3. OBSTETRICAL EMERGENCY MEANS IMMEDIATE
MANAGEMENT IS REQUIRED INCLUDING
EARLY DETECTION AND PROMPT ACTION
FOR BETTER
OUTCOME OF PREGNANCY.
4. âĸ 1. VASA PRAEVIA.
âĸ 2. PRENSENTATION AND PROLAPSE OF THE UMBILICAL
CORD.
âĸ 3. SHOULDER DYSTOCIA.
âĸ 4. RUPTURE OF THE UTERUS.
âĸ 5.AMNIOTIC FLUID EMBOLISM.
âĸ 6.ACUTE INVERSION OF THE UTERUS.
âĸ 7.SHOCK IN OBSTETRICS.
âĸ 8. DIC
THE IMPORTANT EMERGENCY
CONDITIONS IN
OBSTETRICS
7. VASA PREVIA
INCIDENCE
The actual incidence is extremely difficult to
estimate, it appears that vasa previa
complicates approximately 1 in 2,500 births.
8. ī It is an abnormality of the cord that occurs when
one or more blood vessels from the umbilical
cord or placenta cross the cervix but it is not
covered by Whartonâs jelly.
ī This condition can cause hypoxia to the baby
due to pressure on the blood vessels.
ī It is a life threatening condition.
9.
10.
11. ETIOLOGY
These vessels may be from either
ī Velamentous insertion of umbilical cord
ī placental lobe joined to the main disk of the
placenta.
ī Low-lying placenta
ī Previous delivery by C-section.
12. SYMPTOMS
ī The babyâs blood is a darker red color
due to lower oxygen levels of a fetus
âĸ Fetal distress can be seen.
ī Sudden onset of painless vaginal
bleeding, especially in their second and
third trimesters
ī If very dark burgundy blood is seen
when the water breaks, this may be an
indication of vasa previa
14. MANAGEMENT
Antepartum
ī The patient should be monitored closely for
preterm labor, bleeding or rupture of
membranes.
ī Steroids should be administered at about 32
weeks.
ī Hospitalization at 32 weeks is reasonable .
ī Take patient for emergency cesarean
section if membranes are ruptured.
ī Fetal growth ultrasounds should be performed
at least every 4 weeks.
ī Cervical length evaluations may help in
assessing the patient's risk for preterm delivery
or rupture of the membranes
15. Intrapartum
ī The patient should not be allowed to labor. She
should be delivered by elective cesarean at about
35 weeks.
ī Delaying delivery until after 36 weeks increases the
risk of membrane rupture.
ī Care should be taken to avoid incising the fetal vessels
at the time of cesarean delivery.
ī If vasa previa is recognized during labor in an
undiagnosed patient, she should be delivered by
emergency cesarean. The placenta should be
examined to confirm the diagnosis.
16. Postpartum
ī Routine postpartum management
as for cesarean delivery.
ī If the fetus is born after blood loss,
transfusion of blood without delay
may be life-saving.
ī It is important to have O negative
blood or type-specific blood
available immediately for neonatal
transfusion
17. NURSINGMANAGEMENT
ī Assess bleeding, color, amount
ī Administer iv fluids.
ī Administer oxygen.
ī Strict vitals and FHS
monitoring.
ī Prepare patient for caesarean
section.
ī Reserve blood if (Hct >30%)
19. CORD PROLAPSE
ī There are three clinical types of abnormal
descent of the umbilical cord by the side
of the presenting part:
ī Cord presentation
ī Occult prolapse
ī Cord prolapse
20. ī Cord presentation- When cord is slipped down
below the presenting part and is felt lying in the
intact bag of membranes.
ī Occult prolapse- the cord is placed by the side of the
presenting part and is not felt by the fingers on
internal examination.
ī Cord prolapse- the cord is lying inside the vagina or
outside the vulva following rupture of the
membranes
**The incidence of cord prolapse is about 1 in 300
deliveries
23. ETIOLOGY
Anything which interferes
with perfect adaptation of
the presenting part to the
lower uterine segment,
disturbing the ball valve
action may favour cord
prolapse.
24. PREDISPOSING FACTORS
ī§ MALPRESENTATION:-
ī§ Transverse lie
ī§ Breech
ī§ Compound presentation
ī§ HIGH HEAD:-
ī§ Membranes rupture but fetalhead
ishigh.
ī§ PREMATURITY:-
ī§ LBW BABY <1500g.
ī§ POLYHYDRAMNIOS:-
ī§ Cord is swept down in thegush
of liquor.
25. PREDISPOSING FACTORS CONT..
īąTwins or multiple pregnancy
īąLong cord (90-100 cm)
īąPROM
īąCPD
īą Placental factor- minor degree placenta
praevia
īą Iatrogenic- low rupture of the
membranes, manual rotation of the
head.
īą Contracted pelvis
26. DIAGNOSIS
ī OCCULT PROLAPSE
ī Difficult to diagnose.
ī Persistence of variable deceleration of fetal heart
rate pattern.
ī CORD PRESENTATION
ī Feeling the pulsation of the cord through the
intact membrane.
27. ī CORD PROLAPSE
ī The cord is palpated directly by the fingers
and its pulsation can be felt if the fetus is
alive.
ī Cord pulsation may cease during uterine
contraction, however returns after the
contraction passes away.
29. MANAGEMENT
ī Protocol is guided by:
ī Baby living or dead
ī Maturity of the baby
ī Degree of dilatation of the cervix
30. CORD PRESENTATION
ī Once the diagnosis is made, no attempt should be
made to replace the cord.
ī If immediate vaginal delivery is not possible or
contraindicated , caesarean section is the best
method of delivery.
ī A rare occasion when multipara with longitudinal
lie having good uterine contractions with cervix 7-
8cm dilated without fetal distress- watchful
competency and delivery by forceps or breech
extraction
31. MANAGEMENT OF CORD PROLAPSE
īDISCONTINUE THE VAGINAL EXAMINATION to reduce the risk of
rupturing the membranes.
īMONITOR CONTINUOUSLY THE FHR AND FETAL WELL-BEING.
īLIFT PRESENTING PART OFF THE CORD
īINSTRUCT NOT TO PUSH
īPOSITION PATIENT
Knee chest OR
Exaggerated position To minimise the cord compression.
34. CORD PROLAPSE
BABYALIVE
VAGINAL DELIVERY
NOT POSSIBLE
FIRSTAID
DEFINITE-
CAESAREAN SEC.
CAESAREAN
SECTION
VAGINAL DELIVERY
POSSIBLE
VERTEX
FORCEPS OR
VENTOUSE
BREECH
BY EXPERT HAND
BABY DEAD
USG AND VAGINAL
DELIVERY
MANAGEMENT
OFCORD
PROLAPSE
35. CORD PROLAPSE
ī Living baby
ī Immediate take the mother for Caesarean section.
ī Immediate safe vaginal delivery if- head is engaged
ī Immediate safe vaginal delivery not possible- FirstAid
ī First aid
ī Bladder filling is done to raise the presenting part off the
compressed cord.It is done by 400-750ml of NS with a
foleyâs catheter, the ballon is inflated and catheter is
clamped.
ī Lift the presenting part off the cord.
ī Postural treatment- exaggerated and elevated sims
position or trendelenburg or knee chest position.
ī Replace the cord into the vagina to minimize vasospasm
due to irritation.
36. ī Dead baby
ī Labour is allowed to proceed awaiting
spontaneous delivery
40. INCIDENCE
ī Amniotic fluid embolism syndrome is rare.
Most studies indicate that the incidence rate
is between 1 and 12 cases per 100,000
deliveries
41. The body respond in 2 phases
ī The initial phase is one of pulmonary vasospasm
causing hypoxia, hypotension, pulmonary edema and
cardiovascular collapse.
ī The second phase sees the development of left
ventricular failure, with hemorrhage and
coagulation disorders and further uncontrollable
hemorrhage
42.
43. CAUSES
A maternal age of 35 years or older
Caesarean or instrumental vaginal delivery
Polyhydramnios
Cervical laceration or uterine rupture
Placenta previa or abruption
Amniocentesis
Eclampsia
Abdominal trauma
Ruptured uterine or cervical veins
Ruptured membranes
46. SIGNS AND SYMPTOMS
ī Sudden shortness of breath
ī Excess fluid in the lungs
ī Sudden low blood pressure
ī Sudden circulatory failure Life-
threatening problems with blood
clotting (disseminated intravascular
coagulopathy)
ī Altered mental status
ī Nausea or vomiting
ī Chills
ī Rapid heart rate
ī Fetal distress
ī Seizures
ī Coma
47. DIAGNOSIS
ī Chest X-ray: May show an enlarged right atrium and ventricle
and prominent proximal pulmonary artery and pulmonary
edema.
ī Lung scan: May demonstrate some areas of reduced radioactivity
in the lung field.
ī Central venous pressure (CVP) with an initial rise due to
pulmonary hypertension and eventually a profound drop due to
severe hemorrhage.
ī Coagulation profile: decreased platelet count, decreased
fibrinogen and a fibrinogenemia, prolonged PT and PTT, and
presence of fibrin degradation products.
ī Cardiac enzymes levels may be elevated;
ī Echocardiography may demonstrate acute left heart failure,
acute right heart failure or severe pulmonary hypertension
48. MANAGEMENT
ī Maintain systolic blood pressure > 90 mm Hg.
ī Urine output > 25 ml/hr
ī Re-establishing uterine tone
ī Correct coagulation abnormalities
īAdminister oxygen to maintain normal
saturation.
ī Intubate if necessary.
ī Initiate cardiopulmonary resuscitation (CPR) if
the patient arrests. If she does not respond to
resuscitation, perform a cesarean delivery.
49. ī Treat hypotension with crystalloid and blood products.
ī Consider pulmonary artery catheterization in patients who are
haemodynamically unstable. Continuously monitor the fetus.
ī trauma to the uterus must be avoided during maneuvers such
as insertion of a pressure catheter or rupture of membranes.
ī Incision of the placenta during caesarean delivery should also be
avoided
50. NURSINGMANAGEMENT
ī Give immediate and vigorous treatment.
ī Give oxygen by face mask.
ī Maintain normal blood volume through
administration of plasma and intravenous
fluids.
ī Prevent development of disseminated
intravascular coagulation (DIC). Serious
complications can occur. (Disseminated
intravascular coagulation (DIC) is a condition in which blood
clots form throughout the body, blocking small blood vessels.
Symptoms may include chest pain, shortness of breath, leg
pain, problems speaking, or problems moving parts of the body.)
ī Administer whole blood and fibrinogen.
ī Monitor the patientâs vital signs.
ī Deliver the fetus as soon as possible
51.
52. SHOULDER DYSTOCIA
It occurs when anterior shoulder become trapped behind the
symphysis pubis, while the posterior shoulder may bein the hollow
of the sacrum or high above thesacral promontory.
īąINCIDENCE:-
THE INCIDENCE VARY BETWEEN 0.37%- 1.1%
53. RISK FACTORS OF SHOULDER
DYSTOCIA
īFETALMACROSOMIA.
īOBESITY MOTHER.
īMATERNAL DIABETES.
īPOSTMATURITY OF
FETUS.
īMULTIPARITY.
īANENCEPHALY.
īFETALASCITES.
54.
55. MANAGEMENT (HELPERR)
Help â obstetrician, pediatrician
Episiotomy
Legs â elevate
Pressure - suprapubic
Enter vagina â (internal rotation).
Roll the woman over and try again.
Remove posterior arm
56. McRoberts Maneuver
âĸ Hyperflexion of maternal hips Increases
intrauterine pressure
(1,653mmhg- 3,262mmhg)
âĸ Increases amplitude of
contractions
(103mmhg to 129mmhg)
58. Rubinâs Maneuver
âĸ Adduction of the most accessible shoulder
âĸ Moves the fetus into an oblique position and decreases
the bisacromial diameter
59. Woodsâ Cork Screw Maneuver
âĸ Abduct posterior shoulder exerting pressure on anterior
surface of posterior shoulder
60. Deliver posterior arm
(Barnum Maneuver)
âĸ Grasp the posterior arm and
sweep it across the anterior
Chest to deliver
63. OBSTETRIC SHOCK
ī Shock is a critical condition and a life threatening
medical emergency.
ī Shock results from acute, generalized,
inadequate perfusion of tissues, below that
needed to deliver the oxygen and nutrients for
normal function
67. DIAGNOSIS
ī A high index of suspicion and physical
signs of inadequate tissue perfusion and
oxygenation are the basis for initiating
prompt management.
ī Initial management does not rely on
knowledge of the underlying cause.
68. INITIAL MANAGEMENT
ī MaintainABC
ī Airway should assured - oxygen 15
lt/min.
ī Breathing â ventilation should be checked
and support if inadequate
ī Circulation- (with control of
hemorrhage) â Two wide bore canulla
â Restore circulatory volume
ī Reverse hypotention with crystalloid.
â Crossmatch,
ī Arrange and give blood if necessary.
ī See for response such as , vital signs.
Position of patient - Head down and left lateral tilt
to avoid aortocaval compression which may further
worsen the hypotension
69.
70. HYPOVOLEMIC SHOCK
ī The normal pregnant woman can withstand
blood loss of 500 ml and even up to 1000 ml
during delivery without obvious danger due to
physiological cardiovascular and haematological
adaptations during pregnancy.
īą DEFINITION:- THE RESULT OF
A REDUCTION IN
INTRAVASCULAR VOLUME
SUCHAS IN SEVERE
OBSTETRIC
HAEMORRHAGE.
72. SIGN AND SYMPTOMS
Severe symptoms, include:-
ī§ī cold or clammy skin
ī§ī pale skin
ī§ī rapid, shallow breathing
ī§ī rapid heart rate
ī§ī little or no urine output
ī§ī confusion
ī§ī weakness
ī§ī weak pulse
ī§ī blue lips and fingernails
ī§ī Lightheadedness
ī§ī loss of consciousness
Mild symptoms can
include:
ī headache
ī fatigue
ī nausea
ī profuse sweating
ī dizziness
73. PRESENTING FEATURES OF
HYPOVOLUMIC SHOCK
ORGAN SYSTEM EARLY LATE
BP NORMOTENSIVE
OR
HYPOTENSIVE.
HYPOTENSION
PULSE TACHYCARDIA. SAME.
RESPIRATION NORMAL TACHYPNOEA.
RENAL OLIGURIA ACUTE
RENAL
FAILURE
SKIN COLD & CLAMMY COLD & CLAMMY.
MENTAL STATUS NORMAL DISORIENTATION
74. MANAGEMENT
ī Basic shock management then treat specific
cause.
ī Laparotomy for ectopic pregnancy
ī Suction evacuation for incomplete abortion
ī management of uterine atony
ī Repair of laceration
ī Management of uterine rupture â Stop
oxytocin infusion if running
ī Continuous maternal and fetal monitoring
75. ī Emergency laparotomy with rapid operative delivery
ī Cesarean hysterectomy may need to perform if hemorrhage is not
controlled.
ī Management of uterine inversion. â Replacement of the uterus needs
to be undertaken quickly as delay makes replacement more difficult.
ī Administer tocolytics to allow uterine relaxation. â Replacement under
taken ( with placenta if still attached)-manually by slowly and steadily
pushing upwards, with hydrostatic pressure or surgically.
76. CARDIOGENIC SHOCK
ī Cardiogenic shock in pregnancy is a life-
threatening medical condition resulting from an
inadequate circulation of blood.
ī Pregnancy puts progressive strain on the
heart as progresses.
ī Preexisting cardiac disease places the
parturient at particular risk.
ī Cardiac related death in pregnancy is the
second most common cause of death in
pregnancy
77. SIGN AND SYMPTOMS
ī Chest pain
ī Nausea and vomiting
ī Dyspnoea
ī Profuse sweating
ī Confusion/disorientation
ī Palpitations
ī Faintness/syncope
ī Pale, mottled, cold skin with slow capillary refill and poor
peripheral pulses.
ī Hypotension (remember to check BP in both arms in case of
aortic dissection).
ī Tachycardia/bradycardia.
ī Raised JVP/distension of neck veins.
ī Peripheral oedema.
ī Quiet heart sounds or presence of third and fourth heart
sounds.
ī Heaves, thrills or murmurs may be present and may indicate
the cause, such as valve dysfunction.
ī Bilateral basal pulmonary crackles or wheeze may occur.
ī Oliguria
78. MANAGEMENT
ī Re-establishment of circulation to the
myocardium,
ī Minimising heart muscle damage and
improving the heartâs effectiveness as a pump.
ī Administer Oxygen (O2) therapy to reduces the
workload of the heart by reducing tissue
demands for blood flow.
ī Administration of cardiac drugs such as
Dopamine, dobutamine, epinephrine,
norepinephrine,
79. SEPTIC SHOCK
DEFINITION:-
It occurs with a severe generalised infection.
This is sepsis with hypotension despite adequate fluid
resuscitation.
To diagnose septic shock following two criteria must be
met
ī Evidence of infection through a positive blood culture.
ī Refractory hypotension- hypotension despite of
adequate fluid resuscitation.
80. ETIOLOGY
ī Post cesarean delivery
ī Prolonged rupture of membranes
ī Retained products of conception
ī rupture uterus
ī Intra-amniotic infusion
ī Water birth
ī Urinary tract infection
ī Toxic shock syndrome
ī Necrotizing Fasciitis
82. PRESENTING FEATURES OF SEPTIC
SHOCK
ORGEN SYSTEM EARLY LATE
BP NORMOTENSIVE
OR HYPOTENSIVE
HYPOTENSIVE
PULSE TACHYCARDIA TACHYCARDIA
RESPIRATION TACHYPNO
EA,
PULMONAR
Y EDEMA.
TACHYPNOEA
SKIN WARM COLD & CLAMMY.
RENAL OLIGURIA ACUTE
RENAL
FAILURE.
MENTAL STATUS NORMAL DISORIENTED
83. MANAGEMENTOF SEPTICSHOCK
īŧReplacement of fluid volume.
īŧIdentify the sourse of infection.
īŧInfection screening should be carried
out- vaginal swab, urine and blood
cultures
īŧAseptic technique should be maintain.
84. MANAGEMENT
ī Transfer to a higher level facility.
ī Invasive monitoring should be done
ī Obtain blood culture , wound swab culture
and vaginal swab culture.
ī Start broad spectrum antibiotics.
ī Removal of infected tissues.
85. ANAPHYLYTIC SHOCK
ī A serious rapid onset of allergic reaction
that is rapid onset and may cause death.
ī It is a relatively uncommon event in
pregnancy but has serious implications for
both mother and fetus.
87. SIGN ANDSYMPTOMS
ī Cutaneous â Flushing, pruritus, urticaria , rhinitis, conjunctiva
erythema, lacrimation.
o Cardiovascular â Cardiovascular collapse, hypotension, vasodilation
and erythema, pale clammy cool skin, diaphoresis, nausea and
vomiting
ī Respiratory â Stridor, wheezing, dyspnea, cough, chest tightness,
cyanosis.
ī Gastrointestinal â Nausea vomiting , abdominal pain , pelvic pain .
ī Central nervous system â Hypotension â collapse with or without
unconsciousness, dizziness, incontinence.
o Hypoxiaâ causes confusion
88. MANAGEMENT
ī Immediate â
ī Stop administration of suspected agent and call for
help
ī Airway maintenance
ī Circulation â Give epinephrine IM and repeat every 5-
15min in titrated until improvement.
In severe hypotension intravenous
epinephrine should be given.
ī Rapid intravascular volume expansion with
crystalloid solution.
89. Secondary
ī If hypotension persist alternative vasopressor agent
should use. â Atropine if persistent bradycardia
ī If bronchospasm persist nebulize with salbutamol
ī Antihistaminic
ī Steroids
ī All patient with anaphylactic shock should referred to
critical care
90. DISTRIBUTIVESHOCK
ī In distributive shock there is no loss in
intravascular volume or cardiac function.
ī The primary defect is massive vasodilation leading to
relative hypovolemia, reduced perfusion pressure, so
poorer flow to the tissues.
92. SIGN ANDSYMPTOMS
ī Hypotension
ī Bradycardia
ī Hypothermia
ī Shallow breathing
ī Nausea vomiting
ī No response to stimuli
ī Unconscious
ī Blank expression of patient
93. MANAGEMENT
ī Resuscitation
ī Vasopressor agent and atropine may required in management
because spinal injury leads bradycardia due to unopposed vagal
stimulation.
ī Anesthesia -High spinal block
ī Basic ABC management â
īą
īą
īą
Ventilation if needed
Administer iv fluids
Iv steroid such as methylprednisolone
ī Immobilize the patient to prevent further damage
94.
95. UTERINE INVERSION
ī It occurs when the placenta fails to detach from
the uterus as it exits, pulls on the inside surface,
and turns the organ inside out.
ī Uterine inversion is a potentially fatal
childbirth complication with a maternal
survival rate of about 85%
ī The incidence is about 1 in 20,000 deliveries.
96.
97. ETIOLOGY
ī The exact cause of uterus inversion is
unclear.
ī The most likely cause is strong traction on the
umbilical cord, particularly when the placenta is in
a fundal location, during the third stage of labor
98. Causes:
âĸ uterine atony (40%)
âĸ Increase in intra abdominal
pressure
âĸ Fundal attachment of
placenta (75%)
âĸ Short cord
âĸ Placenta accreta
âĸ Excessive cord traction
99.
100. DIAGNOSIS
Prompt diagnosis is crucial and possibly lifesaving.
Some of the signs of uterine inversion could include:
ī The uterus protrudes from the vagina.
ī The fundus doesnât seem to be in its proper position when the
doctor palpates (feels) the motherâs abdomen.
ī The mother experiences greater than normal blood loss.
ī The motherâs blood pressure drops (hypotension).
ī The mother shows signs of shock (blood loss).
ī Scans (such as ultrasound or MRI) may be used in some cases
to confirm the diagnosis
101. Management
âĸ Uterine relaxant (terbutaline 0.25 mg IV
followed by 2 g of MgSO4 over 10 min)
âĸ Treat hypovolaemeia
âĸ Without placenta: Repositioning
102. MANAGEMENT
Before shock
ī Urgent manual replacement
ī After replacement, the hand should remain inside the uterus
until the uterus become contracted by parentral oxytocics.
ī The placenta should be removed manually only after the
uterus becomes contracted.
ī Usual treatment of shock including blood transfusion
should be arranged.
103.
104. Aftershock
ī Morphine 15mg IM , dextrose saline drip and arrangement
of blood transfusion.
ī Push the uterus inside the vagina if possible and pack the
vagina with roller gauze
ī Raised foot end of bed.
ī Replacement of uterus under general anaesthesia
to be done.
ī Emergency hysterectomy (surgical removal of the uterus) in
extreme cases where the risk of maternal death is high.
105. NURSING MANAGEMENT
ī Monitor for signs
of hemorrhage and shock and
treat shock
ī Prepare patient to reposition the
uterus to the correct position via
the vagina or laprotomy if
unsuccessful.
106.
107. RUPTUREUTERUS
ī The most serious complication in midwifery
and obstetrics.
ī It is often fatal for the fetus and may also be
responsible for the death of the mother.
108. DEFINITION
ī Disruption in the continuity of the all uterine
layers( endometrium, myometrium and serosa)
any time beyond 28 weeks of pregnancy is called
rupture of uterus.
INCIDENCE
ī The prevalence widely varies from 1 in 2000 to 1
in 200 deliveries.
111. Completerupture:-
ī The peritoneum tears and the contents of the
motherâs uterus can spill into her peritoneal cavity.
ī It is suggested that delivery via cesarean section (C-
section) should occur within approximately 10 to 35
minutes after a complete uterine rupture occurs.
ī The fetal morbidity rate increases dramatically after
this period
112. Incomplete:-
ī The motherâs peritoneum remains intact.
ī The peritoneum acts as a channel for blood
vessels and nerves.
ī An incomplete uterine rupture is significantly less
dangerous with fewer complications to the delivery
process
113. Causes /Risk
factors
ī§ Obstructed labour
ī§ Separation of previous C/S
scar
ī§ Trauma due to operative
manipulation
ī§ The unwise use of
oxytocin
ī§ The extension of an old
cervical tear.
ī§ Neglected labour
ī§ High parity
115. īSpontaneous
ī During pregnancy-
ī Previous damage to the uterine walls following
D& C procedure.
ī Manual removal of placenta
ī Thin uterine wall
ī Congenital malformation of uterus.
ī During labour-
ī Obstructive rupture due to obstructed labour
ī Non obstructive rupture due to weakening of
walls due to repeated previous birth
117. īIatrogenic
ī During pregnancy-
ī Injudicious administration of oxytocin
ī Use of prostaglandin for induction of abortion or
labour
ī Forcible external version
ī Fall or blow on the abdomen.
ī During labour
ī Internal podalic version.
ī Destructive operation.
ī Manual removal of placenta.
ī Application of forceps or breech extraction
through incomplete dilated cervix.
ī Injudicious administration of oxytocin for
augmentation of labour
118. SIGN ANDSYMPTOMS
ī Abdominal pain and tenderness
ī Shock
ī Vaginal bleeding
ī Undetectable fetal heart beat
ī Palpable fetal body parts
ī Cessation of contractions
ī Signs of intra-peritoneal bleeding
ī The most common sign is the sudden
appearance of fetal distress during labor.
ī Complete laceration of uterine wall.
119. ī Sharp pain between contractions - Contractions that slow down
or become less intense
ī Recession of the fetal head (babyâs head moving back up into
the birth canal)
ī Bulging under the pubic bone (babyâs head has protruded
outside of the uterine scar) Sharp onset of pain at the site of
the previous scar.
ī Uterine atony (loss of uterine muscle tone)
ī Maternal tachycardia (rapid heart rate) and hypotension
120. DIAGNOSIS
ī Ultrasonography is probably the safest and most
useful imaging technique during pregnancy.
sonographic findings associated with includes:
âĸ Extra peritoneal hematoma
âĸ intrauterine bleed
âĸ free peritoneal blood
âĸ empty uterus
âĸ gestational sac above the uterus
âĸ large uterus mass with gas
ī Painful bleeding.
ī Loss of FHS
121. MANAGEMENT
ī Principles for the treatment of uterine
rupture includes:
ī Intensive resuscitation
ī Emergency laparotomy
ī Broad spectrum antibiotics
ī Adequate post operative care
122. ī Intensive resuscitation
ī Correct hypovolaemia from-
# Haemorrhage
#Sepsis
#Dehydration
ī Intravenous broad spectrum antibiotics
#Cephalosporin + Metronidazole combination
ī Monitor to ensure adequate fluid and blood
replacement
ī Blood volume expansion may worsen the bleeding
from damaged vessel and so the laparotomy should not
be delay, once patient condition has improved.
123. ī Surgical options
ī Hysterectomy -Treatment of choice except any
other compelling reasons to preserve the uterus
# Total
# Sub-total
ī Rupture repair
# Occasionally one may be forced to repair
# Repair with sterilization
124. NURSING MANAGEMENT
ī Monitor for the possibility of uterine rupture.
ī In the presence of predisposing factors, monitor maternal labor
pattern closely for hyper tonicity or signs of weakening uterine
muscle.
ī Recognize signs of impending rupture, immediately
notify the physician, and call for assistance.
ī Assist with rapid intervention.If the client has signs of possible
uterine rupture, vaginal delivery is generally not attempted.
īMonitor maternal blood pressure, pulse, and
respirations; also monitor fetal heart tones.
125. ī If the client has a central venous pressure catheter in place,
monitor pressure to evaluate blood loss and effects of fluid and
blood replacement.
ī Insert a urinary catheter for precise determinations of fluid
balance.
ī Obtain blood to assess possible acidosis.
ī Administer oxygen, and maintain a patent airway.
ī Restore circulating volume using one or more IV lines.
ī Evaluate the cause, response to therapy, and fetal condition
126. Preventionofruptureuterus
ī§ Constant and careful antenatal care
ī§ Refer to hospital - mother who has obstructed labour
ī§ Detect high risk mothers and select them for hospital
delivery
ī§ Previous section must always delivery in Hospital
ī§ Care during manipulation
ī§ Careful observation of the mother in labour to
exclude obstructed labour
ī§ Avoid giving pitocin for previous classical c/s scar
127. ī Conclusions: It was concluded that obstetric
emergencies are more common in unbooked cases
and women with low socioeconomic status with
pooraccess to antenatal care.
128.
129.
130. BIBLIOGRAPHY
âĸ D.c Dutta Textbook of Obstetrics7th edition, New
central book agency
private limited London.
âĸ Anamma Jacob Midwifery and Gynaecological
nursing 4th edition, Jaypee brothers and
medical publishers, New Delhi.
âĸ Ajit virkud, Modern Obstetrics, APC
Publishers Mumbai, 3rd edition 2017.