Hyponatraemia Dr Samir Sahu Sr Consultant Critical Care & Pulmonology Apollo Hospitals, Bhubaneswar.
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Transcript of Hyponatraemia Dr Samir Sahu Sr Consultant Critical Care & Pulmonology Apollo Hospitals, Bhubaneswar.
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Hyponatraemia
Dr Samir Sahu
Sr Consultant
Critical Care & Pulmonology Apollo Hospitals, Bhubaneswar
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• Definition:– Commonly defined as a serum sodium concentration
135 meq/L
– Hyponatremia represents a relative excess of water in relation to sodium.
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• Epidemiology:– Frequency
• Hyponatremia is the most common
electrolyte disorder• incidence of approximately 1%• prevalence of approximately 2.5%• surgical ward, approximately 4.4%• 30% of patients treated in the intensive care unit• 15 to 22% in tertiary care setting
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• Epidemiology Cont.
– Mortality/Morbidity• Acute hyponatremia (developing over 48 h or less) are
subject to more severe degrees of cerebral edema
– sodium level is less than 105 mEq/L, the mortality is over 50%
• Chronic hyponatremia(developing over more than 48 h) experience milder degrees of cerebral edema
– Brainstem herniation has not been observed in patients with chronic hyponatremia
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Normal Water Metabolism• Na+ metabolism is primarily controlled by renin-
angiotension-aldoserone mechanism• Water is controlled by arginine vasopressin
(ADH)• Hypothalmic osmoreceptors • Osmoreceptors maintain serum osmolality
between 280 – 295 mOsm/kg• Increase of 2% can increase urine osmolality
due to water reabsorption & stimulate thirst. Decrease of 2% cause maximal dilution of urine
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Normal Water Metabolism• Baroreceptors in cardiac atria, aorta &
carotid arteries, carotid bodies & area postrema
• Non-osmotic stimulus from CVS requires a change of 10-20% in circulating volume or BP to influence ADH
• ADH production is also stimulated by nausea, hypoxia, hypercapnea, stress, hypoglycaemia, IPPV & diminished by opoids
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Pathogenesis• The main factor that contributes to development of
hyponatremia is impaired ability to excrete free water generated in response to ADH excess.
• Hypertonic urinary losses of electrolytes will result in hyponatremia in the absence of fluid administration - thiazide diuretics, cerebral salt wasting
• Excretion of free water will be impaired when there is a marked reduction in GFR, renal hypoperfusion or ADH excess
• ADH increases the permeability of the collecting duct to water, leading to retention of free water.
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Pathogenesis
• Hypovolemic and hypervolemic states of ADH excess are usually associated with avid salt and water retention; administration of hypotonic fluids results in dilutional hyponatremia
• In euvolemic states of ADH excess, hyponatremia results from a combination of free water retention and urinary sodium losses due to a natriuresis that preserves volume at the expense of serum sodium
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Physiology of vasopressin
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PATHOPHYSIOLOGY(cont.)
PathophysiologyPathophysiology
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• Types– Hypovolemic hyponatremia– Euvolemic hyponatremia– Hypervolemic hyponatremia– Redistributive hyponatremia– Pseudohyponatremia
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• Develops as sodium and free water are lost and/or replaced by inappropriately hypotonic fluids
• Sodium can be lost through renal or non-renal routes
www.grouptrails.com/.../0-Beat-Dehydration.jpg
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• Nonrenal loss– GI losses
• Vomiting, Diarrhea, fistulas, pancreatitis– Excessive sweating– Third spacing of fluids
• ascites, peritonitis, pancreatitis, and burns – Cerebral salt-wasting syndrome
• traumatic brain injury, aneurysmal subarachnoid hemorrhage, and intracranial surgery
• Must distinguish from SIADH
www.jupiterimages.com
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• Renal Loss– Acute or chronic renal
insufficiency– Diuretics
www.ct-angiogram.com/images/renalCTangiogram2.jpg
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• Normal sodium stores and a total body excess of free water.– Psychogenic polydipsia, often in psychiatric patients – Administration of hypotonic intravenous or irrigation
fluids in the immediate postoperative period – Administration of hypotonic maintenance intravenous
fluids– Infants who may have been given inappropriate
amounts of free water – Bowel preparation before colonoscopy or colorectal
surgery
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• High levels of ADH are secreted intermittently at an abnormally low threshold or continuously despite low osmolality from Post. Pituitary
• Reduced ability to excrete dilute urine <20mq/l• Ingested fluid is retained• Extracellular fluid Expands (hyposm<290)• Mild natruresis by water expansion• Excrete daily ingested Na (Na balance zero)• Plasma osmolality Aldosterone
Hypokalaemia
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SIADH - CAUSES
• DRUGS - Thiazides, Frusemide- NSAIDS-Brufen, Piroxican Diclofenac - Narcotic Analgesics -Morphine- Anti-depressant Fluoxetine SSRI- Anti Neoplastic-Vincristine Cis-platin Cyclophospamide- Amiodarone, Carbamazepine
• Pulmonary Diseases Pneumonia, Asthma, Carcinoma.• CNS Dis-CVA, Brain Surg, Head Inj. • Malignancy, Stress.
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• Total body sodium increases, and TBW increases to a greater extent.
• Can be renal or non-renal– acute or chronic renal failure
• dysfunctional kidneys are unable to excrete the ingested sodium load
– cirrhosis, – congestive heart failure,– nephrotic syndrome
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Clinical Diagnosis of Acute & Chronic Hyponatremia
Symptoms related to degree of Na insufficiency:
ACUTE121-130 mEq/L Nausea, malaise, headache, lethargy, muscle cramps disorientation, restlessness <120 mEq/L Obtundation, seizures, respiratory arrest, coma, death
CHRONIC Usually Asymptomatic / Non-SpecificNausea, fatigue, gait disturbance, forgetfulness, muscle cramps, confusion, lethargy
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Thiazides• Hyponatraemia with low doses (12.5-25 mg/day)
• Usually evident within 14 days of onset of therapy, but can occur up to 2 years later.
• More common in women and elderly with low body wt
• Initial volume depletion induced by thiazides can stimulate the release of ADH, susceptible patients appear to have a reduced innate ability to excrete water load. These patients may not have clinical features of volume depletion & can be also classified as euvolaemic hypotonic hyponatraemia.
• Cerebral oedema is extremely rare
• In many of these patients, hyponatraemia is reproducible with a thiazide rechallenge
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APPROACH TO CAUSE OF HYPONATRAEMIA
S.Na< 130 Assess ECV
______________________________________
LOW NOR MAL HIGH Ur. Na Urine Na Ur. Na
_______________ _________________ _______________ >20 < 20 > 20 < 20 > 20 <
20 DIURETIC DIARR SIADH PSY POL RENAL F. CCF
ADRENAL Insf RENAL FAIL. PR.DIL Hypothyroidism CIRRHOSIS
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MANAGEMENT
LOW ECV-Diarrhoea, Diuresis, Adrenal Insufficiency
Plasma NS 5%DNS RLNa 141 154 154 130K 4.5 - - 4.0
- Rapid correction is necessary in Acute & Severe Hyponatraemia(S.Na<120) where there is severe symptoms-seizure, coma
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MANAGEMENT
II. HIGH ECV-Renal Failure CCF, Cirrhosis
• Frusemide induced diuresis till S.Na>120
• ACE inhibitors in CCF-Inhibits ADH directly
• Sometimes Oral Salts & Isotonic Saline may be necessary
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HYPONATREMIA - TREATMENT
CHARACTERISTICS OF INFUSATES
Infusate
Infusate Na(meq/L)
Extracellular Fluid
Distribution (%)
5% Sodium chloride in water 855 100
3% Sodium chloride in water 513 100
0.9% Sodium chloride in water 154 100
Ringer’s Lactate solution 130 97
0.45% Sodium chloride in water 77 67
0.2% Sodium chloride in 5% dextrose in water
34 47
5% Dextrose saline 154 100
5% Dextrose in water 0 33
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Less severe symptoms – 0.9% Nacl Soln.
(154meq/L)
Severe Symptoms – 3% Nacl
(250ml bottle – 513 meq/L)
HYPONATREMIA- TREATMENT
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Normal Saline
• Use of 0.9% saline (308 mOsm/l) alone may make the hyponatraemia worse, depending on the patient's serum and urine osmolality.
• 0.9% saline may be attempted in selected patients with urine osmolality of < 500 mOsm/kg water.
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MANAGEMENTNORMAL ECV-SIADH• Free water intake from all sources should be restricted
to less than 1-1.5 l/day• Mild symptoms- Isotonic Saline
- Fluid Restriction (<1500 ml/d)
- Oral Salts-No 5D or free water
Salt therapy is generally contraindicated in patients with hypertension and oedema, as it leads to exacerbation of both conditions
• Severe symptoms - Frusemide diuresis (delivers more dilute urine by inhibiting ADH effect in the collecting tubule) followed by 3% saline infusion.
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TREATMENT OF ACUTE HYPONATREMIA
• Patients with symptomatic hyponatremia need aggressive management with 3% NaCl (513 mmol/l, 1026 mOsm/l)
• Patients with severe symptoms such as seizures, respiratory arrest or neurogenic pulmonary edema should receive 100 ml of 3% NaCl as a bolus over 10 min in order to rapidly reverse brain edema.
• Patients with less-severe symptoms, such as headache, nausea, vomiting or lethargy, can be treated via an infusion pump to achieve a correction of 4–8 mmol/l in the first 4 h.
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TREATMENT OF ACUTE HYPONATREMIA
• To prevent complications arising from excessive therapy, 3% NaCl should be discontinued when symptoms subside or rise is > 10 mmol/l in 5 hours
• The rate of correction should not exceed 20 mmol/l in the first 48 h, and correction should be to mildly hyponatremic values(120), avoiding normonatremia and hypernatremia in the first 48 h.
• In general, 1 ml/kg body weight of 3% NaCl will increase the serum sodium level by about 1 mmol/l. Continuous infusion of 3% NaCl at a rate of 50–100 ml/h administered over 4 h is usually sufficient to reverse symptoms
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CHRONIC HYPONATREMIA
Slow correction
Usually Not > 8meq/L/day
Oral route is better – Salt
NaCl 1gm = 17 meq of Na
If symptomatic –
↑ Plasma Na > 1meq/Lhr then slowly
HYPONATREMIA - TREATMENT
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Tolvaptan: Vasopressin Antagonist
Dose & Administration:
•Blocks the V2 receptors in the kidney that mediate the diuretic effect of ADH
Can be administered without regard to meals . The recommended starting dose is 15 mg once daily. Dosage may be increased at intervals ≥24 hr to 30 mg once daily, and to a maximum of 60 mg once daily. No dosage adjustments necessary based on Age/Gender Patients can take water in response to thirst. No dosage adjustments are necessary based on cardiac, hepatic or renal function. Tolvaptan is not recommended in patients with creatinine clearance <10 ml/min.
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Tolvaptan: Adverse Effects
ThirstDry mouthFrequent urinationNauseaConstipationLoss of AppetiteFeverWeakness
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Tolvaptan:
ContraindicationsndicationsUrgent need to raise serum sodium levels
Inability of the patients to sense or appropriately respond to thirst
HypovolemicConcomitant use with CYP3A
inhibitors.Anuric patients.
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Central (Pontine) Myelinolysis• Patients with chronic gradual onset
hyponatraemia are typically asymptomatic because of the brain adaptation to changes in osmolality.
• This adaptation occurs at the expense of loss of intracellular osmolytes, which normally protect the brain from a sudden increase in osmolality of the ECF.
• In these patients, rapid increase in plasma osmolality results in water moving out of neurons, leading to shrinkage of cerebral tissue.
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Central (Pontine) Myelinolysis• Central myelinolysis, which was first described in the pons,
but can occur diffusely throughout the brain.
• Neurological deterioration typically develops over several days with fluctuating consciousness, convulsions, hypoventilation and hypotension.
• Eventually, patients may develop pseudobulbar palsy with difficulty in swallowing, inability to speak and quadriparesis.
• Recovery from this syndrome is variable, and many neurological complications are permanent.
• The magnetic resonance imaging (MRI) scans demonstrate the demyelinated lesions 3-4 weeks after the correction of hyponatraemia.
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CLASSICAL CASE15.10.99
• GP 72 yrs, M,-COPD, BEP• On Thiazide for oedema feet• Devoloped AcGE & became unconscious• GCS-7, No localized neurological deficit• S.Na-110, S.K-2.9, CT-normal• Stopped thiazide, corrected Hyponatraemia by
isotonic saline and fluid restrictions• Discharged in 5 days
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Case
• 10/04/2000• Took Ditide for oedema feet for 5 days• Vomiting-Seizure-Unconscious• Admitted at DHH / given Mannitol suspecting Stroke• GCS-5, no localized deficit• S.Na-101-103-112-119-123• S.K -2.3- 2.3- 3.- 3.0• Urinary Spot Na-96mEq/l• Stopped thiazide, corrected Hyponatraemia by isotonic
saline and fluid restrictions• Discharged in 7 days
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2006
• Post cataract operation seizure & drowsiness
• Na 100 mEq/l
• Improved with NS & fluid restriction
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HYPONATRAEMIA PRECIPITATING CAUSES
• Elderly Age• - Exaggerated response to ADH release• - Attenuated response to RAS• Fever, Vomiting, Inadequate intake• Salt restriction due to HTN/Oedema• Thiazides, Frusemide.• Fluid replacement with 5D • Mannitol suspecting Stroke.
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Thanks for Kind Attention
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Hypokalaemia
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Potassium Balance
Physiology
Normal a) 98% potassium - Intracellular
(151 meq/L)
b) 2% potassium - E.CF
(3.5 - meq/L)
ICF / ECF = 38;1
Total body content 2500 - 4500 mmol
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Potassium Balance
• Total Body Potassium – 45-50 mmol/Kg males, 35-40 mmol/Kg females
• 95% exchangeable
• 90% intracellular
• 2% ECF, 8% bones, 70% skelatal muscles
• Total body content 2500 - 4500 mmol
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Potassium Balance
Small loss or gain by cells
Large changes in serum K+
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Potassium Balance
Daily K+ intake 1meq/kg/day
50-150- meq/day
Normally - 90% excreted by kidney secretion by CCT
10% excreted through gut
Renal failure GIT losses > 30% sweat
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Potassium Balance
Secretion of K+ by cortical collecting Duct
Increases Decreases1. Aldosterone 1. Absence of aldosterone2. High serum K+ level 2. Low serum K+ level3. High urine flow 3. Low urine flow (osmotic diuresis)4. High sodium delivery 4. Low sodium delivery to to CCT CCT
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Potassium Shift
Shift from ECF to ICF
• Alkalosis
• Insulin
• B-adrenergics
Shift from ICF to ECF
• Acidosis
• Alfa-agonists
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Potassium excretion
1. Renal excretion is the major route of
elimination
2. Filtered load of K+ = 720
GFR x plasma K+ concentration
180 x 4 = 720 mmol/d
3. 90% is reabsorbed in the proximal
convoluted tubule and loop of henle
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Hypokalemia
Defined as a plasma K+ concentration
< 3.5 meq/lt
Decreased Redistribution Increasedintake into cells loss. Elderly. Starvation. Total parenteral nutrition
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HYPOKALEMIA DUE TOEXCESS POTASSIUMLOSS IN STOOL
PhenolphthaleinSodium polystyrenesulfonate
HYPOKALEMIA DUE TOTRANSCELLULARPOTASSIUM SHIFT
Adrenergic agonistsAdrenalineBronchodilatorsSalbutamol
HYPOKALEMIA DUE TOINCREASED RENALPOTASSIUM LOSS
DiureticsThiazidesMetolazoneFurosemideTorsemideMineralocorticoidsFludrocortisoneSubstances with mineralocorticoid effectsHigh-dose glucocorticoids
TheophyllineInsulin overdose
AminoglycosidesAmphotericin B
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Hypokalemia
Normal - 3.5-5 meq /lt
20% of the hospitalized patients have
hypokalemia
75% patients of Hypokalemia - 3-3.5
25% patients of Hypokalemia less than 3 meq/l
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Clinical Features
Vary between different individuals
Severity depend on degree of hypokalemia
Asymptomatic >3 meq/lit
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Clinical Features
Skeletal - Fatigue- Myalgia- Weakness of lower extremities - Cramps
More severe
Progressive weakness Complete paralysis Rhabdomyolysis
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Clinical Features
GI Tract - Nausea, vomiting, constipation,
distension, paralytic ileaus
Renal - Polyuria, Polydipsia
Respiratory - Respiratory Fatigue,
Hypoventilation
(Usually less than 2 meq/l)
Psychiatry – Psychosis, Delirium, Depression,
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Physical examination
Hypotension Signs of ileus Bradycardia, Tachycardia Premature ventricular beats, Cardiac arrest Hypoventilation, Respiratory distress Lethargy, Decreased muscular strength Decreased tendon reflexes
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Hypokalemia clinical features
Usually Present with serum K+ < 2.5 meq/L With rapid fall of serum K+
(1) Cardiac Predisposition of digoxin toxicity Ventricular irritability Abnormal ECG - T wave flattening
- U wave / ST- Ectopics
Cardiac necrosis
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Lab examination »Serum electrolytes »Urine analysis routine»Urine K+» Na+»24 hr urinary K+»Serum Mg»Arterial blood gases»Calcualtion of transtubular Potassium gradient
(TTKG)»Blood sugar»Creatine kinase
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Treatment of Hypokalemia
Basic Aim - to avoid life threatening
consequences
No need to correct entire deficit immediately
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Treatment of Hypokalemia
Estimation of potassium deficit
Assessment of the physiologic effect
a. Electrocardiography
b. Muscle strength
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Speed of potassium repletion
Potassium repletion is rarely an urgent
undertaking.
Always err on the lower side of estimate
to avoid hyperkalemia
Ideal - Administer from mouth over days
to weeks to correct deficits.
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Selecting appropriate rate of administration
Mild hypokalemia 3-3.5 mEq/lWell tolerated except patients - on digitalis - severe hepatic disease
No urgent treatment Prevent further lossOral KCl - 60-80 mEq/dayIf loss persistent - 100 mEq/day
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Route of administration Oral - Preferred in general if bowel sounds positive.Less chances of hyperkalemia.KCl 15 ml - 1.5 g KCl = 20meq KCl
Intravenous - severe hypokalemia Can not take orallyLife threatening situationsa) Paralysisb) Digitalis toxicity c) arrhythmiad) ECG abnormalitye) hypokalemia - hepatic complaints
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Intravenous administration
KCl - 2 meq/ml (10ml )ampoules
1. Do not give more than 40 meq/l by peripheral
vein, 60 meq/l by central vein
2. Prepare KCl in normal saline solution
3. Do not use dextrose, use glucose free
solution
4. Higher concentration can cause irritation,
pain or sclerosis of vein.
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Selecting appropriate rate of administration
Severe hypokalemia requiring emergent therapy
1. Patient to go for emergent surgery
2. Known CAD
3. Patient on digitalis
4. Acute MI with Ectopic
can give I/V 5-10 meq over 15-20 min. Repeat as
needed to achieve K+ > 3.0 Meq/l.
Rapid correction is always in ICU with cardiac
monitor.
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Correction of severe hypokalemia
1.Rapid correction should only be done in life
threatening situations - rarely
2.Frequent potassium estimation 4-6 hr
continuous ECG monitoring
3.Concentrated solutions should contain limited
amount of potassium per container.
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Correction of associated fluid and electrolyte disorders
Potassium depletion is rarely an isolated
phenomenon
Correct - Volume, Acid base equilibrium
Metabolic alkalosis
Magnesium
Hypophosphatemia
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Correction of hypomagnesemia
• Hypomagnesemia
- Renal potassium wasting
- Refractoriness to potassium
replacement
- Unexplained hypokalemia always look
for Hypomagnesemia
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Hypokalemia
Elimination of the cause of potassium loss
- Eliminate cause (eg. Diarrhea ) will repair
potassium deficit from diet (50-150 mmol/day)
- Spontaneous recovery, removal of tumors
- Alkalotic patient - dietary low chloride, potassium
not enough
-Correct kaliureteric mechanism
Primary aldosteronism - K+ sparing diuretic
- TTKG
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Hypokalaemic Periodic Paralysis
• Autosomal-dominant
• Ion channels in muscle sarcolema
• Adolescence
• Transcellular shift
• Needs K+ replacement
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Increased Renal Loss: increase mineralocorticoid effect
• Conn Syndrome – increase aldosterone production
• Cushings Syndrome – generalized adrenal hyperplasia
• Congenital Adrenal hyperplasia
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Increased Renal Loss
• Increased delivery of Na+ to distal segment
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