d) Thiazides may reduce polyuria due to NDI Occasionally (NSAIDs) have been used to treat polyuriaassociated with NDI
  36. 36. A two-pronged approach: Addressing the underlying cause Correcting the prevailing hypertonicityRATE OF CORRECTION:Hypernatremia that developed over a period of hours (accidentalloading) Rapid correction improves prognosis without cerebral edema Reducing Na+ by 1 mmol/L/hr appropriateHypernatremia of prolonged or unknown duration a slow pace of correction prudent maximum rate 0.5 mmol/L/hr to prevent cerebral edema A targeted fall in Na+ of 10 mmol/L/24 hr
  37. 37.  Reduce serum sodium concentration to 145 mmol/L Make allowance for ongoing obligatory or incidental losses ofhypotonic fluids that will aggravate the hypernatremia In patients with seizures prompt anticonvulsant therapy andadequate ventilationAdministration of Fluids Water ideally should be administered by mouth or bynasogastric tube as the most direct way to provide free water, i.e.,water without electrolytes. Alternatively, patients can receive free water in dextrose-containing IV solutions such as 5% dextrose
  38. 38.  Hypernatremia with ECF vol contraction-Isotonic saline is given initially till ECF vol is restored.Subsequently water deficit can be replaced with water bymouth or I.V. 5% dextrose or 0.45% NaCl Hypernatremia with increased ECF volume: sincehypernatremia is secondary to solute administration it canbe rapidly corrected . Patients are volume overloaded- loopdiuretic is given along with water to remove sodium excess
  39. 39.  If at all possible, hyponatremia, especially ifsymptomatic, should be corrected prior to surgery.Level above 130mEq/L is considered safe If lower than 130 mEq/L it can be the cause of :- 1. Cerebral edema 2. Decreased MAC 3. Post op agitation and confusion 4. Problems of hypervolemia If the surgery is urgent, then appropriate correctivetreatment should continue throughout the surgeryand into the postoperative period.
  40. 40.  Frequent measurement of serum sodium is necessary toavoid overly rapid correction of hyponatremia withresultant osmotic demyelination or overcorrectionresulting in hypernatremia. Treatment of the underlying cause of the hyponatremiashould also continue throughout the perioperative period. Induction and maintenance of anesthesia in patients withhypovolemic hyponatremia are fraught with the risk ofhypotension. In addition to fluid therapy, vasopressorsand/or inotropes may be required to treat the hypotension Hypovolemic patients are sensitive to the vasodilating andnegative inotropic effects of the volatileanesthetics, barbiturates, and agents associated withhistamine release(morphine, meperidine, curare, atracurium).
  41. 41.  Dosage requirements for other drugs must also be reducedto compensate for decreases in their volume ofdistribution. Hypovolemic patients are particularlysensitive to sympathetic blockade from spinal or epiduralanesthesia. If an anesthetic must be administered prior to completecorrection of the hypovolemia, ketamine may be theinduction agent of choice for general anesthesia; etomidatemay be a suitable alternative.
  42. 42.  It involves the resection of the prostate via acystoscope with continuous irrigation of thebladder. The irrigating fluid is a nonelectrolyte fluidcontaining glycine, sorbitol, or mannitol, and thisfluid may be absorbed rapidly causing volumeoverload, hyponatremia, and hypo-osmolality. An awake patient permits detection of the signs ofhyponatremia, including nausea, vomiting, visualdisturbances, depressed level of consciousness,agitation, confusion, coma, seizures, musclecramps, and death.
  43. 43.  Cerebral edema occurs at or below a serum level of 123mEq/L, and cardiac symptoms occur at 100 mEq/L. Itcan result in pulmonary edema, hypertension, andheart failure.[19] Monitoring - direct neurologic assessment in thepatient under regional anesthesia- Measurement of serum sodium concentration andosmolality in the patient under general anesthesia. Treatment -Terminating the surgical procedure-Diuretics if needed for relief of cardiovascularsymptoms- Hypertonic saline administration if severe neurologicsymptoms are present or the serum sodiumconcentration is less than 120 mEq/L.
  44. 44.  Overly rapid correction of hyponatremia (>8–10 mM in 24 h or 18mM in 48 h) also is associated with a disruption in integrity ofthe blood-brain barrier. The lesions of ODS classically affect the pons Clinically, patients with central pontine myelinolysis can presentone or more days after overcorrection of hyponatremia withpara- or quadraparesis, dysphagia, dysarthria, diplopia, a"locked-in syndrome," and/or loss of consciousness. Other regions of the brain also can be involved in ODS. In order of frequency, the lesions of extrapontine myelinolysiscan occur in the cerebellum, lateral geniculate body, thalamus,putamen, and cerebral cortex or subcortex.
  45. 45.  Development of ataxia, mutism, parkinsonism, dystonia,and catatonia is seen in these Relowering of plasma Na+ concentration after overly rapidcorrection can prevent or attenuate ODS However, even appropriately slow correction can beassociated with ODS, particularly in patients withadditional risk factors; these factors include alcoholism,malnutrition, hypokalemia, and liver transplantation.
  46. 46. Severehyponatremiafollowed byextrapontinemyelinolysis
  47. 47.  Osmolar gap is considered significant when the differencebetween the measured and calculated osmolarity is > 10 Some critically ill patients have an unexplained osmolar gapwhich is thought to result from escape of osmotically activeintracellular solutes into extracellular fluid Increased membrane permeability to Na and decreased activeremoval of sodium from the cells by energy dependent cationexchange pump leads to redistribution hyponatremia withincreased osmolar gap- a concept called sick cell syndrome. This state has been described during a great variety of humandiseases such as traumatic shock, diabetic ketoacidosis, lacticacidosis and multiple organ failure Both the osmolar gap and hyponatremia correct simultaneouslyin this condition as the primary illness is treated
  48. 48.  If at all possible, surgery should be delayed untilthe hypernatremia has been corrected or at leastuntil symptoms have abated. Frequent serum sodium measurements will berequired perioperatively, and invasivehemodynamic monitoring may be useful. Hypovolemia will be exacerbated by inductionand maintenance of anesthesia and promptcorrection of hypotension with fluids,vasopressors, and/or inotropes may be required. Increased MAC seen in animal studies