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.

Hypodipsic hypernatremia after long-standing polydipsia in a cat with suspect neonatal head trauma.

A 16-month-old neutered male domestic shorthair cat weighing 2.7 kg was referred for further evaluation of acute generalized muscle weakness and paraparesis after a long-standing history of polyuria-polydipsia. The diagnosis of hypodipsic/adipsic hypernatremia relied on the key findings of absent spontaneous drinking despite hypernatremia and a hyperosmolar state (444.8 mOsm/kg, reference interval 280 to 310 mOsm/kg). Brain MRI revealed severe multifocal anatomic anomalies of the rostral calvarium and the forebrain, suggestive of encephaloclastic porencephaly. Involvement of the thalamic and hypothalamic regions could have been responsible for the cat's adipsic hypernatremia. The unique aspects of this case were the rare description of central nervous system disease leading to hypodipsia, and the history of chronic polydipsia before the acute onset of hypodipsia. Key clinical message: Multifocal abnormalities of the forebrain can present with polyuria-polydipsia syndrome, hypodipsia/adipsia, or both, depending on the stage of the disease. This likely happens when the hypothalamic and thalamic regions are affected, since they regulate antidiuretic hormone release and thirst, respectively.

Hypernatrémie hypodipsique après polydipsie ancienne chez un chat suspect de traumatisme crânien néonatal. Un chat domestique à poil court mâle castré âgé de 16 mois et pesant 2,7 kg a été référé pour une évaluation plus approfondie de faiblesse musculaire aiguë généralisée et de paraparésie après une longue histoire de polyurie-polydipsie. Le diagnostic d'hypernatrémie hypodipsique/adipsique reposait sur les principales conclusions de l'absence d'abreuvement spontané malgré l'hypernatrémie et un état hyperosmolaire (444,8 mOsm/kg, intervalle de référence de 280 à 310 mOsm/kg). L'IRM du cerveau a révélé des anomalies anatomiques multifocales sévères de la calotte crânienne rostrale et du prosencéphale évoquant une porencéphalie encéphaloclastique. L'atteinte des régions thalamique et hypothalamique pourrait être responsable de l'hypernatrémie adipsique du chat. Les aspects uniques de ce cas étaient la description rare d'une maladie du système nerveux central conduisant à l'hypodipsie, et l'histoire de la polydipsie chronique avant l'apparition aiguë de l'hypodipsie.Message clinique clé :Les anomalies multifocales du cerveau antérieur peuvent présenter un syndrome de polyurie-polydipsie, une hypodipsie/adipsie, ou les deux, selon le stade de la maladie. Cela se produit probablement lorsque les régions hypothalamique et thalamique sont affectées, car elles régulent respectivement la libération d'hormone antidiurétique et la soif.(Traduit par Dr Serge Messier).

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.

Holoprosencephalia, hypoplasia of corpus callosum and cerebral heterotopia in a male belted Galloway heifer with adipsia.

BACKGROUND: Specialized neurons in the diencephalon detect blood hypernatremia in dehydrated animals. These neurons are connected with the pituitary gland, subsequently producing antidiuretic hormone to reabsorb water from urine in the kidneys, and to the forebrain to generate thirst and trigger drinking behavior. CASE PRESENTATION: This is the first case report describing clinical findings, magnetic resonance imaging (MRI) and necropsy results of a Belted Galloway heifer with severe clinical signs of dehydration and hypernatremia, but concurrent adipsia and isosthenuria. Due to insufficient recovery with symptomatic treatment, owners elected euthanasia. Postmortem MRI and necropsy revealed a complex forebrain malformation: mild abnormal gyrification of the forebrain cortex, lobar holoprosencephaly, and corpus callosum hypoplasia. The affected brain structures are well known to be involved in osmoregulation and generation of thirst in dogs, humans and rodents. CONCLUSIONS: Complex forebrain malformation can be involved in the pathogenesis of hypernatremia and adipsia in bovines.

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.

The successful treatment of multiple organ dysfunction syndrome and severe hypernatremia, secondary to joint supplement toxicity in a dog.

OBJECTIVE: To describe a case of the successful management of hypernatremia and multiple organ dysfunction syndrome secondary to joint supplement toxicity in a dog. CASE SUMMARY: A 6-year-old neutered male Dachshund was presented for severe hypernatremia and neurological abnormalities after ingestion of a large quantity of joint supplements. The patient developed evidence of multiple organ dysfunction in the form of increased hepatocellular enzymes, prolongation of prothrombin and partial thromboplastin times, azotemia, and thrombocytopenia. Treatment was successful at correcting the hypernatremia and restoring neurological function, and organ dysfunction was successfully managed. Following multiple days of hospitalization and aggressive supportive care, the patient survived to discharge. NEW OR UNIQUE INFORMATION PROVIDED: This case report describes the successful management and survival of multiple organ dysfunction associated with joint supplement toxicity. It also serves to highlight the potential for joint supplement overdose in veterinary patients, which is currently believed to be underrecognized.

Short communication: Hypernatremia in diarrheic calves associated with oral electrolyte administration in water and milk replacer in absence of access to water.

A major goal in treatment of calves with diarrhea is to restore hydration and to correct metabolic acidosis. This can be achieved by the administration of oral electrolyte solutions (OES). However, the composition of OES products and the administration protocols in practice vary widely, which can potentially compromise the efficacy and safety of these treatments. In particular, administration of OES in milk replacer (MR) and the absence of water supply in young calves are not unusual and these conditions could compromise calf health. In this light, the objective of this study was to evaluate the efficacy and safety of OES administered in MR and in water without access to water. Forty-five male Holstein calves (16.6 ± 1.6 d of age and 45.4 ± 2.2 kg at arrival) were purchased from a collection center located in the Netherlands. After arrival, calves went through an adaptation period of 4 d. Calves that developed diarrhea within 6 d after the end of the adaptation period were enrolled in the study, and the remaining calves were sold after being weaned. Upon morning detection of abnormal fecal scores (d 1 starting point), calves were blocked based on initial BW. Within each block, calves were randomly assigned to 1 of 2 treatments, including a control consisting of a small dose of whey (CON; n = 12) and an OES treatment (OES; n = 14). Treatments were blinded to the farm staff by randomly assigning a letter to each treatment. Treatments were simultaneously administered for 4 d in MR (2.5 L at 0800 and 1730 h) and in water (3 L at 1300 and 2200 h). Calves had no supplemental access to plain water. Blood samples were taken at 0600 h for 4 d, and fecal scores (0 = normal; 1 = watery feces) were assessed daily at 0900 h for 15 consecutive days. Additionally, skin turgor and degree of enophthalmos were assessed at 1000 h from d 1 to 4 using a 3-level scoring system. Calves fed OES had a higher prevalence of diarrhea on d 3, 4, and 5 as well as higher prevalence of delayed skin turgor and increased degree of enophthalmos over the 4 monitoring days. Diarrhea duration was longer in calves receiving OES than in calves receiving CON (4.2 d vs. 2.1 d, respectively). The OES treatment resulted in hypernatremia (serum Na+ >145 mmol/L) within 48 h after the first OES administration. Hypernatremia was linked with higher serum Cl- and urea concentrations and thus higher serum osmolarity in OES calves compared with CON calves. Administered under these conditions, OES resulted in various degrees of hypernatremia and a delayed recovery from diarrhea, thus defeating the purpose of OES administration.

Severe hypernatremia and transient azotemia in a cat following inadvertent intravenous administration of a commercial polyethylene glycol solution.

OBJECTIVE: To describe the clinical signs, clinicopathologic abnormalities, treatment, and outcome after IV administration of polyethylene glycol 3350 (PEG3350) in a cat. CASE SUMMARY: A cat was inadvertently administered 6 g/kg of PEG3350 in electrolyte solution, IV, resulting in severe hypernatremia (203 mmol/L), diffuse encephalopathy, hemolysis, and moderate azotemia. The hemolysis and acute kidney injury observed immediately following PEG3350 administration resolved with supportive care. Administration of IV and oral electrolyte-free water slowly corrected the hypernatremia and the neurologic signs subsequently improved. Complete resolution of clinical signs was documented one month following hospital discharge. The PEG3350 concentrations in serum, plasma, and urine samples confirmed toxic exposure to PEG3350. Efficacy of treatment was evident by decreasing concentrations of PEG3350 in serum after the first 24 hours of treatment. Renal elimination of PEG3350 was significant and PEG3350 was still detected in the urine 17 days after exposure. NEW INFORMATION PROVIDED: This is the first report to describe the clinical signs and clinicopathologic abnormalities in a cat intoxicated with IV PEG3350. Potential pathophysiologic mechanisms are discussed, and the successful supportive medical treatment is outlined.

Hypernatraemia in 39 hospitalised foals: clinical findings, primary diagnosis and outcome.

OBJECTIVE: To evaluate hypernatraemia in foals presenting as medical emergencies to an intensive care unit (ICU) to determine the prevalence, clinical findings, primary diagnosis and outcome. METHODS: Retrospective case study of records from Thoroughbred foals aged less than 3 months that presented to an ICU as medical emergencies in 2002-12. Data retrieved included signalment, clinical findings, laboratory results, primary diagnosis and outcome. Foals with hypernatraemia (serum sodium > 145 mmol/L) on admission laboratory data were identified and further evaluated. RESULTS: A total of 39 of 1718 foals (2.3%) were diagnosed with hypernatraemia; all foals were less than 7 days of age. The most common primary diagnoses in the foals with hypernatraemia were neonatal syndrome (19/39, 48.7%) and sepsis (15/39, 38.5%). Foals with hypernatraemia at presentation were more likely to die or be euthanased during their hospitalisation than foals with a normal serum sodium concentration on ICU admission (33.3% vs 16.1%; odds ratio, 2.3; 95% confidence interval, 1.2-4.6; P = 0.02). CONCLUSION: Admission hypernatraemia was an uncommon but important electrolyte abnormality in this population of hospitalised foals. Although the short-term outcome in survivors was most likely dependent on the underlying disease process, hypernatraemia was negatively associated with outcome in hospitalised foals.

Food engorgement in 35 dogs (2009-2013) compared with 36 dogs with gastric dilation and volvulus.

The clinical features and management of food engorgement (FE) in dogs have not been previously described. This retrospective observational study describes characteristics and outcome of 35 dogs with FE, and compares features on presentation to 36 dogs with gastric dilation and volvulus (GDV). Cases were retrospectively reviewed for history, clinical findings and outcome. Gastric distension was measured by caudal gastric margin (CGM), level with lumbar vertebrae, on a lateral abdominal radiograph. Frequent characteristics of dogs with FE included tachycardia, tachypnoea, hyperproteinaemia, increased base excess (BE), mild hypernatraemia and hyperlactataemia. There was overlap in CGM between dogs with GDV (CGM range L3 to >L6) and dogs with FE (CGM range

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.

The muscular dystrophic chicken is hypernatremic.

1. The E3 ubiquitin protein ligase 1 (WWP1) gene, the mutation of which causes muscular dystrophy in chickens, is expressed not only in the pectoral muscle, but also in a number of tissues such as the kidney. Therefore, this study examined some parameters related to kidney function in muscular dystrophic (MD) chickens. 2. Plasma osmolality, Na+ and K+ concentrations, aldosterone levels, and the expression of aquaporin (AQP) 2, AQP3, and α subunits of the amiloride-sensitive epithelial sodium channel (αENaC) were analysed in the kidneys of 5-week-old MD chickens and White Leghorn (WL) chickens under physiological conditions or after one day of water deprivation. 3. Plasma osmolality, Na+ concentrations, and plasma aldosterone levels were significantly higher in MD chickens than in WL chickens. αENaC mRNA expression levels were lower in MD chickens than in WL chickens. AQP2 and AQP3 mRNA expression levels were similar in the two strains of chickens. 4. Plasma osmolality correlated with aldosterone levels and AQP2 and αENaC mRNA levels in WL chickens. In MD chickens, plasma osmolality correlated with AQP2 mRNA levels, but not with plasma aldosterone or αENaC mRNA levels. 5. These results suggest that neither water reabsorption nor the expression of AQP2 and AQP3 is impaired in MD chickens and that a WWP1 gene mutation may or may not directly induce an abnormality in Na+-reabsorption in the kidneys of MD chickens, potentially through αENaC.

A Quick Reference on Hypernatremia.

Hypernatremia most commonly is associated with water loss in excess of sodium or salt gain (typically associated with restriction of access to water). Most of the signs of hypernatremia arise from the central nervous system; the more rapid the development of hypernatremia, the more severe the neurologic signs are likely to be. Anorexia, lethargy, vomiting, muscular weakness, behavioral changes, disorientation, ataxia, seizures, coma, and death have been identified in dogs and cats with hypernatremia and hypertonicity.

Disorders of Sodium and Water Homeostasis.

This review article discusses normal and abnormal sodium balance in small animals. The terms and concepts central to understanding normal sodium and water balance are presented as well as of the physiology of body fluid compartments and the movement of fluid between those compartments. As dysnatremia is a very common disorder across the spectrum of critically ill patients, the main focus of the article is to present several clinical examples of both acute and chronic hypernatremia and hyponatremia and their practical, clinical management.

Cerebral Disorders of Calves.

Neurologic diseases of the cerebrum are relatively common in cattle. In calves, the primary cerebral disorders are polioencephalomalacia, meningitis, and sodium toxicity. Because diagnostic testing is not always readily available, the practitioner must often decide on a course of treatment based on knowledge of the likely disease, as well as his or her own clinical experience. This is particularly true with neurologic diseases in which the prognosis is often poor and euthanasia may be the most humane outcome. This article reviews the most common diseases affecting the cerebrum of calves with a focus on pathophysiology, diagnosis, and treatment.

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.

Perioperative Acid-Base and Electrolyte Disturbances.

Obtaining and interpreting blood gas and electrolyte levels is essential in the management of perioperative veterinary patients. Metabolic and electrolyte alterations are common in critically ill surgical patients, and can lead to alterations in cardiovascular function, neurologic status, respiratory function, and even response to various drug therapies. Several common perioperative conditions are discussed in this article, including metabolic disturbances, electrolyte abnormalities (hyponatremia and hypernatremia, hyperkalemia), and respiratory abnormalities.

Incidence, severity and prognosis associated with hypernatremia in dogs and cats.

BACKGROUND: Hypernatremia has been associated with substantial morbidity and death in human patients. The incidence and importance of hypernatremia in dogs and cats has not been determined. HYPOTHESIS/OBJECTIVES: To describe the incidence of and prognosis associated with hypernatremia in dogs and cats at a university teaching hospital. ANIMALS: A total of 16,691 dogs and 4,211 cats with measured blood or serum sodium concentration. METHODS: Retrospective study. Medical records of animals with a blood or serum sodium concentration measured during a 60-month period were reviewed to determine the severity of hypernatremia and its associated case fatality rate. Cases with moderate (11-15 mmol/L above the reference range) or severe hypernatremia (≥16 mmol/L above the reference range) were further reviewed. RESULTS: A total of 957 dogs (5.7%) and 338 cats (8.0%) were diagnosed with hypernatremia. Case fatality rates of dogs and cats with hypernatremia was 20.6 and 28.1%, respectively compared to 4.4 and 4.5% with a normal blood or serum sodium concentration (P < .0001). The magnitude of hypernatremia was linearly associated with a higher case fatality rate (P < .0001). Hypernatremia was associated with a higher case fatality rate than hyponatremia. Among the animals with moderate or severe hypernatremia, 50% of dogs and 38.5% of cats presented with community-acquired hypernatremia, and 50% of dogs and 61.5% of cats developed hospital-acquired hypernatremia. CONCLUSIONS AND CLINICAL IMPORTANCE: Hypernatremia was found infrequently in this population but was associated with increased case fatality rates in dogs and cats. Presence and severity of hypernatremia might be useful as a prognostic indicator.