Pediatrics_Nelson

Pediatrics_Nelson. In situations with combined sodium and water deficits, analysis of the urine differentiates renal and nonrenal etiologies. When the losses are extrarenal, the kidney responds to volume depletion with low urine volume, a concentrated urine, and sodium retention (urine sodium <10 mEq/L). With renal causes, the urine volume is usually high, the urine is not maximally concentrated, and the urine sodium may be inappropriately elevated. Ingestion of seawater Inadequate intake Ineffective breastfeeding Child neglect or abuse Adipsia (lack of thirst) (Urine not maximally concentrated) Osmotic diuretics (mannitol) Diabetes mellitus Chronic kidney disease Polyuric phase of acute Figure 35-2 Differential diagnosis of hypernatremia by mechanism. GI, Gastrointestinal; NG, nasogastric.


Pediatrics_Nelson

Pediatrics_Nelson. Figure 35-2 Differential diagnosis of hypernatremia by mechanism. GI, Gastrointestinal; NG, nasogastric. Most children with hypernatremia are dehydrated and have the typical signs and symptoms of dehydration (see Chapter 33). Children with hypernatremic dehydration tend to have better preservation of intravascular volume owing to the shiftof water from the intracellular space to the extracellular space. Hypernatremic infants potentially become more dehydrated before seeking medical attention. Probably because of intracellular water loss, the pinched abdominal skin of a dehydrated, hypernatremic infant has a doughy feel.


Pediatrics_Nelson

Pediatrics_Nelson. Hypernatremia, even without dehydration, causes central nervous system symptoms that tend to parallel the degree of sodium elevation and the acuity of the increase. Patients are irritable, restless, weak, and lethargic. Some infants have a high-pitched cry and hyperpnea. Alert patients are very thirsty, although nausea may be present. Hypernatremia causes fever, although many patients have an underlying process that contributes to the fever. Brain hemorrhage is the most devastating consequence of hypernatremia. As the extracellular osmolality increases, water moves out of brain cells, resulting in a decrease in brain volume. This decrease in volume can result in tearing of intra-cerebral veins and bridging blood vessels as the brain moves away from the skull and the meninges. Patients may have sub-arachnoid, subdural, and parenchymal hemorrhage. Seizures and coma are possible sequelae of the hemorrhage.


Pediatrics_Nelson

Pediatrics_Nelson. As hypernatremia develops, the brain generates idiogenic osmoles to increase the intracellular osmolality and prevent the loss of brain water. This mechanism is not instantaneous and is most prominent when hypernatremia has developed gradually. If the serum sodium concentration is lowered rapidly, there is movement of water from the serum into the brain cells to equalize the osmolality in the two compartments. The resultant brain swelling manifests as seizures or coma. Because of these dangers, corrected hypernatremia should be treated gradually. The goal is to decrease the serum sodium by less than 12 mEq/L every 24 hours (see Fig. 33-1). The most important component of correcting moderate or severe hypernatremia is frequent monitoring of the serum sodium to allow adjustment of fluid therapy and provide adequate correction that is neither too slow nor too fast.


Pediatrics_Nelson

Pediatrics_Nelson. In a child with hypernatremic dehydration, as in any childwith dehydration, the first priority is restoration of intra-vascular volume with isotonic fluid. Figure 33-1 outlines a general approach for correcting hypernatremic dehydrationsecondary to gastroenteritis. If the hypernatremia and dehydration are secondary to water loss, as occurs with diabetes insipidus, a more hypotonic IV fluid is appropriate. A child with central diabetes insipidus should receive an ADH analog to prevent further excessive water loss. A child withnephrogenic diabetes insipidus requires a urine replacementsolution to offset ongoing water losses. Chronically, reducedsodium intake, thiazide diuretics, and nonsteroidal anti-inflammatory drugs can decrease water losses in nephrogenic diabetes insipidus.


Pediatrics_Nelson

Pediatrics_Nelson. Acute, severe hypernatremia, usually secondary to sodium administration, can be corrected more rapidly because idiogenic osmoles have not had time to accumulate; this balances the high morbidity and mortality from severe, acute hypernatremia with the dangers of overly rapid correction. When hypernatremia is due to sodium intoxication, and the hypernatremia is severe, it may be impossible to administer enough water to correct the hypernatremia rapidly without worsening volume overload. Some patients require use of a loop diuretic or dialysis.


Pediatrics_Nelson

Pediatrics_Nelson. The kidneys are the principal regulator of potassium balance, adjusting excretion based on intake. Factors affecting renal potassium excretion include aldosterone, acid-base status, serum potassium concentration, and renal function. The intracellular potassium concentration is approximately 30 times the extracellular potassium concentration. A variety of conditions alter the distribution of potassium between the intracellular and extracellular compartments, potentially causing either hypokalemia or hyperkalemia. The plasma concentration does not always reflect the total body potassium content. Available @ StudentConsult.com


Pediatrics_Nelson

Pediatrics_Nelson. Available @ StudentConsult.com Hypokalemia is common in children, with most cases related to gastroenteritis. Spurious hypokalemia occurs in patients with leukemia and elevated white blood cell counts if plasma for analysis is left at room temperature, permitting the white blood cells to take up potassium from the plasma. There are four basic mechanisms of hypokalemia (Table 36-1). Low intake, nonrenal losses, and renal losses all are associated with total body potassium depletion. With a transcellular shift, total body potassium is normal unless there is concomitant potassium depletion secondary to other factors.


Pediatrics_Nelson

Pediatrics_Nelson. The transcellular shift of potassium after initiation of insulin therapy in children with diabetic ketoacidosis (see Chapter 171) can be dramatic. These patients have reduced total bodypotassium because of urinary losses, but they often have a normal serum potassium level before insulin therapy from a trans-cellular shift into the extracellular space secondary to insulin deficiency and metabolic acidosis. Children receiving aggressive doses of β-adrenergic agonists (albuterol) for asthma can have hypokalemia resulting from the intracellular movement of potassium. Poor intake is an unusual cause of hypokalemia, unless also associated with significant weight loss (anorexia nervosa).


Pediatrics_Nelson

Pediatrics_Nelson. Diarrhea has a high concentration of potassium, and the resulting hypokalemia usually is associated with a metabolic acidosis secondary to stool losses of bicarbonate. With emesis or nasogastric suction, there is gastric loss of potassium, but this is fairly minimal given the low potassium content of gastric fluid (approximately 10 mEq/L). More important is the gastric loss of hydrochloride, leading to a metabolic alkalosis and a state of volume depletion. Metabolic alkalosis and volume depletion increase urinary losses of potassium.


Pediatrics_Nelson

Pediatrics_Nelson. Urinary potassium wasting may be accompanied by a metabolic acidosis (proximal or distal renal tubular acidosis) (see Chapter 37). Loop and thiazide diuretics lead to hypokalemia and a metabolic alkalosis. Bartter syndrome and Gitelman syndrome are autosomal recessive disorders resulting from defects in tubular transporters. Both disorders are associated with hypokalemia and a metabolic alkalosis. Bartter syndrome is usually associated with hypercalciuria, often with nephrocalcinosis; children with Gitelman syndrome have low urinary calcium losses, but hypomagnesemia secondary to urinary losses.


Pediatrics_Nelson

Pediatrics_Nelson. In the presence of a high aldosterone level, there is urinary loss of potassium, hypokalemia, and a metabolic alkalosis. There also is renal retention of sodium, leading to hypertension. A variety of genetic and acquired disorders can cause high aldosterone levels. Liddle syndrome, an autosomal dominant disorder caused by constitutively active sodium channels, has the same clinical features as hyperaldosteronism, but the serum aldosterone level is low. The heart and skeletal muscle are especially vulnerable to hypokalemia. Electrocardiographic (ECG) changes include a flattened T wave, a depressed ST segment, and the appearance of a U wave, which is located between the T wave (if still visible) and P wave. Ventricular fibrillation and torsades de pointes may occur, although usually only in the context of underlying heart disease. Hypokalemia makes the heart especially susceptible to digitalis-induced arrhythmias.


Pediatrics_Nelson

Pediatrics_Nelson. The clinical consequences in skeletal muscle include muscle weakness and cramps. Paralysis is a possible complication (generally only at potassium levels <2.5 mEq/L). Paralysis usually starts with the legs, followed by the arms. Respiratory paralysis may require mechanical ventilation. Some hypokalemic patients develop rhabdomyolysis, especially following exercise. Hypokalemia slows gastrointestinal motility; potassium levels less than 2.5 mEq/L may cause an ileus. Hypokalemia impairs bladder function, potentially leading to urinary retention. Hypokalemia causes polyuria by producing secondary nephrogenic diabetes insipidus. Chronic hypokalemia may cause kidney damage, including interstitial nephritis and renal cysts. In children, chronic hypokalemia, as in Bartter syndrome, leads to poor growth.


Pediatrics_Nelson

Pediatrics_Nelson. It is important to review the child’s diet, history of gastrointestinal losses, and medications. Emesis and diuretic use can be surreptitious. The presence of hypertension suggestsexcess mineralocorticoids. Concomitant electrolyte abnormalities are useful clues. The combination of hypokalemiaand metabolic acidosis is characteristic of diarrhea, distal renal tubular acidosis, and proximal renal tubular acidosis.A concurrent metabolic alkalosis is characteristic of gastriclosses, aldosterone excess, diuretics, Bartter syndrome, orGitelman syndrome. Factors that influence the therapy of hypokalemia include the potassium level, clinical symptoms, renal function, presence of transcellular shifts of potassium, ongoing losses, and the patient’s ability to tolerate oral potassium. Severe, symptomatic hypokalemia requires aggressive treatment. Supplementation Causes of Hypokalemia


Pediatrics_Nelson

Pediatrics_Nelson. Causes of Hypokalemia Transcellular shifts Alkalemia Insulin β-Adrenergic agonists Drugs/toxins (theophylline, barium, toluene) Hypokalemic periodic paralysis Refeeding syndrome Without specific acid-base disturbance Tubular toxins (amphotericin, cisplatin, aminoglycosides) Interstitial nephritis Diuretic phase of acute tubular necrosis Postobstructive diuresis Hypomagnesemia High urine anions (e.g., penicillin or penicillin derivatives) With metabolic alkalosis RTA, renal tubular acidosis.


Pediatrics_Nelson

Pediatrics_Nelson. RTA, renal tubular acidosis. is more cautious if renal function is decreased because of the kidney’s limited ability to excrete excessive potassium. The plasma potassium level does not always provide an accurate estimation of the total body potassium deficit because there may be shifts of potassium from the intracellular space to the plasma. Clinically, this shift occurs most commonly with metabolic acidosis and as a result of the insulin deficiency of diabetic ketoacidosis; the plasma potassium underestimates the degree of total body potassium depletion. When these problems are corrected, potassium moves into the intracellular space, and these patients require more potassium supplementation to correct the hypokalemia. Patients who have ongoing losses of potassium need correction of the deficit and replacement of the ongoing losses.


Pediatrics_Nelson

Pediatrics_Nelson. Because of the risk of hyperkalemia, intravenous (IV) potassium should be used cautiously. Oral potassium is safer in nonurgent situations. The dose of IV potassium is 0.5 to 1 mEq/kg, usually given over 1 hour. The adult maximum dose is 40 mEq. Conservative dosing is generally preferred. For patients with excessive urinary losses, potassium-sparing diuretics are effective. When hypokalemia, metabolic alkalosis, and volume depletion are present, restoration of intravascular volume decreases urinary potassium losses. Available @ StudentConsult.com


Pediatrics_Nelson

Pediatrics_Nelson. Available @ StudentConsult.com Three basic mechanisms cause hyperkalemia (Table 36-2). Inthe individual patient, the etiology is sometimes multifactorial.Factitious hyperkalemia is usually due to hemolysis during phlebotomy, but it can be the result of prolonged tourniquetapplication or fist clenching, which causes local potassiumrelease from muscle. Falsely elevated serum potassium levels can occur when serum levels are measured in patients withmarkedly elevated white blood cell or platelet counts; a promptlyanalyzed plasma sample usually provides an accurate result. Because of the kidney’s ability to excrete potassium, it is unusual for excessive intake, by itself, to cause hyperkalemia. This mechanism can occur in a patient who is receiving large quantities of IV or oral potassium for excessive losses that are no longer present. Frequent or rapid blood transfusions can increase the potassium level acutely secondary to the high Causes of Hyperkalemia


Pediatrics_Nelson

Pediatrics_Nelson. Causes of Hyperkalemia ACE, Angiotensin-converting enzyme; IV, intravenous; NSAIDs, nonsteroidal anti-inflammatory drugs; PO, oral. potassium content of stored blood. Increased intake may precipitate hyperkalemia if there is an underlying defect in potassium excretion. The intracellular space has a high potassium concentration, so a shift of potassium from the intracellular space to the extracellular space can have a significant impact on the plasma potassium. This shift occurs with acidosis, cell destruction (rhabdomyolysis or tumor lysis syndrome), insulin deficiency, medications (succinylcholine, β-blockers), malignant hyperthermia, and hyperkalemic periodic paralysis.


Pediatrics_Nelson

Pediatrics_Nelson. Hyperkalemia secondary to decreased excretion occurs with renal insufficiency. Aldosterone deficiency or unresponsiveness to aldosterone causes hyperkalemia, often with associated metabolic acidosis (see Chapter 37) and hyponatremia. A form of congenital adrenal hyperplasia, 21-hydroxylase deficiency, is the most frequent cause of aldosterone deficiency in children. Male infants typically present with hyperkalemia, metabolic acidosis, hyponatremia, and volume depletion. Female infants with this disorder usually are diagnosed as newborns because of ambiguous genitalia.


Pediatrics_Nelson

Pediatrics_Nelson. Renin, via angiotensin II, stimulates aldosterone production. A deficiency in renin, resulting from kidney damage, can lead to decreased aldosterone production. These patients typically have hyperkalemia and a metabolic acidosis, without hyponatremia. Some patients have impaired renal function, partially accounting for the hyperkalemia, but the impairment in potassium excretion is more extreme than expected for the degree of renal insufficiency.


Pediatrics_Nelson

Pediatrics_Nelson. Children with pseudohypoaldosteronism type 1 have hyperkalemia, metabolic acidosis, and salt wasting, leading to hyponatremia and volume depletion; aldosterone levels are elevated. In the autosomal recessive variant, there is a defect in the renal sodium channel that is normally activated by aldosterone. In the autosomal dominant form, patients have a defect in the aldosterone receptor, and the disease is milder, often remitting in adulthood. Pseudohypoaldosteronism type 2, also called Gordon syndrome, is an autosomal dominant disorder characterized by hypertension secondary to salt retention and impaired excretion of potassium and acid leading to hyperkalemia and metabolic acidosis. The risk of hyperkalemia secondary to medications that decrease renal potassium excretion is greatest in patients with underlying renal insufficiency.


Pediatrics_Nelson

Pediatrics_Nelson. The most import effects of hyperkalemia are due to the role of potassium in membrane polarization. The cardiac conduction system is usually the dominant concern. ECG changes begin with peaking of the T waves. As the potassium level increases, an increased P-R interval, flattening of the P wave, and widening of the QRS complex occur; this eventually can progress to ventricular fibrillation. Asystole also may occur. Some patients have paresthesias, weakness, and tingling, but cardiac toxicity usually precedes these clinical symptoms.


Pediatrics_Nelson

Pediatrics_Nelson. The etiology of hyperkalemia is often readily apparent. Spurious hyperkalemia is common in children, so a repeat potassium level is often appropriate. If there is a significant elevation of the white blood cells or platelets, the repeat sample should be from plasma that is evaluated promptly. The history initially should focus on potassium intake, risk factors for transcellular shifts of potassium, medications that cause hyperkalemia, and the presence of signs of renal insufficiency, such as oliguria or an abnormal urinalysis. Initial laboratory evaluation should include serum creatinine and assessment of acid-base status. Many causes of hyperkalemia, such as renal insufficiency and aldosterone insufficiency or resistance, cause a metabolic acidosis. Cell destruction, as seen in rhabdomyolysis or tumor lysis syndrome, can cause concomitant hyperphosphatemia, hyperuricemia, and an elevated serum lactate dehydrogenase.


Pediatrics_Nelson

Pediatrics_Nelson. The plasma potassium level, the ECG, and the risk of the problem worsening determine the aggressiveness of the therapeutic approach. A high serum potassium level with ECG changes requires more vigorous treatment. An additional source of concern is a patient with increasing plasma potassium despite minimal intake. This situation can occur if there is cellular release of potassium (tumor lysis syndrome), especially in the setting of diminished excretion (renal failure). The first action in a child with a concerning elevation of plasma potassium is to stop all sources of additional potassium (oral and IV). If the potassium level is greater than 6.5 mEq/L, an ECG should be obtained to help assess the urgency of the situation. Therapy of hyperkalemia has two basic goals: 1. Prevent life-threatening arrhythmias. 2. Remove potassium from the body (Table 36-3). Rapidly decrease the risk of life-threatening arrhythmias


Pediatrics_Nelson

Pediatrics_Nelson. Prevent life-threatening arrhythmias. 2. Remove potassium from the body (Table 36-3). Rapidly decrease the risk of life-threatening arrhythmias Remove potassium from the body Loop diuretic (IV or PO) Sodium polystyrene (PO or rectal) Dialysis IV, Intravenous; PO, oral. Treatments that acutely prevent arrhythmias all work quickly (within minutes), but do not remove potassium from the body. Long-term management of hyperkalemia includes reducing intake via dietary changes and eliminating or reducing medications that cause hyperkalemia. Some patients require medications, such as sodium polystyrene sulfonate and loop or thiazide diuretics, to increase potassium losses. The disorders due to a deficiency in aldosterone respond to replacement therapy with fludrocortisone, a mineralocorticoid.


Pediatrics_Nelson

Pediatrics_Nelson. Close regulation of pH is necessary for cellular enzymes and other metabolic processes, which function optimally at a normal pH (7.35 to 7.45). Chronic, mild derangements in acid-base status may interfere with normal growth and development, whereas acute, severe changes in pH can be fatal. Control of acid-base balance depends on the kidneys, the lungs, and intracellular and extracellular buffers. The lungs and the kidneys maintain a normal acid-base balance. Carbon dioxide (CO2) generated during normal metabolism is a weak acid. The lungs prevent an increase in the partial pressure of CO2 (Pco2) in the blood by excreting the CO2. Production of CO2 varies depending on the body’s metabolic needs. The rapid pulmonary response to changes in CO2 concentration occurs via central sensing of the Pco2 and a subsequent increase or decrease in ventilation to maintain a normal Pco2 (35 to 45 mm Hg).


Pediatrics_Nelson

Pediatrics_Nelson. The kidneys excrete endogenous acids. An adult normally produces about 1 to 2 mEq/kg/day of hydrogen ions, whereas a child produces 2 to 3 mEq/kg/day. The hydrogen ions from endogenous acid production are neutralized by bicarbonate, potentially causing the bicarbonate concentration to fall. The kidneys regenerate this bicarbonate by secreting hydrogen ions, maintaining the serum bicarbonate concentration in the normal range (20 to 28 mEq/L). Available @ StudentConsult.com


Pediatrics_Nelson

Pediatrics_Nelson. Available @ StudentConsult.com Acidemia is a pH below normal (<7.35), and alkalemia is a pH above normal (>7.45). Acidosis is a pathologic process thatcauses an increase in the hydrogen ion concentration, and alkalosis is a pathologic process that causes a decrease in the hydrogen ion concentration. A simple acid-base disorder is a singleprimary disturbance. During a simple metabolic disorder, there is respiratory compensation; the Pco2 decreases during a metabolic acidosis and increases during a metabolic alkalosis. Withmetabolic acidosis, the decrease in the pH increases the ventilatory drive, causing a decrease in the Pco2. The fall in the CO2 concentration leads to an increase in the pH. This appropriate respiratory compensation for a metabolic process happensquickly and is complete within 12 to 24 hours.


Pediatrics_Nelson

Pediatrics_Nelson. During a primary respiratory process, there is metaboliccompensation mediated by the kidneys. The kidneys respondto a respiratory acidosis by increasing hydrogen ion excretion, increasing bicarbonate generation, and raising the serumbicarbonate concentration. The kidneys increase bicarbonateexcretion to compensate for a respiratory alkalosis; the serum bicarbonate concentration decreases. In contrast to a rapidrespiratory compensation, it takes 3 to 4 days for the kidneysto complete appropriate metabolic compensation. However, there is a small and rapid compensatory change in the bicarbonate concentration during a primary respiratory process. Theexpected appropriate metabolic compensation for a respiratorydisorder depends on whether the process is acute or chronic.


Pediatrics_Nelson

Pediatrics_Nelson. A mixed acid-base disorder is present when there is morethan one primary acid-base disturbance. An infant with bronchopulmonary dysplasia may have a respiratory acidosis fromchronic lung disease and a metabolic alkalosis from a diureticused to treat the chronic lung disease. Formulas are available for calculating the appropriate metabolic or respiratory compensation for the six primary simple acid-base disorders (Table 37-1). Appropriate compensation is expected in a simple disorder; it is not optional. If a patient does not have appropriatecompensation, a mixed acid-base disorder is present. Available @ StudentConsult.com Metabolic acidosis occurs frequently in hospitalized children; diarrhea is the most common cause. For a patient with


Pediatrics_Nelson

Pediatrics_Nelson. Available @ StudentConsult.com Metabolic acidosis occurs frequently in hospitalized children; diarrhea is the most common cause. For a patient with Metabolic acidosis PCO2 = 1.5 × [HCO3–] + 8 ± 2 Metabolic alkalosis PCO2 increases by 7 mm Hg for each 10-mEq/L increase in the serum [HCO3–] Respiratory acidosis Acute [HCO3–] increases by 1 for each 10-mm Hg increase in the PCO2 Chronic [HCO3–] increases by 3.5 for each 10-mm Hg increase in the PCO2 Respiratory alkalosis Acute [HCO3–] falls by 2 for each 10-mm Hg decrease in the PCO2 Chronic [HCO3–] falls by 4 for each 10-mm Hg decrease in the PCO2 an unknown medical problem, the presence of a metabolic acidosis is often helpful diagnostically because it suggests a relatively narrow differential diagnosis (Table 37-2).


Pediatrics_Nelson

Pediatrics_Nelson. Diarrhea causes a loss of bicarbonate from the body. The amount of bicarbonate lost in the stool depends on the volume of diarrhea and the bicarbonate concentration of the stool, which tends to increase with more severe diarrhea. Diarrhea often causes volume depletion because of losses of sodium and water, potentially exacerbating the acidosis by causing hypoperfusion (shock) and a lactic acidosis. There are three forms of renal tubular acidosis (RTA):


Pediatrics_Nelson

Pediatrics_Nelson. In distal RTA, children may have accompanying hypokalemia, hypercalciuria, nephrolithiasis, and nephrocalcinosis; rickets is a less common finding. Failure to thrive, resulting from chronic metabolic acidosis, is the most common presenting complaint. Autosomal dominant and autosomal recessive forms of distal RTA exist. The autosomal dominant form is relatively mild. Autosomal recessive distal RTA is more severe and often associated with deafness secondary to a defect in the gene for a H+-ATPase that is present in the kidney and the inner ear. Distal RTA also may be secondary to medications or congenital or acquired renal disease. Patients with distal RTA cannot acidify their urine and have a urine pH greater than 5.5, despite a metabolic acidosis.


Pediatrics_Nelson

Pediatrics_Nelson. Proximal RTA is rarely present in isolation. In most patients,proximal RTA is part of Fanconi syndrome, a generalized dysfunction of the proximal tubule. Along with renal wasting of bicarbonate, Fanconi syndrome causes glycosuria, aminoaciduria, and excessive urinary losses of phosphate and uric acid.The chronic hypophosphatemia is more clinically significantbecause it ultimately leads to rickets in children. Rickets orfailure to thrive may be the presenting complaint. Fanconisyndrome is rarely an isolated genetic disorder, with pediatriccases usually secondary to an underlying genetic disorder, mostcommonly cystinosis. Medications, such as ifosfamide or valproate, may cause Fanconi syndrome. The ability to acidify theurine is intact in proximal RTA, and untreated patients have aurine pH less than 5.5. However, bicarbonate therapy increasesbicarbonate losses in the urine, and the urine pH increases.


Pediatrics_Nelson

Pediatrics_Nelson. In hyperkalemic RTA, renal excretion of acid and potassium is impaired because of either an absence of aldosterone Lactic acidosis (shock) Ketoacidosis (diabetic, starvation, or alcoholic) Kidney failure Poisoning (e.g., ethylene glycol, methanol, or salicylates) Inborn errors of metabolism *[HCO3–] is expressed in mEq/L. or an inability of the kidney to respond to aldosterone. Insevere aldosterone deficiency, as occurs with congenital adrenal hyperplasia secondary to 21α-hydroxylase deficiency, the hyperkalemia and metabolic acidosis are accompanied byhyponatremia and volume depletion from renal salt wasting.Incomplete aldosterone deficiency causes less severe electrolytedisturbances; children may have isolated hyperkalemic RTA,hyperkalemia without acidosis, or isolated hyponatremia.


Pediatrics_Nelson

Pediatrics_Nelson. Lactic acidosis most commonly occurs when inadequate oxygen delivery to the tissues leads to anaerobic metabolism and excess production of lactic acid. Lactic acidosis may be secondary to shock, severe anemia, or hypoxemia. Inborn errors of carbohydrate metabolism produce a severe lactic acidosis (see Chapter 52). In diabetes mellitus, inadequate insulin leads to hyperglycemia and diabetic ketoacidosis (see Chapter 171). Renal failure (see Chapter 165) causes a metabolic acidosis because the kidneys are unable to excrete the acid produced by normal metabolism.


Pediatrics_Nelson

Pediatrics_Nelson. A variety of toxic ingestions cause a metabolic acidosis. Acute salicylate intoxication occurs after a large overdose.Chronic salicylate intoxication is possible because of the gradualbuildup of the drug. In addition to a metabolic acidosis, somepatients may have a respiratory alkalosis. Other symptoms ofsalicylate intoxication include fever, seizures, lethargy, andcoma. Hyperventilation may be particularly marked. Tinnitus,vertigo, and hearing impairment are more likely with chronicsalicylate intoxication. Ethylene glycol, a component of antifreeze, is converted in the liver to glyoxylic and oxalic acids,causing a severe metabolic acidosis. Excessive oxalate excretion causes calcium oxalate crystals to appear in the urine, andcalcium oxalate precipitation in the kidney tubules can cause renal failure. The toxicity of methanol ingestion also depends on liver metabolism; formic acid is the toxic end product thatcauses the metabolic acidosis and other sequelae, which includedamage to


Pediatrics_Nelson

Pediatrics_Nelson. renal failure. The toxicity of methanol ingestion also depends on liver metabolism; formic acid is the toxic end product thatcauses the metabolic acidosis and other sequelae, which includedamage to the optic nerve and central nervous system.


Pediatrics_Nelson

Pediatrics_Nelson. There are many inborn errors of metabolism that maycause a metabolic acidosis (see Section 10). The metabolic acidosis may be due to excessive production of ketoacids, lactic acid, or other organic anions. Some patients have accompanying hyperammonemia. In most patients, acidosis occurs only episodically during acute decompensations, which may be precipitated by ingestion of specific dietary substrates (proteins), the stress of a mild illness (fasting, catabolism), or poor compliance with dietary or medical therapy.


Pediatrics_Nelson

Pediatrics_Nelson. The underlying disorder usually produces most of the signs andsymptoms in children with a mild or moderate metabolic acidosis. The clinical manifestations of the acidosis are related to the degree of acidemia; patients with appropriate respiratory compensation and less severe acidemia have fewer manifestations than patients with a concomitant respiratory acidosis. At a serumpH less than 7.20, there is impaired cardiac contractility andan increased risk of arrhythmias, especially if underlying heartdisease or other predisposing electrolyte disorders are present.With acidemia, there is a decrease in the cardiovascular responseto catecholamines, potentially exacerbating hypotension in children with volume depletion or shock. Acidemia causes vasoconstriction of the pulmonary vasculature, which is especiallyproblematic in neonates with primary pulmonary hypertension of the newborn (see Chapter 61). The normal respiratory response to metabolic acidosis—compensatory hyperventilation—may be


Pediatrics_Nelson

Pediatrics_Nelson. is especiallyproblematic in neonates with primary pulmonary hypertension of the newborn (see Chapter 61). The normal respiratory response to metabolic acidosis—compensatory hyperventilation—may be subtle with mild metabolic acidosis, but it causesdiscernible increased respiratory effort with worsening acidemia. Chronic metabolic acidosis causes failure to thrive.


Pediatrics_Nelson

Pediatrics_Nelson. The plasma anion gap is useful for evaluating patients with a metabolic acidosis. It divides patients into two diagnostic groups: normal anion gap and increased anion gap. The following formula determines the anion gap:


Pediatrics_Nelson

Pediatrics_Nelson. A normal anion gap is 3 to 11. A decrease in the albuminconcentration of 1 g/dL decreases the anion gap by roughly 4mEq/L. Similarly, albeit less commonly, an increase in unmeasured cations, such as calcium, potassium, or magnesium, decreases the anion gap. Conversely, a decrease in unmeasuredcations is a rare cause of an increased anion gap. Because ofthese variables, the broad range of a normal anion gap, and other factors, the presence of a normal or increased anion gapis not always reliable in differentiating the causes of a metabolicacidosis, especially when the metabolic acidosis is mild. Somepatients have more than one explanation for their metabolic acidosis, such as a child with diarrhea and lactic acidosis secondaryto hypoperfusion. The anion gap should not be interpreted indogmatic isolation; consideration of other laboratory abnormalities and the clinical history improves its diagnostic utility.


Pediatrics_Nelson

Pediatrics_Nelson. The most effective therapeutic approach for patients with a metabolic acidosis is correction of the underlying disorder, if possible. The administration of insulin in diabetic ketoacidosis or restoration of adequate perfusion in lactic acidosis from shock eventually results in normalization of acid-base balance. The use of bicarbonate therapy is indicated when the underlying disorder is irreparable; examples include RTA and chronic renal failure. In salicylate poisoning, alkali administration increases renal clearance of salicylate and decreases the amount of salicylate in brain cells. Short-term base therapy is often necessary in other poisonings and inborn errors of metabolism.


Pediatrics_Nelson

Pediatrics_Nelson. The causes of a metabolic alkalosis are divided into two categories based on the urinary chloride (Table 37-3). The alkalosis in patients with a low urinary chloride is maintained by volume depletion. They are called chloride responsive because volume repletion with fluid containing sodium chloride and potassium chloride is necessary to correct the metabolic alkalosis. Emesis, which causes loss of hydrochloride and volume depletion, is the most common cause of a metabolic alkalosis. Diuretic use increases chloride excretion in the urine. Consequently, while a patient is receiving diuretics, the urinary chloride is typically high (>20 mEq/L). After the diuretic effect resolves, the urinary chloride is low (<15 mEq/L), because of appropriate renal chloride retention in response to volume depletion. Categorization of diuretics based on urinary chloride depends on the timing of the measurement. The metabolic alkalosis from diuretics is clearly chloride responsive; it corrects only after


Pediatrics_Nelson

Pediatrics_Nelson. Categorization of diuretics based on urinary chloride depends on the timing of the measurement. The metabolic alkalosis from diuretics is clearly chloride responsive; it corrects only after adequate volume repletion. This is the rationale for including it among the chloride-responsive causes of a metabolic alkalosis.


Pediatrics_Nelson

Pediatrics_Nelson. The chloride-resistant causes of metabolic alkalosis can be subdivided based on blood pressure. Patients with the rare disorders that cause a metabolic alkalosis and hypertension either have increased aldosterone or act as if they have increased aldosterone. Patients with Bartter syndrome or Gitelman syndrome (Chapter 36) have metabolic alkalosis, hypokalemia, and normal blood pressure secondary to renal tubular defects that cause continuous urinary losses of chloride.


Pediatrics_Nelson

Pediatrics_Nelson. The symptoms in patients with a metabolic alkalosis often are related to the underlying disease and associated electrolyte disturbances. Hypokalemia is often present, and occasionally severe, in the diseases that cause a metabolic alkalosis (see Chapter 36). Children with chloride-responsive causes of metabolic alkalosis often have symptoms related to volume depletion (see Chapter 33). In contrast, children with chloride-unresponsive causes may have symptoms related to hypertension. Severe alkalemia may cause arrhythmias, hypoxia secondary to hypoventilation, or decreased cardiac output. Gastric losses (emesis or nasogastric suction) Pyloric stenosis Diuretics (loop or thiazide) Chloride-losing diarrhea Chloride-deficient formula Cystic fibrosis (sweat losses of chloride) Posthypercapnia (chloride loss during respiratory acidosis)


Pediatrics_Nelson

Pediatrics_Nelson. Measurement of the urinary chloride concentration is the most helpful test in differentiating among the causes of a metabolic alkalosis. The history usually suggests a diagnosis, although no obvious explanation may be present in the patient with bulimia, surreptitious diuretic use, or an undiagnosed genetic disorder, such as Bartter syndrome or Gitelman syndrome.


Pediatrics_Nelson

Pediatrics_Nelson. The approach to therapy of metabolic alkalosis depends on theseverity of the alkalosis and the underlying etiology. In childrenwith a mild metabolic alkalosis ([HCO3–] < 32 mEq/L), intervention is often unnecessary. Patients with chloride-responsivemetabolic alkalosis respond to correction of hypokalemia andvolume repletion with sodium and potassium chloride, butaggressive volume repletion may be contraindicated if mildvolume depletion is medically necessary in the child receiving diuretic therapy. In children with chloride-resistant causesof a metabolic alkalosis that are associated with hypertension,volume repletion is contraindicated because it exacerbatesthe hypertension and does not repair the metabolic alkalosis.Treatment focuses on eliminating or blocking the action of theexcess mineralocorticoid. In children with Bartter syndromeor Gitelman syndrome, therapy includes oral potassium supplementation and potassium-sparing diuretics.


Pediatrics_Nelson

Pediatrics_Nelson. During a respiratory acidosis, there is a decrease in the effectiveness of CO2 removal by the lungs. The causes of a respiratory acidosis are either pulmonary or nonpulmonary (Table 37-4). A respiratory alkalosis is an inappropriate reduction in the blood CO2 concentration. A variety of stimuli can increase the ventilatory drive and cause a respiratory alkalosis (Table 37-5). Treatment of respiratory acid-base disorders focuses on correction of the underlying disorder. Mechanical ventilation may be necessary in a child with a refractory respiratory acidosis. overdose) Disorders of the spinal cord, peripheral nerves, or neuromuscular junction (botulism or Guillain-Barré syndrome) Colletti JE, Brown KM, Sharieff GQ, et al: The management of children with gastroenteritis and dehydration in the emergency department, J Emerg Med 38:686–698, 2010 Friedman A: Fluid and electrolyte therapy: a primer, Pediatr Nephrol 25:843–846, 2010


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Pediatrics_Nelson. Med 38:686–698, 2010 Friedman A: Fluid and electrolyte therapy: a primer, Pediatr Nephrol 25:843–846, 2010 Gennari FJ: Pathophysiology of metabolic alkalosis: a new classification based on the centrality of stimulated collecting duct ion transport, Am J Kidney Dis 58:626–636, 2011 Greenbaum LA: Pathophysiology of body fluids and fluid therapy. In Kliegman RM, Stanton BF, St. Geme JW, et al, editors: Nelson textbook of pediatrics, ed 19, Philadelphia, 2011, Elsevier Science, pp 212–249 Kraut JA, Madias NE: Differential diagnosis of nongap metabolic acidosis: value of a systematic approach, Clin J Am Soc Nephrol 7:671–679, 2012 Pepin J, Shields C: Advances in diagnosis and management of hypokalemic and hyperkalemic emergencies, Emerg Med Pract 14:1–17, 2012 Simpson JN, Teach SJ: Pediatric rapid fluid resuscitation, Curr Opin Pediatr 23:286–292, 2011


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Pediatrics_Nelson. Simpson JN, Teach SJ: Pediatric rapid fluid resuscitation, Curr Opin Pediatr 23:286–292, 2011 Unwin RJ, Luft FC, Shirley DG: Pathophysiology and management of hypo kalemia: a clinical perspective, Nat Rev Nephrol 7:75–84, 2011 The Acutely Ill or K. Jane Lee Initial assessment (the ABCs—airway, breathing, and circulation) of an acutely ill or injured child includes rapid identification of physiologic derangements in tissue perfusion and oxygenation. Once identified, immediate resuscitation must be implemented before pursuing the usual information needed to develop a differential diagnosis. Initial resuscitation measures are directed at achieving and maintaining adequate tissue perfusion and oxygenation. Oxygen delivery depends on cardiac output, hemoglobin concentration, and hemoglobin-oxygen saturation. The last mentioned depends on air movement, alveolar gas exchange, pulmonary blood flow, and oxygen-hemoglobin binding characteristics.


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Pediatrics_Nelson. In the resuscitation phase, access to historical information may be limited. Characterization of the onset of symptoms, details of events, and a brief identification of underlying medical problems should be sought by members of the team not actively involved in the resuscitation. Attempts at identifying historical issues that affect the ABCs are useful but should not delay intervention if tissue oxygenation and perfusion are markedly impaired.


Pediatrics_Nelson

Pediatrics_Nelson. Initial examination must focus rapidly on the ABCs (Table 38-1) to address the issues of oxygen delivery to tissues systematically. Airway patency is the first to be addressed, including assessment of the neurologically injured child’s ability to protect the airway. Protection of the cervical spine also should be initiated at this step in any child with traumatic injury or who presents with altered mental status of uncertain etiology. Assessment of breathing includes auscultation of air movement and application of a pulse oximeter (when available) to identify current oxygenation status. Circulatory status is assessed by palpation for distal and central pulses, focusing on the presence and quality of the pulses. Bounding pulses and a wide pulse pressure are often the first sign of the vasodilatory phase of shock and require immediate resuscitation measures. Weak, thready, or absent pulses are indicators for fluid resuscitation, initiation of chest compressions, or both. When assessment


Pediatrics_Nelson

Pediatrics_Nelson. phase of shock and require immediate resuscitation measures. Weak, thready, or absent pulses are indicators for fluid resuscitation, initiation of chest compressions, or both. When assessment of the ABCs is complete and measures have been taken to achieve an acceptable level of tissue oxygenation, a more complete physical examination is performed. The sequence of this examination depends on whether the situation involves an acute medical illness or trauma. In trauma patients, the examination follows the ABCDE pathway. D stands for disability and prompts assessment of the neurologic system and evaluation for major traumatic injuries. E stands for exposure; the child is disrobed and examined for evidence of any life-threatening or limb-threatening problems. For the acutely ill and the injured child, the subsequent physical examination should identify evidence of organ dysfunction, starting with areas suggested in the chief complaint and progressing to a thorough and systematic


Pediatrics_Nelson

Pediatrics_Nelson. the injured child, the subsequent physical examination should identify evidence of organ dysfunction, starting with areas suggested in the chief complaint and progressing to a thorough and systematic investigation of the entire patient.


Pediatrics_Nelson

Pediatrics_Nelson. The physiologic responses to acute illness and injury are mechanisms that attempt to correct inadequacies of tissue oxygenation and perfusion. When initial changes, such as increasing heart and respiratory rates, fail to meet the body’s needs, other manifestations of impending cardiopulmonary failure occur (Table 38-2). Respiratory failure, the most common cause of acute deterioration in children, may result in inadequate tissue oxygenation and in respiratory acidosis. Signs and symptoms of respiratory failure (tachypnea, tachycardia, increased work of breathing, abnormal mentation) progress as tissue oxygenation becomes more inadequate. Inadequate perfusion (shock) leads to inadequate oxygen delivery and a resulting metabolic acidosis. Shock is characterized by signs of inadequate tissue perfusion (pallor, cool skin, poor pulses, delayed capillary refill, oliguria, and abnormal mentation). The presence of any of these symptoms demands careful assessment and intervention to correct


Pediatrics_Nelson

Pediatrics_Nelson. perfusion (pallor, cool skin, poor pulses, delayed capillary refill, oliguria, and abnormal mentation). The presence of any of these symptoms demands careful assessment and intervention to correct the abnormality and to prevent further deterioration.


Pediatrics_Nelson

Pediatrics_Nelson. During the initial phase of resuscitation, monitoring vital signs and physiologic status is the key screening activity. Continuous monitoring with attention to changes may indicate response to Able to be maintained independently Maintainable with positioning, suctioning Unmaintainable, requires assistance Use of accessory muscles Responsiveness (AVPU) Recognition of parents or caregivers Pupil size Posturing AVPU, Alert, responds to voice, responds to pain, unresponsive. therapy or further deterioration requiring additional intervention. During the initial rapid assessment, diagnostic evaluation often is limited to pulse oximetry and bedside measurement of glucose levels. The latter is important in any child with altered mental status or at risk for inadequate glycogen stores (infants, malnourished patients). After resuscitation measures, further diagnostic tests and imaging are often necessary.


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Pediatrics_Nelson. The choice of appropriate diagnostic tests and imaging is determined by the mechanism of disease and results of evaluation after initial resuscitation. The initial evaluation of major Central nervous Lethargy, agitation, delirium, obtundation, system Respiratory Apnea, grunting, nasal flaring, dyspnea, retracting, tachypnea, poor air movement, stridor, wheezing Cardiovascular Arrhythmia, bradycardia, tachycardia, weak pulses, poor capillary refill, hypotension Skin and mucous Mottling, pallor, cyanosis, diaphoresis, poor membranes membrane turgor, dry mucous membranes *Action would seldom be taken if only one or two of these signs and symptoms were present, but the occurrence of several in concert foreshadows grave consequences. Intervention should be directed at the primary disorder.


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Pediatrics_Nelson. trauma patients is focused on identifying evidence of hemorrhage and organ and tissue injury. For an acutely ill child with respiratory distress, a chest x-ray is important. Appropriate cultures should be obtained when sepsis is suspected. Children with historical or physical evidence of inadequate intra-vascular volume should have serum electrolyte levels obtained, including bicarbonate, blood urea nitrogen, and creatinine.


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Pediatrics_Nelson. Resuscitation is focused on correcting identified abnormalities of oxygenation and perfusion and preventing further deterioration. Oxygen supplementation may improve oxygen saturation but may not completely correct tissue oxygenation. When oxygen supplementation is insufficient or air exchange is inadequate, assisted ventilation must be initiated. Inadequate perfusion is usually best managed initially by providing a fluid bolus. Isotonic crystalloids (normal saline, lactated Ringer solution) are the initial fluid of choice. A bolus of 10 to 20 mL/kg should be delivered in monitored conditions. Improvement, but not correction, after an initial bolus should prompt repeated boluses until circulation has been re-established. Because most children with shock have noncardiac causes, fluid administration of this magnitude is well tolerated. If hemorrhage is known or highly suspected, administration of packed red blood cells is appropriate. Monitoring for deteriorating physiologic status


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Pediatrics_Nelson. of this magnitude is well tolerated. If hemorrhage is known or highly suspected, administration of packed red blood cells is appropriate. Monitoring for deteriorating physiologic status during fluid resuscitation (increase in heart rate, decrease in blood pressure) identifies children who may have decreased cardiac function. Fluid resuscitation increases preload, which may worsen pulmonary edema and cardiac function. If deterioration occurs, fluid administration should be interrupted, and resuscitation should be aimed at improving cardiac function.


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Pediatrics_Nelson. When respiratory support and fluid resuscitation are insufficient, introduction of vasoactive substances is the next step. The choice of which agent to use depends on the type of shock present. Hypovolemic shock (when further volume is contraindicated) and distributive shock benefit from drugs that increase systemic vascular resistance (drugs with αagonist activity, such as epinephrine or norepinephrine). The treatment of cardiogenic shock is more complex. To improve cardiac output by increasing the heart rate, drugs with positive chronotropy are used (epinephrine, norepinephrine, and dopamine). Afterload reduction, using drugs such as dobutamine, nitroprusside, or milrinone, also may be needed. Measuring mixed venous oxygen saturation, central venous pressure, and regional oxygen saturations helps guide therapy.


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Pediatrics_Nelson. The outcome of cardiopulmonary arrest in children is poor; survival to hospital discharge is about 6% for out-of-hospital arrest and about 27% for in-hospital arrest, with most survivors having permanent neurologic disability. The ability to anticipate or recognize pre–cardiopulmonary arrest conditions and initiate prompt and appropriate therapy not only is lifesaving, but also preserves the quality of life (see Table 38-2).


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Pediatrics_Nelson. Children who need cardiopulmonary resuscitation (CPR) usually have a primary respiratory arrest. Hypoxia usually initiates the cascade leading to arrest and also produces organ dysfunction or damage (Table 38-3). The approach to cardiopulmonary arrest extends beyond CPR and includes efforts to preserve vital organ function. The goal in resuscitating a pediatric patient following a cardiopulmonary arrest should be to optimize cardiac output and tissue oxygen delivery, which may be accomplished by using artificial ventilation and chest compression and by the judicious administration of pharmacologic agents. In 2010 the American Heart Association revised the recommendations for resuscitation for adults, children, and infants. The biggest change is the recommendation to start chest compressions immediately, rather than beginning with airway and breathing.


Pediatrics_Nelson

Pediatrics_Nelson. Chest compressions should be initiated if a pulse cannot be palpated or if the heart rate is less than 60 beats/min with signs of poor systemic perfusion. Chest compressions should be performed immediately by one person while a second person prepares to begin ventilation. Ventilation is extremely important in pediatric arrests because of the high likelihood of a primary respiratory cause; however, ventilation requires Brain Seizures, cerebral edema, infarction, herniation, anoxic damage, SIADH, diabetes insipidus Cardiovascular Heart failure, myocardial infarct Lung and pulmonary Acute respiratory distress syndrome, vasculature pulmonary hypertension Liver Infarction, necrosis, cholestasis Kidney Acute tubular necrosis, acute cortical Gastrointestinal Gastric ulceration, mucosal damage tract Hematologic Disseminated intravascular coagulation SIADH, Syndrome of inappropriate secretion of antidiuretic hormone.


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Pediatrics_Nelson. Gastrointestinal Gastric ulceration, mucosal damage tract Hematologic Disseminated intravascular coagulation SIADH, Syndrome of inappropriate secretion of antidiuretic hormone. equipment and is, therefore, sometimes delayed. For this reason the recommendation is to start chest compressions first while preparing for ventilation. For optimal chest compressions, the child should be supine on a flat, hard surface. Effective CPR requires a compression depth of one third to one half of the anterior-posterior diameter of the chest with complete recoil after each compression. The compression rate should be at least 100/min with breaths delivered 8 to 10 times per minute. If an advanced airway is in place, compressions should not pause for ventilation; both should continue simultaneously.


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Pediatrics_Nelson. Ventilation requires a patent airway. In children, airway patency often is compromised by a loss of muscle tone, allowing the mandibular block of tissue, including the tongue, bony mandible, and the soft surrounding tissues, to rest against the posterior pharyngeal wall. The head tilt–chin lift maneuver should be used to open the airway in children with no sign of head or neck trauma. In children with signs of head or neck trauma, the jaw thrust maneuver should be used.


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Pediatrics_Nelson. Bag-mask ventilation can be as effective as, and possibly safer than, endotracheal intubation for short periods of time in an out-of-hospital setting. If skilled personnel and proper equipment are available, pediatric patients requiring resuscitation should be endotracheally intubated. Before intubation, the patient should be ventilated with 100% oxygen using a bag and mask. Cricoid pressure should be used to minimize inflation of the stomach. Many conscious patients may benefit from the use of induction medications (sedatives, analgesics, and paralytics) to assist intubation, but caution is necessary to prevent further cardiovascular compromise from vasodilating effects of many sedatives. The correct size of the tube may be estimated according to the size of the child’s mid-fifth phalanx or the following formula: 4 + (patient age in years/4).


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Pediatrics_Nelson. When the endotracheal tube is in place, the adequacy of ventilation and the position of the tube must be assessed. Use of both clinical assessment and confirmatory devices is recommended. Clinical assessment may include looking for adequate chest wall movement and auscultation of the chest to detect bilateral and symmetric breath sounds. Confirmatory devices such as end-tidal carbon dioxide (CO2) monitoring devices are useful for validation of endotracheal placement, but low levels of detected CO2 may be seen secondary to lack of pulmonary circulation. If the patient’s condition fails to improve or deteriorates, consider the possibilities of tube Displacement or Obstruction, Pneumothorax, or Equipment failure (mnemonic DOPE).


Pediatrics_Nelson

Pediatrics_Nelson. The major role of endotracheal intubation is to protect or maintain the airway and ensure the delivery of adequate oxygen to the patient. Because hypoxemia is the final common pathway in pediatric cardiopulmonary arrests, providing oxygen is more important than correcting the respiratory acidosis. The clinician should deliver 100% oxygen at a rate of 8 to 10 breaths/min during CPR, or 12 to 20 breaths/min for a patient who has a perfusing rhythm. Use only the tidal volume necessary to produce visible chest rise. Care should be taken not to hyperventilate the patient. When mechanical means fail to re-establish adequate circulation, pharmacologic intervention is essential (Table 38-4).If intravascular access is not present or rapidly established, administration through an intraosseous route is recommended. Some drugs can also be administered effectively through the endotracheal tube.


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Pediatrics_Nelson. Epinephrine, a catecholamine with mixed α-agonist and β-agonist properties, constitutes the mainstay of drug therapy for CPR. The α-adrenergic effects are most important during acute phases of resuscitation, causing an increase in systemic vascular resistance that improves coronary blood flow. Standard dose therapy is recommended for the first and subsequent boluses. There is no benefit offered by high-dose epinephrine. Vasopressin, an endogenous hormone, causes constriction of capillaries and small arterioles and may be useful. Insufficient data support its routine use, but vasopressin may be considered in children failing standard medication administration.


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Pediatrics_Nelson. The routine use of sodium bicarbonate is currently not recommended. Sodium bicarbonate may be judiciously used to treat toxidromes or hyperkalemic arrest; however, oxygen delivery and elimination of CO2 must be established first. Side effects include hypernatremia, hyperosmolality, hypokalemia, metabolic alkalosis (shifting the oxyhemoglobin curve to the left and impairing tissue oxygen delivery), reduced ionized calcium level, and impaired cardiac function. Routine administration of calcium is not recommended. It may be useful in cases of documented hypocalcemia, calcium channel blocker overdose, hypermagnesemia, or hypokalemia, but is otherwise not beneficial and potentially harmful. Hypoglycemia is not uncommon in infants and children who sustain cardiac arrest. Blood glucose should be checked and hypoglycemia should be promptly treated with glucose.


Pediatrics_Nelson

Pediatrics_Nelson. Prompt electrical defibrillation is indicated when ventricular fibrillation or pulseless ventricular tachycardia is noted (Table 38-5). CPR should continue until immediately before defibrillation and resume immediately afterward, minimizing interruptions in compressions. If a second attempt at defibrillation is necessary, it should be followed by a dose of epinephrine. Children failing two episodes of defibrillation may benefit from administration of amiodarone. Defibrillation should be distinguished from cardioversion of supraventricular tachycardias, which also may compromise cardiac output. Cardioversion requires a lower starting dose and synchronization of the discharge to the electrocardiogram to prevent discharging during a susceptible period, which may convert supraventricular tachycardia to ventricular tachycardia or fibrillation. Place self-adhesive defibrillation pads or paddles with electrode gel at the apex of the heart and the upper right side of the chest


Pediatrics_Nelson

Pediatrics_Nelson. Place self-adhesive defibrillation pads or paddles with electrode gel at the apex of the heart and the upper right side of the chest Notify all participating personnel before discharging paddles so that no one is in contact with patient or bed Begin with 2 J/kg; resume chest compressions immediately If unsuccessful, increase to 4 J/kg and repeat Higher energy levels may be considered, not to exceed 10 J/kg or the adult maximum dose For symptomatic supraventricular tachycardia* or ventricular tachycardia with a pulse, synchronize signal with ECG Choose paddles, position pads, and notify personnel as above Begin with 0.5–1 J/kg If unsuccessful, use 2 J/kg ECG, Electrocardiogram. *Consider adenosine first (see Table 38-4) Table 38-4 Drug Doses for Cardiopulmonary Resuscitation DRUG INDICATION DOSE Adenosine Supraventricular tachycardia 0.1 mg/kg (maximum 6 mg); second dose: 0.2 mg/kg (maximum 12 mg)


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Pediatrics_Nelson. Table 38-4 Drug Doses for Cardiopulmonary Resuscitation DRUG INDICATION DOSE Adenosine Supraventricular tachycardia 0.1 mg/kg (maximum 6 mg); second dose: 0.2 mg/kg (maximum 12 mg) Atropine Supraventricular or junctional 0.02 mg/kg (minimum dose 0.1 mg); up to 0.5 mg; higher doses needed in bradycardia organophosphate poisoning Bicarbonate Hyperkalemia, some toxidromes 1 mEq/kg bolus; ensure adequate ventilation; monitor ABGs; can repeat every 10 min Calcium chloride Hypocalcemia, calcium 20 mg/kg; maximum single dose 2 g; administer slowly channel blocker overdose, hypermagnesemia, hyperkalemia Epinephrine Hypotension, chronotropy, 0.01 mg/kg IV/IO; 0.1 mg/kg ET; may repeat every 3–5 minutes; may promote inotropy arrhythmias Fluid Hypovolemia, sepsis Administer crystalloid in 20 mL/kg boluses titrated to patient’s physiologic needs Glucose Hypoglycemia Newborns: 5–10 mL/kg 10% dextrose; infants and children: 2–4 mL/kg 25% dextrose; adolescents: 1–2 mL/kg 50% dextrose


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Pediatrics_Nelson. Glucose Hypoglycemia Newborns: 5–10 mL/kg 10% dextrose; infants and children: 2–4 mL/kg 25% dextrose; adolescents: 1–2 mL/kg 50% dextrose Data from 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 14: Pediatric Advanced Life Support, Circulation 122 [suppl 3]:S876-S908, 2010. ABG, Arterial blood gas; ET, endotracheal; IO, intraosseous; IV, intravenous; VF, ventricular fibrillation; VT, ventricular tachycardia.


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Pediatrics_Nelson. Acute respiratory failure occurs when the pulmonary system is unable to maintain adequate gas exchange to meet metabolic demands. The resulting failure can be classified as hypercarbic (Paco2 >50 mm Hg in previously healthy children), hypoxemic (Pao2 <60 mm Hg in previously healthy children without an intracardiac shunt), or both. Hypoxemic respiratory failure is frequently caused by ventilation-perfusion mismatch (perfusion of lung that is not adequately ventilated) and shunting (deoxygenated blood bypasses ventilated alveoli). Hypercarbic respiratory failure results from inadequate alveolar ventilation secondary to decreased minute ventilation (tidal volume × respiratory rate) or an increase in dead space ventilation (ventilation of areas receiving no perfusion).


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Pediatrics_Nelson. Respiratory failure may occur with acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). The definitions of these are in the process of revision; however, currently ALI isdefined as having the following four clinical features: acute onset,bilateral pulmonary edema, no clinical evidence of elevated leftatrial pressure, and a ratio of Pao2 to Fio2 ≤ 300 mm Hg regardlessof the level of positive end-expiratory pressure (PEEP). ARDSis a subset of ALI with more severe hypoxemia (Pao2/Fio2 of ≤ 200 mm Hg). These syndromes can be triggered by a variety ofinsults, including sepsis, pneumonia, shock, burns, or traumaticinjury, all resulting in inflammation and increased vascular permeability leading to pulmonary edema. Numerous mediators ofinflammation (tumor necrosis factor, interferon-γ, nuclear factor κB, and adhesion molecules) may be involved in the development of ARDS. Surfactant action also may be affected.


Pediatrics_Nelson

Pediatrics_Nelson. Respiratory failure is frequently caused by bronchiolitis (often caused by respiratory syncytial virus), asthma, pneumonia, upper airway obstruction, and sepsis/ARDS. Respiratory failure requiring mechanical ventilation develops in 7% to 21% of patients hospitalized for respiratory syncytial virus. Asthma is increasing in prevalence and is the most common reason for unplanned hospital admissions in children 3 to12 years of age in the United States. Environmental factors (exposure to cigarette smoke) and prior disease characteristics (severity of asthma, exercise intolerance, delayed start of therapy, andprevious intensive care unit admissions) affect hospitalizationand near-fatal episodes. The mortality rate of asthma for childrenyounger than 19 years of age has increased by nearly 80% since1980. Deaths are more common in African-American children.


Pediatrics_Nelson

Pediatrics_Nelson. Chronic respiratory failure (with acute exacerbations) is often due to chronic lung disease (bronchopulmonary dysplasia, cystic fibrosis), neurologic or neuromuscular abnormalities, and congenital anomalies. Early signs of hypoxic respiratory failure include tachypnea and tachycardia in attempt to improve minute ventilation and cardiac output and to maintain delivery of oxygenated blood to the tissues. Further progression of disease may result in dyspnea, nasal flaring, grunting, use of accessory muscles of respiration, and diaphoresis. Late signs of inadequate oxygen delivery include cyanosis and altered mental status (initially confusion and agitation). Signs and symptoms of hypercarbic respiratory failure include attempts to increase minute ventilation (tachypnea and increased depth of breathing) and altered mental status (somnolence).


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Pediatrics_Nelson. A chest radiograph may show evidence of the etiology ofrespiratory failure. The detection of atelectasis, hyperinflation, infiltrates, or pneumothoraces assists with ongoingmanagement. Diffuse infiltrates or pulmonary edema maysuggest ARDS. The chest radiograph may be normal whenupper airway obstruction or impaired respiratory controlsare the etiology. In patients presenting with stridor or otherevidence of upper airway obstruction, a lateral neck filmor computed tomography (CT) may delineate anatomicdefects. Direct visualization through flexible bronchoscopy allows identification of dynamic abnormalities of theanatomic airway. Helical CT helps diagnose a pulmonaryembolus.


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Pediatrics_Nelson. Pulse oximetry allows noninvasive, continuous assessment of oxygenation but is unable to provide information about ventilation abnormalities. Determination of CO2 levels requires a blood gas measurement (arterial, venous, or capillary). An arterial blood gas allows measurement of CO2 levels and analysis of the severity of oxygenation defect through calculation of an alveolar-arterial oxygen difference. A normal Pco2 in a patient who is hyperventilating should heighten concern about the risk of further deterioration. Hypoxic respiratory failure resulting from impairment of alveolar-capillary function is seen in ARDS; cardiogenic pulmonary edema; interstitial lung disease; aspiration pneumonia; bronchiolitis; bacterial, fungal, or viral pneumonia; and sepsis. It also can be due to intracardiac or intrapulmonary shunting seen with atelectasis and embolism.


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Pediatrics_Nelson. Hypercarbic respiratory failure can occur when the respiratory center fails as a result of drug use (opioids, barbiturates, anesthetic agents), neurologic or neuromuscular junction abnormalities (cervical spine trauma, demyelinating diseases, anterior horn cell disease, botulism), chest wallinjuries, or diseases that cause increased resistance to airflow(croup, vocal cord paralysis, post-extubation edema). Maintenance of ventilation requires adequate function of the chestwall and diaphragm. Disorders of the neuromuscular pathways, such as muscular dystrophy, myasthenia gravis, andbotulism, result in inadequate chest wall movement, development of atelectasis, and respiratory failure. Scoliosis rarelyresults in significant chest deformity that leads to restrictivepulmonary function. Similar impairments of air exchangemay result from distention of the abdomen (postoperativelyor due to ascites, obstruction, or a mass) and thoracic trauma(flail chest).


Pediatrics_Nelson

Pediatrics_Nelson. Mixed forms of respiratory failure are common andoccur when disease processes result in more than one pathophysiologic change. Increased secretions seen in asthma often lead to atelectasis and hypoxia, whereasrestrictions of expiratory airflow may lead to hypercarbia.Progression to respiratory failure results from peripheralairway obstruction, extensive atelectasis, and resultant hypoxemia and retention of CO2.


Pediatrics_Nelson

Pediatrics_Nelson. Initial treatment of patients in respiratory distress includes addressing the ABCs (see Chapter 38). Bag/mask ventilationmust be initiated for patients with apnea. In other patients, oxygen therapy is administered using appropriate methods (e.g., simple mask). Administration of oxygen by nasal cannula allows the patient to entrain room air and oxygen, making it an insufficient delivery method for most children in respiratory failure. Delivery methods, including intubation and mechanical ventilation, should be escalated if there is inability to increase oxygen saturation appropriately.


Pediatrics_Nelson

Pediatrics_Nelson. Patients presenting with hypercarbic respiratory failure are often hypoxic as well. When oxygenation is established, measures should be taken to address the underlying cause of hypercarbia (reversal of drug action, control of fever, or seizures). Patients who are hypercarbic without signs of respiratory fatigue or somnolence may not require intubation based on the Pco2 alone; however, patients with marked increase in the work of breathing or inadequate respiratory effort may require assistance with ventilation.


Pediatrics_Nelson

Pediatrics_Nelson. After identification of the etiology of respiratory failure,specific interventions and treatments are tailored to the needsof the patient. External support of oxygenation and ventilation may be provided by noninvasive ventilation methods (heated humidified high-flow nasal cannula, continuouspositive airway pressure, biphasic positive airway pressure, or negative pressure ventilation) or through invasive methods (traditional mechanical ventilation, high-frequencyoscillatory ventilation, or extracorporeal membrane oxygenation). Elimination of CO2 is achieved through manipulationof minute ventilation (tidal volume and respiratory rate).Oxygenation is improved by altering variables that affectoxygen delivery (fraction of inspired oxygen) or mean airway pressure (PEEP, peak inspiratory pressure, inspiratorytime, gas flow).


Pediatrics_Nelson

Pediatrics_Nelson. The major complication of hypoxic respiratory failure is the development of organ dysfunction. Multiple organ dysfunction includes the development of two or more of the following: respiratory failure, cardiac failure, renal insufficiency/failure, gastrointestinal or hepatic insufficiency, disseminated intravascular coagulation, and hypoxic-ischemic brain injury. Mortality rates increase with increasing numbers of involved organs (see Table 38-3). Complications associated with mechanical ventilation include pressure-related and volume-related lung injury. Both overdistention and insufficient lung distention (loss of functional residual capacity) are associated with lung injury. Pneumomediastinum and pneumothorax are potential complications of the disease process and overdistention. Inflammatory mediators may play a role in the development of chronic fibrotic lung diseases in ventilated patients.


Pediatrics_Nelson

Pediatrics_Nelson. Prognosis varies with the etiology of respiratory failure. Fewerthan 1% of previously healthy children with bronchiolitis die.Asthma mortality rates, although still low, have increased. Despiteadvances in support and understanding of the pathophysiologyof ARDS, the mortality rate remains approximately 30%. Prevention strategies are explicit to the etiology of respiratoryfailure. Some infectious causes can be prevented through activeimmunization against organisms causing primary respiratorydisease (pertussis, pneumococcus, Haemophilus influenzae type b) and sepsis (pneumococcus, H. influenzae type b). Passiveimmunization with respiratory syncytial virus immunoglobulins prevents severe illness in highly susceptible patients (prematurity, bronchopulmonary dysplasia). Primary prevention oftraumatic injuries may decrease the incidence of ARDS. Compliance with appropriate therapies for asthma may decrease thenumber of episodes of respiratory failure (see Chapter 78).


Pediatrics_Nelson

Pediatrics_Nelson. Shock is the inability to provide sufficient perfusion of oxygenated blood and substrate to tissues to meet metabolic demands. Oxygen delivery is directly related to the arterial oxygen content (oxygen saturation and hemoglobin concentration) and to cardiac output (stroke volume and heart rate). Changes in metabolic needs are met primarily by adjustments in cardiac output. Stroke volume is related to myocardial end-diastolic fiber length (preload), myocardial contractility (inotropy), and resistance of blood ejection from the ventricle (afterload) (see Chapter 145). In a young infant whose myocardium possesses relatively less contractile tissue, increased demand for cardiac output is met primarily by a neurally mediated increase in heart rate. In older children and adolescents, cardiac output is most efficiently augmented by increasing stroke volume through neurohormonally mediated changes in vascular tone, resulting in increased venous return to the heart (increased preload),


Pediatrics_Nelson

Pediatrics_Nelson. output is most efficiently augmented by increasing stroke volume through neurohormonally mediated changes in vascular tone, resulting in increased venous return to the heart (increased preload), decreased arterial resistance (decreased afterload), and increased myocardial contractility.


Pediatrics_Nelson

Pediatrics_Nelson. Acute hypovolemia is the most common cause of shock in children. It results from loss of fluid from the intravascular space secondary to inadequate intake or excessive losses (vomiting and diarrhea, blood loss, capillary leak syndromes, or pathologic renal fluid losses) (Table 40-1). Reduced blood volume decreases preload, stroke volume, and cardiac output. Hypovolemic shock results in increased sympathoadrenal activity, producing an increased heart rate and enhanced myocardial CNS, Central nervous system.


Pediatrics_Nelson

Pediatrics_Nelson. CNS, Central nervous system. contractility. Neurohormonally mediated constriction of the arterioles and capacitance vessels maintains blood pressure, augments venous return to the heart to improve preload, and redistributes blood flow from nonvital to vital organs. If hypovolemic shock remains untreated, the increased heart rate may impair coronary blood flow and ventricular filling, while elevated systemic vascular resistance increases myocardial oxygen consumption, resulting in worsening myocardial function. Ultimately, intense systemic vasoconstriction and hypovolemia produce tissue ischemia, impairing cell metabolism and releasing potent vasoactive mediators from injured cells. Cytokines and other vasoactive peptides can change myocardial contractility and vascular tone and promote release of other inflammatory mediators that increase capillary permeability and impair organ function further.


Pediatrics_Nelson

Pediatrics_Nelson. Abnormalities in the distribution of blood flow may result in profound inadequacies in tissue perfusion, even in the presence of a normal or high cardiac output. This maldistribution of flow usually results from abnormalities in vascular tone. Septic shock is the most common type of distributive shock in children. Other causes include anaphylaxis, neurologic injury, and drug-related causes (see Table 40-1). Distributive shock may present with the systemic inflammatory response syndrome (SIRS), defined as two or more of the following: temperature greater than 38° C or less than 36° C; heart rate greater than 90 beats/min or more than two standard deviations above normal for age; tachypnea; or white blood count greater than 12,000 cells/mm3, less than 4000 cells/mm3, or greater than 10% immature forms.


Pediatrics_Nelson

Pediatrics_Nelson. Cardiogenic shock is caused by an abnormality in myocardialfunction and is expressed as depressed myocardial contractility and cardiac output with poor tissue perfusion. Compensatory mechanisms may contribute to the progression of shock bydepressing cardiac function further. Neurohormonal vasoconstrictor responses increase afterload and add to the work of thefailing ventricle. Tachycardia may impair coronary blood flow,which decreases myocardial oxygen delivery. Increased central blood volume caused by sodium and water retention andby incomplete emptying of the ventricles during systole resultsin elevated left ventricular volume and pressure, which impairsubendocardial blood flow. As compensatory mechanisms areovercome, the failing left ventricle produces increased ventricularend-diastolic volume and pressure, which leads to increased leftatrial pressure, resulting in pulmonary edema. This sequence alsocontributes to right ventricular failure because of increased pulmonary artery


Pediatrics_Nelson

Pediatrics_Nelson. volume and pressure, which leads to increased leftatrial pressure, resulting in pulmonary edema. This sequence alsocontributes to right ventricular failure because of increased pulmonary artery pressure and increased right ventricular afterload.


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Pediatrics_Nelson. Primary cardiogenic shock may occur in children who have congenital heart disease. Cardiogenic shock also may occur in previously healthy children secondary to viral myocarditis, dysrhythmias, or toxic or metabolic abnormalities or after hypoxic-ischemic injury (see Chapters 142, 145, and 147, as well as Table 40-1). Obstructive shock results from mechanical obstruction of ventricular outflow. Causes include congenital lesions such as coarctation of the aorta, interrupted aortic arch, and severe aortic valvular stenosis, along with acquired diseases (e.g., hypertrophic cardiomyopathy) (see Table 40-1). For neonates presenting in shock, obstructive lesions must be considered. Dissociative shock refers to conditions in which tissue perfusion is normal, but cells are unable to use oxygen because the hemoglobin has an abnormal affinity for oxygen, preventing its release to the tissues (see Table 40-1).


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Pediatrics_Nelson. All forms of shock produce evidence that tissue perfusion and oxygenation are insufficient (increased heart rate, abnormal blood pressure, alterations of peripheral pulses). The etiology of shock may alter the initial presentation of these signs and symptoms. Hypovolemic shock is distinguished from other causes of shock by history and the absence of signs of heart failure or sepsis. In addition to the signs of sympathoadrenal activity (tachycardia, vasoconstriction), clinical manifestations include signs of dehydration (dry mucous membranes, decreased urine output) or blood loss (pallor). Recovery depends on the degree of hypovolemia, the patient’s preexisting status, and rapid diagnosis and treatment. The prognosis is good, with a low mortality in uncomplicated cases.


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Pediatrics_Nelson. Patients with distributive shock usually have tachycardia and alterations of peripheral perfusion. In early stages, when cytokine release results in vasodilation, pulses may be bounding, and vital organ function may be maintained (an alert patient, with rapid capillary refill and some urine output in warm shock). As the disease progresses untreated, extremities become cool and mottled with a delayed capillary refill time. At this stage, the patient has hypotension and vasoconstriction. If the etiology of distributive shock is sepsis, the patient often has fever, lethargy, petechiae, or purpura, and he or she may have an identifiable source of infection.


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Pediatrics_Nelson. Cardiogenic shock results when the myocardium is unable to supply the cardiac output required to support tissue perfusion and organ function. Because of this self-perpetuating cycle, heart failure progressing to death may be rapid. Patients with cardiogenic shock have tachycardia and tachypnea. The liver is usually enlarged, a gallop is often present, and jugular venous distention may be noted. Because renal blood flow is poor, sodium and water are retained, resulting in oliguria and peripheral edema. Restriction of cardiac output results in an increase in heart rate and an alteration of stroke volume. The pulse pressure is narrow (making pulses harder to feel), and capillary refill is delayed. The liver is often enlarged, and jugular venous distention may be evident. The principal abnormality in dissociative shock is the inability to deliver oxygen to tissues. Symptoms include tachycardia, tachypnea, alterations in mental status, and ultimately cardiovascular collapse.


Pediatrics_Nelson

Pediatrics_Nelson. Shock requires immediate resuscitation before obtaining laboratory or diagnostic studies. Following initial stabilization (including glucose administration if hypoglycemia is present), the type of shock dictates the necessary laboratory studies. All patients with shock may benefit from determination of a baseline arterial blood gas and blood lactate level to assess the impairment of tissue oxygenation. Measurement of mixed venous oxygen saturation aids in the assessment of the adequacy of oxygen delivery. In contrast to other forms of shock, patients with sepsis often have high mixed venous saturation values because of impairment of mitochondrial function and inability of tissues to extract oxygen. A complete blood count can potentially assess intravascular blood volume after equilibration following a hemorrhage. Electrolyte measurements in patients with hypovolemic shock may identify abnormalities from losses. Patients presenting in distributive shock require appropriate bacterial


Pediatrics_Nelson

Pediatrics_Nelson. following a hemorrhage. Electrolyte measurements in patients with hypovolemic shock may identify abnormalities from losses. Patients presenting in distributive shock require appropriate bacterial and viral cultures to identify a cause of infection. If cardiogenic or obstructive shock is suspected, an echocardiogram assists with the diagnosis and, in the case of tamponade, assists with placement of a pericardial drain to relieve the fluid. Patients with dissociative shock require detection of the causative agent (carbon monoxide, methemoglobin). The management of shock also requires monitoring of arterial blood gases for oxygenation, ventilation (CO2), and acidosis, and frequently assessing the levels of serum electrolytes, calcium, magnesium, phosphorus, and blood urea nitrogen (BUN).


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Pediatrics_Nelson. SEE TABLE 40-1. The key to therapy is the recognition of shock in its early,partially compensated state, when many of the hemodynamicand metabolic alterations may be reversible. Initial therapyfor shock follows the ABCs of resuscitation. Later therapycan then be directed at the underlying cause. Therapy shouldminimize cardiopulmonary work, while ensuring cardiacoutput, blood pressure, and gas exchange. Intubation, combined with mechanical ventilation with oxygen supplementation, improves oxygenation and decreases or eliminatesthe work of breathing but may impede venous return if distending airway pressures (positive end-expiratory pressure[PEEP] or peak inspiratory pressure) are excessive. Blood pressure support is crucial because the vasodilation in sepsismay reduce perfusion despite supranormal cardiac output.


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Pediatrics_Nelson. Monitoring a child in shock requires maintaining access to the arterial and central venous circulation to record pressure measurements, perform blood sampling, and measure systemic blood pressure continuously. These measurements facilitate the estimation of preload and afterload. Regional monitoring with near infrared spectroscopy may allow early, noninvasive detection of alterations in perfusion. Alterations in preload have a dramatic effect on cardiac output. In hypovolemic and distributive shock, decreased preload significantly impairs cardiac output. In these cases, early and aggressive fluid resuscitation is important and greatly affects outcome. In cardiogenic shock, an elevated preload contributes to pulmonary edema.


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Pediatrics_Nelson. Selection of fluids for resuscitation and ongoing use is dictated by clinical circumstances. Crystalloid volume expanders generally are recommended as initial choices because they are effective and inexpensive. Most acutely ill children with signs of shock may safely receive, and usually benefit greatly from, a 20-mL/kg bolus of an isotonic crystalloid over 5 to 15 minutes. This dose may be repeated until a response is noted. Colloids contain larger molecules that may stay in the intravascular space longer than crystalloid solutions and exert oncotic pressure, drawing fluid out of the tissues into the vascular compartment. However, long-term risks of colloids may exceed benefits. Care must be exercised in treating cardiogenic shock with volume expansion because the ventricular filling pressures may rise without improvement of the cardiac performance. Carefully monitoring cardiac output or central venous pressure guides safe volume replacement.


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Pediatrics_Nelson. In an effort to improve cardiac output after volume resuscitation or when further volume replacement may be dangerous, a variety of inotropic and vasodilator drugs may be useful (Table 40-2). Therapy is directed first at increasing myocardial contractility, then at decreasing left ventricular afterload. The hemodynamic status of the patient dictates the choice of the agent.


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Pediatrics_Nelson. Therapy may be initiated with dopamine at 3 to 15 mcg/kg/min; however, epinephrine or norepinephrine may be preferable in patients with decompensated shock. In addition to improving contractility, certain catecholamines cause an increase in systemic vascular resistance. The addition of a vasodilator drug may improve cardiac performance by decreasing the resistance against which the heart must pump (afterload). Afterload reduction may be achieved with dobutamine, milrinone, amrinone, nitroprusside, nitroglycerin, and angiotensin-converting enzyme inhibitors. The use of these drugs may be particularly important in late shock, when vasoconstriction is prominent.


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Pediatrics_Nelson. The lung is a target organ for inflammatory mediators inshock and SIRS. Respiratory failure may develop rapidly andbecome progressive. Intervention requires endotracheal intubation and mechanical ventilation accompanied by the useof supplemental oxygen and PEEP. Care must be taken withthe process of intubation, because a child with compensatedshock may suddenly decompensate on administration of sedative medications that reduce systemic vascular resistance.Severe cardiopulmonary failure may be managed with inhalednitric oxide and, if necessary, extracorporeal membrane oxygenation.


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Pediatrics_Nelson. Poor cardiac output accompanied by decreased renal blood flow may cause prerenal azotemia and oliguria/anuria. Severe hypotension may produce acute tubular necrosis and acute renal failure. Prerenal azotemia is corrected when blood volume deficits are replaced or myocardial contractility is improved, but acute tubular necrosis does not improve immediately when shock is corrected. Prerenal azotemia is associated with a serum BUN-to-creatinine ratio of greater than 10:1 and a urine sodium level less than 20 mEq/L; acute tubular necrosis has a BUN-to-creatinine ratio of 10:1 or less and a urine sodium level between 40 and 60 mEq/L (see Chapter 165). Aggressive fluid replacement is often necessary to improve oliguria associated with prerenal azotemia. Because the management of shock requires administering large volumes of fluid, maintaining urine output greatly facilitates patient management.


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Pediatrics_Nelson. Prevention of acute tubular necrosis and the subsequent complications associated with acute renal failure (hyperkalemia, acidosis, hypocalcemia, fluid overload) is important. The use of pharmacologic agents to augment urine output is indicated when the intravascular volume has been replaced. The use of loop diuretics, such as furosemide, or combinations of a loop diuretic and a thiazide agent may enhance urine output. Infusion of low-dose dopamine, which produces renal artery vasodilation, also may improve urine output. Nevertheless, if hyperkalemia, refractory acidosis, hypervolemia, or altered mental status associated with uremia occurs, dialysis or hemofiltration should be initiated.


Pediatrics_Nelson

Pediatrics_Nelson. Shock results in impairment of tissue perfusion and oxygenation and activation of inflammation and cytokine pathways. The major complication of shock is multiple organ system failure, defined as the dysfunction of more than one organ, including respiratory failure, renal failure, liver dysfunction, coagulation abnormalities, or cerebral dysfunction. Patients with shock and multiple organ failure have a higher mortality rate and, for survivors, a longer hospital stay. Early recognition and goal-directed intervention in patients with shock improve survival. However, delays in treatment of hypotension increase the incidence of multiple organ failure and mortality. Goal-directed therapy focused on maintaining mixed venous oxygen saturation may improve survival. *Primarily splanchnic and renal in low doses (3–5 mcg/kg/min). †Low dose (<0.3 mcg/kg/min).


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Pediatrics_Nelson. *Primarily splanchnic and renal in low doses (3–5 mcg/kg/min). †Low dose (<0.3 mcg/kg/min). Prevention strategies for shock are focused, for the most part, on shock associated with sepsis and hypovolemia. Some forms of septic shock can be prevented through use of immunizations (Haemophilus influenzae type b, meningococcal, pneumococcal vaccines). Decreasing the risk of sepsis in a critically ill patient requires adherence to strict hand washing, isolation practices, and minimizing the duration of indwelling catheters. Measures to decrease pediatric trauma do much to minimize hemorrhage-induced shock.


Pediatrics_Nelson

Pediatrics_Nelson. Unintentional injury is the leading cause of death in children 1 to 18 years of age. In 2010, approximately 52% of these deaths were caused by motor vehicle crashes. Most remaining unintentional injury-related deaths were the result of drowning (15%), poisoning (9%), burns (5%), and suffocation (4%). Geography, climate, population density (access to care), and population traits vary by region and affect the frequency, etiology, and severity of injuries. Injury occurs through interaction of the host (child) with the agent (e.g., car and driver) through a vector and an environment (e.g., roadways, weather) that is conducive to exposure. The age of the child may determine the exposure to various agents and environments. For example, most injuries in infants and toddlers occur in the home as the result of exposure to agents found there (water heaters, bathtubs, softbedding). Gender affects exposure to injury, with boys having a fatal injury rate greater than that of girls.


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Pediatrics_Nelson. The recognition that much of the morbidity and mortality are determined at the scene of an injury has stimulated the development of prevention measures. The Haddon matrix combines the epidemiologic components (host, agent, physical and social environments) with time factors (before, during, and after the event) to identify effective interventions focused on different aspects of the injury event. Primary strategies (preventing the event), secondary strategies (minimizing the severity of injury), and tertiary strategies (minimizing longterm impact) can be targeted for each epidemiologic component. Such strategies typically fall into one of three areas: education, enforcement, and environment (including engineering). Education is often the first strategy considered but requires behavioral change and actions on the part of people. Most educational strategies are not well evaluated.


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Pediatrics_Nelson. Education is often the first strategy considered but requires behavioral change and actions on the part of people. Most educational strategies are not well evaluated. Despite the reliance on an action by the individualsinvolved, some active strategies benefit from enforcement.Children wearing bicycle helmets experience a significantly lower incidence of traumatic brain injury and death. Enforcement of seatbelt laws increases seatbelt use and may decreaseinjuries. Automatic strategies require no action on the part ofthe population and often change the environment (speedbumps) or involve engineering (child-resistant pill bottles, air bags). Automatic strategies have more consistentlyresulted in a significant reduction in injuries. The most successful approaches to preventing injury have combined strategies (education, environmental changes, and engineering changes focused on the host, agent, and environment in all three time phases).


Pediatrics_Nelson

Pediatrics_Nelson. The general goal of prehospital trauma care is rapid assessment, support of the ABCs, immobilization, and transportation. Outcomes of patients with major or life-threatening trauma are significantly improved in a pediatric trauma center or in an adult center with pediatric trauma certification compared with level I or II adult trauma centers.


Pediatrics_Nelson

Pediatrics_Nelson. Once the injured child arrives at the emergency department, the trauma team must initiate an organized and synchronized response. The initial assessment of a seriously injured child should involve a systematic approach, including a primary survey, resuscitation, secondary survey, postresuscitation monitoring, and definitive care. The primary survey focuses on the ABCDEs of emergency care, as modified for trauma from the ABCs of cardiopulmonary resuscitation (see Chapter 38). The assessment of the airway and breathing components should include meticulous control of the cervical spine (especially if the patient has an altered mental status), evaluation for anatomic injuries that could impair air entry or gas exchange, and consideration of the likelihood of a full stomach (risk of aspiration pneumonia). Circulation can be assessed via observation (heart rate, skin color, mental status) and palpation (pulse quality, capillary refill, skin temperature) and restored (via two large


Pediatrics_Nelson

Pediatrics_Nelson. pneumonia). Circulation can be assessed via observation (heart rate, skin color, mental status) and palpation (pulse quality, capillary refill, skin temperature) and restored (via two large peripheral intravenous lines, when possible) while control of bleeding is accomplished through the use of direct pressure. Assessment for disabilities (D),including neurologic status, includes examination of pupil size and reactivity, a brief mental status assessment (AVPU—alert; responds to voice; responds to pain; unresponsive), and examination of extremity movement to assess for spinal cord injury. The Glasgow Coma Scale can direct decisions regarding the initiation of cerebral resuscitation in patients with suspected closed head injuries (Table 42-1). E, which stands for exposure,requires a full assessment of the patient by completely disrobing the child for a detailed examination of the entire body. The examiner should ensure a neutral thermal environment to prevent hypothermia.


Pediatrics_Nelson

Pediatrics_Nelson. On completion of the primary survey, a more detailed headto-toe examination (the secondary survey) should ensue along with efforts to obtain a more complete history. The purpose of this careful re-examination is to identify life-threatening and limb-threatening injuries as well as less serious injuries. Coincident with the secondary survey and depending, in part, on the assessed physiologic status of the patient, certain procedures and resuscitative measures are initiated. The prioritization of definitive care needs is determined by the injury findings collected from the primary and secondary surveys, the child’s physiologic response to resuscitation, and data from continuous monitoring. A tertiary survey, including repeat primary and secondary surveys along with review of laboratory tests and radiologic studies, should be performed within 24 hours. SEE CHAPTER 41.


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Pediatrics_Nelson. SEE CHAPTER 41. Screening laboratory studies during initial resuscitation often include the tests listed in Table 42-2. Radiographic studies are determined by the pattern of injuries. A head computed tomography (CT) scan should be obtained in patients with evidence of head trauma or a history of loss of consciousness. Patients with obvious injury to the thorax or abdomen or who have pulmonary or abdominal symptoms may benefit from a CT scan. The focused abdominal sonography for trauma is gaining popularity because of concerns about radiation exposure. Diagnostic peritoneal lavage has limited utility. A spiral Cervical spine films Anteroposterior chest radiograph Radiographs of all apparent fractures Computed tomography scans where indicated for head, chest, AST/ALT, Aspartate aminotransferase/alanine aminotransferase. enhanced CT scan should be performed if there is concern about aortic injuries.


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Pediatrics_Nelson. AST/ALT, Aspartate aminotransferase/alanine aminotransferase. enhanced CT scan should be performed if there is concern about aortic injuries. Head injuries and injuries to the limbs are the most common. Multiple organ involvement is also common, and penetrating trauma is becoming more frequent. After the initial evaluation and stabilization, the team focuses on the involved organ systems. SEE CHAPTER 184.


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Pediatrics_Nelson. SEE CHAPTER 184. Although spinal cord injury is not common in pediatric trauma patients, it is potentially devastating when it occurs. Cervical spine immobilization should be maintained until a spinal cord injury is ruled out. Cervical spine radiographs are not sufficient to rule out a spinal cord injury because the immature vertebral column in children may allow stretching of the cord or nerve roots with no radiologic abnormality (spinal cord injury without radiologic abnormality [SCIWORA]). SCIWORA may occur in a significant percentage of children with a spinal cord injury; when it is suspected, magnetic resonance imaging should be performed.


Pediatrics_Nelson

Pediatrics_Nelson. Thoracic injury is the second leading cause of trauma death. Pulmonary contusion, pneumothorax, and rib fractures occur most commonly, and patients may present without external signs of trauma. Patients with pulmonary parenchymal injury should receive supportive treatment to ensure adequate oxygenation and ventilation. Most pediatric blunt thoracic injuries can be managed without surgery. Injury to the heart and great vessels is rare but requires urgent diagnosis and treatment. Great vessel injury should be suspected if a widened mediastinum is seen on chest radiograph. Injury to the abdomen occurs in approximately 8% of pediatric trauma patients and is the third leading cause of trauma death. The relative size and closer proximity of intra-abdominal organs in children increase the risk of significant injury after blunt trauma. Penetrating trauma may result in a child who is asymptomatic or who presents in hypovolemic shock.