A retrospective analysis of environmental risk factors for the diagnosis of deep stromal abscess in 390 horses in North Central Florida from 1991 to 2013.

PURPOSE: The purpose of this investigation was to identify potential environmental risk factors for the diagnosis of equine deep stromal abscesses (DSA) in the subtropical climate at the University of Florida Veterinary Medical Center (UFVMC). METHODS: Cases included were selected from the UFVMC medical record and imaging database, and included all cases of equine DSA diagnosed during the period from December 1991 to December 2013 in patients residing in north central Florida. Patient date of diagnosis and atmospheric data was obtained for north central Florida for the corresponding time period. Univariate and multivariate general linear models were generated testing effects and interactions between environmental conditions. RESULTS: When year, sulfur dioxide (SO2 ) and wind were analyzed in the presence of each other, a one-mile per hour increase in wind (P = 0.005) significantly increased the number of DSA cases by 1.63 cases per year. When the influence of temperature was evaluated in conjunction with year and nitrogen dioxide (NO2 ), the number of cases decreased by 0.1534 per year for every degree increase in temperature (°C) (P = 0.039). CONCLUSIONS: Wind speed is the first significant atmospheric risk factor to be identified for DSA formation in the horse. The importance of environmental variance in the incidence of DSA indicates that the pathogenesis of DSA formation may be multifactorial, interdependent and provides support in some horses for the micropuncture hypothesis of DSA formation related to the involvement of environmental conditions causing precorneal tear film and epithelial damage.

Use of orally administered dexmedetomidine to induce emesis in cats.

CASE SERIES SUMMARY: This case series describes the use of orally administered dexmedetomidine at a dose of 20 µg/kg to induce emesis in six cats. Emesis was successfully induced in 5/6 cats, with each of the cats vomiting once. The reasons for inducing vomiting included known or suspected ingestion of lilies, onions, acetaminophen (paracetamol) or acetylsalicylic acid. Four of the five cats in which emesis induction was successful did not develop any clinical signs of toxicity associated with the toxin ingested; the fifth cat developed clinicopathological changes consistent with acetaminophen toxicity. All six cats exhibited moderate to profound sedation, as expected, but no other adverse effects were documented. RELEVANCE AND NOVEL INFORMATION: Induction of emesis in cats is notoriously difficult. This case series describes a novel route of administration of dexmedetomidine, a commonly available medication, with a high success rate observed for inducing emesis in this group of cats.

Cats are notoriously more difficult to elicit vomiting in than dogs. This case series describes the use of a novel way of giving cats a commonly available veterinary medication to cause vomiting. The medication, dexmedetomidine, was given by mouth to six cats, of which five vomited. All six cats had eaten toxins: lilies, acetaminophen (paracetamol), aspirin or onions. Four of the five cats that vomited did not develop any signs of toxicity. All six cats that received the medication became sedated, but no other side effects were noted.

Outcomes, including death, in dogs with pneumothorax following nasogastric feeding tube misplacement in the tracheobronchial tree: 13 cases (2017-2022).

OBJECTIVE: Complications of feeding tube placement are uncommon, but life-threatening pneumothorax has been reported in human and veterinary patients during feeding tube placement. This article describes the development of pneumothorax and the outcome associated with misplacement of nasogastric (NG) tubes in the tracheobronchial tree in 13 dogs. ANIMALS: 13 dogs being treated for various medical conditions that had NG tubes placed in 4 hospitals. PROCEDURES: A review was carried out of the medical records of 13 dogs that developed pneumothorax after misplacement of NG tubes between 2017 and 2022. RESULTS: 14 dogs out of 4,777 (0.3%) developed pneumothorax as an adverse effect of NG tube misplacement in the tracheobronchial tree. One dog was excluded due to incomplete medical records. The feeding tube size ranged from 5F to 10F, and the most common tubes utilized were polyurethane tubes with flushing stylets. Nine out of 13 dogs developed evidence of respiratory compromise after the NG tube was placed. Eleven dogs required thoracocentesis, and 5 dogs had thoracostomy tubes placed. Five dogs suffered cardiopulmonary arrest after developing pneumothorax, with 3 of 5 undergoing cardiopulmonary resuscitation. Two out of 3 dogs that underwent cardiopulmonary resuscitation were discharged from the hospital. Five of 13 dogs were successfully discharged from the hospital, while 5 dogs died or were euthanized because of the pneumothorax. CLINICAL RELEVANCE: Pneumothorax is a rare but potentially life-threatening complication of NG tube placement in dogs and may lead to death if not immediately addressed. Practitioners should be aware of this complication and be ready to perform thoracocentesis quickly if appropriate.

A retrospective evaluation of eastern coral snake envenomation and antivenom administration in cats: 30 cases (2012-2019).

Thirty cats were identified to be have been suspected to have a potential coral snake envenomation after searching medical records from 2012 to 2019 at a university teaching hospital. The records were reviewed and evaluated for signalment, date and time of the snake encounter, elapsed time between encounter and hospital examination, presenting complaint, initial physical examination findings, initial laboratory findings, antivenom dose and duration of administration, adverse reactions to antivenom, additional treatments administered, progression of clinical signs, length of hospitalization, and outcome. Thirteen cats presented with clinical signs consistent with envenomation while 17 cats were treated for possible asymptomatic envenomation, as defined by the owner discovering a live or dead coral snake in their home or on their property. Initial physical examination findings included tachypnea with short shallow breaths and use of accessory muscles; tetraparesis with normal or decreased to absent spinal reflexes; cranial nerve deficits including decreased to absent gag, slow pupillary light reflexes, and absent physiologic nystagmus; and normal or altered mentation. Laboratory findings included hypercapnia, hyperglycemia, hypokalemia, increased aspartate aminotransferase activity, increased alanine aminotransferase activity, echinocytosis, leukocytosis, azotemia, and hyperlactatemia. Twenty-eight cats received antivenom; two cats received two vials while twenty-six cats received one vial. Antivenom reaction was suspected in one cat that developed facial swelling during administration of the drug. Average length of hospitalization was 1 day for cats without clinical signs and 3 days for cats with clinical signs. Twenty-nine cats survived to discharge. Due to the inclusion criteria of the study, cats euthanized on presentation or discharged without receiving antivenom may have been unintentionally excluded from the study. Diagnosis of eastern coral snake envenomation should be suspected in the cat that has acute onset of lower motor neuron neuropathy. Prognosis with treatment is considered good with 97% of cats surviving to discharge. Antivenom reaction occurred in 3.5% of administrations with none being fatal. Monitoring of hypercapnia was critical in making the decision to mechanically ventilate patients. Supportive care that includes antivenom administration, recumbency care, and mechanical ventilation if needed are the mainstays of therapy.

Cohen syndrome in the Ohio Amish.

We describe eight members from two large Amish kindreds who share a phenotype characterized by early-onset pigmentary retinopathy and myopia, global developmental delay and mental retardation, microcephaly, short stature, hypotonia, joint hyperextensibility, small hands and feet, common facial appearance, and friendly disposition. Several of the children had intermittent granulocytopenia. The phenotypic occurrence in three siblings coupled with the increased coefficient of inbreeding in the Amish suggested that this disorder is autosomal recessive and due to a single founder allele. Despite similarity to the clinical features of Cohen syndrome, experienced dysmorphologists attending the 23rd David W. Smith Workshop suggested the facial gestalt of the Amish children was inconsistent with this diagnosis. We mapped the locus responsible for these individuals' phenotype to chromosome 8q22-q23, which contains the recently discovered Cohen syndrome gene, COH1. Complete sequencing of the COH1 gene identified a likely disease-causing frameshift mutation and a missense mutation in the Amish patients. A comparison of features among different Cohen syndrome populations with shared linkage to the COH1 locus or known COH1 gene mutations may allow for the determination of improved clinical criteria on which to suspect the diagnosis of Cohen syndrome. We conclude that facial gestalt seems to be an unreliable indicator of Cohen syndrome between ethnic populations, although it is quite consistent among affected individuals within a particular ethnic group. Other features common to almost all individuals with proven COH1 mutations, such as retinal dystrophy, myopia, microcephaly, mental retardation, global developmental delay, hypotonia, and joint hyperextensibility appear to be better clinical indicators of this disorder.