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The following is material that is not all Dr. Ciorciari's original thoughts and not fully referenced to give credit to all information cited. Further this.

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Presentation on theme: "The following is material that is not all Dr. Ciorciari's original thoughts and not fully referenced to give credit to all information cited. Further this."— Presentation transcript:

1 The following is material that is not all Dr. Ciorciari's original thoughts and not fully referenced to give credit to all information cited. Further this is not considered an authoritative source but suggestions and perspectives that may aid in guiding your art of medicine

2 Sodium Disorders: Hyponatremia William Harper, MD, FRCPC Endocrinology & Metabolism Assistant Professor of Medicine McMaster University

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4 P Na (mEq/L) ADH (pM) Thirst↓ ECFv Normal Serum [Na] ( mEq/L) Closely Guarded

5 1)Complete DI 2)Defective osmoreceptor, normal AVP release to ECFv contraction 3)High-set osmoreceptor: AVP release is sluggish/delayed 4)AVP release at normal Posm but subnormal in amount What is Appropriate Urine Concentration?

6 Osmolality Plasma Osmolality: Posm = 2 (Na) + glucose + urea Normal = 2 (140) = 290 ( mM) Urine Osmolality: Normal: mM »Maximal dilution mM (U SG ) »Maximal concentration mM ( U SG ) Concentrated Urine: > 500 mM (at least!), U SG > i.e. U OSM > P OSM is not enough to R/O Diabetes Insipidus

7 Urine Specific Gravity U SG Estimates solute concentration of urine on basis of weight as compared with an equal volume of distilled water Normal Posm is % heavier than water so P SG = Each ↑ in U OSM mM ↑ U SG by 0.1% (0.001) Therefore, U SG of ~ U OSM mM Larger MW urinary OSM (glucose, radiocontrast, carbenicillin) if present will falsely elevate U SG Nothing falsely lowers U SG

8 Hyponatremia Serum OSM Low NormalHigh Hypotonic Hyponatremia ECFv * Low Normal High Hyperglycemia Mannitol Marked hyperlipidemia (lipemia, TG >35mM) Hyperproteinemia (Multiple myeloma) CHF Cirrhosis Nephrosis Hypothyroidism AI SIADH Reset Osmostat Water Intoxication 1° Polydipsia TURP post-op Renal loss (U Na > 20) Diuretics Thiazide K-sparing ACE-I, ARB IV RTA, Hypoaldo Cerebral salt wasting Extra-renal loss (U Na <10) Bleeding Burns GI (N/V, diarrhea) Pancreatitis * Note: all have ↑ADH SIADH: inappropriate Rest: appropriate

9 Rx Hyponatremia Na deficit = 0.6 x wt(kg) x (desired [Na] - actual [Na]) (mmol) When do you need to Rx quickly? –Acute (<24h) severe (< 120 mEq/L) Hyponatremia Prevent brain swelling or Rx brain swelling –Symptomatic Hyponatremia (Seizures, coma, etc.) Alleviate symptoms “Quickly”: 3% NS, 1-2 mEq/L/h until: Symptoms stop 3-4h elapsed and/or Serum Na has reached 120 mEq/L Then SLOW down correction to 0.5 mEq/L/h with 0.9% NS or simply fluid restriction. Aim for overall 24h correction to be < mEq/L/d to prevent myelinolysis

10 Rx Hyponatremia (Example) Na deficit (mmol) = 0.6 x wt(kg) x (desired [Na] - actual [Na]) 60 kg women, serum Na 107, seizure recalcitrant to benzodiazepines. Na defecit = 0.6 x (60) x (120 – 107) = 468 mEq Want to correct at rate 1.5 mEq/L/h: 13/1.5 = 8.7h 468 mEq / 8.7h = 54 mEq/h 3% NaCl has 513 mEq/L of Na 54 mEq/h = x 513 mEq 1L x = rate of 3% NaCl = 105 cc/h over 8.7h to correct serum Na to 120 mEq/h Note: Calculations are always at best estimates, and anyone getting hyponatremia corrected by IV saline (0.9% or 3%) needs frequent serum electrolyte monitoring (q1h if on 3% NS).

11 Rx Hyponatremia Rx slowly (correct < 0.5 mEq/L/h, mEq/L/d) –Symptomatic/Acute: rapid Rx has resolved symptoms and brought serum Na up to 120 mEq/L –Asymptomatic, mild, chronic hyponatremia –Want to prevent myelinolysis Increased risk: Women, alcoholics, malnourished ECFv contracted Bolus NS until BP, HR, JVP stable Then correct slowly with 0.9% NS or po salt ECFv Normal or ECFv Overloaded Fluid Restriction alone (exception: SAH, HI, post-neurosurgery) i.e. they do NOT need any IV or po salt!

12 SIADH Ddx Intracranial disease Pulmonary disease Chest wall disorder (surgery, VZV) Severe pain or emotional distress Severe N/V Ectopic ADH: Small cell lung cancer Drugs: opiods, carbamazepine, chlorpropamide, cyclophosphamide, cisplatin, vincristine, vinblastine, amitriptylline, SSRI, neuroleptics, bromocriptine, ecstasy (MDMA)

13 SIADH Diagnosis Normal ECFv (or slightly increased) Hypothyroidism & AI ruled out ↓ serum Na/OSM U OSM > 100 mM, U Na > 40 mEq/L Low plasma uric acid (< 238 umol/L) (1 mg/dL=59.48 µmol/L) Treatment Fluid Restriction Oral Salt, Hi-protein diet or Urea (30 g/d): promote solute diuresis Lasix 20 mg po od-bid: Loop direct diminishes medullary gradient Demeclocycline mg bid (can be nephrotoxic) Lithium (induces NDI) IV salt solution: Rarely if ever needed (i.e. only if symptomatic with SZ/coma) Solution given must be of greater OSM than U OSM or in long run will just make hyponatremia worse (often IV NS not sufficient)

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15 SIADH: Example U OSM fixed 600 mM due to ADH action 1L NS given: 300 mM (154 mM each of Na and Cl) All sodium will be excreted as renal sodium handling is intact in SIADH. 300 mmoles of osmols given excreted in 500cc urine (300mmoles/500mL = 600 mM) Therefore net gain of 500 cc free water! 1L 3% saline given: 1026 mmoles Excreted in 1.7L to keep U OSM 600 mM Therefore net loss of 700 cc free water! NOT advocating use of any IV NS (0.9% or 3%) in SIADH unless absolutely neccesary (i.e. SZ, coma). Most SIADH hyponatremia is chronic and should be corrected slowly with fluid restriction ONLY.

16 Reset Osmostat 25-30% of circumstances which cause SIADH Downward resetting of the threshold for both ADH release and thirst. Mild asymptomatic hyponatremia (Na mEq/L) Distinguish from SIADH by observing response to water load (10-15 mL/kg po or IV) Normal subjects and those with reset osmostat will secrete the entire water load over 4h without any worsening of the hyponatremia Attempts to correct hyponatremia in reset osmostat are not needed and will cause severe thirst

17 Cerebral Salt Wasting Cerebral disease (particularly SAH) Mimics SIADH with hyponatremia except primary defect is salt wasting not water retention. Circulating factor which impairs renal tubular fn. Atrial natriuretic peptide? Brain natriuretic peptide? Endogenous ouabain? Plasma urate variable (normal or even lower than SIADH) Treatment is NS to correct ECFv contraction

18 SIADH v.s. Cerebral Salt Wasting SIADHCSW Serum Na↓↓ ECFvNormal↓ U Na ↑↑↑ U OSM ↑↑ Urine volumeN or ↓↑ Serum urate↓N or ↓ Urine urate↑N or ↑

19 Rx Hyponatremia: acute SAH/Head injury May have SIADH, CSW or Both! Often difficult to tell which Fluid restriction inappropriate for CSW as may exacerbate ECFv contraction and precipitate cerebral vasospasm and subsequent cerebral infarction IV NS inappropriate for SIADH if U OSM > 300 mM (will make hyponatremia worse) Rx with IV NS: Start with 0.9% NS (as per hypervolemic therapy to prevent cerebral vasospasm) If hyponatremia worsens on 0.9% NS (due to an SIADH component to hyponatremia) consider switch to 3% NS Goal: 0.5 mEq/L/h (only if symptomatic 1-2 mEq/L/h) Fludrocortisone mg/d May also be beneficial in recalcitrant cases to alleviate CSW.

20 Indications for 3% NaCl Symptomatic hyponatremia (SZ, coma) Acute severe hyponatremia (<24h, < 120 mEq/L) SAH with hyponatremia worsening on 0.9% NaCl

21 Sodium Disorders Hypernatremia William Harper, MD, FRCPC Endocrinology & Metabolism Assistant Professor of Medicine McMaster University

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23 Diabetes Insipidus Ddx Diabetes Mellitus Hypercalcemia Solute diuresis: »Volume expansion 2° saline loading »High-protein feeds (urea as osmotic agent) »Post-obstructive diuresis Diabetes Insipidus: »Central (CDI) »Nephrogenic (NDI) Primary (Psychogenic) Polydipsia Polyuria: > 3 L/d +Polydipsia: > 3.5 L/d

24 Diabetes Insipidus Ddx Central (CDI) Idiopathic –autoimmune Neurosurgery, head trauma Cerebral hypoperfusion Tumor –Craniopharyngioma, pituitary adenoma, suprasellar meningioma, pineal gland, metastasis Infiltration –Fe, Sarcoid, Histiocytosis X Nephrogenic (NDI) X-linked recessive Hypokalemia Hypercalcemia (2° to HPT in particular) Renal disease: after ATN, postobstructive uropathy, RAS, renal transplant, amyloid, Sickle cell anemia Sjogren’s Drugs: –Lithium, 20% of chronic users –Demeclocycline, amphotericin, colchicine

25 1)Complete DI 2)Defective osmoreceptor, normal AVP release to ECFv contraction 3)High-set osmoreceptor: AVP release is sluggish/delayed 4)AVP release at normal Posm but subnormal in amount What is Appropriate Urine Concentration?

26 Diabetes Insipidus Intact thirst & access to water Hi-normal serum sodium ( mEq/L) Polydipsia (crave cold fluids) Polyuria, Nocturia  sleep disturbance 1° treatment is pharmacological Impaired thirst or access to water: Hypernatremia Insufficiently concentrated urine 1° treatment is free water (enteral or IV D5W)

27 Diabetes Insipidus Healthy out-patients DI with Intact thirst or access to water Hi-normal serum sodium ( mEq/L) Polydipsia (crave cold fluids) Polyuria, Nocturia  sleep disturbance 1˚ Psychogenic Polydipsia Low-normal serum sodium ( mEq/L) Anxious middle-aged women Psychiatric illness, phenothiazine (dry mouth)

28 1˚ Polydipsia

29 1˚ Polydipsia: “What came first?” The Chicken or the Egg? (Egg) The Polyuria or the Polydipsia?

30 Water Deprivation Test Hold water intake for 2-3h prior to coming in. Continue to hold water & Monitor: Urine volume, U OSM q1h Serum Na, OSM q2h If serum OSM/sodium do not rise above normal ranges & UOSM reaches 600  1˚ Polydipsia If serum OSM reaches mM & U OSM doesn’t ↑ Diabetes Insipidus established Endogenous ADH should be maximal, check serum ADH –2 green rubber stopper tubes, pre-chilled, on ice, need biochemist Give DDAVP 10 ug IN –CDI: U OSM ↑ by % (complete CDI), ↑ by 15-50% (partial CDI) with absolute U OSM > 345mM –NDI: U OSM ↑ by up to < 9%, sometimes ↑ as high as 45% but absolute U OSM always < isotonic (290 mM)

31 Diabetes Insipidus Back to in-patients! Impaired thirst or access to water Elevated serum sodium/OSM U OSM < 500 mM, U SG < If serum sodium/OSM not elevated Not DI! U OSM and U SG are irrelevant

32 Pituitary Surgery Triphasic response to surgery Phase 1: DI Axonal injury 2° surgery/swelling Begins after POD #1 (pre-existing DI can occur earlier) Lasts 1-5d Phase 2: SIADH Axonal necrosis of AVP secreting neurons with uncontrolled AVP release Lasts 1-5 days Phase 3: DI Axonal death with cessation of AVP production Usually permanent

33 1611 POD # P Na (mEq/L) U/O (cc/h) U/O #1 U/O #2

34 1611 POD # P Na (mEq/L) U/O (cc/h) Na #1 U/O #1

35 1611 POD # P Na (mEq/L) U/O (cc/h) Na #2 U/O #2

36 1611 POD # P Na (mEq/L) U/O (cc/h) Na #1 Na #2 U/O #1 U/O #2 #1 DI #2 Normal

37 Treatment of DI Rx Dehydration NS initially if ECFv contraction Then IV D5W or enteral free water to lower serum [Na] »1-2 mEq/h if Na > 160, symptomatic (coma, SZ), acute »Otherwise mEq/h Insensible losses? (0.5 L/d) Do NOT replace U/O if giving DDAVP DDAVP (Desmopressin) Reduces U/O and therefore simplifies fluid therapy Long t½: duration 8-12h, up to 24h Therefore use judiciously »DDAVP 1ug IV/SC x 1 »Only repeat if breaks-thru again (i.e. becomes hypernatremic with dilute polyuria) »Once nasal mucosa stable can switch to intranasal »Also oral form DDAVP now available DDAVP: 1ug IV/SC = 10 ug IN = 0.1 mg PO

38 Treatment of DI AVP, Aqueous vasopressin (Pitressin) Only parenteral form, 5-10 U SC q2-4h Lasts 2-6h Can cause HTN, coronary vasospasm Chlorpropamide (OHA which stimulates AVP secretion) mg po OD-bid Only useful for partial DI, can cause hypoglycemia HTCZ (induces volume contraction which diminishes free water excretion) mg OD-bid Mainstay of Rx for chronic NDI Amiloride (blunts Lithium uptake in distal tubules & collecting ducts) 5-20 mg po OD-bid Drug of choice for Lithium induced DI Indomethacin mg po bid-tid (PGs antagonize AVP action) Clofibrate 500 mg po qid (augments AVP release in partial CDI) Tegretol mg po od (augments AVP release in partial CDI)


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