Final unit one.pptx

Obstetrics II for midwifery students
Course Code – MidW/M3121
ECTS -7 ECTS
By Ritbano Ahmed (BSc, MSc)
Semera University, College of Health science, dep’t
of Midwifery
October, 2016
8/10/2022 1

Chapter one
Abnormalities in pregnancy
2

Introduction
• It is common to some abnormalities during
pregnancy. However some of these are just minor
discomfort but others may become sever and can
complicate more.
3

Minor Disorders of Pregnancy
4

Outlines
Nausea and vomiting
Heart burn
Back pain
Varicosity
Pica
Constipation
Haemorrhoids
Back pain

Minor Disorders of Pregnancy
 Minor disorders are only disorders that occur
during pregnancy
 Are not life threatening.

Nausea And Vomiting
 Approximately 50% of women experience NV in
early pregnancy
 This presents between 4 and 12 weeks gestation.
 Nausea in pregnancy typically peaks at
approximately 9 weeks gestation, with 60% of
cases resolving by the end of the first trimester
 Hormonal influences are listed as the most likely
causes.
 It is usually occurs in the morning but can occur
any time during the day, aggravated by smelling of
food.

Management
Medical History
• Including the pattern of NV, fluid and dietary intake,
factors exacerbating the condition, and current
management.
Note signs of fever, headaches, abdominal pain or other
symptoms that are not characteristic with
uncomplicated nausea and vomiting in pregnancy.
Exclude other medical conditions causing nausea and
vomiting e.g. gastro-intestinal, renal or endocrine

Perform urinalysis including assessment of ketones,
pH, and signs of urine infection such as nitrates,
blood and protein.
 Maternal assessment for signs of dehydration.
 Perform a blood pressure
 Perform temperature, pulse, and respirations if the
medical history indicates risk for infection.
Clinical Assessment

Clinical Assessment…..
If a women presents with a history of NV which is more
than normally expected in pregnancy, perform a baseline
weight (if not available).
Perform a weekly weight until the NV resolves.
 Consider performing full blood picture, urea and
electrolytes, liver function tests, and thyroid function
tests if clinical picture merits further investigation.

Intervention
Non-pharmacological Interventions
 small, frequent meals and snacks
 Bland, low fat, low carbohydrate, high protein diet
 Take more liquids than solids in the diet
 Encourage fluids to prevent dehydration – a least 2
l/day
 Avoid an empty stomach

Non-pharmacological Interventions……..
 Prevent a full stomach e.g. mixing solids with liquids
 Avoid rich, spicy or fatty foods (including smelling
and cooking)
 Ice chips may be beneficial
 Consume a high-protein snack prior to going to bed

Heart Burn
HB: is a burning sensation in the mid chest region.
 Is common in pregnancy, and occurs in two-thirds of
women by the third trimester
 Elevated levels of progesterone cause the lower
oesophageal sphincter to become more relaxed allowing
gastric reflux.
 HB is most troublesome at 30-40 weeks gestation because
at this stage is under pressure from the growing uterus.

Management
Clinical History
 Obtain a current history of symptoms and any previous
history of reflux-type symptoms.
 Exclude diagnosis of pre-eclampsia – check BP and
perform urinalysis.
Dietary and other modifications
 Eat small frequent meals
 Avoid eating and drinking at the same time to reduce
stomach volume
 Decrease fat in the diet, and increase protein consumption

Dietary and other modifications cont.…
 Avoid gastric irritants e.g. chocolate, coffee, citrus
juices, tomato products, alcohol, fizzy drinks, spicy
foods.
 Avoid eating late at night or within 3 hours of going to
bed
 Chewing gum stimulates the salivary glands and may
neutralize acid
 Cease smoking

Positioning
 Elevate the head of the bed by 10-15cm
 Lying on the left side has been shown cause less
frequent reflux
 Encourage an upright position where possible,
avoiding lying down after meals
 For persistence/sever case/ prescribe antacids.

Pica
 This is the term used when mother craves certain
foods of unnatural substances such as coal,
soil...etc.
 The cause is unknown but hormones and changes in
metabolism are blamed.
Management:
o Seek medical advice if the substance craved is
potentially harmful to the unborn baby.

Constipation
Causes:
1. Reduced intestinal motility due to steroid hormones.
2. Increased fluid resorption from the large bowel.
3. Reduced exercise.
4. Mechanical compression by the gravid uterus.
Treatment:
1. Evacuate the bowel at the same time every day.
2. Increase fluid intake/Diet rich in green vegetables,
bran and fruits.
3. Increase the intake of water, fresh fruit, vegetables and
ruphages in the diet.
4. Exercise is helpful especially walking

Backache
Causes:
1. Lumbar lordosis.
2. Relaxation of ligaments and intervertebral joints by
progesterone effect.
Management:
1. Adequate rest and support the back when sitting in a
chair by a pillow.
2. Avoid wearing high heeled shoes.
3. Advice the mother to sleep on firm bed.

Fainting
@ In early pregnancy fainting may be due to the
vasodilation occuring under the influence of
progesterone before there has been a compensatory
increase in blood volume.
@ The weight of the uterine contents presses on the
inferior vena cava and slows the return of blood to
the heart.
• Management
 Avoid long period of standing
 Sit or lie down when she feels slight dizziness
 She would be wise not to lie on her back except
during abdominal examination

Varicosities
1. Progesterone relaxes the smooth muscles of the
veins and result in sluggish circulation.
2. Congenital weakness which will exaggerated by
increased venous pressure by compression with the
pregnant uterus
3. Prolonged standing
 The valves of the dilated veins become insufficient
and varicositis result.
 It occurs in legs, anus (hemorrhoids) and vulva.

Varicosities……….
Management:
1. Exercising the calf muscles by rising on the toes
2. Avoid prolonged standing
3. Elevate the legs in higher level than the body during
sitting and sleeping
4. Support tighs and legs
5. Avoid constipation and advise adequate fluid intake.
6. Sanitary pad give support for vulva varicositis
• Surgical or injection treatment should be avoided
during pregnancy
22

Haemorrhoids
Causes:
1. Laxity of the rectal veins by progesterone effect.
2. Pressure by the gravid uterus.
3. Tendency to constipation.
Conservative management
1. Avoid constipation. .. high fibre diet, increased fluid
intake, exercise.
2. Soothing and astringent agents and Local
anaesthetics/ Mild analgesia.

Conservative management contd….
Avoid straining during defecation, and encourage
defecating in the morning and after meals when
colonic activity is highest.
Skin protection creams may be beneficial for pruritis
and discomfort.
 Topical local anaesthetic and/or corticosteroid agents
may be beneficial
e.g. Rectinol, Proctosedyl ointments.

Surgical Management
 Warmed baths may be used to decrease sphincter tone
or improve venous congestion
 Closed excision haemorrhoidectomy for symptomatic
haemorrhoids using local anaesthetic can be safely
performed during pregnancy.

 Most minor disorders can be advanced into a more
serious complication of pregnancy.
 The disorders require immediate actions are as
follows (Danger signals of pregnancy)
26

Definition
Defn: It is a condition in pregnancy X-ed by
intractable vomiting and nausea that can lead to weight
loss, dehydration, an electrolyte imbalance, acid-base
disturbance, psychological disturbances and
termination of the pregnancy and if severe, hepatic and
renal damage.
 Usually present in T1 the diminishes; persists
through out pregnancy in a minority.
 It is found in only1–20 patients per 1000.
28

Causes of HEG
• It is unclear but it is known to be associated with:
The following theories were postulated:
Hormonal: high hCG stimulates the CTZ in the brain
stem including the vomiting center.
This is the most accepted theory and proved by the
higher frequency in the conditions where the hCG
is high as in :--
• Early in pregnancy,
• Vesicular mole and
• Multiple pregnancy.
• Increased levels of other hormones like thyroid and
estrogen 29

Causes of HEG cont’d
Allergy: to the corpus luteum or the released
hormones.
Deficiency of:
A. adrenocortical hormone and /or
B. vitamin B6 and B1
Nervous and psychological :due to
- Psychological rejection of an unwanted pregnancy
- Fear of pregnancy or labour so it is more common
30

Risk Factors of HEG
Nulliparity
history of HEG in a previous pregnancy
 mothers or sisters with HEG, a female fetus
multiple gestations
increased body weight
history of motion sickness or migraines
31

Pathophysiology
• Poorly understood but there are some most commonly
accepted theory suggests that levels of HCG are associated.
• HCG produced by placenta and corpus luteum its believed
that it results destination of GIT or sometimes because of
HCG’s nature which is similar to TSH it act just like as
TSH & excess TSH in body results gestational
thyrotoxicosis or hyperthyroidism.
• Then hyperthyroidism results sign and symptoms like muscle weakness,
sleeping problem, fast heart rate , poor heat tolerance, diarrhea,
thyroid enlargement & weight loss
32

Pathophysiology ……
• Another estimation is based on hormones estrogen and
progesterone which are produced by placenta specially
increased level of progesterone at 1st trimester may
result
Decreased gut motility
Elevated liver enzyme
Decreased lower esophageal sphincter pressure
Increased level of sex steroid is hepatic portal system
• Another way that results HG is an H.pylori infection.
33

Pathological Changes
• H. Pylori bacteria in lower amount it is common
in many of peoples GIT system but sometimes
may increase steroid level in circulation and
causes hyper emesis.
• And Because of starvation due to vomiting ,
ketone formed from metabolism of fatty acids,
some of the ketone appear in the urine.
• in attempt to restore the PH of the blood the
respiratory rate increase 34

Morning sickness
Excessive
vomiting
Dehydration
Oliguria
Concentrated
urea
Low urinary
chloride
Haemoconcentration Raised blood urea
starvation
Ketosis
Hepatitis
Werncks
encephalopathy
Polyneuritis
emaciation
Ketone urea
Proteinuria
Bile salt

Diagnosis
Symptoms:
1. The patient cannot retain anything in her stomach,
vomiting occurs through the day and night even
without eating.
2. Thirst, constipation and oliguria.
3. In severe cases, vomitus is bile and/ or blood
stained.
4. Finally , there is manifestations of Wernicke's
encephalopathy as drowsiness, nystagmus and loss
of vision then coma.
36

Signs:
Manifestations of starvation and dehydration:
1. Loss of weight.
2. Sunken eyes.
3. Dry tongue and inelastic skin.
4. Pulse: rapid and weak.
5. Blood pressure: low.
6. Temperature: slight rise.
37

DIAGNOSIS
1. Full history and physical examination based on sign
and symptoms
• Continuous and sever nausea and vomiting
particularly if vomiting occur more than 3-4 times
per day.
• Loss of weight (5% or 3kg per day)
• Weakness and fatigue, Sunken eye ball
• Dry tongue and sore throat, Skin in elastic
• Offensive breath or acetone breath
• Rapid pulse
• Low BP
• Dark urine (because of ketone content)
• Constipation due to starvation and dehydrations 38

DIAGNOSIS
2. Laboratory Investigation
• U/A for ketone and proteinuria
• BUN
• LFT
• HCT/HGB
3. Ultrasonography
To rule out twin Px, molar px or trophoblastic mass.
39

Differential Diagnosis
Infections
• UTI
• Hepatitis
• Meningitis
• Gastroenteritis
Gastro intestinal disorders
• Appendicitis
• Pancreatitis
• Fatty liver
• Peptic ulcer
Usually
accompany
with fever
and headache
Usually
accompanied by
abdominal pain

Differential dxs cont.
 Metabolic and endocrine disorders
• Diabetic ketoacidosis
• Hyperparathyroidism
 GTD
 Molar px
 choriocarsinoma
 Pregnancy related disorders
 Preeclampsia
 Drug induced nausea and vomiting
Rule out by
B-HCG

How to manage
Admition criteria
Vomiting greater than 3x a day and persist
irrespective of general measures
Ketone +3
Deranged vital signs
After admition
Limit number of visitors
Open IV line
Stop oral intake for 24 hour
Administer 2 bags of RL in the first 6 hrs if
hypotension occurs
42

How to manage…..
Then 1000 ml NS/RL/DNS every 6 hours alternately by
mixing with 4 capsules of 40%glucose and 2 ampoules
(each 25mg) of vitamin B complex in each bag
Start medications(CPZ, plasil, cemetdin…) as ordered
and some times antibiotics for related signs of infection.
After vomiting stops give solid diet rather than fluid
Perform routine daily U/A, HCT, serum electrolyte
measurement and blood sugar estimation
Perform U/S to rule out R/Fs like
Multiple Px
Molar Px
Trophoblastic disease
Maintain intake – out put chart and strictly follow up
Monitor V/S
43

Management
No pharmacologic Interventions for HG
 Eat small frequent meals. Eat something every 2–3
hours to avoid hunger
Drink fewer liquids with meals. Drinking liquids can
cause a full, bloated feeling. Drink liquids 1/2 to 1
hour after meals
Eat low-fat complex carbohydrates:
 rice , pasta
 potatoes
 bread and cereal
44

Management
No pharmacologic Interventions for HG contd.
• Eat low-fat
protein foods:
• lean meat
• dry roasted nuts
(almonds)
• tofu
• broiled or canned
fish
• boiled beans
45
eggs
 poultry without the skin
Eat fruit and drink fruit
juices (fresh is preferred).
Drink soups and other
liquids between meals
rather than with meals.

 Avoid these foods:
 Fatty, greasy, or fried
Spicy or hot
Very sweet, such as
candy, cake or cookies
With strong odors, like
cooked broccoli,
cabbage, fish, etc.
46
Urinate often.
Avoid warm places
and those with
limited air flow
(stuffy rooms).
 Sit at least
somewhat upright
after meals to reduce
gastric reflux.

• yogurt
• juice
• cheese
• nuts
47
 Fruit
 smoothie
 bread/crackers
 sandwich
• Eat a snack before getting up, going to bed and/or
during the night, such as:

Get out of bed very slowly, sitting for a minute
before you stand. Avoid sudden movements.
Avoid brushing teeth immediately after eating, and
don't use toothpaste if it increases nausea.
 Rest as often as needed, with feet up and head
slightly elevated.
 Get plenty of fresh air, some sunshine, and light
exercise as tolerated.
48

Open windows when cooking or use exhaust fan to
eliminate odors. Grill outdoors when possible.
Avoid stress and ask for help. Consider counseling
to deal with emotions related to being ill.
49

Pharmacological therapy
1. Promethazin
Antidopaminergic agent effective in treating
vomiting. It blocks post synaptic mesolimbic
dopamnergic receptors in the brain and reduce stimuli
to the brain steam reticular system
dose -12.5mg PO TID or
25mg at night or
25mg IV/IM 50

Pharmacological therapy…..
2. Methochloropromide
• Antiemetic by blocking dopamine receptors in the
chemoreceptor trigger zone of the CNS, usually
reserved when other therapies fail to control
symptoms. It stimulates intestinal motility and is
metabolized in the kidneys dose – 10mg orally
QID or 10mg daily IV/IM every 6hrs (30mins
before meals or at bed time)
51

Pharmacological therapy
3. Pyradoxine (vit B6)
dose – 10-20mg orally 6hourely for 3 weeks or
- 10mg IV 4 hourly
4. Thiamine ( vit B1)
Thiamine is used in the Rx of thiamine deficiency including
wrinkles encephalopathy syndrome
dose – 100mg daily IV/IM for up to 2wks
5. Fluid (RL/NS/DNS)
For replacement of electrolytes and fluid in the body
dose – 1000ml every 6 hrs alternatively.
52

Termination of pregnancy:
Indications:
1. Persistent severe vomiting after one week of
treatment.
2. Pulse is persistently above 100/min, temperature
persistently above 38C or the systolic blood
pressure is persistently below 100 mmHg.
3. Jaundice or bile in urine.
4. Anuria, absence of chloride in urine, persistent
5. albuminuria or high blood urea.
6. Retinal haemorrhage or Wernicke's encephalopathy
. 56

Complication
Progress
Can lead to:
 Weight loss
 Dehydration.
 Acidosis from
malnutrition
 Alkalosis from
vomiting
57
• Muscle weakness
• electrocardiographic
abnormalities
disturbances
• Electrolyte depletion
• Vitamin deficiency,
particularly thiamine
• Death from liver failure
or the end processes of
the above.
• Psychological disturbance

Complication….
• Thiamine deficiency
can result in beri-
beri symptoms.
• That include
Fatigue
 loss of appetite
emotional instability
sleep disturbances and
abdominal discomfort.
58
• Advanced neuropathic
manifestations of beri-beri
include:-
Parethesias
Weakness
tenderness and cramps of the lower
extremities.
The cerebral progression of
thiamine deficiency resulting in
Wernicke’s encephalopathy
• Excessive retching during HEG may lead to
esophageal rupture, Mallory Weiss tears,
pneumothorax and pneumomediastinum.

Complication….
• Fetus
 LBW
• Severe malnutrition in pregnancy can lead to:-
 spontaneous abortion
teratogenic effects
poor neurological development
preterm delivery
impaired fetal neuropsychological
development(Ketones)
59

Hypertensive disorders in pregnancy
60

Outline
• Objectives
• Introduction
• Definitions
• Classifications
61
Diagnosis
Intervention
Complication

Objectives
At the end of this section, students will able to:-
 Definition hypertensive disorder of pregnancy
 Discuss pathophysiology of preeclampsia
 List possible complications of preeclampsia
 Discuss the classifications of preeclampsia
 Discuss the management of hypertensive disorder of
pregnancy
62

Introduction
The most common and yet serious conditions seen in
obstetrics
cause substantial morbidity and mortality in the
mother and fetus
Incidence: worldwide: 7-12%
Death due to cerebral hemorrhage, aspiration
pneumonia, hypoxic encephalopathy,
thromboembolism, hepatic rupture, renal failure
63

Classification
I. Pre-existing (chronic) hypertension:
• Presents Before 20 weeks in absence of vesicular
mole and persists beyond 6 wks postpartum
• BP ≥ 140/90 mmHg
Examples:
 Essential hypertension
 Secondary to chronic renal disorders e.g. pyelonephritis
and renal artery stenosis 64

II. Pregnancy-induced hypertension (PIH):
Definition:-Hypertension occurring for the first time
after 20 weeks 'gestation except multiple px and
vesicular mole
Hypertension in pregnancy is defined as one of the
following:
• Diastolic BP ≥90 mmHg
• Systolic BP ≥140 mmHg
• The increased blood pressures be present on at least two
separate occasions, 4/6h apart or Single DBP ≥110mmhg
65

II. PIH……..
Ia. Gestational hypertension
is the development of an elevated BP during
pregnancy or in the first 24 hours postpartum without
other signs or symptoms of preeclampsia or
preexisting HTN
• No proteinuria
 BP > 140/90 mm Hg for 1st time during pregnancy
 The BP must return to normal within 6(12) wks
after delivery
66

II. PIH……..
Ib. Preeclampsia
 It is primarily defined as gestational HTN plus and
proteinuria after 20 weeks of gestation in a
previously normotensive woman.
 Preeclampsia complicates 5–7% of all pregnancies.
 It is divided into mild and severe forms.
67

II. PIH……..
 It is difficult to predict who will develop pre-
eclampsia
Ic. Eclampsia: Seizures that cannot be attributed to
other causes in a woman with preeclampsia
• Pre-eclampsia + convulsions.
68

III. Chronic HTN with Superimposed Preeclampsia
The diagnosis of superimposed preeclampsia is based
on one or more of the following findings:
 New-onset proteinuria 300 mg/24 hours in
hypertensive women but no proteinuria before 20
weeks' gestation
 A sudden increase in proteinuria or blood pressure
or platelet count <100,000/μL in women with
hypertension and proteinuria before 20 weeks'
gestation
69

Pre-eclampsia
Incidence
• 5-10%.
Aetiology
• No definite aetiology is found for pre-eclampsia
and it is still a disease of theories.
70

Theories:
1. The uteroplacental bed:
• In early pregnancy, the cytotrophoblast invade the
decidual arteries making their musculature more
flaccid and dilated.
• During the second trimester of normal pregnancy, a
second wave of invasion occurs into the
myometrial segments of the spiral arteries.
• If the second invasion does not occur pre-
eclampsia develops. 71

II. Immunological factor:
• Stimulation of the maternal immune system by the
early conceptus is essential for production of the
blocking factors that prevent rejection of the foetus
and placenta.
• Hypo immune response results in damage of the
placenta and subsequent pre-eclampsia.
• The evidences is that: Pre eclampsia is less common
in previously stimulated immunity conditions as in:
 Previous pregnancy.
 Previous blood transfusion.
72

II. Immunological factor:….
• Increased maternal anti-HLA (human leucocyte antigen)
antibodies.
III. Genetic factor:
• A maternal autosomal recessive gene or a foetal genetic
component could be responsible.
• An increase in HLA-DR (subtype of human leucocyte
antigen) has been noted in pre-eclamptic women, their
babies and their sisters who developed PIH.
73

IV. Renin- angiotensin system:
• It was found that the vascular sensitivity to
angiotensin II is reduced in normal pregnancy
while it increases in PIH.
• Angiotensin II -binding sites on platelets increase
in women with PIH in comparison with normal
pregnancy.
• This can identify the women in risk of developing
PIH and hence prophylaxis against it can be
achieved by anti-platelets as aspirin.
74

V. Atrial natriuretic peptide (ANP):
• It’s release is stimulated by volume expansion and
increase in atrial pressure. It is increased in normal
pregnancy to ameliorate the effect of the increased
angiotensin II.
• Actually, there is no evidence that there is decrease
in ANP in PIH, but in contrast, it may be increased
as a response to increased blood pressure.
75

VI. Prostaglandins:
• Prostacyclin is a vasodilator and an inhibitor for
platelets aggregation while thromboxane is a
vasoconstrictor and platelets aggregator.
• In PIH, there is imbalance towards an increase in
thromboxane production.
76

VII. Neutrophils:
• Neutrophils activation causes damage and
dysfunction of the vascular endothelium leading to
platelets aggregation, coagulation activation,
hypertension and proteinuria.
77

Predisposing factors:
1. Primigravidae more than multigravidae.
2. Pre-existing hypertension.
3. Previous pre-eclampsia.
4. Family history of pre-eclampsia.
5. Hyperplacentosis i.e. excessive chorionic tissue as in
hydatidiform mole ,multiple pregnancy, uncontrolled
diabetes mellitus and foetal
6. Hemolytic diseases.
7. Obesity.
8. Climatic variations.
9. Race
78

Pathophysiology
Uteroplacental ischemia may be central to the
development of the disease.
 which has been attributed to failure of the
normal physiologic changes in the spiral
and radial arteries of the uterus.
 Uteroplacental ischemia results in the production
and release of toxins that enter the circulation and
cause widespread endothelial dysfunction.
79

 The nature of these toxins has not yet been
identified but may involve oxygen free radicals and
lipid peroxides.
 Endothelial dysfunction leads to an imbalance
between different classes of locally produced
vasoconstrictors and vasodilators
80
Pathophysiology…..

Pathophysiology….
• Preeclampsia is associated with a disturbance in
prostaglandin production, with a decrease in the ratio
of the vasodilators prostaglandin E2 (PGE2) and
prostacyclin to the vasoconstrictor PGF series and
thromboxane.
PGI2 is associated with decreased vascular resistance
and decreased platelet aggregation.
81

Pathophysiology….
 Endothelial changes also appear to involve a
relative deficiency in the production of nitric oxide,
a vasodilator and inhibitor of platelet aggregation,
along with increased production of endothelin-I.
• Endothelin-I is an extremely potent vasoconstrictor
and activator of platelets
82

Pathophysiology….
 This shift in the production of locally acting
vasoactive substances could enhance
vasoconstriction in response to circulating pressor
hormones.
 The net effect would be to cause widespread
arteriolar constriction leading to
hypoxic/ischemic damage in different vascular
beds, systemic hypertension, and worsening
placental ischemia.
83

Pathophysiology….
• The relative severity of the signs and symptoms of
preeclampsia in any given individual afflicted with
the disease would vary on the basis of which
specific organ systems were most affected.
84

Vasospasm :
 Generalized vasospasm in all body systems is the
hallmark of the pathology of preeclampsia and
eclampsia.
 All complications of preeclampsia result from end
organ damage following generalized vasospasm and are
related to its severity.
 As the vasospasm gets severe, it leads to ischemic
damage to microvasculature distal to the site of
vasospasm resulting in further endothelial damage and
leakage of fluid and protein into the surrounding tissue.
85

Vasospasm
1. Liver: subscapular haemorrhage, periportal
necrosis and infarctions.
2. Endocrine glands: necrosis and haemorrhage in
pituitary, pancreas and adrenal glands.
3. Heart and lungs: myocardial and endocardial
haemorrhage and necrosis.
86

Vasospasm …..
4. Lungs shows haemorrhage and secondary
bronchopneumonia.
 Pulmonary capillary endothelial damage and
leakage ( in addition to Hypoproteinemia due to
proteinuria and left ventricular failure)
 Pulmonary edema
87

Pathological Changes……..
Vasospasm …..
5. Kidney: decrease in renal blood flow and
glomerular damage (glomerular endotheliosis ) leading
to:
 Decrease glomerular filtration rate by about 50%,
 Loss of protein in urine (albuminuria)/Proteinuria
 Decreased creatinine and uric acid clearance ---Elevated
serum levels of uric acid, urea and creatinine.
 Serum uric acid level(Hyperuricemia) is diagnostic and
prognostic for severe pre-eclampsia
88

Vasospasm …..
6-Placenta:
• Reduced utero-placental blood flow leading to
intrauterine growth retardation (IUGR) and
even death.
• Placental thrombosis, infarction and abruptio
placentae.
7-Retina: Vascular spasm, haemorrhage, exudate and
rarely retinal detachment in severe cases. Cortical
blindness
89

Vasospasm …..
• Central nervous system
ǣ Cerebral hypoxia due to vasospasm
ǣ focal hemorrhages distal to the vasospasm
ǣ secondary cerebral edema; intracranial
hemorrhages
 Eclampsia
 Hemorrhagic stroke
 Cerebral edema and death Transient blindness –
retinal or cortical
90

Vasospasm …..
• Blood volume
capillary leak---
compromised blood volume-small amount of blood
loss can lead to hypotension
Heamoconcentration
Hematology
 Excessive consumption of platelets to repair
endothelial damage
 RBC damage as they pass through the spastic
arterioles 91

Coagulation status:
1. Fibrin production is increased.
2. Fibrinolytic activity is decreased.
3. Factor VII, factor VIII- related antigen and fibrin/
FDP concentrations in the plasma are all
increased.
4. Fibrin and platelet deposition is increased
particularly in the placental arteries.
5. Thrombocytopenia(due to excessive consumption
of platelets to repair endothelial damage)
92

Coagulation status
• Platelets are activated in the microcirculation of the
placenta, kidney and liver, release their products as
5-hydroxytryptamine and re-enter the circulation in
an exhausted state, unable to respond normally to
aggregating agents and having lower level of 5-
hydroxytryptamine.
• The end result of these changes is
hypercoagulability and disseminated
intravascular coagulation in severe pre-
eclampsia and eclampsia.
93

N.B. HELLP syndrome is described in PIH which
consists of:
• H = Haemolysis, EL= Elevated Liver enzymes, LP=
Low Platelet count.
• All pathologic features of preeclampsia recede upon
delivery of the placenta without any remnant disease
or pathology
94

Diagnosis
Signs
1. Hypertension
Diastolic pressure ≥ 90 mmHg or
Systolic pressure ≥ 140 mmHg or
2. Proteinuria
>300 mg/24-hr urine collection or
+1 or more on dipstick of a random urine
95

Clinical findings contd.
3. Edema
Weight gain: 1-2 lb/wk or 5 lb/wk is considered
worrisome
Degree of edema
Preeclampsia may occur in women with no edema
Most recent reports omit it from the definition
96

Symptoms:
1. Headache: usually frontal but may be occipital. It
is due to cerebral oedema and hypertension.
2. Visual disturbances: blurring of vision, flashes of
light or blindness.
3. Epigastric or right upper quadrant pain: due to
enlargement and subcapsular haemorrhage of the
liver.
4. Nausea and vomiting : due to congestion of
gastric mucosa and/ or cerebral oedema.
5. Oliguria or anuria: due to kidney pathology.
97

Clinical findings
Laboratory findings (1)
• Blood test: elevated Hgb or Hct, in severe cases,
anemia secondary to hemolysis, thrombocytopenia,
decreased coagulation factors
• Urine analysis: proteinuria, specific gravity > 1.020
• Liver function: ALT and AST increase, alkaline
phosphatase increase, LDH increase, serum albumin
• Renal function: uric acid: 6 mg/dl, serum creatinine
may be elevated
98

Laboratory findings (2)
Retinal check:
Other tests: ECG, placenta function, fetal maturity,
cerebral angiography, etc
99

Types:
Mild Preeclampsia
 BP ≥140/90mmHg or ≤ 160/110 mmHg
 Protein ≥ 300mg/24hour, ≥ 1+ dipstick
 No other symptoms, signs or laboratory
findings of severe pre-eclampsia
100

Severe Preeclampsia
 BP ≥160/110 mm Hg
• Proteinuria of > 2g /24hrs or ≥ 2 + 𝑑𝑖𝑝𝑠𝑡𝑖𝑐𝑘
Any of these manifestations of multi organ
involvement
 Headache: -increasing frequency, unrelieved by regular
analgesics (frontal/occipital)
 Hyper-reflexia (exaggerated deep tender reflexes)
 Clouding of vision (blurred vision/photophobia)
 Oliguria (<400 ml urine in 24hrs) (followed by rapid weight
gain)
 Upper abdominal pain (epigastric or right upper quadrant
pain) 101

Severe Preeclampsia contd.
 Pulmonary edema (rapid shallow breathing, cyanosis,
rales).
 Fetal growth restriction
 Abruptio placenta
 Disseminated intravascular coagulation (DIC)
(bleeding)
 HELLP syndrome (hemolysis, elevated liver enzymes &
low platelets)
 Eye changes: arteriolar spasm, edema, retinal
detachment ( by fundoscopy).
 Severe nausea & vomiting
***if one or more found, indicates severe preeclampsia 102

Severe Preeclampsia contd.
 Lab changes include
 Increased hematocrit
(Heamoconcentration)
 Blood smear (>hemolysis)
 Platelets < 1 00,000
103
Serum uric acid (↑ ed)
Serum creatinine (↑ ed)
Significantly altered
liver function tests
Hyperbilirubinemia
 Elevated liver
enzymes (AL T, AST,
LDH)

Classification of Preeclampsia
Criteria Mild preeclampsia Severe preeclampsia
Blood pressure < 160/110 > 160/110
Symptoms Absent Present
Proteinuria ≤ 2 > 3+ on dipstick
Liver and Renal function Normal Abnormal
Platelet count Normal Thrombocytopenia (100,000/μL)
Pulmonary edema Absent Present
Convulsions Absent Present
HEELP 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
104

Complications
Maternal :
1. Convulsions and coma (eclampsia).
2. Cerebral haemorrhage.
3. Renal failure.
4. Heart failure.
5. Liver failure.
6. Disseminated intravascular coagulation.
7. Abruptio placentae.
8. Residual chronic hypertension in about 1/3 of
cases.
9. Recurrent pre-eclampsia in next pregnancies.
107

Complication………
B Foetal :
1. Intrauterine growth retardation (IUGR).
2. Intrauterine foetal death.
3. Prematurity and its complications.
108

Management of Different Stages of PIH
109

Gestational hypertension
Manage on outpatient basis (especially if at <36wks
GA)
@Follow up for increasing BP, urine (for proteinuria)
& fetal condition weekly
@If blood pressure worsens, manage as mild pre-
eclampsia
@If there are signs severe IUGR admit to hospital for
assessment & possible induction of labor/C/S as
indicated.
110

Gestational hypertension ……
Manage on outpatient basis (especially if at <36wks
GA) …
@Counsel the woman & her family about danger
signals indicating sever preeclampsia or
eclampsia.
@If all observations remain stable, allow to proceed
with normal labor & childbirth (but better not to
post term)
111

Mild Pre- Eclampsia
Management may vary depending on the gestational
age
1. Gestational age less than 37 weeks
OP twice weekly follow up is preferable as long as
signs remain unchanged or normalize if it is
convenient for the patient).
Monitor blood pressure, urine protein & fetal
condition, twice weekly.
Counsel about the danger signals (symptoms and
signs of severe pre-eclampsia)
112

Cont….
 Encourage additional periods of bed rest
 Encourage the woman to eat a normal diet (salt
restriction should be discouraged)
 Orient on fetal movement counting (kick chart)
daily, to be reported at ANC visits
No medications (do not give anticonvulsants, anti
hypertensive, sedatives or tranquillizers).
113

Mgt cont’d……
If follow up as an outpatient is not possible or if
close observation is preferred, or pre-eclampsia
progress rapidly, admit to hospital
 Provide a normal diet (no salt restriction)
 Monitor blood pressure (twice daily) & urine protein &
weight (daily)
 Auscultation of FHB & kick chart daily
 Do not give medications (as above)
 Do not give diuretics (diuretics are harmful & only
indicated for use in pre-eclampsia with pulmonary edema
or congestive hear failure)
114

Mgt cont’d……
NB. Weight gain should be : 0.45kg/wk (lesser with
placental dysfunction & excess with fluid retention)
• If the Diastolic blood pressure decreases to normal
levels or her condition remains stable send the
woman home with the following instruction
• Advise her to rest & to watch out for signs of
severity
• Continue follow up twice a week (as above)
• If diastolic blood pressure rises again, readmit her
115

Mgt cont’d……
• If the signs remain unchanged, keep the woman in the
hospital
#Continue the same management & monitor fetal growth
& well-being (by symphysis fundal height, kick chart
& other methods if available).
# If there are signs of growth restriction consider early
delivery
116

Mgt cont’d……
# If not, continue hospitalization until term ( &
consider termination if cervix is favorable)
# If signs worsen (urinary protein level increased etc)
manage as severe pre-eclampsia.
117

Mgt cont’d……
2) Gestation ≥ 37 complete weeks
• If the woman's condition remains stable & there is no
signs of IUGR, Continue monitoring as above & plan
delivery when the cervix is favorable (but before
going post term, better not beyond 40wks)
 If there are signs of fetal compromise, assess the
cervix & hasten delivery.
118

2) Gestation ≥ 37 complete weeks…..
If the cx favorable (soft, thin, partly dilated);
rapture the membranes with an amniotic hook or
kocher clamp & induce labor using oxytocin ( refer
to inducation protocol).
If the cervix is unfavorable (thick, closed), ripen
the cervix using prostaglandin or a folly catheter
(see protocol for induction), or deliver by caesarian
section.
119

Severe pre-eclampsia
The steps of management include:
General measures - supporting the specific
treatments
Prevent convulsion with magnesium sulfate or
valium
 Control hypertension
 Delivery as soon as possible
120

Mgt of Severe pre-eclampsia contd.
General Measures
 Admit the patient urgently, if not done before
 Manage in left lateral position (relieves pressure
on inferior vena cava)
121

 Set up IV line (using cannula) & infuse fluids to
replace estimated loss (from bleeding, vomiting
diarrhea, sweating) ( 500ml in 1st 1/2 hr). then
ongoing loss + urine out put + insensible loss (700
ml/24 hrs (PO & IV).
 Place an indwelling catheter to monitor urine out
put & proteinuria.
122

Urine output should be at least 30 ml/hr. If it is less,
run fluids more rapidly ( if no still improved,
consider renal failure) ..
Maintain a strict fluid balance chart, to avoid fluid
overload
123

Prepare equipment for convulsion management, at
bedside (mouthpiece, airway, suction equipment,
mask & bag, oxygen)
Never leave the patient alone (if convulsion occurs,
aspiration may cause death)
Observe vital signs, FHB & reflexes hourly
124

Osculate the lung bases for crepitation indicating
pulmonary edema. If they occur, with hold fluids
& administer a diuretic (furosemide 40 mg Iv stat)
The immediate treatment should include managing
symptoms
Anti emetic - for nausea & vomiting to minimize
maternal discomfort
Anti pain - for RUQ pain, headache etc
125

2) Stress Reduction
A component of maternal hypertension is
adrenergic & may be modified by stress
reduction
Maternal discomfort must be minimized (as
above & others)
126

Components of stress reduction includes
Quiet, dimly lit, isolate
 Well planned management protocol
Clear explanation of the management plan to
patient and family
 Minimization of negative stimuli
 Consistent, confident team approach
127

• Anticonvulsant therapy (seizure prophylaxis)
 Seizure prophylaxis should be instituted
• Anticonvulsive Drugs
@ Magnesium sulfate
@Diazepam.
@Phenytoin
128

♣ In all pre-eclamptics during labor & continued for
12-24 hrs after delivery
♣ In all severe pre-eclamptics during admission &
continued during period of evaluation &
observation.
♣ This is achieved by proper sedation & cutting off
all peripheral stimuli
129

Magnesium Sulfate
• Use magnesium sulfate in(indication)
@Women with eclampsia
@Women with severe pre-eclampsia necessitating delivery
♣Start magnesium sulfate when decision for delivery is
made
♣Continue for 24 hours postpartum or after last seizure.
130
Magnesium sulfate is the drug of choice
for preventing & treating convulsions
in severe pre-eclampsia & eclampsia

Loading dose
Magnesium sulfate
• 4 gm Mgso4 as 20% solution IV given over 5
minutes
• 10 g of 50% magnesium sulfate solution, 5 g in
each buttock as deep IM injection with 1 mL of
2% lignocaine in the same syringe.
• If convulsions recur after 15 minutes, give 2 g
magnesium sulfate (20% solution) IV over 5
minutes.
131

Magnesium Sulfate protocol:
• Maintenance dose
• 5 g magnesium sulfate (50% solution) + 1 mL
lignocaine 2% IM every 4 hours into alternate
buttocks.
• Continue treatment with magnesium sulfate for
24 hours after delivery or the last convulsion,
whichever occurs last.
132

Magnesium Sulfate protocol:
Before repeat administration, ensure that:
• Respiratory rate is at least 16 per minute.
• Patellar reflexes are present.
• Urinary output is at least 30 mL per hour over 4
hours
WITHHOLD OR DELAY DRUG IF:
• Respiratory rate falls below 16 per minute.
• Patellar reflexes are absent.
• Urinary output falls below 30 mL/hour over
preceding 4 hours.
133

Magnesium Sulfate protocol: contd.
Keep antidote ready
• In case of respiratory arrest:
♣Assist ventilation (mask and bag, anaesthesia
apparatus, intubation).
♣Give calcium gluconate 1 g (10 mL of 10%
solution) IV slowly until respiration begins to
antagonize the effects of magnesium sulfate.
134

Summary
♣There are many manifestations of increased blood
pressure in pregnancy
♣It is not possible to predict which patients are at risk
for severe pre-eclampsia or eclampsia
♣Vigilant care is needed to make the diagnosis
♣Once the diagnosis is made, appropriate treatment
can reduce morbidity and mortality
137

Summary…
♣Anticonvulsants should be used, with magnesium
sulfate being the first line
♣Antihypertensives should be employed as needed
♣Close monitoring is needed for side effects
138

Anti -hypertensive therapy
Goals
• Minimize risk of maternal CVA (but does not
necessarily reduce the risk of seizure or prevent
IUGR)
• Maximize maternal condition for safe delivery
• Gain time for further assessment
• Facilitate vaginal delivery if possible
• Prolong gestation where appropriate / feasible 139

Antihypertensive Drugs
Drugs
•Hydralazine
•Labetolol
•Nifedipine
Principles:
 Initiate antihypertensives if
diastolic blood pressure ≥110 mm
Hg
 The goal is to keep the diastolic
blood pressure 90-100 mm hg) (ll0
mm hg in labor).
140

Hydralazine
• Is the drug of choice for acute therapy (arteriolar
dilator with rapid onset iv)
 Give 5-10 mg iv slowly every 5 minutes until BP is
lowered (to DBP <110mmhg).
 If no response after 20 mg switch to another drug.
Repeat hourly as needed or give 12.5mg 1M every
2hrs as needed.( If IV rout is not possible)
141

Hydralazine
 Cautions -hypotension with fetal compromise may
occur in slow acetylaters &hypovolemic patients
(start with 5 mg iv test dose)-
• Side effects may cause flushing, headache or
tachycardia
142

Nifedipine
@Nifedipine is a calcium channel blocker, oral agent,
with rapid onset of action, if regular capsule used
(relaxes vascular smooth muscle)
@It can be used as alternative for acute therapy (though
less satisfactory) 5-10 mg sublingually (under the
tongue) as initial dose, followed by 5-10mg if
response is inadequate (in 30 minutes). Then continue
as 10-20 mg PO every 6 hours.
143

Nifedipine…
@For maintenance therapy 10-40mg PO bid
Side effects: edema, flushing, headache, palpitation,
MgSo4 toxicity, tocolytic (may stop labor)
144

Methyldopa
• Methyldopa is a centrally acting α:-receptor
agonist, it is an oral agent.
Methyldopa is the drug of choice for
maintenance therapy.
It has a minimal side effect & safe.
 Methyldopa has a long history of safe use in
pregnancy, well tolerated .
145

Methyldopa…
 There is some concern regarding ability to control
blood pressure (additional drug may be needed)
Dosage - 500 - 3000mg PO in 2-4
divided doses per 24 hrs
Other alternative (or supplementary) drugs for
maintenance therapy. Include -nifedipine (PO),
hydralazine (PO) or atenolol (50 - 100 mg PO once
daily)
146

Labetalol hydrochloride
 Nonselective β1- and α1-blocker
Dosage:
 Start with 20 mg IV bolus. If inadequate response
after 10 min, give 40 mg IV followed by 80 mg IV
every 10 min × two more doses if needed to lower
BPs to 140-150/90-100 mm Hg. Total dose not to
exceed 220 mg.
• S/E: Nausea, vomiting, heart block, burning
sensation in throat, dizziness
147

Delivery
 Delivery should take place as soon as the woman's
condition has stabilized, regardless of the
gestational age
 Eclamptic usually proceed to labor spontaneously
while having convulsions
148

Delivery….
 Delivery should occur within 72hrs of the onset of
symptoms in severe pre-eclmapsia, & within 12
hrs of the onset of convulsions, in eclampsia.
 If vaginal delivery is not anticipated within this
time limit, delivery should be by cesarean section.
149

Route of delivery
 Depends on gestation age to cesarean section for
women with PE (even if with sever disease).
 It is desirable, if possible, to avoid the added stress
of surgery & anesthesia, because of multiple
physiologic abnormalities , fetal condition &
presentation, cervical condition & maternal condition
 Vaginal delivery is preferable
150

Route of delivery
• Aim for vaginal delivery by induction using
artificial rupture of membranes ( ARM) & Oxytocin
where needed under the following condition :
 If the cervix is ripe (soft, thin, dilated)
 If the fetus is dead or extremely premature for
survival With rapid progress in labor
 After cervical ripening with prostaglandin E2
gel, under appropriate circumstances 151

Route of delivery
 As trial of induction - warranted because even though
the cervix may feel unfavorable, labor can be induced
& progress fairly (CIS can be performed if labor has
not begin within 6-12hrs or if the progress of labor is
poor).
NB: Eclampsia is not a contraindication to such trial
of induction. In fact it is usually successful with short
induction delivery interval.
152

Route of delivery
Cesarean delivery is indicated
 If the cervix is unfavorable (firm, thick, closed)
esp. in seriously ill patients With poor progress of
labor
 If patient has not entered active labor within 8hrs of
induction of labor
 If there is evidence of fetal distress, or there
obstetric indications,&
153

Post partum Care …..
 Anticonvulsive therapy should be maintained for
24hrs after delivery or the last convulsion, whichever
occurs last
 Continue anti-hypertensive therapy as long as the
DBLOOD PRESSURE is ≥ 110mmhg
 Continue to monitor urine output & check for
coagulation failure, LFT,RFT if possible
154

Post partum Care ……
• Consider referral of women who have:
• Oliguria that persists for 48 hours after delivery
• Coagulation failure [e.g. coagulopathy or
haemolysis, elevated liver enzymes and low
platelets (HELLP) syndrome];
• Persistent coma lasting more than 24 hours after
convulsion.
• If heart, kidney or liver failure is suspected
• If there is increasing drowsiness or coma
155

Eclampsia: Typical signs
 It is the development of convulsions in a pre-
existing pre-eclampsia.
Incidence
 About 1/1000 pregnancies.
Aetiology
 The exact cause is unknown but cerebral
ischaemia and oedema were suggested.
156

Eclampsia…..
 Patients with severe preeclampsia are at the greatest
risk of developing seizures.
 Eclamptic seizures can also occur prior to classic
signs of preeclampsia.
 In general, 25% of patients with eclampsia develop
the seizures before labor, 50% during labor, and
25% after delivery (usually within the first 24 to 48
hours' postpartum).
157

Clinical Picture/The stages of an eclamptic fit
1. Premonitory stage (lasts 10-20 seconds)
The mother is restless and rapid eye movements
can be noted.
The head may be drawn to one side and twitching
of the facial muscles may occur
 The mother has no perception of the impending fit
and shows altered awareness.
158

The stages of an eclamptic fit contd.
2. Tonic stage (lasts 10-20 seconds)
 The muscles of the mother’s body go into spasm
and become rigid and her back may become
arched.
 Her teeth will become tightly clenched and her
eyes staring
159

The stages of an eclamptic fit contd
The Clonic stage (lasts 60-90 seconds)
 Violent contraction and intermittent relaxation of
the mother’s muscles produces conversions
movements
 Salivation increases and foaming at the mouth
occurs.
 The mother’s face becomes congested and bloated
and the features become distorted. 160

The stages of an eclamptic fit contd.
 She is unconscious, her breathing detorous and her
pulse full and bounding.
 Gradually the convulsion subsides.
Stage of coma
 Stertorous breathing continues and coma may persist
for minutes or hours.
 Further convulsions may occur before the mother
regains consciousness. 161

Severity of Eclampsia
Eclampsia is considered severe if one or more of the
following is present (Eden’s criteria):
1. Coma of 6 or more per hours.
2. Temperature 39℃ or more.
3. Pulse over 120/min.
4. Systolic blood pressure over 200 mmHg.
5. Respiratory rate over 40/min.
6. More than 10 convulsions.
162

Differential Diagnosis:
1. Epilepsy.
2. Intracranial haemorrhage.
3. Meningitis.
4. Brain tumours.
163

Strategies for Preventing Eclampsia
 Antenatal care and recognition of hypertension
 Identification and treatment of pre-eclampsia by
skilled attendant
 Timely delivery
•3.4% of women with severe pre-eclampsia will have a
convulsion
•Eclampsia is abrupt in onset, without warning signs in about
20% of women
164

Management of Eclampsia
 Shout for help - mobilize personnel
 Rapidly evaluate breathing and state of
consciousness
• If not breathing, assist ventilation using Ambu
bag and mask
 Check airway, blood pressure and pulse
• Give oxygen at 4–6 L per minute via nasal
catheter;
 Position on left side
 Protect from injury but do not restrain 165

Management of Eclampsia cond.
 Start IV infusion with large bore needle (16-gauge)
 If eclampsia is diagnosed, initiate magnesium
sulfate
If the cause of convulsions has not been
determined, manage as eclampsia and continue to
investigate other causes.
166

Comparison
CLINICAL
FINDINGS
CHRONIC
HYPERTENSION
GESTATIONAL
HYPERTENSIO
N[*] PREECLAMPSIA
Time of onset of
hypertension
<20 weeks Usually in third
trimester
≥20 weeks
Degree of
hypertension
Mild or severe Mild Mild or severe
Proteinuria Absent Absent Usually present
Serum urate >5.5
mg/dl (0.33 mmol/L)
Rare Absent Present in almost all cases
Hemoconcentration Absent Absent Severe disease
Thrombocytopenia Absent Absent Severe disease
Hepatic dysfunction Absent Absent Severe disease
169

Outline
 Definitions
 Aetiology of APH
 Diagnosis of APH
 Clinical manifestations of APH
 Management of APH
 Complications of APH
 Summary 171

Session Objective
• By end of session, participants will be able to:
 Describe APH
 Identify major causes of APH
 Discuss the evaluation Pts with of APH
 Discuss management of APH
 Describe complications of APH
172

Definition
APH is bleeding from genital tract in late pregnancy,
after the 28 week of gestation till the end of Second
Stage of Labour.
 Obstetric hemorrhage is one of the five leading cause
of MMR.
 Vaginal bleeding in the third trimester complicates 4%
of all pregnancies.
 The incidence is 2-3% of all pregnancies 173

Aetiology
• No definite cause is diagnosed in about 40% of
all women who present with APH:
Classification
174
Obstetric Causes
Placental causes
• Abruptio placenta
• Placenta praevia
• Vasa praevia; placenta
membranacea; circumvallate
placenta; marginal separation
of the placenta.

Aetiology
Non placental causes
• Decidual bleeding
• Heavy show
• Uterine rupture
• Bleeding disorder
• Unknown causes
175
Nonobstetric Causes
Cervical cancer or
dysplasia
Cervicitis
Cervical polyps
Cervical eversion
Vaginal laceration
Vaginitis

Abruptio Placentae (Accidental Haemorrhage)
Premature separation of a normally situated placenta
after the 28th week of pregnancy and before delivery
of the foetus.
Types of hemorrhage
• Concealed form (20%)
• External form (80%)
• Combined Haemorrhage
176
It might also be
• Partial abruption
• Total abruption
• Marginal separation

Incidence
• 1/75 to 1/225 births
• 1/3 of all APH
• Sever AP that kills the fetus = 1/830
• Abruption increases PNMR by 25%
• 15% - neurological deficit in the 1st yr. of life.
177

1. Concealed haemorrhage is
 Least common
 No vaginal bleeding instead a
retro placental clot is formed
 Related when separation starts
centrally (Schultz method)
 DIC is common due to collection
of retro placental clots.
 Pain also a feature of concealed
bleeding
178

2. External or Revealed Haemorrhage
 Most common
 Blood escapes through the vagina. (
Trickling of blood is seen)
 Related when separation starts at
the edge of the placenta ( Matthews
Duncan)
 Abdominal pain may or may not
present ( uterus is not distend by
retro placental clots) 179

3. Combined Haemorrhage
 The haemorrhage primarily concealed and then
becomes revealed.
 Uterus became tender
180

Classification of Abruption placenta
A. Mild Abruption placenta (Grade 1)
• Usually develop gradually
• Produce mild to moderate dark vaginal bleeding
• Uterine tenderness is not common
• No sign of foetal distress
B. Moderate abruption placenta (Grade 2)
• Can develop gradually or abruptly
• Produce persistent abdominal pain which
accompanied by visible dark vaginal bleeding.
• Foetal distress and sign of maternal shock is present.
181

Classification of Abruption placenta cnt -
C. Severe Abruption placenta (Grade 3)
• Usually develops suddenly causing severe,
unremitting abdominal pain (knife like pain)
• Uterus is tender and rigid
• Profuse bleeding results
• Shock is common
• There is also sign of foetal distress – foetal death may
result.
• DIC is common due to formation of retro placental
clot. 182

Etiology
Unknown , but the following factors may be
associated with :
• Hypertensive disorders of pregnancy (30%) due to
spasm and degenerative changes in the decidual
arterioles.
• Trauma as during external version.
• Sudden drop of intrauterine pressure as rupture of
membranes in polyhydramnios.
184

Etiology….
• Folate deficiency and may be vitamin C,K, or E
deficiency.
• Passive congestion of the uterus due to pressure of
the gravid uterus on the inferior vena cava.
• Torsion of the uterus.
• Smoking.
185

Initially hemorrhage into decidua basalis
Decidual hematoma & decidua splits
1. Further separation more blood loss SHOCK
and/ or
2. Compression & destruction of adjacent placenta
Acute placental insufficiency
Fetal demise
• Uterus is still distended from product of conception- don’t
contract and compress the torn vessels that supply the
placental bed.
188
Pathogenesis

Diagnosis
Symptoms:
• Acute constant severe abdominal pain which may be
localized or diffuse.
• Dark vaginal bleeding results from escape of blood
from the retroplacental haematoma.
• Cessation of foetal movement is common.
193

Diagnosis
Signs:
A. General examination:
• Shock is usually present and may be marked and not
proportionate to the amount of visible bleeding due to :-
concealed and/ or revealed haemorrhage,
• over distension of the uterus and damage of the
myometrium causing neurogenic shock.
194

Diagnosis…..
Signs:
• Blood pressure is; subnormal due to haemorrhage,
• normal due to falling from previous hypertension
or
• high due to slight bleeding in hypertensive patient.
 Pulse - rapid, weak, irregular
195

Diagnosis……
B. Abdominal examination:
• Uterus is large for date and increasing gradually in size
due to retained blood.
• Uterus is very tender and hard (board-like).
• Foetal parts are difficult to be felt.
• FHS may be absent due to foetal death in severe cases or
distressed in mild cases.
196

C. Investigations:
• Ultrasonography
• Appearance depend on time of scanning
• Most important is to R/O placenta previa
• Importantly, negative findings with ultrasound
examination do not exclude placental abruption.
Ultrasound only shows 25% of abruptions.
• Laboratory testes
• Non are diagnostic
• FDP & thrombomoduline levels
• Fibrinogen level, platelet count/Tests for DIC.
• Pathologic examination
• After delivery
197

Diagnosis….
• Vaginal examination can be done after placenta
previa is R/O
Differential diagnosis
 Placenta previa in labor
 Uterine rupture
 Sepsis / DIC
 Scar dehiscence 198

Management
• Principles:
Admit or Refer all patients to a hospital
NEVER DO PV- before placenta p. is R/O
Take resuscitative measures
Plan further management depending on GA &
severity of clinical presentation.
199

Grade I AP
Expectant Mx. If preterm
Secure IV line
hct, BG &RH, X- match blood
Platelet, PT, PTT, fibrinogen, FDP
Continuous FHR monitoring (CTG)
Follow maternal hemodynamic status
• V/S q 15’, bleeding, S-hct, labor, coagulopathy, uterine tenderness
Steroid therapy
Terminate – any deterioration in mother or fetus or
Term
200

Grade II/ III
 No place for expectant management
 Normalize the blood volume
 Correct anemia
 Correct acid base imbalance
 Prevent or correct coagulopathy
 Monitor the renal function
 Continuous FHR monitoring
201

Mode of delivery
Vaginal
 Depends on the cervical status, maternal & fetal condition.
 Rule out PP by U/S or double set up examination
 Amniotomy and Induction / augmentation
 IU- pressure monitoring
 Internal electronic FHR monitoring
 Frequent V/S monitoring
202

Mode of delivery
Cesarean section
• Indication:
• Uncontrolled hemorrhage
• Protracted labor suspected
• Fetal distress
• No coagulopathy
• Other obstetric indications
203
Termination if there is:
Heavy or recurrent bleeding
Fetal distress
Congenital anomaly
Term
Intra uterine fetal death
(IUFD)
Ongoing separation
Avoid regional anesthesia in hypotension and DIC

Complication
Maternal
 Hypovolemic shock
 Acute renal failure
 DIC
 PPH
 Anemia
 Sheehan syndrome
(pituitary necrosis)
 Maternal death 204
Fetal/ Neonatal
 Prematurity
 IUGR
 PNM(35%)
 Still birth(15%)
 Future neurological
sequels

Prevention
@Avoid all substances during pregnancy including
cigarettes, alcohol, medicines (unless prescribed by
your doctor) and street drugs.
@Reduce your risk of trauma – for example, wear a
seatbelt when travelling in a car and avoid the
possibility of falls
205

Prevention….
@Control high blood pressure. Consult with your
doctor for information, advice and treatment.
@Talk to your doctor if you have had placental
abruption in a previous pregnancy.
@ Take folic acid as recommended by your doctor
or midwife.
206

Placenta Previa
Definition
• The placenta is partially or totally attached to the
lower uterine segment.
• Incidence:0.5% of pregnancies .
• It is more common in multiparas and in twin
pregnancy due to the large size of the placenta.
Bleeding from a placenta previa accounts for
approximately 20% of all cases of antepartum
hemorrhage. 207

Types of PP
Four types
1. Low lying placenta previa/Type I = P.P. lateralis
2. Partial placenta previa/Type II= P.P. marginalis
3. Marginal placenta previa/Type III= P.P. incomplete
centralis
4. Total placenta previa/Type IV = P.P. complete
centralis
208

Type 1 placenta praevia
♣The placenta is implanted in the
LUS such that the placental edge
does not reach the internal os, but
is in close proximity to it
 Vaginal delivery is possible
 Blood loss is usually mild
 The mother and the fetus remains
in good condition
209

Type 2 placenta praevia (marginal placenta pravia)
 The lower edge of the
placenta reaches the margin of
the internal os but does not
cover it.
 Vaginal delivery is possible
particularly if the placenta is
implanted anteriorly
Blood loss is usually moderate
Fetal hypoxia is more likely to be
present 210

Type 3 placenta pravia (Partial placenta previa)
• The internal os is partially
covered by placenta and
Bleeding is likely to be sever
particularly when the lower
segment stretches and the
cervix begins to efface and
dilate in late pregnancy
211
Vaginal delivery is in appropriate.

Type 4 placenta praevia(Total placenta previa)
 The internal os is covered
completely by placenta and sever
haemorrhage is very likely
Vaginal delivery should not be
considered
ƒ caesarean section is essential
in order to save the life of the
mother and fetus.
212

cont.
N.B. Placenta praevia marginalis posterior is
of bad prognosis than marginalis anterior
because:
• It encroaches on the true conjugate diameter
delaying engagement of the head.
• Engagement of the head will compress the
placenta against the sacrum, causing foetal
asphyxia
213

Mechanism of bleeding
 Progressive stretching of the lower uterine segment
normally occurs during the 3rd trimester and labour,
but the inelastic placenta cannot stretch with it. This
leads to inevitable separation of a part of the placenta
with unavoidable bleeding.
 The closer to term, the greater is the amount of
bleeding.
214

Etiology
• The specific cause is unknown
• Many factors may affect placental implantation
 Defective decidual vascularization (ex PID)
 Prior trauma to the endometrium
 Placental hypertrophy
215

Associated factors
• Increased maternal age 1/1500 =teenagers :1/100
>35yrs
• Multiparty
- 1/1500=nullipara vs 1/20= grand multipara
3. Prior uterine scar
-c/s-- 5fold increased incidence
--- 2%with 2 prior c/s
--- 4% with >/=2 prior c/s
-risk of TAH increased with repeat c/s for
PP(25%VS 6%)
216

Associated factors
217
• Smoking = CO hypoxemia ----placental
hypertrophy
• Twins = increased surface area is needed
• Prior placenta previa(4% to 8%)

Clinical course and diagnosis
The mean gestational age at Dx =35wks
PAINLESS ,CAUSELESS ,BRIGHT RED vaginal
bleeding
Why bleeding ?
-formation of the LUS --- detachment of the
placenta
-placentitis
-direct trauma ---coital ,PV exam, douching
Can also remain asymptomatic
1st episode usually slight -- get more sever later on
The GA at 1st episode --- ass. With perinatal outcome
218

Diagnosis
• When placenta previa is diagnosed in the second
trimester, a repeat sonogram is indicated at 30 to 32
weeks for follow-up evaluation.
Symptoms:
• Causeless, painless and recurrent bright-red vaginal
bleeding in the 3rd trimester is PP!!!
• It is causeless, but may follow sexual intercourse or
vaginal examination. 219

Diagnosis
Symptom….
• It is painless, but may be associated with labour
pains .
• It is recurrent, but may occur once in slight placenta
praevia lateralis.
• Fortunately, the first attack usually not severe.
220

Diagnosis…
Signs:
General examination:
• The general condition of the patient depends upon the
amount of blood loss.
Shock develops if there is acute severe blood loss and
anaemia develops if there is recurrent slight blood loss.
221

Diagnosis…
Abdominal examination:
• The uterus is corresponding to the period of amenorrhea,
relaxed and not tender.
• The foetal parts and heart sound (FHS) can be easily
detected.
• Malpresentations, particularly transverse and oblique lie
and breech presentation are more common as well as non-
engagement of the head. This is because the lower
uterine segment is occupied by the placenta
222

Vaginal examination
• Speculum examination to exclude local lesions is only
permissible when placenta praevia has been excluded
by ultrasound.
• P/V is indicated only if active treatment is initiated.
223
Diagnosis….

Diagnosis….
• This may provoke a severe attack of bleeding so it
should be done with the following precautions:
In the operating room, under general
anaesthesia, cross- matched blood is in hand,
operating theatre is ready for immediate
caesarean section.
If the index finger is introduced gently through
the dilated cervix, the placenta can be felt as a
tough fibrous mass.
224

Investigations:
Ultrasound:
• Placenta previa is almost exclusively diagnosed today
by ultrasonography
-abdominal vs vaginal
Transabdominal ultrasonography has an accuracy of
95% for placenta previa detection.
225
Double set up examination
- preparation is needed

Management
• Principles:-
Admit or refer all patients to a hospital
NEVER NEVER NEVER do PV EXAM
Take Resuscitative measures
Plan further management
226

Management of placenta praevia
The Mgt of placenta praevia depends up on:
1. The amount of bleeding
2. The condition of the fetus and mother
3. The location of the placenta
4. The stage of the pregnancy
227

Conservative Mgt
 The objective of conservative management is to
prolong pregnancy and allow the fetus to mature
up to 37 weeks
• If fetus is :
Premature
No labour
No severe bleeding
228

Conservative Mgt
 Complete bed rest
 No vaginal examination
 Monitor maternal & fetal condition
 Beta methasone 12 mg in 2 doses for 28-34 weeks
gestation
 Speculum examination after bleeding stopped (to
exclude incidental bleeding)
 Anaemia should be corrected if present/Blood
transfusion if needed
 Food rich in iron and provide iron tabs
 Termination after 37 completed weeks of gestation
229

Active management
Double set up examination is done
• If GA > 37 wks
 A woman is in labour
 If lung maturity is confirmed
 If fetus is dead
 Lethal congenital malformation
 If bleeding is severe and uncontrollable
230

Active management
231
Vaginal delivery Caesarean section is indicated in :
 PP is lateralis or marginalis anterior  PP 3 and 4 if the foetus is dead and type-
2(poste)
 Bleeding is slight,  Severe bleeding
 Vertex presentation,
 Adequate pelvis with no soft tissue
obstruction.
 Presentation other than vertex/transverse
Partially dilated cervix to allow ARM y
has 2 benefits:
• Allows descent of head so it
compresses the placental site
preventing further bleeding.
• It abolishes the shearing movement of
the placenta during uterine
contractions.
• As the bulging of fore bag of water
during contractions with intact
membranes will drag the edge of the
placenta evoking more bleeding
 Other obstetric indications as contracted
pelvis, cord prolapse and elderly
primigravida.
 Vasa praevia.

Complications
Maternal
♣ Blood loss and shock
♣ Adherent placenta
♣ Transfusion risks
♣ Longer hospital stay
♣ Surgical morbidity
♣ Post partum hemorrhage
232
Fetal/neonatal
♣ Increased PNMR from prematurity
♣ Increased risk of fetal anomalies
(5%)
♣ Increased IUGR(20% vs 5%)
♣ Birth trauma (b/c of
malpresentation )
♣ Neonatal anemia

General basic principles of the Mgt of APH
@ Resuscitation should be started immediately
@ All patients with APH should be admitted to
hospital
@No digital Vx exam until placenta previea has been
ruled out except under the condition of double set up
@ Confirmation of specific Dx
@ AMTSL
233

Summary
APH- bleeding from genital tract after the 28th
weeks of gestation up to delivery of the fetus
 The cause are mainly placental in origin and some
unexplained cause
 Mgt is based on the type
234

Ruptured Vasa Praevia
• In vellamentous insertion of the cord, some of the
foetal vessels in the membranes cross the region of the
internal os.
• When the membranes ruptures, the foetal vessels are
torn and bleeding occurs which is usually slight.
• Foetal heart rate abnormalities are detected .
238

Ruptured Vasa Praevia
Investigations:
The foetal blood can be detected by :
• Apt’s test:4-6 drops of the antepartum haemorrhage blood is
added to 10 ml of water then 2 ml of sodium hydroxide is
added.
1. The foetal blood remains red/ pink for at least 2
minutes and turns green/brown after 10-20 minutes
due to resistance to alkali in formation of alkaline
haematin.
2. If the blood is maternal in origin it turns green/
brown within 10 seconds
239
Treatment:
Immediate caesarean section.

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