OB Hemorrhage - DIC/Blood Products Resources

OBJECTIVE: The objective of this retrospective study is to reflect on our experience on an optimal management for major postpartum hemorrhage, which would prevent the occurrence and complications of disseminated intravascular coagulation and minimize maternal mortality and morbidity.
METHODS: Ten cases out of the 30,000 of total deliveries of severe obstetric hemorrhage associated with disseminated intravascular coagulation were studied. This study was carried out over a 7 year period, October 1988 through to September 1995, at the Obstetric Unit, King Khalid University Teaching Hospital, Riyadh, Kingdom of Saudi Arabia.
RESULTS: All of the 10 women received packed red blood cells, 8 had fresh frozen plasma, and 6 received platelet transfusion. The 10 cases developed disseminated intravascular coagulation following medical and surgical management, all women needed hysterectomy, 4 subtotal, 6 total, and 5 women had relaparotomy and pelvic packing. Two had bladder injuries. There was no maternal death.
CONCLUSION: An early resort to hysterectomy when conservative measures fail, will minimize maternal morbidity and mortality. In case of continuous bleeding after hysterectomy, pelvic packing proved to be effective.

This article presents current understanding of the causes, pathophysiology, clinical, and laboratory diagnosis, and management of fulminant and low-grade DIC, as they apply to obstetric, pregnant, and gynecologic patients. General medical complications leading to DIC, which may often be seen in these patients, are also discussed. Considerable attention has been given to interrelationships within the hemostasis system. Only by clearly understanding these pathophysiologic interrelationships can the obstetrician/gynecologist appreciate the divergent and wide spectrum of often confusing clinical and laboratory findings in patients with DIC. Objective clinical and laboratory criteria for diagnosis of DIC have been outlined to eliminate unnecessary confusion and the need to make empiric decisions regarding the diagnosis. Particularly in the obstetric patient, if a condition is observed that is associated with DIC, or if any suspicion of DIC arises from either clinical or laboratory findings, it is imperative to monitor the patient carefully with clinical and laboratory tools to assess any progression to a catastrophic event. In most instances of DIC in obstetric patients, the disease can be ameliorated easily at early stages. Many therapeutic decisions are straightforward, particularly in obstetric and gynecologic patients. For more serious and complicated cases of DIC in these patients, however, efficacy and choices of therapy will remain unclear until more information is published regarding response rates and survival patterns. Also, therapy must be highly individualized according to the nature of DIC, patient's age, origin of DIC, site and severity of hemorrhage or thrombosis, and hemodynamic and other clinical parameters. Finally, many syndromes that are often categorized as organ-specific disorders and are sometimes identified as independent disease entities, such as AFE syndrome, HELLP syndrome, adult shock lung syndrome, eclampsia, and many others, either share common pathophysiology with DIC or are simply a form of DIC. These entities represent the varied modes of clinical expression of DIC and illustrate the diverse clinical and anatomic manifestations of this syndrome.

The pathophysiologic mechanisms, clinical, and laboratory manifestations of DIC are complex in part due to interrelationships within the hemostasis system. Only by clearly understanding these extraordinarily complex pathophysiologic interrelationships can the clinician and laboratory scientist appreciate the divergent and wide spectrum of often confusing clinical and laboratory findings in patients with DIC. Many therapeutic decisions to be made are controversial and lack validation. Nevertheless, newer antithrombotic agents, and agents that can block, blunt, or modify cytokine activity and the activity of vasoactive substances appear to be of value. The complexity and variable degree of clinical expression suggests that therapy should be individualized depending on the nature of DIC, age, etiology of DIC, site and severity of hemorrhage or thrombosis and hemodynamics and other appropriate clinical parameters. At present, treatment of the triggering event, low-dose heparin or antithrombin concentrate and wise choice of components when indicated appear to be the most effective modes of therapy.

In the UK, maternal mortality due to haemorrhage appears to be rising, with obstetric haemorrhage accounting for 3-4% of the red cells transfused. Allogeneic blood transfusion carries risks such as administration errors, transmitted infections and immunological reactions. The supply of blood is decreasing, partly due to the exclusion of donors who have themselves received a blood transfusion since 1980, in order to stop transmission of variant-Creutzfeldt-Jakob disease. The cost of blood is significantly increasing, partly because it is now leucocyte-depleted to minimize viral transmission. Various blood conservation techniques can reduce exposure to allogeneic blood thereby reducing risk and conserving the blood supply. These include preoperative autologous donation, acute normovolaemic haemodilution and intra-operative cell salvage. Preoperative autologous donation may produce anaemia, does not eliminate transfusion risk, cannot be used in an emergency and is not acceptable to Jehovah's Witnesses. It should be reserved for exceptional circumstances (rare blood type or unusual antibodies). Acute normovolaemic haemodilution may induce anaemia and cardiac failure and cannot be used in an emergency. It may have a limited role in combination with other techniques. Intra-operative cell salvage is more effective and useful in obstetrics than the other techniques, overcomes their shortcomings and is endorsed by CEMACH, OAA/AAGBI Guidelines, the National Blood Service and NICE.

When caring for patients receiving massive transfusion, the nurse will be required to perform ongoing assessments and apply critical thinking to provide optimum care and avoid further complications. The perianesthesia nurse must be aware of the hemodynamic and coagulation changes of pregnancy when caring for an obstetric patient in the PACU to optimize patient outcomes. Understanding the causes of obstetric hemorrhage, which may result in the need for massive transfusion, will enable the nurse to anticipate and prevent potentially deadly complications.

Acute postpartum hemorrhage is the leading worldwide cause of maternal mortality, such deaths being usually related to the development of hemorrhagic shock and its consequences, especially the multiple organ dysfunction syndrome. Obstetricians should be aware of the clinical manifestations and principles of management of hemorrhagic shock. Initial assessment of the bleeding patient requires monitoring blood pressure, pulse, capillary refill, mental status and urinary output. This allows estimation of the amount and the rate of blood loss and helps direct treatment. Hemorrhagic shock is a condition in which inadequate perfusion of organs results in insufficient availability of oxygen to satisfy the metabolic needs of the tissues. A catabolic state develops. The consequences of these changes are inflammation, endothelial dysfunction, and disruption of normal metabolic processes in vital organs. Once these events become established, the process of shock is often irreversible, even if volume and red cell deficits are corrected. The principal goals of management are controlling the source of the blood loss; restoring adequate oxygen carrying capacity; and maintaining adequate tissue perfusion. Patients with severe postpartum hemorrhage are at risk of developing hypothermia, an insidious complication that contributes substantially to morbidity and mortality. It must be prevented or treated promptly. Successful treatment of exsanguinating postpartum hemorrhage depends on efficient collaboration among all members of the patient care team, and a management plan based on an understanding of the pathophysiology of shock and tailored to the individual patient's situation.

Obstetric hemorrhage is still a significant cause of maternal morbidity and mortality. Prevention, early recognition, and prompt intervention are the keys to minimizing complications. Resuscitation can be inadequate because of under-estimation of blood loss and misleading maternal response. A young woman may maintain a normal blood pressure until sudden and catastrophic decompensation occurs. All members of the obstetric team should know how to manage hemorrhage because timing is of the essence. Good communication with the blood bank ensures timely release of appropriate blood products. A well-coordinated team is one of the most important elements in the care of a compromised fetus. If fetal anoxia is presumed, there is less than 10 minutes to permanent fetal brain damage. Antepartum anesthesia consultation should be encouraged in parturients with medical problems.

Obstetric hemorrhage continues to be a significant cause of maternal mortality and morbidity. Blood transfusion in such circumstances may be life saving but involves exposing the patient to additional risks. Limiting blood transfusion and using autologous blood when possible may reduce some of these risks. This article outlines the techniques that may be used to limit and more effectively treat hemorrhage in the obstetric patient, with particular attention paid to reducing the use of allogeneic blood transfusion.

Hemorrhage is the leading cause of intensive care unit admission and one of the leading causes of death in the obstetric population. This emphasizes the importance of a working knowledge of the indications for and complications associated with blood product replacement in obstetric practice. This article provides current information regarding preparation for and administration of blood products, discusses alternatives to banked blood in the obstetric population, and introduces pharmacological strategies for treatment of hemorrhage.

Postpartum hemorrhage (PPH) is one of the top 5 causes of maternal mortality in developed and developing countries. The incidence of PPH is 40% after vaginal delivery and 30% after cesarean section. Criteria for PPH are based on the amount of blood loss. In clinical obstetrics, exact measurement of blood loss is often difficult. The most important treatment of PPH is red blood cell (RBC) transfusion. In the past few years, increasing concern has arisen about this treatment. Despite the introduction of several new guidelines, transfusion criteria still vary widely between clinicians. The decision whether to prescribe RBC transfusion is mostly based on postpartum hemoglobin (Hb) values. RBC transfusion should be aimed to reduce morbidity and especially to improve health-related quality of life (HRQoL). In this review, etiology, epidemiology, treatment, and prevention of postpartum hemorrhage are described. Special attention is given to the role of RBC transfusion in the treatment of PPH and the effects of RBC transfusion on HRQoL.
TARGET AUDIENCE:: Obstetricians & Gynecologists, Family Physicians. LEARNING OBJECTIVES.: After completion of this article, the reader should be able to summarize the new guidelines related to transfusion criteria, explain the importance of reducing morbidity related to improving quality of life issues, and list infectious and noninfectious complications of a red blood cell transfusion.

Obstetrical disseminated intravascular coagulation (DIC) is usually a very acute, serious complication of pregnancy. The DIC diagnostic criteria in obstetrics (the obstetrical DIC score) help with making a prompt diagnosis and starting treatment early. These DIC diagnostic criteria, in which higher scores are given for clinical parameters than for laboratory parameters, have three components: (1) the underlying disease, (2) clinical symptoms, and (3) laboratory findings. It is justified that it is appropriate to initiate therapy for DIC when the obstetrical DIC score reaches 8 points or more before obtaining the results of coagulation tests. Management: (1) Control of the underlying disease: because prolongation of exposure to the triggering factors worsens DIC, it is important to eliminate the etiologic factors as rapidly as possible. Elimination of the cause of DIC can be easily performed in obstetrics, for example, by cesarean section. (2) Antithrombin (AT) therapy: AT monotherapy (1,500 to 3,000 units/day, 2 days) is preferably employed instead of heparin monotherapy or heparin-AT therapy because of the hemorrhagic side effects of heparin. (3) Synthetic serine protease inhibitors: continuous infusion ofgabexate mesilate (FOY) or nafamostat mesilate (FUT) is effective for DIC. Controlled multicenter trials showed a significant improvement not only in clinical response but also in platelet counts and prothrombin time (PT) in the AT group compared with the FOY group. (4) Activated protein C (APC) can inhibit thrombin generation and accelerate fibrinolytic activity. APC (5,000 to 10,000 units) is administered for 2 days in patients with placental abruption complicated by DIC. APC is a very safe, effective, and useful agent for the treatment of DIC.

Healthy pregnancy is accompanied by changes in the haemostatic system which convert it into a hypercoagulable state vulnerable to a spectrum of disorders ranging from venous thromboembolism to disseminated intravascular coagulation (DIC). This latter is always a secondary phenomenon triggered by specific disorders such as abruptio placentae and amniotic fluid embolism due to release of thromboplastin intravascularly or endothelial damage resulting from pre-eclampsia and sepsis. In modern obstetric practice the most common cause is haemorrhagic shock with delay in resuscitation leading to endothelial damage. The initial management of massive obstetric haemorrhage is the same whether associated with coagulopathy initially or not. Low-grade DIC, associated with pre-eclampsia, is monitored haematologically by serial platelet counts and serum fibrin degradation products (FDPs). Supportive measures and removal of the triggering mechanism are the key to successful management. Outcome depends primarily on our ability to deal with the trigger and not on direct attempts to correct the coagulation deficit

In pregnancy and puerperium disseminated intravascular coagulopathy may accompany abruptio placenta, intrauterine fetal demise with retained dead fetus, amniotic fluid embolism, endotoxin sepsis, preecalampsia with HELLP and massive transfusion. Clinical signs and symptoms of DIC can include oozing from venipuncture sites and/or mucous membranes, red cell lysis from activation of the complement system, hemorrhage from coagulopathy and possible uterine atony, hypotension from hemorrhage and/or bradykinin release, and oliguria from end-organ insult and hypovolemia/hypotension. Treatment of DIC consists of replacement of volume, blood products, and coagulation components and cardiovascular and respiratory support with elimination of underlying triggering mechanism.

Postpartum haemorrhage remains an important cause of maternal death in the developed and especially in the developing world. An appreciation of the physiological changes of pregnancy that predispose to rapid development of severe haemorrhage and DIC help maintain a level of vigilance. Although routine antenatal assessment can identify women with factors associated with an increased risk of severe postpartum haemorrhage, a significant proportion of women will develop intrapartum complications that cause severe haemorrhage. Prompt recognition and treatment of women with severe ongoing blood loss is essential to prevent morbidity and mortality. In addition to surgical correction of bleeding, replacement of plasma components to reverse coagulopathy and red cells to maintain tissues oxygenation are the basic aims of management. The haemostatic agent, recombinant Factor VIIa is a potentially useful addition to management of massive, life-threatening obstetric haemorrhage but its safety and efficacy remains untested in clinical trials.

Every year, about 210 million women become pregnant. Postpartum hemorrhage (PPH) is one of the major complications of pregnancy, accounting for 14 million cases annually. Of these, it is estimated that around 140,000 women die, resulting in a case fatality rate of 1%. PPH is defined by WHO as a blood loss > or = 500 mls. Most instances of PPH occur suddenly and without warning even in women without any of the known risks for this condition. If women do not receive timely medical treatment, as is often the case in many parts of the world, death can occur within two hours. The chance of receiving a safe blood transfusion as part of the therapy for PPH varies enormously from country to country, depending on whether a safe blood transfusion program has been set up as a part of the national health policy. The increasing realization of the potential deleterious effects of blood transfusion, including exposure to HIV and other viral agents, has changed the practices that were previously acceptable for the transfusion of blood, as has the recent recognition of specific patients who will benefit from a single unit of blood. In countries with limited resources, where a majority of women have anemia at the onset of their pregnancies, the slightest deviation from normality during labor and/or delivery leading to excessive hemorrhage can put a women's life at risk. In these instances, the patient needs urgent resuscitation, stabilization and transfer to a nearby center. Available blood, preferably typed cross matched and screened for infections, should be given until the patient receives specific treatment. This is especially true in bled- out obstetrics patients, where one unit may make the difference between a near death state and the possibility of slow recovery and survival.

BACKGROUND: Amniotic fluid embolism (AFE) is a rare syndrome that can complicate pregnancy and labor. It often has debilitating and lethal consequences. One serious sequela of AFE is disseminated intravascular coagulation (DIC).
CASE: This report describes an atypical presentation of AFE manifested by sudden fetal bradycardia and complicated by maternal DIC. The DIC was eventually successfully treated with the use of recombinant activated factor VIIa.
CONCLUSION: The use of recombinant activated factor VIIa in cases of massive hemorrhage, such as in our patient, is controversial but has been shown, in some cases, to reverse DIC and be successful. The use of recombinant activated factor VIIa should be considered in patients with massive obstetric hemorrhage in whom standard measures of stabilization are unsuccessful.

OBJECTIVE: To analyze the accuracy of postpartum hemorrhage risk factors to determine patients at risk of severe postpartum hemorrhage and transfusion.
POPULATION AND METHODS: Retrospective cohort study from a database in one high-risk obstetric unit over a 7-year period.
RESULTS: In a cohort of 19,204 deliveries, 44 patients were transfused of whom five were given frozen fresh plasma only. Of the 39 who received red blood cells, 35 received at least three units. Multivariate analysis of postpartum hemorrhage risk factors revealed a significant role of placenta previa/accreta, cesarean section, multiple pregnancy, prematurity and vascular disease. Nevertheless 28% of women transfused had none of these risk factors.
CONCLUSION: The percentage of patients transfused has probably decreased markedly with improved prevention, surveillance and treatment. This study emphasizes that the transfusion risk in the presence of anomalous placental insertion justifies special obstetrical and anesthetic management.

OBJECTIVE: To evaluate risks for intraoperative or postoperative packed red blood cell transfusion in women who underwent cesarean delivery.
METHODS: This was a 19-university prospective observational study. All primary cesarean deliveries from January 1, 1999, to December 31, 2000, and all repeat cesareans from January 1, 1999, to December 31, 2002, were included. Trained, certified research nurses performed systematic data abstraction. Primary and repeat cesarean deliveries were analyzed separately. Univariable analyses were used to inform multivariable analyses.
RESULTS: A total of 23,486 women underwent primary cesarean delivery, of whom 762 (3.2%) were transfused (median 2 units, 25th% to 75th% 2-3 units). A total of 33,683 women underwent repeat [corrected] cesarean delivery, and 735 (2.2%) were transfused (median 2 units, 25th% to 75th% 2-4 units). Among primary cesareans, general anesthesia (odds ratio [OR] 4.2, 95% confidence interval [CI] 3.5-5.0), placenta previa (OR 4.8, CI 3.5-6.5) and severe (hematocrit less than 25%) preoperative anemia (OR 17.0, CI 12.4-23.3) increased the odds of transfusion. Among repeat cesareans, the risk was increased by general anesthesia (OR 7.2, CI 5.9-8.7), a history of five or more prior cesareans (OR 7.6, CI 4.0-14.3), placenta previa (OR 15.9, CI 12.0-21.0), and severe preoperative anemia (OR 19.9, CI 14.5-27.2).
CONCLUSION: Overall, the risk of transfusion in association with cesarean is low. However, both severe preoperative maternal anemia and placenta previa are associated with markedly increased risks. The former argues for optimizing maternal antenatal iron status to avoid severe anemia and the latter for careful perioperative planning when previa complicates cesarean.
LEVEL OF EVIDENCE: II-2

This review describes disseminated intravascular coagulation (DIC) as a syndrome in which hemostatic factors are activated. The syndrome ranges in severity from a decompensated coagulopathy (overt-DIC) to the subclinical compensated activation of hemostatic factors (nonovert DIC). The first part of this review emphasizes two points. First, activation of the hemostatic system is controlled by a vast network of capillaries and venules through anticoagulant and anti-inflammatory regulatory factors that operate from the endothelium (e.g., protein C and thrombomodulin, tissue factor pathway inhibitor). These hemostatic regulators can be overridden by procoagulant disorders such as amniotic fluid embolism or degraded by proinflammatory disorders such as sepsis. Second, because this link between the microvascular endothelium and circulating hemostatic factors is so close, even a relatively mild disturbance of the microvasculature targeted by the inflammatory process may be reflected systemically by changes in molecular biomarkers of hemostatic activity. Therefore, application of criteria for the diagnosis of nonovert DIC should be of value in detecting a compensated response to inflammatory stress of the microvasculature in patients who are at risk before they develop an uncompensated over DIC response and organ failure. The second part of this review covers the recent experience investigators have had in diagnosing and following the response of patients to treatment with biomarkers.