Blood, urine, and ruminal fluid changes associated with metabolic alkalosis induced by duodenal obstruction

Two Holstein heifers and a steer fitted with ruminal and duodenal cannulas were used to determine acid-base and electrolyte changes associated with metabolic alkalosis induced by duodenal obstruction. Obstruction was induced distally to the pylorus, but proximally to the common bile duct entrance. Ruminal fluid, blood, and urine samples were obtained before and after obstruction was induced. Duodenal obstruction resulted in increased blood pH, bicarbonate concentration, and base-excess values. Severe hypochloremia and hypokalemia were evident in 48 hours. Serum sodium concentration decreased only slightly. Packed cell volume and serum concentrations of urea nitrogen, creatinine, glucose, and inorganic phosphate increased, whereas calcium concentration showed no change. Renal chloride excretion reached near zero in 24 hours, whereas sodium and potassium excretions decreased in the steer, but were unchanged in the heifers. Urine creatinine concentration increased markedly in the heifers and steers. Acid urine was not evident up to 96 hours. Ruminal fluid pH decreased and chloride concentration increased in the steer, but remained unaffected in the heifers. Duodenal obstruction had no effect on rumen sodium, calcium, and magnesium concentrations, but the potassium concentration increased in the heifers. The degrees of alkalosis and electrolyte changes were greater in the steer than in the heifers.     

The influence of crystalloid type on acid–base and electrolyte status of cats with urethral obstruction

Objective: To compare the effect of a balanced isotonic crystalloid solution with that of 0.9% sodium chloride on the acid–base and electrolyte status of cats with urethral obstruction.
Design: Randomized prospective clinical trial.
Setting: Academic veterinary emergency room.
Animals: Sixty-eight cats with naturally occurring urethral obstruction.
Interventions: Cats were randomized to receive either a balanced isotonic crystalloid solution (Normosol-R, n =39) or 0.9% sodium chloride ( n =29) for fluid therapy. Baseline venous blood gas and blood electrolyte values were obtained at the time of admission and at intervals during the course of therapy.
Measurements and main results: Baseline values were similar between groups. Cats receiving Normosol-R had a significantly higher blood pH at 12 hours, a significantly greater increase in blood pH from baseline at 6 and 12 hours, as well as a significantly higher blood bicarbonate concentration at 12 hours and a significantly greater increase in blood bicarbonate from baseline at 6 and 12 hours. Conversely, the increase in blood chloride from baseline was significantly higher at 2, 6, and 12 hours in cats receiving 0.9% sodium chloride. There were no significant differences in the rate of decline of blood potassium from baseline between groups. Subgroup analysis of hyperkalemic cats (K⁺>6.0 mmol/L) and acidemic cats (pH<7.3) yielded similar findings.
Conclusions: While both crystalloid solutions appear safe and effective for fluid therapy in cats with urethral obstruction, the use of a balanced electrolyte solution may allow more rapid correction of blood acid–base status within the first 12 hours of fluid therapy. The use of a potassium-containing balanced electrolyte solution does not appear to affect the rate of normalization of blood potassium in treated cats with urethral obstruction.     

Poisoning induced by administration of a phosphate-containing urinary acidifier in a cat

Signs of depression, hyperphosphatemia, azotemia, high anion gap metabolic acidosis, and renal failure developed in an adult cat following administration of an excessive dose of a phosphate-containing urinary acidifier. After extracellular fluid volume expansion, diuresis, and administration of a phosphate binder, serum phosphorus concentration returned to normal in 12 hours; the cat recovered fully. The urinary acidifier had been given as part of treatment for a urinary tract infection. Findings suggest that phosphate-containing urinary acidifiers should be administered cautiously because, like other sources of phosphate, they are capable of causing life-threatening metabolic disturbances.     

Clinical features and treatment of renal tubular acidosis in two horses

Two horses were admitted separately for evaluation and treatment of profound hyperchloremic metabolic acidosis without azotemia. One, an 11-year-old Quarter Horse mare, had been depressed and ataxic for 2 days. The other, a 2-year-old Quarter Horse colt, had a 6-week history of depression, anorexia, and weight loss. Both horses responded to fluid and electrolyte therapy, but required daily oral administration of sodium bicarbonate for maintenance. In each case, the diagnosis was renal tubular acidosis.     

Characterization of the clinical characteristics, electrolytes, acid–base, and renal parameters in male cats with urethral obstruction

Objective: To characterize the clinical characteristics, electrolyte changes, acid–base changes, and renal parameters in a consecutive population of cats with urethral obstruction. Design: Retrospective clinical study. Setting: University Veterinary Teaching Hospital. Animals: Two hundred and twenty‐three male cats that presented consecutively with urethral obstruction between 1997 and 1999. Interventions: None. Measurements and main results: The medical records of 223 cats with urethral obstruction were reviewed for signalment, previous medical history, indoor/outdoor status, body weight, clinical signs, physical examination findings, renal function tests (blood urea nitrogen and creatinine), and blood gas and electrolyte analysis. The majority of cats were relatively stable without serious metabolic derangements. Only 12% (24/199) of cats had severe hyperkalemia (>8.0 mmol/L). Hyperkalemia did not occur in isolation; the majority of these cats had concurrent acidemia and low ionized calcium concentrations. Potassium was significantly inversely correlated with pH, bicarbonate, pCO₂, sodium, chloride, and ionized calcium, but positively correlated with blood urea nitrogen and creatinine. Ionized calcium was positively correlated with pH and bicarbonate. Of the animals with a potassium concentration greater than 8.0 mmol/L, 75% (18/24) had an ionized calcium concentration of less than 1.0 mmol/L. Seventy‐nine percent (19/24) of cats with a potassium concentration greater than 8.0 mmol/L had a blood pH<7.20. Similarly, 74% (23/31) of cats with a pH<7.20 had an ionized calcium concentration <1.00 mmol/L. Conclusions: The majority of cats with urethral obstruction presented with mild electrolyte and blood gas changes and were relatively stable, although 12% of cats had multiple, life‐threatening metabolic derangements. Of 219 cats in this study, 205 (93.6%), where it could be determined, survived to discharge from the hospital, supporting the fact that most cats with urethral obstruction survive the acute episode with emergency treatment.     

Feline ureteral obstructions Part 1: medical management

Feline ureteral obstructions are an increasingly recognised and challenging diagnostic and management problem. Many cats with ureteral obstructions are critically ill at the time of diagnosis, especially if there is dysfunction of the contralateral kidney. They may present with varying severities of acute kidney injury, electrolyte disturbances, and may have comorbidities such as heart disease that complicate perioperative and long‐term management. Medical management, which may consist of rehydration and restoration of intravascular volume with intravenous fluid therapy, osmotic diuresis, ureteral muscle relaxation, and antimicrobials for infection, is important in feline ureteral obstruction patients. Despite medical management, many cats with ureteral obstructions will require decompression of the obstructed kidney to relieve pressure‐nephropathy and restore urine flow. However, some cats may be too unstable for traditional medical management and require more emergent intervention to relieve the obstruction and address the life‐threatening sequelae to acute kidney injury, such as hyperkalaemia and fluid overload. Both surgical and interventional methods to address ureteral obstructions have been described in veterinary medicine, though debate continues as to the ideal approach.     

Comparison of two oral electrolyte solutions for the treatment of dehydrated calves with experimentally-induced diarrhoea

We compared the ability of two oral electrolyte solutions to resuscitate calves with experimentally induced diarrhoea and dehydration. Sucrose solution, furosemide, spironolactone, and hydrochlorothiazide were administered to 18 male Holstein-Friesian calves to induce diarrhoea and dehydration. Clinical changes after 24 h included severe diarrhoea, moderate dehydration (8-10% body weight), azotemia, and clinical depression. Calves were then randomly assigned to one of three treatment groups (milk replacer, 2 L every 12 h; hyperosmotic oral electrolyte solution, 2 L every 12 h; iso-osmotic oral electrolyte solution, 1.5 L every 6 to 12 h) and followed for an additional 48 h.Compared to feeding milk replacer, the hyperosmotic solution significantly (P< 0.05) improved hydration status, increased body weight, maintained urine production, decreased the degree of clinical depression and prevented development of metabolic acidosis, although serum glucose concentration was decreased at 24 h and 48 h. The hyperosmotic solution produced a similar resuscitative response to the iso-osmotic solution, but maintained higher serum glucose concentrations and lower serum beta-OH butyrate and non-esterified fatty-acid concentrations, indicating that the hyperosmotic solution provided greater nutritional support. The hyperosmotic solution rehydrated calves faster and more effectively than feeding equivalent volumes of milk replacer and can, therefore, be recommended as part of the initial treatment of dehydrated calves with diarrhoea.     

Hyperlipemia and Ketonuria in an Alpaca and a Llama

An alpaca and a llama in late stages of gestation were evaluated for lethargy, anorexia, and recumbency. Both camelids had cloudy, white, turbid serum, elevated serum triglyceride (1564, 5658 mg/dL, respectively) and cholesterol (158, 297 mg/dL, respectively) concentrations, and ketonuria. Signs of fetal stress were evident ultrasonographically in the alpaca, and a live cria was delivered by Cesarean section performed under general anesthesia. The alpaca developed severe metabolic acidosis, hepatic lipidosis, and acute renal failure secondary to renal lipidosis and died 36 hours after admission despite medical therapy. Histopathology revealed renal and hepatic lipidosis and neutrophilic pancreatitis. The cria died 72 hours after birth. The llama responded to IV electrolyte, dextrose, and regular crystalline insulin therapy. The pregnancy was maintained, and the llama was discharged from the hospital 20 days after admission. Two months after discharge, the llama gave birth to a live, 5 kg cria. Findings of hypertriglyceridemia, hypercholesterolemia, elevated sorbitol dehydrogenase activity, metabolic acidosis, azotemia, and ketonuria occurred in these two camelids. Based on this report, camelids appear to be similar to both horses and cattle in their response to severe energy imbalances in late gestation.     

Effect of a 24-hour infusion of an isotonic electrolyte replacement fluid on the renal clearance of electrolytes in healthy neonatal foals

OBJECTIVE: To determine the effects of a 24-hour infusion of an isotonic electrolyte replacement fluid (IERF) on weight, serum and urine electrolyte concentrations, and other clinicopathologic variables in healthy neonatal foals. ANIMALS: 4 healthy 4-day-old foals. DESIGN: Prospective study. PROCEDURE: An IERF was administered to each foal at an estimated rate of 80 mL/kg/d (36.4 mL/lb/d) for 24 hours. Body weight was measured before and after the infusion period. Urine was collected via catheter during 4-hour periods; blood samples were collected at 4-hour intervals. Variables including urine production; urine and serum osmolalities; sodium, potassium, and chloride concentrations in urine and serum; urine and serum creatinine concentrations; urine osmolality-to-serum osmolality ratio (OsmR); transtubular potassium gradient (TTKG); and percentage creatinine clearance (Cr(cl)) of electrolytes were recorded at 0, 4, 8, 12, 16, 20, and 24 hours during the infusion period. Immediately after the study period, net fluid and whole-body electrolyte changes from baseline values were calculated. RESULTS: Compared with baseline values, urine and serum sodium and chloride serum concentrations, urine and serum osmolalities, OsmR, and percentage Cr(cl) of sodium and chloride were significantly increased at various time points during the infusion; urine production did not change significantly. After 24 hours, weight, TTKG, serum creatinine concentration, and whole-body potassium had significantly decreased from baseline values. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that administration of an IERF containing a physiologic concentration of sodium may not be appropriate for use in neonatal foals that require maintenance fluid therapy.     

Assessment of blood pressure in cats presented with urethral obstruction

Objective: To determine the arterial blood pressure at presentation in male cats with acute urethral obstruction, and to determine whether there was any correlation between these measurements and concurrent metabolic abnormalities. Design: Prospective, single cohort, observational study. Setting: Private, small animal, after‐hours emergency clinic. Animals: Twenty‐eight client‐owned male cats with acute urethral obstruction and no other known coexisting disease. Interventions: Indirect oscillometric blood pressure measurements obtained before blood sampling and treatment. Measurements and main results: Mean arterial blood pressure (MAP) measurements, physical examination parameters, serum blood urea nitrogen (BUN), creatinine, potassium, phosphorus, total calcium and magnesium concentration, venous pH, lead II electrocardiogram, and urine volume in bladder were evaluated. No cats were hypotensive at presentation; 71% (20/28) were normotensive (median MAP=100 mmHg, range 93–140 mmHg); and 29% (8/28) were hypertensive (median MAP=153 mmHg, range 145–176 mmHg). Compared with hypertensive cats, normotensive cats had significantly lower heart rates (P=0.0201) and lower calcium (P=0.0152). For all 28 cats, MAP correlated with serum potassium and total calcium (P=0.0033). Conclusions: Though potassium and total calcium were inversely and directly correlated respectively with blood pressure in cats with urethral obstruction, none of the cats were hypotensive on presentation. Normotension on admission does not support the absence of biochemical and physical abnormalities in obstructed cats.     

Phosphate enema toxicosis in a pygmy goat wether

Phosphate enema toxicity was diagnosed in a 7-month-old, castrated male, pygmy goat. On presentation, clinical findings included mild depression, tachycardia, tachypnea, rumen stasis, muscle tremors, hypocalcemia, hypokalemia, hypochloremia, hyperphosphatemia, azotemia, and metabolic acidosis. Fluid diuresis and parenteral antimicrobial therapy resulted in recovery after 3 d of treatment.     

Ruminal lactic acidosis in sheep and goats.

The clinical findings in 37 sheep and goats with acute ruminal lactic acidosis included a disturbed general condition characterised by anorexia, apathy, teeth grinding and muscle twitching, ruminal stasis, and the excretion of soupy or watery faeces. The ruminal fluid of affected animals was milky, had a sour odour and a low pH. There was a predominance of Gram-positive bacteria in smears of ruminal fluid. In comparison with 10 control animals, the rumen fluid of 23 sheep with ruminal lactic acidosis had higher lactic acid and lower volatile fatty acid concentrations. In addition, the affected animals often had haemoconcentration and metabolic acidosis. Treatment included single or repeated transfer of ruminal fluid from healthy cows and, depending on the severity, the administration of antacids, yeast and chlortetracycline, and the intravenous infusion of isotonic sodium chloride and 5 per cent sodium bicarbonate solutions. Of the 37 treated sheep and goats, four died within 24 hours, and three others were euthanased after one, two and three days because their condition rapidly deteriorated. Thirty animals were discharged one to nine days after treatment. Twenty-nine of them (78.4 per cent) recovered completely but one was euthanased later.     

Management of ureteral obstruction.

The most common cause of ureteral obstruction in dogs and cats is ureteral calculi. Common clinical signs associated with ureteral obstruction include abnormalities in urination, persistent urinary tract infection, abdominal pain, vomiting, anorexia, weight loss,and depression or lethargy. Medical management of ureteral obstruction includes fluid diuresis, muscle relaxants, and treatment of azotemia using nephrostomy tubes or hemodialysis. Surgical techniques used to restore patency to the ureter include ureterotomy,partial ureterectomy and ureteroneocystostomy, and ureteral resection and anastomosis. Lithotripsy has been used in dogs to remove ureteral calculi. Renal function can be preserved if complete ureteral obstruction is relieved within several days of onset.     

Lactobacillus GG does not affect D-lactic acidosis in diarrheic calves, in a clinical setting

D-lactate, produced by gastrointestinal fermentation, is a major contributor to metabolic acidosis in diarrheic calves. Lactobacillus rhamnosus GG survives gastrointestinal transit in the neonatal calf and does not produce D-lactate. To determine whether this probiotic reduces gastrointestinal D-lactate production or severity of diarrhea or both, 48 calves (mean, 11 days old; range, 2-30 days) admitted to the clinic for treatment of diarrhea were randomly allocated to 2 groups. The experimental group was given Lactobacillus rhamnosus GG (1 x 10(11) cfu/d) PO, dissolved in milk or oral electrolyte solution, in addition to clinic treatment protocols; the other group served as a control. Serum and fecal samples were obtained at admission and at 24 and 48 hours after initial administration of Lactobacillus rhamnosus GG. All samples were analyzed for D- and L-lactate by using high-pressure liquid chromatography. Feces were also analyzed for pathogens, Lactobacillus rhamnosus GG recovery, and dry matter. D-lactic acidemia (>3 mmol/L) was present in 37/48 calves at admission. Lactobacillus rhamnosus GG was recovered in the feces of 13 experimental calves and 0 control calves 24 hours after administration. No difference in serum or fecal D- or L-lactate between the groups was detected at any time point. After therapy, D-lactic acidosis was absent at 48 hours in all but 1 calf. No relation between fecal pathogen (viral, bacterial, or protozoal) and degree of D-lactic acidosis was observed. The reduction in mortality and greater fecal dry matter in Lactobacillus rhamnosus GG-treated calves was not statistically significant.     

Biochemical alterations in serum and cerebrospinal fluid in experimental acidosis in goats

Experimental acidosis was induced in six goats aged between one and two years by administration of whole wheat grain at 100 g kg-1 bodyweight given intraruminally. Blood and cerebrospinal fluid (CSF) samples were collected from these goats before administration of wheat grain (0 hour) and thereafter at 12, 24, 48, 72, 96 and 120 hour intervals. These were analysed for serum enzyme activities and physicochemical characters of CSF. Significantly (P less than 0.05) higher activities of amylase (at 12 hours), lactate dehydrogenase (12 to 48 hours), creatine phosphokinase (12 to 48 hours), aspartate aminotransferase (12 to 24 hours), and gamma-glutamyl transferase (12 to 96 hours) were found in serum samples of acidotic goats. Changes in CSF included decrease of pH and chloride content and higher glucose values. No difference was seen in the physical character of CSF collected at different time intervals from acidotic goats.     

Experimentally induced lactic acidosis in the goat

Lactic acidosis was produced experimentally twice in each of 4 adult, female goats, by giving sucrose orally at the rate of 18 g/kg bodyweight. Changes in pH, osmolality, lactic acid concentration, and other constituents in ruminal fluid, plasma and blood were monitored over a period of 48 h. Also changes in urinary pH and sediment were examined. To ameliorate the metabolic disturbance, calcium hydroxide and bicarbonate treatment was employed after the 24 h samples had been collected and their acid-base status determined. A feature of the disturbance in the goats was that a metabolic alkalosis preceded the onset of lactic acidosis.     

Determination of synovial fluid and serum concentrations, and morphologic effects of intraarticular ceftiofur sodium in horses

OBJECTIVES: To determine the serum and synovial fluid concentrations of ceftiofur sodium after intraarticular (IA) and intravenous (IV) administration and to evaluate the morphologic changes after intraarticular ceftiofur sodium administration. STUDY DESIGN: Strip plot design for the ceftiofur sodium serum and synovial fluid concentrations and a split plot design for the cytologic and histopathologic evaluation. ANIMALS: Six healthy adult horses without lameness. METHODS: Stage 1: Ceftiofur sodium (2.2 mg/kg) was administered IV. Stage 2: 150 mg (3 mL) of ceftiofur sodium (pHavg 6.57) was administered IA into 1 antebrachiocarpal joint. The ceftiofur sodium was reconstituted with sterile sodium chloride solution (pH 6.35). The contralateral joint was injected with 3 mL of 0.9% sterile sodium chloride solution (pH 6.35). Serum and synovial fluid samples were obtained from each horse during each stage. For a given stage, each type of sample (serum or synovial fluid) was collected once before injection and 12 times after injection over a 24-hour period. All horses were killed at 24 hours, and microscopic evaluation of the cartilage and synovium was performed. Serum and synovial fluid concentrations of ceftiofur sodium were measured by using a microbiologic assay, and pharmacokinetic variables were calculated. Synovial fluid was collected from the active joints treated during stage 2 at preinjection and postinjection hours (PIH) 0 (taken immediately after injection of either the ceftiofur sodium or sodium chloride), 12, and 24, and evaluated for differential cellular counts, pH, total protein concentration, and mucin precipitate quality. RESULTS: Concentrations of ceftiofur in synovial fluid after IA administration were significantly higher (P = .0001) than synovial fluid concentrations obtained after IV administration. Mean peak synovial fluid concentrations of ceftiofur after IA and IV administration were 5825.08 microg/mL at PIH .25 and 7.31 microg/mL at PIH 4, respectively. Mean synovial fluid ceftiofur concentrations at PIH 24 after IA and IV administration were 4.94 microg/mL and .12 microg/mL, respectively. Cytologic characteristics of synovial fluid after IA administration did not differ from cytologic characteristics after IA saline solution administration. White blood cell counts after IA ceftiofur administration were < or =3,400 cells/ML. The mean synovial pH of ceftiofur treated and control joints was 7.32 (range, 7.08-7.5) and 7.37 (range, 7.31-7.42), respectively. Grossly, there were minimal changes in synovium or cartilage, and no microscopic differences were detected (P = .5147) between ceftiofur-treated joints and saline-treated joints. The synovial half-life of ceftiofur sodium after IA administration joint was 5.1 hours. CONCLUSIONS: Synovial concentrations after intraarticular administration of 150 mg of ceftiofur sodium remained elevated above minimal inhibitory concentration (MIC90) over 24 hours. After 2.2 mg/kg IV, the synovial fluid ceftiofur concentration remained above MIC no longer than 8 hours. CLINICAL RELEVANCE: Ceftiofur sodium may be an acceptable broad spectrum antimicrobial to administer IA in septic arthritic equine joints.     

Clinical efficacy of intravenous hypertonic saline solution or hypertonic bicarbonate solution in the treatment of inappetent calves with neonatal diarrhea

BACKGROUND: The clinical efficacy of IV administered hypertonic saline solution and hypertonic bicarbonate solution (HBS) in the treatment of inappetent diarrheic calves has not been compared yet. HYPOTHESIS: HBS is more advantageous than hypertonic saline in the treatment of calves with severe metabolic acidosis. ANIMALS: Twenty-eight dehydrated, inappetent calves with neonatal diarrhea. METHODS: In 2 consecutive clinical studies, calves were initially treated with saline (5.85%; 5 mL/kg body weight [BW] over 4 minutes; study I: N = 16) or bicarbonate solution (8.4%; 10 mL/kg BW over 8 minutes; study II: N = 12), respectively, followed by oral administration of 3 L isotonic electrolyte solution 5 minutes after injection. Clinical and laboratory variables were monitored for 72 hours. RESULTS: Treatment failed in 6 calves of study I and in 1 calf of study II as indicated by a deterioration of the general condition. All treatment failures had more severe metabolic acidosis compared with successfully treated calves before treatment. In the latter, rehydration was completed within 18 hours after injection; metabolic acidosis was corrected within 24 hours (study I) and 6 hours (study II) after injection. CONCLUSIONS AND CLINICAL IMPORTANCE: Diarrheic calves with slight metabolic acidosis (base excess [BE] >-10 mM) can be treated successfully with hypertonic saline. HBS is appropriate in calves without respiratory problems with more severe metabolic acidosis (BE up to -20 mM). Intensive care of the calves is required to ensure a sufficient oral fluid intake after the initial IV treatment.     

Presumptive pseudohypoaldosteronism secondary to chronic urinary tract obstruction from sloughed urinary bladder mucosa and urinary tract infection in a cat

Objective – To describe a case of presumptive secondary pseudohypoaldosteronism (PHA) in a cat with urinary tract infection and chronic urethral obstruction. The obstruction was believed to have resulted from sloughed urinary bladder mucosa secondary to pressure necrosis. Case Summary – A 5‐year‐old, 4 kg, castrated male Siamese cat presented for vomiting and stranguria. Medical history included a perineal urethrostomy for urethral obstruction. Physical examination revealed a large, painful, nonexpressible urinary bladder. Point‐of‐care testing demonstrated electrolyte derangements consistent with a postrenal azotemia and metabolic acidosis. Results of urine culture was positive for bacterial growth. Diagnostic imaging revealed presence of retroperitoneal fluid, marked urinary bladder wall thickening, bilateral hydroureter, mild bilateral pyelectasia, and small nephroliths. The patient was treated for a urinary tract obstruction and infection. In the 3 weeks following initial discharge, the patient was evaluated on multiple occasions for lethargy, intermittent vomiting, inappropriate urination, and progressive polyuria and polydipsia. Although the urinary bladder was easily expressed during repeat examinations, it was persistently distended and subjectively thickened upon palpation. Repeat ultrasound of the urinary tract showed evidence of sloughed tissue in the bladder lumen, likely secondary to chronic urethral obstruction and pressure necrosis. A cystotomy was performed to remove the necrotic tissue, and a revised perineal urethrostomy was done due to a partial urethral stricture. Bladder biopsies were obtained at this time. Postoperatively, the cat was reported by the owners to be urinating normally but continued to be polyuric and polydipsic in the week following discharge. One week after surgery, the cat presented in hypovolemic shock with laboratory findings consistent with a presumptive diagnosis of secondary PHA. New or Unique Information Provided – PHA has not been reported previously in a cat. This case report suggests that aldosterone resistance should be considered in cats with consistent laboratory findings and a history of documented obstructive uropathy and urinary tract infection.     

Blood and ruminal fluid profiles in carbohydrate-foundered cattle.

The relationships of acetylhistamine and histamine to the clinical signs of carbohydrate-induced acidosis were investigated in beef steers. Blood pH and plasma L-lactic acid decreased and serum sodium, serum potassium, ruminal fluid L-lactic acid, ruminal fluid histamine, and ruminal fluid and blood acetylhistamine increased in carbohydrate-engorged steers as compared with the changes in the steers while feeding on pasture (forage-fed steers). Twelve to 14 hours after the steers had become engorged, clinical signs of laminitis ("feedlot founder") were observed in three of six steers. These signs appeared 4 to 6 hours after blood acetylhistamine attained maximal concentration (2.9997 +/- 1.7054 microgram of histamine base/ml of blood) and blood pH decreased to 7.260 +/- 0.026 at 8 hours after engorgement. Blood histamine value reached 0.1298 +/- 0.1095 microgram of histamine base/ml 4 hours after engorgement (8 to 10 hours before the appearance of clinical illness), but had reached maximal concentration 32 hours after engorgement (0.3300 +/- 0.028 microgram of histamine base/ml of blood).