Acute hypernatremia and hypocalcemia after oral sodium phosphate administration to a dog.

A 15-year-old male neutered mixed breed dog weighing 28 kg presented to a referral center after developing severe tremors and altered mentation. There was hypocalcemia and hypernatremia after oral administration of sodium phosphate as a bowel cleansing agent in preparation for colonoscopy. The dog was treated intravenously with low sodium fluids and calcium gluconate. Neurologic status and electrolyte derangements normalized over the next 12 hours. Oral administration of sodium phosphate appeared to cause clinical electrolyte derangements in this dog.

Occurrence and clinical relevance of postoperative hypernatremia in dogs undergoing cholecystectomy.

BACKGROUND: Patients undergoing cholecystectomy have not been reported previously to develop clinically relevant postoperative hypernatremia. OBJECTIVES: Describe the frequency of postoperative hypernatremia in dogs undergoing cholecystectomy and its clinical relevance (duration of hospitalization and survival). ANIMALS: Thirty-seven dogs undergoing cholecystectomy at 2 private referral hospitals. METHODS: Retrospective study of dogs undergoing cholecystectomy with available preoperative and postoperative serum sodium concentrations. RESULTS: Postoperative hypernatremia (>150 mEq/L) was common (56%; 95% confidence interval [CI], 40%-70%) and was associated with significantly higher mortality compared to nonhypernatremic patients (52%; 95% CI, 30%-70% vs 12.5%; 95% CI, 2%-40%; P = .02). Nonsurvivors had higher mean postoperative peak serum sodium concentrations (155 mEq/L; range, 146-172) than survivors (150 mEq/L; range, 142-156; P = .01). Dogs developing hypernatremia within 6 hours after surgery had 7.7 higher odds of nonsurvival (odds ratio [OR], 7.7; 95% CI, 5.9-9.4). A delta value (serum sodium concentration on admission [T0] - serum sodium concentration 6 hours postoperatively [T2]) of ≥10 mEq/L carried 3.3 higher odds of mortality (OR, 3.3; 95% CI, 1.6-5.1). All dogs with a postoperative peak sodium concentration >160 mEq/L did not survive. Admission acute patient physiologic laboratory evaluation fast (APPLEfast ) scores were not different between survivors and nonsurvivors or between postoperative hypernatremic and normonatremic patients. Hospitalization time was no different between hypernatremic and normonatremic patients (6 days vs 4.5 days; P = .15). Dogs with gallbladder mucocele were more likely to develop postoperative hypernatremia and have poorer outcomes. CONCLUSIONS: Hypernatremia was a common and clinically relevant postoperative complication in dogs after cholecystectomy. Detection of hypernatremia within 6 hours after surgery may be associated with poorer outcomes.

Primary adipsia and severe hypernatremia in a Pit Bull dog / Adipsia primária e hipernatremia severa em um cão Pit Bull

Primary adipsia is a rare condition in which there is failure in the activation threshold of the hypothalamic osmoreceptors, leading to osmolality imbalance. Here, we reported the case of a Pit Bull dog with an altered level of consciousness (started after weaning) and adipsia. There was an increase in plasma osmolality (444 mOsm/kg), sodium (223.7 mg/dL), and chlorine (173 mg/dL) levels. Based on the suspicion of primary adipsia, water was administered via a nasogastric tube, with clinical improvement. The owner was instructed to supply water with food. Eight months after discharge, the dog returned with parvovirus and died. In the anatomopathological examination, no structural changes were observed in the central nervous system. To our knowledge, this is the first report of hypernatremia due to adipsia in a Pit Bull dog, showing that this is a differential diagnosis that should be considered in this breed.

Adipsia primária é uma rara condição em que há falha no limiar de ativação dos osmoreceptores hipotalâmicos, levando ao desequilíbrio da osmolalidade. Este artigo tem como objetivo relatar o caso de um cão da raça Pit Bull apresentando alteração no nível de consciência (iniciado após o desmame) e adipsia. Foi verificado aumento da osmolalidade plasmática (444 mOsm/kg), sódio (223,7 mg/dL) e cloro (173 mg/dL). Baseado na suspeita de adipsia primária, iniciou-se administração de água via sonda nasogástrica, com melhora clínica. O tutor foi orientado a fornecer água junto a alimentação. Oito meses após alta, o paciente retornou com parvovirose e veio a óbito. No exame anatomopatológico, não foram observadas alterações estruturais no sistema nervoso central. Este é o primeiro relato de hipernatremia por adipsia em um cão Pit Bull, mostrando que este é um diagnóstico diferencial que deve ser considerado nesta raça.

Clinical signs, profound acidemia, hypoglycemia, and hypernatremia are predictive of mortality in 1,400 critically ill neonatal calves with diarrhea.

Profound acidemia impairs cellular and organ function and consequently should be associated with an increased risk of mortality in critically ill humans and animals. Neonatal diarrhea in calves can result in potentially serious metabolic derangements including profound acidemia due to strong ion (metabolic) acidosis, hyper-D-lactatemia, hyper-L-lactatemia, azotemia, hypoglycemia, hyperkalemia and hyponatremia. The aim of this retrospective study was to assess the prognostic relevance of clinical and laboratory findings in 1,400 critically ill neonatal calves with diarrhea admitted to a veterinary teaching hospital. The mortality rate was 22%. Classification tree analysis indicated that mortality was associated with clinical signs of neurologic disease, abdominal emergencies, cachexia, orthopedic problems such as septic arthritis, and profound acidemia (jugular venous blood pH < 6.85). When exclusively considering laboratory parameters, classification tree analysis identified plasma glucose concentrations < 3.2 mmol/L, plasma sodium concentrations ≥ 151 mmol/L, serum GGT activity < 31 U/L and a thrombocyte count < 535 G/L as predictors of mortality. However, multivariable logistic regression models based on these laboratory parameters did not have a sufficiently high enough sensitivity (59%) and specificity (79%) to reliably predict treatment outcome. The sensitivity and specificity of jugular venous blood pH < 6.85 were 11% and 97%, respectively, for predicting non-survival in this study population. We conclude that laboratory values (except jugular venous blood pH < 6.85) are of limited value for predicting outcome in critically ill neonatal calves with diarrhea. In contrast, the presence of specific clinical abnormalities provides valuable prognostic information.

Glioblastoma Multiforme with Hypodipsic Hypernatremia in a Seven-Month-Old Golden Retriever.

Primary hypodipsic hypernatremia is a rarely reported disease in dogs. Reported underlying causes associated with this disease in dogs include congenital malformations, encephalitis, intracranial neoplasia, and pressure atrophy of the hypothalamus secondary to hydrocephalus. The dog in this report had an infiltrative neoplastic disorder, likely causing damage to the hypothalamic osmoreceptors responsible for the thirst generation. The neoplastic process was identified histopathologically as glioblastoma multiforme, an unusual tumor to occur in a dog this young. A tumor of the central nervous system causing physical destruction of the osmoreceptors has rarely been reported in dogs and none of the previously reported cases involved a glial cell tumor.

Hypernatremia in a Cat with Toxoplasma-Induced Panencephalitis.

A 12 yr old female neutered Carthusian crossbreed cat was presented due to progressive neurological signs. Clinical signs included dehydration, stupor, and anisocoria. Laboratory examination revealed severe hypernatremia, azotemia, hyperglobulinemia, and an erythrocytosis. Clinical signs and hypernatremia suggested an intracranial process. Imaging studies revealed a loss of structure in the cerebrum, hypothalamus, and pituitary gland. Due to a poor prognosis, the cat was euthanatized. Histopathological examination revealed a subacute granulomatous and necrotizing panencephalitis with Toxoplasma-typical protozoa. The Toxoplasma-induced dysfunction of the hypothalamus and pituitary gland led to diabetes insipidus, which was, in combination with insufficient water intake, the most likely cause for the hypernatremia.

Severe hyperthermia, hypernatremia, and early postoperative death after transethmoidal cavitron ultrasonic surgical aspirator (CUSA)-assisted diencephalic mass removal in 4 dogs and 2 cats.

OBJECTIVE: To report clinical findings including severe hyperthermia and hypernatremia after transethmoidal Cavitron ultrasonic surgical aspirator (CUSA)-assisted diencephalic mass removal. STUDY DESIGN: Retrospective case series. ANIMALS: Dogs (n = 4) and 2 cats. METHODS: Medical records (1997-2003) of dogs and cats that had transethmoidal CUSA-assisted diencephalic mass removal were reviewed. Retrieved data were: history, signalment, blood work, neurologic examination findings, MRI results, histopathology, postoperative complications, pre- and postoperative medical therapy, and outcome. RESULTS: Tumor types included: meningioma (n = 3), choroid plexus papilloma (1), astrocytoma (1), and pituitary macroadenoma (1). Median onset of hyperthermia was 3.5 hours (range: 1-6 hours) after extubation; median high temperature at onset was 40.3°C, (range: 39.6-41.7°C). Median onset of hypernatremia (median, 172 mmol/L; range: 168-196 mmol/L) was 4.5 hours (range: 1-9 hours) after extubation. Median time of death after hyperthermia was 10.5 hours (range: 6-13 hours) and after extubation was 13.5 hours (range: 11-15 hours). CONCLUSIONS: Transethmoidal CUSA-assisted diencephalic mass removal is associated with early postoperative hyperthermia, hypernatremia, and death, and cannot be recommended.

Primary hypodipsia in a cat with severe hypernatremia.

CLINICAL SUMMARY: A 4.5-year-old male castrated domestic shorthair cat presented with a 2-month history of muscle tremors progressing to weakness, pelvic limb ataxia, mild facial twitching, poor appetite and polyuria. Primary hypodipsia and resultant hypernatremia was diagnosed. Intensive fluid therapy and monitoring were initially required for stabilization, and the cat's condition was successfully managed long-term using canned food supplemented with additional water. PRACTICAL RELEVANCE: Primary hypodipsia is rare in clinical practice, but experience with this case suggests that associated hypernatremia can be successfully managed using a water-enriched diet to provide maintenance hydration.

Polioencephalomalacia secondary to hypernatremia in squirrel monkeys (Saimiri sciureus).

Squirrel monkeys (Saimiri spp) are one of the most consistently used New World primates in biomedical research and are increasingly being used in neuroscience research, including models of drug abuse and addiction. Spontaneous neurologic disease in the squirrel monkey is uncommonly reported but includes various infectious diseases as well as cerebral amyloidosis. Hypernatremia is an extremely serious condition of hyperosmolarity that occurs as a result of water loss, adipsia, or excess sodium intake. Neurologic effects of hypernatremia reflect the cellular dehydration produced by the shift of water from the intracellular fluid space into the hypertonic extracellular fluid space. Severe hypernatremia may result in cerebrocortical laminar necrosis (polioencephalomalacia) in human patients as well as in a number of domestic species, including pigs, poultry, and ruminants. We report the clinical, histopathologic, and immunohistochemical findings of polioencephalomalacia in 13 squirrel monkeys. Polioencephalomalacia in these animals was associated with hypernatremia that was confirmed by serum levels of sodium greater than 180 mmol/L (reference range, 134.0-154.0 mmol/L [mEq/L]). All animals had concurrent diseases or experimental manipulation that predisposed to adipsia. Immunohistochemical investigation using antibodies to neuronal nuclei (NeuN), CNPase, Iba-1, and CD31 revealed necrosis of predominantly cerebral cortical layers 3, 4, and 5 characterized by neuronal degeneration and loss, oligodendrocytic loss, microglial proliferation, and vascular reactivity. The squirrel monkey is exquisitely sensitive to hyperosmolar metabolic disruption and it is associated with laminar cortical necrosis.

[Disturbances of water metabolism in two dogs and one cat with central nervous system disorders]. / Störungen des Wasserhaushaltes bei zwei Hunden und einer Katze mit ZNS-Erkrankungen.

Hypernatremia due to different pathophysiological mechanisms results in a rise in plasma osmolality. Dependent on its severity and on the speed of its development hyperosmolality can be life-threatening. This article describes 2 dogs and 1 cat with central nervous system disorders (adenoma of the pituitary gland, cerebral trauma). All patients developed normovolemic hypernatremia due to pituitary gland and hypothalamus dysfunction, respectively. Plasma sodium concentrations ranged from 163 to 185 mmol/l. Neurological examinations revealed lethargy, disturbances of consciousness, and ataxia, respectively. The dogs had to be euthanased due to the grave prognosis, the cat with cerebral trauma survived.

Le développement d'une hypenatrémie peut avoir plusieurs mécanismes patho-physiologiques. Dans ces cas, il se produit toujours une élévation de l'osmolarité du plasma. Selon l'importance de l'hypernatrémie et la vitesse de l'apparition, une hyperosmolarité peut mettre la vie en danger. Dans le présent article, on décrit des affections du système nerveux central chez deux chiens (adénome de l'hypophyse) et un chat (trauma crânien) ayant développé une hypernatrémie normovolémique suite à un dysfonctionnement de l'hypophyse ou de l'hypothalamus. Les concentrations plasmatiques de sodium étaient comprises entre 163 et 185 mmol/l. Les animaux présentaient de la léthargie, des troubles de la conscience et de l'ataxie. Vu le mauvais pronostic, les chiens ont dû être euthanasiés, le chat victime d'un traumatisme crânien a survécu.

Efeitos do polietilenoglicol 3350 e de soluções acidificantes e alcalinizantes sobre o perfil bioquímico de éguas hígidas / Effects of polyethylene glycol 3350 and alkalizing and acidifying solutions on the biochemical profile of healthy mares

Avaliou-se o perfil bioquímico de cinco éguas hígidas tratadas com polietilenoglicol 3350 (PEG); ou com polietilenoglicol 3350+Ringer lactato (PEG+RL); ou com solução isotônica poliônica enteral (SIPE); ou com solução isotônica poliônica enteral associada ao Ringer lactato intravenoso (SIPE+RL); ou com solução de cloreto de sódio a 0,9% (NaCl 0,9%). Os parâmetros avaliados foram: sódio, cloreto, potássio, cálcio ionizado, fósforo, magnésio total, proteínas totais, albumina, creatinina, ureia e osmolaridade calculada no soro de sangue venoso. O tratamento PEG não alterou os parâmetros bioquímicos. O PEG+RL diminuiu o fósforo. O SIPE diminuiu o fósforo e aumentou o cloreto. O SIPE+RL aumentou o sódio, e o NaCl 0,9% ocasionou o aumento do cloreto e a redução da osmolaridade sérica. Concluiu-se que o tratamento PEG associado ao Ringer lactato pode provocar o aparecimento de hipofosfatemia, o SIPE ocasiona hipercloremia, o NaCl 0,9% diminui a osmolaridade sérica e o SIPE+RL provoca hipernatremia.

The biochemical profile of five healthy mares treated with polyethylene glycol 3350 (PEG); or polyethylene glycol 3350+Ringer lactate intravenous (PEG+RL); or enteral polionic isotonic solution (EPIS); or enteral polionic isotonic solution associated with Ringer lactate intravenous (EPIS+RL); or chloride sodium solution 0.9% (NaCl 0.9%) was evaluated. The parameters evaluated were: sodium, chloride, potassium, ionized calcium, phosphorus, total magnesium, total protein, albumin, creatinine, urea, and calculated serum osmolality of venous blood. PEG treatment did not alter biochemical parameters. PEG+RL decreased phosphorus. SIPE decreased phosphorus and increased chloride. The EPIS+RL caused an increase of sodium and NaCl 0.9% caused an increase of chloride and a reduction of serum osmolarity. It is concluded that PEG treatment associated with Ringer lactate solution can cause the appearance of hypophosphatemia, EPIS causes hyperchloremia, NaCl 0.9% decreases the serum osmolality and EPIS+RL causes hypernatremia.

Hypernatremia associated with intracranial B-cell lymphoma in a cat.

An 8-year-old, spayed female, domestic shorthair cat with a history of hyperthyroidism, anorexia, dehydration, cervical ventroflexion, and behavioral changes was referred to the Iowa State University College of Veterinary Medicine. The cat was obtunded, with severe dehydration (15%) and hypothermia (86 degrees F), and severe muscle atrophy and fasciculations. Serum biochemical abnormalities included severe hypernatremia (195 mmol/L, reference interval 155-165 mmol/L), hyperchloridemia (161 mmol/L, reference interval 123-131 mmol/L), and hypokalemia (3.6 mmol/L, reference interval 4.0-5.7 mmol/L). Calculated osmolality was 418 mOsm/kg (reference interval 280-305 mOsm/kg), attributable to the hypernatremia. The cat was kept warm and given fluid and glucocorticoid therapy and supportive measures but remained unresponsive. Hypernatremia and hyperosmolality improved through day 3, when the cat died suddenly. At necropsy, a 1.25-cm mass was found in the area of the thalamus and interthalamic adhesion that extended to the ventral aspect of the cerebrum. The histologic and immunohistochemical diagnosis was B-cell lymphoma. Hypernatremia and hyperosmolality in this cat were attributed to primary adipsia and hypothalamic dysfunction secondary to effacement of central nervous system tissue by neoplastic lymphocytes. To the authors' knowledge, this is the first reported case of central nervous system lymphoma, confirmed by use of immunohistochemical analysis as a B-cell phenotype, associated with hypernatremia. It also is the first reported case of lymphoma in animals limited to the thalamus, hypothalamus, and cerebrum, with no involvement of the spinal cord.

Adipsia and hypernatraemia in a dog with focal hypothalamic granulomatous meningoencephalitis.

A 7-year-old Doberman was presented with a history of progressive neurological disease of 4 weeks duration. Initially there were episodes of aimless wandering and uncharacteristic aggression, however, the dog was obtunded at presentation. Serum biochemical analysis revealed profound hypernatraemia and moderate hyperproteinaemia. Despite correction of the hypernatraemia by the infusion of hypotonic fluids, the dog continued to periodically exhibit pacing and head pressing. A patchy, ill-defined contrast-enhancing area was evident in the ventral midbrain on computed tomography of the brain. Analysis of the cerebrospinal fluid revealed a mild increase in protein concentration, positive Pandy's test and mild pleocytosis. Because of the poor prognosis, euthanasia and necropsy were performed. Histopathological analysis of the brain revealed a severe focal meningoencephalitis affecting hypothalamic nuclei and mammillothalamic tracts. Destruction of osmoreceptors in the hypothalamus responsible for recognition of thirst is believed to have resulted in adipsia and subsequent hypernatraemia.

Ependymoma of the neurohypophysis and hypernatremia in a horse.

A 2-year-old Standardbred gelding was examined because of prolapse of the third eyelid; myoclonus of the muscles of the head, neck, and forelimbs; and persistent tail swishing. The horse had a high plasma sodium concentration but was not drinking water. The hypernatremia could not be corrected by means of IV administration of fluids, and the horse became worse and, 6 days later, died. At necropsy, a tumor was found to be compressing the neurohypophysis and the area in the brain in which the thirst centers are believed to be located. It is believed that hypernatremia in this horse was a result of altered thirst.

Hypodipsic hypernatremia and associated myopathy in a hydrocephalic cat with transient hypopituitarism.

Hypodipsic hypernatremia developed in association with hypopituitarism and hydrocephalus in a 7-month-old cat. Initial clinical signs (generalized weakness, cervical ventroflexion) were related to a hypernatremia-induced polymyopathy. Forced water intake and dietary sodium restriction corrected the hypernatremia and signs of muscle dysfunction. After restoration of eunatremia, secretion of pituitary hormones normalized. It was speculated that hypothalamic dysfunction, possibly related to hydrocephalus, induced both hypodipsia and transient hypopituitarism.