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Emergency lectures - Electrolyte disturbances

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  • However sensitivities may be between 18-51% (CJN 2008) Fewer than ½ of patients who experienced arrhythmias or cardiac arrest were noted to have new onset peaked T waves Reports from 1950s where ventricular fibrillation was first cardiac manifestation of hyperkalemia Also, Szerlip et al. Am J Kidney Dis 1986 reports two cases of K >9.0 without ECG manifestations
  • Remember, hyperkalemia can cause many different types of cardiac/ECG abnormalities including others than just classic as listed AV block with slow junctional & ventricular escape rhythm Any kind of conduction block: bundle branch block or fascicular block Sinus bradycardia Source: http://lifeinthefastlane.com/ecg-library/basics/hyperkalemia
  • Hyperkalemia Bottom rhythm strip shows progression from peaked T waves gradually to sine wave
  • Peaked T waves in hyperkalemia
  • Potassium quintiles by presence of strict criteria for electrocardiogram (ECG) changes.
  • Calcium directly antagonizes myocardial effects of hyperkalemia without lower plasma levels – reduces threshold potential of cardiac myocytes thus restoring normal gradient with the resting membrane potential
  • 3 times more calcium in CaCl vs. calcium gluconate Caution if pt is taking digoxin – should perhaps give it over 30min in D5W as Calcium can precipitate myocardial digoxin toxicity - Hypercalcemia can potentiate digitalis toxicity so calcium should be given in pts on dig only if there is loss of P waves or widened QRS Calcium: normally membrane resting potential is -90mV and threshold potential might be -75mV In hyperkalemia, the resting membrane potential moves towards more positive (more likely to achieve threshold potential) For e.g. resting potential might go from -90 to -80. With calcium, it causes the threshold potential to become less negative So it may move from -75 to -65, thus ensuring there’s still -15mV required for myocytes to excite
  • D50 represents 50g in 100cc of fluid – but 1 amp is actually 50cc (therefore 25g) Sodium bicarb works only if acidosis since bicarb pulls H+ out of cell, K+ goes in) that’s why only works with acidosis
  • SIADH: inappropriately concentrated urine despite normal circulating volume
  • Renal losses include: diuretics, renal tubular acidosis, salt-wasting nephropathy SIADH: often the most common cause in euvolemic hyponatremia should only be made as a diagnosis of exclusion
  • Some evidence suggests that even 8-10mEq per day correction is too much and risks osmotic demyelination syndrome. Newer recommendations from nephrology literature suggest goal of 6mEq correction
  • Drugs: either cause intracellular shift (catecholamines, salbutamol, verapamil, chloroquine) increased renal losses (acetazolamide, thiazide, loop diuretics, ampho B, penicillins, aminoglycosides)
  • Key causes: Conn’s syndrome caused by hyperaldosteronism causes hypertension & hypokalemia Hypokalemic periodic paralyses are associated with thyroid disease & cause symmetrical proximal muscle weakness
  • U waves & ST depression
  • Less frequently, hypernatremia is caused by increase in total serum sodium
  • Less frequently, hypernatremia is caused by increase in total serum sodium
  • Less frequently, hypernatremia is caused by increase in total serum sodium
  • Less frequently, hypernatremia is caused by increase in total serum sodium
  • Dermal losses include sweating & burn injuries In euvolemic patients with hypernatremia, there are two main mechanisms: Patients have impaired intake of fluid with increased insensible losses (mechanical ventilation) or renal losses Patients lose free water from inability of the kidney to concentrate urine (either a kidney problem or a hormonal signalling problem) – diabetes inspidius Hypervolemic patients actually are the rare patients with increased total body sodium can occur if patient is administered hypertonic electrolyte solutions like sodium bicarbonate Can occur if patient is ingesting sodium tablets or near-drowning in oceans
  • Central Diabetes Insipidus occurs in CNS disease or pituitary/hypothalamus surgery – stroke subarachnoid aneurysm granulomatous diseases (TB, sarcoidosis) infection, trauma systemic diseases Nephrogenic Diabetes insipidus : Renal failure sickle cell drugs (lithium, amphotericin B, aminoglycosides, ofloxacin), hypokalemia & hypercalcemia
  • Central: occurs in CNS disease or pituitary/hypothalamus surgery – stroke, infection, trauma & systemic diseases can all cause this Nephrogenic: Renal failure, sickle cell, drugs (lithium, amphotericin B, aminoglycosides), hypokalemia & hypercalcemia
  • Central: occurs in CNS disease or pituitary/hypothalamus surgery – stroke, infection, trauma & systemic diseases can all cause this Nephrogenic: Renal failure, sickle cell, drugs (lithium, amphotericin B, aminoglycosides), hypokalemia & hypercalcemia
  • Rapid correction will cause the extracellular tonicity to decrease, and water will shift into the brain cells cause cerebral edema and eventually herniation/permanent neurological deficits
  • Rapid correction will cause the extracellular tonicity to decrease, and water will shift into the brain cells cause cerebral edema and eventually herniation/permanent neurological deficits
  • Percent total body water depends on the person young men = 0.6 young women & elderly men = 0.5 elderly women = 0.4
  • Percent total body water depends on the person young men = 0.6 young women & elderly men = 0.5 elderly women = 0.4
  • Transcript

    • 1. Electrolyte Disturbances Andrew Petrosoniak PGY2 Emergency Medicine University of Toronto Canada May 25, 2010
    • 2.
      • Overview of hyperkalemia & hyponatremia
      • Important diagnostic tests
      • Management
      • This presentation also includes hypokalemia & hypernatremia – but for youre own reading!
      Objectives May 25, 2010
    • 3.
      • Case
      • 74 y female with shortness of breath and weakness
      • BP 135/58 HR 105bpm SpO2 96% RR 24
      • Additional history, she just started ACE inhibitor last week for hypertension
      May 25, 2010
    • 4. Hyperkalemia: Overview
      • 90% of potassium is intracellular
      • Ratio of extracellular to intracellular potassium (K) essential for cell membrane potential
      • Most K is eliminated via kidneys (95%)
      • K excretion occurs at distal nephron (collecting duct)
      May 25, 2010
    • 5. May 25, 2010
    • 6. Hyperkalemia: Causes
      • Lab/Human error (e.g. hemolysis)
      • Renal Failure +/- acidosis
      • Cell death (burns, tumor lysis syndrome)
      • Drugs/Toxins/Medications
        • Potassium supplements
        • Non-selective beta-blockers (propanolol)
        • Succinylcholine
        • Digoxin
        • K-sparing diuretic
        • ACE inhibitors
        • Pentamidine & Trimethroprim
      May 25, 2010
    • 7. Pseudohyperkalemia
      • Related to collection and storage of specimen
      • Difficulty in collecting sample
      • Patient clenched fist when sample was taken
      • Sample was shaken or squirted through needle into collection tube
      • Cooling
      • Deterioration of specimen due to length of storage
      • Thrombocytosis
      • Severe leucocytosis (which can also produce pseudohypokalaemia)
      May 25, 2010 Smellie BMJ 2007; 334: 693
    • 8. May 25, 2010 HYPERKALEMIA = ECG ECG may not correlate with potassium levels and so may NOT accurately predict likelihood for cardiac arrest
    • 9. Hyperkalemia: ECG
      • Peaked T waves
      • Widening QRS
      • Loss of P wave
      • Sine wave
      • Ventricular fibrillation/Asystole
      May 25, 2010
    • 10. May 25, 2010
    • 11. May 25, 2010
    • 12. May 25, 2010
    • 13. Potassium quintiles by presence of strict criteria for electrocardiogram (ECG) changes. Montague B T et al. CJASN 2008;3:324-330 ©2008 by American Society of Nephrology
    • 14. Hyperkalemia: Management
      • Membrane antagonism
      • Intracellular shift of potassium
      • Elimination of K from body
      May 25, 2010
    • 15. When does the patient need calcium?
      • Decision to treat emergently varies among clinicians
      • Consider some will ONLY treat if ECG changes
      • SAMPLE GUIDELINES
      • Plasma K > 6.5
      • EKG manifestations regardless of plasma level
      • * Consider acuity of rise
      May 25, 2010 Weisberg Crit Care Med 2008
    • 16. Membrane antagonism: calcium
      • Patient in cardiac arrest, sine wave or central venous access
      • IV Calcium Chloride (10%) 5ml over 2min*
      • *irritates veins, risk of extravasation
      • All other situations
      • IV Calcium gluconate (10% - 1amp) 10ml over 2-10min
    • 17. Intracellular potassium shift
      • IV Insulin R 10U and 2 amps D50 (50g)
        • Effect: 10-20min; Decr K level by 0.6-1.0mEq/L
      • Albuterol/Salbutamol 20mg in 4ml NS nebulized
        • Effect may last 1-2hrs: Decr K level by 0.6mEq/L
      • IV Sodium Bicarbonate (NaHCO3) 1-2 amps (50-100mEq/L)
        • Only if acidosis
    • 18. Elimination of K from body
      • Kayexalate 20-40mg PO/PR
        • Onset 2-6hrs; studies show mild effects
        • Risk of colonic necrosis
      • Furosemide 40-80mg IV
      • Dialysis
    • 19.
      • Case
      • 74 y female with shortness of breath and weakness
      • BP 135/58 HR 105bpm SpO2 96% RR 24
      • Additional history, she just started ACE inhibitor last week for hypertension
      May 25, 2010
    • 20.
      • Case
      • 74 y female with shortness of breath and weakness
      • BP 135/58 HR 105bpm SpO2 96% RR 24
      • Additional history, she just started ACE inhibitor last week for hypertension
      • Management
      • Calcium
      • Insulin & D50
      • Ventolin
      • Kayexalate
      • Consider HCO3 if acidosis
      • Lab calls and K=9.5
      May 25, 2010
    • 21.
      • Causes of hyperkalemia
      • Make sure it is TRUE hyperkalemia
      • ECG manifestations
      • If >6.5 or any ECG changes give calcium
      Recap: Hyperkalemia May 25, 2010
    • 22. Sodium
      • Primarily extracellular cation
      • Closely related to total body water
      • Sodium moves into cells
      • Na/K ATPase transports Na back out of cells
    • 23. Sodium Balance
      • Renin = released with low intravascular volume
        • Triggers sodium reabsorption & potassium excretion in distal nephron (via aldosterone)
      • ADH = released with high serum osmolality
        • Enhances renal water reabsorption
        • Other triggers: angiotensin, catecholamines, opiates, caffeine, stress, hypoglycemia, hypoxia
      May 25, 2010
    • 24. Case
      • 85 y male found with decreased level of consciousness at home
      • History of dementia but still functions at home
      • Found in his own urine, appears to have bit his tongue
      • BP 105/58, HR 74 RR 16 SpO2 94%
      • GCS 12 (E3V3M6)
      • Lab calls you because his serum Na = 103
      May 25, 2010
    • 25. Hyponatremia
      • Serum sodium <135mmol/L
      • Establish whether true hyponatremia (check glucose)
        • Na drops 3 mEq for every 10mmol increase of glucose
      May 25, 2010
    • 26. Hyponatremia
      • Two KEY questions
      • Does the patient have any neurologic symptoms possibly related to hyponatremia?
      • What is the patient’s volume status?
      • 3 Other considerations
      • Is there a sample error? E.g. IV near D5W infusion
      • Is it pseudohyponatremia? Hyperlipidemia/hyperproteinemia
      • Is there another osmole? E.g. Mannitol or Hyperglycemia
    • 27.
      • Hypovolemic: Loss of sodium more than water
      • Euvolemic: Most commonly SIADH = inappropriately concentrated urine
      • Hypervolemic: Both sodium & water retained but water >> Na
    • 28. Volume Status Hyponatremia
      • HYPOVOLEMIC
      • Renal losses
      • GI losses
      • Excess sweating
      • Addison’s disease
      • 3 rd spacing (burns)
      • EUVOLEMIC
      • SIADH
      • Psychogenic polydipsia
      • HYPERVOLEMIC
      • CHF
      • Hepatic cirrhosis
      • Nephrotic syndrome
    • 29. SIADH: causes
      • CNS disease (tumor, infection, trauma)
      • Pulmonary disease (pneumonia, TB, lung abscess)
      • Drugs (diuretics, chemotherapy)
    • 30. Hyponatremia: Clinical features
      • Lethargy, confusion, agitation
      • Weakness
      • Focal neuro deficits
      • Seizures
      • Altered level of consciousness
    • 31.
      • KEY POINTS
      • Always consider sodium abnormality in patient with altered level of consciousness
      • Acute hyponatremia: usually symptoms if <120mEq/L
      • Patients with chronic hyponatremia may tolerate lower levels without symptoms
    • 32. Investigations
      • CBC
      • Electrolytes
      • Serum osmolality
      • Uric acid
      • Consider TSH & cortisol
      • Urine: urinalysis, urine electrolytes, urine osmolality, urine creatinine
      May 25, 2010
    • 33. May 25, 2010
    • 34. Hyponatremia: work-up
      • Serum osmolality: Normal or elevated suggests presence of additional osmole (e.g. glucose, hyperlipidemia)
        • If hypotonic (low serum osmolality) then assess patient’s volume status
      • Urine osmolality & urine electrolytes
      May 25, 2010
    • 35. When does the patient require emergent treatment?
      • Neurologic impairment
      • Currently seizing or post-ictal
      • Altered level of consciousness or comatose
      May 25, 2010
    • 36. May 25, 2010 Immediate treatment is only required if the patient has neurological symptoms
    • 37. Hyponatremia: Emergency therapy
      • Goals of treatment: Rule of 6s
      • Increase serum Na by 6mEq per day
      • Increase serum Na by 6mEq in 6hrs if neurologic symptoms
      May 25, 2010 www.emcrit.org Sterns et al. 2010 Am J Kidney Dis 56:774
    • 38. Hyponatremia: Emergency therapy
      • IV 100cc of 3% saline over 20 minutes
      • If patient does not improve, then repeat 10 minutes later
      • Each 100cc will raise sodium by ~2mmol/L
      • Then STOP! Fluid restriction and admit to hospital
      • If persistent neurologic deficits, consider CT head
      May 25, 2010 www.emcrit.org Sterns et al. 2010 Am J Kidney Dis 56:774
    • 39. Hyponatremia: Over correction
      • Rapidly overcorrection of serum sodium can cause osmotic demyelination syndrome
      • Risk if >10mEq/L correction in 24hr period
      • Risk factors include:
        • Chronic hyponatremia
        • Serum Na <105mEq/L
        • Alcoholism
        • Malnutrition, liver disease
      • If concern about overcorrection then DDAVP 1-2mcg IV and consult nephrology
      May 25, 2010
    • 40.
      • Hypovolemic hyponatremia: volume deficits can be corrected with IV NS 0.9%
      • Euvolemic hyponatremia: free water restriction (500cc-1L/day)
      • Hypervolemic hyponatremia: fluid restriction, cautiously use diuretics (may increase Na urine excretion)
      May 25, 2010
    • 41. Case
      • 85 y male found with decreased level of consciousness at home
      • Found in his own urine, appears to have bit his tongue
      • BP 105/58, HR 74 RR 16 SpO2 94%
      • GCS 12 (E3V3M6)
      • Lab calls you because his serum Na = 103
      • Management
      • Neurologic impairment & probable seizure = 3% saline, start with 100cc, may require 2 nd dose
      • Monitor electrolytes every 4hrs, and give no additional fluid
      May 25, 2010
    • 42. Recap: Hyponatremia
      • Only correct serum Na levels if neurological symptoms
      • IV 100cc 3% saline (consider repeat)
      • Rule of 6s
      • Risk of osmotic demyelination syndrome
      • Overcorrection: DDAVP & nephrology
      May 25, 2010
    • 43. Hypokalemia
      • Assess muscle weakness/need for increased respiratory muscle use (e.g. metabolic acidosis)
      • Is this an emergency? (ECG changes)
      • Usually ABG also helpful
    • 44. Causes
      • Drugs (often thiazides, furosemide)
      • GI losses (vomiting/diarrhea)
      • Hormones
      • Bicarb abnormalities
      • Renal tubular defects
      • Magnesium deficiency
    • 45.
      • Decreased intake
      • Increased loss
        • Renal (CHF, nephrotic syndrome, dehydration)
        • Renal tubular defects (RTA)
        • GI losses (Vomiting, laxatives, diarrhea)
        • Drugs (Diuretics, Ampho B, mannitol, Aminoglycosides
      • Transcellular shifts
        • Alkalosis (vomiting, diuretics)
        • Insulin
        • Beta agonists
      Causes
    • 46. Clinical Manifestations
      • Cardiovascular: Arrhythmias, ECG changes, Digitoxicity
      • Skeletal muscle: weakness, cramps, tetany, paralysis (K<2.0)
      • Smooth muscle: constipation, urinary retention
      • Metabolic alkalosis
    • 47. May 25, 2010 HYPOKALEMIA = ECG
    • 48. Hypokalemia: ECG changes
      • Usually occurs when K <2.7mmol/L
      • PR prolongation
      • T wave flattening or inversion
      • ST depression
      • U waves
      • Apparent long QT interval (T & U waves fuse together)
      http://lifeinthefastlane.com/ecg-library/basics/hypokalaemia/
    • 49. http://lifeinthefastlane.com/ecg-library/basics/hypokalaemia/
    • 50.  
    • 51. Management
      • PO replacement is preferred unless IV is indicated
      • Indications for IV therapy
      • Dysrhythmias
      • Prominent symptoms
      • Unable to tolerate PO
      • Likely if K<2.5mEq/L
      • IV dose 10- 20mEq/hr (upto 40mEq/hr if central line)
    • 52. Management
      • Goal of therapy
      • K = 4.0 – 4.5
      • Probably reasonable to increase serum Mg levels to >1.0
    • 53. Management: Formulations
      • Formulation depends on etiology & other electrolyte levels
      • 1mEq drop in serum level = 100-200mEq total body store
      • KCl 20-40mEq PO 2-4 times/day (available in liquid, powder, pill)
      • KCl 20-40mEq IV in NS/RL
      • Other formulations include K-phos, K-bicarb, K-citrate
    • 54. Recap hypokalemia
      • Causes: think diuretics, diarrhea
      • Get an ECG
      • Clinically not an issue until <2.0 then think paralysis/weakness
      • Always check Mg, and likely replace it
    • 55. Hypernatremia: Overview
      • Serum Na >145mEq/L
      • Hypernatremia is a state of hyperosmolality
      • In general, causes are:
        • Thirst or water access related
        • Renal concentrating problems (kidney or hormone related)
        • Free water losses
      • In normal conditions:
        • water intake = losses
        • Salt intake = losses
      • One or both of these are disrupted in hypernatremia
      May 25, 2010
    • 56. Hypernatremia: Overview May 25, 2010 Hypernatremia is a “water problem” Each litre of free water loss causes 3-5mEq rise in sodium
    • 57. Hypernatremia: Etiologies
      • Reduced water intake
        • Inability to obtain water
        • Disorders of thirst perception
      • Increased water loss
        • GI losses: vomiting, diarrhea, third spacing
        • Renal losses: diabetes insipidus, renal tubular defects
        • Dermal losses: sweating, severe burns
      • Increased sodium
        • Exogenous sodium: salt tablets, hypertonic saline,
        • Increased reabsorption: Cushing’s disease, Exogenous corticosteroids, congenital adrenal hyperplasia
      May 25, 2010
    • 58. Hypernatremia
      • Two questions
      • What is the patient’s volume status?
      • Is the problem acute or chronic?
      May 25, 2010
    • 59. May 25, 2010 Hypernatremia Hypovolemia Euvolemia Hypervolemia
      • GI losses
      • Diuretics
      • Acute & chronic kidney disease
      • Hyperosmolar non-ketotic coma
      • Dermal losses
      • Diabetes insipidus
      • Fever
      • Mechanical ventilation
      • Iatrogenic
      • Hyperaldosteronism
      eMedicine. Hypernatremia 2010 Reynolds et al. BMJ 2006;332(7543):702-705
    • 60. Hypernatremia: Diabetes insipdus
      • Loss of large amounts of dilute urine
      • Lack of concentrating ability in distal nephron
      • Two main classifications
        • Central: Lack of ADH secretion
        • Nephrogenic: Kidneys no longer respond to ADH
      • sdf
      May 25, 2010
    • 61. Hypernatremia: Investigations
      • CBC
      • Serum electrolytes
      • Serum glucose
      • BUN, Creatinine
      • Urine electrolytes
      • Urine osmolality
      • Plasma osmolality
      • Measure urine output
      May 25, 2010
    • 62. Hypernatremia: Diagnosis
      • Establish volume status of the patient
      • Hypovolemia
        • Urine Na <10mEq/L: extrarenal fluid loss
        • Urine Na >20mEq/L: renal losses (diuretics, osmotic diuresis)
      • Euvolemia
        • High urine osmolality (>600-700 mOsm/kg): increased insensible losses
        • Low urine osmolality (<300 mOsm/kg): diabetes insipidus
      May 25, 2010
    • 63. Hypernatremia: Clinical features
      • Dehydration
      • Anorexia, nausea, vomiting, fatigue
      • Lethargy, confusion, coma
      • Hyperreflexia, spasticity, tremor, ataxia
      • Focal findings: upgoing toes, hemiparesis
      May 25, 2010
    • 64. Hypernatremia: Clinical features
      • Serum Osmolality
      • > 350 = excessive thirst
      • > 375 = weakness & lethargy
      • > 400 = ataxia, tremor
      • > 420 = focal neurological deficits, hyperreflexia
      • > 430 = coma & seizures
      May 25, 2010
    • 65. Management
      • Rate of sodium correction depends on how acutely hypernatremia developed & symptom severity
      • Acute: <48hrs
      • Chronic: >48hrs – requires slower correction because of risks of cerebral edema
      May 25, 2010
    • 66. Management May 25, 2010 Acute hypernatremia can be corrected at 1mmol/L per hour Chronic hypernatremia can be corrected at 0.5mmol/L per hour and no more than 10mmol/L per 24hrs
      • replace 50% of free water deficit in 12-24hrs and remaining deficit over next 24hrs
      • routinely check serum & urine electrolytes
      • perform serial neurological examinations
    • 67. Management
      • Hypovolemic: Restore volume deficits with IV NS 0.9% until hemodynamically stable then replace free water deficits
      • Euvolemic: Treat with hypotonic fluids with steps below
      • Calculate Total body water
        • Weight x % body water
        • Calculate change in serum Na after 1L of fluid (e.g. D5W or 0.45NS)
          • Change in serum Na = (infusate Na – serum Na) / (TBW + 1)
      • Amount of solution required = Serum sodium goal decrease / change in serum Na after 1L of fluid
      May 25, 2010
    • 68. Management
      • Case Example
      • 75 year male, obtunded, dry mucous membranes, fever, otherwise normal vital signs. Serum Na = 165 mmol/L; weight = 70kg
      • Total body water = 70kg x 0.5% = 35L
      • Change in serum Na (using 1L of D5W) = (0 – 165) / (35 + 1) = -4.6mmol
      • Goal over 24hrs, decrease by 10mmol/L
      • 10/4.6 = 2.17 L required plus 1L estimation of obligatory water loss = 3.17L
      • Thus over 24hrs, he’ll require D5W at 132cc/hr
      May 25, 2010 Lukitsch I. eMedicine. Hypernatremia 2010
    • 69. Hypernatremia: complications
      • Coma & seizures
      • Cerebral edema (if rapid correction)
      • Intracerebral hemorrhage especially in neonates
      May 25, 2010
    • 70. References
      • eMedicine
      • Rosen’s Emergency Medicine 7 th edition
      • Medscape
      • Listed literature sources
      • Emcrit.org
      • EMRap
      May 25, 2010