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Postpartum hemorrhage

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• 1. Postpartum Haemorrhage “A Study of Case" Norseen Hosameldeen Lotfy 221101448
• 2. List of contents Introduction Reasons Treatment Methodology 01 02 03 04 Conclusion 05
• 3. Introduction Do you know what is the reason for the death of one quarter of all women giving birth around the world? Postpartum Hemorrhage (PPH) is considered to be leading cause of maternal mortality, holding an account for 25–43% of maternal deaths. Every year 14 million women suffer from PPH. It causes 44,000 to 86,000 deaths per year. Introduction Reasons Treatment Methodology Conclusion
• 4. Mostcommo reasonsforPP areknowforth fourTs Reasons Accueil Reasons Treatment Methodology Conclusion Postpartum Hemorrhage (PPH) occurs commonly when there is loss of blood of 500 ml to 1000 ml within the first 24 hours after birth followed by the death of the mother, the ratio of incidence is higher with a c-section. PPH usually happens when there’s an error during placenta delivery. And there’re top 4 reasons for it:
• 5. 1. Uterine atony: considered to be the primary cause of PPH, holds account for 70% to 80% of all hemorrhage. Uterine atony refers to the weakness of the uterus after delivery, when the muscle can't contract enough to clamp the placental blood vessel shunt and this leads to steady blood hemorrhage. 2. Uterine trauma: Bleeding due to a damage to your uterus 3. Retained placental tissue: This happens when the placenta does not separate from the uterine wall 4. Blood clotting condition (thrombin): This is when there is reduced body ability of forming a clot due to coagulation problem, that can make even a tiny bleed uncontrollable
• 6. Treatment Physiological Approaches Pharmacological Therapy (Uterotonics) Blood transfusion: Fastest and most effective physiological method to prevent further complications like coma or death. Surgical interference: Often used with retained placenta First and second line agents: Oxytocin (10UI, IM/IV) Methylergonovine (0.2mg, IM) Misoprostol (600mcg Orally) Introduction Reasons Treatment Methodology Conclusion
• 7. Oxytocin (10UI, IM/IV): Oxytocin is considered to be the first-line agent. It’s a natural hormone works rapidly to cause uterine contraction with no contraindications and minimal side effects. It’s often used when hemorrhage is due uterine atony Recommended drug for prevention of PPH in caesarean section. where oxytocin is not available, second-line agents is used. Methylergonovine (0.2mg, IM): It works rapidly for sustained uterine contraction. Misoprostol (600mcg Orally): Used for its delayed onset than the above medications. Oxytocin is more effective than misoprostol for prevention and treatment of uterine atony and has fewer adverse effects.
• 8. Methodology A quantitative questionnaire investigating 4 main sections: Prevalence Most common causes Treatment Awareness It was conducted among university students and their families in Egypt A total number of 63, 10 Males and 53 females, age group: 17 to 22 of private university students.
• 9. Introduction Reasons Treatment Methodology Conclusion Data Interpretation Prevalence and Awareness
• 10. Data Interpretation Causes and Treatment
• 11. Coclusion 05 Introduction Reasons Treatment Methodology Conclusion  Doctors should be more cautious given the possibility that the frequency and severity of PPH has in fact increased. This applies particularly to the small hospitals with relatively few deliveries where management protocols and drugs or equipment may not be on hand to deal with unexpected severe PPH.  Results have been showing an increasing trend in PPH.  Uterine atony is still the most common cause for postpartum hemorrhage.  A low level of PPH awareness has been noted.  There is a growing demand for effective education and awareness enhancement within the context of local and global imperatives.  Also to encourage women to look for early symptoms and get checked if needed, have a healthy lifestyle and provide health care for themselves throughout their pregnancy.
• 12. Refrences: ● Evensen, A., Anderson, J. M., & Fontaine, P. (2017). Postpartum Hemorrhage: Prevention and Treatment. American family physician, 95(7), 442–449. ● World Health Organization. WHO recommendations for the prevention and treatment of postpartum hemorrhage. Geneva: WHO; 2012. Available from: https://apps.who.int/iris/bitstream/handle/10665/75411/9789241548502_eng.pdf ● Wormer KC, Jamil RT, Bryant SB. Acute Postpartum Hemorrhage. [Updated 2022 May 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499988/
• 13. Thank You

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Claire McLintock; Prevention and treatment of postpartum hemorrhage: focus on hematological aspects of management. Hematology Am Soc Hematol Educ Program 2020; 2020 (1): 542–546. doi: https://doi.org/10.1182/hematology.2020000139

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Visual Abstract

Postpartum hemorrhage (PPH) is the leading cause of global maternal mortality and accounts for approximately one-quarter of all maternal deaths worldwide. Prevention of excess maternal deaths requires a coordinated approach to prevention, early recognition, and intervention by a multidisciplinary team. Although some women have risk factors for PPH that can be identified during pregnancy or during labor or birth, most women with severe PPH do not have any risk factors. Therefore, all pregnant women must be considered to be at risk of PPH. Common causes include uterine atony, retained placenta, trauma to the genital tract or uterus, and coagulopathy. The pivotal role of fibrinogen and hyperfibrinolysis in the evolution and as a treatment target for PPH is increasingly recognized. Coagulopathy can be an early feature in PPH that may be unrecognized, as it can be present before massive transfusion has occurred. Identification of coagulopathy by viscoelastic point-of-care testing or conventional laboratory assays can be helpful in guiding management of PPH and preventing severe maternal outcomes.

Recognize the importance of risk assessment of pregnant women to identify PPH risk factors in the antenatal period and during labor and birth

Recognize the importance of coagulation tests in women with PPH, to enable early identification and treatment of coagulopathy and hyperfibrinolysis

The patient was a 29-year-old Black woman in her first pregnancy. Her body mass index was 33 kg/m 2 . She had no other medical history of note, and antenatal care had been uncomplicated, apart from iron deficiency treated with oral iron supplements from 28 weeks’ gestation. At the 38-week scan, the fetus was well developed (estimated weight, 4100 g).

The patient had spontaneous onset of labor at 39 +5 weeks’ gestation. Her admission observations were normal: afebrile, pulse 88 per minute, blood pressure (BP) 110/68 mm Hg, and respiratory rate 14 per minute. A complete blood count on admission showed hemoglobin (Hb) 10.4 × 10 9 /L, platelets 152, white blood cell count 7.8 × 10 9 /L. She made slow progress in the first stage of labor, requiring augmentation with IV oxytocin. At 11 hours, an epidural was placed after the IV oxytocin was started. The first stage of labor was complete at 17 hours, and initial effective pushing occurred in the second stage, with the head on the perineum at 65 minutes with no further advancement. A successful vacuum extraction (ventouse) was performed after episiotomy by the senior resident, with birth of the infant after 80 minutes in the second stage. Active management of the third stage of labor appeared complete, with controlled cord traction, intramuscular oxytocin, and delivery of the placenta. Immediate postpartum blood loss was estimated at 1200 mL. The pediatric team was called to review the infant, who had a 3990-g birth weight and some initial floppiness but responded rapidly to basic resuscitation.

Ongoing vaginal blood loss continued in the postpartum period. The patient’s uterus remained atonic but responded well to “rubbing up,” and IV oxytocin infusion was started. The team agreed to move her to an operating room (OR) for examination under anesthesia to determine whether there were any retained products of conception or any genital tract trauma that would explain the ongoing blood loss. Maternal observations were pulse, 106 per minute; BP, 98/60 mm Hg; and respiratory rate, 18 per minute.

On arrival in the OR, the observations were pulse, 114 per minute; BP, 94/60 mm Hg; and respiratory rate, 20 per minute. Vaginal blood loss continued, with estimated blood loss of 400 mL on new drapes and swabs in the OR.

Blood taken in the OR and tested on the blood gas analyzer showed Hb of 8.2 g/dL. Two units of packed red cells were ordered from the blood bank. The uterus remained atonic, and there were some abrasions of the vaginal wall and bleeding from the episiotomy; no other cause was identified. Ongoing vaginal blood loss was noted, with loss estimated at 1600 mL. Uterine atony persisted and further uterotonics were given, after which the maternal observations were pulse, 118 per minute; BP, 90/58 mm Hg; and respiratory rate, 22 per minute.

A senior obstetrician and anesthesiologist were called for support.

Obstetric hemorrhage is the leading cause of maternal mortality and bleeding after childbirth. Postpartum hemorrhage (PPH) accounts for two-thirds of cases of obstetric hemorrhage and for approximately one-quarter of all maternal deaths worldwide. There is no universally accepted definition of PPH, with some suggesting that blood loss volume >500 or 1000 mL represents standard or severe PPH. 1   Most otherwise fit and healthy pregnant women will have minimal physiological response to this degree of blood loss, leading some clinicians to suggest more relevant clinical definitions, such as persistent PPH: ongoing active bleeding >1000 mL occurring within 24 hours after birth that continues despite the use of measures such as first-line uterotonic therapy and uterine massage. 2  

Maternal deaths represent only the tip of the iceberg in terms of the overall impact of major bleeding on maternal health. Women who have life-threatening hemorrhage but do not die of PPH can face long-term health complications including loss of fertility and psychological trauma. Although nearly all women with severe PPH live in countries with limited economic resources, PPH and its complications can affect women living in any resource setting. Data from the United States show that rates of severe PPH are increasing. 3   Well-resourced health care settings with access to skilled practitioners, drugs, and blood banks offer the best opportunity to provide optimal care for women. In any care setting, early recognition of abnormal postpartum bleeding and mobilization of appropriate staff and resources is essential to stop the bleeding promptly and minimize morbidity and mortality.

Postpartum hemorrhage should not be viewed as a diagnosis but rather a clinical manifestation of an underlying condition or conditions that require identification and treatment. The differential diagnosis is not wide and includes one or more of the following: uterine atony, retained placenta, and placental malimplantation (previa, accreta, increta, or percreta), and genital tract trauma or coagulopathy, often referred to as the “4 T’s” (tone, tissue, trauma, and thrombin). Some women enter pregnancy with risk factors for PPH or develop these risk factors during the course of pregnancy or labor and birth ( Table 1 ). Women with risk factors identified antenatally should be managed in the appropriate setting with access to skilled staff and a blood bank and with precautionary steps taken during labor and childbirth to minimize the risk of PPH and respond early if it occurs ( Figure 1 ). However, it is critical that all staff caring for women in labor and childbirth be aware that most women who have severe PPH have no identifiable antenatal risk factors and that a high level of awareness be maintained. Risk factors should be reassessed frequently during labor and birth.

Risk factors for PPH

How urgently is red cell transfusion needed?

Setting the scene for the “PPH perfect storm”

Most women with PPH respond to initial measures of uterine massage and therapeutic uterotonics. However, if bleeding continues despite these interventions, the situation can rapidly escalate with more severe blood loss, maternal morbidity, and even mortality. Failure to recognize and respond to an evolving situation of severe PPH is frequently described in reviews of adverse outcomes caused by hemorrhage. This delay in response can be explained by several factors that create the “perfect storm” where the clinical team fails to recognize the severity of the blood loss and to take the appropriate steps.

Potential for rapid loss of a large volume of blood

In pregnancy, the total blood volume is ∼5 to 7 L (70-80 mL/kg lean body mass). By term, the blood supply to the uterine arteries is ∼500 to 600 mL per minute, increased from its normal level of 10 to 15 mL per minute outside of pregnancy. 4   After delivery of the placenta, the uterine muscles contract, effectively staunching blood flow from the uteroplacental bed. Uterine atony, retained placental tissue, and abnormal placental implantation impede the normal action of the uterus in completing this critical mechanical hemostatic process. Given the high blood flow to the uterine arteries, it is easy to appreciate how rapidly a large volume of blood can be lost in a short time.

Underestimation of the degree of blood volume loss

In many clinical settings the volume of blood loss is estimated by using visual assessment rather than objective measurement, which significantly underestimates the actual blood volume, especially at higher volumes. 5   Accurate measurements of blood volume using graduated containers and gravimetric measurement of blood-soaked pads and swabs reported to the clinicians in real time can help alert them to the development of severe continued bleeding. Providing a cumulative total of blood volume loss is especially important when women are moved during the process of PPH management (for example, from the delivery room to the OR) if required for an examination while the patient is under anesthesia, to assess for retained products of conception or genital tract trauma.

Most pregnant women are healthy and physiologically robust

Healthy pregnant women show minimal physiological response to blood loss of 1000 to 1500 mL, perhaps only becoming slightly tachycardic with a minor decline in systolic BP. By the time women have significant hypotension or tachycardia or an increased respiratory rate or become distracted or agitated, they usually have lost in excess of 2000 to 2500 mL. Careful and repeated clinical assessments and documentation of vital signs, such as pulse rate, BP, temperature, and respiratory rate is essential for identifying a trend indicating physiological decompensation in response to hypovolemia. The use of maternity early warning scoring to improve early detection of clinically deteriorating patients and escalation of the clinical response is increasing. 6,7   These systems assign a score to a range of clinical vital signs to form a total maternity early warning score. An increasing score suggests a deviation from a normal physiological state and indicates clinical deterioration, which should prompt an escalation in response by clinicians who have the appropriate level of skill to care for the patient.

Lack of anticipation of the presence of early coagulopathy with PPH, before a massive transfusion is needed

Dilutional coagulopathy is common in patients with hemorrhage after multiple transfusions. Urgent red cell transfusion is preferred to infusion of significant volumes of crystalloid, but in an unstable patient, volume replacement with up to 2 to 3 L of crystalloid may be necessary prevent severe hypotension. 2   Coagulopathy resulting from conditions, such as amniotic fluid embolism, placental abruption, and sepsis, can be present early, before administration of IV fluids or blood products. Early identification of coagulopathy by testing basic hemostatic function, with either laboratory-based assays or point of care (POC) testing, can help identify coagulopathy early and enable directed transfusion of the appropriate blood products.

Standard thrombin-based functional clotting assays for fibrinogen, such as the Clauss fibrinogen assay, measure the time it takes for a fibrin clot to form. In most clinical settings the final result will not be available for at least 45 to 60 minutes. Viscoelastic point of care (VE-POC) tests, such as rotational thromboelastometry (ROTEM) and thromboelastography, are increasingly used to assess global hemostasis, determining the activity of the coagulation factors and the amount of fibrinogen available to form a fibrin clot, as well the resistance of the clot to fibrinolysis. 8   In the setting of PPH, hyperfibrinolysis is not uncommon, especially in more severe PPH. The results of POC tests are usually available within 15 to 20 minutes, especially if the instrument is available in the OR.

Fibrinogen and fibrinolysis in PPH

The importance of fibrinogen and fibrinolysis in major postpartum bleeding has been brought into focus in recent years. Fibrinogen levels in pregnant women at term are increased at ∼4 to 6 g/L, compared with levels of 2 to 4 g/L in nonpregnant patients. In 2007, Charbit et al showed that fibrinogen levels were lower in women who developed severe PPH than in women with nonsevere PPH (median levels, 3.3 and 4.4 g/L, respectively). 9   Importantly, this difference was evident early in the evolution of PPH and before any blood or blood products had been administered. Other studies have confirmed this finding 10,11  

Although these studies suggested that a low level of fibrinogen is predictive of development of severe PPH, they did not ascertain whether early fibrinogen replacement could modify the degree of blood loss. A controlled study of women with moderate PPH (blood loss >1000 mL after Cesarean section [CS], >500 mL in women who required manual removal of placenta, and >1000 mL in women who required exploration of the uterus) randomized women to 2 g of fibrinogen or placebo. 12   Transfusion rates were the same in women (n = 25 of 123; 20%) given fibrinogen as in those who received placebo (n = 26 of 121; 22%). Of note, the mean fibrinogen level in each group was normal (4.5 g/L) and the median blood loss was <1500 mL, indicating that perhaps fibrinogen would not be a key factor in this population.

A second multicenter, double-blind, randomized, placebo-controlled trial of early fibrinogen replacement in women with severe PPH (>1000-1500 mL measured blood loss, with ongoing bleeding and reduced fibrinogen on ROTEM: FIBTEM A5 <15 mm, equivalent to ∼3 g/L fibrinogen). 13   Of 606 women eligible for inclusion, only 57 (9.4%) were randomized, with 55 women analyzed for the primary outcome (the number of allogeneic units transfused: red blood cells and plasma products). There was no difference in blood products transfused or in any of the secondary outcomes, such as invasive procedures for control of blood loss or transfer to intensive care. Analysis of prespecified subgroups showed that, in women with fibrinogen >2 g/L (n = 22), there was no difference in blood loss or blood transfusion after administration of the study medication, whereas the median blood loss was lower in the fibrinogen arm than in the placebo arm in women with fibrinogen <2 g/L. The researchers concluded that a fibrinogen level of >2 g/L appeared sufficient for hemostasis in the setting of PPH. Too few women in the cohort had very low fibrinogen (<2 g/L) for them to determine whether early administration of fibrinogen would modify outcomes in that patient group.

Although Collins et al 13   did not demonstrate an improvement in outcomes in women who were given fibrinogen concentrate, they observed that, over the course of the clinical trial, their approach of routine risk assessment for PPH, objective measurement of cumulative blood loss, and early involvement of senior staff enabled early recognition and intervention in the course of the PPH to take steps to respond to and control blood loss. The prompt recognition allowed for timely and appropriate escalation of care and involvement of senior staff at an early stage. Also, the study led to the practice of early assessment of hemostasis, Hb, and lactate by using POC tests. The clinicians used the study protocol to inform the development of a nationwide interventional program for standardized management of PPH, “OBS Cymru,” which has been effectively implemented across all obstetric units in Wales. 14  

Approach to transfusion of blood and plasma products in management of PPH

Using empiric fixed ratios of red blood cells, fresh frozen plasma (FFP), and platelets in women with PPH >1500 mL has been shown to reduce progression to severe PPH. Most women with PPH <2000 mL do not have low levels of fibrinogen or other clotting factors, and fibrinogen does not appear to decrease to <2 g/L until blood volumes of >4000 mL are lost, although early coagulopathy is a feature of placental abruption and amniotic fluid embolism. Empiric transfusion in the absence of hemostatic testing may lead to overtransfusion of blood and plasma products increased risk of complications, such as transfusion-associated circulatory overload and transfusion-associated lung injury. Collins et al advocate using targeted transfusion protocols with viscoelastic-POC (VE-POC) testing. 15   They reported that fibrinogen levels decrease sooner than other coagulation factors, so that correction of low fibrinogen levels may be a more important therapeutic target.

The International Society on Thrombosis and Haemostasis (ISTH) recommends using either cryoprecipitate (∼15 g/1000 mL) or fibrinogen concentrate (20 g/1000 mL) to maintain fibrinogen >2 g/L when managing PPH. 16   The fibrinogen concentration of FFP is much lower (2 g/1000 mL), and its use for fibrinogen replacement could lead to hemodilution.

Deficiencies of other clotting factors tend to occur at a later stage in PPH, suggesting that there is a more limited requirement for FFP. When VE-POC testing is not available, conventional laboratory testing may be helpful and the ISTH Scientific and Standardization Committee recommends targeting using 15 mL/kg FFP to maintain activated partial thromboplastin time/prothrombin time >1.5 × normal. 16  

Severe thrombocytopenia is uncommon in most women with PPH, leading to a recommendation (ISTH) to limit platelet transfusions, unless platelet count is <75 × 10 9 /L. 16  

Inhibition of fibrinolysis

Over the past 20 years or so, the impact of hyperfibrinolysis in major bleeding has been recognized. The CRASH-2 study demonstrated tranexamic acid, a potent inhibitor of fibrinolysis, reduction in death related to bleeding by 21% (risk ratio [RR], 0.79; 95% confidence interval [CI], 0.64-0.97) in trauma patients who received it within 3 hours and by 32% (RR, 0.68; 95% CI, 0.57-0.82) in patients who received it within 1 hour. 17  

The WOMAN study is a placebo-controlled trial conducted in 21 countries that assessed the impact of tranexamic acid in 20 021 women with PPH >500 mL after vaginal birth or >1000 mL after CS. 18   The maternal mortality rate was 2.4% (n = 483) with 72% (n = 346) of deaths caused by hemorrhage. Administration of 1 g of tranexamic acid (with a second dose given for ongoing bleeding) resulted in an overall reduction in death related to bleeding of 19% (RR, 0.81; 95% CI, 0.65-1.00) when given within 3 hours.

As a result of this study, the World Health Organization now strongly recommends early use of IV tranexamic acid (within 3 hours of birth) in addition to standard care for women with clinically diagnosed PPH after vaginal birth or CS. 19  

Recognition and response to major PPH also requires rapid response with transfusion of red blood cells to maximize oxygen delivery and prevent tissue hypoxia, development of acidosis, organ failure, and worsening of shock. The urgency of red cell transfusion depends on the degree of maternal clinical instability and rapidity of blood loss. Transfusion of O − red blood cells may be required in women who are clinically unstable or who are losing blood rapidly when cross-matched blood is not available.

Antenatal risk factors

In the clinical case, the only identifiable antenatal risk factors for PPH were increased body mass index and fetal macrosomia. Although the patient was iron deficient, she was not anemic. However, during labor she needed augmentation with oxytocin and had prolonged first and second stages of labor, with an assisted delivery. The immediate estimated postpartum blood loss was high, confirming a PPH, and importantly, the bleeding did not stop after initial interventions of uterine massage and therapeutic uterotonics.

An opportunity for escalation of intervention and a call for backup was missed at the time the patient was transferred to the OR. The degree of tachycardia and the increase in the respiratory rate were signs that this otherwise healthy, physiologically robust woman had lost a significant amount of blood. As a rule of thumb, a pulse rate higher than the systolic BP indicates a problem.

Estimated rather than measured blood loss

It is likely given the drop in the Hb that the woman had lost >1600 mL blood. Accurate cumulative measurement of blood loss would have alerted the clinicians to the severity of blood loss and the potential for progression.

Failure to perform an early coagulation test

A test of coagulation is helpful in identifying unanticipated coagulopathy. If available, a VE-POC test (ROTEM or thromboelastography) can provide a result within 15 minutes. Even though a conventional laboratory-based fibrinogen assay may be delayed by 60 minutes, it could still provide additional help if the PPH is not being controlled by initial maneuvers.

Ongoing significant postpartum bleeding in a woman with a well-contracted uterus with no evidence of genital tract trauma or retained placenta should alert the clinicians to the possible presence of coagulopathy.

Claire McLintock, Auckland City Hospital, Grafton Road, Auckland 1143, New Zealand; e-mail: e-mail [email protected] .

Competing Interests

Conflict-of-interest disclosure: The author declares no competing financial interests.

Author notes

Off-label drug use: None disclosed.

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Postpartum Hemorrhage (PPH)

Jan 05, 2020

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Postpartum Hemorrhage (PPH). Family Medicine Specialist CME University of Health Sciences. Clinical Case.

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• risk factors
• postpartum hemorrhage
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Postpartum Hemorrhage(PPH) Family Medicine Specialist CME University of Health Sciences

Clinical Case 25 year-old G7P2 female presents for delivery, which occurs very rapidly after arriving at the District Hospital. Her baby was delivered without difficulty but then the placenta was retained and she began to hemorrhage. What is your definition of a postpartum hemorrhage? What are the risk factors this patient has for a postpartum hemorrhage? What are you going to do to manage this patient?

Objectives • Define postpartum hemorrhage (PPH) • Discuss the risk factors and possible causes for PPH • Describe the preventative measures to take to prevent a PPH • Discuss the management of PPH • Explain the risks to maternal morbidity and mortality of PPH

Definitions • Primary/immediate PPH • Excessive bleeding during the 24 hours after a delivery • Most often due to uterine atony • Secondary/late PPH • Excessive bleeding between 24 hours and up to 6 weeks after delivery • Most often due to retain products of conception, infection or both

What is excessive bleeding or a PPH? • Vaginal delivery • >500 cc of blood loss • Cesarean section • >1000 cc of blood loss • Clinically • Any blood loss that causes the patient to be hemodynamically unstable

Hypovolemia Clinical Presentation • Moderate (20–40% of blood volume) • Heart rate - >110 bpm • Tachycardia - >30 rpm • BP – Normal in supine position/significant postural hypotension • Skin - marked pallor; conjuntiva, palms and mucous • Neurologic status – increasingly anxious Mild (<20% of blood volume) • Heart rate - mild tachycardia • Skin – mottled, cool extremities due to increased systemic vascular resistance and prolonged capillary refilling • Urinary output - decreased • Neurologic status – may report dizziness but usually remains normal Severe (>40% of blood volume) • Heart rate - marked tachycardia • BP – declines/unstable even in supine position • oliguria or anuria • Neurologic status – agitation, confusion, possible loss of consciousness

Estimating blood loss • Usually underestimated • Ongoing trickling can cause significant blood loss • Underestimation can lead to delayed or inadequate treatment • If patient is anemic, then the ability to compensate for blood loss may not be possible and patient cannot tolerate any blood loss

PPH Etiology • Tone – uterine atony • Tissue – retained placenta • Trauma – vaginal/cervical lacerations, rupture, inversion of uterus • Thrombin - coagulopathy

Tone: Risk Factors Etiologic processClinical risk factors Overdistended uterus Polyhydramnios Multiple gestation Macrosomia Uterine muscle Rapid labour exhaustion Prolonged labour High parity Intraamniotic infection Fever Prolonged rupture of membranes (PROM)

Tone – Risk Factors (2) Etiologic processClinical risk factors Functional or anatomic Fibroid uterus distortion of the uterus Placenta previa or abruptio Uterine anomalies Uterine-relaxing Halogenated medications anesthetics nitroglycerin, magnesium sulphate

Tissue – Risk FactorsRetained Placental tissue Etiologic process Clinical risk factors Retained products, Incomplete delivery of placenta abnormal placentation, Previous uterine surgery retained cotyledon or High Parity succinuriate lobe Abnormal placenta on ultrasound Retained blood clotsAtonic uterus

Trauma (Genital Tract) – Risk Factors Etiologic processClinical risk factors Tears (lacerations) of the Precipitous delivery cervix, vagina, or perineum Operative delivery Ruptured vulvar varicosities Mistimed or inappropriate use of episiotomy Extensions, lacerations Malposition at cesarean section Deep engagement Uterine rupturePrevious uterine surgery Uterine inversion High parity Fundal placenta

Thrombin (Abnormalities of Coagulation) – Risk Factors Etiologic processClinical risk factors Pre-existing states History of hereditary coagulopathies History of liver disease Therapeutic History of thrombotic anticoagulation disease

Thrombin (Abnormalities of Coagulation) – Risk Factors (2) Etiologic processClinical risk factors States acquired in pregnancy • idiopathic thrombocytopenic bruising purpura elevated blood pressure • thrombocytopenia with fetal demise preeclampsia fever • disseminated intravascular elevated white blood cells coagulation antepartum hemorrhage • preeclampsia sudden collapse • dead fetus in utero • severe infection/sepsis • placental abruption • amniotic fluid embolus

Prevention of PPH – Active Management of the Third Stage of Labor • prophylactic administration of oxytocin with delivery of anterior shoulder or immediately after delivery • 10 U IM OR 5 U IV bolus • clamp and cut cord after pulsating has stopped • palpate the uterine fundus and confirm the uterus is contracted • perform controlled cord traction with suprapubic counter traction with next strong contraction • perform uterine massage after delivery of the placenta, as appropriate • examine placenta for completeness

Controlled cord Traction

Uterotonics - Oxytocin • stimulates smooth muscle tissue of the upper segment of the uterus causing it to contract rhythmically, constricting blood vessels, and decreasing blood • safe and effective first choice for prevention and treatment • acts almost immediately for IV injections, and within 3 to 5 minutes for IM injections • should be stored in a cool, dry place • uncommon side effects: nausea, vomiting, and headache

Uterotonics – Ergot Alkaloids “Ergometrine” • causes the smooth muscle of both the upper and lower uterus to contract tetanically • takes 5 to 7 minutes to take effect when given intramuscularly • effects last approximately 2 to 4 hours • should be stored in a refrigerator between 2°C – 8°C and away from light • adverse effects include nausea and vomiting

Uterotonics – Prostaglandins “Misoprostol” • causes vasoconstriction and enhances contractibility of the uterine muscles • administered orally or sublingually (rapid action), or rectally (acts fir greater period of time) for prevention or treatment of PPH • relatively inexpensive, easy to store, stable at room temperature • side effects: shivering and fever are generally mild

Management of Postpartum Hemorrhage • Prevention is the key! • Identify and manage risk factors identified for potential PPH • Active management of the third stage of labor

Management of Postpartum Hemorrhage • Active management of the Third Stage of Labor • REMEMBER the ABCs • Call for HELP • Estimate blood loss. • Ask the woman to urinate or catheterize • Put the baby to the breast • Give Oxygen • Assess the uterus using external or internal bimanual massage • Give uterotonic - Oxytocin, Misoprostol, ergotamine • Observe the woman, and consider transport if unstable or bleeding continues

Management of PPH ABC A = airway B = breathing C = circulation

External Bimanual Uterine Massage

Internal Bimanual Uterine Massage

Examine the placenta for completeness Examination of fetal side Examination of maternal side

Manual removal of placenta 1. 2. 3. 4.

Management of Postpartum Hemorrhage • Examine the genitals for trauma and repair as required ie. vulva, vagina, cervix • If bleeding continues may require uterine tamponade or aortic compression • Ensure no uterine inversion or rupture • Manage possible coagulopathy with blood transfusion (if possible) • Consider transfer to facility for surgical management of PPH

Aortic Compression

Uterine Tamponade

Management of secondary PPH Associated with: • retained placental fragments or membranes • infection • shedding of dead tissue following an obstructed labour • breakdown of a uterine wound after a cesarean section or ruptured uterus

Management of secondary PPH (2) • assess the woman’s condition carefully • control blood loss • treat for shock, if necessary • administer antibiotics prophylactically for infection • provide anti-tetanus prophylaxis, if necessary • if there is no improvement with the above treatments, refer the woman promptly for further assessment and treatment

Continued care of woman Once the bleeding is controlled, and the woman is stable, careful monitoring over the next 24–48 hours is required, including: • monitoring uterine tone • monitoring vital signs • estimating ongoing blood loss • ensuring adequate fluid intake • monitoring blood transfusions • monitoring urinary output • ensuring the continuous presence of a skilled attendant, who maintains good documentation

Before discharge from hospital • check hemoglobin, and provide supplements as required • examine for hookworm infestation, malaria, HIV/AIDS or other co-existing conditions, provide treatmentas required • provide the mother and her family with information about her experience of PPH • ensure that lactation has been established, and that a well baby care plan is in place

Conclusion • Assess patient for PPH risk factors and manage accordingly • Prevention is the key: Active management of the third stage of labor • Management of bleeding is essential for saving a woman’s life • Refer to center as required for advanced care

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Postpartum Hemorrhage. Postpartum Hemorrhage. รองศาสตราจารย์วราภรณ์ เชื้ออินทร์ ภาควิชาวิสัญญีวิทยา คณะแพทยศาสตร์ มหาวิทยาลัยขอนแก่น. การประชุมวิชาการวิสัญญีวิทยามอ.-มข.-มช. ครั้งที่ 3 17 กรกฎาคม 2551 ณ. รร.ป่าตอง รีสอร์ท จ.ภูเก็ต.

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Postpartum Hemorrhage Treatment Market

Amongst the PPH devices, Uterine balloon tamponade segment accounted for almost half of the overall market in 2015 and it is also poised to grow at the highest CAGR of 6.1% from 2016 to 2022. This is primarily due to the growing number of PPH cases as well as large number of product approvals and increasing positive clinical outcomes of the treatment devices.

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Postpartum Hemorrhage (PPH) Devices Market

Postpartum hemorrhage is the most common form of obstetric hemorrhage and is one of the leading cause of maternal mortality.

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Postpartum hemorrhage

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Stopping Acute Bleeds, Starting With Severe Postpartum Hemorrhage

From Biopharma Deal Makers .

Acute bleeding associated with traumatic injury is the leading cause of death between ages 1 to 46. Although 20–40% of hemorrhage-related deaths are potentially preventable with rapid hemostatic control, safe and effective pharmaceutical treatments to address this $20 billion market are lacking.

Coagulant Therapeutics—a privately held biotech company of seasoned drug developers specializing in biologics and the coagulation cascade—is here to fill that void. Drawing on over 100 years of collective experience in biopharmaceutical development, the company is leveraging the full range of biological formats to develop novel therapeutics that treat acute bleeds.

Engineering fit-for-purpose treatments

Although the European Medicines Agency (EMA) recently approved a recombinant FVIIa (rFVIIa) for the treatment of acute bleeding in postpartum hemorrhage (PPH), its use is associated with risks of serious thromboembolic events such as clots in the heart or brain. “The coagulation cascade is composed of a set of exquisitely controlled cofactors and proteases,” explained Coagulant’s founder and CEO, Terry Hermiston. “Although FVIIa is essential to stop bleeding, it must be tightly regulated to prevent unwanted thromboembolic events.”

The team at Coagulant Therapeutics has addressed this problem by designing and developing CT-001, a next-generation FVIIa molecule. CT-001 contains key substitutions for greater affinity and activity, and for safety, the engineering of exposed terminal galactose residues tap into the bodies natural recycling center, the liver, for rapid, active clearance from circulation (Fig. 1). Coagulant has shown that this rapid clearance occurs without compromising its life-saving activity.

Superior potency

“Compared to rFVIIa, the potency of our FVIIa molecule is two-to-five times higher, depending on the assay, and its half-life has been reduced from two hours to three minutes,” said Hermiston. “The enzyme doesn’t have to be in the body long to be effective, and any that isn’t used where it’s needed is rapidly removed, thus making it considerably less likely to form unwanted clots elsewhere.”

The entry indication for CT-001 is severe PPH (sPPH), the leading cause of maternal morbidity and mortality globally, with most cases occurring in low- or middle-income countries. Ex vivo studies on postpartum blood samples confirm the activity seen in the preclinical studies relative to rFVIIa3.

Furthermore, administration of CT-001 is straightforward, making it accessible to a considerably greater population than current treatments. “While almost all PPH originates in the uterus or from birth trauma, failure of normal hemostasis occurs when the process is massive, resulting in even greater blood loss and possible death. The ability to manage an sPPH, especially when accompanied by failure of coagulation, is difficult or impossible in rural hospitals or low-resource settings, where treatment options are limited,” said Andra James, professor emeritus of obstetrics and gynecology at Duke University School of Medicine. “Importantly, CT-001 can be given intravenously and without specialized training, facilitating its use outside of the tertiary-care setting and even outside of the hospital, enabling its further use in ambulances or on the battlefield.”

Diverse pipeline and partnering opportunities

Coagulant Therapeutics has a pipeline of well-differentiated molecules that uniquely not only stop bleeding but also address endotheliopathy, a process by which the endothelial barrier is compromised, which can lead to morbidity and mortality in the acute-bleeding setting.

Clinical trials of CT-001 in treating sPPH are expected to begin in 2026. Proof of safety and activity may allow expansion into additional bleeding indications, such as traumatic brain injury, intracranial hemorrhage and trauma, which have high mortality and significant unmet need for highly differentiated treatments.

“Our FVIIa is a highly potent molecule envisioned for the safe treatment of uncontrollable, fatal severe postpartum hemorrhage. It is easy to administer, and addresses the known limitations and liabilities of currently available rFVIIa in this indication,” said Hermiston. “As we transition towards the clinic, we are looking for partners to advance CT-001 and our other exciting programs for the benefit of patients and their families regardless of their location.”

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• v.2020(1); 2020 Dec 4

Prevention and treatment of postpartum hemorrhage: focus on hematological aspects of management

Visual abstract.

Postpartum hemorrhage (PPH) is the leading cause of global maternal mortality and accounts for approximately one-quarter of all maternal deaths worldwide. Prevention of excess maternal deaths requires a coordinated approach to prevention, early recognition, and intervention by a multidisciplinary team. Although some women have risk factors for PPH that can be identified during pregnancy or during labor or birth, most women with severe PPH do not have any risk factors. Therefore, all pregnant women must be considered to be at risk of PPH. Common causes include uterine atony, retained placenta, trauma to the genital tract or uterus, and coagulopathy. The pivotal role of fibrinogen and hyperfibrinolysis in the evolution and as a treatment target for PPH is increasingly recognized. Coagulopathy can be an early feature in PPH that may be unrecognized, as it can be present before massive transfusion has occurred. Identification of coagulopathy by viscoelastic point-of-care testing or conventional laboratory assays can be helpful in guiding management of PPH and preventing severe maternal outcomes.

Learning Objectives

• Recognize the importance of risk assessment of pregnant women to identify PPH risk factors in the antenatal period and during labor and birth
• Recognize the importance of coagulation tests in women with PPH, to enable early identification and treatment of coagulopathy and hyperfibrinolysis

Clinical case

The patient was a 29-year-old Black woman in her first pregnancy. Her body mass index was 33 kg/m 2 . She had no other medical history of note, and antenatal care had been uncomplicated, apart from iron deficiency treated with oral iron supplements from 28 weeks’ gestation. At the 38-week scan, the fetus was well developed (estimated weight, 4100 g).

The patient had spontaneous onset of labor at 39 +5 weeks’ gestation. Her admission observations were normal: afebrile, pulse 88 per minute, blood pressure (BP) 110/68 mm Hg, and respiratory rate 14 per minute. A complete blood count on admission showed hemoglobin (Hb) 10.4 × 10 9 /L, platelets 152, white blood cell count 7.8 × 10 9 /L. She made slow progress in the first stage of labor, requiring augmentation with IV oxytocin. At 11 hours, an epidural was placed after the IV oxytocin was started. The first stage of labor was complete at 17 hours, and initial effective pushing occurred in the second stage, with the head on the perineum at 65 minutes with no further advancement. A successful vacuum extraction (ventouse) was performed after episiotomy by the senior resident, with birth of the infant after 80 minutes in the second stage. Active management of the third stage of labor appeared complete, with controlled cord traction, intramuscular oxytocin, and delivery of the placenta. Immediate postpartum blood loss was estimated at 1200 mL. The pediatric team was called to review the infant, who had a 3990-g birth weight and some initial floppiness but responded rapidly to basic resuscitation.

Ongoing vaginal blood loss continued in the postpartum period. The patient’s uterus remained atonic but responded well to “rubbing up,” and IV oxytocin infusion was started. The team agreed to move her to an operating room (OR) for examination under anesthesia to determine whether there were any retained products of conception or any genital tract trauma that would explain the ongoing blood loss. Maternal observations were pulse, 106 per minute; BP, 98/60 mm Hg; and respiratory rate, 18 per minute.

On arrival in the OR, the observations were pulse, 114 per minute; BP, 94/60 mm Hg; and respiratory rate, 20 per minute. Vaginal blood loss continued, with estimated blood loss of 400 mL on new drapes and swabs in the OR.

Blood taken in the OR and tested on the blood gas analyzer showed Hb of 8.2 g/dL. Two units of packed red cells were ordered from the blood bank. The uterus remained atonic, and there were some abrasions of the vaginal wall and bleeding from the episiotomy; no other cause was identified. Ongoing vaginal blood loss was noted, with loss estimated at 1600 mL. Uterine atony persisted and further uterotonics were given, after which the maternal observations were pulse, 118 per minute; BP, 90/58 mm Hg; and respiratory rate, 22 per minute.

A senior obstetrician and anesthesiologist were called for support.

Obstetric hemorrhage is the leading cause of maternal mortality and bleeding after childbirth. Postpartum hemorrhage (PPH) accounts for two-thirds of cases of obstetric hemorrhage and for approximately one-quarter of all maternal deaths worldwide. There is no universally accepted definition of PPH, with some suggesting that blood loss volume >500 or 1000 mL represents standard or severe PPH. 1 Most otherwise fit and healthy pregnant women will have minimal physiological response to this degree of blood loss, leading some clinicians to suggest more relevant clinical definitions, such as persistent PPH: ongoing active bleeding >1000 mL occurring within 24 hours after birth that continues despite the use of measures such as first-line uterotonic therapy and uterine massage. 2

Maternal deaths represent only the tip of the iceberg in terms of the overall impact of major bleeding on maternal health. Women who have life-threatening hemorrhage but do not die of PPH can face long-term health complications including loss of fertility and psychological trauma. Although nearly all women with severe PPH live in countries with limited economic resources, PPH and its complications can affect women living in any resource setting. Data from the United States show that rates of severe PPH are increasing. 3 Well-resourced health care settings with access to skilled practitioners, drugs, and blood banks offer the best opportunity to provide optimal care for women. In any care setting, early recognition of abnormal postpartum bleeding and mobilization of appropriate staff and resources is essential to stop the bleeding promptly and minimize morbidity and mortality.

Postpartum hemorrhage should not be viewed as a diagnosis but rather a clinical manifestation of an underlying condition or conditions that require identification and treatment. The differential diagnosis is not wide and includes one or more of the following: uterine atony, retained placenta, and placental malimplantation (previa, accreta, increta, or percreta), and genital tract trauma or coagulopathy, often referred to as the “4 T’s” (tone, tissue, trauma, and thrombin). Some women enter pregnancy with risk factors for PPH or develop these risk factors during the course of pregnancy or labor and birth ( Table 1 ). Women with risk factors identified antenatally should be managed in the appropriate setting with access to skilled staff and a blood bank and with precautionary steps taken during labor and childbirth to minimize the risk of PPH and respond early if it occurs ( Figure 1 ). However, it is critical that all staff caring for women in labor and childbirth be aware that most women who have severe PPH have no identifiable antenatal risk factors and that a high level of awareness be maintained. Risk factors should be reassessed frequently during labor and birth.

Risk factors for PPH

How urgently is red cell transfusion needed?

Setting the scene for the “PPH perfect storm”

Most women with PPH respond to initial measures of uterine massage and therapeutic uterotonics. However, if bleeding continues despite these interventions, the situation can rapidly escalate with more severe blood loss, maternal morbidity, and even mortality. Failure to recognize and respond to an evolving situation of severe PPH is frequently described in reviews of adverse outcomes caused by hemorrhage. This delay in response can be explained by several factors that create the “perfect storm” where the clinical team fails to recognize the severity of the blood loss and to take the appropriate steps.

Potential for rapid loss of a large volume of blood

In pregnancy, the total blood volume is ∼5 to 7 L (70-80 mL/kg lean body mass). By term, the blood supply to the uterine arteries is ∼500 to 600 mL per minute, increased from its normal level of 10 to 15 mL per minute outside of pregnancy. 4 After delivery of the placenta, the uterine muscles contract, effectively staunching blood flow from the uteroplacental bed. Uterine atony, retained placental tissue, and abnormal placental implantation impede the normal action of the uterus in completing this critical mechanical hemostatic process. Given the high blood flow to the uterine arteries, it is easy to appreciate how rapidly a large volume of blood can be lost in a short time.

Underestimation of the degree of blood volume loss

In many clinical settings the volume of blood loss is estimated by using visual assessment rather than objective measurement, which significantly underestimates the actual blood volume, especially at higher volumes. 5 Accurate measurements of blood volume using graduated containers and gravimetric measurement of blood-soaked pads and swabs reported to the clinicians in real time can help alert them to the development of severe continued bleeding. Providing a cumulative total of blood volume loss is especially important when women are moved during the process of PPH management (for example, from the delivery room to the OR) if required for an examination while the patient is under anesthesia, to assess for retained products of conception or genital tract trauma.

Most pregnant women are healthy and physiologically robust

Healthy pregnant women show minimal physiological response to blood loss of 1000 to 1500 mL, perhaps only becoming slightly tachycardic with a minor decline in systolic BP. By the time women have significant hypotension or tachycardia or an increased respiratory rate or become distracted or agitated, they usually have lost in excess of 2000 to 2500 mL. Careful and repeated clinical assessments and documentation of vital signs, such as pulse rate, BP, temperature, and respiratory rate is essential for identifying a trend indicating physiological decompensation in response to hypovolemia. The use of maternity early warning scoring to improve early detection of clinically deteriorating patients and escalation of the clinical response is increasing. 6,7 These systems assign a score to a range of clinical vital signs to form a total maternity early warning score. An increasing score suggests a deviation from a normal physiological state and indicates clinical deterioration, which should prompt an escalation in response by clinicians who have the appropriate level of skill to care for the patient.

Lack of anticipation of the presence of early coagulopathy with PPH, before a massive transfusion is needed

Dilutional coagulopathy is common in patients with hemorrhage after multiple transfusions. Urgent red cell transfusion is preferred to infusion of significant volumes of crystalloid, but in an unstable patient, volume replacement with up to 2 to 3 L of crystalloid may be necessary prevent severe hypotension. 2 Coagulopathy resulting from conditions, such as amniotic fluid embolism, placental abruption, and sepsis, can be present early, before administration of IV fluids or blood products. Early identification of coagulopathy by testing basic hemostatic function, with either laboratory-based assays or point of care (POC) testing, can help identify coagulopathy early and enable directed transfusion of the appropriate blood products.

Standard thrombin-based functional clotting assays for fibrinogen, such as the Clauss fibrinogen assay, measure the time it takes for a fibrin clot to form. In most clinical settings the final result will not be available for at least 45 to 60 minutes. Viscoelastic point of care (VE-POC) tests, such as rotational thromboelastometry (ROTEM) and thromboelastography, are increasingly used to assess global hemostasis, determining the activity of the coagulation factors and the amount of fibrinogen available to form a fibrin clot, as well the resistance of the clot to fibrinolysis. 8 In the setting of PPH, hyperfibrinolysis is not uncommon, especially in more severe PPH. The results of POC tests are usually available within 15 to 20 minutes, especially if the instrument is available in the OR.

Fibrinogen and fibrinolysis in PPH

The importance of fibrinogen and fibrinolysis in major postpartum bleeding has been brought into focus in recent years. Fibrinogen levels in pregnant women at term are increased at ∼4 to 6 g/L, compared with levels of 2 to 4 g/L in nonpregnant patients. In 2007, Charbit et al showed that fibrinogen levels were lower in women who developed severe PPH than in women with nonsevere PPH (median levels, 3.3 and 4.4 g/L, respectively). 9 Importantly, this difference was evident early in the evolution of PPH and before any blood or blood products had been administered. Other studies have confirmed this finding 10,11

Although these studies suggested that a low level of fibrinogen is predictive of development of severe PPH, they did not ascertain whether early fibrinogen replacement could modify the degree of blood loss. A controlled study of women with moderate PPH (blood loss >1000 mL after Cesarean section [CS], >500 mL in women who required manual removal of placenta, and >1000 mL in women who required exploration of the uterus) randomized women to 2 g of fibrinogen or placebo. 12 Transfusion rates were the same in women (n = 25 of 123; 20%) given fibrinogen as in those who received placebo (n = 26 of 121; 22%). Of note, the mean fibrinogen level in each group was normal (4.5 g/L) and the median blood loss was <1500 mL, indicating that perhaps fibrinogen would not be a key factor in this population.

A second multicenter, double-blind, randomized, placebo-controlled trial of early fibrinogen replacement in women with severe PPH (>1000-1500 mL measured blood loss, with ongoing bleeding and reduced fibrinogen on ROTEM: FIBTEM A5 <15 mm, equivalent to ∼3 g/L fibrinogen). 13 Of 606 women eligible for inclusion, only 57 (9.4%) were randomized, with 55 women analyzed for the primary outcome (the number of allogeneic units transfused: red blood cells and plasma products). There was no difference in blood products transfused or in any of the secondary outcomes, such as invasive procedures for control of blood loss or transfer to intensive care. Analysis of prespecified subgroups showed that, in women with fibrinogen >2 g/L (n = 22), there was no difference in blood loss or blood transfusion after administration of the study medication, whereas the median blood loss was lower in the fibrinogen arm than in the placebo arm in women with fibrinogen <2 g/L. The researchers concluded that a fibrinogen level of >2 g/L appeared sufficient for hemostasis in the setting of PPH. Too few women in the cohort had very low fibrinogen (<2 g/L) for them to determine whether early administration of fibrinogen would modify outcomes in that patient group.

Although Collins et al 13 did not demonstrate an improvement in outcomes in women who were given fibrinogen concentrate, they observed that, over the course of the clinical trial, their approach of routine risk assessment for PPH, objective measurement of cumulative blood loss, and early involvement of senior staff enabled early recognition and intervention in the course of the PPH to take steps to respond to and control blood loss. The prompt recognition allowed for timely and appropriate escalation of care and involvement of senior staff at an early stage. Also, the study led to the practice of early assessment of hemostasis, Hb, and lactate by using POC tests. The clinicians used the study protocol to inform the development of a nationwide interventional program for standardized management of PPH, “OBS Cymru,” which has been effectively implemented across all obstetric units in Wales. 14

Approach to transfusion of blood and plasma products in management of PPH

Using empiric fixed ratios of red blood cells, fresh frozen plasma (FFP), and platelets in women with PPH >1500 mL has been shown to reduce progression to severe PPH. Most women with PPH <2000 mL do not have low levels of fibrinogen or other clotting factors, and fibrinogen does not appear to decrease to <2 g/L until blood volumes of >4000 mL are lost, although early coagulopathy is a feature of placental abruption and amniotic fluid embolism. Empiric transfusion in the absence of hemostatic testing may lead to overtransfusion of blood and plasma products increased risk of complications, such as transfusion-associated circulatory overload and transfusion-associated lung injury. Collins et al advocate using targeted transfusion protocols with viscoelastic-POC (VE-POC) testing. 15 They reported that fibrinogen levels decrease sooner than other coagulation factors, so that correction of low fibrinogen levels may be a more important therapeutic target.

The International Society on Thrombosis and Haemostasis (ISTH) recommends using either cryoprecipitate (∼15 g/1000 mL) or fibrinogen concentrate (20 g/1000 mL) to maintain fibrinogen >2 g/L when managing PPH. 16 The fibrinogen concentration of FFP is much lower (2 g/1000 mL), and its use for fibrinogen replacement could lead to hemodilution.

Deficiencies of other clotting factors tend to occur at a later stage in PPH, suggesting that there is a more limited requirement for FFP. When VE-POC testing is not available, conventional laboratory testing may be helpful and the ISTH Scientific and Standardization Committee recommends targeting using 15 mL/kg FFP to maintain activated partial thromboplastin time/prothrombin time >1.5 × normal. 16

Severe thrombocytopenia is uncommon in most women with PPH, leading to a recommendation (ISTH) to limit platelet transfusions, unless platelet count is <75 × 10 9 /L. 16

Inhibition of fibrinolysis

Over the past 20 years or so, the impact of hyperfibrinolysis in major bleeding has been recognized. The CRASH-2 study demonstrated tranexamic acid, a potent inhibitor of fibrinolysis, reduction in death related to bleeding by 21% (risk ratio [RR], 0.79; 95% confidence interval [CI], 0.64-0.97) in trauma patients who received it within 3 hours and by 32% (RR, 0.68; 95% CI, 0.57-0.82) in patients who received it within 1 hour. 17

The WOMAN study is a placebo-controlled trial conducted in 21 countries that assessed the impact of tranexamic acid in 20 021 women with PPH >500 mL after vaginal birth or >1000 mL after CS. 18 The maternal mortality rate was 2.4% (n = 483) with 72% (n = 346) of deaths caused by hemorrhage. Administration of 1 g of tranexamic acid (with a second dose given for ongoing bleeding) resulted in an overall reduction in death related to bleeding of 19% (RR, 0.81; 95% CI, 0.65-1.00) when given within 3 hours.

As a result of this study, the World Health Organization now strongly recommends early use of IV tranexamic acid (within 3 hours of birth) in addition to standard care for women with clinically diagnosed PPH after vaginal birth or CS. 19

Recognition and response to major PPH also requires rapid response with transfusion of red blood cells to maximize oxygen delivery and prevent tissue hypoxia, development of acidosis, organ failure, and worsening of shock. The urgency of red cell transfusion depends on the degree of maternal clinical instability and rapidity of blood loss. Transfusion of O − red blood cells may be required in women who are clinically unstable or who are losing blood rapidly when cross-matched blood is not available.

Comments on the case

Antenatal risk factors.

In the clinical case, the only identifiable antenatal risk factors for PPH were increased body mass index and fetal macrosomia. Although the patient was iron deficient, she was not anemic. However, during labor she needed augmentation with oxytocin and had prolonged first and second stages of labor, with an assisted delivery. The immediate estimated postpartum blood loss was high, confirming a PPH, and importantly, the bleeding did not stop after initial interventions of uterine massage and therapeutic uterotonics.

An opportunity for escalation of intervention and a call for backup was missed at the time the patient was transferred to the OR. The degree of tachycardia and the increase in the respiratory rate were signs that this otherwise healthy, physiologically robust woman had lost a significant amount of blood. As a rule of thumb, a pulse rate higher than the systolic BP indicates a problem.

Estimated rather than measured blood loss

It is likely given the drop in the Hb that the woman had lost >1600 mL blood. Accurate cumulative measurement of blood loss would have alerted the clinicians to the severity of blood loss and the potential for progression.

Failure to perform an early coagulation test

A test of coagulation is helpful in identifying unanticipated coagulopathy. If available, a VE-POC test (ROTEM or thromboelastography) can provide a result within 15 minutes. Even though a conventional laboratory-based fibrinogen assay may be delayed by 60 minutes, it could still provide additional help if the PPH is not being controlled by initial maneuvers.

Ongoing significant postpartum bleeding in a woman with a well-contracted uterus with no evidence of genital tract trauma or retained placenta should alert the clinicians to the possible presence of coagulopathy.

Finished Papers

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