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What are the causes of hypomagnesemia?
The causes of magnesium depletion and hypomagnesemia are decreased gastrointestinal (GI) absorption and increased renal loss. Decreased GI absorption is frequently due to diarrhea, malabsorption, and inadequate dietary intake. Common causes of excessive urinary loss are diuresis due to alcohol, glycosuria, and loop diuretics.
Medical conditions putting persons at high risk for hypomagnesemia are alcoholism, congestive heart failure, diabetes, chronic diarrhea, hypokalemia, hypocalcemia, and malnutrition (strength of recommendation: C, based on expert opinion, physiology, and case series). Evidence suggests that magnesium deficiency is both more common and more clinically significant than generally appreciated.
Evidence summary
Prevalence and incidence. In general, studies are limited by variations in analytic techniques and differences in defining the lower limit for normal serum magnesium.1 Estimates of the prevalence of hypomagnesemia in the general population range from 2.5% to 15%. A study of 11,000 white urban Americans aged 45 to 64 years (probability sampling) found 2.5% with magnesium <0.7 mmol/L and 5% with magnesium <0.75 mmol/L; rates for 4000 African Americans were twice as high.2
Some authors have proposed a higher range for normal serum magnesium, asserting that dietary magnesium deficiency is endemic in developed countries where acid rain reduces the magnesium content of crops and food processing causes further large reductions in the magnesium content of the diet.1 Moreover, common diseases are associated with hypomagnesemia and likely contaminate studies of “normal” populations. Thus, a study of 16,000 German subjects (including blood donors, outpatients, and children) found a 14.5% prevalence of hypomagnesemia using a lower limit of 0.76 mmol/L1; however, applying the more commonly cited lower limit of 0.70 mmol/L (1.7 mg/dL) to the same data yielded aprevalence of 2%.
Numerous studies agree that the prevalence of hypomagnesemia is much higher (10%–65%) in subpopulations defined by severity of illness (hospitalization, in intensive care unit [ICU] or pediatric ICU), increasing age (elderly/in nursing home), or specific diseases. For example, of 94 consecutive patients admitted to the ICU, 65% had hypomagnesemia.3 Likewise, for 127 consecutive patients admitted with a diagnosis of alcoholism, the prevalence was 30%.4
Because of limitations noted above, as well as the lack of control groups, the relative prevalence in these groups (compared with the general population) is uncertain, but the studies do identify high-risk populations. A single study, which included a control group, demonstrated an 11% prevalence of hypomagnesemia among 621 randomly selected hospitalized patients compared with 2.5% among 341 hospital employees.5 Other diseases associated with a high prevalence of hypomagnesemia include cardiovascular disease (hypertension, congestive heart failure, coronary artery disease), diabetes, diarrhea, diuretics use, hypokalemia, hypocalcemia, and malabsorption.6-9
Common causes. We found no high-quality studies to establish the relative probabilities of various causes in the general population or any subpopulation.10 The most common causes of significant hypomagnesemia in developed countries are said to be diabetes, alcoholism, and the use of diuretics. In a group of 5100 consecutive patients (predominantly outpatient, middle-aged, and female) presenting to a diagnostic lab, the most common diagnoses associated with hypomagnesemia were diabetes (20% of cases) and diuretic use (14% of cases); however, other potential causes, including alcoholism, were not identified.11 A complete list of causes is in the Table.
Serious causes. A critical serum magnesium level is less than 0.5 mmol/L and is associated with seizures and life-threatening arrhythmias.6 Very low magnesium levels typically result when an acute problem is superimposed on chronic depletion. For example, critical levels can occur among patients with diabetes during correction of ketoacidosis or alcoholics who develop vomiting, diarrhea, or pancreatitis.
Magnesium in the 0.5 to 0.7 mmol/L range may be life-threatening in certain disease contexts, such as acute myocardial infarction or congestive heart failure, where there is already a risk of fatal arrhythmia.8
Impact. The impact of hypomagnesemia is underestimated largely because clinicians fail to measure magnesium.12 Since magnesium is a cofactor for more than 300 enzymes and is involved in numerous transport mechanisms, it is not surprising that hypomagnesemia is associated with significant morbidity.
For example, in a study of 381 consecutive admissions at an inner-city hospital,13 approximately half the admissions went to ICUs and half to regular wards. Despite similar Acute Physiology and Chronic Health Evaluator (APACHE) scores at admission, hospital mortality was twice as high for hypomagnesemic patients in both care settings.
TABLE
Causes of hypomagnesemia
| Gastrointestinal |
| Diarrhea, dietary deficiency (including protein-calorie malnutrition, parenteral and enteral feeding with inadequate magnesium, alcoholism, and pregnancy), familial magnesium malabsorption, gastrointestinal fistulas, inflammatory bowel disease, laxative abuse, malabsorption (sprue, steatorrhea, chronic pancreatitis), nasogastric suction, surgical resection, vomiting |
| Renal |
| Alcoholism, diabetes, diuretics (thiazide, loop, and osmotic/hyperglycemia), other medications, hormones (hypoparathyroidism, hyperthyroidism, hyperaldosteronism, SIADH (syndrome of inappropriate antidiuretic hormone secretion), excessive vitamin D, ketoacidosis, renal disease (acute tubular necrosis, interstitial nephritis, glomerulonephritis, post-obstructive diuresis, post-renal transplantation), hypercalcemia/hypophosphatemia, tubular defects (primary magnesium wasting, Welt’s syndrome, Gitelman’s syndrome, renal tubular acidosis) |
| Shifts from extracellular to intracellular fluid |
| Acidosis (correction of), blood transfusions (massive), epinephrine, hungry bone syndrome, insulin/glucose/refeeding syndrome, pancreatitis (acute) |
| Transdermal losses |
| Excessive sweating, massive burns |
Recommendations from others
Several review articles include a comprehensive differential diagnosis for causes of magnesium deficiency based on physiologic principles as listed in the Table, but none provide data on the relative frequency of the various causes in the general population or specific subgroups.6-9
We need to know when magnesium replacement improves patient outcomes
John Hickner, MD, MSc
Department of Family Medicine, The University of Chicago Pritzker School of Medicine, Chicago, Ill
Treating the underlying cause of hypomagnesemia makes sense. However, even though clinicians often treat “the numbers,” it is not clear that magnesium replacement therapy is beneficial in the absence of symptoms caused by the hypomagnesemia. For example, hypomagnesemia is common for patients with acute myocardial infarction, but magnesium replacement therapy has not been shown to improve outcomes in 2 large randomized trials, the Fourth International Study of Infarct Survival (ISIS 4)14 and Magnesium in Coronaries (MAGIC).15 We need better-designed randomized trials to know for what clinical conditions magnesium replacement leads to improved patient-oriented outcomes.
1. Schimatschek HF, Rempis R. Prevalence of hypomagnesemia in an unselected German population of 16,000 individuals. Magnes Res 2001;14:283-290.
2. Ma J, Folsom AR, Melnick SL, et al. Associations of serum and dietary magnesium with cardiovascular disease, hypertension, diabetes, insulin, and carotid arterial wall thickness: the ARIC study. Atherosclerosis Risk in Communities Study. J Clin Epidemiol 1995;48:927-940.
3. Ryzen E, Wagers PW, Singer FR, Rude RK. Magnesium deficiency in a medical ICU population. Crit Care Med 1985;13:19-21.
4. Elisaf M, Merkouropoulos M, Tsianos EV, Siamopoulos KC. Pathogenic mechanisms of hypomagnesemia in alcoholic patients. J Trace Elem Med Biol 1995;9:210-214.
5. Wong ET, Rude RK, Singer FR, Shaw ST, Jr. A high prevalence of hypomagnesemia and hypermagnesemia in hospitalized patients. Am J Clin Pathol 1983;79:348-353.
6. Topf JM, Murray PT. Hypomagnesemia and hypermagnesemia. Rev Endocr Metab Disord 2003;4:195-206.
7. Whang R, Hampton EM, Whang DD. Magnesium homeostasis and clinical disorders of magnesium deficiency. Ann Pharmacother 1994;28:220-226.
8. Kelepouris E, Agus ZS. Hypomagnesemia: renal magnesium handling. Semin Nephrol 1998;18:58-73.
9. Dacey MJ. Hypomagnesemic disorders. Crit Care Clin 2001;17:155-173.
10. Richardson WS, Wilson MC, Guyatt GH, Cook DJ, Nishikawa J. Users’ Guides to the Medical Literature: XV. How to use an article about disease probability for differential diagnosis. Evidence-Based Medicine Working Group. JAMA 1999;281:1214-1219.
11. Jackson CE, Meier DW. Routine serum magnesium analysis. Correlation with clinical state in 5,100 patients. Ann Intern Med 1968;69:743-748.
12. Whang R, Ryder KW. Frequency of hypomagnesemia and hypermagnesemia. Requested vs routine. JAMA 1990;263:3063-3064.
13. Rubeiz GJ, Thill-Baharozian M, Hardie D, Carlson RW. Association of hypomagnesemia and mortality in acutely ill medical patients. Crit Care Med 1993;21:203-209.
14. ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected acute myocardial infarction. Lancet 1995;345:669-685.
15. Magnesium in Coronaries (MAGIC) Trial Investigators. Early administration of intravenous magnesium to highrisk patients with acute myocardial infarction in the Magnesium in Coronaries (MAGIC) Trial: a randomised controlled trial. Lancet 2002;360:1189-1196.
The causes of magnesium depletion and hypomagnesemia are decreased gastrointestinal (GI) absorption and increased renal loss. Decreased GI absorption is frequently due to diarrhea, malabsorption, and inadequate dietary intake. Common causes of excessive urinary loss are diuresis due to alcohol, glycosuria, and loop diuretics.
Medical conditions putting persons at high risk for hypomagnesemia are alcoholism, congestive heart failure, diabetes, chronic diarrhea, hypokalemia, hypocalcemia, and malnutrition (strength of recommendation: C, based on expert opinion, physiology, and case series). Evidence suggests that magnesium deficiency is both more common and more clinically significant than generally appreciated.
Evidence summary
Prevalence and incidence. In general, studies are limited by variations in analytic techniques and differences in defining the lower limit for normal serum magnesium.1 Estimates of the prevalence of hypomagnesemia in the general population range from 2.5% to 15%. A study of 11,000 white urban Americans aged 45 to 64 years (probability sampling) found 2.5% with magnesium <0.7 mmol/L and 5% with magnesium <0.75 mmol/L; rates for 4000 African Americans were twice as high.2
Some authors have proposed a higher range for normal serum magnesium, asserting that dietary magnesium deficiency is endemic in developed countries where acid rain reduces the magnesium content of crops and food processing causes further large reductions in the magnesium content of the diet.1 Moreover, common diseases are associated with hypomagnesemia and likely contaminate studies of “normal” populations. Thus, a study of 16,000 German subjects (including blood donors, outpatients, and children) found a 14.5% prevalence of hypomagnesemia using a lower limit of 0.76 mmol/L1; however, applying the more commonly cited lower limit of 0.70 mmol/L (1.7 mg/dL) to the same data yielded aprevalence of 2%.
Numerous studies agree that the prevalence of hypomagnesemia is much higher (10%–65%) in subpopulations defined by severity of illness (hospitalization, in intensive care unit [ICU] or pediatric ICU), increasing age (elderly/in nursing home), or specific diseases. For example, of 94 consecutive patients admitted to the ICU, 65% had hypomagnesemia.3 Likewise, for 127 consecutive patients admitted with a diagnosis of alcoholism, the prevalence was 30%.4
Because of limitations noted above, as well as the lack of control groups, the relative prevalence in these groups (compared with the general population) is uncertain, but the studies do identify high-risk populations. A single study, which included a control group, demonstrated an 11% prevalence of hypomagnesemia among 621 randomly selected hospitalized patients compared with 2.5% among 341 hospital employees.5 Other diseases associated with a high prevalence of hypomagnesemia include cardiovascular disease (hypertension, congestive heart failure, coronary artery disease), diabetes, diarrhea, diuretics use, hypokalemia, hypocalcemia, and malabsorption.6-9
Common causes. We found no high-quality studies to establish the relative probabilities of various causes in the general population or any subpopulation.10 The most common causes of significant hypomagnesemia in developed countries are said to be diabetes, alcoholism, and the use of diuretics. In a group of 5100 consecutive patients (predominantly outpatient, middle-aged, and female) presenting to a diagnostic lab, the most common diagnoses associated with hypomagnesemia were diabetes (20% of cases) and diuretic use (14% of cases); however, other potential causes, including alcoholism, were not identified.11 A complete list of causes is in the Table.
Serious causes. A critical serum magnesium level is less than 0.5 mmol/L and is associated with seizures and life-threatening arrhythmias.6 Very low magnesium levels typically result when an acute problem is superimposed on chronic depletion. For example, critical levels can occur among patients with diabetes during correction of ketoacidosis or alcoholics who develop vomiting, diarrhea, or pancreatitis.
Magnesium in the 0.5 to 0.7 mmol/L range may be life-threatening in certain disease contexts, such as acute myocardial infarction or congestive heart failure, where there is already a risk of fatal arrhythmia.8
Impact. The impact of hypomagnesemia is underestimated largely because clinicians fail to measure magnesium.12 Since magnesium is a cofactor for more than 300 enzymes and is involved in numerous transport mechanisms, it is not surprising that hypomagnesemia is associated with significant morbidity.
For example, in a study of 381 consecutive admissions at an inner-city hospital,13 approximately half the admissions went to ICUs and half to regular wards. Despite similar Acute Physiology and Chronic Health Evaluator (APACHE) scores at admission, hospital mortality was twice as high for hypomagnesemic patients in both care settings.
TABLE
Causes of hypomagnesemia
| Gastrointestinal |
| Diarrhea, dietary deficiency (including protein-calorie malnutrition, parenteral and enteral feeding with inadequate magnesium, alcoholism, and pregnancy), familial magnesium malabsorption, gastrointestinal fistulas, inflammatory bowel disease, laxative abuse, malabsorption (sprue, steatorrhea, chronic pancreatitis), nasogastric suction, surgical resection, vomiting |
| Renal |
| Alcoholism, diabetes, diuretics (thiazide, loop, and osmotic/hyperglycemia), other medications, hormones (hypoparathyroidism, hyperthyroidism, hyperaldosteronism, SIADH (syndrome of inappropriate antidiuretic hormone secretion), excessive vitamin D, ketoacidosis, renal disease (acute tubular necrosis, interstitial nephritis, glomerulonephritis, post-obstructive diuresis, post-renal transplantation), hypercalcemia/hypophosphatemia, tubular defects (primary magnesium wasting, Welt’s syndrome, Gitelman’s syndrome, renal tubular acidosis) |
| Shifts from extracellular to intracellular fluid |
| Acidosis (correction of), blood transfusions (massive), epinephrine, hungry bone syndrome, insulin/glucose/refeeding syndrome, pancreatitis (acute) |
| Transdermal losses |
| Excessive sweating, massive burns |
Recommendations from others
Several review articles include a comprehensive differential diagnosis for causes of magnesium deficiency based on physiologic principles as listed in the Table, but none provide data on the relative frequency of the various causes in the general population or specific subgroups.6-9
We need to know when magnesium replacement improves patient outcomes
John Hickner, MD, MSc
Department of Family Medicine, The University of Chicago Pritzker School of Medicine, Chicago, Ill
Treating the underlying cause of hypomagnesemia makes sense. However, even though clinicians often treat “the numbers,” it is not clear that magnesium replacement therapy is beneficial in the absence of symptoms caused by the hypomagnesemia. For example, hypomagnesemia is common for patients with acute myocardial infarction, but magnesium replacement therapy has not been shown to improve outcomes in 2 large randomized trials, the Fourth International Study of Infarct Survival (ISIS 4)14 and Magnesium in Coronaries (MAGIC).15 We need better-designed randomized trials to know for what clinical conditions magnesium replacement leads to improved patient-oriented outcomes.
The causes of magnesium depletion and hypomagnesemia are decreased gastrointestinal (GI) absorption and increased renal loss. Decreased GI absorption is frequently due to diarrhea, malabsorption, and inadequate dietary intake. Common causes of excessive urinary loss are diuresis due to alcohol, glycosuria, and loop diuretics.
Medical conditions putting persons at high risk for hypomagnesemia are alcoholism, congestive heart failure, diabetes, chronic diarrhea, hypokalemia, hypocalcemia, and malnutrition (strength of recommendation: C, based on expert opinion, physiology, and case series). Evidence suggests that magnesium deficiency is both more common and more clinically significant than generally appreciated.
Evidence summary
Prevalence and incidence. In general, studies are limited by variations in analytic techniques and differences in defining the lower limit for normal serum magnesium.1 Estimates of the prevalence of hypomagnesemia in the general population range from 2.5% to 15%. A study of 11,000 white urban Americans aged 45 to 64 years (probability sampling) found 2.5% with magnesium <0.7 mmol/L and 5% with magnesium <0.75 mmol/L; rates for 4000 African Americans were twice as high.2
Some authors have proposed a higher range for normal serum magnesium, asserting that dietary magnesium deficiency is endemic in developed countries where acid rain reduces the magnesium content of crops and food processing causes further large reductions in the magnesium content of the diet.1 Moreover, common diseases are associated with hypomagnesemia and likely contaminate studies of “normal” populations. Thus, a study of 16,000 German subjects (including blood donors, outpatients, and children) found a 14.5% prevalence of hypomagnesemia using a lower limit of 0.76 mmol/L1; however, applying the more commonly cited lower limit of 0.70 mmol/L (1.7 mg/dL) to the same data yielded aprevalence of 2%.
Numerous studies agree that the prevalence of hypomagnesemia is much higher (10%–65%) in subpopulations defined by severity of illness (hospitalization, in intensive care unit [ICU] or pediatric ICU), increasing age (elderly/in nursing home), or specific diseases. For example, of 94 consecutive patients admitted to the ICU, 65% had hypomagnesemia.3 Likewise, for 127 consecutive patients admitted with a diagnosis of alcoholism, the prevalence was 30%.4
Because of limitations noted above, as well as the lack of control groups, the relative prevalence in these groups (compared with the general population) is uncertain, but the studies do identify high-risk populations. A single study, which included a control group, demonstrated an 11% prevalence of hypomagnesemia among 621 randomly selected hospitalized patients compared with 2.5% among 341 hospital employees.5 Other diseases associated with a high prevalence of hypomagnesemia include cardiovascular disease (hypertension, congestive heart failure, coronary artery disease), diabetes, diarrhea, diuretics use, hypokalemia, hypocalcemia, and malabsorption.6-9
Common causes. We found no high-quality studies to establish the relative probabilities of various causes in the general population or any subpopulation.10 The most common causes of significant hypomagnesemia in developed countries are said to be diabetes, alcoholism, and the use of diuretics. In a group of 5100 consecutive patients (predominantly outpatient, middle-aged, and female) presenting to a diagnostic lab, the most common diagnoses associated with hypomagnesemia were diabetes (20% of cases) and diuretic use (14% of cases); however, other potential causes, including alcoholism, were not identified.11 A complete list of causes is in the Table.
Serious causes. A critical serum magnesium level is less than 0.5 mmol/L and is associated with seizures and life-threatening arrhythmias.6 Very low magnesium levels typically result when an acute problem is superimposed on chronic depletion. For example, critical levels can occur among patients with diabetes during correction of ketoacidosis or alcoholics who develop vomiting, diarrhea, or pancreatitis.
Magnesium in the 0.5 to 0.7 mmol/L range may be life-threatening in certain disease contexts, such as acute myocardial infarction or congestive heart failure, where there is already a risk of fatal arrhythmia.8
Impact. The impact of hypomagnesemia is underestimated largely because clinicians fail to measure magnesium.12 Since magnesium is a cofactor for more than 300 enzymes and is involved in numerous transport mechanisms, it is not surprising that hypomagnesemia is associated with significant morbidity.
For example, in a study of 381 consecutive admissions at an inner-city hospital,13 approximately half the admissions went to ICUs and half to regular wards. Despite similar Acute Physiology and Chronic Health Evaluator (APACHE) scores at admission, hospital mortality was twice as high for hypomagnesemic patients in both care settings.
TABLE
Causes of hypomagnesemia
| Gastrointestinal |
| Diarrhea, dietary deficiency (including protein-calorie malnutrition, parenteral and enteral feeding with inadequate magnesium, alcoholism, and pregnancy), familial magnesium malabsorption, gastrointestinal fistulas, inflammatory bowel disease, laxative abuse, malabsorption (sprue, steatorrhea, chronic pancreatitis), nasogastric suction, surgical resection, vomiting |
| Renal |
| Alcoholism, diabetes, diuretics (thiazide, loop, and osmotic/hyperglycemia), other medications, hormones (hypoparathyroidism, hyperthyroidism, hyperaldosteronism, SIADH (syndrome of inappropriate antidiuretic hormone secretion), excessive vitamin D, ketoacidosis, renal disease (acute tubular necrosis, interstitial nephritis, glomerulonephritis, post-obstructive diuresis, post-renal transplantation), hypercalcemia/hypophosphatemia, tubular defects (primary magnesium wasting, Welt’s syndrome, Gitelman’s syndrome, renal tubular acidosis) |
| Shifts from extracellular to intracellular fluid |
| Acidosis (correction of), blood transfusions (massive), epinephrine, hungry bone syndrome, insulin/glucose/refeeding syndrome, pancreatitis (acute) |
| Transdermal losses |
| Excessive sweating, massive burns |
Recommendations from others
Several review articles include a comprehensive differential diagnosis for causes of magnesium deficiency based on physiologic principles as listed in the Table, but none provide data on the relative frequency of the various causes in the general population or specific subgroups.6-9
We need to know when magnesium replacement improves patient outcomes
John Hickner, MD, MSc
Department of Family Medicine, The University of Chicago Pritzker School of Medicine, Chicago, Ill
Treating the underlying cause of hypomagnesemia makes sense. However, even though clinicians often treat “the numbers,” it is not clear that magnesium replacement therapy is beneficial in the absence of symptoms caused by the hypomagnesemia. For example, hypomagnesemia is common for patients with acute myocardial infarction, but magnesium replacement therapy has not been shown to improve outcomes in 2 large randomized trials, the Fourth International Study of Infarct Survival (ISIS 4)14 and Magnesium in Coronaries (MAGIC).15 We need better-designed randomized trials to know for what clinical conditions magnesium replacement leads to improved patient-oriented outcomes.
1. Schimatschek HF, Rempis R. Prevalence of hypomagnesemia in an unselected German population of 16,000 individuals. Magnes Res 2001;14:283-290.
2. Ma J, Folsom AR, Melnick SL, et al. Associations of serum and dietary magnesium with cardiovascular disease, hypertension, diabetes, insulin, and carotid arterial wall thickness: the ARIC study. Atherosclerosis Risk in Communities Study. J Clin Epidemiol 1995;48:927-940.
3. Ryzen E, Wagers PW, Singer FR, Rude RK. Magnesium deficiency in a medical ICU population. Crit Care Med 1985;13:19-21.
4. Elisaf M, Merkouropoulos M, Tsianos EV, Siamopoulos KC. Pathogenic mechanisms of hypomagnesemia in alcoholic patients. J Trace Elem Med Biol 1995;9:210-214.
5. Wong ET, Rude RK, Singer FR, Shaw ST, Jr. A high prevalence of hypomagnesemia and hypermagnesemia in hospitalized patients. Am J Clin Pathol 1983;79:348-353.
6. Topf JM, Murray PT. Hypomagnesemia and hypermagnesemia. Rev Endocr Metab Disord 2003;4:195-206.
7. Whang R, Hampton EM, Whang DD. Magnesium homeostasis and clinical disorders of magnesium deficiency. Ann Pharmacother 1994;28:220-226.
8. Kelepouris E, Agus ZS. Hypomagnesemia: renal magnesium handling. Semin Nephrol 1998;18:58-73.
9. Dacey MJ. Hypomagnesemic disorders. Crit Care Clin 2001;17:155-173.
10. Richardson WS, Wilson MC, Guyatt GH, Cook DJ, Nishikawa J. Users’ Guides to the Medical Literature: XV. How to use an article about disease probability for differential diagnosis. Evidence-Based Medicine Working Group. JAMA 1999;281:1214-1219.
11. Jackson CE, Meier DW. Routine serum magnesium analysis. Correlation with clinical state in 5,100 patients. Ann Intern Med 1968;69:743-748.
12. Whang R, Ryder KW. Frequency of hypomagnesemia and hypermagnesemia. Requested vs routine. JAMA 1990;263:3063-3064.
13. Rubeiz GJ, Thill-Baharozian M, Hardie D, Carlson RW. Association of hypomagnesemia and mortality in acutely ill medical patients. Crit Care Med 1993;21:203-209.
14. ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected acute myocardial infarction. Lancet 1995;345:669-685.
15. Magnesium in Coronaries (MAGIC) Trial Investigators. Early administration of intravenous magnesium to highrisk patients with acute myocardial infarction in the Magnesium in Coronaries (MAGIC) Trial: a randomised controlled trial. Lancet 2002;360:1189-1196.
1. Schimatschek HF, Rempis R. Prevalence of hypomagnesemia in an unselected German population of 16,000 individuals. Magnes Res 2001;14:283-290.
2. Ma J, Folsom AR, Melnick SL, et al. Associations of serum and dietary magnesium with cardiovascular disease, hypertension, diabetes, insulin, and carotid arterial wall thickness: the ARIC study. Atherosclerosis Risk in Communities Study. J Clin Epidemiol 1995;48:927-940.
3. Ryzen E, Wagers PW, Singer FR, Rude RK. Magnesium deficiency in a medical ICU population. Crit Care Med 1985;13:19-21.
4. Elisaf M, Merkouropoulos M, Tsianos EV, Siamopoulos KC. Pathogenic mechanisms of hypomagnesemia in alcoholic patients. J Trace Elem Med Biol 1995;9:210-214.
5. Wong ET, Rude RK, Singer FR, Shaw ST, Jr. A high prevalence of hypomagnesemia and hypermagnesemia in hospitalized patients. Am J Clin Pathol 1983;79:348-353.
6. Topf JM, Murray PT. Hypomagnesemia and hypermagnesemia. Rev Endocr Metab Disord 2003;4:195-206.
7. Whang R, Hampton EM, Whang DD. Magnesium homeostasis and clinical disorders of magnesium deficiency. Ann Pharmacother 1994;28:220-226.
8. Kelepouris E, Agus ZS. Hypomagnesemia: renal magnesium handling. Semin Nephrol 1998;18:58-73.
9. Dacey MJ. Hypomagnesemic disorders. Crit Care Clin 2001;17:155-173.
10. Richardson WS, Wilson MC, Guyatt GH, Cook DJ, Nishikawa J. Users’ Guides to the Medical Literature: XV. How to use an article about disease probability for differential diagnosis. Evidence-Based Medicine Working Group. JAMA 1999;281:1214-1219.
11. Jackson CE, Meier DW. Routine serum magnesium analysis. Correlation with clinical state in 5,100 patients. Ann Intern Med 1968;69:743-748.
12. Whang R, Ryder KW. Frequency of hypomagnesemia and hypermagnesemia. Requested vs routine. JAMA 1990;263:3063-3064.
13. Rubeiz GJ, Thill-Baharozian M, Hardie D, Carlson RW. Association of hypomagnesemia and mortality in acutely ill medical patients. Crit Care Med 1993;21:203-209.
14. ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected acute myocardial infarction. Lancet 1995;345:669-685.
15. Magnesium in Coronaries (MAGIC) Trial Investigators. Early administration of intravenous magnesium to highrisk patients with acute myocardial infarction in the Magnesium in Coronaries (MAGIC) Trial: a randomised controlled trial. Lancet 2002;360:1189-1196.
Evidence-based answers from the Family Physicians Inquiries Network
What is the best way to evaluate and manage diarrhea in the febrile infant?
Routine infant diarrhea requires no lab work or cultures (strength of recommendation [SOR]: C); the degree of dehydration can be determined reliably by percent body weight change (SOR: B). However, bicarbonate may help rule out dehydration (SOR: B); electrolytes and blood urea nitrogen may be useful in evaluating complicated diarrhea with severe dehydration or when intravenous fluids are required; stool cultures are indicated for bloody or prolonged diarrhea, suspected food poisoning, or recent travel abroad (SOR: C).
Oral rehydrating solution is adequate fluid replacement for diarrhea associated with mild to moderate dehydration, followed by prompt refeeding with an age-appropriate diet (SOR: A); intravenous fluids are recommended for severe dehydration (SOR: C). Probiotics have been shown to safely reduce the duration and frequency of diarrhea (SOR: A).
Evidence summary
Evidence is summarized in the Table. Evaluation of an infant with diarrhea usually requires only a thorough history and physical exam. While no clinical trials have tested the impact of blood or stool testing on patient outcome, a recent systematic review suggested the only blood test reliable for ruling out dehydration is a serum bicarbonate greater than 15 to 17 mEq/L.1 Consensus reports have suggested laboratory studies are unnecessary unless dehydration is severe or IV fluids are required; stool cultures are necessary only for bloody or prolonged diarrhea, systemically ill infants, suspected food poisoning, or recent travel abroad.2,3
Effective management of infant diarrhea is based on the degree of dehydration, which can be estimated by percent body weight loss—the difference between the baseline and acute weights, divided by the baseline weight.3 If the baseline weight is not known, prolonged capillary refill time, abnormal skin turgor, and abnormal respiratory pattern are more reliable indicators of dehydration; other physical findings are less precise.1
Infants with diarrhea who are not dehydrated should continue age-appropriate nutrition.4 For infants with mild to moderate dehydration, however, rehydration using oral rehydrating solution is the initial therapy, followed by continued hydration to replace ongoing losses.2,3 A meta-analysis of randomized controlled trials (RCTs) in developed countries demonstrated equivalent efficacy of oral fluids compared with IV fluids, with an overall failure rate of only 3.6% for infants and children treated with oral rehydrating solution (95% confidence interval [CI], 1.4–5.8). There was no significant difference between oral rehydrating solution of varying sodium concentrations, and no increased risk of hypernatremia or hyponatremia compared with the IV treatment arm.5 Continued breastfeeding during the rehydrating phase significantly reduced dehydration (based on case control studies; odds ratio [OR]=5.23; 95% CI, 1.37–19.99; P=.016, limited by sample size).3,6 Breastfeeding also significantly reduced the number of diarrheal stools (found in a small-scale RCT).7 For obtunded or severely dehydrated infants, or those with an ileus or persistent vomiting, expert opinion suggested IV fluids.2,4
In a systematic review of RCTs comparing lower-concentration oral rehydrating solution with standard World Health Organization solution, lower-concentration solution showed superior efficacy. These resulted in fewer unscheduled infusions of IV fluids (OR=0.59; 95% CI, 0.45–0.79) and less stool output without increasing the incidence of hyponatremia.8
Unrestricted diets may reduce the duration of diarrhea compared with oral or IV fluids alone, and age-appropriate diets should be resumed immediately after hydration (based on a review of variable-quality RCTs and prospective trials or case series).2 No studies supported the effectiveness of BRAT (bananas, rice cereal, applesauce, toast) diets over the infant’s usual diet.2,4 A meta-analysis of variable-quality RCTs demonstrated no significant difference in stool frequency between lactose-containing and lactose-free diets.9 Comparisons of undiluted lactose-milk with diluted milk or delayed reintroduction of milk revealed no significant differences in treatment failure or duration of diarrhea, although stool output increased slightly with the undiluted diet. However, undiluted milk was superior for restoring body weight.9
Multiple RCTs showed that Lactobacillus supplementation shortened the duration of diarrhea for infants and young children10,11 and reduced the risk of diarrhea persisting more than 3 days (relative risk [RR]=0.43; 95% CI, 0.34–0.53; P<.001; number needed to treat [NNT]=4).11 This probiotic can be reconstituted in oral rehydrating solution and administered 1 to 8 times daily, depending on the formulation.
Antidiarrheal agents are not recommended (based on limited reviews and consensus reports).2-4,12
TABLE
Evaluative strategies and therapeutic interventions for infant diarrhea
| Routine diarrhea* | Complicated diarrhea† | SOR | ||||
|---|---|---|---|---|---|---|
| Recommended | Not recommended | Recommended | Not recommended | |||
| Evaluation | Serology | X | X | B1, C2-3 | ||
| Stool culture | X | X | C2-3 | |||
| Intervention | WHO ORS (Osm 311 mmol/L) | X | X‡ | A8 | ||
| ORS (Osm 250 mmol/L) | X | X | A8 | |||
| Age-appropriate diet after hydration | X | X | C2 | |||
| Continued breast-feeding | X | X | B6,7 | |||
| BRAT diet | X | X | C2,4 | |||
| Lactose-free or dilute lactose diet | X | X | B9 | |||
| Lactobacillus (probiotic) | X | X | A10,11 | |||
| Antidiarrheal agents | X | X | C2,4,12 | |||
| * Mild to moderate dehydration, diarrhea of short duration without bloody stools, severe systemic illness, suspected food poisoning, or recent foreign travel. | ||||||
| † Severe dehydration, prolonged diarrhea, or diarrhea with bloody stools, severe systemic illness, suspected food poisoning, or recent foreign travel. | ||||||
| ‡ Recommended for treatment of cholera. | ||||||
| ORS, oral rehydration solution; SOR, strength of recommendation; BRAT, bananas, rice cereal, applesauce, and toast. | ||||||
Recommendations from others
The Centers for Disease Control and Prevention (CDC) recommends oral rehydrating solution for mild to moderate dehydration, and boluses of normal saline or Lactated Ringer’s (20 cc/kg) for severe dehydration. For frail or malnourished infants, boluses of 10 cc/kg should be given until hydrated.
The CDC also recommended against nutrition containing simple sugars (soft drinks, juice, gelatin desserts) due to high osmotic loads, but noted that diets containing some fats may have a beneficial effect on intestinal motility. They also recommended age-appropriate use of complex carbohydrates, meats, yogurt, fruits and vegetables. Zinc supplementation may also be beneficial (SOR: C).12
Exam should note fever, weight loss, abdominal tenderness, blood in the stool
Lettie Carter, MD
North Shore University Hospital at Glen Cove, Glen Cove, NY
The evaluation and management of an infant with diarrhea as always, begins with history. The length and severity of the illness, sick contacts, oral intake, travel, and characteristics of the stool are all important factors to consider. The physical exam should note presence of fever, weight loss, abdominal tenderness, and blood in the stool. Laboratory studies such as electrolytes, stool culture, and Wright stain are really only indicated if the child is severely dehydrated, unable to maintain hydration with oral intake and requires IV fluids, or if the episode is unusually protracted or the stool bloody.
A regular age-appropriate diet is essential, but parents should be counseled to avoid adding too much juice to the diet in an effort to rehydrate.
1. Steiner MJ, DeWalt DA, Byerley JS. Is this child dehydrated? JAMA 2004;291:2746-2754.
2. Cincinnati Children’s Hospital Medical Center. Evidence based clinical practice guideline for children with acute gastroenteritis (AGE). Cincinnati, Ohio: Cincinnati Children’s Hospital Medical Center; 2001. Available at www.guideline.gov. Accessed on April 5, 2004.
3. Armon K, Stephenson T, MacFaul R, Eccleston P, Werneke U. An evidence and consensus based guideline for acute diarrhea management. Arch Dis Child 2001;85:132-142.
4. Practice parameter: the management of acute gastroenteritis in young children. American Academy of Pediatrics, Provisional Committee on Quality Improvement, Subcommittee on Acute Gastroenteritis. Pediatrics 1996;97:424-435.
5. Gavin N, Merrick N, Davidson B. Efficacy of glucose-based oral rehydration therapy. Pediatrics 1996;98:45-51.
6. Faruque AS, Mahalanabis D, Islam A, Hoque SS, Hasnat A. Breast feeding and oral rehydration at home during diarrhoea to prevent dehydration. Arch Dis Child 1992;67:1027-1029.
7. Khin MU, Nyunt NW, Myo K, Mu MK, Tin U, Thane T. Effect on clinical outcome of breast feeding during acute diarrhoea. Br Med J (Clin Res Ed) 1985;290:587-589.
8. Hahn S, Kim Y, Garner P. Reduced osmolarity oral rehydration for treating dehydration caused by acute diarrhoea in children (Cochrane Review). In: The Cochrane Library., Issue 4, 2004. Chichester, UK: John Wiley & Sons.
9. Brown KH, Peerson JM, Fontaine O. Use of nonhuman milks in the dietary management of young children with acute diarrhea: a meta-analysis of clinical trials. Pediatrics 1994;93:17-27.
10. Van Niel CW, Feudtner C, Garrison MM, Christakis D. Lactobacillus therapy for acute infectious diarrhea in children: a meta-analysis. Pediatrics 2002;109:678-684.
11. Szajewska H, Mrukowicz JZ. Probiotics in the treatment and prevention of acute infectious diarrhea in infants and children: a systematic review of published randomized, double-blind, placebo-controlled trials. J Pediatr Gastroenterol Nutr 2001;33(Suppl 2):S17-S25.
12. King CK, Glass R, Bresee JS, Duggan C. Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep 2003;52(RR-16):1-16.
Routine infant diarrhea requires no lab work or cultures (strength of recommendation [SOR]: C); the degree of dehydration can be determined reliably by percent body weight change (SOR: B). However, bicarbonate may help rule out dehydration (SOR: B); electrolytes and blood urea nitrogen may be useful in evaluating complicated diarrhea with severe dehydration or when intravenous fluids are required; stool cultures are indicated for bloody or prolonged diarrhea, suspected food poisoning, or recent travel abroad (SOR: C).
Oral rehydrating solution is adequate fluid replacement for diarrhea associated with mild to moderate dehydration, followed by prompt refeeding with an age-appropriate diet (SOR: A); intravenous fluids are recommended for severe dehydration (SOR: C). Probiotics have been shown to safely reduce the duration and frequency of diarrhea (SOR: A).
Evidence summary
Evidence is summarized in the Table. Evaluation of an infant with diarrhea usually requires only a thorough history and physical exam. While no clinical trials have tested the impact of blood or stool testing on patient outcome, a recent systematic review suggested the only blood test reliable for ruling out dehydration is a serum bicarbonate greater than 15 to 17 mEq/L.1 Consensus reports have suggested laboratory studies are unnecessary unless dehydration is severe or IV fluids are required; stool cultures are necessary only for bloody or prolonged diarrhea, systemically ill infants, suspected food poisoning, or recent travel abroad.2,3
Effective management of infant diarrhea is based on the degree of dehydration, which can be estimated by percent body weight loss—the difference between the baseline and acute weights, divided by the baseline weight.3 If the baseline weight is not known, prolonged capillary refill time, abnormal skin turgor, and abnormal respiratory pattern are more reliable indicators of dehydration; other physical findings are less precise.1
Infants with diarrhea who are not dehydrated should continue age-appropriate nutrition.4 For infants with mild to moderate dehydration, however, rehydration using oral rehydrating solution is the initial therapy, followed by continued hydration to replace ongoing losses.2,3 A meta-analysis of randomized controlled trials (RCTs) in developed countries demonstrated equivalent efficacy of oral fluids compared with IV fluids, with an overall failure rate of only 3.6% for infants and children treated with oral rehydrating solution (95% confidence interval [CI], 1.4–5.8). There was no significant difference between oral rehydrating solution of varying sodium concentrations, and no increased risk of hypernatremia or hyponatremia compared with the IV treatment arm.5 Continued breastfeeding during the rehydrating phase significantly reduced dehydration (based on case control studies; odds ratio [OR]=5.23; 95% CI, 1.37–19.99; P=.016, limited by sample size).3,6 Breastfeeding also significantly reduced the number of diarrheal stools (found in a small-scale RCT).7 For obtunded or severely dehydrated infants, or those with an ileus or persistent vomiting, expert opinion suggested IV fluids.2,4
In a systematic review of RCTs comparing lower-concentration oral rehydrating solution with standard World Health Organization solution, lower-concentration solution showed superior efficacy. These resulted in fewer unscheduled infusions of IV fluids (OR=0.59; 95% CI, 0.45–0.79) and less stool output without increasing the incidence of hyponatremia.8
Unrestricted diets may reduce the duration of diarrhea compared with oral or IV fluids alone, and age-appropriate diets should be resumed immediately after hydration (based on a review of variable-quality RCTs and prospective trials or case series).2 No studies supported the effectiveness of BRAT (bananas, rice cereal, applesauce, toast) diets over the infant’s usual diet.2,4 A meta-analysis of variable-quality RCTs demonstrated no significant difference in stool frequency between lactose-containing and lactose-free diets.9 Comparisons of undiluted lactose-milk with diluted milk or delayed reintroduction of milk revealed no significant differences in treatment failure or duration of diarrhea, although stool output increased slightly with the undiluted diet. However, undiluted milk was superior for restoring body weight.9
Multiple RCTs showed that Lactobacillus supplementation shortened the duration of diarrhea for infants and young children10,11 and reduced the risk of diarrhea persisting more than 3 days (relative risk [RR]=0.43; 95% CI, 0.34–0.53; P<.001; number needed to treat [NNT]=4).11 This probiotic can be reconstituted in oral rehydrating solution and administered 1 to 8 times daily, depending on the formulation.
Antidiarrheal agents are not recommended (based on limited reviews and consensus reports).2-4,12
TABLE
Evaluative strategies and therapeutic interventions for infant diarrhea
| Routine diarrhea* | Complicated diarrhea† | SOR | ||||
|---|---|---|---|---|---|---|
| Recommended | Not recommended | Recommended | Not recommended | |||
| Evaluation | Serology | X | X | B1, C2-3 | ||
| Stool culture | X | X | C2-3 | |||
| Intervention | WHO ORS (Osm 311 mmol/L) | X | X‡ | A8 | ||
| ORS (Osm 250 mmol/L) | X | X | A8 | |||
| Age-appropriate diet after hydration | X | X | C2 | |||
| Continued breast-feeding | X | X | B6,7 | |||
| BRAT diet | X | X | C2,4 | |||
| Lactose-free or dilute lactose diet | X | X | B9 | |||
| Lactobacillus (probiotic) | X | X | A10,11 | |||
| Antidiarrheal agents | X | X | C2,4,12 | |||
| * Mild to moderate dehydration, diarrhea of short duration without bloody stools, severe systemic illness, suspected food poisoning, or recent foreign travel. | ||||||
| † Severe dehydration, prolonged diarrhea, or diarrhea with bloody stools, severe systemic illness, suspected food poisoning, or recent foreign travel. | ||||||
| ‡ Recommended for treatment of cholera. | ||||||
| ORS, oral rehydration solution; SOR, strength of recommendation; BRAT, bananas, rice cereal, applesauce, and toast. | ||||||
Recommendations from others
The Centers for Disease Control and Prevention (CDC) recommends oral rehydrating solution for mild to moderate dehydration, and boluses of normal saline or Lactated Ringer’s (20 cc/kg) for severe dehydration. For frail or malnourished infants, boluses of 10 cc/kg should be given until hydrated.
The CDC also recommended against nutrition containing simple sugars (soft drinks, juice, gelatin desserts) due to high osmotic loads, but noted that diets containing some fats may have a beneficial effect on intestinal motility. They also recommended age-appropriate use of complex carbohydrates, meats, yogurt, fruits and vegetables. Zinc supplementation may also be beneficial (SOR: C).12
Exam should note fever, weight loss, abdominal tenderness, blood in the stool
Lettie Carter, MD
North Shore University Hospital at Glen Cove, Glen Cove, NY
The evaluation and management of an infant with diarrhea as always, begins with history. The length and severity of the illness, sick contacts, oral intake, travel, and characteristics of the stool are all important factors to consider. The physical exam should note presence of fever, weight loss, abdominal tenderness, and blood in the stool. Laboratory studies such as electrolytes, stool culture, and Wright stain are really only indicated if the child is severely dehydrated, unable to maintain hydration with oral intake and requires IV fluids, or if the episode is unusually protracted or the stool bloody.
A regular age-appropriate diet is essential, but parents should be counseled to avoid adding too much juice to the diet in an effort to rehydrate.
Routine infant diarrhea requires no lab work or cultures (strength of recommendation [SOR]: C); the degree of dehydration can be determined reliably by percent body weight change (SOR: B). However, bicarbonate may help rule out dehydration (SOR: B); electrolytes and blood urea nitrogen may be useful in evaluating complicated diarrhea with severe dehydration or when intravenous fluids are required; stool cultures are indicated for bloody or prolonged diarrhea, suspected food poisoning, or recent travel abroad (SOR: C).
Oral rehydrating solution is adequate fluid replacement for diarrhea associated with mild to moderate dehydration, followed by prompt refeeding with an age-appropriate diet (SOR: A); intravenous fluids are recommended for severe dehydration (SOR: C). Probiotics have been shown to safely reduce the duration and frequency of diarrhea (SOR: A).
Evidence summary
Evidence is summarized in the Table. Evaluation of an infant with diarrhea usually requires only a thorough history and physical exam. While no clinical trials have tested the impact of blood or stool testing on patient outcome, a recent systematic review suggested the only blood test reliable for ruling out dehydration is a serum bicarbonate greater than 15 to 17 mEq/L.1 Consensus reports have suggested laboratory studies are unnecessary unless dehydration is severe or IV fluids are required; stool cultures are necessary only for bloody or prolonged diarrhea, systemically ill infants, suspected food poisoning, or recent travel abroad.2,3
Effective management of infant diarrhea is based on the degree of dehydration, which can be estimated by percent body weight loss—the difference between the baseline and acute weights, divided by the baseline weight.3 If the baseline weight is not known, prolonged capillary refill time, abnormal skin turgor, and abnormal respiratory pattern are more reliable indicators of dehydration; other physical findings are less precise.1
Infants with diarrhea who are not dehydrated should continue age-appropriate nutrition.4 For infants with mild to moderate dehydration, however, rehydration using oral rehydrating solution is the initial therapy, followed by continued hydration to replace ongoing losses.2,3 A meta-analysis of randomized controlled trials (RCTs) in developed countries demonstrated equivalent efficacy of oral fluids compared with IV fluids, with an overall failure rate of only 3.6% for infants and children treated with oral rehydrating solution (95% confidence interval [CI], 1.4–5.8). There was no significant difference between oral rehydrating solution of varying sodium concentrations, and no increased risk of hypernatremia or hyponatremia compared with the IV treatment arm.5 Continued breastfeeding during the rehydrating phase significantly reduced dehydration (based on case control studies; odds ratio [OR]=5.23; 95% CI, 1.37–19.99; P=.016, limited by sample size).3,6 Breastfeeding also significantly reduced the number of diarrheal stools (found in a small-scale RCT).7 For obtunded or severely dehydrated infants, or those with an ileus or persistent vomiting, expert opinion suggested IV fluids.2,4
In a systematic review of RCTs comparing lower-concentration oral rehydrating solution with standard World Health Organization solution, lower-concentration solution showed superior efficacy. These resulted in fewer unscheduled infusions of IV fluids (OR=0.59; 95% CI, 0.45–0.79) and less stool output without increasing the incidence of hyponatremia.8
Unrestricted diets may reduce the duration of diarrhea compared with oral or IV fluids alone, and age-appropriate diets should be resumed immediately after hydration (based on a review of variable-quality RCTs and prospective trials or case series).2 No studies supported the effectiveness of BRAT (bananas, rice cereal, applesauce, toast) diets over the infant’s usual diet.2,4 A meta-analysis of variable-quality RCTs demonstrated no significant difference in stool frequency between lactose-containing and lactose-free diets.9 Comparisons of undiluted lactose-milk with diluted milk or delayed reintroduction of milk revealed no significant differences in treatment failure or duration of diarrhea, although stool output increased slightly with the undiluted diet. However, undiluted milk was superior for restoring body weight.9
Multiple RCTs showed that Lactobacillus supplementation shortened the duration of diarrhea for infants and young children10,11 and reduced the risk of diarrhea persisting more than 3 days (relative risk [RR]=0.43; 95% CI, 0.34–0.53; P<.001; number needed to treat [NNT]=4).11 This probiotic can be reconstituted in oral rehydrating solution and administered 1 to 8 times daily, depending on the formulation.
Antidiarrheal agents are not recommended (based on limited reviews and consensus reports).2-4,12
TABLE
Evaluative strategies and therapeutic interventions for infant diarrhea
| Routine diarrhea* | Complicated diarrhea† | SOR | ||||
|---|---|---|---|---|---|---|
| Recommended | Not recommended | Recommended | Not recommended | |||
| Evaluation | Serology | X | X | B1, C2-3 | ||
| Stool culture | X | X | C2-3 | |||
| Intervention | WHO ORS (Osm 311 mmol/L) | X | X‡ | A8 | ||
| ORS (Osm 250 mmol/L) | X | X | A8 | |||
| Age-appropriate diet after hydration | X | X | C2 | |||
| Continued breast-feeding | X | X | B6,7 | |||
| BRAT diet | X | X | C2,4 | |||
| Lactose-free or dilute lactose diet | X | X | B9 | |||
| Lactobacillus (probiotic) | X | X | A10,11 | |||
| Antidiarrheal agents | X | X | C2,4,12 | |||
| * Mild to moderate dehydration, diarrhea of short duration without bloody stools, severe systemic illness, suspected food poisoning, or recent foreign travel. | ||||||
| † Severe dehydration, prolonged diarrhea, or diarrhea with bloody stools, severe systemic illness, suspected food poisoning, or recent foreign travel. | ||||||
| ‡ Recommended for treatment of cholera. | ||||||
| ORS, oral rehydration solution; SOR, strength of recommendation; BRAT, bananas, rice cereal, applesauce, and toast. | ||||||
Recommendations from others
The Centers for Disease Control and Prevention (CDC) recommends oral rehydrating solution for mild to moderate dehydration, and boluses of normal saline or Lactated Ringer’s (20 cc/kg) for severe dehydration. For frail or malnourished infants, boluses of 10 cc/kg should be given until hydrated.
The CDC also recommended against nutrition containing simple sugars (soft drinks, juice, gelatin desserts) due to high osmotic loads, but noted that diets containing some fats may have a beneficial effect on intestinal motility. They also recommended age-appropriate use of complex carbohydrates, meats, yogurt, fruits and vegetables. Zinc supplementation may also be beneficial (SOR: C).12
Exam should note fever, weight loss, abdominal tenderness, blood in the stool
Lettie Carter, MD
North Shore University Hospital at Glen Cove, Glen Cove, NY
The evaluation and management of an infant with diarrhea as always, begins with history. The length and severity of the illness, sick contacts, oral intake, travel, and characteristics of the stool are all important factors to consider. The physical exam should note presence of fever, weight loss, abdominal tenderness, and blood in the stool. Laboratory studies such as electrolytes, stool culture, and Wright stain are really only indicated if the child is severely dehydrated, unable to maintain hydration with oral intake and requires IV fluids, or if the episode is unusually protracted or the stool bloody.
A regular age-appropriate diet is essential, but parents should be counseled to avoid adding too much juice to the diet in an effort to rehydrate.
1. Steiner MJ, DeWalt DA, Byerley JS. Is this child dehydrated? JAMA 2004;291:2746-2754.
2. Cincinnati Children’s Hospital Medical Center. Evidence based clinical practice guideline for children with acute gastroenteritis (AGE). Cincinnati, Ohio: Cincinnati Children’s Hospital Medical Center; 2001. Available at www.guideline.gov. Accessed on April 5, 2004.
3. Armon K, Stephenson T, MacFaul R, Eccleston P, Werneke U. An evidence and consensus based guideline for acute diarrhea management. Arch Dis Child 2001;85:132-142.
4. Practice parameter: the management of acute gastroenteritis in young children. American Academy of Pediatrics, Provisional Committee on Quality Improvement, Subcommittee on Acute Gastroenteritis. Pediatrics 1996;97:424-435.
5. Gavin N, Merrick N, Davidson B. Efficacy of glucose-based oral rehydration therapy. Pediatrics 1996;98:45-51.
6. Faruque AS, Mahalanabis D, Islam A, Hoque SS, Hasnat A. Breast feeding and oral rehydration at home during diarrhoea to prevent dehydration. Arch Dis Child 1992;67:1027-1029.
7. Khin MU, Nyunt NW, Myo K, Mu MK, Tin U, Thane T. Effect on clinical outcome of breast feeding during acute diarrhoea. Br Med J (Clin Res Ed) 1985;290:587-589.
8. Hahn S, Kim Y, Garner P. Reduced osmolarity oral rehydration for treating dehydration caused by acute diarrhoea in children (Cochrane Review). In: The Cochrane Library., Issue 4, 2004. Chichester, UK: John Wiley & Sons.
9. Brown KH, Peerson JM, Fontaine O. Use of nonhuman milks in the dietary management of young children with acute diarrhea: a meta-analysis of clinical trials. Pediatrics 1994;93:17-27.
10. Van Niel CW, Feudtner C, Garrison MM, Christakis D. Lactobacillus therapy for acute infectious diarrhea in children: a meta-analysis. Pediatrics 2002;109:678-684.
11. Szajewska H, Mrukowicz JZ. Probiotics in the treatment and prevention of acute infectious diarrhea in infants and children: a systematic review of published randomized, double-blind, placebo-controlled trials. J Pediatr Gastroenterol Nutr 2001;33(Suppl 2):S17-S25.
12. King CK, Glass R, Bresee JS, Duggan C. Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep 2003;52(RR-16):1-16.
1. Steiner MJ, DeWalt DA, Byerley JS. Is this child dehydrated? JAMA 2004;291:2746-2754.
2. Cincinnati Children’s Hospital Medical Center. Evidence based clinical practice guideline for children with acute gastroenteritis (AGE). Cincinnati, Ohio: Cincinnati Children’s Hospital Medical Center; 2001. Available at www.guideline.gov. Accessed on April 5, 2004.
3. Armon K, Stephenson T, MacFaul R, Eccleston P, Werneke U. An evidence and consensus based guideline for acute diarrhea management. Arch Dis Child 2001;85:132-142.
4. Practice parameter: the management of acute gastroenteritis in young children. American Academy of Pediatrics, Provisional Committee on Quality Improvement, Subcommittee on Acute Gastroenteritis. Pediatrics 1996;97:424-435.
5. Gavin N, Merrick N, Davidson B. Efficacy of glucose-based oral rehydration therapy. Pediatrics 1996;98:45-51.
6. Faruque AS, Mahalanabis D, Islam A, Hoque SS, Hasnat A. Breast feeding and oral rehydration at home during diarrhoea to prevent dehydration. Arch Dis Child 1992;67:1027-1029.
7. Khin MU, Nyunt NW, Myo K, Mu MK, Tin U, Thane T. Effect on clinical outcome of breast feeding during acute diarrhoea. Br Med J (Clin Res Ed) 1985;290:587-589.
8. Hahn S, Kim Y, Garner P. Reduced osmolarity oral rehydration for treating dehydration caused by acute diarrhoea in children (Cochrane Review). In: The Cochrane Library., Issue 4, 2004. Chichester, UK: John Wiley & Sons.
9. Brown KH, Peerson JM, Fontaine O. Use of nonhuman milks in the dietary management of young children with acute diarrhea: a meta-analysis of clinical trials. Pediatrics 1994;93:17-27.
10. Van Niel CW, Feudtner C, Garrison MM, Christakis D. Lactobacillus therapy for acute infectious diarrhea in children: a meta-analysis. Pediatrics 2002;109:678-684.
11. Szajewska H, Mrukowicz JZ. Probiotics in the treatment and prevention of acute infectious diarrhea in infants and children: a systematic review of published randomized, double-blind, placebo-controlled trials. J Pediatr Gastroenterol Nutr 2001;33(Suppl 2):S17-S25.
12. King CK, Glass R, Bresee JS, Duggan C. Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep 2003;52(RR-16):1-16.
Evidence-based answers from the Family Physicians Inquiries Network