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Satu dari bagian yang sangat penting dari penanganan perdarahan obstetric adalah
mengetahui beratnya perdarahan. Seperti yang dibahas pada halaman 781,
estimasi perdarahan secara visual,terutama jika terlalu banyak, sangat tidak akurat,
dan jumlah perdarahan yang sebenarnya sering 2 sampai 3 kali lebih banyak dari
perkiraan klinis. Pertimbangkan juga dalam obstetrik, sebagian atau bahkan
kadang-kadang seluruh perdarahan dapat tersembunyi. Perkiraan lebih lanjut lebih
rumit pada perdarahan peripartum,dimana kebanyakan kasus berat ditemui dan
juga mencakup peningkatan volume darah akibat kehamilan. Jika hipovolemia
pada kehamilan bukan suatu faktor, maka kehilangan darah 1000 mL, akan
menurunkan hematokrit menurun 3 sampai 5 persen volume dalam waktu satu
jam. Rendahnya hematokrit bergantung pada kecepatan resusitasi menggunakan
infus kristaloid . ingat bahwa
MANAGEMENT OF HEMORRHAGE
One of the most crucial elements of obstetrical hemorrhage management is
recognition of its severity. As discussed on page 781, visual estimation of blood
loss, especially when excessive, is notoriously inaccurate, and true blood loss is
often two to three times the clinical estimates. Consider also that in obstetrics, part
and sometimes even all of the lost blood may be concealed. Estimation is further
compli- cated in that peripartum hemorrhagewhen most severe cases are
encounteredalso includes the pregnancy-induced increased blood volume. If
pregnancy hypervolemia is not a factor, then following blood loss of 1000 mL, the
hema- tocrit typically falls only 3 to 5 volume percent within an hour. The
hematocrit nadir depends on the speed of resusci- tation using infused intravenous
crystalloids. Recall that with abnormally increased acute blood loss, the real-time
hematocrit is at its maximum whenever measured in the delivery, operat- ing, or
recovery room.
A prudent rule is that any time blood loss is considered more than average by an
experienced team member, then the hema- tocrit is determined and plans are made
for close observation for physiological deterioration. Urine output is one of the
most important vital signs with which to monitor the woman with obstetrical
hemorrhage and who were now isovolemic and not actively bleeding, there were
no benefits of red cell transfusions when the hematocrit was between 18 and 25
volume percent (Morrison, 1991). The number of units transfused in a given
woman to reach a target hematocrit depends on her body mass and on
expectations of additional blood loss.
Blood Component Products. Contents and effects of trans- fusion of various
blood components are shown in Table 41-8. Compatible whole blood is ideal for
treatment of hypovolemia from catastrophic hemorrhage. It has a shelf life of 40
days, and 70 percent of the transfused red cells function for at least 24 hours
following transfusion. One unit raises the hematocrit by 3 to 4 volume percent.
Whole blood replaces many coagulation factorswhich is important in obstetrics
especially fibrino- genand its plasma treats hypovolemia. A collateral
derivative is that women with severe hemorrhage are resuscitated with fewer
blood donor exposures than with packed red cells and components (Shaz, 2009).
There are reports that support the preferable use of whole blood for massive
hemorrhage, including our experiences at Parkland Hospital (Alexander, 2009;
Hernandez, 2012). Of more than 66,000 deliveries, women with obstetrical
hemor- rhage treated with whole blood had significantly decreased incidences of
renal
failure,
acute
respiratory
distress
syndrome,
pulmonary
edema,
of fibrinogen or platelets. If time does not permit this, however, the massive
transfusion protocol is activated.
Dilutional Coagulopathy. A major drawback of treatment for massive
hemorrhage with crystalloid solutions and packed red blood cells is depletion of
platelets and clotting factors. As discussed on page 808, this can lead to a
dilutional coagulopa- thy clinically indistinguishable from disseminated
intravascular coagulation (Hossain, 2013). In some cases, impaired hemosta- sis
further contributes to blood loss.
Thrombocytopenia is the most frequent coagulation defect found with blood loss
and multiple transfusions (Counts, 1979). In addition, packed red cells have very
small amounts of soluble clotting factors, and stored whole blood is deficient in
platelets and in factors V, VIII, and XI. Massive replacement with red cells only
and without factor replacement can also cause hypofibrinogenemia and
prolongation of the prothrom- bin and partial thromboplastin times. Because many
causes of obstetrical hemorrhage also cause consumptive coagulopathy, the
distinction between dilutional and consumptive coagulopa- thy can be confusing.
Fortunately, treatment for both is similar.
A few studies have assessed the relationship between massive transfusion and
resultant coagulopathy in civilian trauma units and military combat hospitals
(Bochicchio, 2008; Borgman, 2007; Gonzalez, 2007; Johansson, 2007). Patients
undergoing massive transfusiondefined as 10 or more units of bloodhad
much higher survival rates as the ratio of plasma to red cell units was near 1.4,
that is, one unit of plasma given for each 1.4 units of packed red cells. By way of
contrast, the highest mortality group had a 1:8 ratio. Most of these studies found
that component replacement is rarely necessary with acute replacement of 5 to 10
units of packed red cells.
From the foregoing, when red cell replacement exceeds five units or so, a
reasonable practice is to evaluate the platelet count, clotting studies, and plasma
fibrinogen concentration. In the woman with obstetrical hemorrhage, the platelet
count should be maintained above 50,000/L by the infusion of platelet concentrates. A fibrinogen level 100 mg/dL or a sufficiently pro- longed
erythrocytes. Further, because some red blood cells are invariably transfused
along with the plate- lets, only units from D-negative donors should be given to
D-negative recipients. If necessary, however, adverse sequelae are unlikely. For
example, transfusion of ABO-nonidentical platelets in nonpregnant patients
undergoing cardiovascular surgery had no clinical effects (Lin, 2002).
Fresh-Frozen Plasma. This component is prepared by separating plasma from
whole blood and then freezing it. Approximately 30 minutes are required for
frozen plasma to thaw. It is a source of all stable and labile clotting factors,
including fibrinogen. Thus, it is often used for treatment of women with
consumptive or dilutional coagulopathy. Plasma is not appropriate for use as a
volume expander in the absence of specific clotting factor deficiencies. It should
be considered in a bleeding woman with a fibrinogen level 100 mg/dL or with
an abnormal prothrombin or partial thromboplastin time.
An alternative to frozen plasma is liquid plasma (LQP). This never-frozen plasma
is stored at 1 to 6oC for up to 26 days, and in vitro, it appears to be superior to
thawed plasma (Matijevic, 2013).
Cryoprecipitate and Fibrinogen Concentrate. Each unit of cryoprecipitate is
prepared from one unit of fresh-frozen plasma. Each 10- to 15-mL unit contains at
least 200 mg of fibrinogen, factor VIII:C, factor VIII:von Willebrand factor, factor
XIII, and fibronectin (American Association of Blood Banks, 2002). It is usually
given as a pool or bag using an aliquot of fibrinogen concentrate taken from 8
to 120 donors. Cryoprecipitate is an ideal source of fibrinogen when levels are
dangerously low and there is oozing from surgical incisions. Another alternative is
virus-inactivated fibrinogen concentrate. Each gram of this raises the plasma
fibrinogen level approxi- mately 40 mg/dL (Ahmed, 2012; Kikuchi, 2013). Either
is used to replace fibrinogen. However, there are no advantages to these compared
with fresh-frozen plasma for general clotting factor replacement. Exceptions are
general factor deficiency replacement for women in whom volume overload may
be a probleman unusual situation in obstetricsand for those with a specific
factor deficiency.
Recombinant Activated Factor VII (rFVIIa). This syn- thetic vitamin K-
cal patients (Pacheco, 2011; Rainaldi, 1998). That said, Allam and associates
(2008) reported the lack of prospective trials but also found no reports of serious
complications.
Complications with Transfusions. During the past sev- eral decades, substantial
advances have been achieved in blood transfusion safety. Although many risks are
avoided or miti- gated, the most serious known risks that remain include errors
leading to ABO-incompatible blood transfusion, transfusion- related acute lung
injury (TRALI), and bacterial and viral trans- mission (Lerner, 2010).
The transfusion of an incompatible blood component may result in acute
hemolysis. If severe, this can cause dis- seminated intravascular coagulation, acute
kidney injury, and death. Preventable errors responsible for most of such reactions
frequently include mislabeling of a specimen or transfusing an incorrect patient.
Although the rate of such errors in the United States has been estimated to be 1 in
14,000 units, these are likely underreported (Lerner, 2010; Linden, 2001). A
transfu- sion reaction is characterized by fever, hypotension, tachycardia, dyspnea,
chest or back pain, flushing, severe anxiety, and hemo- globinuria. Immediate
supportive measures include stopping the transfusion, treating hypotension and
hyperkalemia, provoking diuresis, and alkalinizing the urine. Assays for urine and
plasma hemoglobin concentration and an antibody screen help confirm the
diagnosis.
The syndrome of transfusion-related acute lung injury (TRALI) can be a lifethreatening complication. It is charac- terized by severe dyspnea, hypoxia, and
noncardiogenic pul- monary edema that develop within 6 hours of transfusion
(Triulzi, 2009). TRALI is estimated to complicate at least 1 in 5000 transfusions.
Although the pathogenesis is incom- pletely understood, injury to the pulmonary
capillaries may arise from anti-human leukocyte antigen (HLA) antibodies in
donor plasma (Lerner, 2010; Schubert, 2013). These antibod- ies bind to
leukocytes that aggregate in pulmonary capillaries and release inflammatory
mediators. A delayed form of TRALI syndrome has been reported to have an onset
6 to 72 hours following transfusion (Marik, 2008). Management is with supportive
therapy that may include mechanical ventilation (Chap. 47, p. 944).