Obsterical Emmergencies and Shock

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Time Specific Content Teaching Learning Av- aids Evaluation

No Objective activity Activity
1. 1min To OBSTETRICAL EMERGENCIES T L P What is
introduce I obstetrical
Introduction E P
the S emergencies
obstetrical An emergency is a situation that poses an immediate risk A P ?
T
emergency
to health, life, property or environment. Most emergencies C T
E
require urgent intervention to prevent the worsening of the H
N
situation, although in some situations, mitigation may not I
I
be possible and agencies may only be able to offer N
N
palliative care for the aftermath. One such kind of G
G
emergency is obstetric emergency. M
Obstetrical emergencies may also occur during active E
labor, & after delivery (postpartum). The first principal of T
dealing with obstetric emergencies are the same as for any H
emergency (see to the airway, breathing & circulation) but O
remember that in obstetrics there are two patients; the fetus D
is very vulnerable to maternal hypoxia.
There are a number of illnesses and disorder of pregnancy
that can threaten the well-being of both mother and child.
Sl. Time Specific Content Teaching Learning Av- aids Evaluation
2. 1min To define DEFINITIONS T L P What is the
the I P definition of
Obstetrical emergencies are life threatening medical E
obstetrical T obstetrical
emergencies conditions that occur in pregnancy or during or after labour A S emergencies
To enlist the T and types of
and delivery C
types of obstetrical
obstetrical TYPES OF OBSTETRIC EMERGENCIES H E emergencies
emergencies N
1)obstetric emergencies of pregnancy I
I
•Ectopic pregnancy N N
G
An ectopic, or tubal, pregnancy occurs when the fertilized G
egg implants itself in the fallopian tube rather than the M
uterine wall. E
 If the pregnancy is not terminated at an early stage, T
the fallopian tube will rupture, causing internal H
hemorrhaging and potentially resulting in O
permanent infertility. D
PLACENTAL ABRUPTION T L P
P
Also called abruption placenta, placental abruption occurs E I
T
when the placenta separates from the uterus prematurely, A S
causing bleeding and contractions. If over 50% of the C T
placenta separates both the fetus and mother are at risk. H E
I N
N I
G N
M G
E
T
PLACENTA PREVIA H
When the placenta attaches to the mouth of the uterus and O
partially or completely blocks the cervix, the position is D
termed placenta Previa (or low-lying placenta)
Placenta Previa can result in premature bleeding and
possible postpartum hemorrhage.

•PREECLAMPSIA / ECLAMPSIA PREECLAMPSIA
(toxemia) or pregnancy induced high blood pressure causes
severe edema(swelling due to water retention) and can
impair kidney and liver function. The condition occurs in
approximately 5% of all United States pregnancies. If it
progresses to eclampsia, toxemia is potentially fatal for
mother and child.
Premature rupture of membranes Premature rupture of

membranes is the breaking of the bag of waters (amniotic
fluid) before contractions or labor begins. The situation is
only considered an emergency if the break occurs before
thirty-seven weeks and results in significant leakage of
amniotic fluid and/or infection of the amniotic sac.
T L P
E I P
S T
A
T
C E
N
H
I
I N
3. G
N
1min To explain OBSTETRIC EMERGENCIES DURING LABOUR & What is
about the G obstetrical
DELIVERY
obstetrical emergencies
M
emergencies •Amniotic fluid embolism A rare but frequently fatal during labour
during labour E
complication of labor, this condition occurs when amniotic
and delivery
T
fluid embolisms from the amniotic sac and through the
H
veins of the uterus and into the circulatory system of the
O
mother. The fetal cells present in the fluid then blocker
D
clothe pulmonary artery, resulting in heart attack. This
complication can also happen during pregnancy, but
usually occurs in the presence of strong contractions.
INVERSION OR RUPTURE OF UTERUS DURING T L P
E I P
LABOR, a weak spot in the uterus (such as a scar or a
A S T
uterine wall that is thinned by a multiple pregnancy) may C T
H E
tear,resulting in a uterine rupture. In certain circumstances,
I N
a portion of the placenta may stay attached to thewall and N I
G N
will pull theuterus out with it during delivery. This is called
M G
uterine inversion. E
T
H
O
D
•PLACENTA ACCRETE
Placenta accrete occurs when the placenta is implanted too
deeply into the uterine wall, and will not detach during the
late stages of childbirth, resulting in uncontrolled bleeding.
Prolapsed umbilical cord A prolapse of the umbilical cord

occurs when the cord is pushed down into the cervix or
vagina. If the cord becomes com pressed, the oxygen
supply to the fetus could be diminished, resulting in brain
damage or possible death.

•SHOULDER DYSTOCIA T L P
I P
Shoulder dystocia occurs when the baby' s shoulder(s)
E S T
becomes wedged in the birth canal after the head has been A T
C E
delivered. ```
H N
`Vasa Previa0 ````` I I
N N
‘’’cord prolapse’’’
G G
M
E
T
H
O
D
4. What is
1min To explain the obstetrical
OBSTETRIC EMERGENCIES POSTPARTUM
obstetrics emergencies
emergencies •PPH Severe bleeding or uterine infection occurring after during post
during post partum
delivery is a serious, potentially fatal situation.
partum
Obstetrical emergencies can be caused by a number of T L P
E I P
factors, including-
A S T
•Stress C T
H E
•Trauma
I N
•Genetic and other variables In some cases, past medical N I
G N
history, including previous pregnancies & deliveries, may
M G
help an obstetrician anticipate the possibility of E
T What is the
complications.
H signs and
5. 1min To describe Signs and symptoms of obstetrical emergencies O symptoms of
the signs and D obstetrical
signs and symptoms of an obstetrical emergency include,
symptoms of emergencies
obstetrical but are n ot limited to: •Diminished fetal activity. In the
emergencies
late third trimester, fewer than ten movements in a two
hour period may indicate that the fetus is in distress.
•Abnormal bleeding. During pregnancy, brown or white to
pink vaginal discharge is normal, bright red blood or blood
containing large clots is not. After delivery, continual
blood loss of over 500 ml indicates hemorrhage. •Leaking
amniotic fluid. Amniotic fluid is straw- colored and may
easily be confused with urine leakage, but can be
differentiated by its slightly sweet odor. Signs and
symptoms of obstetrical emergencies
•Severe abdominal pain. Stomach or lower back pain can T L P
E I P
indicate preeclampsia or an undiagnosed ectopic
A S T
pregnancy. Postpartum stomach pain can be a sign of C T
H E
infection or hemorrhage. •Contractions. Regular
I N
contractions before 37 weeks of gestation can signal the N I
G N
onset of preterm labor due to obstetrical complications.
M G
•Abrupt and rapid increase in blood pressure. Hypertension E
T
is one of the first signs of toxemia •Edema. Sudden and
H
significant swelling of hands and feet caused by fluid O
D
retention from toxemia. •Unpleasant smelling vaginal
discharge. A thick, malodorous discharge from the vagina
can indicate a postpartum infection .
Fever.
Fever may indicate an active infection.
•Loss of consciousness.
Shock due to blood loss (hemorrhage) or amniotic
embolism can precipitate a loss of consciousness in the
mother.
•Blurred vision and headaches. Vision problems and
headache are possible symptoms of preeclampsia.
6. 1min To explain the DIAGNOSIS OF OBSTETRICAL EMERGENCIES T L P
diagnosis and E I P What is the
Diagnosis of an obstetrical emergency typically takes place
treatment of A St T diagnosis and
obstetrical in a hospital or other urgent care facility. Diagnosis C E treatment of
emergencies H N obstetrical
includes:-
I I emergencies
•Medical history N N
G G
•General physical examination
M
•Pelvic examination E
T
•Mother’s vital sign taken - If preeclampsia is suspected,
H
BP may be monitored over a period of time. O
D
•Fetal heartbeat assessed with a Doppler stethoscope
•Blood & urine tests •Abdominal sonography
•Biophysical profile (BPP) may also be performed to
evaluate the health of the fetus.
TREATMENT
1)Obstetrical emergencies of pregnancy
•Ectopic pregnancy –
Treatment of an ectopic pregnancy is laparoscopic surgical
removal of the fertilize d ovum.
If the fallopian tube has burst or been damaged, f further
surgery will be necessary.
• Placental abruption – T L P
E I P
In mild cases of placental abruption, bed rest may prevent
A S T
further separation of the placenta and stem bleeding. If a C T
H E
significant abruption (over 50%) occurs, the fetus may
I N
have to be delivered immediate and a blood transfusion N I
G N
may be required.
M G
PLACENTA PREVIA- E
T
Hospitalization or highly restricted at home bed rest is
H
usually recommended if placenta Previa is diagnosed after O
D
the twentieth week of pregnancy. If the fetus is at least 36
weeks old and the lungs are mature, a cesarean section is
performed to deliver the baby.
PREECLAMPSIA / ECLAMPSIA –
Treatment of preeclampsia depends upon the age of the
fetus and the acuteness of the condition. A woman near full
term that has only mild toxemia may have labor induced to
deliver the child as soon as possible. Severe preeclampsia
in a woman
near term also calls for immediate delivery of the child, as
this is the only known cure for the condition.However, if
the fetus is under 28weeks, the mother may be hospitalized
and steroids may be administered to try to hasten lung T L P
development in the fetus. If the life of the mother or fetus I
E P
appears to be in danger, the baby is delivered i mmediately, A S T
usually by cesarean section. C T
•PREMATURE RUPTURE OF MEMBRANE- H E
If PROM occurs before 37 weeks and/or results in I N
significant le adage of amniotic fluid, a course of N I
intravenous antibiotics is started. A culture of the cervix G N
may be taken to analyze for the presence of bacterial infe M G
ction. If the fetus is close to term, labor is typically induced E
if co tractions do not start within 24 hours of rupture. T
7. 1min To describe What is the
OBSTETRICAL EMERGENCIES DURING H
the obstetrical obstetrical
emergencies LABOUR & DELIVERY O emergencies
treatment and treatment
•Amniotic fluid embolism – D
during labour
delivery The stress of contractions can cause this complication;
which h has a high mortality rate. Administering steroids
to the mother and delivering the fetus as soon as p possible
is the standard treatment
Inversion or rupture of uterus –
An inverted uterus is either manually or surgical replaced
to the proper position
A ruptured uterus is repaired if possible, although if the T L P
E I P
damage is extreme, a hysterectomy (removal of the uterus)
A S T
may be performed. A blood transfusion may be required in C T
H E
either case if hemorrhaging occurs.
I N
Shoulder dystocia N I
G N
- The mother is usually positioned with her knees to he r
M G
chest, known as the McRoberts maneuver, in an effort to E
T
free the child's shoulder.
H
An episiotomy is also pe reformed to widen the vaginal O
D
opening.
If the shoulder cannot be dislodged from the pelvis, the
baby's clavicle le (collarbone) may have to be broken to
complete the delivery before a lack of oxygen causes brain
damage to the infant.
Obstetrical emergencies postpartum
Postpartum hemorrhage or infection - The source of the
hemorrhage is determined, and blood transfusion n and IV
fluids are given as necessary.
Oxytocic drugs may be administered to encourage
contraction of the uterus
Retained placenta is a frequent cause of persistent L P
T I P
bleeding, and surgical removal of the remaining
E S T
fragments (curettage) may be required A T
C E
Surgical repair of lacerations to the birth canal or uterus
H
may be required. Drugs that encourage coagulation I N
N I
(clotting) of the blood may be administered to stem the
G N
bleeding. Infrequently, hysterectomy is required. In cases M G
E
of infection, a cour se of intravenous antibiotics is
T
prescribed. Most postpartum infect ions occur in the H
O
endometrium, or lining of the uterus, and may be also
D
caused by a piece of retained placenta. If this is the case, it
will also require surgical removal.
8. 1min To explain the What is the
Prevention of PREVENTION prevention of
obstetrical obstetrical
•Proper prenatal care is the best prevention for obstetrical
emergencies emergencies
emergencies.
•When complications of pregnancy do arise, pregnant
women who see their Ob/GYN on a regular basis are more
likely to get an early diagnosis, & with it, the best chances
for fast & effective treatment.
•In addition, eating right & taking prenatal vitamins and T L P
I P
supplements as recommended by a physician will also
E S T
contribute to the health of both mother & child A T
C E
Role of Obstetric Nurse in Preparing the hospital for
9. 1min To explaining H N
Role of nurse Clinical Emergencies I I What is the
in obstetrical N N role of nurse
emergencies G G in obstetrical
1. Planning M emergencies
E
2. Advance Provision of Resources in the Outpatient T
Setting H
O
3. Early Warning Systems in the Inpatient Setting D
4. Rapid Response Team
5. Emergency Drills and Simulation
PLANNING –
Assessment of actual/potential risks.
Outpatient Setting – Medications given Procedures

performed
Inpatient Setting – Risk management data Common AND
Uncommon emergencies occurred
Nursing Care: T L P
E I P
Perform a complete assessment on any pregnant mother
A S T
who presents with painless bright red vaginal bleeding C T
H E
Vital signs
I N
Continuous Fetal monitoring, N I
G N
 Measure abdominal girth
M G
 Uterine characteristics and activity E
T
 EFM-Continuously For development coagulation
H
problems O
D
 Review lab values:
 CBC, Coagulation studies, PT, PTT
 Insert large IV Catheter(18-gauge or bigger) and
maintain IV infusion
 Provide Oxygen at 8-12 L/min
 Prepare for Transfusion Therapy
 Anticipate Expedited Delivery :Virginally
Cesarean section
 Administer oxygen via face mask at 10L/min P
T L P
 Star IV fluids and monitor for potential fluid
E I T
overload A S
C T
 Use suction as needed
H E
 Give magnesium sulfate or anticonvulsant drug as H N
I
ordered
I N
 Monitor blood pressur Monitor fetal and uterine N G
G
status
M
 Expedite laboratory work as ordered to monitor E
T
kidney liver function Deliver by 6 – 8 hrs.
H
 I/V infusion with big bore needle O
D
 Transfusing blood products
 Administering oxygen
 Assisting with the preparation for immediate
surgery
 Supporting the woman’s family and providing
information
Sl. Time Specific content Teaching Learning Av- aids Evaluation
 Insert 2 fingers into the cervix. With one finger on T L P
E I P
either side of the cord exert upward pressure
S T
against the presenting part to relieve compression A T
C E
of the cord. Place a rolled towel under the
H N
woman’s right/left hip I I
N N
 Place the woman into the Trendelenburg position
G G
or modified sim’s position or knee-chest position. M
E
 If the cord is protruding out wrap in sterile towel
T
saturated with normal saline H
O
 Administer oxygen
D
 Monitor FHR
 Prepare for vaginal delivery if cervix is fully
dilated or cesarean birth if it is not
1, 1min To introduce OBSTETRICAL SHOCK T L P What is the
and definition E I P introduction
DEFINITION.
the obstetrical A S T and definition
shock ‘’Shock is defined as a state of circulatory inadequacy C T of obstetrical
H E shock
with poor tissue perfusion resulting in generalized
I N
cellular hypoxia.” N I
N
 Circulatory inadequacy is due to a disparity
G G
between the circulating blood volume and the M
E
capacity of the circulatory bed.
T
 The net effect of this disparity is inadequate H
O
exchange of oxygen and carbon dioxide between
D
the intra and extravascular compartments.
 The stagnation of carbon dioxide and other
metabolites in the tissue leads to metabolic
acidosis and cellular death.
 The series of changes observed in shock and their
clinical manifestations, are therefore, dependent
on two sets of changes:
 a) Circulatory inadequacy at the 'filtration
level'
 b) Cellular damage and ultimately death.
2. 1min To enlist the T L P What is the
classification E I P classification
of obstetrical A S T of obstetrical
shock C T shock
H E
I N
N I
H N
Circulating blood volume is inadequate resulting from G G
acute depletion. M
NON HAMORRHAGIC E
SHOCK T
HAMORRHAGIC H
SHOCK O
D
Hemorrhagic shock
o Associated with postpartum or post
aborted hemorrhage, ectopic pregnancy,
placenta Previa, abruption placenta,
rupture of the uterus and obstetric surgery
o Shock associated with disseminate
intravascular coagulation, intrauterine
dead fetus syndrome and amniotic fluid
embolism
Non Hemorrhagic shock T L P
E I P
Fluid Shock: -
S T
 Associated with excessing vomiting, diarrhea, A T
C E
diuresis or too rapid removal of amniotic
H N
fluid. I I
N N
Supine Hypotensive Syndrome: -
G G
 Due to compression of inferior vena cava by M
E
the pregnant uterus.
T
septic shock (endotoxin shock) H
O
 Hypotension is due to sepsis resulting in
D
derangements in cellular and organ system
dysfunction.
 hypotension persists in spite of adequate fluid
resuscitation.
3. 1min  associated typically with septic abortion,
Explain the
chorioamnionitis and rarely postpartum
Cardiac shock What is the
endometriosis.
cardiac shock
CARDIAC SHOCK
Decreased systolic pressure ( <80 mm Hg)Decreased
Cardiac Index (<1.8 L /min/m2) Increased left ventricular
filling pressure (> 18 mm Hg)
Massive pulmonary embolism, amniotic fluid embolism, T L P
E I P
anaphylaxis, drug overdose, neurogenic.
A S T
. Chemical injury: - C T
H E
 Associated with aspiration of gastrointestinal
I N
contents during general anesthesia (Mendelson's N I
G N
syndrome) Drug induced:
M G
 Associated with spinal anesthesia. E
T
Pathophysiological changes in obstetric shock are
H
predominantly associated with.. O
D
a) General changes due to hypovolemia
b) Specific changes due to liberation of endotoxin
Hypotension stimulates release of neuroendocrine
mediators like adrenocorticotropic hormone (ACTH),
Growth hormone (GH), β endorphin, cortisol and
glucagon.
 There is also sympathy adrenal response.
 Presence of endotoxin (lipopolysaccharide), in
septic shock activates the leucocytes through
complement system
 There is release of inflammatory mediators T L P
E I P
such as protease, superoxide (o2 - ), hydroxyl
A T
(OH- ) radicals, cytokines, prostaglandins and C S
H T
many cytotoxic enzymes.
I E
 These interfere with the function of a number N N
G I
of enzyme systems and increase capillary
M N
permeability. E G
T
 Cytokines such as interleukins (ILS) and
H
tumor necrosis factor ( INF) interact by O
D
autocrine and paracrine mechanism to cause
cellular or organ dysfunction.
 In presence of hypoxia, sepsis and acidosis,
lysosomal enzymes which are cytotoxic, are
released.
 They can cause myocardial depression and
coronary vasoconstriction.
 Prostacyclin is a vasodilator and inhibits
platelet aggregation.
 Thromboxane A2 causes pulmonary
vasoconstriction and platelet aggregation.
4.  Leukotrienes cause vasoconstriction, platelet T L P
E I P
activation and increased vascular permeability.
A S T
Endothelium derived relaxing factor ( EDRF) C T
H E
which is identified as an nitric oxide (NO) is found
I N
to produce sustained vasodilation and N I
G N
hypotension.
M G
 Thrombosis is increased due to inhibition of ant E
T
thrombin
H
 Thrombocytopenia is common. O
D
 Hepatic glycogenosis due to increased level of
glucagon, catecholamine and cortisol leads to
hyperglycemia.
 There is diminished peripheral utilization of
glucose due to increased level of insulin
antagonist like cortisol and growth hormone.
 Inadequate oxygen supplies to issue initiates
anaerobic metabolism.
 Consequently, there is metabolic acidosis,
production of lactic acid and H+ irons.
 Sodium pump fails to operate. Finally, the
lysosomal enzymes are released.
 These lead to cell death
4. 1min Describe PHASES T L P What is the
briefly about E I P phases of
There are four phases of changes.
phases cardiac A S T cardiac shock
shock The first two phases are reversible, the C T
H E
third one probably correctable and fourth is
I N
irreversible N I
G N
 Sympathetic impulses and the level of circulating
M G
catecholamine’s increase in response to E
T
hypovolemia, cardiogenic or neurogenic
H
stimulus. O
D
 Stretch receptors monitoring blood pressure in
the carotid sinus and aortic arch supply
information to the vasomotor center via the night
and tenth cranial nerves.
 The vasomotor center responds by sending
efferent impulses through the sympathetic
nervous system.
 As a result of excessive sympathetic stimulus,
there is constriction of the pre and post capillary
sphincters, resulting in inadequate venous return
leading to diminished cardiac output, clinical
manifestations of which are hypotension and
tachycardia.
 The mechanisms attempt to correct hypovolemia, T L P
E I P
improve cardiac output and the perfusion of vital
A S T
organs. C T
H E
 At this stage, transfusion and control of
I N
hemorrhage are usually effective in restoring the N I
G N
normal circulatory balance and tissue perfusion.
G
 On the other hand, if bleeding continues or M
E
treatment is delayed, the changes at
T
microcirculatory unit will continue to persist and H
O
will pass into the third and fourth phases of shock.
D
 Prolonged anoxia of the tissues will lead to
excessive production of lactic acid (acidosis).
 Lactic acid and anoxia cause relaxation of the
precapillary sphincters.
 In addition, thromboxane A2 and leukotrienes
(endogenous mediators) cause damage to the
endothelial cells of the capillaries of the
microcirculatory beds.
 These lead to formation of thrombus within the
capillaries (diffuse intravascular coagulation and
increased capillary permeability.
 Consequent to persistent constriction of the T L P
E I P
post capillary sphincter, blood remains
A S T
stagnant within the capillary bed. C T
H E
 Fluid from the capillaries leaks in to the tissue
I N
spaces due to increased permeability. N I
G N
 All fluids administered intravenously will go
M N
into the tissue spaces and circulatory blood E G
T
volume cannot be restored.
H
 Clinically, this is the stage of irreversible O
D
shock. There is severe loss of systemic
vascular resistance, severe myocardial
depression, (decreased cardiac output),
unresponsive hypotension and ultimately
multiple organ system failure.
 Endotoxic shock usually follows infection
with Gram-negative organism (75-80 %).
 The most common organism involved is
Escherichia coli (50 %).
 Other organism occasionally responsible for
endotoxin shock are, Pseudomonas
aeruginosa, klebsiella, proteus, bactericides
and aerobatic aero genes.
 Gram positive organisms, anaerobes, T L P
E I P
clostridium group are less common (20%).
A S T
 Bacterial endotoxin causes selective C T
H E
vasospasm at the post capillary end. I N
 Blood is pooled in the capillary bed. N I
G N
 There is inhibition of myocardial function and M G
cellular damage through complex E
T
biochemical changes H
 The patient in early septic shock feels warm O
D
due to vasoconstriction.
 This is called Warm shock.
 In the late phase, the patient feels cold due
vasoconstriction.
 This is called cold shock or late shock.
 Patient's skin becomes cold, clammy and
ashen gray.
5. 1min Explain VARIOUS BIOCHEMICAL AND PATHOLOGICAL T L P What is the
about I P changes in
CHANGES IN ENDOTOXIC SHOCK
The E S T endogenic?
Various  Diffuse intravascular coagulation A T Shock
pathological C E
 Increased capillary permeability
Changes in H N
endogenic  Metabolic acidosis I I
shock N N
 Release of superoxide and hydroxyl radicals
G G
 Failure of sodium pump operation M
E
 Water and electrolyte imbalance
T
 Excessive and uncontrolled systemic inflammatory H
O
response (SIR) - leads to organ changes
D
 Organ changes depends on the degree of hypo perfusion
and extent of the underlying pathology:
 Kidney: Patchy and massive cortical necrosis leading
to oliguria, anuria and azotemia.
 Persistent hypotension leads to acute tubular necrosis
and ultimately renal failure.
 Liver: Hepatocellular necrosis and degeneration
ultimately leading to hepatic failure.
 GI Tract: L P
I Pp
 Hypoxic mucosal injury increases systemic sepsis by S T
translocation of intraluminal microbes. T
E
 Congestion, hemorrhage and ulceration are responsible N
for hematemesis. T I
E N
 Lungs: Congestion or atelectasis leads to tachypnea, A I
progressive hypoxemia and reduced pulmonary C G
H
compliance. ARDS results from increased capillary I
permiability and thickening of the alveolar capillary N
G
membranes. Arterial PaO2 is low. M What is the
 Mechanical ventilation is needed E hemorrhagic
1min T shock
Describe the HEMORRHAGIC SHOCK H
6. hemorrhagic Early Phase (Compensatory Phase): O
shock D
 In the really phase there is mild vasoconstriction and
with the compensatory mechanism operating, the
patient has relatively normal blood pressure, tachy-
cardia and diaphoresis.
 Extremities remain warm.
 Patient appears restless and anxious.
 This phase can be easily managed by volume
replacement.
Intermediate Phase (Reversible Phase): T L P
E I P
 If the early phase remains untreated, the patient passes
A S T
in to the state of hypotension. C T
H E
 Patient progressively becomes pale, tachycardia
I N
persists and due to intense vasoconstriction, the N I
G n
periphery becomes cold and there may be sweating.
M G
 Due to diversion of blood to vital organs, the patient E
T
remains conscious and the urine output is within normal
H
limits. O
D
 Still with the adequate management, the shock state can
be reversed.
Late Phase (Irreversible Phase):
 Hypotension continues and can not be reversed by fluid
replacement because of stagnation of blood at the micro
vascular level.
 Extremities becomes cold and clammy because of For
the same reason, color of the skin becomes ashen gray.
 For the same reason, color of the skin becomes ashen
gray.
 Metabolic acidosis, coagulopathy and T L P
E I P
thrombocytopenia are associated.
A S T
 Practically imperceptible low volume pulse, oliguria, C T
H E
mental confusion (multiple organ failure) are the I N
combined results of circulatory failure and anaerobic N I
G N
metabolism. M G What is the
1min Explain the  Treatment of any kind is practically useless in this phase neurogenic
7. neurogenic E shock
shock and mortality varies between 3% and 100%. T
NEUROGENIC SHOCK H
O
 The basic pathological factors in both hemorrhagic and D
neurogenic shock are more or less the same except for
the fact that hemorrhagic shock is hypovolemic and
neurogenic shock, initially is normovolemic, though
this becomes hypovolemic in the later phase due to
pooling and stagnation of blood in the micro vascular
capillaries.
 The compensatory phase in neurogenic shock, however,
very transient.
 In the reversible phase, unlike hypovolemic shock,
pallor is absent, on the contrary, the face may be
flushed.
8. 1min Explain the ENDOTOXIC SHOCK L P What is the
endotoxic T I P endotoxic
 In the initial phase of endotoxin shock because of
shock and its E S T shock and
management precapillary dilatation and diversion of blood through A T its
C E management
met arteriolar shunt, the patient remains alert, there is
H N
marked flushing of the face and the skin feels warm. I I
N N
 There are temperature change >38℃ or < 36℃,
G G
bounding pulse, heart rate >100 beats per min, M
E
respiratory rate > 20/min, WBC > 12000/mL3
T
 When, however, the state of shock persists, there is H
O
intense constriction of sphincters at either end of the
D
capillary bed.
 The patient becomes pale and there is profuse sweating.
Extremities are cold and clammy.
 Urine output is markedly reduced.
 If the shock condition does not improve, the patient
passes clinically to the stage of 'irreversible shock'.
HEMORRHAGIC SHOCK: MANAGEMENT T Basic
management of hemorrhagic shock is to stop the bleeding and
replace the volume which has been lost. Restoring circulatory
volume
Maintenance of cardiac efficiency
Administration of oxygen to avoid metabolic acidosis L P
T I P
Pharmacological agents- corticosteroids
E S T
Control of hemorrhage A T
C E
ENDOTOXIC SHOCK INVESTIGATIONS:
H N
CBC I I
N N
Hematocrit
G G
Coagulation Profile M
E
Liver and Renal function test
T
Chest radiography H
O
USG, CT, MRI
D
ECG monitoring
What is the
PRINCIPLE OF MANAGEMENT:
9. 1min principle of
Describe the  To correct the hemodynamic unstability due to sepsis management
principle of
Appropriate supportive care
management
 To remove the source of sepsis
 Two wide bore cannulas sited.
 Folly’s catheter.
 Oxygenation with face mask is to be given.
 Mechanical ventilation may be needed in severe cases.
Antibiotics T L P
E I P
IV fluids and electrolytes
A S T
Correction of acidosis C T
H E
Maintenance of blood pressure
I N
Vasodilator therapy N I
G N
Diuretic therapy
M G
Corticosteroids E
T
Treatment of diffuse intravascular coagulopathy
H
Treatment of myocarditis O
D
Elimination of source of infection
Intensive insulin therapy What is the
10. Explain nursing
NURSING ASSESSMENT
1min about the management
nursing CABs: Circulation, Airway, breathing, and Focused of obstetric
Management shock
assessment of tissue perfusion;
of obstetric
shock • Vital signs
• Peripheral pulses
• Level of consciousness • Capillary refill
•Skin (e.g., temperature, color, moisture)
•Urine output •Brief history Taking
•Events leading to shock
•Onset and duration of symptoms
•Allergies
IMMEDIATE NURSING CARE OF SHOCK T L P
E I P
• Check for a response.
A S T
• Give Rescue Breaths or CPR as needed. C T
H E
• Lay the person flat, face-up, but do not move him or her if you
I N
suspect a head, back, or neck injury. N I
G N
• Raise the person's feet about 12 inches. Use a box, etc.
M G
If raising the legs will cause pain or further injury, keep him or E
T
her flat. Keep the person still.
H
• Do not raise the feet or move the legs if hip or leg bones are O
D
broken.
Keep the person lying flat.
• Check for signs of circulation.
If absent, begin CPR.
• Keep the person warm and comfortable. Loosen belt (s) and
tight clothing and cover the person with a blanket.
NPO: Even if the person complains of thirst, give nothing by
mouth
If the person wants water, moisten the lips. • Reassure the
person. Make him or her as comfortable.
• Fluid and blood replacement: T L P
E I P
Open IV line on both hands with two wide bore cannulas and
A S T
start fluid rapidly as advised. C T
H E
• Administer oxygen via face mask.
I N
• Identify the cause and treat accordingly. N I
G N
• Vasoactive medications to improve cardiac contractility, i.e.
M G
Dopamine, Dobutamine, Noradrenaline. E
T
H
O
D
Summary
By this we have many topic such as obstetric emergencies ,
And obstetric shock about definition , phases types , sign and
symptoms of medical management and surgical
management
Conclusion
I hope that we have understand about the obstetric
emergencies ,and obstetric shock it very conscious during
labour .
Bibliography
1. Text book of comprehensive midwifery and
gynecological nursing,
annamma Jacob ,5th edition ,pub –jaypee, page no358, 216-218.
2. Text book of obstetrics Dc dutta , Hiralal konar, 9th
edition ,
pub jyapee ,page no287,569.
3. Text book for midwifery myles , diane m. fraser
,margaret a. cooper .
14th edition , pub international edition page no 236-
237,160,266.
4. Text book of maternity nursing ,av raaman 20th edition
pub wolters kluwers page no-549,550
, https://www.slideshare.net/priyankagohil10/obstetrical-shock-
159376566
https://www.slideshare.net/lisachadha/obstetrical-
emergencies-130964508
LESSON PLAN
ON
OBSTERICAL EMSRGENCIES
AND OBSTERICAL SHOCK
SUBMITTED TO SUBMITTED BY
MRS. ANCHULA ESTALLA MAM SHEELABAI
ASSISTANT PROFESSOR MSC 2ND YEAR
EBMCON EBMCON
OBJECTIVES
GENERAL OBJECTIVES;
• At the end of this sessions students are able to gain knowledge and skill development, collaborative exchange of ideas
, furthering student able to learn about obstetrical emergencies and obstetrical shock
SPECIFIC OBJECTIVES.
At end of this presentation the student will be able to
To Introduce. Obstetrical emergencies and obstetrical shock
To define the. Obstetrical emergencies and obstetrical shock
To enlist the causes of and signs and symptoms Obstetrical emergencies and obstetrical shock
To explain the risk factors and principles of Obstetrical emergencies and obstetrical shock
To enlist the complication of Obstetrical emergencies and obstetrical shock
To explain briefly about the intrapartum management , medical , surgical during labour of Obstetrical emergencies and obstetrical shock
To describe the nursing management Obstetrical emergencies and obstetrical shock
IDENTIFICATION DATA/
Name of the student teacher: Sheela Bai.
Group: M SC (n)2nd year
Date :
Subject; nursing management
Topic : electronic medical management
Venue ; Msc ( N) students
Duration ; 45 min
Av -aids ; OHP, BLACK BOARD , PPT
Previous knowledge ; Group is having some knowledge regarding obstetrical emergencies obstetrical shock
Name of the evaluator : Mrs. estallamam

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Time Specific Content Teaching Learning Av- aids Evaluation

possible postpartum hemorrhage.

Premature rupture of membranes Premature rupture of

Prolapsed umbilical cord A prolapse of the umbilical cord

damage or possible death.

4. Rapid Response Team

5. Emergency Drills and Simulation

Outpatient Setting – Medications given Procedures

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