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loss from a disconnected catheter port.

       Risk factors

       Large gauge, jugular vein catheters

       Catheters placed above heart level (for air embolism)

       Pathogenesis

      Vascular air embolism may occur during catheter placement before the injection cap is attached to the catheter or it may occur after placement if the injection cap or extension set becomes dislodged from the catheter. Air may be passively aspirated into the catheter because of the negative pressure within the jugular vein when the horse’s head is elevated. The total volume and rate of air aspiration are related to the development and severity of clinical signs. Reportedly, up to 0.25 ml/kg body weight of air may be aspired in horses before clinical signs develop [6, 27] Pulmonary edema results from the inflammatory response and vascular resistance induced by air in the pulmonary microvasculature. Cardiac dysrhythmias or neurological signs occur when the pulmonary vasculature is saturated and air enters the systemic circulation and embolizes to the coronary or cerebral microvasculature or if air moves retrograde (cranially) in the jugular vein [1, 27–31]. Cardiovascular collapse can occur if a large air embolus creates an air‐lock in the right ventricle, reducing cardiac output [29].

      Passive aspiration of air is not a significant concern with catheters that are placed below heart level or in horses with lowered head positions (hemorrhage would be a complication of dislodgement of injection caps or ports from these catheters). Blood loss from a disconnected catheter port is rare, because most horses will clot before life‐threatening amounts of blood are lost [1, 2].

       Prevention

      Risk of vascular air embolism or blood loss following disconnection of catheter attachment can be minimized by securing injection caps or extension sets with luer lock ports. Regular monitoring of horses with indwelling catheters will minimize the length of time that a catheter is disconnected. Theoretically, placement of catheters in the vein against the direction of blood flow (i.e. up the jugular vein) would prevent air embolism, but would create additional problems (increased catheter thrombosis, resistance to injection, and potential for exsanguination if catheter is disconnected) [31].

       Diagnosis

      Clinical signs of vascular air embolism are tachycardia, tachypnea, muscle fasciculations, agitation, respiratory distress and pulmonary edema and may include neurological signs and cardiovascular collapse [1, 27–31]. The signs may be attributed to vascular air embolism if they occur in association with disconnection of the injection cap or extension set from the catheter. The diagnosis may be supported by arterial blood gas analysis and auscultation of a mill‐wheel murmur [27–29]. Echocardiography can also be used to confirm the diagnosis, but most cases are diagnosed presumptively [27–29]. Diagnosis of exsanguination from the catheter is obvious due to the external blood loss.

       Treatment

      Treatment of vascular air embolism starts with immediate replacement of the injection cap or extension set to prevent further aspiration of air. Nasal insufflation of oxygen can help treat respiratory distress and can speed resorption of air emboli by changing pressure gradients to help diffusion of nitrogen out of the air bubbles and reducing their size [1, 29]. Pulmonary edema can be managed with furosemide, corticosteroids, and non‐steroidal anti‐inflammatory drugs. Similarly, neurological signs can be managed with anti‐inflammatory (dimethyl sulfoxide, corticosteroids, non‐steroidal anti‐inflammatory drugs), neuroprotective (thiamine, Vitamin E) and anti‐convulsant (benzodiazepines, barbiturates) treatments, as necessary [1, 30, 31].

      Intravenous fluids should be administered if cardiovascular compromise is evident, but they may exacerbate pulmonary or cerebral edema. The volume of blood loss may be significant in hypocoagulable patients or small‐sized patients [1, 2]. Treatment includes replacement of the injection port and administration of intravenous fluids or whole blood, if signs of hypovolemia are present or severe [1].

       Expected outcome

      If recognized promptly and vascular air aspiration is limited, clinical signs can improve and horses can return to normal after vascular air emboli. In one study, 19% of horses were euthanized or died subsequent to vascular air embolism [27–31]. Similarly, blood loss from a disconnected catheter was unlikely to be significant or affect prognosis, unless the hemorrhage was not recognized or treated.

References

      1 1. Higgins, J. (2015). Preparation, supplies, and catheterization. In: Equine Fluid Therapy (ed. C.L. Fielding and K.G. Magdesian), 127–141. Ames: John Wiley & Sons.

      2 2. Tan, R.H.H., Dart, A.J., and Dowling, B.A. (2003). Catheters: a review of the selection, utilization and complications of catheters for peripheral venous access. Aust. Vet. 81: 136–139.

      3 3. Spriet, M., Trela, J.M., and Galuppo, L.D. (2015). Ultrasound‐guided injection of the median artery in the standing sedated horse. Equine Vet. J. 47: 245–248.

      4 4. Barakzai, S. and Chandler, K. (2003). Use of indwelling intravenous catheters in the horse. In. Pract. 25: 264–271.

      5 5. Hardy, J. (2009). Venous and arterial catheterization and fluid therapy. In: Equine Anesthesia: induction, maintenance and recovery phases of anesthesia. In: Equine Anesthesia: Monitoring and Emergency Therapy, 2e (ed. W.W. Muir and J.A.E. Hubbell), 131–148. St. Louis: Elsevier Saunders.

      6 6. Muir, W.W. (1991). Complication: induction, maintenance and recovery phases of anesthesia. In: Equine Anesthesia: Monitoring and Emergency Therapy, 1e (ed. W.W. Muir and J.A.E. Hubbell), 419–443. St. Louis: Mosby Year Book,

      7 7. Sweeney, R.W. and Sweeney, C.R. (1984). Transient Horner’s syndrome following routine intravenous injection in two horses. J. Am. Vet. Med. Assoc. 185: 802–803.

      8 8. Lorello, O. and Orsini, J.A. (2014). Intravenous catheter placement. In: Equine Emergencies: Procedures and Treatments, 4e (ed. J.A. Orsini and T.J. Divers), 9–11. St. Louis: Elsevier Saunders.

      9 9. Gabel, A.A. and Koestner, A. (1963). The effects of intracarotid artery injection of drugs in domestic animals. J. Am. Vet. Med. Assoc. 142: 1397–1403.

      10 10. Divers, T.J. (2014). Appendix 4 – Adverse drug reactions, air emboli, and lightning strike. In: Equine Emergencies: Procedures and Treatments, 4e (ed. J.A. Orsini and T.J. Divers), 812–816. St. Louis: Elsevier Saunders

      11 11. Dolente, B.A., Beech, J., Lindborg, S. et al. (2005). Evaluation of risk factors for developments of catheter‐associated jugular thrombophlebitis in horses: 50 cases. J. Am. Vet. Med. Assoc. 227: 113–1141.

      12 12. Spurlock, S.L., Spurlock, G.H., Parker, G. et al. (1990). Long‐term jugular vein catheterization in horses. J. Am. Vet. Med. Assoc. 196: 425–430.

      13 13. Ettlinger, J.J., Palmer, J.E., and Benson, C. (1992). Bacteria found on intravenous catheters removed from horses. Vet. Rec. 130: 248–249.

      14 14. Fiege, K., Schwarzwald, C.C., and Bombeli, T. (2003). Comparison of unfractioned and low molecular weight heparin for prophylaxis of coagulopathies in 52 horses with colic: a randomized double‐blind clinical trial. Equine Vet. J. 35: 506–513.

      15 15. Geraghty, T.E., Love, S., Taylor, D.J. et al. (2009). Assessment of subclinical venous catheter‐related diseases in horses and associated risk factors. Vet. Rec. 164: 227–231.

      16 16. Russell, T.M., Kearney, C., and Pollock, P.J. (2010). Surgical treatment of septic jugular thrombophlebitis in nine horses. Vet. Surg. 39: 627–630.

      17 17. Mair, T.S. and Smith, L.J. (2005). Survival and complication rates in 399 horses undergoing surgical treatment of colic. Part 2: short‐term complications. Equine Vet. J. 37: 303–309.

      18 18. Lankveld, D.P.K., Ensink, J.M., Dijk, P.V. et al. (2001). Factors influencing

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