- Email: [email protected]
Hypernatremic Dehydration
HYPERNATREMIC DEHYDRATION HAROLD E. HARRISON, M.D. LAURENCE FINBERG, M.D.
Early recognition of the hypernatremic* state is of great importance in the treatment of this problem, since delay in treatment may lead to an irreversible state resulting in either death or severe brain damage with permanent sequelae. Knowledge of the factors which may predispose to hypernatremic dehydration is of value in the diagnosis, and, perhaps of even more importance, can lead to recommendations for the prevention of this disturbance. PREDISPOSING FACTORS IN GENESIS OF HYPERNATREMIC DEHYDRATION Early Infancy and Prematurity
The relatively large evaporative water losses per kilogram of body weight of this group of infants, and the inefficiency of renal conservation of water due to renal immaturity, explain their susceptibility to hypernatremia. 7 Interference with Oral Intake of Water
This may occur as a result of the anorexia or nausea and vomiting of acute infections. Reduced intake may also be due to neglect of water administration to infants. A special group of hypernatremic patients is accounted for almost solely by this mechanism, namely, those with cerebral defect who either have insufficient access to water or whose From the Pediatric Division, Baltimore City Hospital, and the Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland. " We -have classified patients as hypematremic if serum sodium concentrations are 150 mEq. per- liter or higher.
193
194
HYPERNATREMIC DEHYDRATION
cerebral impairment leads to a lack of thirst response in the presence of the usual stimuli.10 Clinically these patients have to be distinguished from those whose brain damage is secondary to hypernatremic dehydration. At times this distinction may be difficult. Excessive Losses of Electrolyte-Free Water because of Increased Evaporative Water Loss through Skin and Lungs
This is seen in febrile states, environmental heat stress, and in salicylism and other causes of hyperventilation.8 Profuse sweating may also contribute, since normal sweat has a concentration of sodium only 10 to 35 per cent that of extracellular water. Excessive Losses of Water in Stools
The concentration of sodium in the water of normal stools and often in diarrheal stools is considerably less than that in extracellular fluid. 9 However, there is great variation in the concentration of sodium in the water of diarrheal stools, and we have not been able to demonstrate any good correlation between the concentration of sodium in stool water and the development of hypernatremia. This factor, then, appears highly variable in etiologic significance, since no significant difference can be found between the concentrations of sodium in stool water of hypernatremic patients and normonatremic patients who have a similar degree of water loss due to diarrhea. Probably the volume of water lost in the stools is the important factor. Excessive Administration of Solute (Electrolyte and/or Protein) to Sick Infantsl
An infant who is being subjected to a dehydrating influence, be it diarrheal disease, anorexia or fever, has a smaller margin of safety for water conservation. The intake of high protein and electrolyte feedings, or large volumes of saline solutions, orally or parenterally, increase the renal water requirement obligatory for excretion of excess electrolyte and urea. This water may have been easily spared in health, but its loss now serves to increase water deficit. The feeding of undiluted and unmodified cow's milk to a two-month-old infant is an example of a high solute load which is easily tolerated by a well infant, but may cause water deficit in a sick infant.1 In infants with diarrhea the total quantity of sodium intake is important as well as the concentration of sodium in the solution. Even though a fairly dilute electrolyte solution (50 mEq. per liter of sodium) is given orally to infants with diarrhea, hypernatremia may result if it is given in unphysiologically large quantities. 1 Such patients have been noted to produce copious watery stools which
HAROLD E. HARRISON, LAURENCE FINBERG
195
are apparently very dilute in sodium. Only a few actual measurements are available on these infants, but no other explanation is at hand except that of large losses of water in the stool. Salt Poisoning, Either Inadvertently by Addition of Salt to Feedings, or Iatrogenically by Injudicious Therapy, so that Excessive Amounts of Sodium Salts Are Given to Dehydrated Infants 3 , 4, 9
Excessive intake of salt produces an increased body sodium content, and because of attendant anorexia or vomiting plus the usual evaporative water losses there may be dehydration as well. Excessive Renal Water Loss as in Diabetes Insipidus and "Nephrogenic" Diabetes Insipidus
Any interference with the necessary large water intake of these patients quickly leads to hypernatremic dehydration. PHYSIOLOGY AND PATHOLOGY OF HYPERNATREMIA
Hypernatremia can be associated with an increased total sodium content of the extracellular fluid as in patients given excessive amounts of salt. In subjects with severe water deficit, however, total extracellular sodium is reduced despite high concentrations of sodium because of reduction of extracellular fluid volume. All patients with hypernatremia show certain manifestations which are thought to be the result of intracellular dehydration secondary to the increased osmotic concentration of extracellular water. During experimental hypematremia the muscle cells take up sodium, as well as lose water. In addition they reach osmotic equilibrium by apparent dissociation of intracellular complex particles into smaller units. This latter reaction appears to occur to a much greater extent in brain cells, where little or no sodium enters.5 This special behavior of brain cells possibly accounts for the severe functional central nervous system changes seen in hypematremia.
Intracranial bleeding occurs at times in hypernatremic patients and also in animals made acutely hypernatremic. This is apparently the result of injury or rupture of capillaries and venules secondary to reduction in cerebrospinal fluid pressure. 3 , 5, 6 Subdural effusions have also been encountered. 3 These phenomena are probably not responsible for the common symptoms and signs of this disorder, but may in occasional instances cause death or severe residual damage. 3 , 4,5,9 The composition of the extracellular fluid may show other derangements because of the underlying disease, and such secondary phenomena as metabolic acidosis and the biochemical changes of renal insufficiency are seen in addition to the effects of the hypernatremia itself. The most
196
HYPERNATREMIC DEHYDRATION
important of the biochemical disorders secondary to hypernatremia are changes in concentration of potassium and calcium. Potassium deficits are often large in these patients because of losses in gastrointestinal secretions and in the urine. At times the serum potassium concentration will be low in the face of evidences of renal insufficiency;4 this phenomenon may represent an extrarenal adjustment to hypernatremia as well as being a reflection of a reduced body potassium content. If renal impairment persists, serum potassium levels, of course, will rise. Serum calcium levels are frequently reduced in hypernatremic patients. The equilibrium of this ion is affected by multiple factors, but it seems probable from studies in patients and experimental animals that the calcium level is in some way altered by hypernatremia, particularly if associated with potassium deficiency.s.4 In addition, acute renal insufficiency leads to phosphate retention, which may playa contributing role. The metabolic acidosis present in some patients may protect against overt tetany, but when the acidosis is corrected before correcting the hypernatremia, hypocalcemic tetany may occur, as may occasionally be true in untreated hypernatremic dehydration if acidosis is minimal or absent. CLINICAL RECOGNITION OF HYPERNATREMIC STATES
This topic is of paramount importance in any discussion of therapy, since in many situations there is a considerable time lag in obtaining chemical data from the laboratory. The condition can be deceptive because the dehydration, though marked, may seem inapparent to one looking for signs of classic dehydration. The first step toward recognition of hypernatremic dehydration begins with the history of the etiologically disposing factors discussed above. An objective criterion is loss of 10 to 15 per cent of the body weight without the signs of classic dehydration such as loss of skin elasticity and turgor, or circulatory impairment. The hypernatremic patient may have lost 10 per cent of his body weight without evidence of circulatory embarrassment and look deceptively well for a time. These infants are often extremely thirsty, and this is one of the reasons why excessively large intakes of sodium may result if they are given electrolyte solutions ad lib. As they become sicker, however, nausea and vomiting limit the fluid intake. Fever is commonly associated with hypernatremia, so that it may be both a predisposing factor and a manifestation of this state. The presence of signs and symptoms referable to the nervous system has been most important in the diagnosis. Disturbances in consciousness ranging from lethargy to coma have been common. Hyperirritability to stimuli despite extreme lethargy when undisturbed has been characteristic. Other signs such as tremors, exaggerated deep tendon reflexes and
HAROLD E. HARRISON, LAURENCE FINBERG
197
muscle rigidity, including nuchal rigidity, have been common, and occasionally convulsions are seen. The concentration of protein in the cerebrospinal fluid is usually elevated.5 Hypernatremic dehydration when extreme may also be accompanied by reduction in extracellular fluid volume, with the associated circulatory disturbances. Such a "mixed" clinical picture is difficult or impossible to diagnose by clinical criteria alone, and in such instances the laboratory remains the sine qua non of diagnosis. However, this latter type of patient has a greater sodium deficit than the group previously described, so that administration of solutions with the usual concentrations of sodium salts given to dehydrated patients would not be so harmful as in the more common form of hypernatremia. TREATMENT
The goal of treatment is not the rapid restoration of serum sodium levels to normal, but rather the safe return of the patient to optimum physiologic balance without undue risk of complications. Experience in the treatment of hypernatremic subjects has indicated that administration of water rapidly in large quantities in an effort to bring the sodium concentration into the normal range is dangerous. Such an approach may precipitate a severe convulsive state. It has been pointed out that certain adjustments of brain cells to the increased extracellular sodium concentration have occurred, and rapid reduction of extracellular sodium evidently precipitates another disturbance of equilibrium. Since these patients are usually not in circulatory collapse, the pressure for rapid replacement of fluid volume is removed, and the rehydration process may safely be carried out gradually. It is important, however, that fluid administration be started promptly when the diagnosis is suspected and that it be continued at the proper rate. The composition of the fluid to be administered should, of course, be hypotonic with respect to sodium and chloride. Theoretically, it might be possible to eliminate these ions completely and give electrolytefree glucose water. This has two drawbacks: first, many patients do have some extracellular electrolyte deficits, and, secondly, the addition of some sodium makes slightly more rapid administration of fluids possible and safe. Concentrations of sodium above 40 mEq. per liter have been found to be excessive for these patients. Current information suggests that sodium concentrations of 15 to 20 mEq. are the most suitable. Since most patients have a greater deficit of sodium than of chloride (metabolic acidosis), it is customary in our clinic to use 1 part of sixthmolar sodium lactate to 2 parts of 0.85 per cent saline solution in preparing the sodium-containing portion of the solution. The desired concentration indicated above may be reached by combining 1 part of sixth-
198
HYPERNATREMIC DEHYDRATION
molar sodium lactate, 2 parts of 0.85 per cent sodium chloride and 21 parts of 5 per cent glucose in water. If the acidosis is severe (indicated by carbon dioxide contents of less than 8 mEq. per liter), sixth-molar sodium lactate may be used in place of the saline, and thus 3 parts of sixth-molar sodium lactate and 21 parts of 5 per cent glucose in distilled water are given. (Final concentration of sodium lactate is M/48.) Solutions such as these should be given intravenously. The rate of administration to an infant should be such that 200 ml. per kilogram are given during the first 24 hours (0.14 ml. per kilogram per minute). This provides for the deficit of water of about 10 to 15 per cent of the body weight as well as for the continued water requirements of 70 to 100 ml. per kilogram per day for infants. Fluid therapy for the second and subsequent days can be reassessed daily. If tolerated, glucose water may be given orally together with the appropriate electrolyte by the end of 12 to 24 hours or even earlier in milder cases. Although potassium deficits may be severe, it is wise to withhold administration of potassium initially, since many of these patients are oliguric or temporarily anuric. Once it is apparent that urinary output is adequate, potassium replacement should be started. The oral route is preferable when feasible, and 3 to 5 mEq. per kilogram per day are advised initially (10 per cent potassium citrate solution provides 1 mEq. of potassium per milliliter and can be given orally diluted with fruit juice or other fluid). If the parenteral route is necessary, the usual precautions for parenteral potassium administration should be carefully followed. The concentration of potassium chloride in the solution given intravenously should not exceed 20 mEq. per liter (0.15 per cent potassium chloride). A daily weight is important in assessing the previous day's fluid replacement. It is common for these patients to show evidences of overexpanded extracellular fluid with visible edema even before they are completely rehydrated because of the lag in intracellular uptake of water. Part of the therapy should be directed to controlling nervous system complications. Should convulsions occur, the usual anticonvulsant drugs are indicated. We have used subcutaneous phenobarbital sodium and rectal paraldehyde as agents which seem particularly safe in infants. The dose of phenobarbital sodium used is 5 mg. per kilogram repeated once in 20 minutes if necessary. Subsequent maintenance phenobarbital therapy is continued as in any acute convulsive state. When paraldehyde is required to control convulsions, 2 to 4 ml. are given rectally with an equal volume of cottonseed oil. If instilled through a small catheter and the buttocks taped tightly together with adhesive, the paraldehyde is usually retained. It is disconcerting to have nervous system manifestations develop while the patient is receiving therapy, but present knowledge indicates that this occurrence may be inevitable after a certain
r HAROLD E. HARRISON, LAURENCE FINBERG
199
amount of damage has occurred during the hypernatremic phase. Thus some nervous system damage may be irreversible before convulsions occur. Subdural effusions may be suspected and diagnosed by needle aspiration. Our experience to date has not shown any improvement in these patients from paracentesis or surgical drainage of subdural effusions over simple expectant watching. It would seem wise, until better criteria are established, to regard and assess each case individually. Intracranial bleeding may occur in several different sites, and here again individual consideration of treatment is indicated. Hypocalcemia may be averted or treated when present by the administration of 10 to 30 cc. of 10 per cent calcium gluconate per day in the intravenous fluids. In summary, the treatment of hypernatremic dehydration consists in administering an appropriate fluid volume of low (15 to 20 mEq. per liter) sodium concentration at a slow rate until water deficit is overcome. At the same time attention should be paid to needs for potassium and calcium. Meanwhile the nervous system complications must be managed symptomatically. In rare instances aspiration of subdural effusion or hematoma may be indicated. REFERENCES
1. Colle, E., Ayoub, E., and Raile, R.: Hypertonic Dehydration (Hypernatremia): The Role of Feedings High in Solutes. Pediatrics, 22:5,1958. 2. Finberg, L.: Experimental Studies of the Mechanisms Producing Hypocalcemia in Hypernatremic States. ,. Clin. Investigation, 36:434, 1957. 3. Idem: The Pathogenesis of the Nervous System Lesion in Hypernatremic States. I. Clinical Observations of Infants. Pediatrics, in press. 4. Finberg, L., and Harrison, H. E.: Hypernatremia in Infants. Pediatrics, 16:1, 1955. 5. Finberg, L., Luttrell, C., and Redd, H.: Pathogenesis of Lesions in the Nervous System in Hypernatremic States. II. Experimental Studies of Gross Anatomic Changes and Alterations of Chemical Composition of the Tissues. Pediatrics, in press. 6. Girard, F.: Les hematomes sous-duraux. Etude experimentale. Acta paediat., 45: 618, 1956. 7. Pratt, E. L., and Snyderman, S. E.: Renal Water Requirements of Infants Fed Evaporated Milk with and without Added Carbohydrate. Pediatrics, 11 :65, 1953. 8. Rapoport, S.: The Role of Overventilation in Diseases of Infancy. Ann. paediat., 176:137,1951. 9. Weil, W. B., and Wallace, W. M.: Hypertonic Dehydration in Infancy. Pediatrics, 17: 171, 1956. 10. Welt, L. G., Seldin, D. W., Nelson, W. P., III, German, W. J., and Peters, J. P.: Role of Central Nervous System in Metabolism of Electrolytes and Water. Arch. Int. Med., 90:355, 1952. 4940 Eastern Avenue Baltimore 24, Maryland
Early recognition of the hypernatremic* state is of great importance in the treatment of this problem, since delay in treatment may lead to an irreversible state resulting in either death or severe brain damage with permanent sequelae. Knowledge of the factors which may predispose to hypernatremic dehydration is of value in the diagnosis, and, perhaps of even more importance, can lead to recommendations for the prevention of this disturbance. PREDISPOSING FACTORS IN GENESIS OF HYPERNATREMIC DEHYDRATION Early Infancy and Prematurity
The relatively large evaporative water losses per kilogram of body weight of this group of infants, and the inefficiency of renal conservation of water due to renal immaturity, explain their susceptibility to hypernatremia. 7 Interference with Oral Intake of Water
This may occur as a result of the anorexia or nausea and vomiting of acute infections. Reduced intake may also be due to neglect of water administration to infants. A special group of hypernatremic patients is accounted for almost solely by this mechanism, namely, those with cerebral defect who either have insufficient access to water or whose From the Pediatric Division, Baltimore City Hospital, and the Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland. " We -have classified patients as hypematremic if serum sodium concentrations are 150 mEq. per- liter or higher.
193
194
HYPERNATREMIC DEHYDRATION
cerebral impairment leads to a lack of thirst response in the presence of the usual stimuli.10 Clinically these patients have to be distinguished from those whose brain damage is secondary to hypernatremic dehydration. At times this distinction may be difficult. Excessive Losses of Electrolyte-Free Water because of Increased Evaporative Water Loss through Skin and Lungs
This is seen in febrile states, environmental heat stress, and in salicylism and other causes of hyperventilation.8 Profuse sweating may also contribute, since normal sweat has a concentration of sodium only 10 to 35 per cent that of extracellular water. Excessive Losses of Water in Stools
The concentration of sodium in the water of normal stools and often in diarrheal stools is considerably less than that in extracellular fluid. 9 However, there is great variation in the concentration of sodium in the water of diarrheal stools, and we have not been able to demonstrate any good correlation between the concentration of sodium in stool water and the development of hypernatremia. This factor, then, appears highly variable in etiologic significance, since no significant difference can be found between the concentrations of sodium in stool water of hypernatremic patients and normonatremic patients who have a similar degree of water loss due to diarrhea. Probably the volume of water lost in the stools is the important factor. Excessive Administration of Solute (Electrolyte and/or Protein) to Sick Infantsl
An infant who is being subjected to a dehydrating influence, be it diarrheal disease, anorexia or fever, has a smaller margin of safety for water conservation. The intake of high protein and electrolyte feedings, or large volumes of saline solutions, orally or parenterally, increase the renal water requirement obligatory for excretion of excess electrolyte and urea. This water may have been easily spared in health, but its loss now serves to increase water deficit. The feeding of undiluted and unmodified cow's milk to a two-month-old infant is an example of a high solute load which is easily tolerated by a well infant, but may cause water deficit in a sick infant.1 In infants with diarrhea the total quantity of sodium intake is important as well as the concentration of sodium in the solution. Even though a fairly dilute electrolyte solution (50 mEq. per liter of sodium) is given orally to infants with diarrhea, hypernatremia may result if it is given in unphysiologically large quantities. 1 Such patients have been noted to produce copious watery stools which
HAROLD E. HARRISON, LAURENCE FINBERG
195
are apparently very dilute in sodium. Only a few actual measurements are available on these infants, but no other explanation is at hand except that of large losses of water in the stool. Salt Poisoning, Either Inadvertently by Addition of Salt to Feedings, or Iatrogenically by Injudicious Therapy, so that Excessive Amounts of Sodium Salts Are Given to Dehydrated Infants 3 , 4, 9
Excessive intake of salt produces an increased body sodium content, and because of attendant anorexia or vomiting plus the usual evaporative water losses there may be dehydration as well. Excessive Renal Water Loss as in Diabetes Insipidus and "Nephrogenic" Diabetes Insipidus
Any interference with the necessary large water intake of these patients quickly leads to hypernatremic dehydration. PHYSIOLOGY AND PATHOLOGY OF HYPERNATREMIA
Hypernatremia can be associated with an increased total sodium content of the extracellular fluid as in patients given excessive amounts of salt. In subjects with severe water deficit, however, total extracellular sodium is reduced despite high concentrations of sodium because of reduction of extracellular fluid volume. All patients with hypernatremia show certain manifestations which are thought to be the result of intracellular dehydration secondary to the increased osmotic concentration of extracellular water. During experimental hypematremia the muscle cells take up sodium, as well as lose water. In addition they reach osmotic equilibrium by apparent dissociation of intracellular complex particles into smaller units. This latter reaction appears to occur to a much greater extent in brain cells, where little or no sodium enters.5 This special behavior of brain cells possibly accounts for the severe functional central nervous system changes seen in hypematremia.
Intracranial bleeding occurs at times in hypernatremic patients and also in animals made acutely hypernatremic. This is apparently the result of injury or rupture of capillaries and venules secondary to reduction in cerebrospinal fluid pressure. 3 , 5, 6 Subdural effusions have also been encountered. 3 These phenomena are probably not responsible for the common symptoms and signs of this disorder, but may in occasional instances cause death or severe residual damage. 3 , 4,5,9 The composition of the extracellular fluid may show other derangements because of the underlying disease, and such secondary phenomena as metabolic acidosis and the biochemical changes of renal insufficiency are seen in addition to the effects of the hypernatremia itself. The most
196
HYPERNATREMIC DEHYDRATION
important of the biochemical disorders secondary to hypernatremia are changes in concentration of potassium and calcium. Potassium deficits are often large in these patients because of losses in gastrointestinal secretions and in the urine. At times the serum potassium concentration will be low in the face of evidences of renal insufficiency;4 this phenomenon may represent an extrarenal adjustment to hypernatremia as well as being a reflection of a reduced body potassium content. If renal impairment persists, serum potassium levels, of course, will rise. Serum calcium levels are frequently reduced in hypernatremic patients. The equilibrium of this ion is affected by multiple factors, but it seems probable from studies in patients and experimental animals that the calcium level is in some way altered by hypernatremia, particularly if associated with potassium deficiency.s.4 In addition, acute renal insufficiency leads to phosphate retention, which may playa contributing role. The metabolic acidosis present in some patients may protect against overt tetany, but when the acidosis is corrected before correcting the hypernatremia, hypocalcemic tetany may occur, as may occasionally be true in untreated hypernatremic dehydration if acidosis is minimal or absent. CLINICAL RECOGNITION OF HYPERNATREMIC STATES
This topic is of paramount importance in any discussion of therapy, since in many situations there is a considerable time lag in obtaining chemical data from the laboratory. The condition can be deceptive because the dehydration, though marked, may seem inapparent to one looking for signs of classic dehydration. The first step toward recognition of hypernatremic dehydration begins with the history of the etiologically disposing factors discussed above. An objective criterion is loss of 10 to 15 per cent of the body weight without the signs of classic dehydration such as loss of skin elasticity and turgor, or circulatory impairment. The hypernatremic patient may have lost 10 per cent of his body weight without evidence of circulatory embarrassment and look deceptively well for a time. These infants are often extremely thirsty, and this is one of the reasons why excessively large intakes of sodium may result if they are given electrolyte solutions ad lib. As they become sicker, however, nausea and vomiting limit the fluid intake. Fever is commonly associated with hypernatremia, so that it may be both a predisposing factor and a manifestation of this state. The presence of signs and symptoms referable to the nervous system has been most important in the diagnosis. Disturbances in consciousness ranging from lethargy to coma have been common. Hyperirritability to stimuli despite extreme lethargy when undisturbed has been characteristic. Other signs such as tremors, exaggerated deep tendon reflexes and
HAROLD E. HARRISON, LAURENCE FINBERG
197
muscle rigidity, including nuchal rigidity, have been common, and occasionally convulsions are seen. The concentration of protein in the cerebrospinal fluid is usually elevated.5 Hypernatremic dehydration when extreme may also be accompanied by reduction in extracellular fluid volume, with the associated circulatory disturbances. Such a "mixed" clinical picture is difficult or impossible to diagnose by clinical criteria alone, and in such instances the laboratory remains the sine qua non of diagnosis. However, this latter type of patient has a greater sodium deficit than the group previously described, so that administration of solutions with the usual concentrations of sodium salts given to dehydrated patients would not be so harmful as in the more common form of hypernatremia. TREATMENT
The goal of treatment is not the rapid restoration of serum sodium levels to normal, but rather the safe return of the patient to optimum physiologic balance without undue risk of complications. Experience in the treatment of hypernatremic subjects has indicated that administration of water rapidly in large quantities in an effort to bring the sodium concentration into the normal range is dangerous. Such an approach may precipitate a severe convulsive state. It has been pointed out that certain adjustments of brain cells to the increased extracellular sodium concentration have occurred, and rapid reduction of extracellular sodium evidently precipitates another disturbance of equilibrium. Since these patients are usually not in circulatory collapse, the pressure for rapid replacement of fluid volume is removed, and the rehydration process may safely be carried out gradually. It is important, however, that fluid administration be started promptly when the diagnosis is suspected and that it be continued at the proper rate. The composition of the fluid to be administered should, of course, be hypotonic with respect to sodium and chloride. Theoretically, it might be possible to eliminate these ions completely and give electrolytefree glucose water. This has two drawbacks: first, many patients do have some extracellular electrolyte deficits, and, secondly, the addition of some sodium makes slightly more rapid administration of fluids possible and safe. Concentrations of sodium above 40 mEq. per liter have been found to be excessive for these patients. Current information suggests that sodium concentrations of 15 to 20 mEq. are the most suitable. Since most patients have a greater deficit of sodium than of chloride (metabolic acidosis), it is customary in our clinic to use 1 part of sixthmolar sodium lactate to 2 parts of 0.85 per cent saline solution in preparing the sodium-containing portion of the solution. The desired concentration indicated above may be reached by combining 1 part of sixth-
198
HYPERNATREMIC DEHYDRATION
molar sodium lactate, 2 parts of 0.85 per cent sodium chloride and 21 parts of 5 per cent glucose in water. If the acidosis is severe (indicated by carbon dioxide contents of less than 8 mEq. per liter), sixth-molar sodium lactate may be used in place of the saline, and thus 3 parts of sixth-molar sodium lactate and 21 parts of 5 per cent glucose in distilled water are given. (Final concentration of sodium lactate is M/48.) Solutions such as these should be given intravenously. The rate of administration to an infant should be such that 200 ml. per kilogram are given during the first 24 hours (0.14 ml. per kilogram per minute). This provides for the deficit of water of about 10 to 15 per cent of the body weight as well as for the continued water requirements of 70 to 100 ml. per kilogram per day for infants. Fluid therapy for the second and subsequent days can be reassessed daily. If tolerated, glucose water may be given orally together with the appropriate electrolyte by the end of 12 to 24 hours or even earlier in milder cases. Although potassium deficits may be severe, it is wise to withhold administration of potassium initially, since many of these patients are oliguric or temporarily anuric. Once it is apparent that urinary output is adequate, potassium replacement should be started. The oral route is preferable when feasible, and 3 to 5 mEq. per kilogram per day are advised initially (10 per cent potassium citrate solution provides 1 mEq. of potassium per milliliter and can be given orally diluted with fruit juice or other fluid). If the parenteral route is necessary, the usual precautions for parenteral potassium administration should be carefully followed. The concentration of potassium chloride in the solution given intravenously should not exceed 20 mEq. per liter (0.15 per cent potassium chloride). A daily weight is important in assessing the previous day's fluid replacement. It is common for these patients to show evidences of overexpanded extracellular fluid with visible edema even before they are completely rehydrated because of the lag in intracellular uptake of water. Part of the therapy should be directed to controlling nervous system complications. Should convulsions occur, the usual anticonvulsant drugs are indicated. We have used subcutaneous phenobarbital sodium and rectal paraldehyde as agents which seem particularly safe in infants. The dose of phenobarbital sodium used is 5 mg. per kilogram repeated once in 20 minutes if necessary. Subsequent maintenance phenobarbital therapy is continued as in any acute convulsive state. When paraldehyde is required to control convulsions, 2 to 4 ml. are given rectally with an equal volume of cottonseed oil. If instilled through a small catheter and the buttocks taped tightly together with adhesive, the paraldehyde is usually retained. It is disconcerting to have nervous system manifestations develop while the patient is receiving therapy, but present knowledge indicates that this occurrence may be inevitable after a certain
r HAROLD E. HARRISON, LAURENCE FINBERG
199
amount of damage has occurred during the hypernatremic phase. Thus some nervous system damage may be irreversible before convulsions occur. Subdural effusions may be suspected and diagnosed by needle aspiration. Our experience to date has not shown any improvement in these patients from paracentesis or surgical drainage of subdural effusions over simple expectant watching. It would seem wise, until better criteria are established, to regard and assess each case individually. Intracranial bleeding may occur in several different sites, and here again individual consideration of treatment is indicated. Hypocalcemia may be averted or treated when present by the administration of 10 to 30 cc. of 10 per cent calcium gluconate per day in the intravenous fluids. In summary, the treatment of hypernatremic dehydration consists in administering an appropriate fluid volume of low (15 to 20 mEq. per liter) sodium concentration at a slow rate until water deficit is overcome. At the same time attention should be paid to needs for potassium and calcium. Meanwhile the nervous system complications must be managed symptomatically. In rare instances aspiration of subdural effusion or hematoma may be indicated. REFERENCES
1. Colle, E., Ayoub, E., and Raile, R.: Hypertonic Dehydration (Hypernatremia): The Role of Feedings High in Solutes. Pediatrics, 22:5,1958. 2. Finberg, L.: Experimental Studies of the Mechanisms Producing Hypocalcemia in Hypernatremic States. ,. Clin. Investigation, 36:434, 1957. 3. Idem: The Pathogenesis of the Nervous System Lesion in Hypernatremic States. I. Clinical Observations of Infants. Pediatrics, in press. 4. Finberg, L., and Harrison, H. E.: Hypernatremia in Infants. Pediatrics, 16:1, 1955. 5. Finberg, L., Luttrell, C., and Redd, H.: Pathogenesis of Lesions in the Nervous System in Hypernatremic States. II. Experimental Studies of Gross Anatomic Changes and Alterations of Chemical Composition of the Tissues. Pediatrics, in press. 6. Girard, F.: Les hematomes sous-duraux. Etude experimentale. Acta paediat., 45: 618, 1956. 7. Pratt, E. L., and Snyderman, S. E.: Renal Water Requirements of Infants Fed Evaporated Milk with and without Added Carbohydrate. Pediatrics, 11 :65, 1953. 8. Rapoport, S.: The Role of Overventilation in Diseases of Infancy. Ann. paediat., 176:137,1951. 9. Weil, W. B., and Wallace, W. M.: Hypertonic Dehydration in Infancy. Pediatrics, 17: 171, 1956. 10. Welt, L. G., Seldin, D. W., Nelson, W. P., III, German, W. J., and Peters, J. P.: Role of Central Nervous System in Metabolism of Electrolytes and Water. Arch. Int. Med., 90:355, 1952. 4940 Eastern Avenue Baltimore 24, Maryland