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Na /K Disorders. Dr Mojgan Mortazavi. SODIUM. Hyponatremia. Hyponatremia. Hyponatremia defined as a Na+ <135meq/l that usually reflects hypoosmolality . Low plasma osmolality causes water movement into the cells and then cellular overhydration particularly in brain cells.

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na k disorders

Na /K Disorders

Dr MojganMortazavi

hyponatremia
Hyponatremia
  • Hyponatremia defined as a Na+ <135meq/l that usually reflects hypoosmolality.
  • Low plasma osmolality causes water movement into the cells and then cellular overhydration particularly in brain cells
symptoms of hyponatremia
Symptoms of hyponatremia
  • The changes induced by acute hyponatremia (developing over 1-3 days) may result in permanent neurological damage and are primarily duo to cerebral overhydration
  • Nausea and malaise as the plasma Na+ falls acutely below 125 meq/l
  • Headache, lethargy, and obtundation may appear in Na+ between 115-120
symptoms of hyponatremia1
Symptoms of hyponatremia…..
  • The more sever changes of seizures and coma are not seen until the plasma Na+ is less than 110-115 meq/l
  • Women particularly premenopausal women ,appear to be at much greater risk of developing sever neurologic symptoms and of irreversible neurologic damage than men that may be related to differences in cerebral metabolism and sex hormones.
treatment
Treatment
  • There are two basic principles involved in the treatment of hyponatremia: 1-rasing the plasma Na+ at a safe rate 2-treating the underlying cause
treatment with nacl
Treatment with Nacl
  • True volume depletion
  • Diuretics
  • Adrenal insufficiency
treatment with h2o restriction
Treatment with H2O restriction
  • SIADH
  • Edematous state
  • Renal failure
  • Primary polydipsia
the risk factors for developing osmotic demyelination
The risk factors for developing osmotic demyelination
  • 1-More than a 12 meq/l elevation in Na+ in the first day
  • 2-Over correction of the Na+ to above 140 meq/l within the first 2 days
  • 3-Hypoxic or anoxic episodes prior to therapy
treatment of siadh
TREATMENT OF SIADH
  • Acute:

1-water restriction

2-hypertonic saline or Nacl tablets

3-loop diuretics

  • Chronic:

1-water restriction

2-high salt ,high-protein diet

3-loop diuretic

4-demeclocycline ,lithium

treatment of siadh1
TREATMENT OF SIADH
  • Asypmtomatic or Chronic
    • SIADH
      • Water restriction
        • 0.5-1 liter/day
      • Salt tablets
      • Demeclocycline
        • Inhibits the effects of ADH
        • Onset of action may require up to one week
treatment1
Treatment
  • Goal:
    • raise Na by <10 meq/L in the 1st 24 hours
    • raise Na by <18 meq/L in the 1st 48 hours
central pontine myelinosis
Central Pontine Myelinosis
  • Correction of Na too FAST
    • more common w/alcoholism, malnutrition, chronic illness
  • Symptoms: flaccid paralysis, dysarthria, dysphagia
    • Evolve over days – weeks
    • May extend dorsally  Sensory Tracts
      • locked-in syndrome
  • Turn off ADH & prompt diuresis 

Sudden & Dramatic Inc serum Na

hyponatremia1
Hyponatremia
  • Example:
    • a 60 kg women with a plasma sodium of 110 meq/L
    • Formula:
      • ΔSNa = {[Na + K]inf − SNa} ÷ (TBW + 1)
    • What is the TBW?
    • How high will 1 liter of normal saline raise the plasma sodium?
  • Answer:
    • TBW is 30 L
    • Serum sodium will increase by approximately 1.4 meq/L for a total SNa of 111.4 meq/L
hyponatremia2
Hyponatremia
  • Example:
    • a 90 kg man with a plasma sodium of 110 meq/L
    • Formula:
      • ΔSNa = {[Na + K]inf − SNa} ÷ (TBW + 1)
    • What is the TBW?
    • How high will 1 liter of 3% saline raise the plasma sodium?
  • Answer:
    • TBW is 54 L
    • Serum sodium will increase by approximately 7.3 meq/L for a total SNa of 117.3 meq/L
hyponatremia3
Hyponatremia

hollywoodphony.files.wordpress.com

  • Example:
    • 63 y/o female at 75 Kg with N/V/D for 4 days
    • SNa is 108 mEq/L
    • She has had one seizure in the ambulance
        • Plasma osmolality is 251 mosmol/kg
        • Urine osmolality is 47 mosmol/kg
        • Uric acid is 6mg/dl
    • What type of hyponatremia does this patient have?
    • What additional labs/studies would you want?
hyponatremia4
Hyponatremia
  • How will you Tx her?
    • Calculate the total body water
      • 0.5 x weight = 37.5 L
    • What rate of correction do you want?
      • 8 to 10 mEq/L in 6 to 8 hours
    • What fluid will you use?
      • 3% Saline
    • How will you calculate the amount of sodium to give her?
      • ΔSNa = {[Na + K]inf − SNa} ÷ (TBW + 1)
    • How will her sodium increase after 1 liter of 3% saline?
      • By 10.8 mEq/L to 118.8 mEq/L
hyponatremia5
Hyponatremia
  • What other medication will she need?
    • Lasix and a foley
  • Her sodium increases to 118.8 mEq/L over the next 8-10 hours. How will you continue to correct her hyponatremia?
    • ΔSNa = {[Na + K]inf − SNa} ÷ (TBW + 1)
    • ΔSNa = 154mEq/L – 118.8mEq/L ÷ 38.5L = 0.9 mEq/L
  • So 2 liters of normal saline over the next 14 hours
hypernatremia
HYPERNATREMIA
  • Hypernatremia is defined as a plasma Na+>145 meq/l
  • Hypernatremia represent hyperosmolality that results in water movement out of the cells into the extracellular fluid that causes cellular dehydration in the brain that is primarily responsible for the neurologic symptoms.
generation of hypernatremia
Generation of hypernatremia
  • Water loss: hypernatremia due to water loss occurs only in patients who have hypodipsia, in adults with altered mental status, and in infants.
  • Na+ concentration > 150 is virtually never seen in an alert adult with a normal thirst mechanism and access to water.
slide26

Hypernatremia

Fluid volume status assessed by physical eaxam

Hypovolemic

Loss of H2O>Na+ loss

Isovolemic

Loss of H2O

Hypervolemic

Gain H2O and Na+

Check urine Na+

Check urine Na+

Check urine Na+

>20 mEq/L

<10 mEq/L

>20 mEq/L

  • Renal loss
  • Diuretic
  • Glycosuria
  • Renal failure
  • Extrarenal loss
  • GI-vomiting
  • GI-diarrhea
  • Excess
  • sweating
  • Respiratory loss
  • Renal loss
  • Diabetic insipidis
  • Central
  • Nephrogenic
  • Extrarenal loss
  • Insensible losses
  • Skin
  • Respiration
  • Iatrogenic
  • Hypertonic NaHCO3
  • NaCl tablets
  • Hypertonic solutions
  • Mineralocorticoid
  • 1 Hyperaldosteronism
  • Cushing disease
  • Adrenal

o

  • Hypertonicdialysis
  • Hemodilysis
  • Peritoneal dialysis
  • Treatment
  • Water replacement
  • D5W at 1-2 mEq/L/hr
  • ± vasopressin for
  • Central DI
  • Treatment
  • Saline then hypotonic
  • solution
  • Treatment
  • Diuretics ± dialysis
symptoms of hypernatremia
Symptoms of hypernatremia
  • Lethargy ,weakness, irritability, are the earliest findings which can then progress to twitching ,seizures, coma, and death that are more related to cellular dehydration in the brain.
  • Patients with chronic hypernatremia may be relatively asymptomatic despite a plasma Na+ >170
  • The severity of the neurologic symptoms is related to the both the degree and more importantly ,the rate of rise in the effective plasma osmolality.
treatment of hypernatremia
Treatment of hypernatremia
  • Rapid correction of hypernatremia can induce cerebral edema, seizures, permanent neurologic damage, and death therefore the plasma Na+ must be slowly lowered unless the patient has symptomatic hypernatremia.
treatment of hypernatremia1
Treatment of hypernatremia……
  • Water deficit= 0.4 LBW( plasma Na-140/ 140)
  • The maximum safe rate at which the plasma Na+ should be lowered (in the absence of hypernatremic symptoms) is 0.5 meq/L/h or 12 meq/L/per day
formula for managing hypernatremia

CLINICAL USE

Estimate the effect of 1 liter of any infusate on serum Na+

FORMULA*

1. Change in serum Na+ =

2. Change in serum Na+ =

infusate Na+ - serum Na+

total body water + 1

(infusate Na+ + infusate K+) -serum Na+

total body water + 1

Estimate the effect of 1 liter of any infusate containing Na+ and K+ on serum Na+

Formula for Managing Hypernatremia
summary of managing hypernatremia
Summary of Managing Hypernatremia
  • Isotonic saline unsuitable except in ECF volume depletion causing hemodynamic instability
  • Switch to hypotonic solutions as soon as circulatory status stabilized
  • Avoid excessive rapid correction or over correction
  • Select the most hypotonic infusate suitable with appropriate allowances for ongoing fluid losses
  • Most important - reassess infusion prescriptions at regular intervals based on pt’s clinical status and electrolyte values
potassium balance
POTASSIUM BALANCE
  • Potassium is the major intracellular cation that is essential for a variety of cellular and neuromuscular functions.
  • The total body K+ stores in a normal adult are 3000-4000 meq(50-55meq/kg) and the normal plasma concentration is 3.5-5 meq/l and inside cells is about 140 meq/l
regulation of potassium balance
Regulation of potassium balance
  • The maintenance of K+ balance involves two functions: 1-the normal distribution of K+ between the cells and extra cellular fluid 2-the renal excretion of the K+ added to the extra cellular fluid from dietary intake and endogenous cellular breakdown
factors influencing the distribution of k between the cells and extra cellular fluid
Factors influencing the distribution of K+ between the cells and extra cellular fluid
  • Physiologic:

1-Na+k+ ATPase

2-catecholamines

3-insulin

4-plasma potassium concentration

5-exercise

  • Pathologic:

1-chronic disease

2-extra cellular PH

3-hyperosmolality

renal excretion of k
Renal excretion of k+
  • The urine is major route by which the K+ derived from diet and endogenous cellular breakdown , is eliminated from the body.
  • The primary event in urinary K+ excretion is the SECRETION of K+ from the tubular cell in to the lumen in the distal nephron.
renal handling of k
Renal Handling of K+
  • Glomerulus: freely filtered
  • PCT, Thick As limb LOH : reabsorbed
hypokalemia
Hypokalemia
  • Hypokalemia is defined as a K+ <3.5 meq/l, may result from one or more of the following: 1-decreased net intake

2-shift into the cells

3-increased net loss

slide44

Hypokalemia

  • Exclude reredistribution
  • Alkalosis
  • Insulin
  • Periodic paralysis
  • Barium poisoning
  • Vitamin B12 therapy
  • Extrarenal K losses
  • Urine electrolytes
  • K+<20 mEq/day
  • Na+>100 mEq/day
  • (If Na+<100 mEq/day repeat
  • Test after increasing dietary
  • Na+>100 mEq/day)
  • Biliary losses
  • Lower GI losses
  • Fistula
  • Skin losses
  • Renal K losses
  • Urine electrolytes
  • K+>20 mEq/day
  • Na+>100 mEq/day

High blood pressure

Normal blood pressure

Plasma renin levels

Serum HCO3 -

slide45

Plasma renin levels

Serum HCO3 -

  • High plasma renin
  • Malignant HTN
  • Renovascular disease
  • Renin secreting tumor
  • Low HCO3 –
  • RTA

Low plasma renin

High HCO3 -

Aldoserone

Urine chloride

  • High
  • Hyperlado-
  • Steronism
  • Bilateral
  • hyperplasia
  • Low
  • Mineralocorticoid
  • Ingestion
  • Adrenal hyperpasia
  • (congenital)
  • Cushing syndrome
  • <10 mEq/day
  • Vomiting
  • <10 mEq/day
  • Bartter
  • Syndrome
  • Diuretics
  • Magnesium
  • deficiency

T U

T U

symptoms of hypokalemia
Symptoms of hypokalemia
  • Marked symptoms are unusual unless the plasma K+ concentration is below 2.5-3 meq/l ,but in susceptible patients even mild reductions in the plasma potassium can predispose to potential fatal arrhythmia.
clinical features
Clinical Features
  • Mild hypokalemia : generally asymptomatic
  • Increased risk of mortality for pts with cardiovascular disease – trigger ventricular tachycardia / ventricular fibrillation

(decrease K+ : d/t sympathetic stimulation)

  • Digitalis induced arrhythmias – can occur with normal drug levels if hypokalemia is present
  • Diuretic induced hypokalemia & hypomagnesemia must be avoided in pts on drugs that prolong QT interval : as it predisposes to polymorphic VT / Torsade de pointes
  • Hypokalemia < 3 mEq/L : Symptomatic
cardiac
Cardiac
  • Digitalis Intoxication : ventricular extrasystoles

ventricular tachycardia

ventricular fibrillation

partial-complete AV block

bradycardia

atrial flutter

atrial fibrillation

  • Ventricular arrhythmias : tachycardia / fibrillation
neuro muscular
Neuro-muscular
  • Fatigue
  • Myalgia
  • Muscular weakness involving lower limbs

Severe Hypokalemia :

  • Paralysis ( extremities )
  • Weakness of respiratory muscles ( dyspnea )
  • Rhabdomyolysis (exercise induced)
gastro intestinal
Gastro-intestinal
  • Constipation
  • Paralytic ileus
fluid electrolyte
Fluid – Electrolyte
  • Polyuria( nephrogenic diabetes insipidus )
  • Polydipsia ( nephrogenic diabetes insipidus )
  • Increased ammonia production ( intracellular acidosis ) precipitate hepatic coma in pts with advanced liver ds
  • Edema
  • Chloride wasting
  • Metabolic alkalosis
  • Hypercalciuria
  • Phosphaturia
endocrine
Endocrine
  • Glucose intolerance ( decreased insulin secretion )
  • Growth retardation ( Reduced Growth hormone receptors

Reduced IGF-1 )

hemodynamic
Hemodynamic
  • Hypertension ( increased renin secretion )
abnormalities induced by hypokalemia
Abnormalities induced by hypokalemia
  • Muscle weakness or paralysis
  • Cardiac arrhythmias
  • Rhabdomyolysis
  • Renal dysfunction 1-impaired concentrating ability 2-increased ammonia production 3-impaired urinary acidification 4-increased bicarbonate reabsorption 5-renal insufficiency
  • Hyperglycemia
basic investigations
Basic Investigations
  • ECG : Initially : flattening of t wave

depression of ST Segment

development of prominent u waves

Severe hypokalemia : increased amplitude of p wave

increased QRS duration

  • S.Potassium
treatment of hypokalemia
Treatment of hypokalemia
  • Monitoring of ECG and muscle strength, is an essential part of the management of patients with sever hypokalemia
  • There is no definite correlation between the PLASMA k+ and BODY K+ stores.
  • A reduction in the plasma K+ from 4 to 3 meq/l requires the loss of 200-400 meq of K+
renal vs extra renal loss
Renal Vs Extra renal loss
  • Urinary K+: > 20 mEq/L – Renal loss
  • Urinary K + : < 20 mEq/L – Extrarenal loss
  • TTKG : Transtubular Potassium Gradient

( Urine K+ / Plasma K+ )

( Urine Osm / Plasma Osm )

  • TTKG : Renal loss : > 4

Extra renal loss : < 4

renal loss drugs
Renal loss - Drugs
  • Amphotericin B : tubular damage

increased excretion of K+

  • Aminoglycosides : renal wasting of K+
  • Thiazides, Furosemide, Acetazolamide : renal loss K+
  • Cisplatin
  • HYPOMAGNESEMIA : Significant renal K+ wasting
treatment of hypokalemia1
Treatment of hypokalemia…….
  • A variety of potassium preparations are available for oral and IV use including the CL-, HCO3-, phosphate ,gluconate.
  • In metabolic alkalosis and hypokalemia KCL preparation is choice
  • In metabolic acidosis and mild degree of hypokalemia KHCO3 is preferred
  • ORAL: KCL can be given orally in salt substitutes as a liquid or in a slow release tablet or capsule
treatment of hypokalemia2
Treatment of hypokalemia…….
  • IV: the standard IV kcl solution contains 2meq/ml each of k+ and cl-.
  • 20-40 meq of k+(10-20 ml) is added to each liter of saline solution.
  • In general ,no more than 60 meq/l should be given through a peripheral vein ,since higher concentration of k+ are very irritating ,resulting in pain and sclerosis of the vein.
treatment of hypokalemia3
Treatment of hypokalemia……..
  • 1-If k+ is between 3 to 3.5 meq/l treatment is not urgent and these patients can usually be treated with oral kcl at an initial dose of 60-80 meq/day
  • 2-In patients with sever symptoms or marked hypokalemia ,k+ must be give more rapidly. The plasma k+ will acutely rise by as much as 1-1.5meq/l after 40-60 meq oral kcl and by 2.5-3.5 meq/l after 135-160 meq/l but these maximum effect is transient ,why?
rate of potassium repletion
Rate of potassium repletion
  • IV potassium is administered at a maximum rate of 10-20 meq/h although as much as 40-60 meq/h has been given to patients with paralysis or life threatening arrhythmias.
  • This solution containing as much as 200 meq of k+ /L and are best tolerated if given into a large vein such as femoral vein (infusion through a central venous line should probably be avoided, why?
slide68

Rapid administration of k+ is potentially dangerous even in severely k+ depleted patients and should be used only in life threatening situation

hyperkalemia
HYPERKALEMIA
  • Hyperkalemia defined as a k+>5meq/l occurs as a result of either k+ release from cells or decreased renal loss.
  • There is an adaptive response in hyperkalemia
slide71

Hyperkalemia

  • Redistribution
  • Acidosis
  • Diabetic ketoacidosis
  • β-Blockade
  • Succinylcholine
  • Periodic paralysis
  • Digoxin toxicity
  • Spurious
  • Hemolysis
  • Thrombocytosis
  • Leukocytosis
  • Mononucleosis
  • (leaky RBC)

Potassium excess

  • Increased intake/
  • tissue release
  • Interavenous/oral intake
  • Hemolysis
  • Rhabdomyolysis
  • Tumor lysis
  • Stored blood

Renal function

Serum K+

(mEq/L)

Atrial standstill

Intraventricular

block

  • GFR <20 mL/min
  • Acute renal failure
  • Chronic renal failure

GFR >20 mL/min

9

Hyperkalemia

  • Tubular hyperkalemia
  • Without aldosterone
  • Deficient
  • Acquired
  • Obstruction
  • Renal transplants
  • SLE
  • Amyloidosis
  • Sickle cell
  • Drugs
  • K-sparing diuretics
  • Aldosterone Deficient
  • Addison disease
  • Hereditary
  • Adrenal defects
  • Drugs
  • Heparin
  • NSAID
  • ACE inhibitors
  • Cyclosporine
  • spironolactone

7

High T wave

4

Normal

Normal

symptoms of hyperkalemia
Symptoms of hyperkalemia
  • 1-Muscle weakness : most often begins in the lower extremities and ascends to the trunk and upper extremities. *The respiratory muscles and those supplied by the cranial nerves are usually spared
  • 2-Abnormal cardiac conduction: the cardiac toxicity is enhanced by hypocalcemia, hyponatremia, acidemia, and a rapid elevation in the plasma k+ concentration