The case report by Husser et al. describes a situation involving massive transfusion of crystalloid, packed erythrocytes, and platelets in a crisis situation. During the case, our rapid infusion/warmer, the FMS 2000 (Belmont Instrument Corporation, Billerica, MA), detected an over-temperature situation, alarmed, and stopped the infusion. A portion of the heat exchanger seemed to have become very hot, and a portion of the housing seemed to have softened. The authors attribute a brief episode of hypotension, and tachycardia, to the incident.
The FMS 2000 monitors the true temperature of the infusate (not that of a water bath or plate) and alarms whenever the fluid exiting the heat exchanger reaches 42°C, well below the temperature at which blood can be damaged. When the alarm occurs, the system immediately closes the line to the patient and stops the pump and heater, and an alarm message instructs the user to discard the disposable set. There is a substantial volume (45 ml) in our disposable set downstream of the heat exchanger, at lower temperature, so that it is impossible for any fluid above 42°C to reach the patient. When the system involved in the incident was returned to us for evaluation, it was thoroughly tested, and it performed according to specification. The disposable set was returned to us, and the heat exchanger was found to be partially occluded with what seemed to be clotted blood. There was no charred plastic. Blood clots had become trapped in the fine channels of the heat exchanger, preventing blood from flowing through them, and also preventing much of the clot material from being infused into the patient. When sufficient clot material is trapped in the heat exchanger, a portion of the heater can be occluded, trapping infusate fluid, which can get very hot. However, the trapped fluid cannot reach the patient. As soon as any fluid at 42°C or higher exits the heat exchanger, the over-temperature alarm activates, closing off flow to the patient as described above.
The heat exchanger in our system consists of a series of specially treated stainless steel annular rings that are heated indirectly by magnetic induction and are enclosed in plastic housing. The system has been tested multiple times by an independent, university-affiliated laboratory using packed human erythrocytes from a blood bank. Hemolysis and erythrocyte osmotic fragility have been measured both for test samples at all flow rates and for control samples that did not pass through the system. In all measurements, which were repeated on several occasions using different blood samples, no difference between the test samples and controls was ever found. As to the origin of the clots, we know that they were formed downstream of the reservoir filter of our disposable set, which removes all gross particulate matter, suggesting the involvement of a soluble factor. The pore size of the reservoir filter is 160 μm (0.16 mm), which is much smaller than the heat exchanger channel spacing, 760 μm (0.76 mm). At some institutions, lactated Ringer’s solution (containing Ca2+ions) has been infused with citrated blood products, which, in a few cases, has led to clotting within the disposable set. However, in this case report, the authors state that lactated Ringer’s solution was never added to the FMS.
The only way in which we are able to reproduce such high heat as to soften the heat exchanger housing is to completely occlude a section of the heat exchanger with epoxy cement. This causes no flow to occur in the blocked section, which leads to dramatic overheating. (The annular rings of the heat exchanger divide the flow into a series of parallel fine channels. Occluding approximately two thirds of the fluid path for all 17 channels in the heat exchanger and monitoring the fluid temperature just downstream of the blockage with a small thermocouple probe showed only a small increase in temperature to between 42° and 46°C, which does not damage stored erythrocytes.1This makes the scenario in the second to last paragraph of the case report, regarding vasoactive mediators, very unlikely. It is only when several channels were completely blocked that dramatic overheating occurred. This was due to a region of trapped, stagnant fluid being continually heated by the rings. The temperature in the adjacent unblocked channels stayed near normothermic temperature.) If the flow path changes slightly, and some of the overheated fluid can reach the output temperature probe, the system alarms as soon as the output temperature reaches 42°C. In the disposable set returned to us, the occlusion was located very close to the output of the heat exchanger, so that the response would have been very quick.
The authors speculate that the hypotensive incident could have been caused by damage to the small amount of leukocytes contained in the packed erythrocytes. However, the high temperature in the heat exchanger results from complete lack of flow in an area of occlusion. Furthermore, leukocytes in packed erythrocyte suspensions stored under standard conditions are already degraded and are known to release numerous cytokines.2–4In this case report, no laboratory measurements were made relating to leukocytes or cytokines, and no conclusion regarding the involvement of these factors can be made. As for the transient hypotensive incident, Elia and Kang,5in their comprehensive review of rapid transfusion devices, state that “hypotension may occur during massive transfusion because the heart is exposed to a large amount of acidic, hyperkalemic, hypocalcemic, and desaturated blood.” As for the hemolyzed blood in the arterial blood gas samples, many factors are known to produce hemolysis during transfusion, including 5% dextrose–containing solutions,6the effects of massive transfusion, and the process of drawing the blood sample for the measurement.
This incident describes a situation in which our infusion-warming device, the FMS 2000, overheated during a massive transfusion crisis. However, the device alarmed when it sensed 42°C infusate and protected the patient by shutting off the patient line, while maintaining a margin of safety of 45 ml between the device and the patient. We attribute the problem to gross blood clots within the heat exchanger. Our examination of the disposable set indicated that there was no charred plastic, as alleged by the authors. There is no evidence for the involvement of damaged leukocytes or cytokines.
More than 20,000 patients have been helped with the FMS 2000, including a number of cases that involved much higher transfused fluid volumes than that described here, including several in which more than 100 l was transfused.