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Ambo University 
College of Health Sciences 
Department of Medicine 
1 
Obstetric Emergency 
By : Aregahegn T & Aster.A 
July,2014 
Ambo,Ethiopia
Outline 
Before delivery 
-Hyperemesis G 
-PROM 
-Abortion 
-Ectopic P 
-Preeclampsia & E 
-Abreptio P 
-Placenta P 
During delivery 
-Obstructed labour 
-Uterine rupture 
-Cord prolapse 
After delivery 
-Retained P 
-Placenta accreta 
-Injury to the cervix 
2
Hyperemesis Gravidarum 
It is the actual vomiting in the morning , which 
leads to dehydration & significant amount of wt 
loss 
 It is usually start between the 4th and 6th weeks 
of pregnancy and improves or disappears about 
the 12 th week. 
 The vomiting is not confined to the morning but 
it is repeated throughout the day until it affects 
the general condition of the patient 
3
Etiology 
1 Hormonal: 
High human chorionic gonadotrophin (hCG) 
stimulates the chemoreceptor trigger zone in 
the brain stem including the vomiting center 
in the conditions where the hCG is high as in:- 
a. early in pregnancy, 
b. vesicular mole and 
c. multiple pregnancy. 
4
Cont’d 
2.Allergy: to the corpus luteum or the released 
hormones. 
3. Deficiency of: 
a. adrenocortical hormone and /or, 
b. vitamin B6 and B1 
4.Nervous and psychological: 
a due to psychological rejection of an 
unwanted pregnancy, 
b fear of pregnancy or labour so it is more 
common in primigravidae 
5
Diagnosis 
Symptoms: 
>The patient cannot retain anything in her 
stomach, 
> vomiting occurs through the day and night even 
without eating. 
>Thirst, constipation and oliguria. 
>In severe cases, vomitus is bile and/ or blood 
stained. 
> Finally, there is manifestations of Werniche’s 
encephalopathy as drowsiness, nystagmus and 
loss of vision then coma. 
6
Cont’d 
Signs: 
Manifestations of starvation and dehydration: 
*Loss of weight.5% 
* Sunken eyes. 
* Dry tongue and inelastic skin. 
* Pulse: rapid and weak. 
* Blood pressure: low. 
* Temperature: slight rise 
7
Management 
Hospitalization 
For observation, fluid therapy 
Intravenous fluids 
Drugs 
8
PROM 
 Premature ROM is defined as rupture of the 
chorioamnionic membranes prior to the onset 
of labor 
 Prolonged ROM usually refers to ROM for 
more than 24 hours 
 It is a complication in one quarter to one 
third of preterm births 
9
Cont’d 
• May or may not be associated with PTL 
(preterm labor) 
• Complicates 1/3 of all preterm deliveries 
• Around 1-2% of pregnancies 
• Majority of patients delivery within 1 week 
10
Risk Factors 
• Previous preterm PROM 
• Incompetent cervix 
• Alterations in vaginal pH 
– Infections 
• Smoking 
• Multiple gestation 
11
Diagnosis 
History 
– Gush of fluid 
– Constantly wet 
Physical 
– Pooling fluid - posterior fornix 
– Fluid per os 
– Examine with sterile speculum to prevent/limit 
digital exam of cervix, to minimize risk of 
ascending infection and amnionitis 
12
Cont’d 
Test 
– Fern - cervical mucus broad fern vs. amniotic 
fluid narrow fern 
– pH (Nitrazine) - turns blue 
– Cervicovaginal fetal fibronectin > 50 ng/ml 
– Val-salva 
Imaging-Ultrasound 
13
Complication 
Maternal effects 
 Increase in chorioamnionitis 
 Increase in Cesarean delivery 
 Spontaneous labor in ~ 90% within 48 hr. of 
membrane rupture 
 Increased risk of placental abruption 
 Thromboembolic disease 
14
Cont’d 
Fetal effects 
 Increase in RDS 
 Increase in intraventricular hemorrhage 
 Increase in neonatal sepsis and subsequent 
cerebral palsy 
 Increase in perinatal mortality 
 Increase in cord prolapse 
 Abruption 
 Oligohydramnios 
15
Management 
Considerations 
When? 
• If later than 34 weeks, consider induction 
• If <34 weeks, consider tocolysis for steroid 
course, then expectant management or 
delivery? 
• Chorioamnionitis necessitates immediate 
delivery 
16
Cont’d 
Supported Interventions 
- Tocolysis for steroid administration if no 
contraindications and fetus 24 – 34 weeks 
- Prophylactic antibiotics 
 May prolong latent period by an average of 
5-7d 
 May reduce maternal amnionitis and 
neonatal sepsis 
- Ultrasound for fetal weight 
- Expectant management for any gestational age 
17
Cont’d 
• Steroids 
– To enhance fetal lung maturation and 
decrease RDS 
• Tocolytics 
– Randomized trials have shown no pregnancy 
prolongation 
18
ABORTION 
Spontaneous abortion, or “miscarriage,” is 
defined as pregnancy loss before 20 weeks of 
gestation. 
Most of these occur before 12 weeks. 
10-15% of clinically recognized pregnancies 
terminate in spontaneous abortion. 
19
Cont’d 
The causes of spontaneous abortion are both 
fetal and maternal. 
Chromosomal anomalies such as aneuploidy, 
polyploidy, and translocations are present in 
approximately 50% of early abortuses. 
Maternal factors include luteal-phase defect, 
poorly controlled diabetes, and other 
uncorrected endocrine disorders. 
20
Cont’d 
Physical defects of the uterus, such as 
submucosal leiomyomas, uterine polyps, or 
uterine malformations may prevent 
implantation adequate to support fetal 
development. 
Systemic disorders affecting maternal 
vasculature, such as antiphospholipid 
antibody syndrome, coagulopathies, and 
hypertension, may predispose to miscarriage. 
21
Cont’d 
 Finally, infections with bacteria such as 
Toxoplasma, Mycoplasma, and Listeria, as 
well as viral infections, have also been 
implicated as causes of abortion. 
Ascending infection is particularly common in 
second-trimester losses. 
Clinically the patient may have bleeding or 
shock. 
22
Essentials of Diagnosis 
 Suprapubic pain, uterine cramping, and/or back pain 
 Vaginal bleeding 
 Cervical dilatation 
 Extrusion of products of conception. 
 Disappearance of symptoms and signs of pregnancy. 
 Quantitative -HCG 
 Abnormal ultrasound findings 
23
Ectopic pregnancy 
The term applied to implantation of the fetus 
in any site other than a normal intrauterine 
location. 
The most common site is within the fallopian 
tubes (∼90%). 
Other sites include the ovary, the abdominal 
cavity, and the intrauterine portion of the 
fallopian tube (cornual pregnancy). 
24
Cont’d 
 The most important predisposing condition 
are: 
- Prior pelvic inflammatory disease resulting in 
fallopian tube scarring 
- Factors leading to peritubal scarring and 
adhesions such as endometriosis, and 
previous surgery. 
- Intrauterine contraceptive devices 
- Fallopian tube may normal in some cases 
25
Cont’d 
Ovarian pregnancy is presumed to result from 
the rare fertilization and trapping of the ovum 
within the follicle just at the time of its 
rupture. 
Abdominal pregnancies may develop when 
the fertilized ovum fails to enter or drops out 
of the fimbriated end of the tube. 
26
Cont’d 
In all these abnormal locations, the fertilized 
ovum undergoes its usual development with 
the formation of placental tissue, amniotic 
sac, and fetus, and the host implantation site 
may develop decidual changes. 
27
Cont’d 
Morphology. Tubal pregnancy is the most 
common cause of hematosalpinx (blood-filled 
fallopian tube) and should always be suspected 
when a tubal hematoma is present. 
 Initially the embryonal sac, surrounded by 
placental tissue composed of immature chorionic 
villi, implants in the lumen of the fallopian tube. 
 With time trophoblastic cells and chorionic villi 
start to invade the fallopian tube wall as they do 
in the uterus during normal pregnancy. 
28
Cont’d 
 However, proper decidualization is lacking in 
the fallopian tube, and growth of the 
gestational sac distends the fallopian tube 
causing thinning and rupture. 
 Fallopian tube rupture frequently results in 
massive intraperitoneal hemorrhage. 
29
Cont’d 
Less commonly the tubal pregnancy may 
undergo spontaneous regression and 
resorption of the entire conceptus. 
Still less commonly, the tubal pregnancy is 
extruded through the fimbriated end into the 
abdominal cavity (tubal abortion). 
30
Risk Factors 
High risk 
• Tubal surgery 
• Sterilization 
• Previous ectopic pregnancy 
• In utero exposure to diethylstilbestrol 
• Use of IUD 
• Documented tubal pathology 
Moderate risk 
Infertility ,Previous genital infections ,Multiple sexual 
partners 
Slight risk 
• Previous pelvic/abdominal surgery, Cigarette smoking, 
Vaginal douching ,Early age at first intercourse (< 18 years) 
31
Clinical Features 
 The clinical course of ectopic pregnancy is 
punctuated by the onset of severe abdominal 
pain, most commonly about 6 weeks after a 
previous normal menstrual period, when 
rupture of the tube leads to pelvic 
hemorrhage. 
32
Cont’d 
Rupture of a tubal pregnancy constitutes a 
medical emergency. 
 In such cases the patient may rapidly develop 
hemorrhagic shock with signs of an acute 
abdomen, and early diagnosis is critical. 
Chorionic gonadotropin assays, ultrasound 
studies, and laparoscopy may be helpful to 
diagnose. 
33
PREECLAMPSIA AND ECLAMPSIA 
 Preeclampsia refers to a systemic syndrome 
characterized by widespread maternal 
endothelial dysfunction presenting clinically 
with hypertension, edema, and proteinuria 
during pregnancy. 
Preeclampsia should be distinguished from 
gestational hypertension that can develop in 
pregnancy without proteinuria. 
34
Cont’d 
Minimum criteria 
– BP ≥ 140/90 mm Hg after 20 weeks' gestation 
– Proteinuria ≥ 300 mg/24 hours or ≥ 1 + 
dipstick 
Increased certainty of preeclampsia 
– BP ≥ 160/110 mg Hg 
– Proteinuria 5.0 g/24 hours or ≥ 2+ dipstick 
35
Cont’d 
– Serum creatinine > 1.2 mg/dL unless known 
to be previously elevated 
– Platelets 
– Microangio< 100,000/mm3pathic hemolysis 
(increased LDH) 
– Elevated ALT or AST 
– Persistent headache or other cerebral or 
visual disturbance 
– Persistent epigastric pain 
36
Risk factors 
• Primigravida 
• Multipara with change 
of partner 
• Chronic hypertension 
• Chronic renal disease 
• Diabetes mellitus 
• Multifetal gestation 
• Polyhydramnios 
• RH Isoimmunized 
pregnancy 
• Hydatidiform mole 
• Previous history of 
preeclampsia 
• Family history of 
pregnancy induced 
hypertension 
37
Types 
Mild pre-eclampsia: blood pressure ≥ 140/90 mmHg ± oedema. 
Severe pre-eclampsia: 
- blood pressure >140/90 mmHg + proteinuria ± oedema or 
- diastolic blood pressure>110 mmHg or 
- cerebral or visual disturbances. 
N.B. 
Imminent eclampsia : It is a state in which the patient is about to 
develop eclampsia. Usually there are : 
- blood pressure much higher than 160 /110 mmHg , 
- heavy proteinuria (+++or ++++), 
- hyperreflexia, 
- severe continuous headache, 
- blurring of vision, 
- epigastric pain. 
Fulminating pre-eclampsia: a rapidly deteriorating pre-eclampsia to 
be imminent eclampsia. 
38
Classification 
39 
Criteria Mild preeclampsia Severe preeclampsia 
Blood pressure < 160/110 > 160/110 
Symptoms Absent Present 
Proteinuria < 5 g/dl 24 hours collection > 5 g/dl; > 2+ on dipstick 
Liver and Renal function Normal Abnormal 
Platelet count Normal Thrombocytopenia 
Pulmonary edema Absent Present 
Convulsions Absent Present 
HELLP syndrome Absent Present 
Fetal growth restriction Absent Present 
The presence of any one of the above findings is sufficient to lead to a classification of the 
preeclampsia into the severe category
Pathogenesis 
The exact mechanisms leading to 
development of preeclampsia are still being 
investigated; however, it is clear that the 
placenta plays a central role in the 
pathogenesis of the syndrome, since the 
symptoms disappear rapidly after delivery of 
the placenta. 
The placenta reveals various microscopic 
changes, most of which reflect malperfusion, 
ischemia, and vascular injury 
40
Clinical Feature 
The onset is typically insidious, characterized 
by hypertension and edema, with proteinuria 
following within several days. 
Headaches and visual disturbances are 
serious events and are indicative of severe 
preeclampsia, often requiring delivery. 
Eclampsia is heralded by central nervous 
system involvement, including convulsions 
and eventual coma. 
41
Symptoms 
• Visual disturbances: blurring of vision, flashes of 
light or blindness. 
• Epigastric or right upper quadrant pain: due to 
enlargement and subcapsular haemorrhage of 
the liver. 
• Nausea and vomiting : due to congestion of 
gastric mucosa and/ or cerebral oedema. 
• Oliguria or anuria: due to kidney pathology. 5 
42
Investigations 
• Complete urine examination: for proteinuria, 
pus cells, RBCs, casts,specific gravity, culture 
and sensitivity . 
• Kidney function tests: serum uric acid > 6 mg 
% is abnormal during pregnancy. It is more 
specific for pre-eclampsia than creatinine. 
• Coagulation status :Platelet count, fibrinogen 
and FDP as DIC may develop. 
43
cont’d 
• Eye fundus examination. 
• Tests for foetal well being: as 
- ultrasound, 
- daily foetal movement count, 
- non-stress test, 
- oxytocin challenge test (if needed) 
44
Complication 
45 
Fetal 
• IUGR 
• Oligohydramnios 
• Placental infarcts 
• Placental abruption 
• Prematurity 
• Uteroplacental 
insufficiency 
• Perinatal death 
Maternal 
• CNS seizures & stroke 
• DIC 
• ↑↑ CS 
• Renal failure 
• Hepatic failure or 
rupture 
• Death
Management 
46 
Mild preeclampsia Severe preeclampsia 
Management depends on: 
•Gestational age 
•Fetal well being 
If at term : 
•Admission 
•Ascertain fetal maturity 
•Terminate pregnancy via the most appropriate 
route 
If preterm : Conservative management 
•Admission 
•Bed rest 
•Follow vital signs; organ function tests; platelet 
count; development of symptoms; level of 
proteinuria; evidence of hemolysis; fetal well being 
tests 
•If severe disease develops during conservative 
management or achieve fetal maturity; proceed to 
delivery 
If any one of the evidences of severe 
preeclampsia develop or are present, 
conservative management option is 
not possible. 
Conservative management is 
contraindicated. 
Management of severe preeclampsia 
includes: 
•Admission 
•Administration of anticonvulsants-valium; 
magnesium sulphate; 
phenytoin 
•Control of severe hypertension by IV 
antihypertensives such as hydralazine 
or labetalol 
•After mother is stabilized, proceed to 
delivery irrespective of fetal gestational 
age
Abruptio placenta 
Detachment of placenta after 24 weeks of 
gestation and before delivery 
Predisposing factors: 
• Multiparity 
• Hypertension 
• Blunt external abdominal trauma (direct) 
• Cocaine use 
• Previous third trimester bleeding 
• Age older than 35 years 
47
Types 
Revealed (80%) 
- Pain + Vaginal bleeding 
Concealed (20%) 
-Pain/Shock 
-No vaginal bleeding 
48
Management 
• Management is influenced by gestational age 
and degree of abruption 
• Indicators for delivery- 
– Fetal intolerance 
– DIC 
– Labor 
• Vaginal delivery is acceptable 
49
Cont’d 
• Correct SHOCK- IV access – 2 large bore 
cannulae 
-Crystalloids IV – emergency 
-BLOOD as soon as possible 
• Correct DIC - Heparin 
• Catheterize - hourly urine output chart 
• Assess for delivery 
50
Placenta previa 
Placenta attached in the lower segment 
There are four grades 
1) Low lying - lower than upper implantation 
2) Marginal – placental edge approaches 
cervical os 
3) Partial – implantation occludes portion of the 
cervical os 
4) Total – implantation totally obstruct cervical 
os 
51
Cont’d 
52
Types 
• Minor – Enters LUS but does not cover os 
• Major – Covers internal os completely 
53
Etiology 
• Unclear 
• Any damage to endometrium or myometrium 
Scar tissue impedes migration away from 
os 
• Multiple pregnancy- large surface area 
• Cigarette smoking- vasoconstriction 
• Cocaine Use – Vasoconstriction-hypertrophy 
• Rh issoimmunization 
• Syphilis 
54
Cont’d 
• Previous Placenta Praevia 
• Maternal Age – reduced uterine blood flow 
needs greater surface area 
• Parity - 3 previous deliveries 2.6 fold 
Vessels at site of previous placenta reduced 
flow discourage implantation 
55
Presentation 
• Antepartum Haemorrhage 
- Late pregnancy 
- Painless bleeding ( most common) 
• Malpresentation 
-Breech/High Head/Unstable lie in 3rd 
trimester 
56
Diagnosis 
• The clinically important diagnosis of placenta 
previa is therefore a late second or early third 
trimester diagnosis (after 24-26 weeks 
gestation) 
• Ultrasound is the easiest, most reliable way to 
diagnose (95-98% accuracy) 
• Pelvic examination is contraindicated 
57
Management 
Antenatal 
• Bed rest indicated 
• Inpatient vs Outpatient 
• Major Vs minor 
• Anaemia 
-Regular Hb 
-X-match/Transfuse 
58
Cont’d 
• Delivery should depend upon type of previa 
– Complete previa = c/section 
– Low lying = probable attempted vaginal 
delivery 
– Marginal/partial = it depends!Consider 
“double setup” for uncertain cases 
59
Obstructed labor 
Obstructed labor is failure of progressive 
descent of the presenting part of the fetus in 
the birth canal for mechanical reasons inspite 
of good uterine contraction. 
The prevalence in developing countries is 
about 1-2% in the referral hospitals 
60
Risk Factors 
Ht <150 cm 
Previous Hx of prolonged or OL 
Clinical pelvimetry 
Soft tissue anomalies 
Estimate size of fetus late in Pregnancy 
61
Etiology 
A. Maternal causes 
 Cephalo-pelvic disproportion (CPD) 
• Contracted pelvis 
• Bone deformities 
• Soft tissue obstruction 
62
Contracted pelvis 
 Generally contracted pelvis involves contracture 
of:- 
- the pelvic inlet 
- the mid pelvis 
- the pelvic outlet, or by combinations of 
these. 
 Inlet contracture- 
-AP diameter of < 10 cm – normally 11cm 
-Transverse diameter of < 12cm ---normally 
–13.5cm 
-Diagonal conjugate <11.5cm,normally-12.5cm 
63
Cont’d 
 Mid cavity contracture – 
-AP < 11.5cm ---normally -11.5cm 
-Transverse diameter < 9.5cm 
Outlet contracture- 
-Inter tuberous diameter <8cm- normally-10cm 
64
Cont’d 
 Clinical pelvic assessment done after emptying 
the bladder & putting the woman in lithotomy 
position. 
• Then we assess the following:- 
-Reachability of sacrum promontory. 
-Smoothness &concavity of sacrum. 
-Straightness of sidewalls and projection of 
ischial spine. 
-Size of pubic angle & intertuberous distance 
65
Bone deformity 
Small pelvis -developmental or congenital 
Abnormal shape of the pelvis due to: 
-Diseases like rickets & osteomalacia or 
tuberculosis 
-Previous accidents. 
-Tumors of the bones. 
-Childhood poliomyelitis affecting shape of the hips. 
-Spine: -Lumbar kyphosis. 
- Lumbar scoliosis 
66
Soft tissue obstruction 
Tight perineum in primi 
Vaginal abnormalities- septa, scar, tumors 
Cervical stenosis- infection, surgery, tumors 
Uterine factors- fibroids, congenital anomalies 
Ovarian tumor- impacted in the pelvis 
67
B. Fetal causes 
Large sized fetus / Macrocosmic 
 Congenital anomalies- Hydrocephalus 
 Locked and conjoined twins 
 Shoulder dystocia 
 Malpositions and Malprsentation 
– Breech 
– Transverse lie 
– Brow presentation 
– Mento- posterior position (face) 
68
Diagnosis 
History 
– The patient is usually young teenage 
– Abnormally prolonged labor 
 General examination 
– Tired, exhausted and anxious. 
– Tachycardic, tachypenic . 
– Dehiydrated 
-Temprature increase(>38) 
69
Cont’d 
Abdominal examination 
– Hypertonic or hypotonic uterine contraction. 
– Uterus is hard and tender 
– FHR abnormality – tachycadia, bradycardia 
or may be absent 
– Bladder often distended. 
– Catheterization may be often difficult 
and the urine is blood stained. 
70
Cont’d 
Vaginal examination 
-Vulva is edematous. 
- Cervix fully or partially dilate& edematous 
-The liquor is meconium stained and often 
foul smelling. 
-The presenting part is high, not engaged, 
with excessive moulding and Large caput. 
71
Complication 
Maternal 
- Maternal distress 
– Uterine rupture – UNcommon in primi 
– PPH- atonic or traumatic 
– Infection -sepsis, abscess and peritonitis 
– Infertility 
– Psychological trauma 
72
Cont’d 
Fetal 
• Cerebral birth trauma 
• Asphyxia 
• Early neonatal infection 
• Congenital pneumonia 
• Intracranial hemorrhage from excessive 
moulding. 
• Birth injuries 
73
Management 
Prevention 
• Good nutritional supply since childhood 
• Avoid early marriage 
• Universal ANC 
–To screen out the " at risk mothers " 
–Pelvic assessment at 38-39wks 
• Promote family planning services 
• Elective caesarean delivery when 
indicated 
74
Cont’d 
Specific treatment 
• Resuscitation 
• Broad spectrum antibiotics 
• Operative delivery 
– Episiotomies for some primis with tight perineum. 
– Vacum / Forceps delivery 
• Alive fetus and head < 1/5 above pelvic brim (+1) 
• Mild-moderate moulding 
– Destructive delivery 
• Dead fetus, fully dilated cervix and no evidence of 
rupture or imminent rupture of the uterus 
75
Cont’d 
- Caesarean delivery 
• Alive fetus with incomplete cervical dilatation or 
high station. 
• Alive fetus with Brow or Mento posterior 
position or face 
• Alive or dead fetus with evidence of imminent 
uterine rupture. 
- Caesarean Hysterectomy 
• Severely bruised lower uterine segment 
• Major uterine vessels torn 
76
Uterine Rupture 
Tear in the wall of the uterus w/c commonly 
occurs in the lower uterine segment. 
Common in multiparas and rarely occurs in 
primiparas. 
Peak incidence is 3rd /4th pregnancy. 
It can occur anteriorlly , posteriorlly , laterally 
or combination of these. 
-anterior rupture is the commonest 
77
In obstructed labour: 
- It is usually in lower uterine segment. 
- Usually oblique or transverse. 
- More on the left side due to; 
i) dextrorotation of the uterus. 
ii) left occipito-positions are more common. 
 In rupture scar: 
At the site of the scar. 
78
Cont’d 
Can be complete or incomplete 
1 Complete(true) uterine rupture 
-includes the entire thickness of the uterine wall 
and serosa resulting in direct communication 
with peritoneal cavity. 
2 Incomplete (uterine dehiscence) 
-is the defect of the uterine wall that is 
contained by the visceral peritoneum or broad 
ligament. 
-common in patients with prior C/S scar 
79
Cont’d 
Incidence 
0.05% for all pregnancies. 
 0.8% for women with low-transverse uterine 
scar. 
4-8% -prior classic scar. 
all pregnancies following myomectomy may 
be complicated by uterine rupture. 
80
Causes 
• OL specially in multis 
• Rupture or dehiscence of previous c/s scar 
• Excessive stimulation 
• Difficult instrumental delivery 
• Internal podalic version -particularly after 
drainage of the liquor 
• Difficult manual removal of placenta 
• Sharp penetrating trauma 
81
Clinical features 
 History 
• History of prolonged labor 
• Worsening abdominal pain (supra pubic) 
persisting b/n contraction 
• Sudden cessation of uterine contraction 
• Absent fetal movement 
• Variable degree of vaginal bleeding 
• Shoulder pain on lying down due to irritation of the phrenic 
nerve by accumulating blood under the diaphragm 
82
Cont’d 
 P/E-reduced BP 
-feeble and rapid pulse/impalpable 
-Signs of severe anemia-pallor 
• Abdomen -tender & distension 
-Scar of the previous operation. 
-easily palpable fetal parts 
-absent FHB & uterine contraction 
-signs of fluid collection/variable shifting dullness 
• Pelvic examination 
-active vaginal bleeding 
-the presenting part may be impacted or 
retracted in to peritoneal cavity. 
83
Differential Diagnosis 
• Abruptio placentae. 
• Disturbed advanced extrauterine pregnancy. 
• Other causes of acute abdomen. 
84
Management 
1 Supportive management 
• Secure IV line with two lines 
• Vigorous infusion of crystalloids 
• Do HCT ,B/g 
• Broad spectrum IV antibiotics 
• Catheterize 
85
2 Definitive management 
• Repair- If it is amenable for repair and the 
patient did not complete her family. 
-usually with tubal ligation if future 
fertility is not desired. 
• Hysterectomy-total/subtotal if posterior, 
lateral 
• Subtotal hysterectomy is less time consuming 
so it is done if there is no cervical tear. 
86
Cord presentation and prolapse 
Cord presentation and prolapse describe a 
situation in which the umbilical cord is felt 
anterior to the fetal presenting part on vaginal 
examination. 
If the membranes are intact it is a cord 
presentation while with ruptured membranes 
it is identified as a prolapsed cord. 
 As long as the membranes are not ruptured, 
the risk of compression and asphyxia is low. 
87
Cont’d 
Cord prolapse can be: 
1 Overt- being felt inside the cervix, the 
vagina or even hanging outside the introitus. 
2 Occult- with the cord anterior to 
the presenting part in the lower segment but 
not felt on digital vaginal exam 
88
Cont’d 
Cord prolapse can occur in: 
– vertex and frank breech presentations-0.5% 
– complete breech -5% 
– footling breech -15% and 
– shoulder presentation -20%. 
89
Etiology 
• Malpresentations in labor 
• PROM 
• Amniotomy with a high fetal station 
• Polyhydramnios with sudden membrane 
rupture 
• Second twin delivery 
• Internal podalic version 
• Cephalopelvic disproportion in labor 
90
Complications 
• Cord compression and constriction of umbilical 
vessels due to cold exposure outside the introitus 
can lead to fetal asphyxia and death. 
• Partial cord occlusion may give the fetus some 
time but in complete cord occlusion the fetus can 
die of asphyxia in 5-7 minutes if cord 
compression is not immediately relieved. 
• There is increased maternal risk from cord 
prolapse because of emergency operative vaginal 
or abdominal delivery performed in order to 
salvage the fetus 
91
Diagnosise 
• In the vagina or inside the cervix anterior to the presenting 
part 
– Check for pulsation and its rate 
– Replace the cord immediately into the vaginal ( not inside 
the uterus) canal if outside the introitus 
• If membrane is intact, cord presentation is diagnosed 
• In all malpresentations, a careful search for cord presentation 
or prolapse should be made 
• Occult cord prolapse can only be diagnosed by detection of 
abnormal fetal heart rate patterns 
• In cases of malpresentations, sonographic search can also be 
made for cord anterior to the fetal presentation 
92
Management 
Immediate management 
If cord is pulsating: 
• Put mother in knee-chest position 
• Initiate oxygen administration by face mask 
5L/min 
• Insert bladder catheter and infuse the bladder 
with 0.5L of saline 
• Replace the cord into the vaginal canal 
• Push fetal presenting part upwards via the 
examining hand in the vagina to relieve 
compression of the cord by the presentation 
• Prepare for immediate delivery 
93
Cont’d 
Delivery : 
Non-pulsatile cord: 
• Manage as any other labor as the cord prolapse will 
not alter the course of labor (dead fetus) 
Pulsatile cord: 
 Second stage of labor: 
• Expedite delivery by forceps delivery if other 
conditions for forceps delivery are met. 
• Breech extraction if other conditions for breech 
extraction are met (full cervical dilation) 
 First stage of labor: 
• caesarean delivery. 
94
Postpartum hemorrhage 
Excess blood loss after delivery (>500ml ) 
It is the leading cause of maternal mortality 
Types 
- Primary PPH in the first 24 hours 
- Secondary PPH the first 24 hrs to 6 weeks. 
 Massive PPH may be truly terrifying 
95
Etiology 
• The “4 T’ s” : tone, tissue, trauma, and 
thrombosis 
• Uterine atony, i.e., failure of the uterine 
contraction and retraction of myometrial muscle 
fibers following delivery of the baby. 
• PPH in a previous pregnancy is a major risk 
factor and every effort should be made to 
determine its severity and cause. 
• Birth weight, labor induction and augmentation, 
chorioamnionitis 
96
Cont’d 
Primary PPH 
The most important cause of massive PPH is uterine 
atony when the uterus is not contracted 
Steps to stop bleeding 
1. Massaging the uterus to cause it to contract 
2. Bimanual compression-Under general anaesthesia, 
the uterus is firmly compressed for 5-30 minutes 
3. Uterine contraction is maintained by oxyitocin 
4. Prostaglandin -through the anterior abdominal wall. 
97
Aetiology: 
(A) Placental site haemorrhage: 
(I) Atony of the uterus(90%) 
II) Retained placenta. 
(III) Disseminated intravascular coagulation 
(B) Traumatic haemorrhage: 
Rupture uterus, cervical, vaginal , vulval or 
perineal lacerations. 
98
Complications 
1- Maternal death in 10% of postpartum 
haemorrhages. 
2- Acute renal failure. 
3- Embolism. 
4- Sheehan’s syndrome. 
5- Sepsis. 
6- Anaemia. 
7- Failure of lactation 
99
Cont’d 
Secondary PPH 
1. Retained products or conception 
2. Uterine infection 
3. placenta accrete 
4. Injury to cervix 
100
Retained placenta 
Incidence 
Retained placenta is found in 2% of deliveries. 
The frequency of retained placenta is markedly 
increased at gestation <26 weeks 
At term, 90% of placentas will be delivered within 15 
minutes. 
Once the third stage exceeds 30 minutes, there is a 
ten-fold increase in the risk of hemorrhage 
101
Causes: 
• Atony of the uterus :due to causes mentioned 
before. 
• Constriction ring. 
• Rupture uterus :where the placenta passes to the 
peritoneal cavity. 
• Abnormal adherence of the placenta which may be: 
i) Simple adhesion: Manual separation can be done 
easily. 
ii) Morbid adhesion: Placenta accreta 
102
Clinical Picture 
• Bleeding :occurs only if the placenta is separated 
partially or completely. 
• Uterus :is lax in case of atony. 
• Vaginal examinationmay reveal: 
i- Constriction ring. 
ii- Rupture uterus. 
iii- Morbid placental adherence where there is 
no plane of cleavage 
103
Management 
 When the placenta is delivered, it should be 
inspected for completeness. 
 Manual exploration of the uterine cavity as 
required. 
 If the placenta is retained, the operator 
should use the fingers of one hand or 
Curettage with a blunt instrument. 
 Antibiotics should be routinely administered 
104
Manual Removal of The Placenta 
• The procedure is done under general anaesthesia. 
• The right hand is introduced along the umbilical 
cord into the uterus. 
• The lower edge of the placenta is identified and by 
a sawing movement from side to side the placenta 
is separated from its bed. 
• Grasp the placenta and deliver it out. 
• Examine the placenta and membranes for 
completeness. 
• The left hand is supporting the uterus abdominally 
throughout the procedure. 
105
Complications of Retained Placenta 
1- Shock. 
2- Postpartum haemorrhage. 
3- Puerperal sepsis. 
4- Subinvolution 
5- Retained parts with subsequent haemorrhage, 
infection, placental polyp formation or 
choriocarcinoma. 
6- Complications of the methods used for its 
separation 
106
Placenta accreta 
Placenta accreta is a retained placenta that is 
morbidly adherent to the uterine wall. 
Types 
1.Accreta vera (75-85%)- in which the placenta 
adheres to the myometrium without invasion into 
the muscle. 
2.Increta (17%)-, in which it invades into the 
myometrium. 
3.Percreta (5%)- in which it invades the full 
thickness of the uterine wall and possibly other 
pelvic structures, most frequently the bladder 
107
Cont’d 
In a patient with a previous cesarean 
section 
-Previous one has 14% risk of placenta a. 
-Previous two has 24% risk of placenta a. 
-Previous three has 44% risk of placenta a. 
108
Management 
1. Hysterectomy 
2. Simple excision of the site of trophoblast 
invasion with over sewing of the area to the 
uterine 
3. Internal iliac artery ligation 
109
Injury to the cervix 
After a vaginal delivery, the majority of 
women will have lacerations or bruising 
of the cervix. 
Bleeding which continues despite a well-contracted 
uterus is an indication for 
examining the cervix. 
110
Etiology 
• Forceps, ventose or breech extraction before full 
cervical dilatation. 
• Manual dilatation of the cervix. 
• Improper use of oxytocins. 
• Precipitate labour. 
Predisposing Factors: 
• 1- Cervical rigidity. 
• 2- Scarring of the cervix. 
• 3- Oedema as in prolonged labour. 
• 4- Placenta praevia due to increased vascularity. 
111
Types: 
1- Unilateral :more common on the left side due 
to: 
i) Dextro-rotation of the uterus. 
ii) Left occipito-anterior position is the 
commonest. 
2- Lateral. 
3- Stellate:multiple tears extending radially from 
the 
external os like a star. 
4- Annular detachment 
112
Diagnosis: 
• Postpartum haemorrhage,in spite of well 
contracted uterus. 
• Vaginal examination :The tear can be felt. 
• Speculum examination : using a posterior wall self 
retaining speculum or vaginal retractors and 2 ring 
forceps to grasp the anterior and posterior lips of 
the cervix so the tear can be visualised. 
113
Complications 
• Postpartum haemorrhage. 
• Rupture uterus due to upward extension. 
• Infection: cervicitis and parametritis. 
• Cervical incompetence leading to future 
recurrent abortion or preterm labour. 
• Ureteric injury: from the extension of the tear or 
during its repair. 
114
Vaginal Lacerations 
Causes: 
(I) Primary lacerations less common and caused by : 
1- Forceps application. 
2- Destructive operations. 
3- Vacuum extraction if the cup sucks a part from 
the vaginal wall. 
(II) Secondary lacerations :more common and are 
due to extension from perineal or cervical tears. 
115
Management 
Immediate repair :Continuous locked cut gut 
sutures are taken starting from above the 
apex to control bleeding from the retracted 
blood vessels. 
Tight pack :may be needed to control bleeding 
from a raw surface area. Foley's catheter 
should be inserted before packing and both 
are removed after 12-24 hours. 
116
Cont’d 
Deep lacerations, and particularly those that 
involve the vaginal vault, need to be 
managed under anaesthesia. 
A laceration into the vault could extend 
forward to the bladder or laterally towards 
the uterine artery at the base of the broad 
ligament 
117
Management 
• Prompt recognition of the injury and action to 
control the bleeding 
• Repair 
118
References 
Current Obstetrics and Gynecologic diagnosis 
Williams Obstetrics 23rd edition 
Management of common problems in GYN 
and Obs 5th edition 
Simplified Obstetrics 
Aptudate 
119
120

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Obstateric emergencies

  • 1. Ambo University College of Health Sciences Department of Medicine 1 Obstetric Emergency By : Aregahegn T & Aster.A July,2014 Ambo,Ethiopia
  • 2. Outline Before delivery -Hyperemesis G -PROM -Abortion -Ectopic P -Preeclampsia & E -Abreptio P -Placenta P During delivery -Obstructed labour -Uterine rupture -Cord prolapse After delivery -Retained P -Placenta accreta -Injury to the cervix 2
  • 3. Hyperemesis Gravidarum It is the actual vomiting in the morning , which leads to dehydration & significant amount of wt loss  It is usually start between the 4th and 6th weeks of pregnancy and improves or disappears about the 12 th week.  The vomiting is not confined to the morning but it is repeated throughout the day until it affects the general condition of the patient 3
  • 4. Etiology 1 Hormonal: High human chorionic gonadotrophin (hCG) stimulates the chemoreceptor trigger zone in the brain stem including the vomiting center in the conditions where the hCG is high as in:- a. early in pregnancy, b. vesicular mole and c. multiple pregnancy. 4
  • 5. Cont’d 2.Allergy: to the corpus luteum or the released hormones. 3. Deficiency of: a. adrenocortical hormone and /or, b. vitamin B6 and B1 4.Nervous and psychological: a due to psychological rejection of an unwanted pregnancy, b fear of pregnancy or labour so it is more common in primigravidae 5
  • 6. Diagnosis Symptoms: >The patient cannot retain anything in her stomach, > vomiting occurs through the day and night even without eating. >Thirst, constipation and oliguria. >In severe cases, vomitus is bile and/ or blood stained. > Finally, there is manifestations of Werniche’s encephalopathy as drowsiness, nystagmus and loss of vision then coma. 6
  • 7. Cont’d Signs: Manifestations of starvation and dehydration: *Loss of weight.5% * Sunken eyes. * Dry tongue and inelastic skin. * Pulse: rapid and weak. * Blood pressure: low. * Temperature: slight rise 7
  • 8. Management Hospitalization For observation, fluid therapy Intravenous fluids Drugs 8
  • 9. PROM  Premature ROM is defined as rupture of the chorioamnionic membranes prior to the onset of labor  Prolonged ROM usually refers to ROM for more than 24 hours  It is a complication in one quarter to one third of preterm births 9
  • 10. Cont’d • May or may not be associated with PTL (preterm labor) • Complicates 1/3 of all preterm deliveries • Around 1-2% of pregnancies • Majority of patients delivery within 1 week 10
  • 11. Risk Factors • Previous preterm PROM • Incompetent cervix • Alterations in vaginal pH – Infections • Smoking • Multiple gestation 11
  • 12. Diagnosis History – Gush of fluid – Constantly wet Physical – Pooling fluid - posterior fornix – Fluid per os – Examine with sterile speculum to prevent/limit digital exam of cervix, to minimize risk of ascending infection and amnionitis 12
  • 13. Cont’d Test – Fern - cervical mucus broad fern vs. amniotic fluid narrow fern – pH (Nitrazine) - turns blue – Cervicovaginal fetal fibronectin > 50 ng/ml – Val-salva Imaging-Ultrasound 13
  • 14. Complication Maternal effects  Increase in chorioamnionitis  Increase in Cesarean delivery  Spontaneous labor in ~ 90% within 48 hr. of membrane rupture  Increased risk of placental abruption  Thromboembolic disease 14
  • 15. Cont’d Fetal effects  Increase in RDS  Increase in intraventricular hemorrhage  Increase in neonatal sepsis and subsequent cerebral palsy  Increase in perinatal mortality  Increase in cord prolapse  Abruption  Oligohydramnios 15
  • 16. Management Considerations When? • If later than 34 weeks, consider induction • If <34 weeks, consider tocolysis for steroid course, then expectant management or delivery? • Chorioamnionitis necessitates immediate delivery 16
  • 17. Cont’d Supported Interventions - Tocolysis for steroid administration if no contraindications and fetus 24 – 34 weeks - Prophylactic antibiotics  May prolong latent period by an average of 5-7d  May reduce maternal amnionitis and neonatal sepsis - Ultrasound for fetal weight - Expectant management for any gestational age 17
  • 18. Cont’d • Steroids – To enhance fetal lung maturation and decrease RDS • Tocolytics – Randomized trials have shown no pregnancy prolongation 18
  • 19. ABORTION Spontaneous abortion, or “miscarriage,” is defined as pregnancy loss before 20 weeks of gestation. Most of these occur before 12 weeks. 10-15% of clinically recognized pregnancies terminate in spontaneous abortion. 19
  • 20. Cont’d The causes of spontaneous abortion are both fetal and maternal. Chromosomal anomalies such as aneuploidy, polyploidy, and translocations are present in approximately 50% of early abortuses. Maternal factors include luteal-phase defect, poorly controlled diabetes, and other uncorrected endocrine disorders. 20
  • 21. Cont’d Physical defects of the uterus, such as submucosal leiomyomas, uterine polyps, or uterine malformations may prevent implantation adequate to support fetal development. Systemic disorders affecting maternal vasculature, such as antiphospholipid antibody syndrome, coagulopathies, and hypertension, may predispose to miscarriage. 21
  • 22. Cont’d  Finally, infections with bacteria such as Toxoplasma, Mycoplasma, and Listeria, as well as viral infections, have also been implicated as causes of abortion. Ascending infection is particularly common in second-trimester losses. Clinically the patient may have bleeding or shock. 22
  • 23. Essentials of Diagnosis  Suprapubic pain, uterine cramping, and/or back pain  Vaginal bleeding  Cervical dilatation  Extrusion of products of conception.  Disappearance of symptoms and signs of pregnancy.  Quantitative -HCG  Abnormal ultrasound findings 23
  • 24. Ectopic pregnancy The term applied to implantation of the fetus in any site other than a normal intrauterine location. The most common site is within the fallopian tubes (∼90%). Other sites include the ovary, the abdominal cavity, and the intrauterine portion of the fallopian tube (cornual pregnancy). 24
  • 25. Cont’d  The most important predisposing condition are: - Prior pelvic inflammatory disease resulting in fallopian tube scarring - Factors leading to peritubal scarring and adhesions such as endometriosis, and previous surgery. - Intrauterine contraceptive devices - Fallopian tube may normal in some cases 25
  • 26. Cont’d Ovarian pregnancy is presumed to result from the rare fertilization and trapping of the ovum within the follicle just at the time of its rupture. Abdominal pregnancies may develop when the fertilized ovum fails to enter or drops out of the fimbriated end of the tube. 26
  • 27. Cont’d In all these abnormal locations, the fertilized ovum undergoes its usual development with the formation of placental tissue, amniotic sac, and fetus, and the host implantation site may develop decidual changes. 27
  • 28. Cont’d Morphology. Tubal pregnancy is the most common cause of hematosalpinx (blood-filled fallopian tube) and should always be suspected when a tubal hematoma is present.  Initially the embryonal sac, surrounded by placental tissue composed of immature chorionic villi, implants in the lumen of the fallopian tube.  With time trophoblastic cells and chorionic villi start to invade the fallopian tube wall as they do in the uterus during normal pregnancy. 28
  • 29. Cont’d  However, proper decidualization is lacking in the fallopian tube, and growth of the gestational sac distends the fallopian tube causing thinning and rupture.  Fallopian tube rupture frequently results in massive intraperitoneal hemorrhage. 29
  • 30. Cont’d Less commonly the tubal pregnancy may undergo spontaneous regression and resorption of the entire conceptus. Still less commonly, the tubal pregnancy is extruded through the fimbriated end into the abdominal cavity (tubal abortion). 30
  • 31. Risk Factors High risk • Tubal surgery • Sterilization • Previous ectopic pregnancy • In utero exposure to diethylstilbestrol • Use of IUD • Documented tubal pathology Moderate risk Infertility ,Previous genital infections ,Multiple sexual partners Slight risk • Previous pelvic/abdominal surgery, Cigarette smoking, Vaginal douching ,Early age at first intercourse (< 18 years) 31
  • 32. Clinical Features  The clinical course of ectopic pregnancy is punctuated by the onset of severe abdominal pain, most commonly about 6 weeks after a previous normal menstrual period, when rupture of the tube leads to pelvic hemorrhage. 32
  • 33. Cont’d Rupture of a tubal pregnancy constitutes a medical emergency.  In such cases the patient may rapidly develop hemorrhagic shock with signs of an acute abdomen, and early diagnosis is critical. Chorionic gonadotropin assays, ultrasound studies, and laparoscopy may be helpful to diagnose. 33
  • 34. PREECLAMPSIA AND ECLAMPSIA  Preeclampsia refers to a systemic syndrome characterized by widespread maternal endothelial dysfunction presenting clinically with hypertension, edema, and proteinuria during pregnancy. Preeclampsia should be distinguished from gestational hypertension that can develop in pregnancy without proteinuria. 34
  • 35. Cont’d Minimum criteria – BP ≥ 140/90 mm Hg after 20 weeks' gestation – Proteinuria ≥ 300 mg/24 hours or ≥ 1 + dipstick Increased certainty of preeclampsia – BP ≥ 160/110 mg Hg – Proteinuria 5.0 g/24 hours or ≥ 2+ dipstick 35
  • 36. Cont’d – Serum creatinine > 1.2 mg/dL unless known to be previously elevated – Platelets – Microangio< 100,000/mm3pathic hemolysis (increased LDH) – Elevated ALT or AST – Persistent headache or other cerebral or visual disturbance – Persistent epigastric pain 36
  • 37. Risk factors • Primigravida • Multipara with change of partner • Chronic hypertension • Chronic renal disease • Diabetes mellitus • Multifetal gestation • Polyhydramnios • RH Isoimmunized pregnancy • Hydatidiform mole • Previous history of preeclampsia • Family history of pregnancy induced hypertension 37
  • 38. Types Mild pre-eclampsia: blood pressure ≥ 140/90 mmHg ± oedema. Severe pre-eclampsia: - blood pressure >140/90 mmHg + proteinuria ± oedema or - diastolic blood pressure>110 mmHg or - cerebral or visual disturbances. N.B. Imminent eclampsia : It is a state in which the patient is about to develop eclampsia. Usually there are : - blood pressure much higher than 160 /110 mmHg , - heavy proteinuria (+++or ++++), - hyperreflexia, - severe continuous headache, - blurring of vision, - epigastric pain. Fulminating pre-eclampsia: a rapidly deteriorating pre-eclampsia to be imminent eclampsia. 38
  • 39. Classification 39 Criteria Mild preeclampsia Severe preeclampsia Blood pressure < 160/110 > 160/110 Symptoms Absent Present Proteinuria < 5 g/dl 24 hours collection > 5 g/dl; > 2+ on dipstick Liver and Renal function Normal Abnormal Platelet count Normal Thrombocytopenia Pulmonary edema Absent Present Convulsions Absent Present HELLP syndrome Absent Present Fetal growth restriction Absent Present The presence of any one of the above findings is sufficient to lead to a classification of the preeclampsia into the severe category
  • 40. Pathogenesis The exact mechanisms leading to development of preeclampsia are still being investigated; however, it is clear that the placenta plays a central role in the pathogenesis of the syndrome, since the symptoms disappear rapidly after delivery of the placenta. The placenta reveals various microscopic changes, most of which reflect malperfusion, ischemia, and vascular injury 40
  • 41. Clinical Feature The onset is typically insidious, characterized by hypertension and edema, with proteinuria following within several days. Headaches and visual disturbances are serious events and are indicative of severe preeclampsia, often requiring delivery. Eclampsia is heralded by central nervous system involvement, including convulsions and eventual coma. 41
  • 42. Symptoms • Visual disturbances: blurring of vision, flashes of light or blindness. • Epigastric or right upper quadrant pain: due to enlargement and subcapsular haemorrhage of the liver. • Nausea and vomiting : due to congestion of gastric mucosa and/ or cerebral oedema. • Oliguria or anuria: due to kidney pathology. 5 42
  • 43. Investigations • Complete urine examination: for proteinuria, pus cells, RBCs, casts,specific gravity, culture and sensitivity . • Kidney function tests: serum uric acid > 6 mg % is abnormal during pregnancy. It is more specific for pre-eclampsia than creatinine. • Coagulation status :Platelet count, fibrinogen and FDP as DIC may develop. 43
  • 44. cont’d • Eye fundus examination. • Tests for foetal well being: as - ultrasound, - daily foetal movement count, - non-stress test, - oxytocin challenge test (if needed) 44
  • 45. Complication 45 Fetal • IUGR • Oligohydramnios • Placental infarcts • Placental abruption • Prematurity • Uteroplacental insufficiency • Perinatal death Maternal • CNS seizures & stroke • DIC • ↑↑ CS • Renal failure • Hepatic failure or rupture • Death
  • 46. Management 46 Mild preeclampsia Severe preeclampsia Management depends on: •Gestational age •Fetal well being If at term : •Admission •Ascertain fetal maturity •Terminate pregnancy via the most appropriate route If preterm : Conservative management •Admission •Bed rest •Follow vital signs; organ function tests; platelet count; development of symptoms; level of proteinuria; evidence of hemolysis; fetal well being tests •If severe disease develops during conservative management or achieve fetal maturity; proceed to delivery If any one of the evidences of severe preeclampsia develop or are present, conservative management option is not possible. Conservative management is contraindicated. Management of severe preeclampsia includes: •Admission •Administration of anticonvulsants-valium; magnesium sulphate; phenytoin •Control of severe hypertension by IV antihypertensives such as hydralazine or labetalol •After mother is stabilized, proceed to delivery irrespective of fetal gestational age
  • 47. Abruptio placenta Detachment of placenta after 24 weeks of gestation and before delivery Predisposing factors: • Multiparity • Hypertension • Blunt external abdominal trauma (direct) • Cocaine use • Previous third trimester bleeding • Age older than 35 years 47
  • 48. Types Revealed (80%) - Pain + Vaginal bleeding Concealed (20%) -Pain/Shock -No vaginal bleeding 48
  • 49. Management • Management is influenced by gestational age and degree of abruption • Indicators for delivery- – Fetal intolerance – DIC – Labor • Vaginal delivery is acceptable 49
  • 50. Cont’d • Correct SHOCK- IV access – 2 large bore cannulae -Crystalloids IV – emergency -BLOOD as soon as possible • Correct DIC - Heparin • Catheterize - hourly urine output chart • Assess for delivery 50
  • 51. Placenta previa Placenta attached in the lower segment There are four grades 1) Low lying - lower than upper implantation 2) Marginal – placental edge approaches cervical os 3) Partial – implantation occludes portion of the cervical os 4) Total – implantation totally obstruct cervical os 51
  • 53. Types • Minor – Enters LUS but does not cover os • Major – Covers internal os completely 53
  • 54. Etiology • Unclear • Any damage to endometrium or myometrium Scar tissue impedes migration away from os • Multiple pregnancy- large surface area • Cigarette smoking- vasoconstriction • Cocaine Use – Vasoconstriction-hypertrophy • Rh issoimmunization • Syphilis 54
  • 55. Cont’d • Previous Placenta Praevia • Maternal Age – reduced uterine blood flow needs greater surface area • Parity - 3 previous deliveries 2.6 fold Vessels at site of previous placenta reduced flow discourage implantation 55
  • 56. Presentation • Antepartum Haemorrhage - Late pregnancy - Painless bleeding ( most common) • Malpresentation -Breech/High Head/Unstable lie in 3rd trimester 56
  • 57. Diagnosis • The clinically important diagnosis of placenta previa is therefore a late second or early third trimester diagnosis (after 24-26 weeks gestation) • Ultrasound is the easiest, most reliable way to diagnose (95-98% accuracy) • Pelvic examination is contraindicated 57
  • 58. Management Antenatal • Bed rest indicated • Inpatient vs Outpatient • Major Vs minor • Anaemia -Regular Hb -X-match/Transfuse 58
  • 59. Cont’d • Delivery should depend upon type of previa – Complete previa = c/section – Low lying = probable attempted vaginal delivery – Marginal/partial = it depends!Consider “double setup” for uncertain cases 59
  • 60. Obstructed labor Obstructed labor is failure of progressive descent of the presenting part of the fetus in the birth canal for mechanical reasons inspite of good uterine contraction. The prevalence in developing countries is about 1-2% in the referral hospitals 60
  • 61. Risk Factors Ht <150 cm Previous Hx of prolonged or OL Clinical pelvimetry Soft tissue anomalies Estimate size of fetus late in Pregnancy 61
  • 62. Etiology A. Maternal causes  Cephalo-pelvic disproportion (CPD) • Contracted pelvis • Bone deformities • Soft tissue obstruction 62
  • 63. Contracted pelvis  Generally contracted pelvis involves contracture of:- - the pelvic inlet - the mid pelvis - the pelvic outlet, or by combinations of these.  Inlet contracture- -AP diameter of < 10 cm – normally 11cm -Transverse diameter of < 12cm ---normally –13.5cm -Diagonal conjugate <11.5cm,normally-12.5cm 63
  • 64. Cont’d  Mid cavity contracture – -AP < 11.5cm ---normally -11.5cm -Transverse diameter < 9.5cm Outlet contracture- -Inter tuberous diameter <8cm- normally-10cm 64
  • 65. Cont’d  Clinical pelvic assessment done after emptying the bladder & putting the woman in lithotomy position. • Then we assess the following:- -Reachability of sacrum promontory. -Smoothness &concavity of sacrum. -Straightness of sidewalls and projection of ischial spine. -Size of pubic angle & intertuberous distance 65
  • 66. Bone deformity Small pelvis -developmental or congenital Abnormal shape of the pelvis due to: -Diseases like rickets & osteomalacia or tuberculosis -Previous accidents. -Tumors of the bones. -Childhood poliomyelitis affecting shape of the hips. -Spine: -Lumbar kyphosis. - Lumbar scoliosis 66
  • 67. Soft tissue obstruction Tight perineum in primi Vaginal abnormalities- septa, scar, tumors Cervical stenosis- infection, surgery, tumors Uterine factors- fibroids, congenital anomalies Ovarian tumor- impacted in the pelvis 67
  • 68. B. Fetal causes Large sized fetus / Macrocosmic  Congenital anomalies- Hydrocephalus  Locked and conjoined twins  Shoulder dystocia  Malpositions and Malprsentation – Breech – Transverse lie – Brow presentation – Mento- posterior position (face) 68
  • 69. Diagnosis History – The patient is usually young teenage – Abnormally prolonged labor  General examination – Tired, exhausted and anxious. – Tachycardic, tachypenic . – Dehiydrated -Temprature increase(>38) 69
  • 70. Cont’d Abdominal examination – Hypertonic or hypotonic uterine contraction. – Uterus is hard and tender – FHR abnormality – tachycadia, bradycardia or may be absent – Bladder often distended. – Catheterization may be often difficult and the urine is blood stained. 70
  • 71. Cont’d Vaginal examination -Vulva is edematous. - Cervix fully or partially dilate& edematous -The liquor is meconium stained and often foul smelling. -The presenting part is high, not engaged, with excessive moulding and Large caput. 71
  • 72. Complication Maternal - Maternal distress – Uterine rupture – UNcommon in primi – PPH- atonic or traumatic – Infection -sepsis, abscess and peritonitis – Infertility – Psychological trauma 72
  • 73. Cont’d Fetal • Cerebral birth trauma • Asphyxia • Early neonatal infection • Congenital pneumonia • Intracranial hemorrhage from excessive moulding. • Birth injuries 73
  • 74. Management Prevention • Good nutritional supply since childhood • Avoid early marriage • Universal ANC –To screen out the " at risk mothers " –Pelvic assessment at 38-39wks • Promote family planning services • Elective caesarean delivery when indicated 74
  • 75. Cont’d Specific treatment • Resuscitation • Broad spectrum antibiotics • Operative delivery – Episiotomies for some primis with tight perineum. – Vacum / Forceps delivery • Alive fetus and head < 1/5 above pelvic brim (+1) • Mild-moderate moulding – Destructive delivery • Dead fetus, fully dilated cervix and no evidence of rupture or imminent rupture of the uterus 75
  • 76. Cont’d - Caesarean delivery • Alive fetus with incomplete cervical dilatation or high station. • Alive fetus with Brow or Mento posterior position or face • Alive or dead fetus with evidence of imminent uterine rupture. - Caesarean Hysterectomy • Severely bruised lower uterine segment • Major uterine vessels torn 76
  • 77. Uterine Rupture Tear in the wall of the uterus w/c commonly occurs in the lower uterine segment. Common in multiparas and rarely occurs in primiparas. Peak incidence is 3rd /4th pregnancy. It can occur anteriorlly , posteriorlly , laterally or combination of these. -anterior rupture is the commonest 77
  • 78. In obstructed labour: - It is usually in lower uterine segment. - Usually oblique or transverse. - More on the left side due to; i) dextrorotation of the uterus. ii) left occipito-positions are more common.  In rupture scar: At the site of the scar. 78
  • 79. Cont’d Can be complete or incomplete 1 Complete(true) uterine rupture -includes the entire thickness of the uterine wall and serosa resulting in direct communication with peritoneal cavity. 2 Incomplete (uterine dehiscence) -is the defect of the uterine wall that is contained by the visceral peritoneum or broad ligament. -common in patients with prior C/S scar 79
  • 80. Cont’d Incidence 0.05% for all pregnancies.  0.8% for women with low-transverse uterine scar. 4-8% -prior classic scar. all pregnancies following myomectomy may be complicated by uterine rupture. 80
  • 81. Causes • OL specially in multis • Rupture or dehiscence of previous c/s scar • Excessive stimulation • Difficult instrumental delivery • Internal podalic version -particularly after drainage of the liquor • Difficult manual removal of placenta • Sharp penetrating trauma 81
  • 82. Clinical features  History • History of prolonged labor • Worsening abdominal pain (supra pubic) persisting b/n contraction • Sudden cessation of uterine contraction • Absent fetal movement • Variable degree of vaginal bleeding • Shoulder pain on lying down due to irritation of the phrenic nerve by accumulating blood under the diaphragm 82
  • 83. Cont’d  P/E-reduced BP -feeble and rapid pulse/impalpable -Signs of severe anemia-pallor • Abdomen -tender & distension -Scar of the previous operation. -easily palpable fetal parts -absent FHB & uterine contraction -signs of fluid collection/variable shifting dullness • Pelvic examination -active vaginal bleeding -the presenting part may be impacted or retracted in to peritoneal cavity. 83
  • 84. Differential Diagnosis • Abruptio placentae. • Disturbed advanced extrauterine pregnancy. • Other causes of acute abdomen. 84
  • 85. Management 1 Supportive management • Secure IV line with two lines • Vigorous infusion of crystalloids • Do HCT ,B/g • Broad spectrum IV antibiotics • Catheterize 85
  • 86. 2 Definitive management • Repair- If it is amenable for repair and the patient did not complete her family. -usually with tubal ligation if future fertility is not desired. • Hysterectomy-total/subtotal if posterior, lateral • Subtotal hysterectomy is less time consuming so it is done if there is no cervical tear. 86
  • 87. Cord presentation and prolapse Cord presentation and prolapse describe a situation in which the umbilical cord is felt anterior to the fetal presenting part on vaginal examination. If the membranes are intact it is a cord presentation while with ruptured membranes it is identified as a prolapsed cord.  As long as the membranes are not ruptured, the risk of compression and asphyxia is low. 87
  • 88. Cont’d Cord prolapse can be: 1 Overt- being felt inside the cervix, the vagina or even hanging outside the introitus. 2 Occult- with the cord anterior to the presenting part in the lower segment but not felt on digital vaginal exam 88
  • 89. Cont’d Cord prolapse can occur in: – vertex and frank breech presentations-0.5% – complete breech -5% – footling breech -15% and – shoulder presentation -20%. 89
  • 90. Etiology • Malpresentations in labor • PROM • Amniotomy with a high fetal station • Polyhydramnios with sudden membrane rupture • Second twin delivery • Internal podalic version • Cephalopelvic disproportion in labor 90
  • 91. Complications • Cord compression and constriction of umbilical vessels due to cold exposure outside the introitus can lead to fetal asphyxia and death. • Partial cord occlusion may give the fetus some time but in complete cord occlusion the fetus can die of asphyxia in 5-7 minutes if cord compression is not immediately relieved. • There is increased maternal risk from cord prolapse because of emergency operative vaginal or abdominal delivery performed in order to salvage the fetus 91
  • 92. Diagnosise • In the vagina or inside the cervix anterior to the presenting part – Check for pulsation and its rate – Replace the cord immediately into the vaginal ( not inside the uterus) canal if outside the introitus • If membrane is intact, cord presentation is diagnosed • In all malpresentations, a careful search for cord presentation or prolapse should be made • Occult cord prolapse can only be diagnosed by detection of abnormal fetal heart rate patterns • In cases of malpresentations, sonographic search can also be made for cord anterior to the fetal presentation 92
  • 93. Management Immediate management If cord is pulsating: • Put mother in knee-chest position • Initiate oxygen administration by face mask 5L/min • Insert bladder catheter and infuse the bladder with 0.5L of saline • Replace the cord into the vaginal canal • Push fetal presenting part upwards via the examining hand in the vagina to relieve compression of the cord by the presentation • Prepare for immediate delivery 93
  • 94. Cont’d Delivery : Non-pulsatile cord: • Manage as any other labor as the cord prolapse will not alter the course of labor (dead fetus) Pulsatile cord:  Second stage of labor: • Expedite delivery by forceps delivery if other conditions for forceps delivery are met. • Breech extraction if other conditions for breech extraction are met (full cervical dilation)  First stage of labor: • caesarean delivery. 94
  • 95. Postpartum hemorrhage Excess blood loss after delivery (>500ml ) It is the leading cause of maternal mortality Types - Primary PPH in the first 24 hours - Secondary PPH the first 24 hrs to 6 weeks.  Massive PPH may be truly terrifying 95
  • 96. Etiology • The “4 T’ s” : tone, tissue, trauma, and thrombosis • Uterine atony, i.e., failure of the uterine contraction and retraction of myometrial muscle fibers following delivery of the baby. • PPH in a previous pregnancy is a major risk factor and every effort should be made to determine its severity and cause. • Birth weight, labor induction and augmentation, chorioamnionitis 96
  • 97. Cont’d Primary PPH The most important cause of massive PPH is uterine atony when the uterus is not contracted Steps to stop bleeding 1. Massaging the uterus to cause it to contract 2. Bimanual compression-Under general anaesthesia, the uterus is firmly compressed for 5-30 minutes 3. Uterine contraction is maintained by oxyitocin 4. Prostaglandin -through the anterior abdominal wall. 97
  • 98. Aetiology: (A) Placental site haemorrhage: (I) Atony of the uterus(90%) II) Retained placenta. (III) Disseminated intravascular coagulation (B) Traumatic haemorrhage: Rupture uterus, cervical, vaginal , vulval or perineal lacerations. 98
  • 99. Complications 1- Maternal death in 10% of postpartum haemorrhages. 2- Acute renal failure. 3- Embolism. 4- Sheehan’s syndrome. 5- Sepsis. 6- Anaemia. 7- Failure of lactation 99
  • 100. Cont’d Secondary PPH 1. Retained products or conception 2. Uterine infection 3. placenta accrete 4. Injury to cervix 100
  • 101. Retained placenta Incidence Retained placenta is found in 2% of deliveries. The frequency of retained placenta is markedly increased at gestation <26 weeks At term, 90% of placentas will be delivered within 15 minutes. Once the third stage exceeds 30 minutes, there is a ten-fold increase in the risk of hemorrhage 101
  • 102. Causes: • Atony of the uterus :due to causes mentioned before. • Constriction ring. • Rupture uterus :where the placenta passes to the peritoneal cavity. • Abnormal adherence of the placenta which may be: i) Simple adhesion: Manual separation can be done easily. ii) Morbid adhesion: Placenta accreta 102
  • 103. Clinical Picture • Bleeding :occurs only if the placenta is separated partially or completely. • Uterus :is lax in case of atony. • Vaginal examinationmay reveal: i- Constriction ring. ii- Rupture uterus. iii- Morbid placental adherence where there is no plane of cleavage 103
  • 104. Management  When the placenta is delivered, it should be inspected for completeness.  Manual exploration of the uterine cavity as required.  If the placenta is retained, the operator should use the fingers of one hand or Curettage with a blunt instrument.  Antibiotics should be routinely administered 104
  • 105. Manual Removal of The Placenta • The procedure is done under general anaesthesia. • The right hand is introduced along the umbilical cord into the uterus. • The lower edge of the placenta is identified and by a sawing movement from side to side the placenta is separated from its bed. • Grasp the placenta and deliver it out. • Examine the placenta and membranes for completeness. • The left hand is supporting the uterus abdominally throughout the procedure. 105
  • 106. Complications of Retained Placenta 1- Shock. 2- Postpartum haemorrhage. 3- Puerperal sepsis. 4- Subinvolution 5- Retained parts with subsequent haemorrhage, infection, placental polyp formation or choriocarcinoma. 6- Complications of the methods used for its separation 106
  • 107. Placenta accreta Placenta accreta is a retained placenta that is morbidly adherent to the uterine wall. Types 1.Accreta vera (75-85%)- in which the placenta adheres to the myometrium without invasion into the muscle. 2.Increta (17%)-, in which it invades into the myometrium. 3.Percreta (5%)- in which it invades the full thickness of the uterine wall and possibly other pelvic structures, most frequently the bladder 107
  • 108. Cont’d In a patient with a previous cesarean section -Previous one has 14% risk of placenta a. -Previous two has 24% risk of placenta a. -Previous three has 44% risk of placenta a. 108
  • 109. Management 1. Hysterectomy 2. Simple excision of the site of trophoblast invasion with over sewing of the area to the uterine 3. Internal iliac artery ligation 109
  • 110. Injury to the cervix After a vaginal delivery, the majority of women will have lacerations or bruising of the cervix. Bleeding which continues despite a well-contracted uterus is an indication for examining the cervix. 110
  • 111. Etiology • Forceps, ventose or breech extraction before full cervical dilatation. • Manual dilatation of the cervix. • Improper use of oxytocins. • Precipitate labour. Predisposing Factors: • 1- Cervical rigidity. • 2- Scarring of the cervix. • 3- Oedema as in prolonged labour. • 4- Placenta praevia due to increased vascularity. 111
  • 112. Types: 1- Unilateral :more common on the left side due to: i) Dextro-rotation of the uterus. ii) Left occipito-anterior position is the commonest. 2- Lateral. 3- Stellate:multiple tears extending radially from the external os like a star. 4- Annular detachment 112
  • 113. Diagnosis: • Postpartum haemorrhage,in spite of well contracted uterus. • Vaginal examination :The tear can be felt. • Speculum examination : using a posterior wall self retaining speculum or vaginal retractors and 2 ring forceps to grasp the anterior and posterior lips of the cervix so the tear can be visualised. 113
  • 114. Complications • Postpartum haemorrhage. • Rupture uterus due to upward extension. • Infection: cervicitis and parametritis. • Cervical incompetence leading to future recurrent abortion or preterm labour. • Ureteric injury: from the extension of the tear or during its repair. 114
  • 115. Vaginal Lacerations Causes: (I) Primary lacerations less common and caused by : 1- Forceps application. 2- Destructive operations. 3- Vacuum extraction if the cup sucks a part from the vaginal wall. (II) Secondary lacerations :more common and are due to extension from perineal or cervical tears. 115
  • 116. Management Immediate repair :Continuous locked cut gut sutures are taken starting from above the apex to control bleeding from the retracted blood vessels. Tight pack :may be needed to control bleeding from a raw surface area. Foley's catheter should be inserted before packing and both are removed after 12-24 hours. 116
  • 117. Cont’d Deep lacerations, and particularly those that involve the vaginal vault, need to be managed under anaesthesia. A laceration into the vault could extend forward to the bladder or laterally towards the uterine artery at the base of the broad ligament 117
  • 118. Management • Prompt recognition of the injury and action to control the bleeding • Repair 118
  • 119. References Current Obstetrics and Gynecologic diagnosis Williams Obstetrics 23rd edition Management of common problems in GYN and Obs 5th edition Simplified Obstetrics Aptudate 119
  • 120. 120