00:00
aapko basic science topic hemorrhage in
00:02
obstetrics postpartum hemorrhage is
00:04
common the w-h-o reports post-prom
00:06
hemorrhage is the leading cause of
00:08
maternal mortality accounting for 35% of
00:11
all maternal deaths in severe cases of
00:13
hemorrhage is important to consider the
00:15
diagnosis of disseminated intravascular
00:16
coagulation in this video we will review
00:20
the basic principles of normal
00:21
hemostasis review the physiologic
00:24
changes associated with coagulation
00:25
during pregnancy and review the
00:27
pathophysiology and management of di C
00:30
please meet our patient miss Hayne she
00:33
is a 35 year old gravity’ 3 para 2 at 36
00:36
weeks gestational age with chronic
00:37
hypertension she presents with vaginal
00:39
bleeding and abdominal pain to labor and
00:41
delivery on exam vital signs are notable
00:44
for blood pressure 100 over 60 pulse of
00:46
98 abdomen is tender to palpation in M
00:50
pelvic exam there’s significant clot in
00:52
the vagina with active bleeding from the
00:53
cervix to commentary demonstrates
00:56
uterine tachy systole labs demonstrated
00:58
hemoglobin of 8.5 platelet count of
01:01
240,000 per thrombin teen of 12.8
01:04
activated partial thromboplastin time of
01:06
27 and fibrinogen of 450 her symptoms
01:10
are concerning for placental abruption
01:11
and she is presenting with abdominal
01:13
pain and bleeding let’s look more
01:15
closely at her labs what specifically do
01:18
PT PTT and fibrinogen measure these labs
01:21
are useful to assess clotting function
01:23
and patients pta measures the extrinsic
01:25
pathway of the coagulation cascade and
01:27
includes factors 7 10 5 and thrombin
01:30
which is also known as factor 2 PTT
01:33
measures an intrinsic pathway an easy
01:36
way to remember this is that includes
01:37
all factors except for 7 including
01:39
factors 12 11 9 8 10 5 and 2 both
01:45
pathways converge to form thrombin and
01:47
subsequently fiber tension which is
01:48
cleaved to form fibrin necessary for
01:50
Klat formation let’s take a look at
01:52
normal hemostasis to truly understand
01:54
the role clotting factors play in clot
01:56
formation and why coagulation labs are
01:58
helpful in determining if coagulopathy
01:59
is present in our patients in normal
02:03
hemostasis a platelet plug first occurs
02:05
at the site of injury this is a blood
02:07
vessel with epithelial cells
02:09
when injury occurs platelets adhere to
02:11
the site of injury with the help of von
02:12
willebrand factor at the same set of
02:15
injury tissue factors released
02:17
interaction of tissue factor with factor
02:19
7 initiates clotting and is considered
02:22
the primary event of the Cascade the
02:24
subsequently activates factors 10 and 9
02:27
activated factor 9 combines with
02:29
activated factor 8 to activate factor 10
02:32
activated factor 10 with activated
02:34
factor 5 generates a small and minor
02:36
thrombin the small amount of thrombin
02:39
activates platelets as well as factors 5
02:41
8 and 11 which leads to the application
02:43
of thrombin generation the so called
02:46
thrombin burst this propagation accounts
02:48
for the majority of thrombin generated
02:50
in addition activated factor 12
02:52
activates 11 on the surface of activated
02:54
platelets which provides an alternative
02:57
route for generation of thrombin let’s
02:59
take a moment to review how clotting
03:00
factors relate to PT and PTT I’m
03:03
circling was considered the extrinsic
03:05
pathway which again is measured by PT
03:07
and this is the intrinsic pathway
03:09
measured by PTT
03:11
let’s pause read and apply patients with
03:15
hemophilia a have factor 8 deficiency
03:18
what lab findings would you expect for
03:20
PT and PTT in the patient with this
03:22
disorder since factor a is part of the
03:25
intrinsic pathway and not the extrinsic
03:27
pathway we expect an increased PTT and
03:31
normal PT let’s continue with the
03:34
Cascade thrombin then converts
03:36
fibrinogen into fibrin fibrin monomers
03:39
are then cross-linked by factor 13 to
03:41
form a clot what keeps the clot from
03:44
propagating indefinitely termination of
03:46
clotting is an important step in normal
03:48
hemostasis and also prevents clotting
03:50
when it is not required thrombin
03:52
stimulates the activation of
03:53
antithrombin through negative feedback
03:56
thrombin and 10a are inhibited similarly
03:58
tissue factor pathway inhibitor and
04:00
habits tissue factor protein C is also
04:03
activated with the assistance of protein
04:05
s activated protein C then inhibits
04:08
factor 5 finally the clot is removed
04:11
with the activation of plasma plasma
04:13
ningen binds fibrin and tissue
04:15
plasminogen activator which converts
04:17
plasminogen to proteolytic plasma
04:19
plasmon cleaves fibrin releasing fibrin
04:22
degradation products and d-dimer’s let’s
04:26
remember our patient now that we know
04:28
what the labs are measuring what is
04:30
normal for pregnancy during pregnancy
04:33
there’s an increase in some coagulation
04:34
factors and decrease in some anti
04:36
coagulation factors to decrease
04:38
excessive bleeding postpartum the
04:40
changes create a relative
04:41
hypercoagulable state procoagulant
04:43
factors fibrinogen factors 2 7 8 9 10 12
04:49
and 13 increased by 20 to 200 percent in
04:52
addition there’s a decrease in
04:54
anticoagulant protein s in antithrombin
04:57
other proteins such as c 5 and 11 remain
05:00
relatively unchanged in pregnancy the
05:03
placental bed plays a role deciduous
05:06
cells that line the placental bed
05:07
strongly expressed tissue factor when
05:10
this is released at sites of decidua
05:11
Yama initiation of the coagulation
05:13
cascade occurs these factors along with
05:16
my own material contraction all
05:17
contribute to decreasing the risk for
05:19
excessive bleeding at the time of
05:20
delivery factors typically return to
05:23
normal levels six to twelve weeks
05:24
postpartum and how does this affect labs
05:28
in pregnancy PT again measuring the
05:31
extrinsic pathway generally stays the
05:33
same with no market changes PTT
05:35
measuring the intrinsic pathway is
05:37
usually shortened by up to four seconds
05:39
in the third trimester
05:40
in addition fibrinogen is markedly
05:43
elevated with normal levels ranging from
05:45
350 to over 600 milligrams per deciliter
05:48
let’s go back to our patient she
05:51
continues to have heavy vaginal bleeding
05:53
in addition repeat vital signs
05:55
demonstrated blood pressure of 80 over
05:57
40
05:57
pulse of 120 labs are also redrawn her
06:01
hemoglobin is now seven platelets are
06:04
70,000 PT is 15.5 PTT is 39 and
06:08
fibrinogen is 250 what is happening to
06:12
our patient she is hypotensive and
06:15
tachycardic her labs are consistent with
06:17
anemia and thrombocytopenia she has
06:20
evidence of coagulopathy as PT and PTT
06:22
are elevated and fibrinogen is low in
06:25
severe cases of hemorrhage is important
06:28
to consider the diagnosis of di c in d
06:30
IC the processes of coagulation and
06:33
Brunell Isis become abnormally activated
06:35
within the vasculature but what is the
06:38
underlying pathophysiology of di see the
06:41
typical sequence of events is as follows
06:43
endothelial damage may cause release of
06:46
procoagulant enzymes or phospholipids
06:48
activation of the coagulation cascade
06:49
leads to production of thrombi in the
06:51
micro vascular and/or larger vessels
06:54
extensive formation of thrombi in turn
06:56
leads to consumption of platelets
06:58
coagulant and anticoagulant factors
07:00
rapid consumption of factors outpaces
07:03
their production creating a consumptive
07:04
coagulopathy with impaired coagulation
07:08
fibrinolysis is activated at sites the
07:10
thrombus formation with generation of
07:12
fibrin degradation products such as
07:13
d-dimer large amounts of degradation
07:15
products interfere with both fibrin clot
07:18
formation and platelet aggregation
07:19
causing impaired coagulation tissue or
07:22
organ damage may result from reduced
07:23
perfusion thrombosis and or bleeding
07:26
labs demonstrated thrombocytopenia hypo
07:29
fibrinogen amia increased d-dimer’s and
07:31
prolonged PT and PTT it is important to
07:35
note that obstetric complications are
07:36
common causes of di see including
07:39
abruption and fetal demise amniotic
07:41
fluid embolism preeclampsia and help
07:43
syndrome and postpartum hemorrhage let’s
07:45
review the underlying pathophysiology in
07:47
placental abruption and fetal demise
07:49
there’s significant injury and necrosis
07:51
of fetal placental tissue increasing the
07:53
release of pro coagulants in amniotic
07:56
fluid embolism amniotic fluid rich in
07:58
procoagulant in anticoagulants is
08:00
released into the circulation
08:02
preeclampsia and help contributes to
08:04
endothelial cell damage which activates
08:06
coagulation hemorrhage can lead to shock
08:09
resulting in severe tissue hypoxia
08:11
resulting a release of tissue factor
08:12
from damaged cells the treatment of di C
08:15
is focused on correcting the underlying
08:17
cause maintenance of volume status and
08:19
supportive measures and replacement of
08:21
blood products replacement of products
08:23
is justified in patients who have
08:24
serious bleeding or at high risk for
08:26
bleeding red blood cell transfusion is
08:28
necessary for severe bleeding platelet
08:30
transfusions should be given if
08:32
platelets are less than 15,000 with
08:33
serious bleeding
08:34
coagulation factor replacement should be
08:36
given to patients with severe bleeding
08:38
who exhibits signs of coagulopathy let’s
08:40
go back to the clan cascade to see our
08:42
replacement products correct
08:43
coagulopathy fresh frozen plasma
08:45
contains fibrinogen and
08:47
coagulation factors cryoprecipitate on
08:49
the other hand has a smaller volume and
08:51
is rich and fibrinogen factors 8 and 13
08:53
as well as von Willebrand factor if I’m
08:56
Willebrand factor helps platelets adhere
08:57
to the site of injury let’s pause read
09:01
and apply if you suspect di see in a
09:05
patient what lab studies would support
09:07
this diagnosis labs consistent with di C
09:10
include increased PT and PTT and
09:13
decrease fibrinogen and platelets this
09:16
concludes the fqo basic science video on
09:18
hemorrhage in this video we covered
09:20
normal hemostasis physiologic changes
09:23
associated with coagulation during
09:25
pregnancy in the pathophysiology and
09:27
management of di sea
09:29
[Music]

00:01
hello and welcome to this aapko basic
00:04
science objective video about uterine
00:06
atony the objectives of this video are
00:08
to understand the mechanism of uterine
00:10
muscle architecture and contractility
00:12
describe how risk factors for uterine
00:14
atony interfere with myometrium
00:16
contraction appreciate the mechanism of
00:19
action and pharmacology of uterotonic
00:21
agents and describe the physiologic
00:24
mechanism by which mechanical therapy
00:26
improves uterine tone this is miss ghana
00:29
bleat alotta or miss gb and she is
00:32
pregnant with twins miss gb is in labor
00:34
and her uterus is working hard let’s
00:36
quickly review the basics before she
00:38
delivers the layers of the uterine myoma
00:41
trium are made up of millions of smooth
00:43
muscle cells they are organized in
00:45
layers which run in multiple directions
00:47
uterine smooth muscle is made up of
00:49
bundles of myocytes which are organized
00:51
to form a continuous layer and give the
00:53
uterus its contractile function there
00:56
are three layers of fibres stratum some
00:58
vascular a stratum vascular II and
01:00
stratum supra vascular II that runs
01:03
sukham French lis Lajja – de lis and
01:05
obliquely throughout the myometrium
01:08
let’s pause think and apply why is a
01:11
patient with her placenta located in the
01:13
lower uterine segment an increased risk
01:15
for uterine atony the lower uterine
01:18
segment has fewer layers of smooth
01:20
muscle to contract a slow bleeding from
01:21
the spiral arterioles following delivery
01:23
of the placenta nor is the lower uterine
01:25
segment able to generate enough force to
01:27
expel clots that have formed when blood
01:30
collects in the lower uterine segment
01:32
further distension decreases the ability
01:34
of the available actin and myosin
01:35
myofibrils
01:36
to attach and contract on a cellular
01:40
level smooth muscle contraction is
01:42
mediated by an increase in intracellular
01:43
cytoplasmic calcium this activates
01:46
myosin light-chain kinase which
01:48
catalyzes the phosphorylation of light
01:50
chain myosin phosphorylated myosin
01:53
interacts with actin and activase ATPase
01:56
ATP hydrolysis and ATPase generates
01:59
force and the muscle contracts smooth
02:02
muscle relaxation begins with the
02:04
sequestration of calcium in the
02:06
sarcoplasmic reticulum with a
02:08
dephosphorylation of myosin light-chain
02:10
bye phosphatase and inactivation of –
02:13
light chain kinase recall that the
02:16
spiral arterioles are located within the
02:18
wall of the myometrium and act to
02:20
provide circulation to the pregnant
02:21
uterus and it’s placental bed there are
02:24
on average 120 of these arterioles which
02:27
lack a muscular layer do-do and no
02:28
trophoblastic remodeling when the
02:31
placenta separates these vessels are
02:32
avulsed at the WA central site
02:35
hemostasis is achieved when the
02:37
myometrium contracts and compresses
02:38
these vessels eventually leading to
02:40
clotting and obliteration of their lumen
02:43
ms gb is slowly progressing in labor
02:46
after her pitocin was started 18 hours
02:48
ago although she has started on
02:50
antibiotics for chorioamnionitis the
02:53
babies look great and her labor course
02:55
continues right after miss GB delivers
02:58
she quickly begins hemorrhaging the
03:00
cause of the postpartum bleeding is
03:02
determined to be uterine atony but why
03:05
ever did this happen MS GP was so
03:08
healthy there are three main mechanisms
03:11
that lead to uterine atony
03:13
let’s take each one in turn the first
03:16
mechanism is over distension of the
03:18
uterus this can occur with fetal
03:20
macrosomia multiple fetuses
03:22
polyhydramnios and distension with blood
03:25
clots over distension pulls apart actin
03:29
and myosin so they cannot overlap to
03:31
connect and bind which limits the
03:32
contractile ability of the smooth muscle
03:35
the second mechanism is anaesthesia such
03:38
as halogenated agents and conduction
03:40
anesthesia that can lead to hypotension
03:43
the hypotension causes a decrease in
03:46
circulating oxytocin which decreases
03:48
uterine contraction the third mechanism
03:51
is the result of an exhausted myometrium
03:53
this can happen in the setting of a very
03:56
fast labor prolonged labor with oxytocin
03:58
stimulation and chorioamnionitis
04:01
repeated exposure to oxytocin leads to
04:04
oxytocin receptors desensitization and a
04:06
loss in capacity to respond the
04:09
pathophysiology of chorioamnionitis
04:11
leading to uterine atony is not well
04:14
understood likely that inflammation
04:17
leads to dysfunctional myometrium
04:18
contractility
04:20
it is hypothesized that the inflammatory
04:22
process consumes energy that would
04:24
otherwise be readily available for
04:26
uterine smooth muscle contraction
04:28
another hypothesis is that cytokine
04:30
induced nitric acid production inhibits
04:33
mitochondrial energy production and
04:35
impairs contractile function in myocytes
04:37
let’s pause think and apply why does
04:41
prolonged use of magnesium increase the
04:43
risk of uterine atony magnesium competes
04:46
for and blocks the calcium channels
04:48
through which calcium enters the
04:49
intracellular cytoplasm without an
04:52
increase in intracellular calcium to
04:54
activate light-chain kinase the
04:56
mechanism by which smooth muscle fibers
04:57
contract is inhibited thankfully
05:00
although Miss GB had many risk factors
05:02
such as over uterine distension with
05:04
twins and myometrium exhaustion with a
05:06
prolonged labor and chorioamnionitis
05:08
there are many medications and
05:10
procedures to help stop her bleeding
05:13
oxytocin or pitocin is used for both
05:15
prevention and treatment of postpartum
05:17
hemorrhage oxytocin is a non peptide
05:20
produced in the paraventricular nucleus
05:21
of the hypothalamus and released by the
05:24
posterior pituitary gland it can be
05:26
given intravenously or intramuscularly
05:29
however in spite of it being a first
05:31
line of therapy there is no standardized
05:33
rate or optimal dose oxytocin works by
05:36
stimulating myometrium contractility by
05:38
an increase in intracellular calcium the
05:41
rate limiting step is the number of
05:43
oxytocin receptors on the myometrium the
05:46
highest concentration is at the fundus
05:47
and the receptor concentration decreases
05:49
as you move to the lower uterine segment
05:51
and cervix IV onset is almost immediate
05:55
while IM is about three to seven minutes
05:57
the half-life is between 10 to 12
06:00
minutes and there is no difference in
06:01
the efficacy between IV and IM usually
06:05
patients do not have any side effects
06:07
from oxytocin due to its structural
06:10
similarity to vasopressin exceedingly
06:13
high doses could lead to water
06:14
intoxication hyponatremia and coma now
06:18
let’s pause think and apply in a patient
06:21
having an 18-week DNA who encounters
06:24
post abortive uterine atony why might
06:26
oxytocin not be as effective in treating
06:28
uterine atony
06:29
as it is at term
06:31
recruitment of oxytocin receptors and
06:34
the effective hypertrophy on smooth
06:36
muscle cells is sub-optimal at this
06:38
gestational age methyl ergo no vein or
06:41
mother giant is another uterotonic
06:43
commonly used for uterine atony it is a
06:46
semi-synthetic amide
06:48
ergo derivative and the usual dose is
06:51
0.2 milligrams
06:52
intramuscularly every two to four hours
06:54
it can also be given orally methyl
06:57
aergon ovine works by creating a
06:59
sustained contraction by acting as an
07:02
agonist on the 5-ht ii receptor found in
07:05
uterine smooth muscle onset of action is
07:08
usually two to five minutes for
07:09
intramuscular and five to ten for oral
07:11
administration this is a very highly
07:14
effective uterotonic a common
07:16
second-line agent systemic
07:18
vasoconstriction can lead to
07:20
hypertensive urgency especially in those
07:22
with elevated blood pressure due to
07:23
chronic HTN or preeclampsia and should
07:26
not be used in these patients similar
07:29
HTN urgency can also be seen in patients
07:31
using protease inhibitors for HIV
07:33
treatment karma Proust or Hema Bay is a
07:36
third highly effective uterotonic that
07:38
is often used if methyl Erica nouvion is
07:40
contraindicated karma Prost is an
07:43
analogue of 15 methyl prostaglandin F 2
07:45
alpha the 250 microgram dose is
07:47
administered intramuscularly and can be
07:50
repeated every 15 to 90 minutes with a
07:52
maximum of eight doses biomaterial
07:55
intracellular free calcium is increased
07:58
by prusik Landon’s and this increased
07:59
availability of calcium leads to
08:01
increased myosin light-chain kinase
08:03
activity augmenting contractile response
08:05
of the uterus to most common side
08:08
effects include diarrhea due to smooth
08:10
muscle relaxation in the
08:11
gastrointestinal system and bronchospasm
08:13
making it contraindicated in asthmatic
08:15
patients misoprostol or site attack is a
08:19
synthetic analogue of prostaglandin e1
08:21
it is a low-cost easily stored
08:24
medication that can be administered by
08:25
in many routes although not part of an
08:28
initial treatment for acne misoprostol
08:30
has a role in management especially if
08:32
other agents are not available or
08:34
contraindicated misoprostol is given in
08:37
doses of six hundred to a thousand
08:39
micrograms and almost any mucous
08:41
membrane oral buccal SLE badge
08:45
or rectal it stimulates uterine
08:47
contractions similar to oxytocin the per
08:50
oral and buccal roots have the fastest
08:52
onset of 3 to 5 minutes most side
08:54
effects are minimal such as GI upset or
08:57
transient fever in some situations such
09:00
as for MS GB uterotonic are not able to
09:03
control the uterine atony in this
09:05
scenario there are several procedures
09:07
that can also be performed to decrease
09:09
and/or stop the postpartum hemorrhage
09:11
the most common procedure performed in
09:13
the setting of uterine atony is uterine
09:15
massage
09:16
this helps to evacuate the uterus of any
09:19
clots as well as Rhea proximate
09:20
myofilaments to promote contraction this
09:23
can be done while utero tonics are being
09:25
administered another option would be a
09:27
uterine artery ligation this would
09:30
decrease the post pressure to the uterus
09:31
slow bleeding from the spiral arterioles
09:34
in the placental bed decreased blood and
09:36
clot collection in the uterus and
09:37
decrease overall distension of the
09:39
uterus similar to uterine massage by
09:42
decreasing over distension Mya filaments
09:44
are able to really tap remove muscle
09:47
contraction a b-lynch stitch causes
09:50
manual compression of the uterus which
09:52
can also aid in riah proximities smooth
09:54
muscle fibers the manual compression is
09:56
done by using sutures which go over the
09:59
uterus like suspenders the only other
10:01
option to consider short of hysterectomy
10:04
is a bakery balloon it is
10:06
counterintuitive to consider placing
10:08
something to further distend the uterine
10:10
cavity however the main role of the
10:12
balloon is to provide counter pressure
10:14
at the placental site and allow for
10:16
compression of the spiral arterioles
10:18
with eventual decrease in flow and
10:20
improve clotting and eventual hemostasis
10:22
at the site this measure can also be
10:25
used to provide time for utero tonics to
10:28
take effect thankfully from Miss GB she
10:31
had a multidisciplinary team which had
10:33
practiced to handle her obstetric
10:35
emergency she responded well to euro
10:37
tonics and by manual massage and is now
10:40
enjoying time with her two newborns
10:42
this concludes this aapko basic science
10:45
objective video about uterine atony
10:47
you should now be able to understand the
10:50
mechanism of uterine muscle architecture
10:52
and contractility describe how risk
10:54
factors for uterine atony interfere with
10:57
myometrium contraction
10:58
appreciate the mechanism of action and
11:00
pharmacology of uterotonic agents and
11:03
describe the physiologic mechanism by
11:05
which mechanical therapy improves
11:07
uterine tone thanks for watching
11:10
[Music]
11:19
[Music]
11:25
[Music]
11:37
you

00:04
Postpartum hemorrhage is a significant loss of blood after giving birth, and it’s the
00:10
number one reason for maternal morbidity and maternal death around the world.
00:15
Specifically it’s defined as losing more than 500ml of blood after a vaginal delivery
00:20
or more than 1000ml after a cesarean section delivery.
00:26
Of course, deliveries can be messy and it’s impossible to measure the precise amount of
00:29
blood that’s lost.
00:30
In addition, there’s the possibility of internal bleeding.
00:33
So additional criteria to consider for postpartum hemorrhage include a decrease of 10% or more
00:38
in hematocrit from baseline, and changes in a mother’s heart rate, blood pressure, and
00:44
oxygen saturations – all of which suggest a significant blood loss.
00:49
Significant bleeding in the first 24 hours after delivery is called primary postpartum
00:53
hemorrhage, and after that it’s called secondary, or late, postpartum hemorrhage.
00:59
The most common causes of postpartum hemorrhage can be lumped into four groups which can easily
01:04
be remembered as the “4 Ts”: Tone, Trauma, Tissue, and Thrombin.
01:12
Tone refers to a lack of uterine tone or uterine atony – basically a soft, spongy, boggy
01:19
uterus, and this is the main cause of postpartum hemorrhage, generally resulting in a slow
01:24
and steady loss of blood.
01:27
The uterus is a muscular organ wrapped by three layers of smooth muscle called the myometrium,
01:33
which contracts during labor to dilate and efface the cervix and ultimately push out
01:37
the fetus and placenta.
01:40
After delivery, the myometrium continues to contract and this squeezes down on the placental
01:45
arteries at the point where they are attached to the uterine wall, clamping them shut, thereby
01:51
reducing uterine bleeding.
01:53
The contractions continue for a few weeks after the delivery.
01:57
With uterine atony, though, the uterus fails to contract after birth, and those placental
02:02
arteries don’t clamp down, leading to excessive bleeding.
02:10
Uterine atony can be caused by several things, repeated distention of the uterus as a result
02:14
of multiple pregnancies, overstretching from twins or triplets, or any condition that causes
02:19
too much uterine stretching can interfere with efficient uterine contractions and lead
02:24
to diminished tone and eventual uterine atony.
02:29
Uterine atony can also occur when the uterine muscles fatigue during the delivery process
02:33
because of prolonged labor.
02:35
It can also occur when a woman is unable to empty her bladder, since a full bladder can
02:40
push against the uterus and interfere with uterine contractions.
02:43
Finally, some commonly used obstetric medications such as anesthetics (especially halothane),
02:50
magnesium sulfate, nifedipine, and terbutaline can all interfere with uterine contractions
02:57
and increase the risk of uterine atony.
03:01
Uterine atony can be treated by fundal massage, massaging the fundus – the upper section
03:06
of the uterus which is typically near the umbilicus right after birth.
03:10
Fundal massage causes the smooth muscle in the wall uterine wall to contract and harden.
03:15
If a full bladder seems to be interfering with contractions, a woman can urinate or
03:20
have a catheter placed if she’s unable to void by herself.
03:24
Medications to help firm up the uterus can also be given, and if necessary, the bleeding
03:28
may be stopped surgically.
03:30
Alright the next ‘T’, trauma, refers to damage to any of the genital structures – the
03:36
uterus, cervix, vagina, or perineum.
03:40
This can include the incision from a cesarean delivery, incidental trauma from a baby coming
03:45
through the vaginal canal, or trauma from instruments used in the delivery.
03:50
For example, the use of forceps, vacuum extraction, or an episiotomy, a small cut used to enlarge
03:56
the vaginal opening, can all cause unintended bleeding.
04:01
Sometimes the bleeding is in a concealed location and a hematoma can form and go unnoticed for
04:08
hours after delivery.
04:11
A key to recognizing a hematoma is severe pain and persistent bright red vaginal bleeding
04:16
in spite of a firmly contracted uterus.
04:20
In general, any trauma-related bleeding is an emergency and the site of bleeding has
04:24
to be repaired right away – generally by applying pressure and stitching lacerations.
04:33
Tissue refers to placental fragments retained in the uterine cavity.
04:36
The entire placenta normally separates from the uterine wall in the third stage of labor,
04:42
but occasionally a part of the placenta remains behind in the uterus.
04:46
In placenta accreta, the placenta invades the myometrium so it doesn’t easily separate
04:51
from the uterus.
04:54
Placenta accreta or simply too much traction on the umbilical cord can both cause the placenta
04:58
to be retained.
05:00
This in turn prevents effective uterine contractions, and leads to uterine atony.
05:08
The goal here is to prevent this from happening in the first place by making sure that the
05:11
placenta comes out completely intact, and removing any tissue that does get retained
05:16
as soon as possible.
05:19
Thrombin, the final T, refers to the mother having some condition that prevents blood
05:25
clots from forming normally – for example, a genetic disorder like von Willebrand disease
05:30
or an obstetric condition like eclampsia and placental abruption which may result in a
05:35
clotting disorder, the most dangerous of which is disseminated intravascular coagulation
05:40
or DIC.
05:42
These are conditions that prevent a clot from forming normally when there’s a bleed, and
05:46
this can make even a tiny bleed into a serious problem since it won’t easily stop.
05:51
The treatment for each of these is specific to the specific underlying cause.
05:58
Postpartum hemorrhage is an obstetric emergency and maintaining adequate circulating volume
06:03
is a key priority.
06:05
Regardless of the cause, intravenous fluids and blood products may be used to ensure that
06:09
the vital organs are well perfused.
06:13
As a quick recap, postpartum hemorrhage is the most common cause of maternal morbidity
06:17
and mortality around the world, and the causes are the 4 T’s: Tone (atony), Trauma, Tissue,
06:24
and Thrombus (coagulopathy).
06:25
The most common cause – uterine atony – can usually be managed with fundal massage and
06:31
medications to help the uterus contract.

00:14
follow an escalating sequence of actions
00:17
to control postpartum hemorrhage but
00:20
whenever blood loss is significant call
00:22
for additional personnel give IV fluid
00:25
resuscitation and test for coagulopathy
00:28
first give oxytocin and do uterine
00:30
massage routine measures done after
00:33
placental delivery to increase uterine
00:35
tone particularly a funeral tone is poor
00:38
give a second drug to increase uterine
00:41
tone and check for and remove retained
00:43
products of conception particularly a
00:46
few Turan tone is good look for and
00:49
repair bleeding vaginal lacerations
00:51
cervical lacerations are both then if
00:55
needed tamponade the uterus using a
00:57
balloon or gloss packing if bleeding
01:01
persists do a laparotomy to place
01:03
uterine compression sutures removed
01:06
retained products of conception or both
01:08
as a last resort do arterial
01:11
embolisation or ligation or hysterectomy
01:19
if postpartum hemorrhage is significant
01:23
call for additional nursing assistance
01:25
and notify anesthesia due volume
01:28
resuscitation as for other causes of
01:30
hemorrhage as needed with significant
01:33
hemorrhage send labs considering
01:36
disseminated intravascular coagulation
01:38
as well as inherited coagulopathy lay up
01:41
tests should include fibrinogen level as
01:44
well as CBC with platelets PT and PTT
01:48
and type and screen for possible
01:50
transfusion next address the source of
01:53
bleeding most commonly uterine atony
01:56
during delivery of the placenta oxytocin
02:00
is given routinely ideally as an
02:02
infusion using 20 units and 1 liter of
02:04
IV normal saline solution or another
02:07
crystalloid solution beginning at 10
02:09
milliliters per minute which is 600
02:11
milliliters per hour
02:13
you may increase the rate to give as
02:15
much as 500 milliliters over 10 minutes
02:18
uterine fungal massage is also done
02:20
routinely after delivery of the placenta
02:22
if bleeding persists despite these
02:25
routine measures due by manual uterine
02:28
massage simultaneously rubbing the
02:30
uterine fundus and anterior vaginal
02:32
fornix use a sterile glove on your
02:34
inside hand give a second uterotonic
02:37
drug two of the choices are
02:39
intramuscular injections intramuscular
02:42
choices include methyl ergo Naveen 0.2
02:46
milligrams or one milliliter unless the
02:50
woman has hypertension and 16 methyl
02:53
prostaglandin F 2 alpha 250 micrograms
02:57
unless the woman has asthma an
02:59
alternative is rectal miss approach tall
03:01
800 to 1000 micrograms
03:04
kharbut Osen 100 micrograms IV is an
03:08
alternative prostaglandin that is more
03:10
heat stable than 16 methyl prostaglandin
03:14
f2 alpha but is not available in the
03:17
United States because Carbet Osen can be
03:20
used without having been refrigerated as
03:22
can miss a pro stall these drugs can
03:25
often be given in resource-poor areas
03:28
consider retained products of conception
03:30
as a cause if uterine atony
03:33
persists
03:35
if bleeding persists particularly if the
03:38
uterus is firm consider a vaginal or
03:41
cervical laceration so look for and
03:43
repair these be sure to examine the
03:46
patient with proper positioning and
03:47
lighting have an assistant use
03:49
retractors if necessary also
03:52
particularly if the uterus is not firm
03:55
palpate inside the uterus for retained
03:57
products of conception and remove them
03:59
do ultrasound agree if you are unsure
04:01
whether retained products are present if
04:04
measures thus far failed to slow
04:07
bleeding begin full bore volume
04:09
resuscitation has done for other causes
04:11
of hemorrhage replace intravascular
04:13
volume first using crystalloid up to two
04:16
liters
04:16
if further volume is needed Francie’s
04:20
packed red blood cells also insert a
04:23
bladder catheter to monitor urine output
04:25
and closely monitor heart rate and blood
04:27
pressure gather equipment to do uterine
04:30
tamponade to tamponade the uterus insert
04:34
an intrauterine balloon which must be
04:36
placed and filled using ultrasonographic
04:39
guidance the balloon tip should be close
04:41
to the uterine fundus fill a balloon
04:44
with saline until bleeding is controlled
04:45
or the capacity of the balloon is
04:47
reached this commercially available
04:49
Bakri balloon can hold 300 to 500
04:53
milliliters vaginal packing may be
04:55
needed to hold the balloon in place
04:57
remove the balloon gradually and within
05:00
24 hours if a balloon cannot be used use
05:05
ring forceps to pack the uterus with
05:07
gauze
05:09
if significant hemorrhage persists treat
05:12
operatively usually first trying
05:14
compression sutures however before
05:17
placement compressed the uterus manually
05:19
to ensure that the bleeding stops when
05:21
the uterus is compressed
05:23
if retained products of conception or
05:26
intrauterine clots are possible do a
05:28
history Tommy and completely evacuate
05:30
the uterus manually this uterus shows a
05:34
history Tommy incision use a rapidly
05:37
absorbable suture such as 2o chromic on
05:40
a large curved needle various
05:43
compression sutures are effective some
05:46
are shown in this figure the most
05:48
commonly used compression sutures are
05:50
the B Lynch and as shown here the
05:52
modified B Lynch sutures place the
05:56
needle into the uterine cavity at the
05:57
lateral edge of the lower anterior
05:59
uterus and then out the other side do
06:02
this below the histor atomy incision if
06:05
there is one now put the needle in and
06:08
then out of the top of the uterine
06:10
fundus
06:12
next insert the needle and move it from
06:14
one side to the other
06:15
on the lower posterior uterus
06:22
take another bite at the top of the
06:24
fundus
06:27
finish the modified b-lynch suture by
06:30
taking a bite similar to the first one
06:32
but on the opposite lateral side
06:38
cut the needle from the suture tie the
06:42
suture closed an assistant should
06:45
simultaneously compress the uterus
06:49
either after or before doing the
06:51
compression suture close the histor
06:53
atomy incision begin with an anchor
06:56
suture at one end of the histor otta me
07:05
you
07:12
complete the closure using a running
07:14
locked suture
07:21
you
07:23
when finished cut and tie in the usual
07:26
fashion
07:32
you
07:35
put the sutured compressed uterus back
07:37
into the abdominal cavity if bleeding
07:40
persists despite all the described
07:42
interventions options include uterine
07:45
artery ligation hypogastric artery
07:48
ligation arterial embolisation by
07:51
interventional radiology and ultimately
07:53
hysterectomy