Practical Approach Practical Approach to Common to Common Electrolyte Electrolyte

EmergenciesEmergenciesMohammad Tinawi, MD, Mohammad Tinawi, MD,

FACPFACP

mtinawi@pol.netmtinawi@pol.net

Case #1Case #1 73 Y old man with PMHx of DM-II was 73 Y old man with PMHx of DM-II was

admitted with left hip fx after a fall at admitted with left hip fx after a fall at home.home.

He had a successful ORIF.He had a successful ORIF. In hospital medications: Insulin, In hospital medications: Insulin,

esomeprazole, enoxaparin, and IVF: D5W at esomeprazole, enoxaparin, and IVF: D5W at 100 ml/h100 ml/h

POD #3: Urea 84, Cr 1.4. A nephrology POD #3: Urea 84, Cr 1.4. A nephrology consultation was requested due to consultation was requested due to decreased level of consciousness.decreased level of consciousness.

Head CT showed old white matter disease.Head CT showed old white matter disease.

Case #1Case #1

The elevation in urea and creatinine The elevation in urea and creatinine is not the cause of his altered mental is not the cause of his altered mental status.status.

The elevation is prerenal in origin.The elevation is prerenal in origin. The patient was found to have lower The patient was found to have lower

GI bleeding causing the elevation in GI bleeding causing the elevation in urea.urea.

What is the cause of his altered What is the cause of his altered mental status?mental status?

Case #1Case #1

Answer: In hospital hyponatremia.Answer: In hospital hyponatremia. IatrogenicIatrogenic Due to inappropriate use of hypotonic Due to inappropriate use of hypotonic

IVFIVF Avoidable by using 0.9 NS in all patients Avoidable by using 0.9 NS in all patients

except in those with hypernatremiaexcept in those with hypernatremia The patient’s sodium was corrected The patient’s sodium was corrected

slowly to 134 mmol/L (over 72 h) with slowly to 134 mmol/L (over 72 h) with improvement in mental statusimprovement in mental status

Case #1Case #1

Hospitalized patients have numerous stimuli Hospitalized patients have numerous stimuli for arginine vasopressin production and are for arginine vasopressin production and are at risk of developing hyponatremiaat risk of developing hyponatremia

Routine administration of hypotonic Routine administration of hypotonic parenteral fluid to hospitalized patients can parenteral fluid to hospitalized patients can result in fatal hyponatremic encephalopathyresult in fatal hyponatremic encephalopathy

0.9% NaCl (154 mmol/l) should be 0.9% NaCl (154 mmol/l) should be administered as prophylaxis against administered as prophylaxis against hyponatremia, except in the setting of a free hyponatremia, except in the setting of a free water deficit or ongoing free water losseswater deficit or ongoing free water losses

Case #1Case #1

Patients at greatest risk of developing Patients at greatest risk of developing neurological complications secondary neurological complications secondary to hyponatremia are children, to hyponatremia are children, premenopausal females, postoperative premenopausal females, postoperative patients, and those with brain injury, patients, and those with brain injury, brain infection or hypoxemiabrain infection or hypoxemia

3% NaCl (513 mmol/l) is an essential 3% NaCl (513 mmol/l) is an essential treatment for hyponatremic treatment for hyponatremic encephalopathyencephalopathy

HyponatremiaHyponatremia

Na is mainly extracellular, K is intracellularNa is mainly extracellular, K is intracellular Serum osmol = 2(Na)+ BUN/2.8 + Gluc/18Serum osmol = 2(Na)+ BUN/2.8 + Gluc/18

Sodium is the primary determinantSodium is the primary determinant Abnormal ratio of Na to waterAbnormal ratio of Na to water Na < 135Na < 135 Most often due to retention of free waterMost often due to retention of free water

Secondary to impaired excretion of free waterSecondary to impaired excretion of free water Occ. due to Na loss exceeding water lossOcc. due to Na loss exceeding water loss

i.e. thiazide-induced hypoNa (elderly women)i.e. thiazide-induced hypoNa (elderly women)

HyponatremiaHyponatremia

Hyponatremia is Hyponatremia is usually due to too usually due to too much water rather much water rather than too little than too little sodium!sodium!

HyponatremiaHyponatremia Simply, hyponatremia is due to inability to match Simply, hyponatremia is due to inability to match

water excretion with water ingestionwater excretion with water ingestion 1. Defect in 1. Defect in water excretionwater excretion

SIADH SIADH (inappropriate ADH release)(inappropriate ADH release) HypovolemicHypovolemic state (appropriate ADH release) state (appropriate ADH release) HypervolemicHypervolemic (Increased ADH release) (Increased ADH release)

CHF, cirrhosis, nephrotic syndrome, ARF / CHF, cirrhosis, nephrotic syndrome, ARF / CRICRI

HyperglycemiaHyperglycemia (draws water into plasma) (draws water into plasma)

2. System overwhelmed (2. System overwhelmed (water ingestionwater ingestion)) i.e. primary polydipsiai.e. primary polydipsia

ManifestationsManifestations

Mild Sx: anorexia, nausea, lethargyMild Sx: anorexia, nausea, lethargy Mod Sx: disoriented, agitated, neuro Mod Sx: disoriented, agitated, neuro

deficitdeficit Sev Sx: seizures, coma, deathSev Sx: seizures, coma, death

Case #2Case #2

A 50-yr-old man with hemophilia, A 50-yr-old man with hemophilia, HIV/AIDS and cirrhosis caused by HIV/AIDS and cirrhosis caused by hepatitis C is admitted for renal failure. hepatitis C is admitted for renal failure.

Meds: furosemide, spironolactone, Meds: furosemide, spironolactone, sulfamethoxazole and trimethoprim sulfamethoxazole and trimethoprim

BP is 98/62 mmHg, scleral icterus, BP is 98/62 mmHg, scleral icterus, stigmata of cirrhosis, an abdominal stigmata of cirrhosis, an abdominal fluid wave, and pitting edema of his fluid wave, and pitting edema of his lower extremities. He has asterixis.lower extremities. He has asterixis.

Case #2Case #2

Labs: Na 128 mEq/L, K 5.7 mEq/L, Cl 95 Labs: Na 128 mEq/L, K 5.7 mEq/L, Cl 95 mEq/L, CO2 23 mEq/L, BUN 49 mg/dl, mEq/L, CO2 23 mEq/L, BUN 49 mg/dl, glucose 110 mg/dl, and creatinine 2.3 mg/dl.glucose 110 mg/dl, and creatinine 2.3 mg/dl.

Plasma osmolality 290 mOsm/kg. Urine Plasma osmolality 290 mOsm/kg. Urine osmolality is 580 mOsm/kg. Urine Na 53 osmolality is 580 mOsm/kg. Urine Na 53 mEq/L mEq/L

Random serum cortisol 25 g/dl, uric acid Random serum cortisol 25 g/dl, uric acid 14.2 mg/dl, serum triglycerides 50 mg/dl, 14.2 mg/dl, serum triglycerides 50 mg/dl, total cholesterol 95 mg/dl, total protein 11.7 total cholesterol 95 mg/dl, total protein 11.7 gm/dl, albumin 2.4 gm/dl.gm/dl, albumin 2.4 gm/dl.

Case #2Case #2

Which ONE of the following is the Which ONE of the following is the MOSTMOST

likely cause of the patient’s likely cause of the patient’s hyponatremia?hyponatremia?

A. Addison diseaseA. Addison disease

B. Trimethroprim therapyB. Trimethroprim therapy

C. Syndrome of inappropriate antidiureticC. Syndrome of inappropriate antidiuretic

hormone secretion (SIADH)hormone secretion (SIADH)

D. PseudohyponatremiaD. Pseudohyponatremia

Case #2Case #2 Answer: D. PseudohyponatremiaAnswer: D. Pseudohyponatremia Plasma osmolality is 290 which excludes Plasma osmolality is 290 which excludes

the various causes of hypotonic the various causes of hypotonic hyponatremia such as SIADH. hyponatremia such as SIADH.

His pseudohyponatremia is caused by his His pseudohyponatremia is caused by his extremely high serum protein extremely high serum protein concentration, a phenomenon that has concentration, a phenomenon that has been reported in patients with HIV and been reported in patients with HIV and hepatitis C.hepatitis C.

J Gen Intern Med 23:202-5, 2008Clin J Am Soc Nephrol 3:1175-84, 2008

Case #3Case #3 40-yr-old woman is admitted with the worst 40-yr-old woman is admitted with the worst

headache of her life. headache of her life. PE: wt 56 kg, BP 170/60 mmHg. Meningeal PE: wt 56 kg, BP 170/60 mmHg. Meningeal

signs are present.signs are present. Head CT: a small subarachnoid hemorrhage.Head CT: a small subarachnoid hemorrhage. Labs: Na 140 mEq/L, K 3.9 mEq/L, Cl 105 Labs: Na 140 mEq/L, K 3.9 mEq/L, Cl 105

mEq/L, CO2 22 mEq/L,mEq/L, CO2 22 mEq/L, BUN 17 mg/dl, BUN 17 mg/dl, creatinine 1.0 mg/dl, and hematocrit 37%. creatinine 1.0 mg/dl, and hematocrit 37%.

During the first 6 d of hospitalization, she is During the first 6 d of hospitalization, she is treated with nimodipine and 0.9% saline at treated with nimodipine and 0.9% saline at 200 ml/h. 200 ml/h.

Case #3Case #3 Gradually Na falls to 125 mEq/L. Mannitol 12.5 Gradually Na falls to 125 mEq/L. Mannitol 12.5

g is administered, and saline is continued. g is administered, and saline is continued. The next day, BP 148/66, wt: 58 kg. She is alertThe next day, BP 148/66, wt: 58 kg. She is alert

and oriented but complains of a headache. and oriented but complains of a headache. Labs on day 6: Na 124 mEq/L, K 4.2 mEq/L, Cl Labs on day 6: Na 124 mEq/L, K 4.2 mEq/L, Cl

91 mEq/L, CO2 22 mEq/L. BUN 11 mg/dl, 91 mEq/L, CO2 22 mEq/L. BUN 11 mg/dl, creatinine 0.9 mg/dl, glucose 260 mg/dl, and creatinine 0.9 mg/dl, glucose 260 mg/dl, and hematocrit 34. Serum osmolality is 260 hematocrit 34. Serum osmolality is 260 mOsm/kg; urine osmolality is 800 mOsm/kg. mOsm/kg; urine osmolality is 800 mOsm/kg. Urine values : Na 240 mEq/L, K 20 mEq/L, and Urine values : Na 240 mEq/L, K 20 mEq/L, and output 200 ml/h.output 200 ml/h.

Case #3Case #3

Which ONE of the following is the Which ONE of the following is the MOSTMOST

likely cause of her hyponatremia?likely cause of her hyponatremia? A. PseudohyponatremiaA. Pseudohyponatremia B. Translocational hyponatremia as a B. Translocational hyponatremia as a

result ofresult of

mannitolmannitol C. SIADHC. SIADH D. Cerebral salt wastingD. Cerebral salt wasting

Case #3Case #3 Answer Answer C: SIADHC: SIADH The patient has hypotonic hyponatremia with a The patient has hypotonic hyponatremia with a

measured plasma osmolality (260 mOms/kg) measured plasma osmolality (260 mOms/kg) excluding pseudohyponatremia (answer A) or excluding pseudohyponatremia (answer A) or translocational hyponatremia due to mannitol translocational hyponatremia due to mannitol (which raises plasma osmolality) (answer B). (which raises plasma osmolality) (answer B).

The high urine osmolality and urine sodium The high urine osmolality and urine sodium concentrations are consistent with either SIADH concentrations are consistent with either SIADH (answer C) or cerebral salt wasting (answer D). (answer C) or cerebral salt wasting (answer D).

Cerebral salt wasting is associated with volume Cerebral salt wasting is associated with volume depletiondepletion. The patient’s blood pressure is high, she . The patient’s blood pressure is high, she has gained weight, and her hematocrit has fallen, has gained weight, and her hematocrit has fallen, findings that are inconsistent with hypovolemia.findings that are inconsistent with hypovolemia.

J Am Soc Nephrol 19:194-6, 2008Clin J Am Soc Nephrol 2008

Treatment – UrgentTreatment – Urgent

If symptomatic & urgent, give If symptomatic & urgent, give hypertonic salinehypertonic saline

Do not correct more than 8 Do not correct more than 8 mEq /daymEq /day

Risk of central pontine myelinolysis Risk of central pontine myelinolysis (CPM)(CPM)

Treatment of Treatment of HyponatremiaHyponatremia

HypovolemicHypovolemic (diarrhea, diuretics) → (diarrhea, diuretics) → give volume: but never hypotonic give volume: but never hypotonic solutions.solutions.

HypervolemicHypervolemic (CHF) → Na & water (CHF) → Na & water restriction ± loop diureticsrestriction ± loop diuretics

Euvolemic (SIADH)Euvolemic (SIADH) → water → water restrictionrestriction

Case #4Case #4

80 year old woman, wt 60 kg, BP 80 year old woman, wt 60 kg, BP 175/70175/70

PMHx: Ongoing chemo for small cell PMHx: Ongoing chemo for small cell lung CAlung CA

Started on hydrochlorothiazide 25 mg/dStarted on hydrochlorothiazide 25 mg/d One week later she was admitted with One week later she was admitted with

seizuresseizures BP 140/68, Na 112BP 140/68, Na 112 How do we correct her hyponatremia?How do we correct her hyponatremia?

Case #4Case #4 Things to remember:Things to remember:

Na deficitNa deficit (mmol)(mmol) = 0.6 x wt (kg) x (desired = 0.6 x wt (kg) x (desired [Na] - actual [Na]) “in women 0.5”[Na] - actual [Na]) “in women 0.5”

0.9 NS has 154 meq/L of sodium0.9 NS has 154 meq/L of sodium 3% NS has 513 meq/L of sodium3% NS has 513 meq/L of sodium Use 3% in emergencies only and ask for a Use 3% in emergencies only and ask for a

consultconsult Check Na often while correcting q 2-3 hCheck Na often while correcting q 2-3 h Thiazides are associated with hyponatremiaThiazides are associated with hyponatremia Loop diuretics are associated with Loop diuretics are associated with

hypernatremiahypernatremia

Case #4Case #4

Na deficitNa deficit (mmol)(mmol) = 0.5 x wt (kg) x = 0.5 x wt (kg) x (desired [Na] - actual [Na])(desired [Na] - actual [Na])

Na deficit = 0.5 x 60 x (120 – 112) Na deficit = 0.5 x 60 x (120 – 112) = 240 mmol= 240 mmol

Amount of 3% NS: 240/513 = 467 Amount of 3% NS: 240/513 = 467 mlml

Rate 467/8 = 58 ml/ h (for 8 h only Rate 467/8 = 58 ml/ h (for 8 h only for the first 24 h).for the first 24 h).

Case #5Case #5 65-yr-old woman with a history of a 65-yr-old woman with a history of a

schizoaffective disorder has been treated with schizoaffective disorder has been treated with lithium 400 mg/d for the past 20 yr.lithium 400 mg/d for the past 20 yr.

Admitted with fever and a change in mental Admitted with fever and a change in mental status.status.

BP 90/50 mmHg, HR: 120 bpm, temp 39°C, dry BP 90/50 mmHg, HR: 120 bpm, temp 39°C, dry mucous membranes, clear lungs, no edema.mucous membranes, clear lungs, no edema.

Labs: Na 148 mEq/L, K 3.6 mEq/L, Cl 114Labs: Na 148 mEq/L, K 3.6 mEq/L, Cl 114mEq/L, CO2 28 mEq/L, BUN 26 mg/dl, mEq/L, CO2 28 mEq/L, BUN 26 mg/dl, creatininecreatinine0.6 mg/dl, and calcium 13.5 mg/dl. Urine and 0.6 mg/dl, and calcium 13.5 mg/dl. Urine and blood cultures are positive for blood cultures are positive for E. coliE. coli. Abdominal . Abdominal CT shows nonobstructing calcium stones.CT shows nonobstructing calcium stones.

Case #5Case #5

Lithium is discontinued, and she is treated Lithium is discontinued, and she is treated with isotonic saline, antibiotics, and with isotonic saline, antibiotics, and pamidronate.pamidronate.

Five days later, she is alert, normotensive, andFive days later, she is alert, normotensive, and

afebrile. Urine output is 5 L/d. Serum calcium afebrile. Urine output is 5 L/d. Serum calcium isis

9.5 mg/dl, and serum sodium is 148 mEq/L.9.5 mg/dl, and serum sodium is 148 mEq/L.

Urine osmolality is 180 mOsm/kg. Urine osmolality is 180 mOsm/kg. After desmopressin,After desmopressin, urine osmolality urine osmolality

increases to 230 mOsm/kg.increases to 230 mOsm/kg.

Case #5Case #5

Which ONE of the following is the Which ONE of the following is the BESTBEST

explanation for her polyuria?explanation for her polyuria?

A. Psychogenic polydipsiaA. Psychogenic polydipsia

B. Central DIB. Central DI

C. Osmotic diuresisC. Osmotic diuresis

D. Nephrogenic DI as a result of lithiumD. Nephrogenic DI as a result of lithium

Case #5Case #5 Answer D. Nephrogenic DI as a result of lithiumAnswer D. Nephrogenic DI as a result of lithium The urine is dilute indicating that the polyuria is The urine is dilute indicating that the polyuria is

caused by a water diuresis and not an osmotic caused by a water diuresis and not an osmotic diuresis (answer C). diuresis (answer C).

A water diuresis could be caused by psychogenic A water diuresis could be caused by psychogenic polydipsia (answer A), central diabetes insipidus polydipsia (answer A), central diabetes insipidus (answer B) or nephrogenic diabetes insipidus. (answer B) or nephrogenic diabetes insipidus.

Dilute urine despite a high serum sodium Dilute urine despite a high serum sodium concentration excludes psychogenic polydipsia .concentration excludes psychogenic polydipsia .

The limited response to exogenous desmopressin is The limited response to exogenous desmopressin is most consistent with nephrogenic diabetes insipidus, most consistent with nephrogenic diabetes insipidus, an expected complication after 20 years of lithium an expected complication after 20 years of lithium therapy. therapy.

Hypercalcemia can also cause nephrogenic diabetes Hypercalcemia can also cause nephrogenic diabetes insipidus, but the urine is not usually dilute in that insipidus, but the urine is not usually dilute in that condition unless the patient has primary polydipsia.condition unless the patient has primary polydipsia.

Semin Nephrol 26:244-8, 2006Cleve Clin J Med 73:65-71, 2006

Pathophysiology of Pathophysiology of hypernatremiahypernatremia

Free water deficient state Free water deficient state Total Body WaterTotal Body Water deficit > deficit >

Total Body Sodium DeficitTotal Body Sodium Deficit Usually due to excess water loss and Usually due to excess water loss and

not excess sodium retentionnot excess sodium retention Lacks normal physiologic response Lacks normal physiologic response

to free water loss to free water loss ADH secretion (diabetes insipidus)ADH secretion (diabetes insipidus) Thirst Thirst

Symptoms and Signs of Symptoms and Signs of HypernatremiaHypernatremia

Lethargy Lethargy Restlessness Restlessness Hyperreflexia Hyperreflexia Spasticity Spasticity SeizureSeizure

Case #6Case #6

85 year old man is admitted with 85 year old man is admitted with altered metal status due to urosepsisaltered metal status due to urosepsis

Serum Na: 174 mEq/L, weight: 69 kg Serum Na: 174 mEq/L, weight: 69 kg

How do we replace the water deficit?How do we replace the water deficit?

Case #6 Case #6

Water deficit = 0.6 x Wt x ( Serum Na Water deficit = 0.6 x Wt x ( Serum Na – 140) / 140– 140) / 140

Water deficit = 0.6 x 69 x (174-140) / Water deficit = 0.6 x 69 x (174-140) / 140 = 10 L140 = 10 L

Replace Replace Free Water DeficitFree Water Deficit with D5W with D5W over 48 hours (200 ml/h).over 48 hours (200 ml/h).

Monitor electrolytes closely while Monitor electrolytes closely while administering D5W, the above administering D5W, the above formula does not take insensible formula does not take insensible losses into account.losses into account.

Case #7Case #7 62 year old man with a known history of type 62 year old man with a known history of type

II DM and CKD-3 (serum Cr 2.1, K 4.9) is II DM and CKD-3 (serum Cr 2.1, K 4.9) is started on a low Na diet for HTN.started on a low Na diet for HTN.

2 weeks later he is unable to lift himself out of 2 weeks later he is unable to lift himself out of a chair.a chair.

Exam: marked proximal muscle weaknessExam: marked proximal muscle weakness ECG: peaked T waves and widening of P wave ECG: peaked T waves and widening of P wave

and QRS complexesand QRS complexes Labs: Na 130, K 9.8, Cl 98, HCO3 17, Cr 2.2, Labs: Na 130, K 9.8, Cl 98, HCO3 17, Cr 2.2,

arterial pH 7.32arterial pH 7.32 What is the cause for his severe hyperkalemia?What is the cause for his severe hyperkalemia?

Case #7Case #7

Use of a salt substitute (which is Use of a salt substitute (which is KCL).KCL).

Hyporeninemic hypoaldosteronism Hyporeninemic hypoaldosteronism state, which is common in diabetic state, which is common in diabetic patients, this is why hyperkalemia patients, this is why hyperkalemia can be seen in diabetics at an earlier can be seen in diabetics at an earlier stage of their CKD.stage of their CKD.

Clinical Sequelae of Clinical Sequelae of HyperkalemiaHyperkalemia

CardiacCardiac Abnormal conduction, ventricular Abnormal conduction, ventricular

fibrillationfibrillation Pacemaker dysfunctionPacemaker dysfunction

NeuromuscularNeuromuscular Flaccid paralysisFlaccid paralysis

Fluids and ElectrolytesFluids and Electrolytes NHNH33 production, metabolic acidosis production, metabolic acidosis

ECG in HyperkalemiaECG in Hyperkalemia

ECG in HyperkalemiaECG in Hyperkalemia

ECG in HyperkalemiaECG in Hyperkalemia

Differential Diagnosis of Differential Diagnosis of HyperkalemiaHyperkalemia

PseudohyperkalemiaPseudohyperkalemia HemolysisHemolysis ThrombocytosisThrombocytosis LeukocytosisLeukocytosis

RedistributionRedistribution AcidosisAcidosis Insulin deficiencyInsulin deficiency Beta-adrenergic Beta-adrenergic

blockadeblockade SuccinylcholineSuccinylcholine Digitalis overdoseDigitalis overdose Periodic paralysisPeriodic paralysis

Differential Diagnosis of HyperkalemiaDifferential Diagnosis of Hyperkalemia

Potassium RetentionPotassium Retention

GFR < 5-10 ml/minGFR < 5-10 ml/min Oligoanuria (any etiology)Oligoanuria (any etiology) Potassium load: Potassium load:

A. ExogenousA. Exogenous B. Endogenous:B. Endogenous:

Tissue necrosisTissue necrosis HemolysisHemolysis Hypercatabolism Hypercatabolism

Differential Diagnosis of Differential Diagnosis of HyperkalemiaHyperkalemia

Potassium RetentionPotassium RetentionGFR > 20 ml/minGFR > 20 ml/min

Low aldosteroneLow aldosterone Addison’s diseaseAddison’s disease Hyporeninemic Hyporeninemic

hypoaldosteronismhypoaldosteronism DrugsDrugs

PG synthetase PG synthetase inhibitorsinhibitors

ACEIACEI HeparinHeparin

Normal or high aldoNormal or high aldo Renal tubular Renal tubular

acidosisacidosis AcquiredAcquired

Renal transplantRenal transplant Lupus erythematosusLupus erythematosus AmyloidAmyloid Sickle cell diseaseSickle cell disease Obstructive uropathyObstructive uropathy

HereditaryHereditary KK++ sparing diuretics sparing diuretics

Treatment of HyperkalemiaTreatment of Hyperkalemia

SpecificSpecificAntagonize the membrane effects Antagonize the membrane effects

of hyperkalemiaof hyperkalemiaRapidly lower the serum potassium Rapidly lower the serum potassium

by shifting potassium from the by shifting potassium from the extracellular space into cellsextracellular space into cells

Remove potassium from the bodyRemove potassium from the body

Treatment of Treatment of HyperkalemiaHyperkalemia

Mechanism Therapy Dose Onset Duration

Antagonizemembraneeffects

Calcium Calciumgluconate,10% solution,10 ml IV over10 min

1 to 3 min 30 to 60 min

Cellularpotassiumuptake

Insulin Regularinsulin, 10 UIV, withdextrose,50% , 50 ml ifplasmaglucose is<250 mg/dl

30 min 4 to 6 h

ß2agonist

Nebulizedalbuterol, 10mg

30 min 2 to 4 h

Treatment of HyperkalemiaTreatment of Hyperkalemia

Mechanism Therapy Dose Onset Duration

Potassiumremoval

Sodiumpolystyrenesulfonate

Kayexalate, 60g p.o. in 20%sorbitol, orKayexalate, 60g retentionenema withoutsorbitol

1 to 2 h 4 to 6 h

Hemodialysis Immediate Until dialysiscompleted

Case #8Case #8 A 24-yr-old primigravida presents to the

emergency department at 31 wk gestation with a history of progressive fatigue and muscle weakness for 1 mo.

Her prenatal course had been uneventful until 1 month ago.

BP is 106/70 mmHg. Labs: Na 130 mmol/L, K 1.5 mmol/L, Cl 90

mmol/L, HCO3 20 mEq/L, CPK 1800 U/L (24 to 200), pH 7.48, PCO2 30 Torr; urine electrolytes are as follows: Na 79, K 15, Cl 55 (mEq/L).

Case #8Case #8

Which ONE of the following is the BEST explanation for the hypokalemia?

A. Normal value for serum potassium concentration in pregnancy.

B. Hyperemesis gravidarum.C. Activating mutation of mineralocorticoidreceptor.D. Surreptitious laxative use.E. Occult ingestion of Bentonite clay.

Case #8Case #8

Answer E: Answer E: Occult ingestion of Bentonite clay. The patient presents with severe

hypokalemia complicated by evidence of rhabdomyolysis.

The low urinary K suggests an extrarenal cause of hypokalemia.

Bentonite is a clay reported to bind potassium in the gastrointestinal tract accounting for the abnormalities in this patient.

Case #8Case #8 Hypokalemia is not a feature of normal

pregnancy. Hyperemesis gravidarum or vomiting would

produce hypokalemia in association with metabolic alkalosis but there is no such hx.

Choice C is incorrect due to the lack of metabolic alkalosis and hypertension.

Choice D is incorrect since surreptitious laxative abuse would be associated with evidence of a normal gap metabolic acidosis (AG here is 20) and a negative urinary anion gap (AG here is + 39).

Obstet Gynecol 102: 1169-1171, 2003Pediatr Emerg Care 22: 500-502, 2006

Potassium HomeostasisPotassium Homeostasis

Factors Influencing KFactors Influencing K++ Secretion In The Distal Secretion In The Distal

NephronNephron AldosteroneAldosterone

NaNa+ + absorptionabsorption Enhance the activity Enhance the activity

of Naof Na++-K-K++-ATPase -ATPase pumppump

Enhance the number Enhance the number of open Kof open K++ channels channels

Plasma potassiumPlasma potassium aldo secretionaldo secretion Same renal effects Same renal effects

as aldo in CCTas aldo in CCT

Distal flow rateDistal flow rate decreased distal decreased distal

flow rate leads to flow rate leads to decreased Kdecreased K+ + secretion in the secretion in the collecting tubulecollecting tubule

NaNa++ reabsorption reabsorption without Clwithout Cl++

Enhances lumen Enhances lumen negativitynegativity

Clinical Sequelae of Clinical Sequelae of HypokalemiaHypokalemia

CardiacCardiac Sensitivity to digitalis toxicitySensitivity to digitalis toxicity Ventricular arrhythmiasVentricular arrhythmias

NeuromuscularNeuromuscular Constipation, ileusConstipation, ileus Weakness, paralysisWeakness, paralysis RhabdomyolysisRhabdomyolysis

Clinical Sequelae of Clinical Sequelae of HypokalemiaHypokalemia

Renal, Fluids and ElectrolytesRenal, Fluids and ElectrolytesPolyuriaPolyuriaPolydypsiaPolydypsia NHNH33 production, hepatic coma production, hepatic comaMetabolic alkalosisMetabolic alkalosisInterstitial nephritisInterstitial nephritisEdemaEdema

ECG in HypokalemiaECG in Hypokalemia

The following changes may be seen in hypokalemia:

Small or absent T wavesProminent U waves First or second degree AV block Slight depression of the ST segment

ECG demonstrating prominent U waves in a patient with hypokalemia

Hypokalemia Produced by Hypokalemia Produced by Transcellular ShiftTranscellular Shift

AlkalemiaAlkalemia Respiratory alkalosisRespiratory alkalosis Metabolic alkalosisMetabolic alkalosis

Insulin excessInsulin excess Endogenous (glucose administration)Endogenous (glucose administration) ExogenousExogenous

ββAdrenergic catecholamine excessAdrenergic catecholamine excess Endogenous (acute stressful conditions)Endogenous (acute stressful conditions) Exogenous (Exogenous (ββ22-agonists)-agonists)

Hypokalemia Produced by Hypokalemia Produced by Transcellular ShiftTranscellular Shift

IntoxicationsIntoxications TheophyllineTheophylline BariumBarium TolueneToluene

Hypokalemic periodic paralysisHypokalemic periodic paralysis HereditaryHereditary Acquired (thyrotoxicosis)Acquired (thyrotoxicosis)

Case #9Case #9

60 year old man with 2 yr hx of HTN.60 year old man with 2 yr hx of HTN. Labs: Na 142, K 3.4, Cl 101, HCO3 29Labs: Na 142, K 3.4, Cl 101, HCO3 29 BP 180/110 on amlodpine (10 mg/d), BP 180/110 on amlodpine (10 mg/d),

fosinopril (40 mg/d), atenolol (50 mg fosinopril (40 mg/d), atenolol (50 mg bid), and terazosin (5 mg/d)bid), and terazosin (5 mg/d)

Due to his resistant HTN, HCTZ 25 mg Due to his resistant HTN, HCTZ 25 mg was addedwas added

One week later: BP 175/105, K 2.7One week later: BP 175/105, K 2.7 What is the etiology of his What is the etiology of his

hypokalemia?hypokalemia?

Case #9Case #9

Primary hyperaldosteronismPrimary hyperaldosteronism is the is the cause of his resistant hypertension, cause of his resistant hypertension, initially low K and his exaggerated initially low K and his exaggerated hypokalemic response to HCTZ.hypokalemic response to HCTZ.

Think of primary Think of primary hyperaldosternonism in any hyperaldosternonism in any hypertensive patient with chronic hypertensive patient with chronic hypokalemia.hypokalemia.

Differential Diagnosis of Differential Diagnosis of HypokalemiaHypokalemia

< 20 m Eq /da y Extra rena l Loss

L owD iarrh eaL ow er G I fis tu las

N orm a lC ath artic sP ro fu se sw eatin g

H ig hD iscon tin u ed d iu re tic sP reviou s vom itin gG as tric fis tu las

S eru m b ica rb on a te

Urine Potassium

Diet: normal Na

UNa>100 mEq/ day

Differential Diagnosis of Differential Diagnosis of HypokalemiaHypokalemia

h ig h P R A , h ig h a ld oM alig n an t H B PR en ovascu la r H B PR en in -sec re tin g tu m or

low P R A , h ig h a ld oP rim ary a ld os te ron ism

low P R A , low a ld oC u sh in g 's syn d rom eIn g es ted m in era locort ico idC on g en ita l ad ren a l h yp erp las ia

Pla sm a R enin

Urine Potassium

Diet: normal Na

UNa>100 mEq/ day

> 20 mEq /day Renal Loss

HBP

Differential Diagnosis of Differential Diagnosis of HypokalemiaHypokalemia

N orm a l B lood Pressue

L ow b ica rbR en a l tu b u la r ac id os is

H ig h b ica rb , U c l < 1 0 m E q /dV om itin g

H ig h b ica rb , U c l > 1 0 m E q /dD iu re tic s , M g d ep le tionB artte r's s yn d rom eN orm oten s ive H yp era ld os te ron ism

S eru m b ica rb on a te

Urine Potassium

Diet: normal Na

UNa>100 mEq/ day

> 20 mEq /day Renal Loss

Treatment of HypokalemiaTreatment of Hypokalemia

If the patient can take potassium If the patient can take potassium PO, give it POPO, give it PO

If serum K is between 3.0-3.5, If serum K is between 3.0-3.5, replace PO if possiblereplace PO if possible

Replace magnesium if low, Replace magnesium if low, refractory cases of hypokalemia refractory cases of hypokalemia can result from hypomagnesemiacan result from hypomagnesemia

Treatment of HypokalemiaTreatment of Hypokalemia

The recommended rate of IV The recommended rate of IV potassium correction is 10 meq per potassium correction is 10 meq per hourhour

The rate of correction should never The rate of correction should never exceed 20 meq per hourexceed 20 meq per hour

A rate higher than 10 meq per hour A rate higher than 10 meq per hour should only be considered in should only be considered in unstable patients who are on unstable patients who are on telemetrytelemetry

Treatment of HypokalemiaTreatment of Hypokalemia

Consider replacement IV in the Consider replacement IV in the following conditions:following conditions:

Serum K is less than 3.0 meq/lSerum K is less than 3.0 meq/l ECG changesECG changes The patient is on digitalisThe patient is on digitalis Hypokalemia associated with Hypokalemia associated with

DKADKA

Potassium Content of FoodsPotassium Content of FoodsOrange juice 11-13/glass

Grapefruit juice 10-11/glass

Tomato juice 12-14/glass

Bananas 13-15 each

Avocados 25-30 each

Beans 12-14/cup

Cream of tartar (can be added to juice) 10-12/tsp

Bouillon cube (salt-free) 12-13 each

Milk 12-14/cup

Raisins 12-14 1/2/cup

Salt substitute (KCI) 15-16 1/2/tsp

Instant tea9-11/tsp

mEq