Asymptomatic hypovolemic hypernatremia. A variant of essential hypernatremia.
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Adolescent↗
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[Neurogenic hypernatremia. Apropos of a case of neurogenic hypernatremia in the course of an ectopic pinealoma of the chiasma, causing a global pituitary insufficiency. Study of exchangeable sodium and potassium].
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Adolescent↗
Hypernatremia in the intensive care unit: an indicator of quality of care?
OBJECTIVE: To assess the frequency of hypernatremia in patients who were admitted to an intensive care unit (ICU) and to determine the correlation of hypernatremia with the clinical outcomes, durations of the patients' stays in the ICU, and other clinical variables. DESIGN: Retrospective survey. SETTING: University teaching hospital. PATIENTS: All patients (total, 389) who were admitted to the medical ICU of the department of internal medicine during 1 yr. MEASUREMENTS: The database of our hospital's mainframe computer was searched for sodium values > or = 150 mmol/L that were registered in the year 1995. These data were then matched with the registration numbers of all patients who were admitted to our medical ICU between January 1 and December 31, 1995. In this way, we identified all patients in whom hypernatremia was present at admission or those who developed hypernatremia in the course of their stay in our ICU. The prevalence and duration of hypernatremia (defined as a serum sodium concentration of > or = 150 mmol/L or more) were determined; the correlation of hypernatremia with clinical outcome, duration of ICU stay, Acute Physiology and Chronic Health Evaluation II scores, and other clinical variables were evaluated; and changes in fluid administration in response to hypernatremia and fluid regimens in the period preceding hypernatremia were examined. MAIN RESULTS: Of a total of 389 patients who were admitted in 1995, hypernatremia was present at admission in 34 patients (8.9%). The average duration of hypernatremia in these patients was 16.2 (range, 4-56) hrs. A total of 22 patients (5.7%) developed hypernatremia in the course of their stay in the ICU. The average duration of hypernatremia in this group was 34.7 (range, 4-89) hrs. Moderately elevated levels of sodium had been detected in most of these patients (n = 21) in the days before the development of severe hypernatremia; however, adjustments in fluid infusion aimed at preventing the occurrence of hypernatremia were either lacking (n = 7) or inadequate (n = 11). Hospital-acquired hypernatremia vs. hypernatremia present at admission to the ICU was associated with a higher mortality rate (32% vs. 20.3%, respectively; p < .01). CONCLUSIONS: Despite frequent measurement of sodium levels in patients in the ICU, hypernatremia is a relatively common occurrence. Initial treatment of hypernatremia is often inadequate, and sometimes treatment is delayed. The development of hypernatremia is associated with adverse outcomes for patients developing hypernatremia in the ICU. Hypernatremia could potentially be used as an indicator of quality of care in the medical ICU.
APACHE↗
The changing pattern of hypernatremia in hospitalized children.
OBJECTIVES: Past studies have revealed that hypernatremia occurs primarily in infants with diarrheal dehydration. With improved infant feeding practices and the advent of pediatric critical care medicine, the pattern of hypernatremia in children has likely changed. The purpose of this study was to evaluate the current pattern of hypernatremia in hospitalized children. METHODS: Medical records were reviewed for 68 patients admitted to a large urban children's hospital during a 3-year period, all with a serum sodium greater than 150 mEq/L. The etiologies, predisposing factors, and morbidity and mortality associated with hypernatremia were evaluated. RESULTS: The average patient age was 3.9 years (range, 1 day to 19. 7 years), and the peak serum sodium concentration was 159 mEq/L (range, 151-184 mEq/L). Hypernatremia was hospital acquired in 60% of children. The majority of children (71%) were admitted for reasons other than hypernatremia. In 76% of the patients, inadequate fluid intake was the main cause of hypernatremia. Gastroenteritis contributed to the hypernatremia in only 20% (14 out of 68) of children. Eleven of these were infants <1 year of age with hypernatremia on admission. Eighty-eight percent of patients (60 out of 68) suffered from neurologic impairment, critical illness, chronic disease, or prematurity before developing hypernatremia. The overall mortality was 16%. Patients in whom hypernatremia was not corrected had a significantly higher mortality than those in whom hypernatremia was corrected (4 out of 8 [50%] vs 7 out of 60 [12%]). Peak serum sodium was no different for survivors than nonsurvivors. No deaths were attributable to cerebral edema caused by correction of hypernatremia. Neurologic complications related to hypernatremia occurred in 15% of patients. CONCLUSIONS: Hypernatremia occurs in children of all ages, with the vast majority having significant underlying medical problems. Hypernatremia caused by gastroenteritis in infants has become much less common than previously reported. Hypernatremia is primarily a hospital-acquired disease, produced by the failure to administer sufficient free water to patients unable to care for themselves. Failure to correct hypernatremia may result in a high mortality rate.
Adolescent↗
Hypernatremia in hospitalized patients.
OBJECTIVE: To determine the incidence, clinical characteristics, and outcome for general medical-surgical hospital patients with hypernatremia. DESIGN: A prospective cohort study. SETTING: A 942-bed urban university hospital. PATIENTS: All patients who developed a serum sodium concentration of 150 mmol/L or greater during a 3-month observation period. MEASUREMENTS: Daily fluid balance, mental status, and serum and urine electrolytes and osmolality. RESULTS: 103 patients were identified. Eighteen patients were hypernatremic on hospital admission, and 85 developed hypernatremia during hospitalization. Patients who developed hypernatremia during hospitalization were younger than patients who developed hypernatremia before hospital admission (mean age +/- SD, 58.9 +/- 19.2 years compared with 76.6 +/- 16.6 years; P < 0.01) but did not differ in age from the patients of the general hospitalized population. Eighty-nine percent of patients who developed hypernatremia during hospitalization had urine concentrating defects, primarily as the result of the use of diuretics or of solute diuresis, whereas only 50% of patients who were hypernatremic on admission could be shown to have concentrating defects (P < 0.01). Fifty-five percent of all hypernatremic patients had increased insensible water losses, and 35% had increased enteral water losses. Eighty-six percent of patients with hospital-acquired hypernatremia lacked free access to water, 74% had enteral water intake of less than 1 L/d, and 94% received less than 1 L of intravenous electrolyte-free water per day during the development of hypernatremia. No supplemental electrolyte-free water was prescribed during the first 24 hours of hypernatremia in 49% of patients. The duration of hypernatremia was shorter in patients who were hypernatremic on admission (median duration, 3 days) than in patients with hospital-acquired hypernatremia (median duration, 5 days; P < 0.05). Mortality was 41% for all patients, but hypernatremia was judged to have contributed to mortality in only 16% of patients. CONCLUSIONS: Although the development of hypernatremia before hospital admission occurs primarily in geriatric patients, hospital-acquired hypernatremia was more common in our cohort and had an age distribution similar to that of the general hospitalized population. Hospital-acquired hypernatremia was primarily iatrogenic, resulting from inadequate and inappropriate prescription of fluids to patients with predictably increased water losses and impaired thirst or restricted free water intake or both. Treatment of hypernatremia is often inadequate or delayed. Efforts to manage hypernatremia better and altogether avoid hospital-acquired hypernatremia should focus on both physician education and the development of hospital systems to prevent errors in fluid prescription.
Adult↗
Only some septicaemic patients develop hypernatremia in the burn intensive care unit: why?
From April 1993 to January 2000, 105 patients in the burn intensive care unit (BICU) that developed septicaemia in the course of their treatment were studied retrospectively to investigate as to why only 36 septicaemic patients (34%) developed hypernatremia (serum sodium >150mmol/l). Septicaemic burn patients who developed hypernatremia were found to have a higher incidence of inhalation injury and a larger burn area (TBSA) signifying greater free water losses in the face of increasing fluid requirements. Patients who developed hypernatremia showed a characteristic pattern of septicaemia: early onset, multiple episodes, polymicrobial, need for multiple antibiotics, longer duration and a higher mortality, indicating a more severe degree of sepsis. The level of incapacitation either from the burn itself, mechanical ventilation or from impaired mental status leading to an inadequate free water intake was more in septicaemic patients who developed hypernatremia. Increased urinary free water losses and solute diuresis from hyperglycemia were significant factors in the development of hypernatremia. Patients who were treated with early wound excisions were less prone to develop hypernatremia when compared to those who did not undergo early wound excision. The close association between the onset of hypernatremia and the onset of septicaemia noted in this study suggests the use of hypernatremia as a marker for septicaemia in burn patients. Hypernatremia in a septicaemic burn patient is multi-factorial and a thorough understanding of the underlying factors will help prevent the onset and progress of hypernatremia.
Adult↗
Fatal hypernatremia from exogenous salt intake: report of a case and review of the literature.
Hypernatremia is a common electrolyte disturbance, most often caused by volume depletion. Hypernatremia due to sodium excess occurs less frequently, and fatal hypernatremia solely from ingestion of table salt is rare. We describe a 41-year-old man who had seizures and hypernatremia after ingestion of a supersaturated salt water solution intended for gargling. He had consumed approximately a third cup of table salt (approximately 70 to 90 g of salt or 1,200 to 1,500 meq of sodium). His initial serum sodium concentration was 209 meq/liter. Hypotonic fluid therapy was given to provide free water and to correct the hypernatremia gradually. Our patient, however, failed to recover from the initial insult and died 3 days later. Review of the literature revealed 10 adult and 20 pediatric cases of hypernatremia attributable to exogenous intake of salt. The type of therapy (fluid or peritoneal dialysis), the type of fluid used, and the rate of correction of hypernatremia did not influence survival. The age of the patient and the initial serum sodium concentration were the most important prognostic indicators. Both very young patients and those with lesser degrees of hypernatremia had a better rate of survival than did other patients. In addition, our review illustrates the surprisingly small amount of salt that can cause severe hypernatremia and the danger of using salt or saline as an emetic.
Adult↗
[Hyponatremia and hypernatremia in the elderly].
The study aimed at evaluating an incidence of hypo- and hypernatremia in the elderly and the results of therapy. Hyponatremia. The studies involved 18 patients aged 69.8 +/- 5.9 years with hyponatremia of 126.8 +/- 2.7 mmol/L. The main causes of hyponatremia were: diuretics, diarrhoea, and vomiting. Sodium deficit was calculated prior to the treatment in all patients. An analysis of hyponatremia incidence indicates that hyponatremia was diagnosed in 1.39% of patients over 60 years, hospitalized within 1989-1990. Sodium deficit in this group was 495.5 +/- 167.7 mmol. Sodium chloride solution was given intravenously to 12 patients, according to the "free correction" principle (a mean increase in serum sodium level was 0.17 +/- 0.07 mmol/L per hour). Mortality in such treated patients was 33%. Sodium chloride was not given to 6 out of examined patients. In 12 patients (66.6%) hyponatremia developed prior to hospitalization, in 6 patients (33.3%) during hospitalization. Mortality rate was 16.6% and 50%, respectively. This confirms higher mortality rate of the rapidly developing hyponatremia in the hospitalized elderly patients. In some cases hyponatremia may constitute iatrogenic complication, especially in the elderly given diuretics in an uncontrollable way. Own experience suggests that elderly patients with a risk of hyponatremia require close monitoring and early compensation of the electrolyte disorders. Hypernatremia. The studies involved 20 patients aged 71.4 +/- 7.7 years with hypernatremia of 155.6 +/- 8.4 mmol/L. A total water deficit (DH20) was calculated in this group. An analysis of hypernatremia incidence showed that this state was diagnosed in 1.55% of patients treated at the Department of Arterial Blood Hypertension within 1989-1990. Total water deficit was 3.9 +/- 1.9 L. A 5% glucose was given intravenously to 15 patients whereas oral fluid therapy was carried out in 5 patients. A mean corrected DH2O in the first day was 46.0 +/- 21.0%. Mortality rate in this group was 65%. It is worth mentioning that 37% of patients with chronic hypernatremia which developed prior to hospitalization died while in case of the acute hypernatremia developed in the hospital mortality rate was 83%. A significant effect on the results of therapy plays an early correction of hypernatremia. Mortality rate in case of DH2o supplementation below 30% during the first 24 hours is about 66%., if DH2o supplementation is 31-60%, a mortality rate is 63%, and in DH2o supplementation over 60% mortality rate is 100%. The obtained results suggest that hypernatremia in the elderly is related to the high mortality rate (65%). An early decrease of water deficit increases mortality rate in patients with hypernatremia.
Age Factors↗
Prognostic significance of hypernatremia and hyponatremia among patients with aneurysmal subarachnoid hemorrhage.
OBJECTIVE: Abnormal serum sodium levels (hyponatremia and hypernatremia) are frequently observed during the acute period after aneurysmal subarachnoid hemorrhage (SAH) and may worsen cerebral edema and mass effect. We performed this study to determine the prognostic significance of serum sodium concentration abnormalities. METHODS: We analyzed prospectively collected data for the placebo treatment group in a clinical trial conducted at 54 neurosurgical centers in North America. The presence of hypernatremia (serum sodium concentration of >145 mmol/L) and hyponatremia (serum sodium concentration of <135 mmol/L) was determined with serum sodium measurements obtained at admission and 3, 6, and 9 days after SAH. The effects of hypernatremia and hyponatremia on the risk of symptomatic vasospasm and on 3-month outcomes were analyzed after adjustment for the following potential confounding factors: age, sex, preexisting hypertension, admission Glasgow Coma Scale score, initial mean arterial pressure, subarachnoid clot thickness, intraventricular blood or intraparenchymal hematoma, ventricular dilation, and aneurysm size and location. RESULTS: Of 298 patients in the analysis, 58 (19%) developed hypernatremia and 88 (30%) developed hyponatremia. Hypernatremia was significantly associated with poor outcomes (odds ratio, 2.7; 95% confidence interval, 1.2-6.1). A positive correlation was observed between the highest sodium values recorded and Glasgow Outcome Scale scores at 3 months (P < 0.0001 by analysis of variance). Hyponatremia was not associated with 3-month outcomes (odds ratio, 1.9; 95% confidence interval, 0.9-4.3). Neither hypernatremia nor hyponatremia was associated with the risk of symptomatic vasospasm. CONCLUSION: Hyponatremia seems to be more common than hypernatremia after SAH. However, hypernatremia after SAH is independently associated with poor outcomes, and this association is independent of previously identified outcome predictors, including age and admission Glasgow Coma Scale scores. Further studies are needed to define the underlying mechanism of this association.
Adolescent↗
Extracellular volume decreases while cell volume is maintained by ion uptake in rat brain during acute hypernatremia.
1. Regulation of brain extracellular and intracellular water content, regarded as volume, and electrolytes in response to 90 min of hypernatremia has been studied in the cerebral cortex of rats under urethane anaesthetic. 2. Total tissue electrolytes and water were partitioned between extracellular and intracellular compartments based on measurements made in two series of experiments. In one, tissue samples were collected and analysed for total water, Na+, K+ and Cl-. In the other, tissue extracellular volume fraction, [Na+] and [K+] were measured in situ using ion-selective microelectrodes. 3. Osmotically induced water loss from cerebral cortex was less than that predicted for ideal osmotic behaviour, revealing a degree of volume regulation, and this regulation was associated with net tissue uptake of Na+, Cl- and K+. 4. Total water content was 3.77 g H2O (g dry weight)-1 in control cortex and this decreased by 7% after 30 min of hypernatremia and then remained relatively stable at this value. Control extracellular water content, based on an extracellular volume fraction of 0.18, was 0.88 g H2O (g dry weight)-1. Control intracellular water content, estimated as the difference between total and extracellular water contents, was 2.89 g H2O (g dry weight)-1. After 30 min of hypernatremia, extracellular water content decreased by an average of 27% but intracellular water did not change. This indicates selective regulation of cell volume. By 90 min the extracellular water content had decreased by 47% and the loss in extracellular water content appeared to be accompanied by a roughly equivalent increase in intracellular water content. The intracellular volume increase, however, was not statistically significant. The tortuosity of the extracellular space averaged 1.57 and increased to 1.65 during the hypernatremia. 5. Brain extracellular fluid and plasma [Na+] were roughly equal in control tissue. Both increased by 30 mu equiv (g H2O)-1 as a result of the hypernatremia, although extracellular [Na+] lagged behind the plasma value during much of the first 60 min of hypernatremia. Extracellular [K+] was homeostatically regulated at 3 mu equiv (g H2O)-1 independent of changes in plasma electrolytes. 6. Estimates of extracellular and intracellular ion content (mu equiv (g dry weight)-1) indicate that extracellular Na+, Cl- and K+ content decreased during hypernatremia, by 32, 21 and 42% respectively, whereas intracellular ion content increased by 100, 169 and 5% respectively. 7. It is concluded that during acute hypernatremia the extracellular space decreases in volume through the loss of water and electrolytes while the intracellular compartment maintains its water content and gains electrolytes.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
[Hyponatremia--with comments on hypernatremia].
Disorders of the serum sodium concentration (hypo- and hypernatremia) are amongst the most frequent electrolyte disorders in clinical medicine. They are attributable to disturbance of to water metabolism. Hyponatremia is almost always a condition of water excess while hypernatremia is due water deficiency. Physiological normonatremia (normal plasma osmolality) is maintained by an integrated system involving regulated water intake via thirst and control of water excretion via antidiuretic hormone secretion. Therefore hypo- and hypernatremia should be analyzed in terms of dysregulated ADH secretion, fluid intake and renal water excretion. Hyponatremia is usually a disorder of vasopressin excess, due to 'non-osmotic' vasopressin release. The latter may occur in two different settings: (I) SIADH, (II) baroreceptor mediated vasopressin secretion (cardiac failure, liver cirrhosis). This entities are easy to distinguish in clinical practice. SIADH is associated with striking lower plasma concentrations of urate, creatinine and urea. In SIADH the blood pressure is normal and there is no edema. In contrast in the hyponatremia of liver cirrhosis and heart failure the plasma measurements indicated are usually slightly elevated, the blood pressure is low and there is edema. The typical patient with hypernatremia is old and has no thirst sensation. Hypo- or hypernatremia may cause major neurologic symptoms. These symptoms are more related to the rate of change in the serum sodium concentration than to the absolute level of a hypo- or hypernatremia reached. The traditional treatment for hyponatremia used to be water restriction. However V2-Vasopressin-Antagonists may provide a better treatment modality in the future. Hypernatremia is treated by slow rehydratation.
Diagnosis, Differential↗
Effects of hypernatremia on organic brain osmoles.
We studied the effects of varying degrees and durations of hypernatremia on the brain concentrations of organic compounds believed to be important, so-called "idiogenic" osmoles in rats by means of conventional biochemical assays, nuclear magnetic resonance spectroscopy, and high-performance liquid chromatography. There were no changes in the concentrations of these osmoles (specifically myoinositol, sorbitol, betaine, glycerophosphorylcholine [GPC], phosphocreatine, glutamine, glutamate, and taurine) in rats with acute (2 h) hypernatremia (serum Na 194 +/- 5 meq/liter). With severe (serum Na 180 +/- 4 meq/liter) chronic (7 d) hypernatremia, the concentrations of each of these osmoles except sorbitol increased significantly: myoinositol (65%), betaine (54%), GPC (132%), phosphocreatine (73%), glutamine (143%), glutamate (84%), taurine (78%), and urea (191%). Together, these changes account for 35% of the change in total brain osmolality. With moderate (serum Na 159 +/- 3 meq/liter) hypernatremia, more modest but significant increases in the concentrations of each of these osmoles except betaine and sorbitol were noted. When rats with severe chronic hypernatremia were allowed to drink water freely, their serum sodium as well as the brain concentrations of all of these organic osmoles except myoinositol returned to normal within 2 d. It is concluded that: idiogenic osmoles play an important role in osmoregulation in the brain of rats subjected to hypernatremia; the development of these substances occur more slowly than changes in serum sodium; and the decrease in concentration of myoinositol occurs significantly more slowly than the decrease in serum sodium which occurs when animals are allowed free access to water. These observations may be relevant to the clinical management of patients with hypernatremia.
Acute Disease↗
[Hypernatremia. Etiopathogenetic classification and description of a rare clinical case].
On the basis of a rare case of hypernatremia, the essential lines which allow a correct diagnostic and therapeutic approach to hypernatremia are underlined. Hypernatremia is classified according to the patient's state of hydratation and on the content of sodium as: hypovoloemic, euvolemic and hypervolemic. Even the concentrations of sodium in urine are often of great importance for a correct diagnosis. The patient studied suffered from hypernatremia, which is based on genetical factors. The state of dehydration, together with hypovolemia and acute tubular necrosis secondary to rhabdomyolisis, were the causes of hypernatremia. The above mentioned causes were resolved but an enterocutaneous fistula showed to be the cause, quite rare, of hypernatremia. It is suggested that this rare cause should always be mentioned when diagnosing hypernatremia; which it is important since this cause could be solved with an operation. All this was useless in our case since the patient had a drastic deterioration of his general clinical conditions.
Algorithms↗
[A case of severe hypernatremia complicated with rhabdomyolysis].
We report a 45-year-old male patient with severe hypernatremia followed by rhabdomyolysis and acute renal failure. He had developed hypernatremia for two years after a surgery for an intraventricular AVM involving the hypothalamic area, which was fed by the anterior cerebral artery. He was admitted to our hospital because of progressive muscle weakness. Because of loss of water intake due to impaired thirst sensation, he developed severe hypernatremia (191mEq/l) and marked rhabdomyolysis (CK 17,772 IU/l). He was treated with fluid supplement and hemodialysis for acute renal insufficiency. He had no thirst feeling. Blood studies revealed hyporeactivity to ADH in spite of marked hypernatremia and hyperosmorality. Therefore his condition was considered as adipsic hypernatremia. We concluded that rhabdomyolysis of this case was caused by severe hypernatremia. On reviewing the literature, only a few cases of rhabdomyolysis due to hypernatremia have been reported.
Acute Kidney Injury↗
Influence of high donor serum sodium levels on early postoperative graft function in human liver transplantation: effect of correction of donor hypernatremia.
Donor hypernatremia was reported to cause postoperative graft dysfunction in human orthotopic liver transplantation (OLT). However, the effects of the correction of donor hypernatremia before organ procurement have not been confirmed. The aim of this study is to determine whether donor hypernatremia is associated with early graft dysfunction after OLT and to determine the effect of the correction of donor hypernatremia. One hundred eighty-one consecutive OLTs performed between May 1997 and July 1998 were entered onto this study. The cases were divided into three groups according to the donor serum sodium concentration: group A, serum sodium of 155 mEq/L or less before organ procurement (n = 118); group B, peak sodium greater than 155 mEq/L and final sodium 155 mEq/L or less (n = 36); and group C, final sodium greater than 155 mEq/L (n = 27). Graft survival within 90 days after OLT and early postoperative graft function were analyzed. There were no significant differences in donor and recipient variables among the three groups. The frequencies of graft loss were 15 of 118 grafts (12.7%) in group A, 4 of 36 grafts (11.1%) in group B, and 9 of 27 grafts (33.3%; P <.05 v groups A and B) in group C. The liver enzyme values in groups B and C were significantly greater than those in group A postoperatively. The prothrombin times of group C were significantly longer than those of group A for the first 4 postoperative days. Recipients of hepatic allografts from donors with uncorrected hypernatremia had a significantly greater incidence of graft loss compared with recipients of hepatic allografts from normonatremic donors. However, the differences in graft survival were abrogated by the correction of donor hypernatremia before procurement.
Adult↗
Effect of acute and chronic hypernatremia on myoinositol and sorbitol concentration in rat brain and kidney.
In animal models of hypernatremia, increases in brain electrolyte content account for the entire increase in osmolality in acute but not chronic hypernatremia, suggesting that there is generation of additional intracellular solutes ("idiogenic osmoles") in chronic hypernatremic states. In the present study, the concentration of the polyols myoinositol and sorbitol and water content were determined in the brain and kidneys of rats made acutely (2 hours) and chronically (72 hours) hypernatremic by intraperitoneal injection of NaCl and water restriction. Both the brain and the kidney responded to chronic hypernatremia with increased levels of myoinositol. Sorbitol levels increased in the kidney in response to both acute and chronic hypernatremia. Water content dropped in acute hypernatremia, but remained unchanged during chronic hyperosmolar challenge. We conclude that the polyols, myoinositol and sorbitol, may play a significant role in cellular osmoregulation in brain and kidney during chronic hypernatremia in the rat.
Acute Disease↗
Hypernatremia and hypertonic syndromes.
Hypernatremia is the most common cause of hypertonicity in small animal medicine. Despite this fact, severe hypernatremia is an uncommon clinical entity in dogs and cats. The causes of hypernatremia are excessive water loss and increased sodium intake. Clinical signs are most often related to CNS dysfunction. Severe hypernatremia should be considered a life-threatening situation and treated as such. Initial fluid therapy should be given with care according to the rate of onset of hypernatremia, as deterioration of the animal's condition is a common sequela. The determination of the cause of hypernatremia and the treatment can be both challenging and rewarding. The other notable hypertonic syndrome in small animal medicine is hyperosmolar nonketotic diabetes mellitus. Judicious management of this disease with fluid therapy and insulin is the standard therapy. An understanding of the pathophysiology is essential to their diagnosis and appropriate medical management.
Animals↗
Adipsic hypernatremia in two patients with AIDS and cytomegalovirus encephalitis.
In patients with acquired immune deficiency syndrome (AIDS), hypoosmolality is frequently observed, whereas hypernatremia is distinctly rare. We report two patients with advanced AIDS and cytomegalovirus (CMV) encephalitis, who developed severe hypernatremia without any thirst sensation, that is, adipsic hypernatremia. Both developed severe hypernatremia of up to 164 and 162 mmol/L, with serum osmolalities of 358 and 344 mOsmol/kg while remaining alert and denying thirst. Serum antidiuretic hormone (ADH) levels were 0.9 and 1.5 pg/mL, inappropriately low for the concomitant serum osmolalities. Vital signs were stable. During hypernatremia, urine osmolalities were 327 and 340 mOsmol/kg, and urine Na+ levels were 56 and 119 mmol/L, respectively. Periventricular white matter lesions were seen on cerebral nuclear magnetic resonance imaging (NMRI) in case 1, but the pituitary appeared normal in both cases. Survival after onset of hypernatremia was 6 and 4 weeks, respectively. Autopsy in case 1 showed typical findings of CMV encephalitis but normal pituitary, confirming that infection with HIV or CMV most likely caused the dysfunction of the central osmostat.
AIDS-Related Opportunistic Infections↗