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.     

D-lactic acidosis secondary to exocrine pancreatic insufficiency in a cat

An indoor, 2-year-old, spayed female domestic cat was referred to the University of Missouri Veterinary Medical Teaching Hospital (UMC-VMTH) for evaluation of weight loss and polyphagia of 1-year duration, with recent episodes of generalized weakness and lethargy. These episodes occurred approximately once per month over the past 4 months. The cat produced frequent stools, which were occasionally poorly formed. A CBC and serum biochemistry were performed 1 and 5 months before referral, and leukopenia (1,200/μL; reference interval, 3,500-16,000/μL; no differential provided), hypocholesterolemia (64 mg/dL and 46 mg/dL; reference interval, 75–220 mg/ dL), and hypotriglyceridemia (22 mg/dL and 16 mg/dL; reference interval, 26–160 mg/dL) were identified. The most recent serum biochemistry results disclosed mild hypercalcemia (11.3 mg/dL; reference interval, 8.2–10.8 mg/ dL) and hypernatremia (163 mg/dL; reference interval, 145–158 mg/dL). Antibody titers for Toxoplasma were consistent with past exposure (immunoglobulin M [IgM] negative; IgG 1:256).     

What is your diagnosis? Abdominal mass aspirate in a cat with an increased Na:K ratio

Abstract: A 13‐year‐old domestic shorthair cat was presented for evaluation of pollakiuria. Laboratory abnormalities included mild hypercholesterolemia, moderate hypertriglyceridemia, and a mild increase in the Na:K ratio (43, reference interval 32–41). Abdominal ultrasonography revealed urinary calculi and a soft tissue mass between the right caudate liver lobe and the right kidney. Surgery was done to remove the cystic calculi, and aspirates of the mass were obtained. Cytologic specimens contained a population of large, round to angular cells with round nuclei, coarse irregularly stippled chromatin, 1–2 prominent round to angular nucleoli, and abundant pale basophilic cytoplasm distended by numerous well‐delineated vacuoles. Rare binucleated cells and micronuclei, and moderate anisocytosis, anisokaryosis, and anisonucleoleosis were noted. The cytologic interpretation was adrenal neoplasia, consistent with adrenal carcinoma. Approximately 4 months later, the cat developed vomiting, dehydration, weakness, and cervical ventroflexion. Serum biochemical alterations at that time included marked hypokalemia (2.4 mmol/L, reference interval 3.4–5.6 mmol/L) and a markedly increased Na:K ratio (65, reference interval 32–41). Mean systolic blood pressure was 205 mmHg. Surgical removal of the mass was accomplished via right adrenalectomy and a diagnosis of adrenal carcinoma was confirmed histologically. Plasma aldosterone concentration (measured preoperatively) was 1358 pmol/L (reference interval 194–388 pmol/L). Primary hyperaldosteronism caused by a functional adrenal carcinoma is an uncommon condition in cats.     

Successful treatment of severe salt intoxication in a dog

Objective: To report successful treatment of severe salt intoxication and hypernatremia in a dog. Case summary: A 5‐year‐old intact female Doberman Pinscher was admitted to the intensive care unit with a history of seizures and coma. The owner had administered approximately 100 g of cooking salt to induce vomiting following ingestion of a nontoxic dose (10 g) of chocolate. Upon admission, the dog was comatose with intermittent seizures and vomiting. Diagnostic tests confirmed salt intoxication (Na: 200 mEq/L, Cl: 180 mEq/L) and metabolic acidosis (pH: 7.18; pCO₂: 39 mmHg; HCO₃: 14.3 mmol/L). Immediate treatment included intravenous fluid therapy, an anticonvulsant, antiemetic, diuretic, low molecular weight heparin, and supplemental oxygen. A fluid therapy protocol was initiated to decrease serum sodium concentration by approximately 2 mEq/L/hr. After 24 hours of intensive care, the patient regained consciousness and volume and acid‐base abnormalities improved. The patient developed a variety of abnormal clinical signs as a result of the severe hypernatremia. After 5 days of treatment, the serum sodium concentration returned to the established reference range. The patient recovered completely in 10 days. New information provided: Severe hypernatremia due to salt ingestion is a rare condition in dogs. All dogs in previous case reports of salt intoxication have died. This case report is the first to report survival of a dog with severe salt intoxication.     

Hypernatremia in Calves

Hypernatremia (sodium chloride intoxication) is described in two calves due to presumed mixing errors of oral electrolyte solutions while undergoing therapy for neonatal diarrhea. The experimental induction of hypernatremia in two clinically normal calves is also reported. Physical findings in diarrheic calves included depression, weakness, dehydration, and diarrhea. Serum sodium concentrations were found to be 171.6 mEq/l and 208.0 mEq/l, respectively. Treatment with intravenous fluids was attempted in both cases, but one calf died after 6 hours and the other calf died after 2 days and exhibited periodic convulsions before death. Experimental induction with oral administration of 1 l of electrolyte concentrate, which contained approximately 2750 mEq sodium revealed that the normal calves would willingly consume the solution as mixed with milk and develop clinical signs of hypernatremia within 6 hours of administration. Serum sodium concentrations of 176.0 and 179.8 were found in the experimental calves and coincided with the onset of overt depression and weakness, at which time they were euthanatized. Cerebrospinal fluid electrolyte analysis paralleled the serum electrolyte alterations.     

Semilobar holoprosencephaly in a Morgan horse

A6 1/2‐month‐old Morgan filly was examined because of a history of abnormal behavior, teeth grinding, hypothermia, and electrolyte disturbances when weaned. She was from a breeding farm with several other Morgan horses. The 11‐year‐old dam had been purchased the year before as a proven broodmare, which had several previous foals. Breeding, gestation, and birth of this foal were normal. She was raised with 4 other mares and their offspring on pasture with free access to shelter in an open barn. Supplementary feeding consisted of oats and timothy hay. The owners reported that the foal showed unusual behavior, such as lack of apprehension of people, lack of distress from maternal separation, and a higher activity level than other foals of the same age. The foal extensively chewed the dam's tail and mane, masticated oats slowly with rapid jaw movements without actually swallowing them, and ground her teeth. She frequently nibbled the handler's clothes without biting, ate pebbles, and played with the salt block in the paddock. At 4 1/2 months of age, she was treated for suspected gastroduodenal ulcers and weaned. The referring veterinarian examined her 5 days after weaning because of dull demeanor and excessive teeth grinding. The foal was in thin body condition, hypothermic (37°C, 98.6°F), and tachycardic (60 beats per minute [bpm]) and had decreased borborygmi. Major abnormalities on serum biochemistry were severe hypernatremia (166 mmol/L; reference range 136–144 mmol/L) and hyperchloremia (128 mmol/L; reference range 94–104 mmol/L), azotemia (urea, 11.3 mmol/L; reference range 4.2–8.9 mmol/L), and hyperfibrinogenemia (5.2 g/L, reference range 1.6–2.9 g/L). The only abnormality on the CBC was hemoconcentration (PCV, 0.57 L/L; reference range 0.28–0.44 L/L). The foal was treated with penicillin procaine G^a (20,000 IU/kg [9072 IU/1b] IM q12h) and rifampin^b (5 mg/kg [2.7 mg/1b] PO q8h). The next day the tachycardia worsened (120 bpm) and the foal was estimated to be 5–8% dehydrated. IV fluid therapy with lactated Ringer solution^c (LRS) was initiated, and the antibiotic was changed to ceftiofur^d (2 mg/kg [0.91 mg/1b] IV q12h). The foal and dam were rejoined, and the foal's clinical status improved with resumption of nursing. Serial laboratory testing showed persistent hypernatremia 160 mmol/L) and hyperchloremia (123 mmol/L), azotemia urea 11.3 mmol/L and creatinine 168 umol/L; reference range 80–130 μmol/L), hyperglycemia (8.7 mmol/L; reference range 3.7–6.7 mmol/L), high aspartate aminotranferase activity (662 U/L; reference range 259–595 U/L), and high creatine kinase (CK) activity (1,196 U/L; reference range 108–430 U/L). The foal's condition improved and IV fluids were discontinued. Ceftiofur administration was discontinued and trimethoprim‐sulfamethoxazole^e (25 mg/kg [11.3 mg/1b] PO q12h) was administered for 3 days. During the next month the foal was stable but the abnormal behavior persisted. She was weaned again, and within days marked behavior changes such as circling, throwing the head around compulsively, and severe hind‐end shivering recurred. At examination, the foal was dull, tachycardic (60 bpm), was hypothermic (33.6°C, 92.5°F), had dark red mucous membranes, and was estimated to be 5% dehydrated. Laboratory findings were similar to those of the previous tests except for high fibrinogen (7.1 g/L). The foal was again rejoined with the dam, treated with intramuscular penicillin, and referred     

Hypernatremia in neonatal elk calves: 30 cases (1988-1998)

OBJECTIVE: To characterize hypernatremia in neonatal elk calves, including clinical signs, incidence, physical examination findings, and possible causes. DESIGN: Retrospective case series. ANIMALS: 26 neonatal elk calves were examined; 4 calves were evaluated twice, for a total of 30 examinations. PROCEDURE: Medical records were reviewed for signalment, history, physical examination findings, results of diagnostic tests, and response to treatment. Hypernatremia was defined as serum sodium concentration > 153 mEq/L. RESULTS: Hypernatremia was diagnosed in 14 calves and was significantly associated with diarrhea, high WBC count, high anion gap, and high serum concentrations of albumin, chloride, creatinine, and urea. Hypernatremia was not significantly associated with survival, but high serum albumin concentration and rectal temperature were significantly associated with survival of calves. Animals given antibiotics and electrolyte solutions orally prior to evaluation were significantly more likely to die than those untreated. Dehydration was a common reason for evaluation but was not significantly associated with survival. CONCLUSIONS AND CLINICAL RELEVANCE: Hypernatremia was significantly associated with diarrhea. Treatment of diarrheic elk calves is often the same as that used in bovine calves with diarrhea; however, bovine calves are commonly hypo- or normonatremic. Our experience suggests that treatment protocols used in bovine calves are unsatisfactory for elk calves. The rate at which serum sodium concentration is reduced should be < 1.7 mEq Na/L/h to avoid development of neurologic signs associated with iatrogenically induced cerebral edema.     

B-cell conjunctival lymphoma in a cat

A bilateral conjunctival neoplasm was surgically removed from a 13-year-old Domestic Short-haired female cat and examined by histopathology. The neoplasm was infiltrative, nonencapsulated and composed of large sheets of densely packed, round to polygonal cells. Neoplastic cells were variably sized with scant to modest amounts of cytoplasm and oval to round nuclei. On immunohistochemistry the neoplastic cells stained positively for BLA.36 and negative for CD-3 antibodies. On the basis of histopathology and immunohistochemical findings, a diagnosis of conjunctival B-cell lymphoma was made. This is the first case with immunohistochemical characterization of conjunctival lymphoma in a cat.     

Apparent pseudohyperkalemia in a Chinese Shar Pei dog

Whole blood in a serum clot tube and EDTA-anticoagulated samples from an 8-year-old spayed female Chinese Shar Pei dog were submitted by an external clinic to the diagnostic laboratory at Atlantic Veterinary College for routine biochemical and hematologic analysis prior to entropion surgery. Laboratory abnormalities included mild hyperkalemia (6.3 mmol/L, reference interval 3.6-6.0 mmol/L), mild normocytic, hypochromic, nonregenerative anemia (HCT 0.31 L/L, reference interval 0.37-0.55 L/L; MCHC 290 g/L, reference interval 320-360 g/L), and increased red cell distribution width (RDW; 26.2%, reference interval 11-14%). A small subpopulation of macrocytic, slightly hypochromic erythrocytes was noted on Wright's-Giemsa-stained blood smears. Biochemical and hematologic data obtained from this patient over the previous 7.5 years indicated that serum (and in 1 case, heparinized plasma) potassium concentration was increased (range, 6.3-10.9 mmol/L) in 5 of 8 samples (HCT ranged from 0.31-0.43 L/L, Hgb 91-124 g/L, MCHC 280-312 g/L, and RDW 18.2-26.9%). Clinical signs suggestive of hyperkalemia were not observed at any time, suggesting pseudohyperkalemia as the cause of the increased potassium concentrations. An erythrocyte lysate prepared from a heparinized blood sample had a high potassium concentration (16.8 mmol/L) compared with that of a clinically healthy, non-Shiba control dog (6.7 mmol/L). An osmotic fragility test of the patient's erythrocytes showed 50% hemolysis at 0.57% NaCl, compared with 0.48% NaCl for the control dog, indicating increased fragility. On scanning electron microscopy, a small subpopulation of erythrocytes were large, flattened, and had a tendency to fold. These findings supported the provisional diagnosis of pseudohyperkalemia due to increased intracellular RBC potassium concentration. High-potassium erythrocytes have been reported in Akitas, Shibas, Jindos, other East Asian dog breeds, and occasionally, in mixed-breed dogs. Pseudohyperkalemia should also be considered when an otherwise unexplained elevation in serum or plasma potassium concentration is observed in Chinese Shar Pei dogs, and may be accompanied by increased RDW, low MCHC, and increased osmotic fragility with or without mild anemia.     

Presumptive acute lung injury following multiple surgeries in a cat

A 12-year-old, 3.5-kg spayed female domestic shorthair cat had a tracheal mass identified as malignant B-cell lymphoma. The cat had tracheal resection and subsequently developed laryngeal paralysis. Due to multiple episodes of respiratory distress the cat subsequently had tracheal surgeries. Finally, the cat had a sudden onset of severe respiratory distress and collapsed. Computed tomography imaging and arterial blood gas analysis supported a diagnosis of acute lung injury.     

Clinical, biochemical, acid-base, and electrolyte abnormalities in cats after hypertonic sodium phosphate enema administration

Ten clinically healthy cats were allotted into 2 groups. Group A was given the low (60 ml), and group B was given the high (120 ml) recommended dose of a commercial hypertonic sodium phosphate enema. Enema retention was enforced. All cats developed clinical and/or laboratory abnormalities, with group B cats being more severely affected. Clinical signs that occurred rapidly included depression, ataxia, vomition, bloody diarrhea, mucous membrane pallor, and stupor; tetany was not seen. One cat in group B died. Laboratory abnormalities included hypernatremia, hyperphosphatemia, hypocalcemia, hyperglycemia, calculated hyperosmolality, and metabolic acidosis with high anion gap probably due to hyperlacticacidemia. There were no significant gross or microscopic lesions associated with enema administration. Therefore, the use of hypertonic sodium phosphate enema at recommended doses is potentially dangerous to cats.     

Use of the advanced micro-osmometer model 3300 for determination of a normal osmolality and evaluation of different formulas for calculated osmolarity and osmole gap in adult dogs

Objective: To determine a reference interval of whole blood and plasma osmolalities for dogs using the Advanced Micro Osmometer Model 3300, to compare calculated osmolarity to measured osmolality, to determine a reference osmole gap, and to determine the best formula for calculated osmolaity. Design: Prospective, observational. Setting: Tertiary referral and teaching hospital. Animals: One hundred healthy adult dogs. Interventions: None. Measurements: Serum and whole blood biochemistry and osmolality assessments. Results: The mean and median of the measured whole blood osmolality were 323 and 320 mOsm/kg, respectively, with a standard deviation of 13.2 mOsm/kg. The mean and median of the measured plasma osmolality were 313 and 310 mOsm/kg, respectively, with a standard deviation of 13.2 mOsm/kg. The formula that was closest to predicting the measured whole blood and plasma osmolality was ((1.86(Na+K))+(BUN/2.8)+(Glucose/18))/0.93 followed closely by the traditional formula of (2(Na+K))+(BUN/2.8)+(Glucose/18). The mean calculated osmolarities using these formulas were 314.1 and 313.25 mOsm/L, respectively. The mean osmole gap using these formulas was 3.49 and 4.41 mOsm, respectively, for whole blood and ?2.01 and ?1.1 mOsm, respectively, for plasma. Conclusion: The Advanced Micro Osmometer Model 3300 was successful in measuring the osmolality in relative agreement with the current published reference intervals for osmolality. Measured osmolality correlated well with traditional calculated osmolarity.     

Evaluation of the prognostic significance of BCL6 gene expression in canine high-grade B-cell lymphoma

The clinical usefulness of BCL6 gene expression was evaluated as a prognostic indicator in dogs with high-grade B-cell lymphoma. Forty-four dogs were diagnosed with centroblastic or B-cell immunoblastic type lymphoma according to the updated Kiel classification. BCL6 mRNA expression was measured by real-time PCR and its relationship with prognosis was analyzed. Progression-free and overall survival was not significantly different between the high BCL6 expression group (higher than the median) and the low BCL6 expression group (lower than the median) (P=0.99 and P=0.61, respectively). No correlation between BCL6 and prognosis was observed in this study, which is inconsistent with findings reported for human diffuse large B-cell lymphoma. BCL6 protein expression was not detected in the 11 dogs evaluated by immunohistochemistry. Furthermore, BCL6 protein expression was assessed in 13 archived paraffin-embedded high-grade canine lymphoma tissues and all were also negative. The results suggest that most canine high-grade B-cell lymphomas correspond to human diffuse large B-cell lymphoma with no immunohistochemical expression of BCL6.     

Stomatocytosis in 7 related Standard Schnauzers

BACKGROUND: Hereditary canine stomatocytosis has been described in purebred Alaskan Malamutes, Drentse Patrijshonds, and Miniature Schnauzers. In humans, hereditary stomatocytosis is a heterogeneous group of congenital disorders characterized by the presence of stomatocytes in blood, increased osmotic fragility, and frequently, hemolytic anemia. OBJECTIVE: Our objective was to describe hematologic findings and RBC characteristics in 7 closely related Standard Schnauzers with stomatocytosis. METHODS: The following parameters were measured using an automated analyzer: HCT, RBC, hemoglobin (Hb) concentration, MCV, MCH, MCHC, red cell distribution width (RDW), WBC, platelet count, mean platelet volume (MPV), thrombocrit (PCT), and platelet distribution width (PDW). Differential leukocyte count, platelet estimate, reticulocyte count, and the percentage of stomatocytes in blood films were microscopically evaluated. An osmotic fragility test of RBCs and measurement of intracellular Na+, K+, and 2,3-diphosphoglycerate (2,3-DPG) concentrations were also performed. RESULTS: The affected dogs had macrocytosis (80.0 +/- 4.2 fL, reference interval 60-76 fL), decreased MCHC (29.3 +/- 0.8 g/dL, reference interval 32-39 g/dL), slightly increased RDW (17.3 +/- 0.4%, reference interval 12-16%), and an increased reticulocyte count (1.55 +/- 0.77%, reference interval <1%). The percentage of stomatocytes in blood films varied from 0.6 to 18.9% of all RBCs. Erythrocyte osmotic fragility and intracellular Na+ (138.1 +/- 3.2 mmol/L; controls 99 +/- 6.1 mmol/L), K+ (8.1 +/- 0.8 mmol/L; controls 6.1 +/- 0.5 mmol/L), and 2,3-DPG (21.9 +/- 2.0 micromol/g Hb; controls: 14.6 +/- 3.3 micromol/g Hb) concentrations were increased in dogs with stomatocytosis. CONCLUSIONS: Hematologic findings and the metabolic defects in RBCs in these Standard Schnauzers were consistent with a diagnosis of stomatocytosis. Parentage analysis suggests that stomatocytosis in Standard Schnauzers may have a hereditary component.     

Plasma biochemistry reference values of wild-caught southern stingrays (Dasyatis americana).

Stingrays are prominent marine animals; however, there are few published reference values for their blood chemistry and hematology. Twenty-eight southern stingrays (Dasyatis americana) were caught using the bottom trawl nets of fishery-independent boats operated by the South Carolina Department of Natural Resources during June and July 2002 from Winyah Bay, South Carolina, to St. Augustine, Florida. Median values of blood and plasma obtained from live animals promptly after capture are as follows: packed cell volume = 0.22 L/L (22%), total solids (TS) = 56.5 g/L (5.65 g/dl), total protein (TP) = 26 g/L (2.6 g/dl), sodium = 315 mmol/L, potassium = 4.95 mmol/L, chloride = 342 mmol/L, calcium = 4.12 mmol/L (16.5 mg/dl), phosphorus = 1.5 mmol/L (4.7 mg/dl), urea nitrogen = 444 mmol/L (1,243 mg/dl), glucose = 1.69 mmol/L (30 mg/dl), aspartate aminotransferase = 14.5 U/L, creatine phosphokinase = 80.5 U/L, osmolality = 1065 mOsm/kg, and lactate = 3.1 mmol/L. Bicarbonate was less than the low end of the instrument range (5 mmol/L) in all but three samples. Anion gap was negative in all samples. Albumin was less than the low end of the instrument range (1 g/dl) in all except one sample. Osmolality was significantly higher in the rays caught in the southern region. TS and TP values were linearly related to each other, and the equation for the fitted line is TS = (11.61 x TP) + 25.4 (in g/L) [or TS = (1.161 x TP) + 2.54 (in g/dl)]. The reference ranges reported in this study can be used to aid in the management of aquarium stingrays and to create a baseline for health monitoring of the wild Dasyatis spp.     

What is your diagnosis? Marked hyperchloremia in a dog

Abstract: A 5‐year‐old neutered male Cavalier King Charles Spaniel was evaluated for a 3‐week history of progressive paresis. The dog had been receiving potassium citrate capsules to acidify urine for the past 2 years because of an earlier history of urolithiasis. Results of neurologic examination, spinal cord radiography, and magnetic resonance imaging of the skull and spinal cord revealed no lesions that could have accounted for the neurologic signs. The main abnormalities on a clinical chemistry profile were marked hyperchloremia (179 mmol/L, reference interval 108–122 mmol/L) and an anion gap of ?50.4 mmol/L (reference interval 16.3–28.6 mmol/L). Because of the severe hyperchloremia, serum bromide concentration was measured (400 mg/dL; toxic concentration >150 mg/dL; some dogs may tolerate up to 300 mg/dL). Analysis of the potassium citrate capsules, which had been compounded at a local pharmacy, yielded a mean bromide concentration of 239 mg/capsule. Administration of the capsules was discontinued and there was rapid resolution of the dog's neurologic signs. This case of extreme bromide toxicity, which apparently resulted from inadvertent use of bromide instead of citrate at the pharmacy, illustrates the importance of knowing common interferents with analyte methodologies and of pursing logical additional diagnostic tests based on clinical and laboratory evidence, even when a patient's history appears to rule out a potential etiology.     

Hypernatremia and adipsia in a dog

Primary adipsia and defective osmoreceptor function were diagnosed in a 7-month-old female Miniature Schnauzer. Also, the dog was noted to be dehydrated and to have chronic hypernatremia. On multiple occasions the dog's urine osmolality: plasma osmolality was greater than 4. The dog had inappropriate responses to isoosmotic and hypertonic NaCl infusions. Chlorpropamide administration initiated water intake but the volume was insufficient to avoid hypernatremia. The chronic hypernatremia and dehydration were treated successfully by mixing the calculated maintenance fluid volume in canned food. At 25 months of age, the dog died several days after becoming dehydrated and severely hypernatremic. Astrogliosis and neuronal degeneration were noted in both the thalamic and hypothalamic regions, but were believed to be nonspecific degenerative lesions compatible with seizures and severe dehydration.     

Hypernatremia

Hypernatremia is a potentially life-threatening electrolyte abnormality. This problem develops most often because of loss of water from the animal, but in rare cases hypernatremia results from gain of sodium chloride. Important conditions predisposing to hypernatremia include diarrhea, vomiting, heat stroke, fever, limited access to water, excessive diuretic use, renal diseases, and pituitary diabetes insipidus. This condition rarely develops if animals have adequate access to water. Clinical signs relate to central nervous system derangements and can progress to seizures and coma. Diagnosis is based on the serum sodium concentration; treatment should be instituted if it is greater than 170 mEq per L. Treatment is based on knowledge of the volume status of the patient and the probable cause for the hypernatremia. In general, 5 per cent dextrose in water or other hypotonic fluids are given slowly intravenously. The rate of administration should be adjusted so the water deficit is replaced over 48 to 72 h. Too rapid correction of hypernatremia can lead to cerebral edema and worsening of the animal. In cases of salt intoxication, diuretics must be given in addition to slow water replacement to avoid the development of pulmonary edema.     

Hematology and plasma chemistry reference intervals for cultured shortnose sturgeon (Acipenser brevirostrum)

BACKGROUND: The shortnose sturgeon, Acipenser brevirostrum, is an imperiled species distributed along the Atlantic coast of North America. Interest in replenishing wild stocks with hatchery-reared fish has created a need for accurate hematologic and biochemical reference intervals to evaluate the health of both fish raised in aquaculture systems and fish in the wild. OBJECTIVES: The objective of this study was to generate hematologic and biochemistry reference intervals for healthy shortnose sturgeon. METHODS: Blood samples were collected in heparinized tubes from 77 shortnose sturgeon raised in flow-through aquaculture systems. Whole blood and plasma samples were analyzed for hematologic and biochemical variables using standard techniques. Reference intervals were calculated as the central 95% (percentile) of data. RESULTS: Hematologic reference intervals (n = 46) were as follows: PCV 26-46%, hemoglobin 5.7-8.7 g/dL, MCV 307-520 fL, MCH 65.9-107.1 pg, MCHC 15-30 g/dL, plasma proteins (refractometry) 2.8-6.0 g/dL, RBC count 0.65-1.09 x 10(6)/microL, total WBC count 28,376-90,789/microL, small lymphocytes 9063-56,656/microL, large lymphocytes 2122-10,435/microL, neutrophils 3758-33,592/microL, monocytes 0-7137/microL, eosinophils 0-1544/microL, thrombocyte-like cells 6863-23,046/microL, thrombocytes 32,205-122,179/microL, and neutrophil:lymphocyte ratio 0.068-1.026. Plasma chemistry reference intervals (n = 77) were as follows: total protein 2.7-5.3 g/dL, albumin 0.8-1.7 g/dL, globulins 1.8-3.7 mg/dL, creatinine 0-1.4 mg/dL, total bilirubin 0-0.1 mg/dL, alkaline phosphatase 47-497 U/L, aspartate aminotransferase 90-311 U/L, sodium 124-141 mmol/L, potassium 2.9-3.7 mmol/L, chloride 106-121 mmol/L, calcium 6.6-12.1 mg/dL, magnesium 1.6-2.3 mg/dL, phosphorus 5.1-8.1 mg/dL, glucose 37-74 mg/dL, cholesterol 42-133 mg/dL, and osmolality 232-289 mOsm/kg. CONCLUSION: Reference values reported here will be useful for the early detection, identification, and monitoring of disease and sublethal conditions in cultured shortnose sturgeon.