Rebound hyperkalemia in a dog with albuterol toxicosis after cessation of potassium supplementation

Objective

To describe the presentation of rebound hyperkalemia as a delayed side effect of albuterol toxicity in a dog.

Case Summary

A 3-year-old female neutered mixed-breed dog was presented for albuterol toxicosis that led to a severe hypokalemia, hyperlactatemia, and hyperglycemia. The dog also experienced sinus tachycardia and generalized weakness. Treatment was instituted with intravenous fluid therapy and potassium supplementation, and the dog was monitored with a continuous electrocardiogram. Resolution of hypokalemia was documented 12 hours after initial presentation, at which time fluid therapy and potassium supplementation were discontinued. There were no further periods of sinus tachycardia, but instead the dog developed ventricular ectopy with rapid couplets (instantaneous rates of 300/min). An echocardiogram revealed normal cardiac size and function. Twenty-four hours after presentation, the patient developed severe hyperkalemia, despite discontinuation of fluids and potassium supplementation for 12 hours. Serial venous and urinary electrolytes were performed for determination of the fractional excretion of electrolytes. These data confirmed rebound hyperkalemia (7.0 mmol/L), consistent with a markedly increased fractional excretion of potassium, and secondary to the release of potassium from inside the cells. Fluid therapy with dextrose supplementation was provided until 36 hours postpresentation. The hyperkalemia resolved, and the dog was discharged after 44 hours of hospitalization.

New or Unique Information Provided

This case documents rebound hyperkalemia following treatment of albuterol toxicosis in a dog. This case highlights the importance of understanding the distribution of total body potassium when treating serum hypokalemia. Transcellular shifts of potassium, as in the case of albuterol toxicosis, can lead to rebound hyperkalemia even after discontinuation of potassium supplementation. This case further explores the utility of fractional excretion of electrolytes in elucidating the etiology and management of electrolyte disturbances.     

Cutaneous saphenous nerve graft for the treatment of sciatic neurotmesis in a dog

CASE DESCRIPTION: A 2-year-old Griffon Vendéen was examined because of a 1-month history of right hind limb lameness after a traumatic injury. CLINICAL FINDINGS: Neurologic examination revealed monoplegia and anesthesia of the right hind limb distal to the stifle (femorotibial) joint except for the area supplied by the cutaneous saphenous nerve. Results of electromyographic testing were consistent with a severe lesion of the tibial and peroneal nerves at the level of the stifle joint. TREATMENT AND OUTCOME: Exploratory surgery revealed an 80-mm-long gap in both the peroneal and tibial branches of the right sciatic nerve. A section of the left cutaneous saphenous nerve was interposed to graft the nerve defects. The dog received joint mechanotherapy and electrophysiologic therapy during the reinnervation process. Ten months after surgery, the dog had recovered almost completely. Neurologic examination revealed diminished flexion of the tarsal and digital joints. Repeat electromyographic testing revealed no abnormal spontaneous electrical activity in the right hind limb musculature, and small compound muscle action potentials were recorded in the right interosseous and cranial tibial muscles. CLINICAL RELEVANCE: Without surgical treatment, neurotmesis injury results in poor recovery of motor and sensory functions and may result in amputation. If a nerve defect exists, nerve grafting should be considered, even if the procedure is delayed until well after the injury. The sensory portion of the cutaneous saphenous nerve is a potential source of peripheral nerve for grafting in dogs. Reinnervation is a long-term process and physiologic support and owner involvement are necessary, but nearly complete functional recovery is possible.     

Imaging findings and surgical treatment of hemivertebrae in three dogs

CASE DESCRIPTION: 3 immature screw-tailed dogs were evaluated because of progressive pelvic limb paraparesis. CLINICAL FINDINGS: Each dog had marked ataxia and paresis of the pelvic limbs and a palpable deformity of the midthoracic portion of the vertebral column. Pain perception in the pelvic limbs was considered normal, and there was no evidence of fecal or urinary incontinence in any of the 3 dogs. Radiography and magnetic resonance imaging revealed hemivertebrae with severe dorsoventral stenosis of the vertebral canal resulting in spinal cord compression in 2 dogs and lateral compression in the other. TREATMENT AND OUTCOME: Each dog underwent decompressive surgery consisting of dorsal laminectomy or hemilaminectomy and vertebral stabilization by use of combinations of Kirschner wires or threaded external fixator pins plus polymethylmethacrylate bone cement. All dogs regained strong locomotor function with minimal residual pelvic limb ataxia. CLINICAL RELEVANCE: Little detailed information regarding surgical treatment of hemivertebrae in dogs is available; results of treatment in these 3 dogs suggest that spinal cord decompression and stabilization of the vertebral column can achieve a satisfactory, functional outcome.     

Suspected Albuterol Intoxication In A Dog

A suspected case of intoxication of a dog by the beta₂-adrenergic agonist albuterol is discussed. Clinical abnormalities observed included hypokalemia, weakness, tachycardia, tachypnea, hyperthermia, and delirium. Treatment with high-dose potassium supplementation helped to resolve these abnormalities.
Adrenergic control of potassium homeostasis is beta₂-mediated and causes the intracellular uptake of potassium, primarily in liver and muscle. The mechanism of action of albuterol in decreasing serum potassium, its clinical applications in humans, and possible application in dogs are discussed.     

Extradural haematoma secondary to brown snake (Pseudonaja species) envenomation

A 4-year-old Siberian Husky dog was treated with brown snake antivenom by his regular veterinarian after a witnessed episode of brown snake envenomation. The dog was discharged 5 hours post presentation despite an ongoing coagulopathy. The dog was presented to the emergency centre 2 hours later because the owner believed the dog to be in pain. Initial examination revealed an ambulatory but neurologically normal patient with thoracolumbar pain and laboratory evidence of a coagulopathy. Despite correction of the coagulopathy, the signs progressed to bilateral hind limb paresis after approximately 3 hours of hospitalisation, and continued to deteriorate over the next 56 hours to loss of deep pain perception in the right hind limb. Computed tomography imaging identified the presence of an extradural haematoma which was subsequently removed via a hemilaminectomy. Surgical decompression was successful in treating the spinal compression and the dog recovered with minimal complications. To our knowledge this is the first report of extradural haematoma secondary to coagulopathy induced by brown snake envenomation.     

Goitrous hypothyroidism associated with treatment with trimethoprim-sulfamethoxazole in a young dog

CASE DESCRIPTION: A 16-week-old female Boxer that had been treated for 5 weeks with trimethoprim-sulfamethoxazole and chloramphenicol because of aspiration pneumonia was evaluated for bilaterally symmetric masses in the subcutaneous tissues of the ventral neck, in the region of the larynx. CLINICAL FINDINGS: Fine-needle aspirates were obtained from the neck masses; cytologic examination revealed well-differentiated thyroid epithelial tissue. A blood sample was collected for serum biochemical and thyroid function analyses. Mild hyperphosphatemia, severe hypercholesterolemia, mild hyperkalemia, and a mild increase in creatine kinase activity were identified. Serum concentration of total thyroxine was less than the lower reference limit, and that of thyroid-stimulating hormone was greater than the upper reference limit. Findings were consistent with a diagnosis of clinical hypothyroidism in a skeletally immature dog. TREATMENT AND OUTCOME: Treatment with trimethoprim-sulfamethoxazole was discontinued. The dog was reevaluated 3 weeks later, at which time the neck masses were markedly decreased in size. Serum concentrations of cholesterol and potassium were lower; serum concentrations of total thyroxine and thyroid-stimulating hormone were near or within respective reference ranges. Age-appropriate increases in serum phosphorus concentration and serum alkaline phosphatase activity were also detected. CLINICAL RELEVANCE: To the authors' knowledge, this is the first report of antimicrobial-induced goiter in a dog. Cytologic examination of fine-needle aspirates and interpretation of data from serum biochemical and thyroid function analyses were needed to obtain a definitive diagnosis. Practitioners should include goiter among the differential diagnoses for ventral neck swellings in young dogs receiving potentiated sulfonamide antimicrobials.     

Retinopathy associated with ivermectin toxicosis in two dogs

CASE DESCRIPTION: 2 dogs (dogs 1 and 2) were examined for sudden onset of blindness. Both dogs had mild obtundation and mydriasis in both eyes. It was thought that dog 1 may have ingested ivermectin; dog 2 had been treated with ivermectin for demodectic mange. CLINICAL FINDINGS: On initial examination, both dogs had mydriasis and decreased pupillary light reflexes in both eyes. Dog 1 had an absent menace response bilaterally. Fundic examination of both eyes in both dogs revealed regions of multifocal retinal edema and folds with low-lying retinal separation. The electroretinogram was extinguished in dog 1 and attenuated in dog 2. Ivermectin was detected in serum samples from both dogs. TREATMENT AND OUTCOME: Both dogs made a complete clinical recovery following cessation of exposure to ivermectin; electroretinographic findings improved, and retinal edema resolved with some residual chorioretinal scarring. CLINICAL RELEVANCE: To our knowledge, this is the first report of resolution of retinal edema and electroretinographic changes associated with ivermectin toxicosis in dogs. In dogs that develop blindness suddenly, fundic examination, electroretinography, and assessment of serum ivermectin concentration are diagnostically useful, even if exposure to ivermectin is unknown.     

Myocardial damage and paroxysmal ventricular tachycardia in a dog after Albuterol intoxication

Intoxication with the beta2-agonist Albuterol may lead to immediate signs of beta-adrenergic stimulation like excitation, tachypnea and tachycardia. Furthermore, it typically causes severe hypokalemia, which then leads to muscle weakness and which predisposes to ventricular arrhythmias. We describe a dog where albuterol intoxication caused runs of fast paroxysmal ventricular tachycardia that persisted after normalization of the hypokalemia. Based on a markedly elevated serum troponin I level acute myocardial damage was identified as cause of the tachyarrhythmia. Repeated Troponin I measurements and Holter-ECGs were the means to document complete cure.     

Suspected panosteitis in a camel

CASE DESCRIPTION: A 6-month-old male Bactrian camel was examined because of a 3-week history of lameness of the left hind limb. CLINICAL FINDINGS: Lameness was initially detected in the left hind limb but resolved and was detected in the right hind limb during treatment. Lameness increased during periods of rapid growth. Radiography revealed multiple small opacities of the medullary cavity of several long bones throughout treatment. Core bone biopsies of lesions in the tibiae revealed lamellar bone with areas of loose connective tissue, osteoblasts in the medullary cavity, and periosteal new bone formation, all which were consistent with panosteitis. TREATMENT AND OUTCOME: Palliative treatment was attempted with epidural and transdermal administration of analgesics. Flunixin meglumine was administered PO, which coincided with an abrupt increase in serum creatinine concentration. Performance of multiple diagnostic bone biopsies led to remission of clinical signs of pain. CLINICAL RELEVANCE: Panosteitis should be a differential diagnosis for shifting limb lameness in young camels. Bone biopsies can be useful for diagnosis of panosteitis and possible relief of pain associated with the disease. Bactrian camels may be susceptible to the renal toxicity of flunixin meglumine, especially when dehydrated.     

Multiple myeloma with central nervous system involvement in a cat

CASE DESCRIPTION: A 1.5-year-old spayed female domestic shorthair cat was admitted for hind limb locomotor difficulties and signs of pain along the lumbar portion of the vertebral column. At the time of referral, the cat was paraparetic with deficits in the spinal reflexes of the hind limbs. Neuroanatomic localization was at the L6-S2 spinal cord segments, corresponding approximately to the region of the L4-L6 vertebral bodies. CLINICAL FINDINGS: Radiography revealed a mixed osteolytic-proliferative lesion within the body of L5 involving the cranial end plate, as well as punctate radiolucencies in the distal portion of the femur. Magnetic resonance imaging revealed an intramedullary spinal cord lesion along with extensive meningeal and nerve root lesions in the area of the L4-L6 vertebral bodies. Cytologic analysis of a bone marrow aspirate from the right trochanteric fossa revealed a substantial plasma cell infiltrate. Analysis of CSF revealed a high protein concentration and morphologically abnormal plasma cells. Urine, but not serum, protein electrophoresis revealed a sharp gamma-globulin peak consistent with a monoclonal band of Bence-Jones proteins. The diagnosis was multiple myeloma. TREATMENT AND OUTCOME: The cat was treated with melphalan and prednisolone. A rapid clinical response was reported, and by week 3 after diagnosis, the cat's locomotion and behavior had normalized. However, by month 4, multifocal neurologic deficits were evident. The cat was euthanized at 9 months because of tetraparesis and substantial weight loss. CLINICAL RELEVANCE: To our knowledge, this is the first report of myeloma in a cat that had electrophoretically detectable light chain proteinuria but lacked a detectable serum monoclonal gammopathy.     

Arterial thromboembolic disease in a dog with blastomycosis localized in a hilar lymph node

An 8-year-old mixed-breed dog was evaluated for caudal paresis. Transient lameness of the left hind and left forelimbs had developed during the preceding week. Clinical findings included conscious proprioceptive deficits, hyporeflexive tendon reflexes and decreased pain perception, coolness in the hind limbs and left forelimb, and absence of femoral pulses. A fluid-dense mass was radiographically identified adjacent to the left atrium. Echocardiography revealed a mass in the left atrium and spontaneous contrast in the left ventricular lumen and aortic root. The dog was euthanatized because of its deteriorating condition. A large mass was adhered to the dorsal left atrial wall and had eroded into the atrial lumen. A sterile blood clot was attached to this site, and sterile thrombi were in the terminal portion of the aorta. Histologically, the mass was found to be hilar lymph node with chronic pyogranulomatous inflammation containing organisms characteristic of Blastomyces dermatitidis.     

Thoracolumbar vertebral osteochondroma in a young dog.

Osteosarcoma was diagnosed in a 7-month-old female German Shepherd Dog with hind limb paresis. Radiography revealed a circumscribed calcified mass in the dorsal vertebral lamina at T13-L1 resulting in extradural compression of the spinal cord. Surgical excision of the mass resulted in gradual return to normal neurologic function. Four weeks after surgery, the dog became severely atactic after rolling onto its back. A chip fracture of T13 was identified, and the dog was euthanatized at the owners' request.     

Nematode eggs observed in cytology of cerebrospinal fluid diagnostic for intramedullary Spirocerca lupi spinal cord migration

Spinal spirocercosis due to aberrant Spirocerca lupi nematode migration is an emerging etiology for acute myelitis in dogs in Israel, causing severe, mostly nonsymmetrical hind limb paresis or paralysis, and sometimes tetraparesis or tetraparalysis. So far, incidental identification of parasites during spinal surgery or at necropsy provides the only definite diagnosis, while antemortem diagnosis of this condition has been uncertain. Specifically, antemortem diagnosis is based on the typical clinical presentation of acute, progressive, asymmetrical hind limb paresis or paralysis, with moderate to severe eosinophilic to mixed cerebrospinal fluid (CSF) pleocytosis and increased CSF protein concentration. Exclusion of other differential diagnoses also requires using spinal cord imaging. In this novel report, we document a case of an intradural spinal spirocercosis in a dog, diagnosed antemortem, by detecting S lupi eggs in the CSF, and subsequent treatment, resulting in the resolution of the clinical signs.     

Successful use of short‐term mechanical ventilation to manage respiratory failure secondary to profound hypokalemia in a cat with hyperaldosteronism

Objective – To report successful management of respiratory failure due to severe hypokalemia in a cat with hyperaldosteronism, including short‐term mechanical ventilation strategies and aspects of medical and surgical treatment. Case Summary – A cat presented with bilateral pelvic limb weakness that rapidly progressed to tetraparesis and respiratory muscle failure. Point‐of‐care testing revealed severe hypokalemia (1.9 mmol/L) and mild azotemia. Initial management included endotracheal intubation, mechanical ventilation, and aggressive potassium supplementation. Spironolactone was started due to a high index of suspicion for hyperaldosteronism. A right adrenal mass visualized during abdominal ultrasonographic examination and a serum aldosterone level greater than 3329 pmol/L confirmed the diagnosis. The cat made a full recovery following surgical removal of a right adrenal adenoma. New or Unique Information Provided – We report successful management of respiratory failure in a cat with hyperaldosteronism using short‐term mechanical ventilation. Respiratory failure due to severe hypokalemia should be considered a complication of hyperaldosteronism in cats and may require mechanical ventilation. However, full recovery is possible.     

Hypokalemia in cats: 186 cases (1984-1987)

Retrospective review of serum biochemical data obtained from 501 cats over a 3-year period (1984-1987) indicated that 186 (37%) had hypokalemia (serum potassium concentration less than 4.1 mEq/L). After adjusting for disease diagnosis, cats fed either of 2 commercial diets were 4 times more likely to be hypokalemic than cats fed other diets. Odds ratios (OR; measure of association), adjusted for diet type, were calculated to determine the odds of hypokalemia for a given disease, compared with odds of normokalemia for the same disease. Chronic renal failure (OR = 14.4), hepatic disease (OR = 5.7), systemic infectious diseases (viral or bacterial; OR = 2.7), and neuromuscular or CNS disease (OR = 2.4) were all significantly associated (P less than 0.05) with the occurrence of hypokalemia. Significant differences in age or sex between hypokalemic and normokalemic cats were not found. Within the group of 186 hypokalemic cats, hypercholesterolemia (89 cats; 48%), hyperglycemia (88 cats; 47%), high serum urea nitrogen concentration (86 cats; 46%), hyperchloridemia (80 cats; 43%), and high serum creatinine concentration (73 cats; 39%) were the most common biochemical abnormalities. When disease diagnosis was compared among cats with severe hypokalemia (serum potassium concentration less than 3.0 mEq/L) and those with moderate hypokalemia, cats with severe hypokalemia were 3.5 times more likely to have chronic renal failure than cats with less severe hypokalemia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Incomplete rupture of the gastrocnemius and superficial digital flexor muscles in a Quarter Horse stallion

CASE DESCRIPTION: A 16-year-old 500-kg (1,100-lb) Quarter Horse stallion was examined because of acute severe lameness involving the left hind limb. CLINICAL FINDINGS: Examination revealed signs of failure (concurrent flexion of the tarsus and extension of the stifle [femorotibial] joint) of the caudal component of the reciprocal apparatus. Results of radiographic evaluation ruled out fracture or joint injury as causes of the lameness. During the next 48 hours, the reciprocal apparatus on the left hind limb progressively deteriorated until the horse became non-weight bearing on the limb. TREATMENT AND OUTCOME: The horse wore a full-limb splint over a Robert-Jones bandage on the plantar aspect of the limb for 30 days. Thirty-four days after the initial injury, the horse had weak function of the reciprocal apparatus and limited ability to bear weight. Six days after removal of the splint, laminitis developed in the contralateral hind limb. The horse was managed with a sling for 5 weeks, during which time deep digital flexor tendon contracture developed. Eleven weeks after the initial injury, the stallion was discharged from the hospital and walking comfortably with a 1-cm-high block under the heel of the left hind foot. CLINICAL RELEVANCE: Incomplete failure of the caudal component of the reciprocal apparatus is an unusual injury that likely occurs during a fall with a hind limb extended under the body, resulting in forced extension of the muscle while it is engaged in contraction. Conservative management of this injury in a heavily muscled adult horse is possible.     

Effects of hypercalcemia on serum concentrations of magnesium, potassium, and phosphate and urinary excretion of electrolytes in horses

OBJECTIVE: To determine effects of experimentally induced hypercalcemia on serum concentrations and urinary excretion of electrolytes, especially ionized magnesium (iMg), in healthy horses. ANIMALS: 21 clinically normal mares. PROCEDURES: Horses were assigned to 5 experimental protocols (1, hypercalcemia induced with calcium gluconate; 2, hypercalcemia induced with calcium chloride; 3, infusion with dextrose solution; 4, infusion with sodium gluconate; and 5, infusion with saline [0.9% NaCl] solution). Hypercalcemia was induced for 2 hours. Dextrose, sodium gluconate, and saline solution were infused for 2 hours. Blood samples were collected to measure serum concentrations of electrolytes, creatinine, parathyroid hormone, and insulin. Urine samples were collected to determine the fractional excretion of ionized calcium (iCa), iMg, sodium, phosphate, potassium, and chloride. RESULTS: Hypercalcemia induced by administration of calcium gluconate or calcium chloride decreased serum iMg, potassium, and parathyroid hormone concentrations; increased phosphate concentration; and had no effect on sodium, chloride, and insulin concentrations. Hypercalcemia increased urinary excretion of iCa, iMg, sodium, phosphate, potassium, and chloride; increased urine output; and decreased urine osmolality and specific gravity. Dextrose administration increased serum insulin; decreased iMg, potassium, and phosphate concentrations; and decreased urinary excretion of iMg. Sodium gluconate increased the excretion of iCa, sodium, and potassium. CONCLUSIONS AND CLINICAL RELEVANCE: Hypercalcemia resulted in hypomagnesemia, hypokalemia, and hyperphosphatemia; increased urinary excretion of calcium, magnesium, potassium, sodium, phosphate, and chloride; and induced diuresis. This study has clinical implications because hypercalcemia and excessive administration of calcium have the potential to increase urinary excretion of electrolytes, especially iMg, and induce volume depletion.     

Acute monensin toxicosis in Stone sheep (Ovis dalli stonei), blesbok (Damaliscus dorcus phillipsi), and a Bactrian camel (Camelus bactrianus)

Accidental monensin toxicosis developed in 5 Stone sheep (Ovis dalli stonei), 5 blesbok (Damaliscus dorcas phillipsi), and a Bactrian camel (Camelus bactrianus) at the St Louis Zoological Park. Eight animals died acutely and 1 was euthanatized because of chronic hind limb paresis. All affected animals had clinicopathologic evidence of severe muscle necrosis, serum electrolyte disturbances, and hemoconcentration.     

MAGNETIC RESONANCE IMAGING OF PRESUMPTIVE LUMBOSACRAL DISCOSPONDYLITIS IN A DOG

A three-year-old male Boxer dog had hyperesthesia, symmetrical epaxial, gluteal and hind limb muscular atrophy and rear limb ataxia. Neurological deficits included decreased conscious proprioception of the left hind limb, decreased withdrawal and increased patellar reflexes of both hind limbs. The dog had a urinary tract infection with positive culture for Staphylococcus intermedius. On survey radiography of the lumbosacral spine there was active bone proliferation spanning the L7 S1 intervertebral disc space with an epidural filling defect at the ventral aspect of the vertebral canal on epidurography, On magnetic resonance imaging (MRI), findings were similar to those described for human diskospondylitis including altered signal intensity and nonuniform contrast enhancement of the L7-S1 intervertebral disc, adjacent vertebral end plates and epidural and sublumbar soft tissues. Although skeletal radiography is usually sufficient to reach a diagnosis of discospondylitis, MRI of this patient made it possible to reach a presumptive diagnosia of discospondyltis prior to development of definitive radiographic abnormalties.     

Detection of Bartonella henselae DNA in two dogs with pyogranulomatous lymphadenitis

CASE DESCRIPTION: 1 dog evaluated because of inappetence and lameness of the left hind limb of 1 day's duration and 1 dog evaluated because of inappetence, fever, and lymphadenopathy of 2 weeks' duration. CLINICAL FINDINGS: Histologic examination of excisional biopsy specimens from lymph nodes revealed pyogranulomatous lymphadenitis in both dogs. Quantitative real-time PCR assays detected Bartonella henselae DNA in blood samples and affected lymph node specimens from both dogs. Antibodies against B. henselae were not detected via immunofluorescent antibody testing during active disease in either dog. TREATMENT AND OUTCOME: 1 dog recovered after 6 weeks of treatment with doxycycline (5 mg/kg [2.3 mg/lb], p.o., q 12 h), whereas the other dog recovered after receiving a combination of azithromycin (14.5 mg/kg [6.6 mg/lb], p.o., q 24 h for 21 days), doxycycline (17.3 mg/kg [7.9 mg/lb], p.o., q 24 h for 4 weeks), and immunosuppressive corticosteroid (prednisone [3 mg/kg {1.4 mg/lb}, p.o., q 24 h], tapered by decreasing the daily dose by 25% every 2 weeks) treatment. CLINICAL RELEVANCE: B. henselae is implicated as a possible cause or a cofactor in the development of pyogranulomatous lymphadenitis in dogs. In dogs with pyogranulomatous lymphadenitis, immunofluorescent assays may not detect antibodies against B. henselae. Molecular testing, including PCR assay of affected tissues, may provide an alternative diagnostic method for detection of B. henselae DNA in pyogranulomatous lymph nodes.