Needle emboli can occur when the needle breaks off the hub during placement (Figure 3.5). This will be recognized immediately because the hub and syringe will be free from the needle. Catheter fragmentation will not be recognized until the catheter is removed and found to be incomplete. Loss of the guidewire is typically recognized immediately in veterinary medicine [22]; however, delayed recognition is common in human medicine [21]. Catheter breakage is immediately evident if it occurs at the time of catheter removal; however, if the failure occurs in an indwelling catheter, it may not be recognized. During aspiration or injection of the catheter, any evidence that air bubbles are being aspirated or bubbling under the skin during injection is strongly suggestive that there is a defect in the catheter at or near the insertion site. Intravascular foreign bodies should be localized by radiographs starting at the site of penetration and proceeding along the vein toward the thorax (Figure 3.5) [1, 20]. Ultrasound may be needed to evaluate the site of insertion (although manipulation of the tissues makes ultrasound less desirable than radiographs) or to evaluate if the intravascular foreign body is in the heart [1, 20].
Figure 3.5 Lateral radiograph of the cranial cervical region (cranial to the left of the image) in a horse that was referred for treatment and removal of a needle fragment that broke off during attempted venipuncture of the left jugular vein. An intravenous catheter was placed in the contralateral (right) jugular vein. The needle fragment was located medial to the jugular vein in the cranial cervical region.
Source: Courtesy of the University of California, Davis Veterinary Medical Teaching Hospital Diagnostic Imaging Service.
Treatment
For any intravascular foreign bodies, immediate steps to be taken would be occlusion of the vein on the cardiac side of the insertion point to try to prevent migration into the heart and pulmonary vasculature [5]. Defective catheters should be removed immediately. During removal, the vein should be occluded on the cardiac side of the vein so that any catheter fragments can be trapped at the site and prevented from embolization [5]. If the intravascular foreign body is accessible, it should be removed to prevent complications, assuming the risks of removal do not outweigh the benefits [8, 20, 25]. Direct approaches can be made to the jugular vein, but this should be done under general anesthesia with radiographic control to guide dissection. Endovascular retrieval is preferred in humans [25]; however, horse size will be limiting to this technique unless the patient is a foal or pony‐sized or the intravascular foreign body is located in the jugular vein or cranial vena cava [20, 22]. In an experimental study, 5 out of 6 horses with experimental catheter transection had the transected catheter located in the proximal or distal pulmonary arteries at necropsy 30 hours later [26].
Expected outcome
In general, it is believed that intravascular foreign bodies located within the pulmonary vasculature carry a low risk of complications [1, 8].
Vascular Air Embolism/Bleeding
Definition
Vascular air embolism is the aspiration of a significant amount of air from the environment into the vasculature and the resulting systemic effects.
Blood 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
