No abstract

In horses, gastrointestinal (GI) disorders are the main cause of disseminated intravascular coagulation (DIC), a potentially life-threatening condition. Large colon volvulus, colitis, and strangulating small intestinal lesions are the most common GI conditions that cause DIC in horses, 4,12 but DIC is also reported in septicemia, snakebites, rhabdomyolysis, and diffuse clostridial myonecrosis. 11,13,16,19,21,22 Significantly prolonged PT was reported in 58% of horses with acute GI crisis-associated DIC, 12 and was significantly associated with strangulating GI lesions. 3,4 Early diagnosis of subclinical DIC is crucial, and depends on laboratory testing of hemostasis. 3 Prothrombin time (PT) is commonly measured in horses to assess the status of hemostasis, specifically the extrinsic and common pathways. 21 Monitoring changes in PT over time is of diagnostic and prognostic value, as well as a clinical tool to help guide treatment. 3,4 Equine medicine is often practiced at a distance from reference laboratories. Delays in receiving hemostasis test results may be detrimental in treating critically ill horses. A reliable, cost-effective, point-of-care (POC) test to assess hemostasis, such as PT measurement, would be useful under field conditions. The CoaguChek-XS (Roche Diagnostics, Mannheim, Germany) is a small, portable POC PT analyzer, commonly used in human medicine for home monitoring of warfarin therapy, that is suitable for both venous and capillary blood samples, providing results within minutes. 17,20 Studies have assessed the reliability, precision, and suitability of the CoaguChek-XS

ObjectiveTo describe the successful management of ventricular fibrillation (VF) and ventricular tachycardia (VT) using cardiopulmonary resuscitation, including defibrillation, followed by continuous rate infusion of IV amiodarone, in a cat with cardiac arrest secondary to tachyarrhythmia.Case summaryA 12‐year‐old previously healthy neutered male Scottish Fold cat presented following an acute episode of collapse. Initial physical examination revealed severe tachycardia and cardiovascular collapse. Within a few minutes after arrival, the cat experienced cardiopulmonary arrest. Electrocardiographic assessment was suggestive of VF, and CPR was initiated, including 2 rounds of defibrillation (2 joule/kg each), resulting in return of spontaneous circulation with sustained VT. After procainamide and lidocaine failed to result in conversion to normal sinus rhythm (NSR), continuous IV amiodarone therapy was initiated, and NSR was achieved. Echocardiography demonstrated severe systolic dysfunction, and tachycardia‐induced cardiomyopathy (TICM) secondary to chronic VT was suspected; however, dilated cardiomyopathy (DCM) or end‐stage hypertrophic cardiomyopathy could not be ruled out. The patient was discharged the following day with oral amiodarone and pimobendan. During a recheck examination performed 7 months later the cat was in NSR, with no direct evidence of long‐term amiodarone adverse effects. The cat died acutely at home 8 months after discharge.New or unique information providedThis report is the first to describe the successful use of IV amiodarone in a cat to manage sustained VT following CPR.

Introduction: Acute kidney injury (AKI) is a common complication following cardiac arrest (CA) and is associated with poor outcomes. Early detection of AKI is crucial; serum creatinine (sCR) is the most commonly used indicator of AKI, despite low sensitivity and specificity for early detection of AKI. Hypothesis: Kidney-specific serum biomarkers neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and cystatin-C could better predict post-CA AKI than sCR. Methods: Adult CA patients who had kidney-specific biomarkers of AKI collected shortly after return of spontaneous circulation (ROSC) as part of four randomized trials and one observational study were included. Patients with Kidney Disease Improving Global Outcome (KDIGO) stage III AKI or end-stage renal disease, or renal replacement therapy at the time of enrollment were excluded. The association between renal biomarker levels (sCR, NGAL, KIM-1, cystatin-C) shortly after ROSC and the development of KDIGO stage III AKI within 7 days of enrollment were assessed as well as their predictive value of future AKI development. Results: Of 155 patients, 46 (29.7%) developed stage III AKI within 7 days, and 98 (63.2%) died prior to hospital discharge. Patients who developed stage III AKI, compared to those who did not, had higher median levels of sCR (1.4 mg/dL [IQR: 1.2, 1.9] vs. 1.2 [IQR: 1.0, 1.5]; p=0.001), NGAL (868,208 pg/mL [IQR: 412,547.1, 1,341,597] vs. 298,928.3 [IQR: 170,786.6, 594,389.7], p<0.001). and cystatin-C (1,649,202 pg/mL [IQR: 1,184,788, 2,440,583] vs. 1,132,955 [IQR: 795,323.7, 1,580,415]; p<0.001). There was no difference in KIM-1 between groups (150.6 pg/mL [IQR: 150.8, 288.4] vs. 158.9 [IQR: 78.8, 284.7]; p=0.351). There was no significant difference between biomarkers in their ability to predict development of stage III AKI (NGAL AUC=0.75 [95%CI: 0.67-0.83], cystatin-C AUC=0.71 [95%CI: 0.62-0.79], KIM-1 AUC=0.55 [95%CI: 0.45-0.65], sCR AUC=0.67 [95%CI: 0.57-0.76], p>0.05 for all). Both NGAL and cystatin-C performed better than KIM-1 (p<0.01). Conclusion: In post-CA patients, sCR, NGAL, and cystatin-C (but not KIM-1) measured shortly after ROSC were higher in patients who subsequently developed AKI. No biomarker was statistically superior to sCR. Comparison was limited by the small number of patients who developed AKI.

No abstract