Erythrocyte salvage during cesarean section.

McConnell’s Sign in a Patient with Amniotic Fluid Embolism and Severe Right Ventricular Dysfunction

The use of cell salvage during caesarean section has been increasing steadily, although there are concerns relating to cost, a perceived risk of amniotic fluid embolism, and fetal red cell sensitisation. We present observational data from almost a decade of use of intra-operative cell salvage in obstetrics. By the end of this period, we set up cell salvage collection for >98% of all caesarean sections. From 2008 to 2017, 1170 women have had a re-infusion of cell salvaged blood with no clinical safety concerns; the median (IQR [range]) volume was 231 (154-306 [80-1690]) ml. During this time there has been a marked reduction in the number of women who were transfused allogeneic blood, as well as the amount of blood transfused. In total, 647 (55%) women have had alloimmunisation testing, with two positive cases. Quality control data indicate that the quality of blood processed from partial first bowls is no worse than that from full bowls. We discuss the costs of providing this service with regard to: staffing costs; single suction; leucodepletion filters; selectivity in the processing of collected blood; and the use of partial first bowls.

Incidence and risk factors of amniotic fluid embolisms: a population-based study on 3 million births in the United States

To determine the incidence of amniotic fluid embolism and the incidence as modified by cesarean section and age. Data are from the National Hospital Discharge Survey. We examined the number of patients discharged from short-stay nonfederal hospitals throughout the United States, from 1980 through 2005, with a diagnostic code for amniotic fluid embolism. From 1980 through 2005, there were 112,712,000 deliveries, of which 12,000 patients (11/100,000) had amniotic fluid embolism. The incidence of amniotic fluid embolism was lower in 1993-2005 than in 1980-1992 (9/100,000 vs. 12/100,000)(p < 0.0001). The incidence of amniotic fluid embolism was higher with cesarean section, 5,000 of 22,937,000 (22/100,000) than with vaginal delivery, 7,000 of 89,775,000 (8/100,000) (relative risk 2.80, 95% CI 2.70-2.90) (p < 0.0001). The incidence was also higher in women aged 30-39 years, 6,000 of 35,039,000 (17/100,000) than in women aged 15-29 years, 6,000 of 77,673,000 (8/100,000) (relative risk 2.22, 95% CI 2.14-2.30) (p < 0.0001). The incidence of amniotic fluid embolism has decreased since the early 1990s. The risk is higher with cesarean section and higher in women aged > or =30 years.

Amniotic fluid embolism (AFE) is a rare, catastrophic complication of pregnancy that occurs in the setting of a disrupted barrier between the amniotic fluid and maternal circulation. The onset of signs and symptoms is swift and dramatic, classically marked by dyspnea, hypoxemia, and hypotension, followed by cardiopulmonary collapse. Coagulopathy and hemorrhage are common and often occur after the clinical diagnosis is made. Mortality remains high despite aggressive therapeutic interventions. We describe a perplexing case of AFE in which isolated coagulopathy was the initial presentation. Case Report The patient was a healthy, 23 year-old secundigravid, nulliparous woman at 37 wk gestation who was admitted to our labor and delivery unit in active labor. Her antepartum obstetric history was unremarkable. On admission, the patient's arterial blood pressure was 132/87 mm Hg, and her temperature was 36.4[degree sign]C orally. Her initial hematocrit and platelet count were 42% and 241,000 cells/[micro sign]L, respectively. Her cervix was dilated 5 cm, and contractions occurred every 90-120 s. The fetal heart monitor revealed a reassuring tracing. One hour after admission, amniotomy was performed, and clear fluid was noted. Because the external tocodynamometer was unable to detect contractions, an intrauterine pressure catheter was inserted at that time. Thirty minutes later, a continuous lumbar epidural catheter was placed uneventfully, and 0.125% bupivacaine 10 mL and fentanyl 50 [micro sign]g were given incrementally. Analgesia was maintained with a solution of 0.125% bupivacaine and 2 [micro sign]g/mL fentanyl at the rate of 10 mL/h. Approximately 3 h after admission, the patient's cervix was completely dilated, and expulsive efforts were initiated. One hour later, her temperature increased from 38.1[degree sign]C to 39.1[degree sign]C. The patient was given ampicillin 2 g and gentamicin 100 mg IV for presumed chorioamnionitis. At this point, the fetal heart tracing revealed tachycardia and severe variable decelerations during contractions. Gingival and epidural catheter site bleeding in addition to epistaxis were noted on placing the patient in the knee-chest position, which was initiated to improve the fetal dysrhythmias. During this time, the patient's blood pressure and heart rate were 146/86 mm Hg and 133 bpm, respectively. The fetal heart tracing demonstrated no improvement; the patient was then transported to the delivery suite for a trial of forceps delivery. The epistaxis was controlled with direct pressure to her nostrils, and it resolved in the delivery suite. Coagulation studies were obtained and sent to the laboratory. The patient underwent a low-outlet forceps delivery resulting in a viable male infant (Apgar scores of 6 and 8 at 1 and 5 min, respectively). The second stage of labor lasted for 3.5 h. Immediately after the delivery of an intact placenta without evidence of retroplacental clots, postpartum hemorrhage ensued from uterine atony. Over the next 60 min, the patient received oxytocin (100 U IV), methylergonovine (0.2 mg intrauterine), and.15-methylprostaglandin F2-alpha (0.5 mg IM). Laboratory studies were consistent with disseminated intravascular coagulation (DIC): prothrombin time >60 s, partial thromboplastin time >150 s, D-dimer >8.0 [micro sign]g/mL, fibrin split products >40 [micro sign]g/mL, platelets 85,000 cells/[micro sign]L. The patient's condition quickly deteriorated. She became disoriented and unresponsive, for which she underwent endotracheal intubation. Of note, the patient maintained adequate oxygenation throughout this time, with pulse oximetry revealing 98%-100% saturation with 0.5 fraction of inspired oxygen. Packed red blood cells and platelets were administered, followed by fresh-frozen plasma. The patient then became hypotensive despite the rapid administration of crystalloid, colloid, and blood products and incremental dosing of ephedrine and phenylephrine. Resuscitation continued while central venous and arterial catheters were placed. Because of the acuity of events and time course, however, no central venous or pulmonary artery pressure monitoring was obtained, and vasoactive infusions were omitted in favor of bolus injections. The pulse oximetry tracing later diminished, and arterial blood gas analysis confirmed hypoxemia despite ventilation with 1.0 fraction of inspired oxygen. The patient experienced cardiopulmonary arrest immediately thereafter, and despite aggressive resuscitative efforts, including transfusion of multiple blood products (10 U of packed red blood cells, 6 U of fresh-frozen plasma, 6 pack of platelets), IV calcium, atropine, and epinephrine, followed by open chest cardiac massage, the patient died. The postmortem examination determined AFE as the cause of death, with diffuse extensive capillary and large vessel plugging by squamous cells, mucin, lipid material, and lanugo hairs noted in the lungs. No thromboemboli were observed. Similar amniotic fluid contents were present in the liver and parametrium, with markedly prominent plugging noted in the vasculature of the posterior cervix. Evidence of early myocardial infarction was noted in the right ventricle consistent with acute cor pulmonale. The uterus was intact, and the placenta demonstrated prominent microcalcifications without evidence of chorioamnionitis or abruption. Discussion AFE, first described by Meyer [1] in 1926, is a topic of great concern in obstetrics today because of its dramatic presentation and high rate of mortality. The reported incidence of AFE varies from 1:8,000 [2] to 1:80,000, but a rate between the two figures is most likely. Mortality exceeds 80%, with 25%-50% of deaths occurring within the first hour of diagnosis [3]. AFE can occur only when there is a breech in the barrier between the amniotic fluid and maternal circulation. The three most common routes of entry are the endocervical veins, the placental site, and a uterine trauma site [4]. Postmortem examination of our patient revealed marked plugging of the cervical vasculature by amniotic fluid contents, with significant numbers of acute inflammatory cells noted; thus, the posterior endocervical veins were deemed to be the port of entry. It is noteworthy that traumatic intrauterine pressure catheter placement has been implicated as a risk factor for AFE [5], although there was no evidence of traumatic insertion documented in the patient's chart. The onset of AFE is said to be abrupt, heralded by sudden dyspnea, hypoxemia, cyanosis, and hypotension disproportionate to the amount of blood loss [6]. More than 80% of patients [7] experience cardiopulmonary arrest. Invasive hemodynamic monitoring in patients with AFE reveals decreased cardiac output, increased pulmonary artery pressure, and marked systemic vasodilation [8]. Of those patients who survive the initial hemodynamic collapse, approximately 70% develop noncardiogenic pulmonary edema [9], and 45% develop a severe coagulopathy 30 min to 4 h later [10]. Laboratory evidence of coagulopathy can be seen 30-60 min before the onset of the more classic signs and symptoms of AFE, which suggests that a latency period may be necessary [10]. Although there was no laboratory confirmation of coagulopathy in our patient, the spontaneous gingival and epidural catheter site bleeding and epistaxis noted approximately 120 min before hemodynamic collapse support a coagulopathic state at that time. In a review of 272 cases of AFE, Morgan [11] found excess bleeding in 49%-in 12%, it was the first indication of the ensuing catastrophe. It must be noted, however, that Morgan did not differentiate coagulopathy from hemorrhage, and no mention is made concerning the presentation time of coagulopathy relative to the onset of AFE. Although our patient experienced excess bleeding from uterine atony after delivery, we believe that she was coagulopathic before delivery; further, it may have been the initial presentation of AFE. A recent review of the national registry of AFE patients by Porter et al. [12] identified eight patients in whom isolated acute coagulopathy developed without preceding hypotension, hypoxia, or evidence of placental abruption. Acute hemorrhage occurred post-partum in seven of eight patients, five of whom developed uterine atony. Six patients exsanguinated despite appropriate medical management and blood component transfusion, yielding a mortality rate (75%) similar to that in classic AFE. The authors concluded that fatal DIC in pregnant patients may represent a forme fruste of AFE. The cause of coagulopathy from amniotic fluid is multifactorial. Phillips and Davidson [13] described the procoagulant properties of amniotic fluid, specifically noting increased factor X activity when amniotic fluid is mixed with maternal blood. In addition, Yaffe et al. [14] discussed the increase in thromboplastic activity associated with AFE. Furthermore, although amniotic fluid lacks plasmin and plasmin activator, it contains plasmin proactivator. Weiner [10] speculated that thrombin generation in the pulmonary beds leads to plasmin and kinin production, which, in the absence of antiplasmin, perpetuate their own generation. When thrombin generation occurs in an environment of excess plasmin proactivator, a coagulopathy composed of fibrin-fibrinogenolysis-yielding fibrin split products may follow [10]. Excessive production of fibrin split products is implicated in decreased uterine contractility [10], which often occurs in cases of AFE. Indeed, our patient demonstrated evidence of both increased fibrin split products and severe uterine atony with resultant postpartum hemorrhage. AFE is almost always diagnosed on clinical grounds and should not be confused with sepsis, drug reaction, pulmonary aspiration, venous air embolism, pulmonary thromboembolism, or placental abruption [9,15]. Laboratory data may be supportive, but they alone can never diagnose or exclude AFE [9]. Once the diagnosis is made and resuscitative efforts have begun, blood is aspirated from a central venous or pulmonary artery catheter and placed in an anticoagulated test tube. It is then sent for pathologic examination with special stains and dyes (Nile blue A, Papanicolaou, oil red O, and acid mucopolysaccharide) that can demonstrate fetal squamous cells, fat, and mucin [15]. Unfortunately, no differentiation can be made microscopically between fetal and maternal squamous cells. Furthermore, squamous cells have been identified in blood aspirated from pulmonary artery catheters in nonpregnant patients [16]. The identification of mucin, however, seems to be a more sensitive indicator of AFE [15]. Treatment of AFE includes endotracheal intubation and mechanical ventilation with a high inspired concentration of oxygen, inotropic support guided by pulmonary artery catheterization, and correction of coagulopathy. Acute left ventricular dysfunction is the primary hemodynamic insult; thus, therapy should be directed toward improving inotropy [17]. Gillie and Hughes [15] recommend dopamine (2-40 [micro sign]g [center dot] kg-1 [center dot] min-1), dobutamine (2-40 [micro sign]g [center dot] kg-1 [center dot] min-1), and norepinephrine (2-4 [micro sign]g/min) as the drugs of choice for maintaining cardiac output and blood pressure. Fluid therapy should also be guided by central monitoring, avoiding overhydration in these patients, who are predisposed to pulmonary edema. The patient should be ventilated with the highest inspired concentration of oxygen to maintain arterial oxygen saturation greater than 90%. Positive end-expiratory pressure is often helpful in improving oxygenation. Although concern has been raised about "adding fuel to the fire" of DIC [10], blood component therapy remains the first line of treatment for correcting the coagulopathy associated with AFE. Fresh-frozen plasma, cryoprecipitate, and platelet transfusion are indicated [15], with therapy being guided by the laboratory markers of coagulation and clinical evidence of bleeding. Cryoprecipitate is rich in both fibrinogen and fibronectin, the latter facilitating uptake of cellular and particulate matter (e.g., amniotic fluid contents) from the blood via the reticuloendothelial system. Some have advocated heparinization and administration of thrombolytics [11]. Although most authors today do not recomment the administration of thrombolytics, Weiner [10] recommended administering 3000-5000 U of IV heparin once the diagnosis of AFE has been made. We described a case of AFE that presented atypically as an isolated coagulopathy followed by uterine atony. We speculate that a small tear in the posterior cervix during labor caused amniotic fluid to slowly seed the maternal circulation, being inhibited somewhat by the presence of the fetal head. This may explain the fever and coagulopathy she experienced during labor. Once the fetus was delivered, a larger volume of amniotic fluid may have then entered the circulation, leading to cardiovascular collapse. Although we think that a coagulopathy was the first indication of this patient's AFE, other causes of coagulopathy [18-20], such as placental abruption, preeclampsia, and bacteremia/sepsis must be considered. The latter two processes may have been present to some degree, but they were not likely to have contributed to our patient's death from AFE. This case reinforces that coagulation defects in parturients can encompass a wide differential diagnosis. Successful outcome, albeit uncommon, requires aggressive resuscitation and support.

Amniotic fluid embolism (AFE) is one of the catastrophic complications of pregnancy in which amniotic fluid, fetal cells, hair, or other debris enters into the maternal pulmonary circulation, causing cardiovascular collapse. Etiology largely remains unknown, but may occur in healthy women during labour, during cesarean section, after abnormal vaginal delivery, or during the second trimester of pregnancy. It may also occur up to 48 hours post-delivery. It can also occur during abortion, after abdominal trauma, and during amnio-infusion. The pathophysiology of AFE is not completely understood. Possible historical cause is that any breach of the barrier between maternal blood and amniotic fluid forces the entry of amniotic fluid into the systemic circulation and results in a physical obstruction of the pulmonary circulation. The presenting signs and symptoms of AFE involve many organ systems. Clinical signs and symptoms are acute dyspnea, cough, hypotension, cyanosis, fetal bradycardia, encephalopathy, acute pulmonary hypertension, coagulopathy etc. Besides basic investigations lung scan, serum tryptase levels, serum levels of C3 and C4 complements, zinc coproporphyrin, serum sialyl Tn etc are helpful in establishing the diagnosis. Treatment is mainly supportive, but exchange transfusion, extracorporeal membrane oxygenation, and uterine artery embolization have been tried from time to time. The maternal prognosis after amniotic fluid embolism is very poor though infant survival rate is around 70%.

Obstetric anesthesia in China: associated challenges and long-term goals.

To salvage – it means to save – from a shipwreck, a fire, a wrecking ball or other forms of permanent destruction or loss. The act of salvaging implies repurposing, putting to use somewhere else. It makes perfect sense in a world that throws away and loses a lot of things. Cell salvage also makes perfect sense: collect the patient's own blood from the operative field, wash away the impurities and re-infuse it to the patient; thus, avoiding the risks, and costs, of allogeneic transfusion. But a lot of things in medicine that appear to make perfect sense do not actually work as expected. For example, the practice of bloodletting to rid the body of bad humours made perfect sense to our medical colleagues practicing in previous centuries, but it does not work and may cause harm. Similarly, we need to ask, does cell salvage use actually result in lower allogeneic transfusion rates and its associated risks? Specifically, in the obstetric population, does the benefit of routine use of cell salvage outweigh the risks? Postpartum haemorrhage is the leading cause of maternal mortality worldwide. The incidence is increasing, and the incidence of postpartum haemorrhage requiring blood transfusion in the US nearly quadrupled between 1993 and 2014 1. In 2014, 0.4% of all deliveries required a blood transfusion. Importantly, experts estimate that between 70% and 90% of postpartum haemorrhage-related deaths are preventable 2, 3. The morbidity of postpartum haemorrhage often reflects the quality of the clinical response; early recognition and prompt management of haemorrhage are critical to improving maternal outcomes. Recommendations to improve care include: identification of women at high risk for haemorrhage; improved recognition of haemorrhage; and timely management. Yet, identifying at-risk women is challenging; many women who experience postpartum haemorrhage do not have identifiable risk factors 4. Therefore, strategies such as the routine use of cell salvage during caesarean section might improve the timeliness of clinical response and improve outcomes. But does this strategy actually work, and is it safe and cost effective? In this issue of Anaesthesia, Sullivan and Ralph report the results of a retrospective observational study of one UK centre's experience with cell salvage in 6352 obstetric patients 5. Between 2008 and 2017, cell salvage was used routinely for 98% of caesarean deliveries. Salvaged blood was re-infused in 1170 women (18.4%), and only 44 women (3%) required an allogeneic blood transfusion in addition to salvaged blood. In a subset of patients, the investigators assessed the ‘quality’ of the salvaged blood; fetal blood cells were found in all samples; however, the rate of allo-immunisation was very low. Of note, the authors used a single suction catheter to aspirate blood from the surgical field; washed all surgical swabs; and, in the latter years of the study period, did not use a leucocyte depletion filter. They reported no major safety events. The authors concluded that “it is possible to use cell salvage at caesarean section both safely and economically” without the need for additional staff, using one suction device and no leucocyte depletion filter. Although these results are promising, they contrast with the results of the cell salvage in obstetrics (SALVO) trial, a pragmatic, multicentre (26 UK units), randomised controlled trial 6. In the trial, 3028 women at risk for haemorrhage and undergoing a scheduled or intrapartum caesarean section were randomly allocated to receive cell salvage in addition to standard care (experimental group) or standard care alone (control group). The rate of allogeneic transfusion was 2.5% in the cell salvage group and 3.5% in the standard care group, a difference that was not statistically different (adjusted risk difference −1.03, [95%CI: −2.13 to 0.06]) 6. On average, 1 in every 100 women who received routine cell salvage avoided an allogeneic transfusion. Similar to the study by Sullivan and Ralph 5, the SALVO trial investigators concluded that use of cell salvage in obstetric patients was safe 6. Finally, the SALVO investigators used their data to perform a cost effectiveness analysis from the perspective of the NHS, and concluded that cell salvage was more expensive than standard care; the incremental cost effectiveness ratio was £8110 (€9711; $10,303) per transfusion avoided 6. How can we bridge the gap between the Sullivan and Ralph study and the SALVO trial 5, 6? The studies differed methodologically. In the hierarchy of evidence, the findings of randomised controlled trials are normally considered superior to observational studies. The SALVO trial was a large, well-conducted, randomised controlled trial in women at increased risk for haemorrhage 6. The primary outcome was the rate of women receiving allogeneic blood transfusion to manage haemorrhage; secondary outcomes included safety and cost. In contrast, the Sullivan and Ralph study was a retrospective observational trial 5. All women undergoing caesarean section were included. Although outcomes were not defined a priori, the authors reported allogeneic transfusion rates over the 10-year study period, as well as safety data. Although Sullivan and Ralph did not report cost as an outcome of their study, they emphasised key differences between their own practice and that described in the SALVO study 5, 6. Specifically, in the SALVO study, a full setup for both collection and processing of salvaged blood was mandated as part of the study protocol 6. In contrast, in the Sullivan and Ralph study, the cell salvage machine was initially setup for collection only, and the processing kit was opened only if a sufficient amount of blood had collected in the reservoir 5. By protocol, all surgical swabs were washed and a single suction device was used to aspirate blood from the surgical field, rather than using one suction before delivery of the placenta, and a second one afterwards (the use of two suction catheters has been recommended to reduce the volume of amniotic fluid collected into the cell salvage reservoir 7). Leucocyte depletion filters were not used after 2015, and perhaps most importantly, no additional staff were required to operate the cell salvage machine. Operating department practitioners, who are routinely available to assist the anaesthetist, were trained in cell salvage operation and were available 24 h a day, 7 days a week. In contrast, in the SALVO trial, many centres required additional personnel to operate the cell salvage machine, and just over half of the centres used a leucocyte depletion filter, washed swabs and used one suction, rather than two 6. Thus, personnel costs and routine use of the processing kit were likely to have been significant costs in the SALVO trial. Importantly, the cost-saving measures used by Sullivan and Ralph did not appear to reduce the quality of the salvaged blood, or result in any identifiable patient harm, although both studies were underpowered for safety outcomes 5, 6. Although it was once thought that a leucocyte depletion filter was necessary to reduce amniotic fluid contaminants in the salvaged blood 7, many centres, including nearly half of the centres in the SALVO trial 6, have abandoned their use due to reports of acute hypotensive events, as well as slower infusion rates 8. Indeed, 16 out of 18 adverse events reported in the SALVO trial were thought to be related to the leucocyte depletion filter 6. An additional safety concern is maternal allo-immunisation. Among the subset of 647 women in the Sullivan and Ralph study who had subsequent allo-immunisation testing, only two women developed new antibodies 5. Additionally, the authors reported that, in the past 3 years, they observed no increase in the dose of Rho(D) immune globulin administered to Rh-negative women with Rh-positive fetuses, indirect evidence that abandoning the use of leucocyte depletion filters does not increase the risk of fetomaternal haemorrhage 5. In contrast, the SALVO investigators reported a greater incidence of fetomaternal haemorrhage, defined as ≥ 2 ml, in women who received cell salvage compared with those who did not 6. Although the Sullivan and Ralph study was not powered to investigate this safety outcome, the results add reassurance that leucocyte depletion filters may not be necessary for routine cell salvage 5. More studies are needed to fully understand the impact of cell salvage reinfusion on the risk of allo-immunisation. When making the decision to use any medical intervention, the benefits must be weighed against the risks, including cost. Arguably, the primary benefit of cell salvage is a reduction in allogeneic blood transfusion. The SALVO study found no benefit in terms of reduced allogeneic blood transfusion when cell salvage was used routinely for high-risk patients undergoing caesarean section, although in a planned sub-group analysis in women undergoing emergency caesarean section, the allogenic transfusion rate was lower in the cell salvage group at 3.0% vs. 4.6% in the standard care group 6. Although Sullivan and Ralph reported an inverse relationship between cell salvage use and allogenic transfusion over the 10-year study period, the causality of this association must be viewed with scepticism 5. As noted by the authors, other blood conservation strategies were also implemented during the study period that were likely to have contributed to the observed decrease in the allogeneic transfusion rate. However, before we totally dismiss the routine use of cell salvage for obstetric patients, we should consider other possible benefits of its use. These include improved ability to rescue, a reduction in maternal near-miss events and death due to haemorrhage, a leading, but usually preventable cause of maternal mortality. Perhaps, the rate of allogeneic blood transfusion is not the outcome we should be assessing, but rather other important outcomes, such as failure to rescue. As confirmed in the current study as well as in others, the risks of cell salvage are low and the costs could be lower if modelled on the setup described by the authors in their institution 5. The SALVO study cost analysis only considered direct costs from the provider perspective – it did not consider the costs, to both the provider and to society, of serious adverse outcomes such as failure to rescue. The death of a mother due to haemorrhage is a tragedy, all the more so because it is almost always preventable with appropriate and timely management. In the US, the National Partnership for Maternal Safety, an organisation formed with the goal of reducing maternal mortality, published an obstetric haemorrhage safety bundle in 2015 9. A key element of the bundle is readiness. It is possible that using cell salvage in all patients improves the team's preparedness to manage cell salvage, the quality of the salvaged blood and perhaps other components of preventing and treating postpartum haemorrhage. The routine use of cell salvage would certainly improve our ability to initiate treatment early in haemorrhage. It would provide the ‘regular experience’ required by the National Institute for Health and Care Excellence (NICE) guidelines for its use 10. Furthermore, its use might serve as a trigger to focus the team on postpartum haemorrhage diagnosis and treatment, leading to improved outcomes. Many organisations, including the Royal College of Obstetricians and Gynaecologists, the National Institute of Health and Care Excellence (NICE), the American College of Obstetricians and Gynecologists and the American Society of Anesthesiologists, recommend that cell salvage be considered in selected situations, such as when large blood loss is expected (> 20% of blood volume), when patients refuse allogeneic blood or during intractable haemorrhage when banked blood is not available 10-13. These guidelines imply, although they do not directly state, that the routine use of cell salvage in all obstetric patients is not indicated. Indeed, in the first updated guideline published since the SALVO trial, the Association of Anaesthetists state that cell salvage “is not used routinely for caesarean section based on the current evidence, be it elective, urgent or emergency” 14. We suggest that further research is necessary before completely condemning the routine use of cell salvage. The sub-group analysis in emergency caesarean section patients in the SALVO study suggests that the technique may have benefit in this patient group 6. We suggest a randomised controlled trial of the routine use of cell salvage in emergency caesarean section patients, incorporating the paradigm suggested by Sullivan and Ralph, and powered to assess outcomes such as near misses or a composite outcome of adverse outcomes, is a rational next step for further defining the role of cell salvage in obstetric care. No external funding or competing interests declared.

Amniotic fluid embolism – an update

Relationships between docosahexaenoic acid compositions of maternal and umbilical cord erythrocytes in pregnant Japanese women

In 38 of 287 amniocenteses done at the Mayo Clinic the amniotic fluid contained enough erythrocytes to permit blood typing with commercial sera. Simultaneous use of both an acid‐elution technic and the direct Coombs test helped to establish three of the four possibilities for having erythrocytes in bloody amniotic fluid: 1) maternal and fetal erythrocytes of different blood types; 2) maternal erythrocytes only; 3) fetal erythrocytes only; and 4) maternal and fetal erythrocytes of the same blood type. Twenty of the 38 bloody amniotic fluids permitted fetal erythrocyte‐typing that was later verified postnatally in the living newborns. Traumatic amniocentesis in an Rho(D)‐negative mother with an Rho(D)‐positive fetus increases the risk of anamnestic rise in maternal antibody levels. Amniotic epithelial cells from seven different nonbloody amniotic fluids were typed by mixed agglutination technic. Although the ABO groupings were accurate as shown by postnatal typing, Rho(D) typing was unreliable.

Objective To assess the safety and effect of intraoperative cell salvage (ICS) during cesarean section. Methods This was a case-control study in which 60 gravidas who received ICS (ICS group) and 60 gravidas who received allogenic transfusion (control group) during caesarean section in Obstetrics and Gynecology Hospital of Fudan University during January 2014 to December 2016 were enrolled. Subjects in the two groups were matched in age, gestational age, gestational complications (placenta increta, placenta previa, scarred uterine, leiomyomas and anemia) and hemorrhagic volume during cesarean section. Several indicators including complications of transfusion, postoperative recovery, expense of transfusion, as well as the complete blood count and body temperature before and after operation were compared between the two groups. T, rank-sum or Chi-square test was used for statistical analysis. Results (1) No significant difference in age, gestational age, twin gestation, complications, preoperative body temperature, or the volume of hemorrhage or transfusion was observed between the two groups (all P>0.05). (2) The autotransfusion volume was 385 (161-583) ml in the ICS group. Fifteen cases (20.0%) in the ICS group also received additional transfusions of leukocyte-reduced red blood cell (RBC) suspension, fresh frozen plasma and cryoprecipitate and two cases (3.3%) received additional transfusions of leukocyte-reduced RBC suspension and fresh frozen plasma. The two groups showed no significant difference in the cost of transfusion or per-capita transfusion volume of fresh frozen plasma or cryoprecipitate. However, the transfusion volume of leukocyte-reduced RBC suspension was lower in the ICS group as compared with that in the control group [M (P25-P75), 1.9 (1.5-4.5) vs 4.1 (2.8-6.2) U, Z=-2.800, P=0.005]. (3) There was no significant difference in complete blood count or coagulation function between the two groups before the operation. White blood cell (WBC) counts in the two groups were elevated following operation. Postoperative WBC count in the control group was higher than that in the ICS group, while the levels of RBC and hemoglobin were lower than those in the ICS group following operation (all P<0.05). (4) No amniotic fluid embolism was reported in the two groups. Only one case of rash was reported in the ICS group, which was fewer than the transfusion reactions occurred in the control group [1.7% (1/60) vs 13.3% (8/60), χ2=5.886, P=0.016]. (5) The two groups showed no significant difference in preoperative temperature, the highest temperature within three days after operation or incision healing. Compared with the patients in the control group, those in the ICS group had shorter hospital stay [(4.7±1.1) vs (6.3±1.8) d, t=3.341, P<0.05]. Conclusion ICS is a safe and effective measure for gravidas at higher risk of hemorrhage during cesarean section. Key words: Blood transfusion, autologous; Cesarean section; Intraoperative period

In 38 of 287 amniocenteses done at the Mayo Clinic the amniotic fluid contained enough erythrocytes to permit blood typing with commercial sera. Simultaneous use of both an acid-elution technic and the direct Coombs test helped to establish three of the four possibilities for having erythrocytes in bloody amniotic fluid: 1) maternal and fetal erythrocytes of different blood types; 2) maternal erythrocytes only; 3) fetal erythrocytes only; and 4) maternal and fetal erythrocytes of the same blood type. Twenty of the 38 bloody amniotic fluids permitted fetal erythrocyte-typing that was later verified postnatally in the living newborns. Traumatic amniocentesis in an Rho(D)-negative mother with an Rho(D)-positive fetus increases the risk of anamnestic rise in maternal antibody levels. Amniotic epithelial cells from seven different nonbloody amniotic fluids were typed by mixed agglutination technic. Although the ABO groupings were accurate as shown by postnatal typing, Rho(D) typing was unreliable.

Objective To evaluate the reliability of autologous blood withdrawal during cesarean section. Methods Fifteen patients preoperatively diagnosed with pernicious placenta previa and/or accrete by using ultrasound and magnetic resonance imaging, aged 20-35 yr, weighing 55-75 kg, at ≥ 36 weeks of gestation, were enrolled in the study.Blood containing amniotic fluid from the surgical field was collected, and the washed blood was processed using cell-salvage machine and then filtered using a leukocyte depletion filter during cesarean section.The 20 ml blood samples collected included maternal central venous blood after delivery of fetus, unwashed blood, washed blood and filtered blood.The fetal squamous cells were counted using papanicolaou staining.The concentrations of a-fetoprotein, tissue factor, endothelin-1 and histamine were measured by enzyme linked immunosorbent assay.The fetal red blood cells were counted using the acid elution method and HE staining. Results Compared with unwashed samples, the tissue factor concentrations were significantly increased, and the fetal squamous cell count, concentrations of a-fetoprotein and endothelial-1, and fetal red blood cells were decreased in the washed samples.Compared with washed samples, the fetal squamous cell count, concentrations of a-fetoprotein and fetal red blood cells were significantly decreased in filtered samples.Compared with maternal venous blood samples, the tissue factor concentrations were significantly increased, and the fetal squamous cell count and concentrations of a-fetoprotein and endothelial-1 were decreased in filtered samples. Conclusion Autologous blood withdrawn during cesarean section can be used for reinfusion in cesarean section. Key words: Blood transfusion; autologous; Cesarean section

Comparison of mercury levels in maternal blood, fetal cord blood, and placental tissues