Practical Approach to Common Electrolyte Emergencies

Mohammad Tinawi, MD, FACP mtinawi@pol.net

Case #1

73 Y old man with PMHx of DM-II was admitted with left hip fx after a fall at home. He had a successful ORIF. In hospital medications: Insulin, esomeprazole, enoxaparin, and IVF: D5W at 100 ml/h POD #3: Urea 84, Cr 1.4. A nephrology consultation was requested due to decreased level of consciousness. Head CT showed old white matter disease.

Case #1

The elevation in urea and creatinine is not the cause of his altered mental status. The elevation is prerenal in origin. The patient was found to have lower GI bleeding causing the elevation in urea. What is the cause of his altered mental status?

Case #1

Answer: In hospital hyponatremia. Iatrogenic Due to inappropriate use of hypotonic IVF Avoidable by using 0.9 NS in all patients except in those with hypernatremia The patients sodium was corrected slowly to 134 mmol/L (over 72 h) with improvement in mental status

Case #1

Hospitalized patients have numerous stimuli for arginine vasopressin production and are at risk of developing hyponatremia Routine administration of hypotonic parenteral fluid to hospitalized patients can result in fatal hyponatremic encephalopathy 0.9% NaCl (154 mmol/l) should be administered as prophylaxis against hyponatremia, except in the setting of a free water deficit or ongoing free water losses

Case #1

Patients at greatest risk of developing neurological complications secondary to hyponatremia are children, premenopausal females, postoperative patients, and those with brain injury, brain infection or hypoxemia 3% NaCl (513 mmol/l) is an essential treatment for hyponatremic encephalopathy

Hyponatremia

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

Sodium is the primary determinant

Abnormal ratio of Na to water Na < 135 Most often due to retention of free water

Secondary to impaired excretion of free water i.e. thiazide-induced hypoNa (elderly women)

Occ. due to Na loss exceeding water loss

Hyponatremia
Hyponatremia

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

Hyponatremia

Simply, hyponatremia is due to inability to match water excretion with water ingestion 1. Defect in water excretion

SIADH (inappropriate ADH release) Hypovolemic state (appropriate ADH release) Hypervolemic (Increased ADH release) CHF, cirrhosis, nephrotic syndrome, ARF / CRI Hyperglycemia (draws water into plasma)

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

Manifestations

Mild Sx: anorexia, nausea, lethargy Mod Sx: disoriented, agitated, neuro deficit Sev Sx: seizures, coma, death

Case #2

A 50-yr-old man with hemophilia, HIV/AIDS and cirrhosis caused by hepatitis C is admitted for renal failure. Meds: furosemide, spironolactone, sulfamethoxazole and trimethoprim BP is 98/62 mmHg, scleral icterus, stigmata of cirrhosis, an abdominal fluid wave, and pitting edema of his lower extremities. He has asterixis.

Case #2

Labs: Na 128 mEq/L, K 5.7 mEq/L, Cl 95 mEq/L, CO2 23 mEq/L, BUN 49 mg/dl, glucose 110 mg/dl, and creatinine 2.3 mg/dl. Plasma osmolality 290 mOsm/kg. Urine osmolality is 580 mOsm/kg. Urine Na 53 mEq/L Random serum cortisol 25 g/dl, uric acid 14.2 mg/dl, serum triglycerides 50 mg/dl, total cholesterol 95 mg/dl, total protein 11.7 gm/dl, albumin 2.4 gm/dl.

Case #2
Which ONE of the following is the MOST likely cause of the patients hyponatremia? A. Addison disease B. Trimethroprim therapy C. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) D. Pseudohyponatremia

Case #2

Answer: D. Pseudohyponatremia Plasma osmolality is 290 which excludes the various causes of hypotonic hyponatremia such as SIADH. His pseudohyponatremia is caused by his extremely high serum protein concentration, a phenomenon that has been reported in patients with HIV and hepatitis C.
J Gen Intern Med 23:202-5, 2008 Clin J Am Soc Nephrol 3:1175-84, 2008

Case #3

40-yr-old woman is admitted with the worst headache of her life. PE: wt 56 kg, BP 170/60 mmHg. Meningeal signs are present. Head CT: a small subarachnoid hemorrhage. Labs: Na 140 mEq/L, K 3.9 mEq/L, Cl 105 mEq/L, CO2 22 mEq/L, BUN 17 mg/dl, creatinine 1.0 mg/dl, and hematocrit 37%. During the first 6 d of hospitalization, she is treated with nimodipine and 0.9% saline at 200 ml/h.

Case #3

Gradually Na falls to 125 mEq/L. Mannitol 12.5 g is administered, and saline is continued. The next day, BP 148/66, wt: 58 kg. She is alert and oriented but complains of a headache. 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, creatinine 0.9 mg/dl, glucose 260 mg/dl, and hematocrit 34. Serum osmolality is 260 mOsm/kg; urine osmolality is 800 mOsm/kg. Urine values : Na 240 mEq/L, K 20 mEq/L, and output 200 ml/h.

Case #3

Which ONE of the following is the MOST likely cause of her hyponatremia? A. Pseudohyponatremia B. Translocational hyponatremia as a result of mannitol C. SIADH D. Cerebral salt wasting

Case #3

Answer C: SIADH The patient has hypotonic hyponatremia with a measured plasma osmolality (260 mOms/kg) excluding pseudohyponatremia (answer A) or translocational hyponatremia due to mannitol (which raises plasma osmolality) (answer B). The high urine osmolality and urine sodium concentrations are consistent with either SIADH (answer C) or cerebral salt wasting (answer D). Cerebral salt wasting is associated with volume depletion. The patients blood pressure is high, she has gained weight, and her hematocrit has fallen, findings that are inconsistent with hypovolemia.

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

Treatment Urgent

If symptomatic & urgent, give hypertonic saline

Do

not correct more than 8 mEq /day

Risk of central pontine myelinolysis (CPM)

Treatment of Hyponatremia

Hypovolemic (diarrhea, diuretics) give volume: but never hypotonic solutions. Hypervolemic (CHF) Na & water restriction loop diuretics Euvolemic (SIADH) water restriction

Case #4

80 year old woman, wt 60 kg, BP 175/70 PMHx: Ongoing chemo for small cell lung CA Started on hydrochlorothiazide 25 mg/d One week later she was admitted with seizures BP 140/68, Na 112 How do we correct her hyponatremia?

Case #4

Things to remember: Na deficit (mmol) = 0.6 x wt (kg) x (desired [Na] actual [Na]) in women 0.5 0.9 NS has 154 meq/L of sodium 3% NS has 513 meq/L of sodium Use 3% in emergencies only and ask for a consult Check Na often while correcting q 2-3 h Thiazides are associated with hyponatremia Loop diuretics are associated with hypernatremia

Case #4
Na deficit (mmol) = 0.5 x wt (kg) x (desired [Na] - actual [Na]) Na deficit = 0.5 x 60 x (120 112) = 240 mmol Amount of 3% NS: 240/513 = 467 ml Rate 467/8 = 58 ml/ h (for 8 h only for the first 24 h).

Case #5

65-yr-old woman with a history of a schizoaffective disorder has been treated with lithium 400 mg/d for the past 20 yr. Admitted with fever and a change in mental status. BP 90/50 mmHg, HR: 120 bpm, temp 39C, dry mucous membranes, clear lungs, no edema. Labs: Na 148 mEq/L, K 3.6 mEq/L, Cl 114 mEq/L, CO2 28 mEq/L, BUN 26 mg/dl, creatinine 0.6 mg/dl, and calcium 13.5 mg/dl. Urine and blood cultures are positive for E. coli. Abdominal CT shows nonobstructing calcium stones.

Case #5

Lithium is discontinued, and she is treated with isotonic saline, antibiotics, and pamidronate. Five days later, she is alert, normotensive, and afebrile. Urine output is 5 L/d. Serum calcium is 9.5 mg/dl, and serum sodium is 148 mEq/L. Urine osmolality is 180 mOsm/kg. After desmopressin, urine osmolality increases to 230 mOsm/kg.

Case #5
Which ONE of the following is the BEST explanation for her polyuria?

A. Psychogenic polydipsia B. Central DI C. Osmotic diuresis D. Nephrogenic DI as a result of lithium

Case #5

Answer D. Nephrogenic DI as a result of lithium The urine is dilute indicating that the polyuria is caused by a water diuresis and not an osmotic diuresis (answer C). A water diuresis could be caused by psychogenic polydipsia (answer A), central diabetes insipidus (answer B) or nephrogenic diabetes insipidus. Dilute urine despite a high serum sodium concentration excludes psychogenic polydipsia . The limited response to exogenous desmopressin is most consistent with nephrogenic diabetes insipidus, an expected complication after 20 years of lithium therapy. Hypercalcemia can also cause nephrogenic diabetes insipidus, but the urine is not usually dilute in that condition unless the patient has primary polydipsia.
Semin Nephrol 26:244-8, 2006 Cleve Clin J Med 73:65-71, 2006

Pathophysiology of hypernatremia

Free water deficient state

Total Body Water deficit > Total Body Sodium Deficit Usually due to excess water loss and not excess sodium retention

Lacks normal physiologic response to free water loss

ADH secretion (diabetes insipidus) Thirst

Symptoms and Signs of Hypernatremia

Lethargy Restlessness Hyperreflexia Spasticity Seizure

Case #6

85 year old man is admitted with altered metal status due to urosepsis Serum Na: 174 mEq/L, weight: 69 kg How do we replace the water deficit?

Case #6

Water deficit = 0.6 x Wt x ( Serum Na 140) / 140 Water deficit = 0.6 x 69 x (174-140) / 140 = 10 L Replace Free Water Deficit with D5W over 48 hours (200 ml/h). Monitor electrolytes closely while administering D5W, the above formula does not take insensible losses into account.

Case #7

62 year old man with a known history of type II DM and CKD-3 (serum Cr 2.1, K 4.9) is started on a low Na diet for HTN. 2 weeks later he is unable to lift himself out of a chair. Exam: marked proximal muscle weakness ECG: peaked T waves and widening of P wave and QRS complexes Labs: Na 130, K 9.8, Cl 98, HCO3 17, Cr 2.2, arterial pH 7.32 What is the cause for his severe hyperkalemia?

Case #7

Use of a salt substitute (which is KCL). Hyporeninemic hypoaldosteronism state, which is common in diabetic patients, this is why hyperkalemia can be seen in diabetics at an earlier stage of their CKD.

Clinical Sequelae of Hyperkalemia

Cardiac
Abnormal

conduction, ventricular fibrillation Pacemaker dysfunction

Neuromuscular
Flaccid

paralysis

Fluids and Electrolytes

NH3 production, metabolic acidosis

ECG in Hyperkalemia

ECG in Hyperkalemia

ECG in Hyperkalemia

Differential Diagnosis of Hyperkalemia

Pseudohyperkalemia Hemolysis Thrombocytosis Leukocytosis Redistribution Acidosis Insulin deficiency Beta-adrenergic blockade Succinylcholine Digitalis overdose Periodic paralysis

Differential Diagnosis of Hyperkalemia Potassium Retention GFR < 5-10 ml/min Oligoanuria (any etiology) Potassium load:
A. Exogenous B. Endogenous:

Tissue necrosis Hemolysis Hypercatabolism

Differential Diagnosis of Hyperkalemia Potassium Retention GFR > 20 ml/min

Low aldosterone Addisons disease Hyporeninemic hypoaldosteronism Drugs

Normal or high aldo Renal tubular acidosis

Acquired

PG synthetase inhibitors ACEI Heparin

Renal transplant Lupus erythematosus Amyloid Sickle cell disease Obstructive uropathy

Hereditary

K+ sparing diuretics

Treatment of Hyperkalemia

Specific Antagonize the membrane effects of hyperkalemia Rapidly lower the serum potassium by shifting potassium from the extracellular space into cells Remove potassium from the body

Treatment of Hyperkalemia
Mechanism Antagonize membrane effects Cellular potassium uptake Therapy Calcium Dose Onset Duration 30 to 60 min Calcium 1 to 3 min gluconate, 10% solution, 10 ml IV over 10 min Regular 30 min insulin, 10 U IV, with dextrose, 50% , 50 ml if plasma glucose is < 250 mg/dl Nebulized 30 min albuterol, 10 mg

Insulin

4 to 6 h

2 to 4 h

agonist

Treatment of Hyperkalemia
Mechanism Potassium removal Therapy Sodium polystyrene sulfonate Dose Onset Duration 4 to 6 h Kayexalate, 60 1 to 2 h g p.o. in 20% sorbitol, or Kayexalate, 60 g retention enema without sorbitol Hemodialysis Immediate

Until dialysis completed

Case #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 #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 mineralocorticoid receptor. D. Surreptitious laxative use. E. Occult ingestion of Bentonite clay.

Case #8

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 #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, 2003 Pediatr Emerg Care 22: 500-502, 2006

Potassium Homeostasis

Factors Influencing K+ Secretion In The Distal Nephron

Aldosterone

Distal flow rate

Na+ absorption Enhance the activity of Na+-K+-ATPase pump Enhance the number of open K+ channels

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

Plasma potassium

aldo secretion Same renal effects as aldo in CCT

Na+ reabsorption without Cl+

Enhances lumen negativity

Clinical Sequelae of Hypokalemia

Cardiac Sensitivity to digitalis toxicity Ventricular arrhythmias Neuromuscular Constipation, ileus Weakness, paralysis Rhabdomyolysis

Clinical Sequelae of Hypokalemia

Renal, Fluids and Electrolytes Polyuria Polydypsia NH3 production, hepatic coma Metabolic alkalosis Interstitial nephritis Edema

ECG in Hypokalemia

The following changes may be seen in hypokalemia:

Small

or absent T waves Prominent 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 Transcellular Shift

Alkalemia Respiratory alkalosis Metabolic alkalosis Insulin excess Endogenous (glucose administration) Exogenous Endogenous (acute stressful conditions) Exogenous (2-agonists)

Adrenergic catecholamine excess

Hypokalemia Produced by Transcellular Shift

Intoxications Theophylline Barium Toluene Hypokalemic periodic paralysis Hereditary Acquired (thyrotoxicosis)

Case #9

60 year old man with 2 yr hx of HTN. Labs: Na 142, K 3.4, Cl 101, HCO3 29 BP 180/110 on amlodpine (10 mg/d), fosinopril (40 mg/d), atenolol (50 mg bid), and terazosin (5 mg/d) Due to his resistant HTN, HCTZ 25 mg was added One week later: BP 175/105, K 2.7 What is the etiology of his hypokalemia?

Case #9

Primary hyperaldosteronism is the cause of his resistant hypertension, initially low K and his exaggerated hypokalemic response to HCTZ. Think of primary hyperaldosternonism in any hypertensive patient with chronic hypokalemia.

Differential Diagnosis of Hypokalemia

Urine Potassium

Diet: normal Na

UNa>100 mEq/ day

< 20 mEq /day Extrarenal Loss

Serum bicarbonate

Low Diarrhea Lower GI fistulas

Normal Cathartics Profuse sweating

High Discontinued diuretics Previous vomiting Gastric fistulas

Differential Diagnosis of Hypokalemia

Urine Potassium

Diet: normal Na

UNa>100 mEq/ day

> 20 mEq /day

Renal Loss

HBP
Plasma Renin
high PRA, high aldo Malignant HBP Renovascular HBP Renin-secreting tumor low PRA, high aldo Primary aldosteronism low PRA, low aldo Cushing's syndrome Ingested mineralocorticoid Congenital adrenal hyperplasia

Differential Diagnosis of Hypokalemia

Urine Potassium

Diet: normal Na UNa>100 mEq/ day

> 20 mEq /day

Renal Loss

Normal Blood Pressue

Serum bicarbonate

Low bicarb Renal tubular acidosis

High bicarb, Ucl < 10 mEq /d Vomiting

High bicarb, Ucl > 10 mEq /d Diuretics, Mg depletion Bartter's syndrome Normotensive Hyperaldosteronism

Treatment of Hypokalemia
If

the patient can take potassium PO, give it PO If serum K is between 3.0-3.5, replace PO if possible Replace magnesium if low, refractory cases of hypokalemia can result from hypomagnesemia

Treatment of Hypokalemia
The

recommended rate of IV potassium correction is 10 meq per hour The rate of correction should never exceed 20 meq per hour A rate higher than 10 meq per hour should only be considered in unstable patients who are on telemetry

Treatment of Hypokalemia
Consider replacement IV in the following conditions: Serum K is less than 3.0 meq/l ECG changes The patient is on digitalis Hypokalemia associated with DKA

Potassium Content of Foods

mEq
Orange juice Grapefruit juice Tomato juice Bananas Avocados Beans Cream of tartar (can be added to juice) Bouillon cube (salt-free) Milk Raisins Salt substitute (KCI) Instant tea 11-13/glass 10-11/glass 12-14/glass 13-15 each 25-30 each 12-14/cup 10-12/tsp 12-13 each 12-14/cup 12-14 1/2/cup 15-16 1/2/tsp 9-11/tsp