OBSTETRICAL

EMERGENCIES

IMS Murah Manoe

 EMERGENCIES

BLEEDING
UMBLICAL CORD PROLAPS
SHOULDER DYSTOCIA
AMNIOTIC FLUID EMBOLISM
UTERUS INVERSION
Fetal distress
SHOCK
SEPSIS
Bleeding Prepartal /Antepartum
bleding

 Placenta praevia - Polyp

 Placental - E rosio portionis
Abruption - Trauma
 Uterine rupture - Dehiscence of
cesarean scar
- Carcinoma
 PLACENTA PRAE VIA

 The placenta covers the internal cervical

os completely or partially:
Placenta praevia totalis
Placenta praevia partialis
Placenta praevia marginalis
 0.5% -1% of all births.
 Risk factors : previous cesarean section (x
6)- Multiparity(x 2.6) –previous D&C-
S moking
 PLACENTA PRAE VIA

 Manifestations: painless bleeding of

maternal origin
 Diagnosis:1. S onography
2.If cervical os dilated
cautious inspection
 Risks: placental abruption,Anomalies of
fetal presentation,postpartal
bleeding
 Management: Bed rest, Anti-D and
Thrombosis prophylaxis
 PLACENTA PRAE VIA
DE LIVE RY MODUS
 Practically all women do need cesarean section.
 There are four different constellations:
1.The fetus is preterm and there is no
indication for delivery.(observe)
2.The fetus is mature and the bleeding does not
stop.(cesarean S )
3.The patient is in labor (cesarean S )
4.The bleeding severe,and the fetus immature
(cesarean S ection )
PLACE NTA PRE V.TOTALIS
PLACE NTA PRAE VIA
PLACE NTA PRE V. PARTIALIS
PLACENTA PRE V.MARGINALIS
 PLACENTAL ABRUPTION

 One of the leading causes of the perinatal

mortality
 Incidence: 0.5% - 1% of all deliveries
 Pathophysiology: The villi are seperated
from decidua basalis due to:
 Abdominal trauma
 Hypoxia & Ischemia
 Infections
 CLINICAL STAGING

 Grade 0: asymptomatic;diagnosis often

postnatal or by sonography
 Grade 1 :scant external & internal bleeding.No
maternal circulatory changes;No fetal distress.
 Grade 2 :heavy bleeding (external –internal)
F etal distress (CTG )
 Grade 3 :severe external & internal bleeding.The
uterus very painfull; fetal demise;maternal shock
in 30% of cases associated with coagulation
disorders.
 RIS KFACTORS :

I. Previous abruption (x 10)

II. Myoms
III. Uterusseptum
IV. Maternal diseases: Hypertension,
Thrombophilia , Hyperhomocysteinemia
V. Abnormal Placentation :for example: Plac.
Circumvallata
VI. Nicotine & Cocaine Abuse
VII. Blunt Abdominal Trauma
 ABRUPTIO PLACENTAE
DIAGNOSIS
 Painfull vaginal bleeding

 Tetanic contractions of uterus

 Pathological CTG

 S onography: ( S ensitivity : 50%)

 ABRUPTIO PLACENTAE
MANAGEMENT
 No symptoms(no bleeding ) :observe the mother
and the fetus .
 S evere bleeding +the fetus is alive: Cesarean
section.
 Clinical symptoms (bleeding)+the fetus is dead :
Amniotomy +packed red cells+coagulation
factors +labor induction (vaginal birth),but if the
bleeding too severe then cesarean section
PLACENTA CIRCUMVALLATA
Risk factor for pl.abruption
PLACENTA CIRCUMVALLATA
 BLE E DING INTRAPARTAL/
Intra partum bleeding
 BLOODY S HOW

 VAS A PR AE VIA

 INS E R TIO VE LAME NTOS A

 ABR UPTIO PLACE NTAE

 UTE R INE R UPTUR E

 VASA PRAE VIA
Think of it if bleeding occurs
after Amniotomy!!!
 INSE RTIO VE LAMENTOSA
May cause intrapartal bleeding
INS E RTIO VE LAME NTOS A
PLACENTA BILOBATA
A RISK FACTOR
 UTRINE RUPTURE
 Definition :
 Uterine rupture during pregnancy is a rare
occurrence that frequently results in life-
threatening maternal and fetal
compromise, whereas uterine scar
dehiscence is a more common event that
seldom results in major maternal or fetal
complications.
 Uterine rupture
 Uterine rupture in pregnancy is a rare and
often catastrophic complication with a high
incidence of fetal and maternal morbidity
 Incidence of uterine rupture is low.
 1 in 1514 pregnancies (0.07%).
 The initial signs and symptoms typically
nonspecific, a condition that makes
diagnosis difficult, which sometimes
delays definitive therapy
 Uterine rupture
 From the time of diagnosis to delivery,
only 10-37 minutes are available before
clinically significant fetal morbidity
becomes inevitable.
 Fetal morbidity invariably occurs because
of catastrophic hemorrhage, fetal anoxia,
or both..
 Uterine rupture is associated with clinically
significant uterine bleeding; fetal distress;
expulsion or protrusion of the fetus,
placenta, or both into the abdominal cavity;
and the need for prompt cesarean
delivery, uterine repair, or hysterectomy.
 Incidence and risk factors
 Congenital uterine anomalies, multiparity,
previous uterine myomectomy, the
number and type of previous cesarean
deliveries, fetal macrosomia, labor
induction, uterine instrumentation, and
uterine trauma
 All increase the risk of uterine rupture,
whereas previous successful vaginal
delivery and a prolonged interpregnancy
interval after a previous cesarean delivery
Major patient characteristic categories for
determining risk of uterine rupture:
 Uterine status
 Native (unscarred)
 S carred
 Previous cesarean delivery
 Single low transverse (further subcategorized by 1-layer
or 2-layer hysterectomy closure)
 Single low vertical
 Classic vertical
 Multiple previous cesarean deliveries
 Previous myomectomy
 Transabdominal
 Laparoscopic
 Uterine configuration
 Normal

 Congenital uterine anomaly

 Pregnancy considerations
 Grand multiparity

 Maternal age

 Placentation (accreta, percreta, increta, previa,

abruption)
 Cornual (or angular) pregnancy

 Overdistension (multiple gestation, polyhydramnios)

 Dystocia (fetal macrosomia, contracted pelvis)

 Trophoblastic invasion of the myometrium

(hydatidiform mole, choriocarcinoma)
 Previous pregnancy and delivery history
 Previous successful vaginal delivery

 No previous vaginal delivery

 Interdelivery interval

 Labor status
 Not in labor

 Spontaneous labor

 Induced labor

 With oxytocin

 With prostaglandins

 Augmentation of labor with oxytocin

 Duration of labor

 Obstructed labor
 Obstetric management considerations
 Instrumentation (forceps use)

 Intrauterine manipulation (external cephalic version,

internal podalic version, breech extraction, shoulder
dystocia, manual extraction of placenta)
 Fundal pressure

 Uterine trauma
 Direct uterine trauma (motor vehicle accident, fall)

 Violence (gunshot wound, blunt blow to abdomen)

The normal, unscarred uterus is least
susceptible to rupture.
 Grand multiparity, neglected labor,
malpresentation, breech extraction, and
uterine instrumentation are all
predisposing factors for uterine rupture
 Oxytocin augmentation and induction of
labor in the unscarred uterus
 Congenital uterine anomalies
 Signs and S ymptoms of
Uterine Rupture During
Pregnancy
 Largely depend on the timing, site, and
extent of the uterine defect.
 Uterine rupture at the site of a previous
uterine scar is typically less violent and
less dramatic than a spontaneous or
traumatic rupture because the scar is
relatively avascular
 The classic signs and symptoms of
uterine rupture are :
 fetal distress (as evidenced most often by
pattern of abnormalities in fetal heart rate/
fetal bradycardias ), diminished baseline
uterine pressure, loss of uterine
contractility, abdominal pain, recession of
the presenting fetal part, hemorrhage, and
shock.
 DIAGNOS IS
 Uterine rupture is most appropriately diagnosed
on the basis of standard signs and symptoms

 S everal reports have suggested that

transabdominal, transperineal, transvaginal, or
sonohysterographic ultrasonography may be
useful for detecting uterine-scar defects after
cesarean delivery.
 In a study of 722 women, Gotoh et al
reported that a cervical wall thinner than 2
mm, as determined with usg performed
within 1 week of delivery, significantly
increased the risk of uterine rupture.
Positive and negative predictive values
were 73.9% and 100%, respectively.
 Fetal and neonatal
consequences of uterine
rupture
 Fetal hypoxia or anoxia
 Fetal acidosis
 Admission to a neonatal intensive care
unit
 Fetal or neonatal death
 Maternal consequences of
uterine rupture
 Maternal bladder injury
 Severe maternal blood loss or anemia
 Hypovolemic shock
 Need for hysterectomy
 Maternal death Maternal death as a
consequence of uterine rupture occurs at
a rate of 0-1% in modern developed
nations, but the mortality rates in
developing countries are 5-10%.
Management of the Ruptured
Uterine Treatment
 The most critical aspects of treatment in
the case of uterine rupture are
establishing a timely diagnosis and
minimizing the time from the onset of
signs and symptoms until the start of
definitive surgical therapy.
 Once a diagnosis of uterine rupture is
established, the immediate stabilization of
the mother and the delivery of the fetus
are imperative
 After the fetus is delivered, the type of
surgical treatment for the mother should
depend on the following factors:
 Type of uterine rupture
 E xtent of uterine rupture
 Degree of hemorrhage
 General condition of the mother
 Mother's desire for future childbearing
 Uterine bleeding is typically most profuse when
the uterine tear is longitudinal rather than
transverse.
 Hysterectomy should be considered the
treatment of choice when intractable uterine
bleeding occurs or when the uterine rupture
sites are multiple, longitudinal, or low lying.
 As a rule, the time available for successful
intervention after frank uterine rupture and
before the onset of major fetal morbidity is only
10-37 minutes
 Because of the short time available for
successful intervention, the following 2 premises
should always be kept firmly in mind:
 (1) Maintain a suitably high level of suspicion
regarding a potential diagnosis of uterine
rupture, especially in high-risk patients.
 (2) When in doubt, act quickly and definitively
 PRE VE NTION
 The absolute risk of uterine rupture in
pregnancy is low, but it is highly variable
depending on the patient subgroup

 The most direct prevention strategy for

minimizing the risk of pregnancy-related
uterine rupture is to minimize the number
of patients who are at highest risk
The categories of patients that exceed this critical
value are those with the following:

 S everal previous cesarean deliveries

 Previous classic midline cesarean delivery
 Previous low vertical cesarean delivery
 Previous low transverse cesarean delivery with a
single-layer hysterotomy closure
 Previous cesarean delivery with an interdelivery
interval of less than 2 years
 Previous low transverse cesarean delivery with a
congenitally abnormal uterus
 Previous cesarean delivery without a previous
history of a successful vaginal birth
 Previous cesarean delivery with either labor
induction or augmentation
 Previous cesarean delivery in a woman carrying a
macrosomic fetus who weighs more than 4000 gr
 Previous uterine myomectomy accomplished by
means of laparoscopy or laparotomy
 Conclusion
 Uterine rupture is a rare but often catastrophic
obstetric complication
 The vast majority of uterine ruptures occur in
women who have uterine scars, most of which
are the result of previous cesarean deliveries. A
single cesarean scar increases the overall
rupture rate to 0.51%, with the rate for women
with 2 or more cesarean scars increasing to 2%
 S urgical intervention after uterine rupture in less
than 10-37 minutes is essential to minimize the
risk of permanent perinatal injury to the fetus. .
 Conclusion
 The most consistent early indicator of uterine rupture is
the onset of a prolonged, persistent, and profound fetal
bradycardia. Other signs and symptoms of uterine
rupture, such as abdominal pain, abnormal progress in
labor, and vaginal bleeding, are less consistent and less
valuable than bradycardia in establishing the appropriate
diagnosis.
 The general guideline that labor-and-delivery suites
should be able to start cesarean delivery within 20-30
minutes of a diagnosis of fetal distress is of minimal
utility with respect to uterine rupture
 Postpartal / Postpartum
Bleeding
 ACCOR DING TO WHO: WOR LDWIDE ONE
WOMAN DIE S PR O MINUTE DUE TO
POS TPAR TAL BLE E DING.
 BLE E DING MOR E THAN 500 ml IN THE F IR S T
24 HOUR S AF TE R LABOR .
 THINK OF 4 T,s :TONUS -TIS S UE -
TR AUMA-THR OMBIN.
 LATE S Y MPTOMS DUE TO PR E GNANCY
CHANGE S OF BLOOD VOLUME .
 WHO:WOR LD HE ALTH OR GANIS ATION
 TONUS
If the uterus not contracted,the
blood vessels are not
compressed
 TISSUE
(PLACENTA RE ST)
 TRAUMA
CE RVIX TE AR
 POSTPARTAL BLE E DING
MANE GEMENT
 LAR GE BOR E VE NOUS CATHE TE R
 UTE R OTONICA(Methergin-Oxytocin)
 MAS S AGE THE UTE R US
 BIMANUAL COMPR E S S ION
 VOLUME S UBS TITUTION
 S PE CULUM: CE R VIX OR VAGINAL TE AR ?
 PLACE NTAL TIS S UE ? CUR E TTAGE
 NO INJUR Y :LAPAR ATOMY -LIGATION OF THE
UTE R INE AR TE R Y -ILIACA INTE R NA
 ULTIMA R ATIO : HY S TR E CTOMY
BIMANUAL COMPRE S S ION
 S HOCK
 S hock is the reversible phase of death.
 Circulatory failure characterized by
disorder of microcirculation.
 Centralisation results in hypoxia.
 Hypoxia causes acute tubular necrosis
and endothelium injury of pulmonary
capillary vessels that in turn causes renal
failure and adult respiratory distress
syndrome(ARDS ) .
 SHOCK FORMS

 HY POVOLUE MIC

 CAR DIAL

 ANAPHY LACTIC

 NE UR OGE NIC

 S E PTIC
 SHOCK MANAGEMENT
HYPOVOLUMIC
 DO NOT FOR GE T :THE TIME IS GOLD
IN THE E AR LY S TAGE S THE S HOCK
CAN BE MANAGE D E F F E CTIVE LY WITH
S IMPLE ME AS UR E S :INFUS IONS BUT IN
THE ADVANCE D S TAGE S YOU MAY
NE E D CONS IDE R ABLY MORE ;A LONG
TIME IN INTENS IVE CAR E UNIT AND
VE R Y HIGH COS TS .
AMNIOTIC FLUID E MBOLIS M
 R are: 1:8,000 to 1:30,000 labors
 Very high Mortality
 Misnomer: false name, because it is an
 Anaphylactic reaction to the fetal antigens.
 Mainly subpartu : under delivery
 R isk factors : Multiparity, Abruptio
placentae,Blunt Abdominal Trauma E xternal
version ,fetal death, Amniocentesis
AMNIOTIC FLUID E MBOLIS M
 Manifestations: R igors,Perspiration,
R estlessness , Coughing , Cyanosis,
Hypotension, Bronchospasm, Tachypnea ,
Tachycardia , Arrhythmia,Convultions,
Myocardial infarkt, DIC
 Diagnosis: Clinical manifestations+chest X-R ay
+E CG +Blood gas analysis
 Therapy: Intensive Care Unit.
 NOTICE : S UDDE N COUGHING ATTACK
AF TE R CE S AR E AN OR VAGINAL
BIR TH.
 Umbilical cord prolaps
 Define the key terms: cord prolaps.
 Identify risks factors of cord prolaps.
 Understand the current intervention to
treat cord prolaps.
 Discuss the nursing care and treatment for
women experienced cord prolaps,
 Definition
 If the umbilical cord presents in front of
the fetal presenting part and the
membranes rupture, the risk that the cord
will prolapse through the cervix into the
vagina is significant.
 UMBILICAL CORD PROLAPS
 Incidence: 0.2% -0.6%of births
 Risk factors : long umblical cord,breech
+transverse lie, small fetus ,multiparity
,twins ,amniotomy
 ATTENT ION:
CTG changes after amniotomy are
suspect of umblical cord prolaps until
the contrary is proven.
 Causes include

- abnormal presentation
- a long umbilical cord
- polyhydramnios
- prematurity
- an unengaged presenting part.
As a result, oxygen and blood supplies to
the fetus are diminished or cut-off and the
baby must be delivered quickly.
 UMBILICAL CORD PROLAPS

 DIAGNOS IS : Inspection +Palpation

 MANAGE MENT :
Determine if the fetus is alive:
1. YE S : elevate the presenting
part and cesaraen section
2. NO: labor induction

During labor : FHR bradycardia

 Nursing Intervention for
Prolapsed Cord
 Position change, trendelenburg or
modified sims position, the knee-elbow
position
 S terile towel wrap the cord
 Oxygen 8-10 L/min
 IV fluid
 Monitoring FHR
 Do not place cord back into cervix
 Prepare emergency birth (vaginal or
cesarean)
 If attempts to deliver the baby prompty fail,
the fetus' air and blood supply are
occluded and brain damage or death will
occur
UMBILICAL CORD PROLAPS
UMBILICAL CORD PROLAPS
 S HOULDE R DYS TOCIA
 INCIDE NCE :0.2 %of all births,increases
however to 10% if the fetus weighs 4000 G and
even to 22% if the fetus weighs more than
4500G.

 R IS K F ACTOR S : Makrosomia
Previous dystocia
Overweight mother
Multyparity
Diabetes mellitus
 S HOULDE R DYS TOCIA
 THE FE TAL HE AD IS BOR N.
 AFTE R THE CONTR ACTION CE AS E S ,THE FE TAL
HE AD S LIPS BACK INTO THE VAGINA.
(TUR TLE PHENOMENE N).
 BLUE LIVID COLOR OF THE FACE .
 THIS DIS COLOR ATION IS CAUS E D BY VE NOUS
CONGE S TION AND IS NOT DUE TO HYPOXIA,
 THE R E F OR E :
NO HAS TINE S S ,DO NOT ENDANGE R THE FE TUS
THR OUGH UNWISE HAS TY ACTIONS.
SHOULDE R DYSTOCIA
MANAGEMENT
 McR oberts maneuver:
1.flexing the thighs
sharply up onto the
abdomen.
2.suprapubic
pressure.
SHOULDE R DYSTOCIA
MANAGEMENT
 Woods Maneuver:
the posterior shoulder
is rotated 180
degrees in a
corkscrew manner so
that the anterior
shoulder is released.
SHOULDE R DYSTOCIA
MANAGEMENT
 Delivery of the
posterior shoulder.
Jacqumiere
Maneuver.
SHOULDE R DYSTOCIA
MANAGEMENT
R UBIN MANE UVE R :
THE IMPACTE D
ANTE R IOR
S HOULDE R IS
R OTATE D IN
ABDOME N
DIR E CTION.
 SHOULDE R DYSTOCIA
MANAGEMENT
 If no success after all of the mentioned
maneuvers ,then : 1.Fracture
of the clavicula (upward direction).
2.Zavanelli maneuver: put the fetal head
into the vagina and cesarean section.
3.Abdominal Rescue after O,Leary &
Cuva.
Abdominal Rescue

 If you are not able to

put the fetal head into
the vagina then:
 Lap+uterotomy
:release the impacted
anterior shoulder
abdominally,and the
posterior shoulder
vaginal and deliver
the fetus vaginally.
 Complication
 There are two major types of brachial plexus
injury: E rb palsy and Klumpke palsy.
 E rb palsy, the more commonly occurring of the
two forms of brachial plexus injury, involves the
upper trunk of the brachial plexus (nerve roots
C5 through C7).
 This palsy affects the muscles of the upper arm
and causes abnormal positioning of the scapula
called "winging".
 Cont …
 Klumpke palsy involves lower trunk
lesions from nerve roots C7, C8, and T1.
 In this injury the elbow becomes flexed
and the forearm supinated (opened up,
palm-upwards) with a characteristic
clawlike deformity of the hand. S ensation
in the palm of the hand is diminished.
UTE RUS INVE RS ION
 IF THE F UNDAL
PLACE NTA IS
PULLE D OUT
INCAUTIOUS AND
F OR CE F ULLY .
UTE RUS INVE RS ION
 UTE RUS INVE RS ION
 Rare: 1 /2000 -1/20,000
 Can results in death due to vasovagal
shock and massive bleeding.
 Can be complete or partial.
 If the blood loss does not correspond to
the shock symptoms think of the partial
form.
 RE POS ITION OF INVE R S ION :
IN GENE R AL ANE S THE S IA
 RE POS ITION of INVE RS ION
 IF THE PLACE NTA IS S TILL ATTACHE D DO
NOT R E MOVE IT.
 MANUAL R E POS ITION OF UTE R US ;
THE HAND R E MAINS IN THE UTE R US UNTIL
IT IS E F F E CTIVLY CONTR ACTE D.
 IF THE R E POS ITION IS NOT POS S IBLE ,
THE N R E MOVE THE PLACE NTA.
(DANGE R OF HE AVY BLE E DING) AND TR Y
TO R E POS E THE UTE R US .
 AS ULTIMA R ATIO :HYS TR E CTOMY
RE POS ITION OF UTE RUS
 S epsis
 Definisi
 Infeksi adalah reaksi inflamasi yang disebabkan oleh
adanya mikroorganisme atau invasi organ steril oleh
mikroorganisme.
 2. Bakteriemia adalah adanya bakteria dalam darah.
 3. Systemic Inflamatory Response Syndrome ( S IR S )
adalah reaksi inflmasi sebagai reaksi terhadap adanya
berbagai penyakit/ kondisi dengan diagnosis seperti
telah disebutkan diatas.
 4. S epsis ( SIR S + infeksi ) adalah SIR S yang
disebabkan oleh faktor infeksi.
 5. S epsis berat / severe sepsis adalah sepsis dengan
tanda - tanda disfungsi organ atau penurunan perfusi
organ ( asidosis laktat, oliguri < 30 ml/jam atau 0,5
ml/kg berat badan/jam, hipotensi < 90 mmHg, atau
penurunan > 40 mmHg ) dan perubahan mental.
 6. Syok septik adalah sepsis berat dan hipotensi yang
persisten, meskipun telah diberikan cairan yang
adekuat, dan setelah menyingkirkan penyebab hipotensi
yang lainnya.
 7. Sindrom disfungsi organ multipel ( MODS ) adalah
adanya gangguan fungsi multi organ pada pasien
dengan sakit berat akut dimana hemostasis tidak dapat
dipertahankan tanpa intervensi
 Terapi harus dimulai secara agresif dan adekuat dalam
waktu kurang dari 6 jam. Patokan yang disebut
dengan”early goal directed therapy” telah terbukti dapat
mPendekatan tersebut terdiri dari pemberian cairan intra
vena, peningkatan pemberian oksigen, pemberian obat
obat vasopresor, pemberian obat - obat inotropik,
pemberian tranfusi darah, pemberian ventilasi mekanik,
dan pemakaian kateter arteri.
Pendekatan ini bertujuan untuk melakukan penyesuaian
kembali, cardiac preload, afterload dan kontraktilitas
jantung untuk tujuan akhir yaitu tercapainya
keseimbangan antara oxygen delivery dan oxygen
demand.
 TE RAPI
A ANTIBIOTIKA
B. CAIR AN MAP
C. Pengobatan Mencegah Gagal Nafas
D. Pemberian kortikosteroid
Meskipun masih kontroversi penggunaan kortikosteroid
dosis kecil jangka panjang menunjukkan perbaikan
hemodinamik dan menurunkan kebutuhan obat
vasopressor serta menurunkan secara bermakna angka
kematian pasien di ruang intensif serta mengurangi hari
rawat pasien.
C. Pengobatan mencegah gagal nafas
 Mekanikal :

 Kapasitas Vital < 15 mL/kg

 Maternal inspiratory force (MIF) < - 25 cm H20

 Frekuensi nafas > 35 kali/menit

 Oksigenasi :

 Pa 02 < 70 mmHg dengan FiO2 0,4

 P(A-a)02 > 350 mmHg dengan FiO2 1,0

 Ventilasi :

 Pa CO2 > 55 mmHg (pada keadaan akut)

 Dead space/ tidal volume ( Vd/Vt > 0,6)

 4. End Respiratory lung inflation inadequate for

adequate gas exchange.


E PE MBE R IAN ANTIKOAGULAN
F PE ENG ENDALIAN GULA DARAH
G.Penatalaksanaan koagulasi intravaskuler
diseminata
H.Pengakhiran kehamilan
YOU WILL REMEMBE R A LITTLE
OF WHAT YOU HE AR,SOME OF
WHAT YOU
RE AD,CONSIDE RABLY MORE
OF WHAT YOU SE E ,BUT
ALMOST ALL OF WHAT YOU
UNDE RSTAND.