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Electrolyte Abnormalities in The Hospitalized Patient
Electrolyte Abnormalities in The Hospitalized Patient
Electrolyte Abnormalities in The Hospitalized Patient
Cynthia Seitz MD
Potassium
Phosphorus
Sodium Homeostasis
Principal determinant of extracellular osmolality. The low intracellular sodium concentration, approximately 10 mEq/L, is maintained by Na+, K+-ATPase, which exchanges Na+ for K+
Sodium is necessary for the maintenance of intravascular volume. Sodium excretion occurs in stool and sweat, but the kidney regulates sodium balance and is the principal site of sodium excretion. Plasma VOLUME- not osmolality determines the excretion of sodium by the kidney
renin-angiotensin-aldosterone system In hyponatremia or hypernatremia, the underlying pathophysiology determines urinary Na+, not the serum sodium concentration
When extracellular sodium s plasma tonicity water efflux from cells cellular dehydration ( cell volume) (to maintain equal osmolality inside and outside the cell)
Sodium is unique among electrolytes because water balance, not sodium balance, usually determines its concentration.
Hyponatremia
The most common electrolyte abnormality in children: 1.5% of all pediatric hospitalizations Causes: Increased Free water Increased sodium loss Decreased salt intake Most common cause in children is extrarenal GI losses like diarrhea.
Diuretic Use Urinary tract obstruction and/or urinary tract infection Autosomal recessive polycystic kidney disease Tubulointerstitial nephritis Cerebral salt wasting Lack of aldosterone effect (serum K+, Na+) / Deficient aldosterone (CAH)
Gastrointestinal (emesis, diarrhea) Skin (CF, sweating, or burns) Third space losses (pancreatitis, burns, effusions, ascites)
Hypervolemic Hyponatremia
Hypoalbuminemia due to gastrointestinal disease/ Nephrotic syndrome/ Cirrhosis Congestive heart failure Renal failure Capillary leak due to sepsis
Hyponatremia- types
Euvolemic Hyponatremia
Usually ADH secreted due to vol osm. Can be released due to pain, nausea, vomiting, morphine
Glucocorticoid deficiency Hypothyroidism Water intoxication diluted formula, swimming, child abuse Water enemas
Pseudohyponatremia
Hyperglycemia Mannitol
Hyponatremia
Clinical Presentation
Degree of symptoms depend on Na+ level and rate of decrease Symptoms:
Anorexia Nausea, emesis Malaise, muscle cramps, and weakness. Lethargy, confusion, agitation, headache, seizures, coma, decreased reflexes, hypothermia Cheyne-Stokes respirations,
Hyponatremia- Diagnosis
History can tell you most of the story Laboratory studies: Urine Na and Osm compared to Serum Na and Osm Calculate Osmolar Gap: Difference between measured & calculated osm Gap is high with mannitol, glycerol, lactate, methanol, EtOH, ethylene glycol Calc Osm= 2( Serum Na + serum K+) + (BUN/2.8) + (glucose/18)
Cause of Hyponatremia by Urine Specimen Cause Urine Na Urine Osmolarity Volume Hypovolemic renal Na loss >20mEq/L Hypovolemic extrarenal loss Hypervolemic HypoNa- CHF,edema <20mEq/L Hypervolemic HypoNa- Renal Failure varies varies SIADH-like syndrome >20mEq/L
Hyponatremia- Treatment
Correction: in chronic hypo Na- correct by no more than 8-12mEq/L each day
In acute hypoNa: brain doesnt have time to adapt. So less risk of CPM
Active CNS symptoms often improve after receiving 46mL/kg of 3% sodium chloride.
Hyponatremia- Treatment
IVF replacement
NS: 154 mEq/ L of Na NS: 77 mEq/ L of Na NS: 38.5 mEq/ L of Na Maintenance needs: Sodium: 23mEq/kg/24hr Deficit Replacement:
Estimate Water = % dehydration X patient's weight Calculated Na deficit from serum
Ongoing Losses:
Diarrhea: Na content 55 mEq/L Gastric fluids: Na content 60mEq/L Sweat: 540 mEq/L of Na
Hyponatremia: Complications
Physiology review: Hyponatremia= decreased plasma osmolarity (except in extreme hyperglycemia)---Water flow from low solute (low osm) to high solute (high osm)--So water flow from extracellular space into intracellular space ---Cells SWELL! Brain adapts to the decreased extracellular osmolality by decreasing its internal osmolality. Initially, through loss of sodium, potassium, and chloride. Chronically there is loss of intracellular osmoles such as amino acids. Treatment complications: overly rapid correction
Fun Facts
67% of cases presenting with Human Ehrlichiosis have hyponatremia
of course, they also have fever (100%), thrombocytopenia (92%), and rash (67%)
Hypernatremia
Serum Na >145 mEq/L [deficit of (TBW) relative to Na] Primarily hospital-acquired in children who have restricted access to fluids. Incidence >1% in hospitalized patients. CAUSES: Water deficit Salt Excess Water depletion exceeding sodium depletion
Sodium is unique among electrolytes because water balance, not sodium balance, usually determines its concentration.
Renal
Central DI Nephrogenic DI
Insensible Losses
Excessive perspiration Fever/ Heat exhaustion/Heatstroke Respiratory Illness Prematurity-large surface area
Inadequate Intake
Hypernatremia-Causes
Water and Sodium Deficit Gastrointestinal losses
Cutaneous losses
Renal losses
Hypernatremia- Causes
Excessive Sodium Improperly mixed formula Excess sodium bicarbonate Ingestion of seawater or sodium chloride Intentional salt poisoning
(child abuse)
Within 1 hour, the brain intracellular Na and K, amino acids, & idiogenic osmoles Within 1 week, the brain regains 98% of its water content. In patients with prolonged hypernatremia, rapid rehydration with hypotonic fluids may cause cerebral edema, which can lead to coma, convulsions, and death.
Irritability or lethargy High-pitched cry or wail Altered sensorium Seizures Increased muscle tone Fever Rhabdomyolysis Oligouria
Categorizing hypernatremia
Hypernatremia: Work-up Serum sodium, glucose, osmolality, BUN, and creatinine levels must be
measured. Urine volume, urine osmolality and urine electrolyte levels
Assess renal concentrating ability Quantify the urinary free water losses
urine osm (<800 mmol/L) with serum hypernatremia = renal concentrating defect
Hypovolemic hypernatremia
Extrarenal losses show urine sodium levels of <20 mEq/L Renal losses urine sodium values are >20 mEq/L.
In euvolemic hypernatremia, urine sodium data vary. In hypervolemic hypernatremia, the urine sodium level is >20 mEq/L. In alert, severely hypernatremic patients: rule out a hypothalamic lesion
Imaging studies
Hypernatremia: Treatment
Correct fluid deficit first Rapid correction can cause cerebral edema. Dehydration should be corrected over 48-72 hours. The rate of sodium correction: 10-12 mEq/L in 24 hours. Calculation of body water deficit: In children, TBW is 60% of lean body weight. TBW = 0.6 X weight.
An exception is babies, with TBW around 80% of their body weight.
1. Water deficit (L) = [(current Na mEq/L 145 mEq/L) - 1] X 0.6 X Wt (kg) or 2. Water deficit(L)= 4ml x Wt(kg) x (desired change in Na mEq/L) Example calculation: A child weighs 10 kg with Na= 160 mEq/L.
With first equation, water deficit (L) = [(160 mEq/L 145 mEq/L) - 1] X 0.6 X 10 = 0.62 L. With second equation, water deficit (L)= 4ml x 10 kg x 15 mEq/L Na change = 600ml= 0.6 L
Hypernatremia: treatment
Cause A. Sodium and water loss B. Primary water loss C. Nephrogenic diabetes insipidus D. Central diabetes insipidus E. Sodium overload D5 NS D5 NS D2.5 1/8 NS (acute management) Desmopressin acetate D5W (may need Diuretics or dialysis) Treatment*
If acutely hypotensive, use NS or LR first to restore some volume. Avoid D5W if hyperglycemia is present
Treatment of Hypernatremic Dehydration RESTORE INTRAVASCULAR VOLUME Normal saline: 20 mL/kg over 20 min (Repeat until intravascular volume restored) DETERMINE TIME FOR CORRECTION BASED ON INITIAL SODIUM [Na]:145157 mEq/L:24 hr [Na]:158170 mEq/L:48 hr [Na]:171183 mEq/L:72 hr [Na]:184196 mEq/L:84 hr ADMINISTER FLUID AT CONSTANT RATE OVER TIME FOR CORRECTION Typical fluid: D5 normal saline (with 20 mEq/L KCl unless contraindicated) Typical rate: 1.251.5 times maintenance FOLLOW SERUM SODIUM CONCENTRATION EVERY 2-4 hrs ADJUST FLUID BASED ON CLINICAL STATUS AND SERUM SODIUM Signs of volume depletion: administer normal saline (20 mL/kg) Sodium decreases too rapidly Increase sodium concentration of IVF, or Decrease rate if IVF Sodium decreases too slowly Decrease sodium concentration of IVF, or Increase rate if IVF
Im not fat Im just really swollen from the salt in my chili cheese fries
Potassium Homeostasis
Most potassium is intracellular Distribution of between the intra- and extracellular compartments alters serum levels Na+, K+-ATPase maintains the high intracellular K+ concentration
Insulin activates the Na+, K+-ATPase- drives K+ into the cell Acidosis (high H+) drives potassium extracellularly; (H+ in for K+ out) Alkalosis drives K+ into the cell -Adrenergic agonists stimulate the Na+, K+-ATPase, cellular uptake of K+ -Adrenergic agonists and exercise cause a net movement of K+ out.
Electrical responsiveness of nerve and muscle cells Contractility of cardiac, skeletal, and smooth muscle.
In distal tubule and collecting duct- K+ absorbed and secreted Tubular secretion that regulates the amount of K+ in the urine Regulating hormone- aldosterone (in hyperkalemia) Acts on cortical collecting duct Moves sodium into cells Creates a negative charge in the lumen K+ excretion. intracellular Na+ stimulates the basolateral Na+, K+-ATPase
Moves K+ into cells lining the cortical collecting duct from blood side.
Glucocorticoids, ADH, high urine flow, and high Na+ delivery to the distal nephron also urine K+. Alkalosis - urine K+. Acidosis urine K+. Excretion is decreased by insulin, catecholamines, and urine ammonia
Hyperkalemia- Pathophysiology
One of the few things you can die from without any symptoms Causes Spurious Increased Intake Decreased Excretion Transcellular shifts
Hemolysis- during heelstick, or clenched fist Tissue ischemia- during blood drawing Thrombocytosis/ Leukocytosis- release of K+ during clot formation Storage of specimen in cold- causes K+ release from cells
Increased Intake
IV fluid administration/ TPN Excess oral dosing Blood transfusions Acidosis- less with organic acids and even less with respiratory causes Cell destruction :Rhabdomyolysis, tumor lysis, tissue necrosis, hemolysis Hematomas/gastrointestinal bleeding Medicines: Succinylcholine/ Digitalis/ Fluoride/ -Adrenergic blockers Exercise Hyperosmolality- water flows out of cells and K+ follows (Mannitol ,etc) Insulin deficiency Malignant hyperthermia - muscles release K+ Hyperkalemic periodic paralysis
Transcellular Shifts
Hyperkalemia- Causes
Decreased Excretion
Acquired Addison disease- metabolic acidosis, salt wasting and hyponatremia 21-hydroxylase deficiency 3-hydroxysteroid dehydrogenase deficiency Met acidosis/Na+ ok Urinary tract obstruction Sickle cell disease Kidney transplant Lupus nephritis Pseudohypoaldosteronism type I- Aldosterone- Met acidosis, Salt wasting (Na) Acquired tubular dysfxn (Sickle cell, lupus)- impaired H+ and K+ excretion Angiotensin-converting enzyme inhibitors/ Angiotensin II blockers Potassium-sparing diuretics Nonsteroidal anti-inflammatory drugs Trimethoprim Heparin
Medications
Hyperkalemia
CLINICAL MANIFESTATIONS. Effects on membrane polarization.
peaked T waves P-R interval flat P wave wide QRS Eventually progress to ventricular fibrillation and Asystole Paresthesias Weakness Tingling.
Hyperkalemia
DIAGNOSIS. Spurious hyperkalemia is very common in children, get repeat value!
If Hyponatremia and volume depletion due to salt wasting- think low aldosterone
If Hyperphosphatemia and hyperuricemia- think causes of cell death Tumor lysis syndrome Rhabdomyolysis- Elevated creatinine phosphokinase (CPK) level and Ca Hemolysis- Hemoglobinuria and a decreasing hematocrit
When no clear etiology - differentiating decreased potassium excretion from the other etiologies
Measuring urinary potassium to assess renal excretion of potassium. The transtubular potassium gradient (TTKG) = [K]urine/[K]plasma (plasma osm/urine osm)
urine osmolality > serum osmolality for the result to be valid.
Aldosterone level
Hyperkalemia- Treatment
K+ level, the ECG, and the risk determine the aggressiveness of therapy.
Stop all sources of additional potassium (oral, intravenous) If K+ level is believable at >6.0 mEq/L, get EKG
Stabilize the heart to prevent life-threatening arrhythmias Calcium-stabilizes the cell membrane of heart cells
Rapidly decrease serum K+ level (even if only temporary) Bicarbonate- K+ to move intracellularly, lowering the plasma K+ level Insulin- K+ to move intracellularly, give with glucose Albuterol neb- stimulates 1-receptorsrapid movement of K+ into cells
Hyperkalemia- Treatment
Remove potassium from the body. Loop diuretic increases renal excretion of K+- only if making urine. Kayexalate- exchange resin that is given either rectally or orally Dialysis for acute potassium removal
necessary if severe renal failure or high rate of endogenous K+ release Hemodialysis better than Peritoneal dialysis reducing dietary intake and eliminating or reducing medications that cause hyperkalemia. May need meds to remove K+
Chronic management
Hypokalemia
Hypokalemia in kids is common Usually associated with gastroenteritis Causes: Decreased intake Increased losses: extrarenal and renal Transcellular shifts *Lab error- spurious
Metabolic acidosis
Renal tubular acidosis (usu distal, rarely proximal) Ureterosigmoidostomy Diabetic ketoacidosis
Metabolic alkalosis
Emesis / nasogastric suctionGastric loss of K+ and HCLkidney secretes HCO3 Na + K lost too
Chloride-losing diarrhea AR D/O with unusual met alkalosis with diarrhea Cystic fibrosis chloride loss in sweat
urinary loss of K+ & Cl- with volume depletion and aldosterone Gitelman (urinary Ca with urinary Mg) Bartter syndrome (Urinary Ca) Loop and thiazide diuretics
17- or11-hydroxylase deficiency 11-hydroxysteroid dehydrogenase def. Cushing syndrome- mineralcorticoid activity of cortisol Licorice ingestion- inhibits 11-hydroxysteroid dehydrogenase Liddle syndrome
(AD mutation of Aldosterone responsive Na channel- upregulated) See low aldosterone levels
ECG changes
flattened T wave depressed ST segment appearance of a U wave Ventricular fibrillation and Torsades de pointes
(if K <2.5 mEq/L) Usually starts with the legs, followed by the arms. Respiratory paralysis may require mechanical ventilation. Rhabdomyolysis
Bladder dysfunction- urinary retention. Chronic hypokalemia may cause kidney damage
Diagnosis- Hypokalemia
Diarrhea and RTA: hypokalemia and non-AG metabolic acidosis Vomiting and NG losses- hypo K and met. Alkalosis Urinary potassium distinguishes between renal and extrarenal losses. Urinary potassium losses
LABS:
24-hr urine spot K+/Creat ratio fractional excretion of K+ Calculation: TTKG = [K]urine/[K]plasma (plasma osm/urine osm) The urine osmolality > serum osmolality for the result to be valid. A TTKG of >4 in the presence of hypokalemia suggests excessive urinary losses of potassium.
Treatment- Hypokalemia
Severe, symptomatic hypokalemia requires aggressive treatment
Because of the risk of hyperkalemia, use IV potassium cautiously 0.51 mEq/kg, usually given over 1 hr. The adult maximum dose is 40 mEq. Oral potassium is safer. Potassium chloride is the usual choice for supplementation. Potassium acetate or potassium citrate for patients with acidosis and hypokalemia Potassium phosphate if hypophosphatemia is present Potassium-sparing diuretics- for patients with excessive urinary losses
If hypokalemia, metabolic alkalosis, and volume depletion are present (with gastric losses): Restore volume with NS to help decrease urinary potassium losses. Disease-specific therapy is effective in many of the genetic tubular disorders.
Unfortunately.
Phosphorus Metabolism
Phosphate is critical for many cellular processes. Major component of the bone, nucleic acids, ATP, acid-base buffers, and enzymes < 1% of body phosphorus is in the plasma The serum concentration of phosphate may not reflect true phosphate stores. VARIES significantly with age!!!
1619 yr
2.74.7 mg/dL
Phosphorus Homeostasis
INTAKE Phosphorus is readily available in food. (Dairy products, meat, & fish). GI absorption is proportional to intake, with 65% of intake absorbed- mostly in the small intestine. Absorption of phosphate can be blocked by aluminum-, calcium-, and magnesiumcontaining antacids. Stool losses can be increased in severe diarrhea or intestinal malabsorption. Bone metabolism of phosphate is affected by bone formation and destruction EXCRETION Excretion matches intake, except for the needs for growth. The kidney regulates phosphorus balance 90% of plasma phosphate is filtered at the glomerulus. A sodium-phosphate cotransporter mediates uptake at the PCT PTH = renal resorption of phos Calcitriol (1,25 Vit D) intestinal absorption of phos and helps renal resorption of phos.
Hypophosphatemia
Causes
Decreased
Nutritional deficiency
Anorexia
Malnutrition
Impaired
Premature infants ( needs compared to term infants) Low phosphorus formula Antacids and other phosphate binders (prevent absorption)
Renal
Increased Excretion
Hyperparathyroidism Parathyroid hormonerelated peptide (malignancy) Tumor-induced osteomalacia Hypophosphatemic rickets Fanconi syndrome Dent disease (x-linked defective chloride channel) Mutations in sodium-phosphate cotransporter Volume expansion and intravenous fluids Metabolic acidosis (phosphorus shifts out of cells then excreted by kidney) Diuretics Others
Transcellular Shifts
Overall- increased intracellular use of phosphorus Glucose infusioninsulin release Insulin shift of glucose and phosphorus into cells Refeeding anabolic state leads to cellular demand for phos
Total parenteral nutrition (insufficient supplementation) Respiratory alkalosis intracellular pH stimulates intracellular
metabolism and increased phos use
Tumor growth (leukemia/lymphoma due to use by tumors) Bone marrow transplantation Hungry bone syndrome (use of phos/ca/mg) after
parathyroidectomy
Multifactorial
Vitamin D deficiency
impaired
Sepsis Dialysis
Clinical Manifestations
hemolysis, cardiac dysfunction and neurologic symptoms. muscle weakness and atrophy
Chronic hypophosphatemia
proximal
Rickets
Short
stature
Diagnostic Testing
The history and basic laboratory evaluation (serum calcium, magnesium, and potassium) often suggests the etiology
Hyperparathyroidism has plasma PTH and calcium levels. Low magnesium = poor nutrition. Arterial blood gas: if respiratory alkalosis is suspected Urinary phosphorus determination confirms the presence of renal phosphate wasting. Urinalysis (fanconi will show renal glycosuria, aminoaciduria, type II renal tubular acidosis, hypouricemia, and hypophosphatemia.)
Treatment
Sodium phosphate or potassium phosphate Choice based on K+ level Starting doses are 0.080.16 mmol/kg over 6 hr.
The oral preparations of phosphorus are available with various ratios of sodium and potassium. Oral maintenance doses are 23 mmol/kg/day in divided doses. (cause diarrhea) Increasing dietary phosphorus is the only intervention needed in infants with inadequate intake. Certain diseases require specific therapy.
Vitamin D supplementation, not phosphorus, is the principal therapy Combination of 1,25-dihydroxyvitamin D and oral phosphorus.
Hyperphosphatemia
Causes
Increased
Increased Intake
Fleet enemas have high phosphorus content Sodium phosphorus laxatives Dont use in small kids! Increased in ileus and hirschprungs disease
Phosphorus excretion is then decreased at kidney phos resorption at proximal convoluted tubule
Decreased Excretion
Acromegaly
Phosphorus resorption at Prox Conv Tubule due to GH thyroxine= Phos resorption at PCT Bone resorption- phos, Ca+
Hyperthyroidism
Increased Increased
Transcellular Shifts
contents
Rhabdomyolysis
Muscle
Acute hemolysis
Red blood cell breakdown phos, K+, indirect bilirubin,
LDH
Clinical Manifestations
Hypocalcemia
Tissue deposition of calcium-phosphorus salt Inhibition of 1,25-dihydroxyvitamin D production Decreased bone resorption.
Systemic calcification
Solubility of phosphorus and calcium in the plasma is exceeded. Inflamed conjunctiva- foreign body feeling, erythema, and injection. (BOBBY) Hypoxia from pulmonary calcification Renal failure from nephrocalcinosis.
Diagnostic Testing
Assess renal function: Bun and creatinine. Focus history on intake of phosphorus and the presence of chronic disease. If suspect rhabdomyolysis, tumor lysis, or hemolysis
Check
CPK
Treatment
Depends on its severity and etiology. Dietary phosphorus restriction- in mild hyperphosphatemia Intravenous fluids- enhance renal excretion if kidney function is intact. Oral phosphorus binder- in significant hyperphosphatemia
Prevents absorption of dietary phos Removes phos from the body by binding what is normally secreted and absorbed by GI tract Binders containing aluminum hydroxide or use calcium carbonate if also hypocalcemic.
Preservation of renal function-high urine flow permits continued excretion Dialysis directly removes phosphorus from the blood in ESRD
only an adjunct to dietary restriction and phosphorus binders dialysis is not efficient enough to keep up with normal dietary intake.
Practice Case
An 8-year-old girl is admitted to the intensive care unit for a severe asthma exacerbation. As part of her management, she is placed on continuous albuterol nebulization at 15 mg/h. Of the following, the MOST likely electrolyte abnormality to expect in this girl is A. hypercalcemia B. hypermagnesemia C. hypernatremia D. hypoglycemia E. hypokalemia
Answer
The most common adverse reactions to beta2-adrenergic agonists are tremor, tachycardia, and palpitations. Administration of therapeutic or multiple doses of a beta2-adrenergic also may cause transient decreases in PaO2, prolonged QTc interval, arrhythmias, and electrolyte abnormalities.
Continuous administration of a beta2-adrenergic agonist, as described in the vignette, can result in hyperglycemia due to glycogenolysis, hypomagnesemia, and hypokalemia. Hypokalemia results from stimulation of the Na+-K+ pump and may be characterized by a decrease in serum potassium concentrations by 0.4 to 0.9 mEq/L (0.4 to 0.9 mmol/L). Patients who have preexisting hypoglycemia or relative hypoglycemia due to diuretic therapy may be at higher risk for arrhythmias during continuous beta2-adrenergic agonist therapy. Hypoglycemia and hypocalcemia have been reported in isolated cases, but hypermagnesemia, hypercalcemia, hyponatremia, and hypernatremia have not been reported during single or continuous beta2-adrenergic agonist administration
Practice Case
A 15-year-old girl is admitted to your facility with severe anorexia nervosa and amenorrhea. She weighs 35 kg and is 160 cm tall. She has bradycardia and orthostatic hypotension. You plan to stabilize her medically and begin nasogastric tube feeding. Of the following, the electrolyte abnormality that is MOST likely to occur during the first week of her treatment is A. hypercalcemia B. hyperphosphatemia C. hypocalcemia D. hyponatremia E. hypophosphatemia
Answer
Preferred Response: E
The girl described in the critique is severely malnourished and about to undergo intensive nutritional rehabilitation with enteral feeding. Although this therapy is lifesaving, it also may result in refeeding syndrome. In this syndrome, malnourished patients given oral, enteral, or intravenous nutrition develop fluid retention and electrolyte abnormalities. The most common electrolyte abnormality reported is hypophosphatemia, which can occur in approximately 25% of patients who have anorexia nervosa during refeeding. Other electrolyte and micronutrient abnormalities, including hyponatremia, hypocalcemia, hypokalemia, hyperglycemia, and thiamine deficiency, also may occur, but are less prevalent than hypophosphatemia. Hypercalcemia and hyperphosphatemia generally do not occur. With careful monitoring of electrolytes and slow refeeding, signs and symptoms of refeeding syndrome can be avoided. However, the clinical manifestations include edema, muscle weakness, and cardiac arrhythmias. The precise mechanism by which phosphorus levels are lowered during refeeding has not yet been characterized fully. Malnourished patients are depleted in total body phosphorus, despite normal serum concentrations. The carbohydrate challenge during refeeding induces the release of insulin, which causes fluid and electrolyte shifts. In addition, malnourished patients being refed synthesize the phosphate-rich compounds creatine phosphokinase, 2,3 diphosphoglycerate, and adenosine triphosphate. Thus, total body stores of phosphorus may be depleted even further during energy synthesis. To minimize the risk of refeeding syndrome, supplemental feedings should be introduced gradually to malnourished patients (beginning at 25% of recommended calories and advancing to full calories over 5 to 7 days). In addition, serum electrolytes, blood glucose, calcium, phosphorus, and magnesium should be measured at least daily for the first week of feeding. Many centers automatically prescribe a phosphorus supplement (500 mg twice a day) to patients who have anorexia nervosa and are being refed.
Practice Case
You are supervising a pediatric resident in her continuity clinic. She is evaluating a 4-weekold male infant who has had projectile vomiting after feeding for the past week. After reviewing the patient's electrolyte levels, she obtains an electrocardiogram (ECG) and asks you to help interpret it. The ECG reveals a T wave abnormality. Of the following, the MOST likely electrolyte abnormality suggested by the electrocardiographic findings is A. hypercalcemia B. hyperkalemia C. hypernatremia D. hypocalcemia E. hypokalemia
Answer
Hypokalemia generally is defined as a serum potassium concentration of less than 3.5 mEq/L (3.5 mmol/L) in infants and children. Potassium is an intracellular cation that is vital in maintaining the normal transmembrane charge in cells. Hypokalemia may be precipitated by gastrointestinal loss from vomiting or diarrhea, especially when there is inadequate oral intake. Other primary causes include aldosterone excess or renal tubular disorders. Abnormalities of potassium homeostasis can affect cardiac conduction and often are observed with defined changes in surface electrocardiography. The typical electrocardiographic findings seen in a child who has hypokalemia include ST segment depression, flattening of the T waves, and the appearance of a U wave as seen for the infant in the vignette. Generally, there are broadened T and U waves, and rarely the QT interval can be prolonged, which places the patient at greater risk for the development of ventricular dysrhythmias. However, arrhythmias with hypokalemia are unusual unless the patient is receiving digoxin, whose arrhythmogenic effects are potentiated by hypokalemia. Hyperkalemia most commonly is due to renal failure, adrenal insufficiency, or an iatrogenic overdose. As levels exceed 5.5 mEq/L (5.5 mmol/L), the T waves on the electrocardiogram may become tall and peaked. Prolonged conduction delay also may develop as potassium concentrations increase. Hypercalcemia may be due to a variety of causes and typically shortens the QT interval by shortening the ST segment. Hypercalcemia also may affect the sinus node, causing sinus slowing or sinus arrest. Hypocalcemia, in contrast, prolongs the ST segment, thereby prolonging the QT interval. Hypernatremia is not associated with electrocardiographic abnormalities.
Practice Case
A 12-month-old boy comes to the emergency department with a 3-day history of intractable vomiting and watery diarrhea. His mother reports decreased urine output for the past 24 hours. His heart rate is 180 beats/min, and his blood pressure is 85/40 mm Hg. He is lethargic but responds to stimulation. His mucous membranes are very dry, his skin turgor is decreased, and his capillary refill is 3 seconds. The remainder of his physical examination findings are unremarkable. Of the following, the laboratory data that are MOST consistent with this patient's clinical presentation are: A. Serum Sodium: High; Serum Osmolality: High; Urine Sodium: Low; Urine Osmolality: Low B. Serum Sodium: Low; Serum Osmolality: Low; Urine Sodium: Low; Urine Osmolality: High C. Serum Sodium: Low; Serum Osmolality: Low; Urine Sodium: High; Urine Osmolality: High D. Serum Sodium: Low; Serum Osmolality: Normal; Urine Sodium: High; Urine Osmolality: High E. Serum Sodium: Normal; Serum Osmolality: Normal; Urine Sodium: Low; Urine Osmolality: Low
Answer
Diarrhea due to acute gastroenteritis usually causes a proportional water and sodium loss, resulting in isonatremic dehydration. Hyponatremic dehydration also may be seen in acute gastroenteritis, especially if the only fluids tolerated are low-sodium fluids, such as water or juice. The clinical signs of both hyponatremic and isonatremic dehydration are due to decreased extracellular fluid, primarily from the intravascular compartment. The signs include decreased skin turgor, delayed capillary refill, decreased tear production and urine output, sunken eyes and anterior fontanelle, and tachycardia. Hypotension is a late finding, indicating decompensated shock. Because the child described in the vignette displays these clinical signs, isonatremia or hyponatremia is likely. With hypernatremic dehydration, intravascular volume is relatively preserved, despite an overall body water loss, so the degree of dehydration may be underestimated. Hyponatremia resulting from gastroenteritis is associated with a low serum osmolality. In contrast, factitious hyponatremia may occur with high osmolar states such as hyperglycemia or hyperlipidemia. In a healthy child who has gastroenteritis, renal sodium-preserving and concentrating mechanisms remain intact, resulting in low urinary sodium concentrations and high urine osmolality, respectively. The findings of hyponatremia with normal-to-high urine sodium and urine osmolality values should alert the clinician to the possibility of the syndrome of inappropriate antidiuretic hormone secretion, which is not likely in the child in the vignette.
Practice Case
An afebrile 5-year-old boy has had a generalized seizure. Findings on his physical examination are normal. Laboratory evaluation reveals a low serum calcium level of 5.5 mg/dL (5.5 mmol/L), an elevated serum phosphorus level of 7.5 mg/dL (7.5 mmol/L), and a normal serum albumin level of 4.0 g/dL (40 g/L).
Of the following, the test that is MOST helpful in establishing the cause of the hypocalcemia is measurement of serum levels of A. alkaline phosphatase B. amylase C. magnesium D. parathyroid hormone E. vitamin D