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901 | as important as the use of activated vitamin D. CALCIUM DEFICIENCY Pathophysiology Rickets secondary to inadequate dietary calcium is a significant problem in some countries in Africa, although there are cases in other regions of the world, including industrialized countries. Because breast milk and formula are excelle... |
902 | dren have diets high in cereal with negligible intake of cows milk, school based milk programs have been effective in reducing the prevalence of rickets. PHOSPHORUS DEFICIENCY Inadequate Intake With the exception of starvation or severe anorexia, it is almost impossible to have a diet that is deficient in phosphorus, b... |
903 | in patients with severe renal impairment. Conventional treatment is a combination of oral phosphorus and 1,25 D (calcitriol). The daily need for phosphorus supplementation is 1 3 g of elemental phosphorus divided into four or five doses. Frequent dosing helps to prevent prolonged decrements in serum phosphorus because ... |
904 | caused by pathologic variants in FAM20C and is an osteosclerotic bone dysplasia that is often fatal in the neonatal period. However, patients who survive into childhood may develop rickets. The three types of ARHR are associated with elevated levels of FGF 23, leading to renal phosphate wasting, hypophosphatemia, and l... |
905 | secrete FGF 23 and produce a biochemical phenotype similar to XLH, including urinary phosphate wasting, hypophosphatemia, ele vated ALP levels, and low or inappropriately normal 1,25 D levels (see Table 69.4). Curative treatment is excision of the tumor. If the tumor cannot be removed, treatment is identical to that fo... |
906 | all patients have low molecular weight pro teinuria and hypercalciuria. Other, less universal abnormalities are aminoaciduria, glycosuria, hypophosphatemia, and hypokalemia. Rickets occurs in approximately 25 of patients, and it responds to oral phosphorus supplements. Some patients also need 1,25 D, but this treatment... |
907 | because 1,25 D stimulates bone resorp tion. Serum levels of calcium are low, normal, or high, and patients often have hypercalciuria. Elevated serum calcium levels and hyper calciuria are secondary to increased intestinal absorption and bone dissolution caused by elevated 1,25 D levels and inability to deposit calcium ... |
908 | on ensuring adequate deliv ery of calcium, phosphorus, and vitamin D. If mineral delivery has been good and there is no evidence of healing, it is important to screen for vitamin D deficiency by measuring serum 25 D. Measurement of PTH, 1,25 D, and urinary calcium and phosphorus may be helpful in some cases. DISTAL REN... |
909 | 25 D. Anemia is sometimes present; the mechanism is unknown. Diagnosis and Differential Diagnosis The diagnosis is based on the presence of hypercalcemia and an ele vated serum 25 D level, although children with excess intake of 1,25 D or another synthetic vitamin D preparation have normal levels of 25 D. With careful ... |
910 | in chronic illnesses. PATHOGENESIS The term vitamin E denotes a group of 8 compounds with simi lar structures and antioxidant activity. The most potent member of these compounds is tocopherol, which is also the main form in humans. The best dietary sources of vitamin E are vegetable oils, seeds, nuts, green leafy veget... |
911 | (AVED), a rare auto somal recessive disorder, there are pathologic variants in TTPA, the gene for tocopherol transfer protein. Patients with this disorder are unable to incorporate vitamin E into lipoproteins before their release from the liver, leading to reduced serum levels of vitamin E. There is no associated fat m... |
912 | deficiency of vitamin K can result in clinically significant bleed ing. Vitamin K deficiency typically affects infants, who experience a transient deficiency related to inadequate intake, or patients of any age who have decreased vitamin K absorption. Mild vitamin K deficiency can affect long term bone and vascular hea... |
913 | In addition, there is high turnover of vitamin K, and the vitamin Kdependent clotting factors have a short half life. Thus symptomatic vitamin K deficiency can develop within weeks when there is inadequate supply because of low intake or malabsorption. There are three forms of vitamin K deficiency bleeding (VKDB) of th... |
914 | Older children with vitamin K deficiency can present with bruising, mucocutaneous bleeding, or more serious bleeding. Laboratory Findings In patients with bleeding as a result of vitamin K deficiency, the prothrombin time (PT) is prolonged. The PT must be interpreted based on the patients age because it is normally pro... |
915 | does not prevent a substantial number of cases of late VKDB. However, a single intramuscular (IM) injection of vitamin K (1 mg), the current practice in the United States, is almost universally effective, except in children with severe malab sorption. This increased efficacy of the IM form is thought to be the result o... |
916 | often have inadequate sources, leading to goiter and hypothyroidism. Iodine deficiency is not a problem in the United States because of the widespread use of iodized salt; however, symptomatic Chapter 72 Micronutrient Mineral Deficiencies Larry A. Greenbaum Table 72.1 Trace Elements ELEMENT PHYSIOLOGY EFFECTS OF DEFICI... |
917 | that facilitates intestinal copper absorption (see Chapters 639.5 and 703). These pathologic variants result in severe copper deficiency; subcutaneous copper is an effective treatment. Nutritional copper deficiency has been reported in children receiving unsupplemented parenteral nutrition and in children on a ketogeni... |
918 | muscle mass of males causes them to have a higher ICF volume than females. There is no significant difference in the ECF volume between postpubertal females and males. The ECF is further divided into the plasma water and the inter stitial fluid (see Fig. 73.2). The plasma water is 5 of body weight. The blood volume, gi... |
919 | of the intravascular volume. In chil dren with hypoalbuminemia, the decreased oncotic pressure of the intravascular fluid contributes to the development of edema. Loss of fluid from the intravascular space may compromise the intravas cular volume, placing the child at risk for inadequate blood flow to vital organs. Thi... |
920 | process is usually a change in the osmolality of the ECF, with resultant shift of water into the ICF if ECF osmolality decreases, or vice versa if ECF osmolality increases. The ECF osmolality can be determined and usually equals ICF osmolality. Plasma osmolality, normally 285 295 mOsmkg, is measured by the degree of fr... |
921 | osmolality and calculated osmolality are within 10 mOsmkg. However, there are some clinical situations in which this difference does not occur. The presence of unmeasured osmoles causes measured osmolality to be significantly elevated in comparison with the calculated osmolality. An osmolal gap is present when the diff... |
922 | results should not be used on an alternating basis when following critical trends (e.g., during correction of hypernatremia or hypona tremia; see Chapter 73.3). Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. 73.2 Regulation of Osmolality and Volume Larry A. Greenbaum The regulation of plasma osmo... |
923 | California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 488 Part VI u Fluid and Electrolyte Disorders the collecting duct, limiting the amount of water that can be excreted. The impairment in the GFR must ... |
924 | In some situations, Cl depletion is consid ered the dominant derangement causing volume depletion (metabolic alkalosis with volume depletion). The kidney determines sodium balance because there is little homeostatic control of sodium intake, even though salt craving does occasionally occur, typically in children with c... |
925 | significantly reduced GFR, the normal intrarenal mechanisms that regulate Na excretion malfunction, causing excessive renal reten tion of Na and volume overload. Renal retention of Na occurs during volume depletion, but this appropriate response causes the severe excess in total body Na that is present in heart failure... |
926 | it is the principal determinant of extracellular osmolality. Na is therefore necessary for the maintenance of intravascular volume. Less than 3 of Na is intracellular. More than 40 of total body Na is in bone; the remainder is in the interstitial and intravascular spaces. The low intracellular Na, approximately 10 mEqL... |
927 | administration. Moder ate or severe hypernatremia has significant morbidity because of the underlying disease, the effects of hypernatremia on the brain, and the risks of overly rapid correction. Table 73.1 Causes of Hypernatremia EXCESSIVE SODIUM Improperly mixed formula Excess sodium bicarbonate Ingestion of seawater... |
928 | often in a primiparous mother, can cause severe hypernatremic dehydration. Adipsia, the absence of thirst, is usually secondary to damage to the hypothalamus, such as from trauma, tumor, hydrocephalus, or histiocytosis. Primary adipsia (essential hypernatremia) is rare but is seen in children with central nervous syste... |
929 | and mild hypocalcemia; the mecha nisms are unknown. Beyond the sequelae of dehydration, there is no clear direct effect of hypernatremia on other organs or tissues, except the brain. Brain hemorrhage is the most devastating consequence of untreated hypernatremia. As the extracellular osmolality increases, water moves o... |
930 | on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 73 u Electrolyte and Acid Base Disorders 491 diabetes insipidus (see Chapters 570 and 596). A water deprivation test is unnecessary if the patient has simultaneous documentation of hype... |
931 | removal of excess Na and water, decreasing the risk of volume overload. With Na over load, hypernatremia is corrected with Na free intravenous (IV) fluid (D5W). Hyperglycemia from hypernatremia is not usually a problem and is not treated with insulin because the acute decrease in glucose may precipitate cerebral edema ... |
932 | to compensate for the volume depletion. The patient has a pathologic increase in fluid loss, and this fluid contains Na. Most fluid that is lost has a lower Na than that of plasma. Viral diarrhea fluid has an average Na of 50 mEqL. Replacing diarrhea fluid, which has Na of 50 mEqL, with formula, which has only approxim... |
933 | of urinary tract obstruction and dur ing the polyuric phase of acute tubular necrosis. Transient tubu lar damage in these conditions further impairs Na conservation. The serum Na in these conditions depends on Na of the fluid used to replace the losses. Hyponatremia develops when the fluid is hypotonic relative to the ... |
934 | nephritis Obstructive uropathy Cerebral salt wasting Proximal (type II) renal tubular acidosis (OMIM 604278) Lack of aldosterone effect (high serum potassium): Absence of aldosterone (e.g., 21 hydroxylase deficiency OMIM 201910) Pseudohypoaldosteronism type I (OMIM 264350177735) Urinary tract obstruction andor infectio... |
935 | SIADH typically occurs with disorders of the CNS (infection, hemorrhage, trauma, tumor, thrombosis, Guillain Barr syndrome), but lung disease (infection, asthma, positive pressure ventilation) and malignant tumors (producing ADH) are other potential causes. A variety of medications may cause SIADH, including recreation... |
936 | on beer, a poor source of Na and protein, causes hyponatremia because of the inability to excrete the high water load (beer potomania). Exercise induced hyponatremia, reported frequently during mar athons, is caused by excessive water intake, salt losses from sweat, and secretion of ADH. The pathogenesis of the hyponat... |
937 | caveat that SIADH is much more likely. Liver disease, nephrotic syndrome, kidney failure, or congestive heart failure may be Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission... |
938 | used but low after the diuretic effect is gone. This becomes an issue only when diuretic use is surreptitious. The urine Na is not useful if a metabolic alkalosis is present; the urine Cl must be used instead (see Chap ter 73.7). Differentiating among the nonrenal causes of hypovolemic hypona tremia is usually facilita... |
939 | edema. Each mLkg of 3 NaCl increases the serum Na by approximately 1 mEqL. A child with active symptoms often improves after receiving 4 6 mLkg of 3 NaCl. The child with hypovolemic hyponatremia has a deficiency in Na and may have a deficiency in water. The cornerstone of therapy is to replace the Na deficit and any wa... |
940 | Subsequent management is dictated by the patients volume status. The hypovolemic child should receive isotonic IV fluids. The child with nonphysiologic stimuli for ADH production should undergo fluid restriction. Prevention of this iatrogenic complication requires judi cious use of IV fluids (see Chapter 74). Specific ... |
941 | net movement of K out of the ICS. An increase in plasma osmolality, as with mannitol infusion, leads to water movement out of the cells, and K follows as a result of solvent drag. The serum K increases by approximately 0.6 mEqL with each 10 mOsm rise in plasma osmolality. The high intracellular concentration of K, the ... |
942 | the cortical collecting duct. Glucocorticoids, ADH, a high urinary flow rate, and high Na deliv ery to the distal nephron also increase urinary K excretion. Insu lin, catecholamines, and urinary ammonia decrease K excretion. Whereas ADH increases K secretion, it also causes water resorp tion, decreasing urinary flow. T... |
943 | patient who is receiving large quantities of IV or oral K for excessive losses that are no longer present. Frequent or rapid blood transfusions can acutely increase the K because of the K content of blood, which is variably elevated. Increased intake may precipitate hyperkalemia if there is an underlying defect in K ex... |
944 | Nonsteroidal antiinflammatory drugs Trimethoprim Heparin Drospirenone (in some oral contraceptives) OMIM, database number from the Online Mendelian Inheritance in Man (http:www.n cbi.nlm.nih.govomim). Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevie... |
945 | tubular dysfunction, with an impaired ability to excrete K, occurs in a number of conditions. These disorders, all characterized by tubulointerstitial disease, are often associated with impaired acid secretion and a secondary metabolic acidosis. In some affected children, the metabolic acidosis is the dominant feature,... |
946 | second measurement should be performed on a plasma sample that is evaluated promptly. The history should initially focus on potassium intake, risk factors for transcellular shifts of K, medications that cause hyperkalemia, and signs of renal insufficiency, such as oliguria and edema. Initial laboratory evaluation shoul... |
947 | may cause arrhythmias. Bicarbonate causes potassium to move intracellularly, lowering the plasma K; it is most efficacious in a patient with a metabolic acidosis. Insulin causes K to move intracellularly but must be given with glucose to avoid hypoglycemia. The combination of insulin and glucose works within 30 minutes... |
948 | the intracellular K. Alkalemia is one of the more com mon causes of a transcellular shift. The effect is much greater with a metabolic alkalosis than with a respiratory alkalosis. The impact of exogenous insulin on K movement into the cells is substantial in patients with DKA. Endogenous insulin may be the cause when a... |
949 | increased aldosterone, which increases urinary K and acid losses, contributing to the hypokalemia and the metabolic alkalosis. Other mechanisms often contribute to both the K losses and the metabolic alkalosis. With emesis or nasogastric suction, there is gastric loss of K, but this is minimal given the low K content o... |
950 | Man (http:www.ncbi.nlm.nih.govomim). Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 500 Part VI u Fluid and Electrolyte... |
951 | function variant in CLCN2 that causes increased aldosterone synthesis. Familial hyper aldosteronism type III, an autosomal dominant disorder, is due to a gain of function variant in KCNJ5 that causes a dramatic increase in aldosterone synthesis and severe hypertension and hypokalemia. Familial hyperaldosteronism type I... |
952 | as supraventricular tachycardia, ventricular tachycardia, and heart block (see Chapter 484). The clinical consequences of hypokalemia in skeletal muscle include muscle weakness and cramps. Paralysis is a possible complication, gen erally only at K 2.5 mEqL. It usually starts in the legs and moves to the arms. Respirato... |
953 | may be shifts of K from the ICS to the plasma. Clinically, such shifts occur most often with metabolic acidosis and the insulin deficiency of DKA; the plasma K measurement underestimates the degree of total body K depletion. When these problems are corrected, K moves into the ICS, so more K supplementation is required ... |
954 | children and adults. Only 1 of body magnesium is extracellular (60 ionized, 15 complexed, 25 protein bound). In the United States, serum magnesium is reported as mgdL (Table 73.6). Values in the left column unit are converted into the right column unit by multiplying the conversion factor (e.g., calcium of 10 mgdL 0.25... |
955 | PA I, pseudohyperaldosteronism type I; PA II, pseudohyperaldosteronism type II; PRA, plasma renin activity; TTKG, transtubular potassium gradient. (From Shoemaker LR, Eaton BV, Buchino JJ. A three year old with persistent hypokalemia. J Pediatr. 2007;1516:696699.) Magnesium is a necessary cofactor for hundreds of enzym... |
956 | a transient receptor potential cation channel. The patients have seizures, tetany, tremor, or restlessness at 2 8 weeks of life because of severe hypomagnesemia (0.2 0.8 mgdL) and secondary hypocalcemia. Renal losses may occur because of medications that are direct tubu lar toxins. Amphotericin frequently causes signif... |
957 | does not occur in hypercalcemia caused by familial hypercalcemic hypocalciuria or lithium. A number of rare genetic diseases cause renal magnesium loss. Gitelman and Bartter syndromes, both autosomal recessive disor ders, are the most common entities (see Chapter 571). Gitelman syndrome, caused by a defect in the thiaz... |
958 | mild. A pathogenic variant in a mitochondrially encoded transfer RNA is associated with hypomagnesemia, hypertension, and hypercho lesterolemia. Hypomagnesemia is occasionally present in children with other mitochondrial disorders. Poor intake is an unusual cause of hypomagnesemia, although it can be seen in children w... |
959 | change according to the serum magnesium concentration. The FEMg ranges from 18 in children with normal magnesium levels. In the patient with hypomag nesemia as a result of extrarenal causes, FEMg should be low because of renal conservation, typically 2. The FEMg is inappropriately elevated in the setting of renal magne... |
960 | reduced GFR. Most pediatric cases not related to maternal hypermagnesemia occur in infants because of excessive use of antacids or laxatives. Mild hypermagnesemia may occur in chronic kidney disease, familial hypocalciuric hypercalcemia, DKA, lithium ingestion, milk alkali syndrome, and tumor lysis syndrome. The hyperm... |
961 | 15, is protein bound. The remainder can be filtered by the glomeru lus, with most existing as free phosphate and a small percentage com plexed with calcium, magnesium, or sodium. Phosphate is the most plentiful intracellular anion, although the majority is part of a larger compound (ATP). More than that of any other el... |
962 | dent of regulatory hormones. Fibroblast growth factor 23 (FGF 23) inhibits renal resorption of phosphorus in the proximal tubule, and its level increases in the setting of hyperphosphatemia. FGF 23 also inhibits synthesis of 1,25 vitamin D in the kidney by decreasing 1 hydroxylase activity. Secreted in response to a lo... |
963 | Glycosuria Glucocorticoids Chemotherapy (cisplatin, ifosfamide) Kidney transplantation MULTIFACTORIAL Vitamin D deficiency Vitamin Ddependent rickets type 1 (OMIM 264700) Vitamin Ddependent rickets type 2 (OMIM 277440) Alcoholism Sepsis Dialysis These are primary genetic causes of Fanconi syndrome. Fanconi syndrome may... |
964 | This process can cause phosphorus deficiency and rickets in growing children. A similar mechanism causes hypo phosphatemia in patients who are overtreated for hyperphosphate mia with phosphorus binders. In children with kidney failure, the addition of dialysis to phosphorus binders increases the risk of iat rogenic hyp... |
965 | renal phosphorus loss is further increased by the osmotic diuresis. With correction of the metabolic acidosis and the adminis tration of insulin, both of which cause a transcellular movement of phosphorus into the cells, there is a marked decrease in the plasma phosphorus level. Volume expansion from any cause, such as... |
966 | paresthesia, ataxia, seizures, delirium, and coma. Diagnosis The history and basic laboratory evaluation often suggest the etiol ogy of hypophosphatemia. The history should investigate nutrition, medications, and familial disease. Hypophosphatemia and rickets in an otherwise healthy young child suggest a genetic defect... |
967 | are hyperuricemia and hypocalcemia, whereas indirect hyperbilirubinemia and elevated lactate dehydroge nase (LDH) values are often present with hemolysis. An elevated CPK level is suggestive of rhabdomyolysis. During lactic acidosis or DKA, use of phosphorus by cells decreases, and phosphorus shifts into the ECS. This ... |
968 | hypocalcemia and systemic calcification. The hypocalcemia is probably caused by tissue deposition of calcium phosphorus salt, inhibition of 1,25 D production, and decreased bone resorption. Symptomatic hypocalcemia is most likely to occur when the phos phorus level increases rapidly or when diseases predisposing to hyp... |
969 | Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. 73.7 Acid Base Balance Larry A. Greenbaum ACID BASE PHYSIOLOGY Terminology 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... |
970 | Buffers The bicarbonate and nonbicarbonate buffers protect the body against major changes in pH. The bicarbonate buffer system is routinely monitored clinically and is based on the relationship between carbon dioxide (CO2) and bicarbonate (HCO3 ): CO2 H2OH HCO3 CO2 acts as an acid in that, after combining with water, i... |
971 | is approximately 6.5. This is close enough to a normal pH (7.4) to make histidine an effective buffer. Hemoglobin and albumin have 34 and 16 histidine molecules, respectively. Phosphate can bind up to three hydrogen molecules, so it can exist as PO4 3, HPO4 2, H2PO4 1, or H3PO4. However, at a physiologic pH, most phosp... |
972 | baseline incomplete metabolism that contributes to endogenous acid production. This factor increases in pathologic conditions, such as lactic acidosis and diabetic ketoacidosis (DKA). Stool loss of bicarbonate is the third major source of endogenous acid produc tion. The stomach secretes H, but most of the remainder of... |
973 | 85 of the fil tered bicarbonate (Fig. 73.8). The final 15 is reclaimed beyond the proximal tubule, mostly in the ascending limb of the loop of Henle. Bicarbonate molecules are not transported from the tubular fluid into the cells of the proximal tubule. Rather, hydrogen ions are secreted into the tubular fluid, leading... |
974 | with filtered bicarbonate to generate carbonic acid. CO2 and water are produced from carbonic acid (H2CO3). This reaction is catalyzed by luminal carbonic anhydrase (3). CO2 diffuses into the cell and combines with OH ions to gener ate bicarbonate. This reaction is catalyzed by an intracellular carbonic anhydrase (4). ... |
975 | of glutamine through the fol lowing reactions: GlutamineNH4 glutamate Glutamate NH4 ketoglutarate3 The metabolism of glutamine generates two ammonium ions. In addition, the metabolism of ketoglutarate generates two bicarbon ate molecules. The ammonium ions are secreted into the lumen of the proximal tubule, whereas the... |
976 | This response to a low serum pH reaches its maxi mum within 5 6 days; ammonia excretion can increase approximately 10 fold over the baseline value. Acid excretion by the collecting duct increases in a number of differ ent clinical situations. The extracellular pH is the most important regu lator of renal acid excretion... |
977 | increase in H, and an alkalosis is a pathologic process that causes a decrease in H. Whereas acidemia is always accompanied by an aci dosis, a patient can have an acidosis and a low, normal, or high pH. For example, a patient may have a mild metabolic acidosis but a simul taneous, severe respiratory alkalosis; the net ... |
978 | 23 2; see Table 73.11). If the patients CO2 is 25 mm Hg, a concurrent respira tory acidosis is present; CO2 is higher than expected. A patient may have a respiratory acidosis despite a CO2 level below the nor mal value of 35 45 mm Hg. In this example, CO2 21 mm Hg indicates a concurrent respiratory alkalosis; CO2 is lo... |
979 | other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 514 Part VI u Fluid and Electrolyte Disorders diagnosed in the second step, and the expected compensation is cal culated (see Table 73.11). If the compensation is appropriate, a simple acid base disorder is present. If the compensation is... |
980 | a low HCO3 occurs only if some degree of respiratory alkalosis is present. In this situation, distinguishing an isolated chronic respiratory alkalosis from a mixed metabolic acidosis and acute respiratory alkalosis may be possible only clinically. In contrast, the combination of a low serum pH and a low HCO3 occurs onl... |
981 | Acid Base Disorders 515 to thrive because of chronic metabolic acidosis is the most common presenting complaint. Patients with distal RTA cannot acidify their urine and thus have a urine pH 5.5 despite a metabolic acidosis. Proximal RTA is rarely present in isolation. In most patients, proximal RTA is part of Fanconi s... |
982 | of a metabolic acidosis. This resolves over 1 2 days through increased acid excretion by the kidneys. Lactic acidosis (l lactic) typically occurs when inadequate oxy gen delivery to the tissues leads to anaerobic metabolism and excess production of lactic acid. Lactic acidosis may be secondary to shock, severe anemia, ... |
983 | insulin leads to hyperglycemia and DKA (see Chapter 629). Production of acetoacetic acid and hydroxybutyric acid causes the metabolic acidosis. Admin istration of insulin corrects the underlying metabolic problem and permits conversion of acetoacetate and hydroxybutyrate into bicar bonate, which helps correct the metab... |
984 | cause a metabolic acidosis (see Chapters 104 107). The metabolic acidosis may be the result of exces sive production of ketoacids, lactic acid, and other organic anions. Some patients have accompanying hypoglycemia or hyperammone mia. In most patients, the acidosis occurs episodically during acute decompensations, whic... |
985 | and ketonuria support a diagnosis of DKA. Starvation causes ketosis, but the metabolic acidosis, if present, is usually mild (HCO3 18 mEqL). Most children with ketosis from poor intake and meta bolic acidosis have a concomitant disorder, such as gastroenteritis with diarrhea, that explains the metabolic acidosis. Alter... |
986 | observed albumin) The number of serum anions must equal the number of serum cat ions to maintain electrical neutrality (Fig. 73.11). The anion gap is the difference between the measured cation (Na) and the measured anions (Cl bicarbonate). The anion gap is also the difference between the unmeasured cations (K, magnesiu... |
987 | anion gap, and other variables, the presence of a normal or an increased anion gap is not always reliable in differentiating among the causes of a meta bolic acidosis, especially when the metabolic acidosis is mild. In some patients, there is more than one explanation for the metabolic acidosis, such as the child with ... |
988 | the generation of CO2, which can accumulate in patients with respiratory failure. Because CO2 readily diffuses into cells, the administration of bicarbonate can lower the intracellular pH, potentially worsening cell function. Base therapy is usually reserved for children with severe acute lactic acidosis and severe DKA... |
989 | also leads to a com pensatory elevation of the serum HCO3 . With a simple metabolic alkalosis, however, the pH is elevated; alkalemia is present. Patients with a respiratory acidosis are acidemic. Decreasing ventilation causes appropriate respiratory compensation for a metabolic alkalosis. Pco2 increases by 7 mm Hg for... |
990 | Acid Base Disorders 519 Emesis or nasogastric suction results in loss of gastric fluid, which has a high content of HCl. Generation of H by the gastric mucosa causes simultaneous release of bicarbonate into the bloodstream. Nor mally, the hydrogen ions in gastric fluid are reclaimed in the small intestine (by neutraliz... |
991 | compensatory mechanisms that cause and maintain a metabolic alkalosis. Many of these patients have a decreased effective intravascular volume before they begin diuretic therapy, increasing the likelihood of diuretic induced met abolic alkalosis. Diuretic use increases chloride excretion in the urine. Conse quently, whi... |
992 | hyper tension. Metabolic alkalosis and hypokalemia result from aldosterone mediated renal excretion of H and K. The urinary Cl level is not low because these patients are volume overloaded, not volume depleted. The volume expansion and hypertension allow normal excretion of Na and Cl despite the presence of aldosterone... |
993 | Cl, metabolic alkalosis, and hypokalemia (see Chapter 571). In Bart ter syndrome, patients have a defect in Na and Cl resorption in the loop of Henle. This leads to excessive urinary losses of Na and Cl, and as in patients receiving loop diuretics, volume deple tion and secondary hyperaldosteronism occur, causing hypok... |
994 | disease and associated electrolyte disturbances. Children with Cl responsive causes of metabolic alkalosis often have symptoms related to volume depletion, such as thirst and lethargy. In contrast, children with Cl unresponsive causes may have symptoms related to hypertension. Alkalemia causes potassium to shift into t... |
995 | abusing diuretics. The Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 73 u Electrolyte and Acid Base Disorders ... |
996 | gastric PPI reduces gastric secretion and losses of HCl. Diuretics are an important cause of meta bolic alkalosis, and if a change is tolerated, they should be eliminated or the dose reduced. Adequate potassium supplementation or the addition of a potassium sparing diuretic is also helpful in a child with a metabolic a... |
997 | (Pco2). CO2 is a by product of metabolism and is removed from the body by the lungs. During a respiratory acidosis, the effective ness of CO2 removal by the lungs is decreased. A respiratory acidosis is secondary to either pulmonary disease, such as severe bronchiolitis, or nonpulmonary disease, such as a narcotic over... |
998 | The patient is alkalemic; this is not a respiratory acidosis. During a mixed disturbance, a patient can have a respiratory acidosis and a normal or even low Pco2. This condi tion may occur in a patient with a metabolic acidosis. A respiratory acidosis is present if the patient does not have appropriate respiratory comp... |
999 | CNS depression and patients who are on the verge of complete respiratory failure secondary to fatigue of the respiratory muscles. The symptoms of respiratory acidosis are related to the severity of the hypercarbia. Acute respiratory acidosis is usually more symptom atic than chronic respiratory acidosis. Symptoms are a... |
1,000 | is unlikely to respond quickly to therapy. In addition, hypercarbia causes cerebral vasodilation, and the increase in ICP can be dangerous in a child with an underlying CNS disease. Readily reversible CNS depression, as from a narcotic overdose, may not require mechanical ventilation. Decisions on mechanical ventilatio... |
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