Few studies have been reported on the usefulness of IABS in emergency surgery for massive hemothorax [1–3]. Although massive hemothorax with significant blood loss and hemodynamic instability ordinarily requires urgent intervention, including emergency surgery and allogeneic blood transfusions, an innovative IABS technique can reduce the overall blood loss and thereby avoid the need for allogeneic transfusion, which is associated with known adverse clinical outcomes and life-threatening complications. IABS can also save time for the preparation of allogeneic blood. IABS was introduced in the early 1980s and rapidly gained clinical acceptance as a safe alternative to allogeneic transfusion. IABS is now commonly used during surgeries with the potential for massive bleeding, such as cardiac surgery, vascular surgery, spinal surgery, or liver transplant [4, 5]. IABS systems, including Haemonetics Cell Saver 5+, which was used in this study, entail the collection and reinfusion of a patient’s own blood that is lost throughout surgery. First, it collects shed blood from the operative field into a centrifuge. Heparin anticoagulant is added, and the contents are filtered to remove platelets, white blood cells (WBCs), free hemoglobin, and concomitants such as clots and lipids from the operating field. RBCs are then washed with saline, separated by differential centrifugation, and reinfused. The final blood consists of washed, concentrated RBCs with a hematocrit count of approximately 53.7‒60% suspended in normal saline solution. The blood processing speed is 3–5 min. IABS systems have been reported to bring about significant attenuation of the inflammatory response in processed blood, demonstrating the effective elimination of several inflammatory cytokines (TNF-α, IL-2, IL-6, IL-8, etc.), WBCs, and markers of leukocyte activation (myeloperoxidase and elastase) [6, 7]. On the other hand, RBCs salvaged from the operating field in IABS have been suggested to result in bleeding due to dilutional coagulopathy caused by the elimination of platelets and coagulation factors [1, 2]. Recent evidence has, however, demonstrated that no significant coagulopathy is associated with IABS . IABS also carries the risk of bacterial contamination from the operating fields, but none of the patients in our study developed an infection.
Adverse clinical outcomes among recipients of allogeneic blood transfusion have been widely reported, such as higher rates of serious perioperative infections, post-injury multiple-organ failure, pulmonary, renal, and cardiac complications, and higher mortality rate . “Blood storage lesions” and subsequent immune suppression are likely important contributors to these morbidities. Older allogeneic blood is known to increase morbidity and mortality as compared with newer blood . Refrigerated storage of blood results in a “storage lesion,” characterized by rheological changes, metabolic derangements, changes in oxygen affinity and delivery, oxidative injury to lipids and proteins, RBC shape change, loss of membrane carbohydrate, and reduced RBC lifespan. These changes become more pronounced with longer storage, promoting in vivo hemolysis [11, 12]. Other known serious adverse events associated with allogeneic blood transfusion include incompatibility reactions and transfusion-transmitted diseases. Furthermore, many countries often face a shortage of allogeneic blood and issues of increasing cost . Another life-threatening complication of allogeneic transfusion includes transfusion-related acute lung injury (TRALI), which was reported in approximately 2.4% of cardiac surgery patients with 13% mortality in a Dutch-nested, case-control cohort study . TRALI is the acute onset of non-cardiogenic pulmonary edema that occurs within 6 hours of transfusion and is the leading cause of transfusion death. TRALI is thought to be a two-event entity. The first event is the presence of an inflammatory condition in the host that causes endothelial activation, which leads to neutrophil sequestration and priming in the lung. The second event is transfusion of an allogeneic blood product containing either donor leukocyte antibody or bioactive lipids (lysophosphatidylcholines) that accumulate during storage of RBCs or platelets, providing additional signals for neutrophil activation, resulting in the clinical syndrome of pulmonary edema. The onset of TRALI correlates with the total volume of RBC products stored for ≥ 14 days [15, 16]. In the present study, Patient 3, who had 4 U of allogeneic and 1227 cc of IABS transfusions, experienced severe ARDS. While severe ARDS was accompanied by massive, watery intra-airway secretion that started intraoperatively in this case, how much this ARDS is attributable to TRALI by allogeneic blood transfusion rather than by re-expansion lung edema following prolonged lung atelectasis (≥ 2.5 days) or a massive fluid infusion to compensate for hemodynamic instability caused by large blood loss (2130 cc) is unclear. Generally, patients with massive hemothorax, who have undergone a large volume overload with both fluid and blood, and especially with a more prolonged period of lung collapse, seem highly vulnerable to re-expansion lung edema. Tension thorax, which is prone to accompany hemopneumothorax rather than simple hemothorax, may partially contributed to re-expansion edema.
Owing to such adverse clinical outcomes and life-threatening complications, allogeneic blood transfusion should be avoided as much as possible. From this standpoint, IABS is an effective blood conservation strategy in surgeries with massive bleeding.
Strong clinical and economic evidence supports the use of IABS in surgeries with massive bleeding, as IABS results in a significant reduction in allogeneic RBC and coagulant product transfusions , earlier discharge from the intensive care unit, and a lower incidence of myocardial infarction in cardiac [5, 8] and pediatric cardiac surgery patients . On the other hand, IABS is believed to be cost-effective only when large blood loss equivalent to1–2 units of RBCs can be salvaged during surgery . While a minimum of 600–800 ml of intraoperative bloodshed is required for the Cell Saver devices to process, only one-third of this amount is returned. In cases where the system is set up and fails to collect enough volume to process, a considerable cost is incurred for zero benefit .
As the blood drained through the chest tube cannot be processed for reinfusion because of its considerable risk of contamination, the greater the preoperative chest tube drainage of intrathoracic shed blood, the less the amount of blood available for IABS, thereby increasing the likelihood of a subsequent allogeneic transfusion in surgery for massive hemothorax. Among the 7 IABS patients in the present study, 3 who did not undergo preoperative chest tube drainage (patients 5, 6, and 8) and/or one who had a chest tube drainage of < 150 cc (Patient 3) showed a trend toward receiving more IABS transfusions (mean, 1162 ± 414 cc), than the 3 patients who had preoperative chest tube drainage of ≥ 150 cc (patients 4, 7, and 9; mean, 666.7 ± 150 cc; P = 0.0574); that is, the amount of IABS transfusion was inversely proportional to the amount of preoperative chest tube drainage and allogeneic transfusion, which means that the lower the amount of chest tube drainage, the larger the amount of IABS autotransfusion, and the fewer units of allogeneic transfusion were required irrespective of the total amount of shed blood. Thus, from the standpoint of promoting maximal IABS utilization and limiting allogeneic blood transfusion, preoperative chest tube drainage should be spared to the maximum possible extent as long as hemodynamics remain stable.
Hemodynamic status at the first hospital visit varied in each patient; some patients who had continuous or vigorous bleeding from the onset of hemothorax might appear with relatively unstable conditions, whereas others who had substantial initial bleeding with the subsequent hemostasis caused by the spasm of torn arteries, or by compression of the intrathoracic clot might show more stable hemodynamic conditions. In the present study, 3 patients who had an onset-to-surgery time of < 10 hours (patient 2, 7, and 9) simultaneously had a mean bleeding rate of ≥ 400 cc/hour and further had a larger total blood loss exceeding 2800 cc. These three patient had a significantly higher mean bleeding rate (mean, 438 ± 21.7 cc/hour; range, 424.0–463.0 cc/hour; P = 0.006; Fig. 2), significantly greater total blood loss (mean, 3533 ± 690 cc; range, 2800–4170 cc; P = 0.0246; Fig. 3), and further significantly shorter onset-to-surgery time (mean, 8.03 ± 1.27 hours; range, 6.6–9.0 hours; P = 0.0091), than the other 6 patients. These results suggest that more vigorous arterial bleeding probably started concurrently with the onset and continued until surgery in these 3 patients. This high mean bleeding rate (mean, 438 ± 21.7 cc/hour, range, 424.0–463.0 cc/hour) could have led to hemodynamic instability sooner, promoting surgical intervention at an earlier timing (Online Resource 1).
As for surgical approaches, all patients in this study were treated with complete thoracoscopic surgery, which is less invasive and can provide far superior vision as compared with thoracotomy alone. It is well-suited for observing the entire pleural cavity following evacuation of shed blood and clot, and for searching and clipping the bleeding torn arteries. The thoracoscopic procedures have been refined over the years, and the incision sizes have decreased. This is partially because it has turned out that the evacuation of massive blood and coagula is feasible even through smaller-sized ports in most cases.
In the present study, the chest radiographs taken at the initial visit to the hospital demonstrated a significant mediastinal shift in all the patients except for Patient 6, who had the lowest net blood loss. Once tension thorax with some hemodynamic instability is demonstrated in patients with hemothorax or hemopneumothorax, immediate chest tube placement is usually required. All the patients in this study except for Patient 8 had spontaneous hemopneumothorax that tended to accompany tension thorax more easily than simple hemothorax, with chest tube placement required more frequently. In these cases, the best practice might be to place the chest tube first and then clamp it when the hemodynamics is stabilized with the relief of the mediastinal shift by the evacuation of air and blood. This can minimize unnecessary blood loss and allow for scheduling of early emergency surgery. On the basis of the results of this study, we propose the following algorithm for treating hemothorax with hemodynamic instability: 1) stabilization of hemodynamics on arrival by fluid infusion, 2) radiological diagnosis (chest radiography and/or computed tomography scan), 3) chest tube placement for the relief of tension thorax as required, 4) preparation of allogeneic blood as needed, and 5) scheduling early emergency thoracoscopic surgery in combination with IABS when ≥ 800 cc of intrathoracic blood is suspected.
In conclusion, utilizing the Cell Saver IABS with the sparing of preoperative chest tube drainage to the maximum possible extent is an efficient strategy to reduce both overall blood loss and subsequent allogeneic blood transfusion in emergency thoracoscopic surgery for massive hemothorax.