Professional Documents
Culture Documents
Electrolyte Disorders: Camiron L. Pfennig and Corey M. Slovis
Electrolyte Disorders: Camiron L. Pfennig and Corey M. Slovis
Electrolyte Disorders
Camiron L. Pfennig and Corey M. Slovis
Electrolyte abnormalities are common in emergency medicine result is cardiac arrest, usually from disintegration into ventricular
and can vary greatly in importance, severity, and symptoms. fibrillation, pulseless electrical activity, or asystole. A serum potas-
Asymptomatic electrolyte abnormalities can usually be gradually sium level of 10.0 mEq/L is usually fatal, but decompensation and
corrected, but those that cause alterations in consciousness or life- death can occur at any level above 7 to 8 mEq/L.
threatening dysrhythmias require immediate therapy to avoid The most common cause of hyperkalemia is spurious elevation
permanent sequelae or death. In some cases, therapy for life- due to hemolysis during or after the blood draw. Thus an ECG
threatening electrolyte disorders may even need to be initiated should be used to assess for true hyperkalemia while another
before laboratory results become available. sample is analyzed. Most causes of true hyperkalemia are due to
release from cells or renal insufficiency. Renal failure is the most
common cause of confirmed hyperkalemia and is often com-
pounded by medications that further impair renal potassium
HYPERKALEMIA handling. Box 125-1 organizes the most common causes of hyper-
Principles of Disease kalemia. The presence of one of these conditions may be the lone
historical clue in hyperkalemia.3
Hyperkalemia, defined as serum potassium level greater than
5.0 mEq/L, is the most dangerous acute electrolyte abnormality, Clinical Features
potentially leading to life-threatening arrhythmias and death.
Although hyperkalemia may have vague and varied symptoms, it Hyperkalemia remains a difficult clinical diagnosis to make on
is usually totally asymptomatic, with cardiac arrest as its first clinical grounds alone. It is not uncommon for a patient with mild
“symptom.”1 Thus the diagnosis of hyperkalemia depends on to moderate hyperkalemia to be identified during routine blood
paying specific attention to risk factors for impaired potassium sampling for an unrelated condition. Patients with moderate to
excretion, such as dehydration and renal failure, along with an severe hyperkalemia may have gastrointestinal effects such as
awareness of medications that cause potassium retention. Evalua- nausea, vomiting, and diarrhea often in association with their
tion of the electrocardiogram (ECG) of patients at risk for this underlying disease. Neuromuscular findings, including muscle
electrolyte disturbance is critical. Hyperkalemia can be rapidly cramps, generalized weakness, paresthesias, tetany, and focal or
progressive, and lifesaving interventions must be instituted at the global paralysis, may be seen in patients with severe hyperkalemia.
earliest suspicion of toxicity. The signs and symptoms of progressive muscle weakness, pares-
Upwards of 98% of potassium in the body is contained intracel- thesias, dyspnea, and depressed deep tendon reflexes are neither
lularly, whereas less than 2% remains circulating in the blood. sensitive nor specific, nor do they appear reliably with a particular
Serum potassium concentration is normally between 3.5 and serum potassium level.3 Patients with severe hypokalemia may
5.0 mEq/L and is tightly regulated by the kidney. In the healthy present with hemodynamic instability and cardiac arrhythmias
state, at least 90% of potassium excretion occurs through the requiring immediate intervention.
kidney; in the renally impaired state, the gastrointestinal tract may
account for roughly 25% of excretion. Hyperkalemia usually Diagnostic Strategies
develops from impaired renal excretion or increased release from
cells; however, in advanced chronic kidney disease or end-stage The ECG is helpful in making the diagnosis of hyperkalemia and
renal disease, dietary intake of potassium may be a significant can be used in unstable patients to initiate treatment (Figs. 125-1
factor in its development.2 to 125-3). Classic electrocardiographic changes—the peaked T
Hyperkalemia causes cardiotoxicity by increasing the resting wave, flattened p wave with prolonged PR interval or a totally
membrane potential of the cardiac myocyte, causing “membrane absent P wave, wide QRS, and sine wave pattern, portending
excitability” and conversely sluggish depolarization as well as imminent cardiac arrest—have been well described as appearing
decreasing the duration of repolarization. At very high levels, sequentially with rising serum potassium levels.4,5 Peaked T waves
potassium causes the depolarization threshold to rise, leading to usually appear as serum potassium levels exceed 5.5 to 6.5 mEq/L;
overall depressed cardiac function. Nearly any cardiac arrhythmia P wave disappearance and PR prolongation are common with
can be seen with hyperkalemia, including heart blocks, bradydys- levels above 6.5 to 7.5 mEq/L; and QRS prolongation is seen with
rhythmias, pseudoinfarction ST segment elevation, and the potassium levels above 7.0 to 8.0 mEq/L. Although these changes
classic “sine wave” pattern. As hyperkalemia advances, the end may occur in only half the patients, recognition of these patterns
1636
Chapter 125 / Electrolyte Disorders 1637
when they are present is vital to rapid diagnosis and initiation hyperkalemia should not be the sole reason to treat a stable patient
of lifesaving treatment.6 A serum potassium level above 5.0 mEq/L not likely to have an elevated potassium concentration until serum
is diagnostic of hyperkalemia, but the value itself does not levels have returned.3
always predict electrocardiographic changes or the degree of car-
diotoxicity. Subtle electrocardiographic changes consistent with Management
Patients with suspected or known hyperkalemia require intrave-
BOX 125-1 Five Most Common Causes of Hyperkalemia nous access and continuous cardiac monitoring. The treatment of
hyperkalemia is based on the clinical scenario combined with the
Spurious elevation Hemolysis due to drawing or storing of the 12-lead ECG and the laboratory potassium value. The treatment
laboratory sample or post–blood sampling strategy consists of three main steps: stabilization of the cardiac
leak from markedly elevated white blood membrane, shifting of potassium into the cells, and then removal
cells, red blood cells, or platelets
Renal failure Acute or chronic
of potassium from the body. In patients who do not require urgent
Acidosis Diabetic ketoacidosis, Addison’s disease, treatment, lowering of total body potassium may be the only step
adrenal insufficiency, type 4 renal tubular necessary. A variety of treatment options are considered for the
acidosis acute management of hyperkalemia, including calcium, insulin,
Cell death Rhabdomyolysis, tumor lysis syndrome, beta2-adrenergic agonists, sodium bicarbonate, resins, and dialysis
massive hemolysis or transfusion, crush (Table 125-1).
injury, burn Intravenous calcium is used to stabilize the cardiac membrane
Drugs Beta-blockers, acute digitalis overdose, by restoring the electrical gradient. Calcium increases the depo-
succinylcholine, angiotensin-converting larization threshold and the calcium gradient across the cardiac
enzyme inhibitors, angiotension receptor membrane, quieting myocyte excitability and increasing cardiac
blockers, nonsteroidal anti-inflammatory
drugs, spironolactone, amiloride,
conduction speed, thus narrowing the QRS. Calcium does not
potassium supplementation decrease serum potassium levels, and its effect is rapid but tran-
sient. The dose is one ampule, or 10 mL of 10% calcium chloride
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
IV
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
VI
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
VI
II
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
ST
Although short periods of mild potassium depletion are typically depression
well tolerated in healthy individuals, severe potassium depletion Flat T wave
can result in serious cardiovascular instability, neurologic dys- U wave
function, glucose intolerance, gastrointestinal symptoms, and
renal failure as well as affect the acid-base balance in the body.27
The likelihood of symptoms appears to correlate with the rapidity
of the decrease in serum potassium. In patients without underly-
ing heart disease, abnormalities in cardiac conduction are
Prolonged Q-T interval
extremely unusual, even when the serum potassium concentration
is below 3.0 mEq/L. Paresthesias, depressed deep tendon reflexes, Hypokalemia
fasciculations, muscle weakness, and confusion can occur when
Figure 125-5. Electrocardiographic changes in hypokalemia.
the serum potassium level is less than 2.5 mEq/L. However, in
patients with cardiac ischemia or heart failure, even mild to mod-
erate hypokalemia increases the likelihood of cardiac arrhythmias
secondary to potassium’s effect on the action potential. The that it may also cause a prolonged QT interval. Once the QT
data linking hypokalemia with arrhythmias and cardiac arrest in interval becomes longer than 500 milliseconds, the risk of malig-
acute myocardial infarction are fairly strong, but the direct myo- nant ventricular arrhythmias and torsades de pointes increases
cardial stimulatory effects of increased circulating epinephrine is dramatically.28 Hypokalemia is also notorious for causing nonspe-
a possible confounder.20 Hypokalemia is an independent risk cific ST and T wave changes. In addition, prolonged potassium
factor contributing to reduced survival of cardiac patients and depletion of even modest proportion can provoke or exacerbate
increased incidence of arrhythmic death. On the basis of available kidney injury or hypertension. A severe degree of hypokalemia
evidence, it appears best to attempt to maintain a serum potas- with paralysis is a potentially life-threatening medical emergency;
sium concentration above 4.5 mEq/L in patients having an acute measurement of relative urinary potassium excretion and an
myocardial infarction. Hypokalemic patients can demonstrate assessment of the acid-base status might help narrow the differ-
first- and second-degree heart block, atrial fibrillation, ventricular ential diagnosis in the emergency setting.
fibrillation, and asystole. Hypokalemia can also promote meta-
bolic acidosis. Management
Hypokalemic periodic paralysis is a rare disorder characterized
by potentially fatal episodes of muscle weakness through the Potassium is an intracellular cation, so a low serum potassium
involvement of the respiratory muscles. Life-threatening cardiac level almost always reflects a significant total potassium deficit.
arrhythmias are managed by restoration of serum potassium levels When treating hypokalemia, one should remember that each
into the normal range.28 0.3 mEq potassium drop below normal correlates with an approx-
imately 100 mEq total body deficit.29 Patients who have mild or
Diagnostic Strategies moderate hypokalemia are usually asymptomatic or present with
minor symptoms. These patients may only need oral potassium
Hypokalemia is rarely suspected on the basis of clinical presenta- replacement therapy if they do not have nausea or vomiting as the
tion, and the diagnosis is typically made by measurement of the cause of their hypokalemia. Oral replacement is available in liquid,
serum potassium concentration during routine laboratory study. powder, and tablet form. Potassium chloride is the most com-
If there is any suspicion for hypokalemia or a patient presents monly used supplementation, and 40 to 60 mEq orally every 2 to
with generalized weakness, palpitations, or arrhythmias, an ECG 4 hours is typically well tolerated. If the cause of hypokalemia is
should be obtained. Just as a tall-peaked T wave is characteristic not clear or the hypokalemia is severe and associated with
of hyperkalemia, a flattened T wave can be seen in hypokalemia. profound weakness, obtain a spot urine potassium level before
U waves, which are small deflections after the T wave, may also be starting therapy to assess whether the patient’s kidneys are inap-
seen (Figs. 125-4 and 125-5). The real danger of hypokalemia is propriately wasting potassium from a renal or endocrine cause.
Chapter 125 / Electrolyte Disorders 1641
Patients in whom severe hypokalemia is suspected should be
immediately placed on a cardiac monitor and intravenous access BOX 125-3 Three Types of Hypernatremia
secured.
Treatment of hypokalemia is essential in multiple populations Hypernatremia with Heatstroke
of patients. Hypokalemia is arrhythmogenic, especially in the set- dehydration and low Increased insensible losses: burns,
total body sodium sweating
tings of acute myocardial infarction, high catecholamine states,
Gastrointestinal loss: diarrhea,
and hypertrophied or dilated ventricles. Hypokalemia is an impor- protracted vomiting, continuous
tant independent risk factor for morbidity and mortality in gastrointestinal suction
patients with heart failure. Correction of serum potassium levels Osmotic diuresis: glucose, mannitol,
to between 4.0 and 5.0 mEq/L is important in these patients.30 enteral feeding
If intravenous infusion is necessary, potassium chloride at a rate Hypernatremia with low Diabetes insipidus
of 10 to 20 mEq/hr is considered safe. Potassium may burn total body water and Neurogenic
patients with small veins, so small amounts of lidocaine can be normal total body Elderly with “reset” osmostat
added to the intravenous solution. In the rare instance in which sodium Hypothalamic dysfunction
intravenous repletion is planned at more than 20 mEq/hr, closely Suprasellar or infrasellar tumors
Renal disease
monitor the patient with continuous cardiac monitoring and Drugs (amphotericin, phenytoin,
establish central line access. lithium, aminoglycosides,
Hypokalemia is associated with hypomagnesemia, and the methoxyflurane)
severity of the hypokalemia correlates with a similar degree of Sickle cell disease
hypomagnesemia.31 Magnesium replacement should usually Hypernatremia with Salt tablet ingestion
accompany potassium repletion. Unless the patient receives at increased total body Salt water ingestion92
least 0.5 g/hr of magnesium sulfate along with potassium replace- sodium Saline infusions
ment, potassium will not move intracellularly and the patient will Saline enemas
lose potassium through excretion.22 Correction of large potassium Intravenous sodium bicarbonate
deficits may require several days, and oral and intravenous replace- Poorly diluted interval feedings
Primary hyperaldosteronism
ment can occur simultaneously. Hemodialysis
Cushing’s syndrome
HYPERNATREMIA Conn’s syndrome
Principles of Disease
Hypernatremia is defined as a serum sodium concentration above
145 mEq/ L and is usually associated with a poor prognosis. It is BOX 125-4 More Common Causes of Diabetes Insipidus
uncommon in previously normal patients, and in adults it is
almost exclusively due to a total body water deficit.32 Most hyper- Central
Idiopathic
natremic patients have either an impaired sense of thirst or no Familial disease
access to water. Thus elders, infants, patients in coma or with Cancer
mental impairment, and those who are intubated and paralyzed Hypoxic encephalopathy
are at highest risk for this disorder.33,34 Hypernatremia can be Infiltrative disorders
divided into three physiologic pairings (Box 125-3). Diabetes Postsupraventricular tachycardia
insipidus, a condition that results in insufficient production of or Anorexia nervosa
lack of response to antidiuretic hormone, can lead to life- Nephrogenic
threatening hypernatremia35 (Box 125-4). Chronic renal insufficiency
Polycystic kidney disease
Clinical Features Lithium toxicity93
Hypercalcemia
Hypernatremia is a disease seen predominantly in elders, but it Hypokalemia
can also be seen in patients who depend on others to provide them Tubulointerstitial disease
with water, including infants, intubated patients, and persons with Hereditary
mental debilitation.36,37 In addition, patients will also have multi- Sickle cell disease
factorial causes leading to severe hypernatremia.38 Patients may
complain of polyuria or polydipsia or have obvious causes of
extrarenal fluid losses; others may have no complaints at all. A patient’s total body water is usually calculated by multiplying
Hypernatremia should be considered in any patient presenting the patient’s body weight in kilograms times 0.6. However, because
with altered mental status, especially individuals with severe of percentage body fat differences based on the age and sex of the
mental retardation, cerebral palsy, and head injury, as well as in patient, it is more accurate to use the correction factors listed in
bed-ridden patients who have no access to water. Table 125-2.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Table 125-4 Clinical Effects of Hypermagnesemia BOX 125-11 Most Common Causes of Hypomagnesemia
EFFECT LEVEL (mg/dL) Dietary
Decreased deep tendon reflexes 4-5 Gastrointestinal
Renal
Hypotension 5-7 Endocrine or metabolic
Respiratory insufficiency 10 Drug induced
Heart block 10-15
Cardiac arrest 10-24
References 31. Hamill-Ruth RJ, McGory R: Magnesium repletion and its effect on
potassium homeostasis in critically ill adults: Results of a double-blind,
1. Glasziou P: Practice corner: The first symptom of hyperkalemia is death. randomized, controlled trial. Crit Care Med 1996; 24:38-45.
ACP J Club 2004; 140:A13. 32. Huang WY, et al: Central pontine and extrapontine myelinolysis after
2. Whang R, et al: Predictors of clinical hypomagnesemia. Hypokalemia, rapid correction of hyponatremia by hemodialysis in a uremic patient.
hypophosphatemia, hyponatremia, and hypocalcemia. Arch Intern Med Ren Fail 2007; 29:635-638.
1984; 144:1794-1796. 33. Adler SM, Verbalis JG: Disorders of body water homeostasis in critical
3. Wrenn KD, Slovis CM, Slovis BS: The ability of physicians to predict illness. Endocrinol Metab Clin North Am 2006; 35:873-894, xi.
hyperkalemia from the ECG. Ann Emerg Med 1991; 20:1229-1232. 34. Jacobson J, Bohn D: Severe hypernatremic dehydration and
4. Ahmed J, Weisberg LS: Hyperkalemia in dialysis patients. Semin Dial hyperkalemia in an infant with gastroenteritis secondary to rotavirus.
2001; 14:348-356. Ann Emerg Med 1993; 22:1630-1632.
5. Semple P, Booth C: Calcium chloride; a reminder. Anaesthesia 1996; 35. Verbalis JG: Diabetes insipidus. Rev Endocr Metab Disord 2003;
51:93. 4:177-185.
6. Singh BS, et al: Efficacy of albuterol inhalation in treatment of 36. Palevsky PM, Bhagrath R, Greenberg A: Hypernatremia in hospitalized
hyperkalemia in premature neonates. J Pediatr 2002; 141:16-20. patients. Ann Intern Med 1996; 124:197-203.
7. Allon M, Dunlay R, Copkney C: Nebulized albuterol for acute 37. Price TG, Kallenborn JC: Infant hypernatremia: A case report. J Emerg
hyperkalemia in patients on hemodialysis. Ann Intern Med 1989; Med 2000; 19:153-157.
110:426-429. 38. Holley AD, Green S, Davoren P: Extreme hypernatraemia: A case report
8. Nair S, et al: A randomized controlled trial to assess the optimal dose and brief review. Crit Care Resusc 2007; 9:55-58.
and effect of nebulized albuterol in acute exacerbations of COPD. Chest 39. Adrogue HJ, Madias NE: Hyponatremia. N Engl J Med 2000;
2005; 128:48-54. 342:1581-1589.
9. Allon M, Copkney C: Albuterol and insulin for treatment of 40. Kaplan LJ, Kellum JA: Fluids, pH, ions and electrolytes. Curr Opin Crit
hyperkalemia in hemodialysis patients. Kidney Int 1990; 38:869-872. Care 2010; 16:323-331.
10. Allon M, Shanklin N: Effect of bicarbonate administration on plasma 41. Pirzada NA, Ali II: Central pontine myelinolysis. Mayo Clin Proc 2001;
potassium in dialysis patients: Interactions with insulin and albuterol. 76:559-562.
Am J Kidney Dis 1996; 28:508-514. 42. Turchin A, Seifter JL, Seely EW: Clinical problem-solving. Mind the gap.
11. Mahoney A, et al: Emergency interventions for hyperkalaemia. Cochrane N Engl J Med 2003; 349:1465-1469.
Database Syst Rev 2005; 2:CD003235. 43. Cheng JC, et al: Long-term neurologic outcome in psychogenic water
12. Gruy-Kapral C, et al: Effect of single dose resin-cathartic therapy on drinkers with severe symptomatic hyponatremia: The effect of rapid
serum potassium concentration in patients with end-stage renal disease. correction. Am J Med 1990; 88:561-566.
J Am Soc Nephrol 1998; 9:1924-1930. 44. Almond CS, et al: Hyponatremia among runners in the Boston
13. Kitabchi AE, et al: Hyperglycemic crises in adult patients with diabetes. Marathon. N Engl J Med 2005; 352:1550-1556.
Diabetes Care 2009; 32:1335-1343. 45. Lien YHH, Shapiro JI: Hyponatremia: Clinical diagnosis and
14. Alfonzo AV, et al: Potassium disorders—clinical spectrum and management. Am J Med 2007; 120:653-658.
emergency management. Resuscitation 2006; 70:10-25. 46. Sterns RH, Hix JK, Silver S: Treatment of hyponatremia. Curr Opin
15. Vanden Hoek TL, et al: Part 12: Cardiac arrest in special situations: 2010 Nephrol Hypertens 2010; 19:493-498.
American Heart Association Guidelines for Cardiopulmonary 47. Verbalis JG, et al: Hyponatremia treatment guidelines 2007: Expert panel
Resuscitation and Emergency Cardiovascular Care. Circulation 2010; recommendations. Am J Med 2007; 120(Suppl 1):S1-S21.
122(Suppl 3):S829-S861. 48. Janicic N, Verbalis JG: Evaluation and management of hypo-osmolality
16. Blumberg A, et al: Effect of various therapeutic approaches on plasma in hospitalized patients. Endocrinol Metab Clin North Am 2003;
potassium and major regulating factors in terminal renal failure. Am J 32:459-481, vii.
Med 1988; 85:507-512. 49. Oren RM: Hyponatremia in congestive heart failure. Am J Cardiol 2005;
17. Roffey P, et al: Implication of epinephrine-induced hypokalemia during 95:2B-7B.
cardiac arrest. Resuscitation 2003; 58:231. 50. Ellison DH, Berl T: Clinical practice. The syndrome of inappropriate
18. Lin JL, et al: Outcomes of severe hyperkalemia in cardiopulmonary antidiuresis. N Engl J Med 2007; 356:2064-2072.
resuscitation with concomitant hemodialysis. Intensive Care Med 1994; 51. Vaidya C, Ho W, Freda BJ: Management of hyponatremia: Providing
20:287-290. treatment and avoiding harm. Cleve Clin J Med 2010; 77:715-726.
19. Buckley MS, Leblanc JM, Cawley MJ: Electrolyte disturbances associated 52. Stewart AF: Clinical practice. Hypercalcemia associated with cancer.
with commonly prescribed medications in the intensive care unit. Crit N Engl J Med 2005; 352:373-379.
Care Med 2010; 38(Suppl):S253-S264. 53. Ziegler R: Hypercalcemic crisis. J Am Soc Nephrol 2001; 12(Suppl
20. Osadchii OE: Mechanisms of hypokalemia-induced ventricular 17):S3-S9.
arrhythmogenicity. Fundam Clin Pharmacol 2010; 24:547-559. 54. Ariyan CE, Sosa JA: Assessment and management of patients with
21. Huang CL, Kuo E: Mechanism of hypokalemia in magnesium deficiency. abnormal calcium. Crit Care Med 2004; 32(4 Suppl):S146-S154.
J Am Soc Nephrol 2007; 18:2649-2652. 55. Nishi SP, Barbagelata NA, Atar S, Birnbaum Y, Tuero E: Hypercalcemia-
22. Whang R, Whang DD, Ryan MP: Refractory potassium repletion. induced ST-segment elevation mimicking acute myocardial infarction.
A consequence of magnesium deficiency. Arch Intern Med 1992; J Electrocardiol 2006; 39:298-300.
152:40-45. 56. Littmann L, Taylor L, Brearley WD: ST-segment elevation: A common
23. Hunt SA, et al: 2009 Focused update incorporated into the ACC/AHA finding in severe hypercalcemia. J Electrocardiol 2007; 40:60-62.
2005 Guidelines for the Diagnosis and Management of Heart Failure in 57. LeGrand SB, Leskuski D, Zama I: Narrative review: Furosemide for
Adults: A report of the American College of Cardiology Foundation/ hypercalcemia: An unproven yet common practice. Ann Intern Med
American Heart Association Task Force on Practice Guidelines: 2008; 149:259-263.
Developed in collaboration with the International Society for Heart and 58. Drake MT, Clarke BL, Khosla S: Bisphosphonates: Mechanism of action
Lung Transplantation. Circulation 2009; 119:e391-e479. and role in clinical practice. Mayo Clinic Proc 2008; 83:1032-1045.
24. Umpierrez GE, et al: Treatment of diabetic ketoacidosis with 59. Major P, et al: Zoledronic acid is superior to pamidronate in the
subcutaneous insulin aspart. Diabetes Care 2004; 27:1873-1878. treatment of hypercalcemia of malignancy: A pooled analysis of two
25. Finsterer J, et al: Malnutrition-induced hypokalemic myopathy in randomized, controlled clinical trials. J Clin Oncol 2001; 19:558-567.
chronic alcoholism. J Toxicol Clin Toxicol 1998; 36:369-373. 60. Stewart AF: Clinical practice. Hypercalcemia associated with cancer.
26. Udezue E, D’Souza L, Mahajan M: Hypokalemia after normal doses N Engl J Med 2005; 352:373-379.
of nebulized albuterol (salbutamol). Am J Emerg Med 1995; 61. Koo WS, et al: Calcium-free hemodialysis for the management of
13:168-171. hypercalcemia. Nephron 1996; 72:424-428.
27. Greenlee M, et al: Narrative review: Evolving concepts in potassium 62. Cooper MS, Gittoes NJ: Diagnosis and management of hypocalcaemia.
homeostasis and hypokalemia. Ann Intern Med 2009; 150:619-625. BMJ 2008; 336:1298-1302.
28. Krahn LE, et al: Hypokalemia leading to torsades de pointes. 63. Aguilera M, Vaughan RS: Calcium and the anaesthetist. Anaesthesia
Munchausen’s disorder or bulimia nervosa? Gen Hosp Psychiatry 1997; 2000; 55:779-790.
19:370-377. 64. Bosworth M, et al: Clinical inquiries: What is the best workup for
29. Gennari FJ: Hypokalemia. N Engl J Med 1998; 339:451-458. hypocalcemia? J Fam Pract 2008; 57:677-679.
30. Coca SG, Perazella MA, Buller GK: The cardiovascular implications of 65. Levine M, Nikkanen H, Pallin DJ: The effects of intravenous calcium in
hypokalemia. Am J Kidney Dis 2005; 45:233-247. patients with digoxin toxicity. J Emerg Med 2011; 40:41-46.
1651.e2 PART III ◆ Medicine and Surgery / Section Eleven • Metabolism and Endocrinology
66. Schelling JR: Fatal hypermagnesemia. Clin Nephrol 2000; 53:61-65. saline from an indwelling catheter. Clin Chem Lab Med 2004;
67. Qureshi T, Melonakos TK: Acute hypermagnesemia after laxative use. 42:107-108.
Ann Emerg Med 1996; 28:552-555. 82. Slovis CM, Meehan PM: Electrolyte abnormalities. In: Roppolo LP, ed.
68. Birrer RB, Shallash AJ, Totten V: Hypermagnesemia-induced fatality Emergency Medicine Handbook: Critical Concepts for Clinical Practice.
following Epsom salt gargles. J Emerg Med 2002; 22:185-188. Philadelphia: Mosby/Elsevier; 2007:1166-1184.
69. Tofil NM, et al: Fatal hypermagnesemia caused by an Epsom salt enema: 83. Martin KJ, Gonzalez EA: Prevention and control of phosphate retention/
A case illustration. South Med J 2005; 98:253-256. hyperphosphatemia in CKD-MBD: What is normal, when to start, and
70. Slovis CM, Meehan PM: Electrolyte abnormalities. In: Roppolo LP, ed. how to treat? Clin J Am Soc Nephrol 2011; 6:440-446.
Emergency Medicine Handbook: Critical Concepts for Clinical Practice. 84. Tonelli M, Pannu N, Manns B: Oral phosphate binders in patients with
Philadelphia: Mosby/Elsevier; 2007:1166-1184. kidney failure. N Engl J Med 2010; 362:1312-1324.
71. Topf JM, Murray PT: Hypomagnesemia and hypermagnesemia. Rev 85. Culleton BF, et al: Effect of frequent nocturnal hemodialysis vs
Endocr Metab Disord 2003; 4:195-206. conventional hemodialysis on left ventricular mass and quality of life:
72. Vanden Hoek TL, et al: Cardiac arrest in special situations: 2010 A randomized controlled trial. JAMA 2007; 298:1291-1299.
American Heart Association Guidelines for Cardiopulmonary 86. Subramanian R, Khardori R: Severe hypophosphatemia.
Resuscitation and Emergency Cardiovascular Care. Circulation 2010; Pathophysiologic implications, clinical presentations, and treatment.
122:S829-S861. Medicine (Baltimore) 2000; 79:1-8.
73. Soliman HM: Development of ionized hypomagnesemia is associated 87. Miller DW, Slovis C: Hypophosphatemia in the emergency department
with higher mortality rates. Crit Care Med 2003; 31:1082-1087. therapeutics. Am J Emerg Med 2000; 18:457-461.
74. Poikolainen K, Alho H: Magnesium treatment in alcoholics: A 88. Shor R, et al: Severe hypophosphatemia in sepsis as a mortality
randomized clinical trial. Subst Abuse Treat Prev Policy 2008; 3:1. predictor. Ann Clin Lab Sci 2006; 36:67-72.
75. Liao F, Folsom AR, Brancati FL: Is low magnesium concentration a risk 89. Kraft MD, Btaiche IF, Sacks GS, Kudsk KA: Treatment of electrolyte
factor for coronary heart disease? The Atherosclerosis Risk in disorders in adult patients in the intensive care unit. Am J Health Syst
Communities (ARIC) Study. Am Heart J 1998; 136:480-490. Pharm 2005; 62:1663.
76. Agus ZS: Hypomagnesemia. J Am Soc Nephrol 1999; 10:1616-1622. 90. Reference deleted in proofs.
77. ISIS-4: A randomized factorial trial assessing early captopril, oral 91. Chiasson JL, et al: Diagnosis and treatment of diabetic ketoacidosis and
mononitrate, and intravenous magnesium sulfphate in 58,050 patients the hyperglycemic hyperosmolar state. CMAJ 2003; 168:859-866.
with suspected acute myocardial infarction. ISIS-4 Collaborative Group. 92. Casavant MJ, Fitch JA: Fatal hypernatremia from saltwater used as an
Lancet 1995; 345:669. emetic. J Toxicol Clin Toxicol 2003; 41:861-863.
78. Broeren MA, Geerdink EA, Vader HL, van den Wall Bake AW: 93. Trepiccione F, Christensen BM: Lithium-induced nephrogenic diabetes
Hypomagnesemia induced by several proton-pump inhibitors. Ann insipidus: New clinical and experimental findings. J Nephrol 2010;
Intern Med 2009; 151:755-756. 23(Suppl 16):S43-S48.
79. Champagne CM: Magnesium in hypertension, cardiovascular disease, 94. Porath A, et al: Dead Sea water poisoning. Ann Emerg Med 1989;
metabolic syndrome, and other conditions: A review. Nutr Clin Pract 18:187-191.
2008; 23:142-151. 95. Liamis G, et al: Medication-induced hypophosphatemia: A review. QJM
80. Kapoor M, Chan G: Fluid and electrolyte abnormalities. Crit Care Clin 2010; 103:449-459.
2001; 17:503-529.
81. Ball CL, Tobler K, Ross BC, Connors MR, Lyon ME: Spurious
hyperphosphatemia due to sample contamination with heparinized