Canine status epilepticus: a retrospective study of 50 cases

The medical records of 50 dogs that exhibited generalised convulsive tonic-clonic (GCTC) status epilepticus (SE) were reviewed and compared with the records of 50 dogs that exhibited non-SE GCTC seizures. The mean age, bodyweight and gender of the patients in both groups were not significantly different. Dogs in the non-SE group were two times more likely to be an idiopathic epileptic than to have secondary epileptic seizures. The SE group was more likely to have abnormalities on cerebrospinal fluid analysis, but not more likely to have abnormalities detected on computed tomography, when compared with the non-SE group. SE was 1.57 times more likely if the cause for the seizures was secondary or reactive epilepsy rather than idiopathic or primary epilepsy. In conclusion, dogs that exhibit SE should be thoroughly investigated for secondary causes.     

Status Epilepticus and Epileptic Seizures in Dogs

Background: A special form of epileptic seizures (ES) is the life-threatening condition of status epilepticus (SE), which requires immediate and specific treatment based on a correct diagnosis of the underlying disease condition.
Hypothesis/Objectives: The objectives of this retrospective study were to determine prevalence of ES and SE in dogs presenting at a veterinary teaching hospital, to identify the etiology and relative risk (RR) for SE in general and at the onset of seizures. Furthermore the outcome for dogs suffering from SE was to be evaluated.
Animals: Three hundred and ninety-four dogs that were admitted to a veterinary teaching hospital (January 1, 2002 to March 31, 2008) with ES.
Methods: All medical records of dogs with ES were identified by screening the clinical documentation system and evaluated for inclusion in this retrospective study.
Results: Dogs with reactive seizures caused by poisoning had a significantly higher risk of developing SE ( P < .001; RR = 2.74), particularly as 1st manifestation of a seizure disorder ( P = .001; RR = 1.97). After SE, dogs with symptomatic epilepsy had a significantly lower probability of survival than dogs with idiopathic epilepsy ( P < .001) and reactive ESs ( P = .005).
Conclusion and Clinical Importance: In dogs showing SE as the 1st manifestation of a seizure disorder, intoxication should always be considered and appropriate investigations undertaken. Dogs with SE owing to toxicosis have more favorable outcomes than dogs with symptomatic epilepsy ( P < .001).     

Clinical, epidemiological and treatment results of idiopathic epilepsy in 54 labrador retrievers: a long-term study

The records of 54 labrador retrievers with idiopathic epilepsy were reviewed. Exogenous factors played a minor role in the transmission of the epilepsy. Prodromal phase and aura were present in the majority of the dogs with generalised seizures. The ictal phase was characterised by long-lasting automatisms. Approximately half of the dogs had seizures more than once a month; the remainder ranged from one every two months to one every 12 months. The average frequency in dogs with generalised seizures (n = 49) was one every 65 days and in dogs with partial seizures (n 5) one every 205 days. Long-term follow-up was performed in 46 dogs, 37 of which followed a strict treatment protocol. Possible causes for the large variations in treatment results were analysed. One goal was identify objective aspects enabling a realistic prognosis prior to treatment. Animals with a high age at onset of seizure (mean, four years) showed an excellent outcome, even if treatment began late. Dogs with low frequency rates and low total numbers of seizures responded well to therapy if treated as early as possible.     

Tremorgenic mycotoxin intoxication with penitrem A and roquefortine in two dogs

In this report, we describe the natural intoxication of 2 dogs that consumed moldy dairy products found in the household garbage and the procedures used to identify and quantify the tremorgenic mycotoxins, roquefortine and penitrem A, in the remaining portions of ingested materials. Following the ingestion of mycotoxins, the dogs of our report developed muscle tremors or seizures that resembled clinical signs of strychnine poisoning. Roquefortine was the predominant mycotoxin in a moldy cream cheese wrapper that was found among scattered garbage consumed by the first dog. Penitrem A was the only mycotoxin detected in discarded moldy macaroni and cheese that was consumed by the second dog. Treatment of dogs with tremorgenic mycotoxin intoxication involves supportive care. Close monitoring is important because the development of aspiration pneumonia is common and has been reported as the cause of death. Clinical signs of intoxication gradually resolve within 24 to 48 hours.     

Clinical, neurological and clinicopathological signs, treatment and outcome of metaldehyde intoxication in 18 dogs

OBJECTIVES: To describe the clinical signs, clinicopathological abnormalities and outcome of metaldehyde intoxication in dogs. METHODS: Medical records of dogs presenting between 1989 and 2005 with a diagnosis of metaldehyde toxicity were reviewed retrospectively. Data obtained from the medical record included signalment, history, clinical signs, laboratory tests results, hospitalisation period length, treatments and outcome. RESULTS: Eighteen dogs fulfilled the inclusion criteria. The most prevalent clinical signs were seizures, hyperthermia, tachycardia and muscle tremors. Serum biochemistry abnormalities included increased serum muscle enzymes activities, acidaemia (six dogs) and decreased blood bicarbonate (eight dogs). Treatment was symptomatic and supportive. Hyperbilirubinaemia was observed in two dogs. Diazepam was the most commonly used anticonvulsant followed by phenobarbitone and pentobarbital. General inhalant anaesthesia was required in nine of 18 dogs with seizures unresponsive to anticonvulsants. The survival was 83 per cent (15 of 18 dogs). CLINICAL SIGNIFICANCE: This clinical study recorded, for the first time in the veterinary literature, several clinicopathological abnormalities from severely intoxicated dogs. Metabolic acidosis was common, while acute or delayed hepatotoxicity was an uncommon complication.     

Case Series: Continuous electroencephalographic monitoring of status epilepticus in dogs and cats: 10 patients (2004–2005)

Objective – To describe the use of continuous electroencephalographic (EEG) monitoring for management of status epilepticus (SE) in dogs and cats. Design – Retrospective study. Setting – University teaching hospital. Animals – Ten patients (7 dogs, 3 cats) with SE of differing etiology (idiopathic epilepsy, n=3; toxicity, n=4; meningoencephalitis, n=2; undefined, n=1). Interventions – The EEG was recorded continuously from 5 stainless‐steel needle electrodes inserted SC. Animals were treated with diazepam and phenobarbital followed by either propofol (n=3) or pentobarbital (n=7) as a continuous rate of infusion. Measurements and Main Results – Clinical seizures stopped after induction of anesthesia in each animal. The EEG, however, still showed distinct epileptiform patterns (spikes, polyspikes) in all animals. Paroxysms were suppressed by increasing the infusion rate of either pentobarbital or propofol. A burst‐suppression pattern was achieved in 5 animals. EEG epileptiform activity reappeared in 4 animals when attempting to taper the dose after >6 hours of anesthesia. This was interpreted as ongoing EEG seizure activity and an increased risk for clinical seizures, and the anesthetic dosage was adjusted accordingly. Conclusion – Continuous EEG monitoring appears to be a useful tool for therapeutic monitoring of SE in dogs and cats. It allows the detection of EEG seizures without the appearance of clinical seizures. Further investigations with blinded investigators and homogeneous animal groups to define therapeutic endpoints are warranted.     

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.     

Evaluation of splenectomy as a risk factor for gastric dilatation-volvulus

Objective-To evaluate whether dogs undergoing splenectomy had an increased risk of gastric dilatation-volvulus (GDV), compared with a control group of dogs undergoing enterotomy. Design-Retrospective case-control study. Animals-219 dogs that underwent splenectomy for reasons other than splenic torsion (splenectomy group; n = 172) or enterotomy (control group; 47) without concurrent gastropexy. Procedures-Medical records were reviewed for information on signalment, date of surgery, durations of surgery and anesthesia, reason for splenectomy, histopathologic findings (if applicable), whether gastropexy was performed, duration of follow-up, and date of death (if applicable). Follow-up information, including occurrence of GDV, was obtained via medical records review and a written client questionnaire. Results-Reasons for splenectomy included splenic neoplasia, nonneoplastic masses, infarction, traumatic injury, and adhesions to a gossypiboma. Incidence of GDV following surgery was not significantly different between dogs of the splenectomy (14/172 [8.1 %]) and control (3/47 [6.4%]) groups. Median time to GDV for the 17 affected dogs was 352 days (range, 12 to 2,368 days) after surgery. Among dogs that underwent splenectomy, sexually intact males had a significantly higher incidence of GDV (4/16) than did castrated males and sexually intact or spayed females (10/156). Incidence of GDV among sexually intact male dogs did not differ between groups. Conclusions and Clinical Relevance-Results did not support a recommendation for routine use of prophylactic gastropexy in dogs at the time of splenectomy. Other patient-specific risk factors should be assessed prior to recommending this procedure.     

Administration of acepromazine maleate to 31 dogs with a history of seizures

Objective: To retrospectively evaluate the incidence of seizures in dogs presenting with a history of seizures that were treated with acepromazine (ACE) during hospitalization. Design: Retrospective study. Setting: Privately owned emergency and referral hospital. Animals: Thirty‐one client‐owned dogs. Interventions: Administration of ACE. Measurements and main results: The medical records from dogs with an acute or chronic seizure history that received ACE were reviewed. Factors evaluated included presenting complaint, seizure history, ACE dosage, duration of observation, seizure activity, and other medications used. Thirty‐one dogs qualified for the study: 20 males and 11 females. Age range was 3 months to 14.9 years. Presenting complaint was seizure in 28/31 dogs. There was a prior history of seizures in 22/31 dogs, and 15/22 were currently on antiseizure medication. ACE was given 1–5 times per dog. Mean ACE dose was 0.029 mg/kg IV (range: 0.008–0.057 mg/kg; n=46), 0.036 mg/kg IM (range: 0.017–0.059 mg/kg; n=14), 0.53 mg/kg PO (n=2). Twenty‐seven dogs did not seizure after administration of ACE within the observation period (mean: 16.4 hours, range: 0.25–66 hours). Twenty‐five dogs received antiseizure medication before ACE. Eight seizure episodes occurred in 4 dogs (all of whom presented for seizures) within 0.3–10 hours after ACE administration. Conclusions: There was no observed correlation between ACE administration in dogs with a seizure history and the recurrence of seizure activity during hospitalization. The time from ACE administration to seizure activity was greater than expected for measurable effects to be seen in 1 dog (10 hour). Further studies with a larger group and alternative ACE doses are needed to more thoroughly evaluate the safety of short‐term ACE use in dogs with a seizure history.     

Canine intracranial neoplasia: clinical risk factors for development of epileptic seizures

Objectives : To identify clinical risk factors for seizures in dogs with intracranial neoplasia. Methods : A cross‐sectional retrospective study of 68 dogs with histopathologically confirmed primary or secondary intracranial neoplasia, complete clinical history and magnetic resonance imaging of the brain was conducted. Signalment and clinical history were retrieved from clinical records and magnetic resonance images of the brain were re‐evaluated. Prevalence of findings was compared between dogs with and without seizures. Results : Forty‐two dogs had tumour‐related seizures, the remaining 26 were seizure‐free. Tumour types included meningioma (23 dogs with and 5 without seizures), glioma (9 dogs with and 6 without seizures), choroid plexus tumour (2 dogs without seizures), neuroblastoma (1 dog with seizures) and metastatic/invasive tumours including lymphoma (9 dogs with and 13 without seizures). On the basis of multi‐variable logistic regression analysis, risk factors for seizures associated with intracranial neoplasia were magnetic resonance imaging findings consistent with the presence of neoplastic tissue in frontal lobe [odds ratio (OR) 9·61; 95% confidence interval (CI) 2·59 to 35·61], marked gadolinium enhancement (OR 10·41; 95% CI 2·07 to 52·30) and magnetic resonance imaging findings of subfalcine and/or subtentorial herniation (OR 3·88; 95% CI 1·10 to 13·71). Clinical Significance : Dogs with primary or secondary intracranial neoplasia are at risk of seizures, particularly those with tumours that affect the frontal lobe, enhance markedly with gadolinium, or cause subfalcine and/or subtentorial herniation.     

Pulmonary metastatectomy in the management of four dogs with hypertrophic osteopathy

The efficacy and outcome of pulmonary metastatectomy in the management of hypertrophic osteopathy (HO) secondary to metastatic osteosarcoma was retrospectively evaluated in four dogs. Metastatectomy was performed by subpleural enucleation, partial lung lobectomy or complete lung lobectomy through either a median sternotomy or thoracoscopically. Perioperative morbidity was minimal. Clinical signs associated with HO resolved within 24 h of pulmonary metastatectomy in all dogs. Durable remission of symptomatic HO was achieved in all dogs (range, 50–294 days), although recurrence of HO was noted in one dog, 246 days postmetastatectomy due to metastasis to the lungs and chest wall. Pulmonary metastatectomy resulted in a rapid and prolonged resolution of HO, and the clinical benefits of metastatectomy potentially exceed the morbidity associated with the surgical procedure.     

Ivermectin toxicity in 17 collies

Ivermectin is widely used in veterinary medicine as an anthelminthic and generally has a wide margin of safety, but Collies are prone to ivermectin toxicity. Two groups of Collies were presented to the University of California Veterinary Medical Teaching Hospital (VMTH) with ivermectin toxicity. The medical records of the 2 groups of Collies were reviewed retrospectively. Group I comprised 5 adult Collies that received at least 400 microg/kg ivermectin p.o. and were presented to the VMTH 3 hours after intoxication. These Collies showed marked clinical signs on presentation. Three of these dogs required mechanical ventilation and were euthanized for financial reasons; the remaining 2 dogs were comatose but recovered in 5-7 days. Group II was comprised of 12 adult Collies presented to the VMTH 2 days (n = 10) and 5 days (n = 2) after subcutaneous injection of 200-250 microg/kg ivermectin. These animals showed greater variation in severity of illness among individuals; 5 animals progressed to stupor or coma, whereas 4 animals remained ambulatory. Most of these dogs' clinical signs deteriorated from the day of intoxication until approximately day 6, from which time they showed gradual but steady improvement. All of the Collies in this group survived, but it took 3 weeks for most of them to recover. Collies suffering from ivermectin toxicity can have a severe and prolonged clinical course requiring intensive nursing care. Respiratory, cardiovascular, and nutritional support may all be required. With appropriate care, however, the prognosis for complete recovery is good.     

Clinical, epidemiologic and therapeutic aspects of idiopathic epilepsy in 25 golden retrievers: results of a long term study]

The records of 25 Golden Retrievers with idiopathic epilepsy were reviewed. One goal was to identify objective aspects enabling a realistic prognosis prior to treatment. In half the dogs seizures occurred for the first time at the age of one to three years and were mostly generalised. The character, feeding habits and confinement of the dogs played a minor role in the clinical manifestation of the fits, but they were seen mostly during sleep in two thirds of the dogs. Because of the long follow-up period some important findings were made. At the beginning of the standardized long-term therapy with phenobarbital a success was observed in two thirds of the dogs, while after four years the symptoms worsened significantly in about half the dogs. We found no better success rate in castrated dogs. Dogs responded well to therapy if treated as early as possible.     

Aetiology and long-term outcome of juvenile epilepsy in 136 dogs

The aetiology and outcome of dogs with juvenile-onset seizures were investigated. One hundred and thirty-six dogs whose first seizure occurred before the age of one year were investigated. One hundred and two dogs were diagnosed with idiopathic epilepsy (IE), 23 with symptomatic epilepsy (SE), nine with reactive seizures (RS) and two with probable symptomatic epilepsy (pSE). The outcome was known in 114 dogs; 37 per cent died or were euthanased as a consequence of seizures. The mean survival time of this population of dogs was 7.1 years. Factors that were significantly associated with survival outcome included the diagnosis of SE and the number of antiepileptic drugs (AEDs) used before investigation. The use of one AED before investigation and a diagnosis of SE were associated with a negative outcome, whereas receiving no AED medications before referral was associated with a longer survival. For dogs with IE, survival time was shortened if the dog was a border collie or with a history of status epilepticus;receiving no AEDs before referral in the IE group was associated with a positive outcome. Seizure-free status was achieved in 22 per cent of dogs diagnosed with IE. While the survival times were longer than previously reported in canine epilepsy, similar remission rates to those reported in childhood epilepsy, where a 70 per cent remission rate is documented, were not seen in the canine juvenile population.     

4-Methylpyrazole as treatment for naturally acquired ethylene glycol intoxication in dogs

Eight dogs with ethylene glycol intoxication were treated with 4-methylpyrazole, an alcohol dehydrogenase inhibitor. Dogs had clinical signs referable to ethylene glycol ingestion including ataxia, depression, vomiting, polyuria, and dehydration. Metabolic abnormalities included high anion gap metabolic acidosis, serum hyperosmolality, isosthenuria, and monohydrate and dihydrate calcium oxalate crystalluria. Serum and urine ethylene glycol concentrations were determined to confirm ingestion of ethylene glycol. A 50-mg/ml solution of 4-methylpyrazole in propylene glycol was administered iv as follows: initial treatment, 20 mg/kg of body weight; at 17 hours after admission, 15 mg/kg; at 25 hours after admission, 5 mg/kg. By 24 hours after admission, all dogs had clinical and metabolic improvement. Of the 8 dogs, 7 were released within 3 days of admission. Four of the 8 dogs returned for follow-up evaluation, at which time biochemical or hematologic abnormalities were not observed.     

An evaluation of activated coagulation time in warfarin-intoxicated dogs

Activated coagulation time, one stage prothrombin time and activated partial thromboplastin time were compared in warfarin-intoxicated dogs. All coagulation tests were significantly prolonged on the third and fourth days following intoxication. Coagulation assays of all dogs except one returned to preintoxication values one day following vitamin K therapy. Significant correlation was found between all coagulation tests in the intoxicated group. Activated coagulation time may provide a useful coagulation screening test to veterinarians with limited laboratory capabilities.     

Clinical findings, treatment, and outcome of dogs with status epilepticus or cluster seizures: 156 cases (1990-1995)

OBJECTIVE: To report clinical findings, treatments, and outcomes of dogs admitted to the hospital for status epilepticus or cluster seizures and evaluate factors associated with outcome. DESIGN: Retrospective study. ANIMALS: 156 dogs admitted for status epilepticus or cluster seizures. PROCEDURE: Medical records were reviewed for seizure and medication history, diagnostic test results, types of treatment, hospitalization costs, and outcome of hospital visits. RESULTS: Dogs were admitted for seizures on 194 occasions. Of 194 admissions, 128 (66%), 2 (1%), 32 (16.5%), 2 (1%), and 30 (15.5%) were of dogs with a history of clusters of generalized seizures, clusters of partial complex seizures, convulsive status epilepticus, partial status epilepticus, and > 1 type of seizure, respectively. Underlying causes of seizures were primary epilepsy (26.8%; 52/194), secondary epilepsy (35.1%; 68), reactive epileptic seizures (6.7%; 13), primary or secondary epilepsy with low serum antiepileptic drug concentrations (5.7%; 11), and undetermined (25.8%; 50). One hundred and eighty-six hospital visits resulted in admission to the intensive care unit (ICU). Treatments with continuous i.v. infusions of diazepam or phenobarbital were initiated during 66.8% (124/186) and 18.7% (35) of ICU hospital stays for 22.3 +/- 16.1 hours (mean +/- SD) and 21.9 +/- 15.4 hours, respectively. Of 194 admissions, 74.7% (145) resulted in discharge from the hospital, 2.1% (4) in death, and 23.2% (45) in euthanasia. A poor outcome (death or euthanasia) was significantly associated with granulomatous meningoencephalitis, loss of seizure control after 6 hours of hospitalization, and the development of partial status epilepticus. CONCLUSIONS AND CLINICAL RELEVANCE: Granulomatous meningoencephalitis, loss of seizure control after 6 hours of hospitalization, or the development of partial status epilepticus may indicate a poor prognosis for dogs with seizures.     

Neutropenia associated with vincristine and L-asparaginase induction chemotherapy for canine lymphoma

Vincristine (VCR) and L-asparaginase (L-ASP) are commonly used to treat canine lymphoma. As single agents, these drugs are not myelosuppressive. However, in combination, VCR and L-ASP cause severe neutropenia in some dogs. It has been recommended that L-ASP be administered 12-24 hours after VCR to minimize toxicity. The purpose of this retrospective study was to determine the prevalence of neutropenia after VCR/L-ASP induction therapy for canine lymphoma and to evaluate risk factors for myelosuppression, especially the interval between VCR and L-ASP administration. Medical records of 147 dogs were reviewed. L-ASP was given 0 (n = 50), 6 (n = 23), 18 (n = 20), or 24 (n = 54) hours after VCR. Forty percent of the dogs were neutropenic 7 days after VCR/L-ASP, and 18% had neutrophil counts of <1,000 cells/microL. The median neutrophil count was 3,712 cells/microL (range 0-30,968 cells/microL). No correlation was found between administration interval and day 7 neutrophil count (P = .84) or development of gastrointestinal signs, including vomiting (P = .80), diarrhea (P = .52), and decreased appetite (P = .30). No significant predictors of neutropenia were identified. Higher clinical stage and substage b were associated with decreased appetite after treatment (P = .04 and .01, respectively). Sixteen percent of the dogs were hospitalized. This study demonstrates that VCR/L-ASP induction for canine lymphoma may result in neutropenia but that separation of VCR and L-ASP administration may not be necessary to avoid toxicity.     

Low concentrations of cerebrospinal fluid GABA correlate to a reduced response to phenobarbital therapy in primary canine epilepsy

In this study, we investigated whether pretreatment cerebrospinal fluid (CSF) neurotransmitter concentrations of gamma-aminobutyric acid (GABA) and glutamate (GLU) were correlated with response to phenobarbital treatment in dogs with primary epilepsy. Eleven untreated dogs, 6 males and 5 females, with a median age of onset of seizures of 3 years (range: 0.5-5 years) were selected for therapy based on progressive or serious seizure patterns. The median interval between the first observed seizure and start of phenobarbital therapy was 485 days (range: 101-1,765 days). All dogs were purebred, with the exception of I male dog. Oral phenobarbital was started at 2.5 mg/kg every 12 hours. Trough serum phenobarbital concentrations were measured at 15, 45, 90, 180, 360, 540, and 720 days after the start of treatment. There was no difference in the mean trough serum concentration or in the mean number of seizures recorded between each time period of phenobarbital measurement over the 2-year evaluation. No correlation was found between CSF GLU, GABA, or GLU: GABA ratio and the total number of seizures recorded before or after initiation of phenobarbital therapy. Lower CSF GABA concentration, however, was correlated with a lower seizure frequency difference (the total number of seizures before phenobarbital therapy minus the total number of seizures after phenobarbital therapy for an identical time period of evaluation) and lower percentage reduction in seizures: ([total number of seizures before phenobarbital therapy minus the total number of seizures after phenobarbital therapy] divided by the total number of seizures before phenobarbital therapy) x 100. There was no correlation between CSF GLU and the seizure frequency difference and percentage reduction in seizures. A negative correlation between the CSF GLU:GABA ratio and seizure frequency difference was found. Thus, dogs with an initial lower CSF GABA concentration before phenobarbital therapy did not respond as well as did dogs with a higher CSF GABA concentration.