ABNORMAL PREGNANCY

Mr Mbaabu

1.CARDIAC DISEASE IN PREGNANCY.

CHANGES IN CARDIOVASCULAR DYNAMICS DURING PREGNANCY.
Blood volume increases by 50%. Maximum increase is in second trimester. Initial increase is due to
increased stroke volume and decreased resistance. Later increase is due to increased heart rate and blood
volume.

Vascular resistance reduces by20-30%

Heart rate increases. Blood pressure may be normal or lower than normal.

Red blood cell mass increases by 30%. White blood cells and Platelets also increase.

Haemodilution may occur leading to physiological gestational anaemia.

Cardiac output increases by 50%. The initial increase is due to reduced vascular resistance and increased
preload while the latter increase is due to increased heart rate and blood volume.

The left ventricle increases in volume. Preload is increased and afterload is reduced.

There is prominent jugular vein pulsation.

Oedema of extremities which is caused by pressure on the vena cava compromising venous return,
sometimes generalized oedema may occur which is known as anasarca.

Angina chest pain may be present.

EFFECTS OF CARDIAC DISEASE IN PREGNANCY.

 Transfer of congenital heart defects. A mother with congenital heart diseases like tetralogy of
fallot and atrial septal defect can pass it to a child.
 Still birth and retarded intrauterine growth mostly in chronic hypertension and gestational
hypertension.
 Thromboembolism due to hypercoagulability of blood occurring in pregnancy and sometimes due
to venous thromboembolism.
 Maternal seizures especially in chronic hypertension.
 Maternal death
 Post partum haemorrhage in atonic uterus, tears and in hypertension.

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 Premature spontaneous delivery especially in pulmonary hypertension secondary to right sided
heart failure.

Specific cardiac diseases in pregnancy.

1. Rheumatic Heart Disease.

Definition.
It is a condition in which the heart valves are damaged by a disease process that begins with a throat
infection caused by group A beta haemolytic streptococcal bacteria.

Etiology.
Untreated sore throat which result to rheumatic fever. Repeated infection leads to rheumatic heart disease
which attack connective tissues especially of the heart valves.

Assessment and diagnosis.

History of characteristic signs and symptoms. History of two weeks post-streptococcal infection like sore
throat/ pharyngitis.

Auscultation will indicate murmurs

Chest X-ray and echocardiogram.

Magnetic resonance imaging.

Signs and symptoms.

Asymptomatic or mild discomfort in some people.

Dizziness or fainting during exertion, shortness of breath, fatigue, murmurs, arrhythmias, stenosis,
cardiomegaly, jugular venous extension, palpitation, fever, raised ESR, leucocytosis, cyanosis, and
arthralgia.

Laboratory studies/ hemodynamic monitoring.

Serological studies. Detect antibodies against beta hemolytic streptococcal- antistreptolysin O positive. Or
immune complexes.

Blood culture and gram staining. Especially if there is active sore throat.

During labor take frequent BP, respiratory rate, body temperature and pulse rate. Monitor electrolytes like
potassium and sodium to prevent arrhythmias.

2. CONGENITAL HEART DISEASE.

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Definition
They are inborn defects in heart structure and vessels. They may obstruct blood flow or result in mixing
of oxygenated and deoxygenated blood. They include:
 Ventricular septal defects which are the most common
 Patent ductus arteriosus
 Mitral stenosis and mitral stenosis with arterial fibrillation.
 Bio-prosthetic valves
 Coarcation of aorta without valvular involvement.
 Coarcation of aorta with valvular involvement.
 Marian’s syndrome with aortic involvement.

Signs and symptoms

Digital clubbing, cyanosis, shortness of breath, syncope, heart murmurs.

Associated signs and symptoms include: vertebral anomalies, anal atresia, cardiovascular anomalies,
tracheoesophageal fistula, esophageal atresia, renal anomalies and limb defects given the acronym
VACTERL.

Investigations.

history taking to elicit signs and symptoms

Echocardiogram will show defects in the heart, MRI, and chest x-ray can also be used.

Management

Infection control eg antibacterial prophylaxis and immunization against influenza or pneumococcal.

Treat co-morbid conditions like anemia.

Health messages on diet, smoking, rest and activities.

Pharmacological intervention with digoxins in heart failure, diuretics like laxis to manage edema. Avoid
warfarin and ACE- inhibitors. Warfarin cause nasal hypoplasia and brain degeneration while ACE-
inhibitors may cause renal failure.

Surgical correction may be done pre-conception.

Admit at thirty eight for complete bed rest.

Hemodynamic monitoring

Check blood pressure, electrolyte and maintain at normal pregnancy ranges.

3. BACTERIAL ENDOCARDITIS
DEFINATION

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A bacterial infection of endothelial surface of the heart.
It is caused by infectious agents like bacteria and fungi.
As a result the valves of the heart do not receive enough blood supply as well as immune supply against
vegetative organisms.
There are three types of bacterial endocarditis:
 Sub-acute caused by low virulence bacteria like streptococci viridians.
 Mild to moderate illness that progresses slowly for weeks
 Acute illness/fulminant illness caused by high virulence bacteria eg staphylococcus aureas.

In another classification there is culture negative where by the organism requires a longer period of time
to grow e.g. coxiella and Chlamydia, and culture positive where by the organism is present in cultures.

It can also be classified as right sided bacterial endocarditis which is mostly introduced by exposure to
intravenous drugs or left sided endocarditis introduced from other sites e.g. lungs.

SIGNS AND SYMPTOMS

Low grade Fever rarely above thirty nine degrees C, new/changing heart murmurs, neurological
anomalies like stroke, intra cerebral haemorrhage and sub arachnoid haemorrhage.extracardiac
manifestations include:petechae,sub-ungue haemorrhage ie dark streaks on the nails of fingers and
nails.hepatoslenomegaly,renal insufficiency and oslaer are also common.in
neonates,osteomyelitis,meningitis,feeding problems and tachycardia may be observed.

INVESTIGATIONS.

 Serology inorder to establish the antibodies to the causative agent or immune complexes.
 Blood culture to rule out the causative agent.
 Echocardiograph is positive.
 MRI.

The duke criteria can be used to rule out endocarditis in which endocarditis is present if one major
procedure and two other minor are present or two major procedures and one minor are present. The major
procedures are: positive blood culture and positive echocardiograph.mninor procedures include:
predisposing factor eg cardiac lesion, Fever above thirty eight degrees c, Evidence of embolism and
immunological problems e.g. glomerulonephritis.

Management.

 Use of drugs like erythromycin, amoxicillin.

 Prophylaxis before procedures.
 Counseling before conception.

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4. Peripartum Cardiomyopathy.

Definition: it is a heart failure with no identifiable cause.

Criteria.

 Occurs in the final month before pregnancy or five months after delivery.
 No identifiable cause of heart failure.
 No previous heart disease by final month of pregnancy.
 Left ventricle dysfunction.

Risk factors.

 Old age above thirty five.

 Multiple gestation.
 Pre ecclampsia

The incidence is about one to three thousand births.

Symptoms.

 Orthopnoea.
 Oedema.
 Chest pain.
 Fatigue.

Signs.

 Pulmonary crackles.
 Rales.
 Hepatomegaly.
 Elevated jugular veins pressure.
 Dizziness.

About twenty percent of the patients require cardiac transplantation, fifty to sixty percent recover, twenty
percent in subsequent pregnancies die.

Classification.

Intrinsic: weakness in heart muscles without identifiable cause e.g, infections, drugs, alcohol toxicity or
genetics.

Extrinsic: primary pathology lies outside myocardium. It is the most common.

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Other functional classifications.

Dilated cardiomyopathy: heart muscles become weak and subsequently the heat chambers dilate.

Hypertrophic cardiomyopathy: muscle is much thicker than normal.

Restrictive cardiomyopathy: muscle becomes stiff and heart can’t fill efficiently.

Investigations.

 ECG-shows left ventricle hypertrophy.

 Chest x-ray-shows cardiomegaly.
 Echocardiography-left ventricular dysfunction.
 Cardiac catheterization.

Management.

Medical intervention: use vasodilators like hydralazine, nitrate or amlodipine to improve preload and
decrease systemic vascular resistance. Diuretics for pulmonary oedema, anticoagulants to prevent
thromboembolism. Use pacemakers and defibrillators if arrhythmias occur. Don’t give ACE- inhibitors or
warfarin in pregnant women. ACE- inhibitors are fetal renal toxic while warfarin cause nasal hypoplasia,
optic atrophy and brain degeneration. Give ACE- inhibitors postpartum as the mainstay drug.

Surgical intervention may involve heart transplant.

Avoid alcohol, salt or smoking.

Perform moderate activity and ensure a balance diet.

Classification of heart disease in pregnancy

According to Newyork Heart Association, heart diseases in pregnancy are classified into four classes.

1. Class one. Uncompromised.

There are no symptoms of cardiac insufficiency or angina pain.
2. Class two. Slight limitation of physical activity. Comfortable at rest, symptoms when
doing ordinary activity
3. Class three. Mild limitation of physical activity. Comfortable at rest, symptoms with less
than ordinary physical activity.
4. Class four. Severely compromised, symptomatic at rest, can’t perform any activity
without surgery.

MANAGEMENT.
Principles of management.
 Maternal health is given priority. Pregnancy may be interrupted incase the mother’s life is at risk.
 Involve a team of professionals eg cardiologist, obstetricians, anaesthesiologists, nurses and
others.

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 Infection control through vaccination against pneumococcal and influenza. Avoid smoking and
illicit drug use. Use prophylaxis against bacterial endocarditis and rheumatic fever
 Activity and diet modification. Ensure client has enough rest and feed on a balance diet.
 Counseling on possible complications to child or mother, on medical and other therapeutic
interventions, on diet, activity and rest. Pre-conception counseling may include contraception.

AIMS OF MANAGEMENT
It is to achieve pregnancy cardiovascular dynamics such as fifty percent increase in pre-pregnancy blood
volume, ten to twenty percent decrease in vascular resistance and hypercoagulability.

Management of class one and class two.

These classes are associated with less morbidity.
Key is to prevent and detect early signs of heart failure. Give cardiac glycosides incase of heart failure
Vaginal delivery is preferred.
For Reduction of labors, epidural anesthesia is recommended.
Good history taking and careful physical examination.
Monitoring of the client is after two weeks for first thirty two weeks. Then admit for complete bed rest at
week thirty eight.
Infection control and treatment of existing diseases eg treat anaemia and vaccinate against pneumococcal
infection
Give health messages on a balanced diet, adequate rest and activity. Discourage tooth removal to avoid
bacterial endocarditis.

MANAGEMENT IN LABOR
Stage one and two
 Let the patient be in semi recumbent position with a lateral tilt.
 Take vital signs frequently between a quarter and half hourly.
 Monitor the fetal heart rate.
 Treat postpartum haemorrhage, anemia, infection and venous thromboembolism.
 Avoid postpartum tubal ligation.
 Administer prophylactic antibiotics.
 Induce mild sedation.
Stage two
 Mother should lie in dorsal position.
 Avoid exhaustion of the mother.
 The paediatrician should be around to check the condition of the child.
 Episiotomy or vacuum extraction can be used.
Stage three
 Don’t use egometrin.
 Controlled cord traction can be applied.
Pueperium
 Complete rest or use of sedatives.
 Keep under strict observation half hourly for two to four hours till stable.
 Treat any infection promptly.
 Monitor for deep venous thrombosis.
 If no complications discharge in the tenth day post delivery.

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GRADE iii AND IV.
General management.
 Refer to high risk cardiologists and obstetricians
 Consider pregnancy termination on onset of gestation or labor.
 The patient may require prolonged hospitalization and bed rest.
 Vaginal delivery should be preferred.
 Nurse the patient on a cardiac bed.
 Monitor fetal heart rate and fetal-placental blood flow.
 Give a diet low in salt.
 Ensure good hygiene and adequate rest.
 Social care by family members or social workers.
 Attend to emotional needs and give counseling on reproductive health.
In first stage of labor
 Avoid exhaustion.
 Prop up the bed to prevent orthopnoea.
 Give oxygen continuously
 Epidural anesthesia should be given.
 Give analgesics but avoid inhalational ones.
 Observe a quarter hourly for vital signs.
In the second stage of labor
 The mother should not push, give episiotomy or vacuum extraction.
 Egometrin should be administered.
 If any postpartum hemorrhage, give syntometrin.
Pueperium
 Nursing should be in ICU for forty eight hours. The following steps should be done in ICU:
i) Ensure complete bed rest and total nursing.
ii) Observe half hourly for vital signs for four hours till stable.
iii) Withhold breastfeeding if the mother is in heart failure.
iv) Admit the baby in a special care unit.
v) Antibiotics and sedatives should be given for two weeks.

ACUTE HEART FAILURE IN PREGNANCY

DEFINATION

Clinical entity characterized by a rapid onset of signs and symptoms due to abnormal cardiac functioning
with reduced cardiac output and pulmonary/systemic congestion.

ETIOLOGY.

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Colonary heart disease which contribute to about sixty to seventy percent.

Less common causes include;

 Myocarditis
 Endocarditis
 Hypertensive crisis

SIGNS AND SYMPTOMS

Rapid irregular pulse rate,

Cyanosis.

Hemoptysis

Cold sweat in extremities.

Pulmonary oedema which is sudden with tachycardia, bronchospasm, cough and frothy mucus.

MANAGEMENT.

Medical intervention; morphine fifteen mg intravenous to relieve anxiety. Digoxin zero point five mg
OD. Lasix as prescribed. If cyanotic administer oxygen. Give aminophylline two fifty mg as slow
infusion incase of bronchospasm. Diazepam five to ten grams nocte for sedation.

Prop up the bed to facilitate breathing/to preventing orthopnea. Avoid exertion, but encourage passive
leg movement to avoid blood stasis.

Provide low salt diet, restrict fluid intake, monitor fluid intake and output, rehydrate slowly, keep
patient warm.

Observe vital signs quarter hourly. Report severe breathlessness for respiration above twenty four.

FIRST STAGE OF LABOR

Give morphine fifteen mg intravenous to relieve anxiety. Digoxin zero point five mg OD. Lasix as
prescribed. If cyanotic administer oxygen. Give aminophylline two fifty mg as slow infusion incase
of bronchospasm. Give Diazepam five to ten grams nocte for sedation.

SECOND STAGE OF LABOR

No pushing to avoid exertion of the cardiac muscle

Carryout episiotomy under pundedal nerve block

Do not give ergometrin which can aggravate heart failure.

Give syntometrin if there is post partum hemorrhage.

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THIRD STAGE OF LABOUR

The patient may collapse

Decrease abdominal pressure by pressing with your two hands on the abdomen.

Discourage over breathing

Give a continuous infusion of syntometrin ten to twenty units. Also give lasix half an hour before
infusing syntometrin. If there is blood transfusion, give lasix before the transfusion.

Pueperium

Complete bed rest, ensure adequate breathing, and give passive exercise to prevent emboli.

Ambulate during the fourth or fifth week.

Continue with antibiotics for two weeks as well as encouraging feeding.

2. ANAEMIA IN PREGNANCY
Definition of anaemia: Anaemia is a disorder characterised by blood haemoglobin concentration lower
than the defined normal level and it is usually associated with decrease in circulating mass of red blood
cells. This may result from decreased generation of red blood cells, or from their premature destruction,
or from loss through chronic blood loss or haemorrhage.

Anaemia is diagnosed when the Hb level of pregnant women is below 10 gm/dl and can be
grouped as;
 Mild: Hb 8.1 – 9.9 g/dl
 Moderate: Hb 5.1 g – 8.0 g/ dl
 Severe: Hb less or equal to 5 g/ dl

Causes of anaemia During pregnancy

The growth of the foetus and the placenta and the larger amount of blood circulating blood in the
expectant mother lead to an increase in the demand for nutrients, especially iron and folic acid.

The fact that most women start pregnancy with depleted body stores of these nutrients mean that their
extra requirements are even higher than usual.

The total iron needed during the whole pregnancy is estimated at 1000mg. The daily requirement of iron
as well folic acid is six times greater for a woman in the last trimester of pregnancy than for a non
pregnant woman. This need cannot be met by diet alone, but it is derived at least partly from maternal

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reserves. In a well nourished woman about half of total requirement of iron may come from iron stores.
When these reserves are already low-due to malnutrition, malaria and /or frequent pregnancies, anaemia
results.

Common causes

(a) Physiological anaemia This is due to the disproportionate increase in plasma volume in relation to
the red blood cell mass during pregnancy.

(b) Dietary causes A low dietary intake of iron, folic acid and proteins Faulty absorption of nutrients
such as iron, folic acid and proteins

(c) Obstetrical and gynaecological reasons Pregnancy related blood loss ( Abortions, Ectopic
Pregnancy, APH, PPH) Menorrhagia Increased demand (multiple pregnancy, frequent child birth)

(d) Non-obstetrical reasons Frequent attacks of malaria Dysentery Hook worm infestation Urinary
tract infections including bilharzia

(e) Chronic illness Bleeding Disorders Pulmonary Tuberculosis Pre -existing medical conditions i.e.
HIV/AIDS, sickle cell disease

Women at risk of developing anaemia in pregnancy

 Low socio economic status
 Young primigravida
 Frequent or too many pregnancies
 Previous history of PPH
 History of APH
 Multiple pregnancy
 Pregnant women in Malaria endemic areas

Effects of anaemia in pregnancy

A.Maternal Effects:

Antenatal period

 Prone to PET
 Heart failure
 Diminished resistance to infection
 Late abortions (20-28 weeks)
 Preterm labour

During labour and delivery

 Predisposed to PPH

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 Maternal death
 Congestive cardiac failure

Peurperium

 Puerperal sepsis
 Uterine sub-involution
 Deep venous thrombosis
 Pulmonary embolism
 Post partum haemorrhage

B.Effects of anaemia on foetus

 Prematurity
 Intra uterine growth retardation (IUGR)
 Foetal malformations esp. in folate deficiency.
 Intra uterine foetal death (IUFD)
 Foetal distress
 Asphyxia at birth
 Meconium aspiration
 Low birth weight
 Still births (may be fresh or macerated)

Diagnosis of anaemia
A comprehensive history and physical examination is imperative to rule out the underlying causes of
anaemia, and to detect any complications that may have occurred.

Basic laboratory work up

1. Haemoglobin and haematocrit Estimation (to know degree of anaemia)

2. Full blood count and peripheral blood film (to know the type of anaemia)

3. Stool examination for ova and cysts, Blood Slide or RDTs for malaria diagnosis, urinalysis /
microscopy etc (to know the cause of anaemia)

4. Blood group and Rhesus factor determination

5. Other tests will be determined by the findings on history and physical examination

Management of anaemia during pregnancy and labour

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General treatment of anaemia during pregnancy Prescribe ferrous sulphate 200 mg and folic acid 5mg by
mouth once daily for 6 months during pregnancy and continue for 3 months postpartum.

Where hookworm is endemic, give mebendazole 500 mg by mouth once or 100 mg two times per day for
3 days

It is important to differentiate between mild, moderate and severe anaemia at the time of diagnosis as the
specific management depends on the degree of anaemia present.

Mild anaemia is to be treated by administration of oral iron and folate.

Moderate anaemia may need parental iron therapy. If detected after 36 weeks, she may need a blood
transfusion.

Women with severe anaemia should be admitted to the hospital for close supervision and intensive
treatment.

Transfuse using packed red cells.

Administer a diuretic (e.g. frusemide 40mg IV) with each unit of blood.

If the woman is in heart failure, transfuse as above slowly, maintain a strict fluid balance chart and
manage the congestive cardiac failure.

Thereafter maintain on iron 120mg plus folate 400mcg orally once a day for six months during pregnancy
and until 3 months post partum .

During Labour and delivery

When a severely anaemic patient is in labour, she should be nursed in a propped up position. Monitoring
of the mother and foetus must be maintained.

The team must always be prepared to manage PPH and for newborn resuscitation.

1. Give oxygen inhalation by mask

2. Transfuse as necessary.

3. Maintain strict aseptic technique in order to minimize puerperal infection.

4. The second stage of labour usually poses no problem, but assisted delivery with forceps or vacuum
extraction is recommended.

5. Active management of third stage of labour is recommended.

6. Prophylactic antibiotics such as Amoxicillin may be given as 500mg orally every 8 hours.

NOTE: In facilities where blood transfusion services are not available, EARLY REFERRAL is
mandatory with an experienced escort

Prevention of Anaemia

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 Pre-pregnancy care for early diagnosis and management of anaemia and any underlying causes
should be encouraged.
 Early ANC attendance is important for prompt diagnosis of anaemia
 Ensure comprehensive obstetric and social history in antenatal clinic to identify factors
predisposing to anaemia
 During the ANC, give routine supplementation of iron and folic acid Deworm the pregnant
mothers as part of ANC care
 Give intermittent preventive treatment of malaria in Malaria endemic areas
 Treat any concurrent infections, infestations and manage medical conditions as appropriate
 Give dietary advice which is appropriate for each woman depending on health status, religious
and cultural preferences
 Advise women on healthy timing and spacing of pregnancy
 Counsel to discourage pica (especially eating of soil) during pregnancy

3. DM IN PREGNANCY

PRISCILLA WHITE CLASSIFICATION OF OBSTETRIC DIABETES

Fasting 2-hour Postprandial

Class Onset Plasma Glucose Glucose Therapy

A1 Gestational <5.8mmol/L <6.7mmol/L Diet

A2 Gestational >5.8mmol/L >6.7mmol/L Insulin

Age of Onset Duration Vascular

Class (Overt) (Years) Disease Therapy

B > 20 < 10 None Insulin

C 10-19 10-19 None Insulin

D <10 > 20 Benign retinopathy Insulin

F Any Any Nephropathy* Insulin

R Any Any Proliferative retinopathy Insulin

H Any Any Coronary artery disease Insulin

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T Any Any Renal transplant Insulin

* When diagnosed during pregnancy: ≥ 500mg/24hrs proteinuria measured

before 20 weeks’ gestation.

A) OVERT DIABETES - DIAGNOSED BEFORE PREGNANCY

Classified according to whether or not the patient requires exogenous insulin to
prevent ketoacidosis

Type 1 (insulin dependent/Juvenile)

Type 1 diabetes is immune mediated and develops in genetically susceptible

persons. This predisposition is permissive rather than causal and disease
presumably is triggered by a viral infection. There is inflammatory insulitis
with lymphocytic infiltration of islets. Subsequently, there is immune
stimulation of antibodies against the β-cell. The β-cell membrane becomes
susceptible to autoimmune cytotoxic antibodies, which leads to eventual
destruction of the cell and resultant diabetes.

Type 2 (noninsulin dependent/maturity onset)

Its pathophysiology is abnormal insulin secretion and insulin resistance

in target tissues. Most patients are overtly obese, and there is speculation
that peripheral insulin resistance induced by obesity leads to β-cell
exhaustion.

Some general characteristics of Insulin-Dependent (Type 1) and Non-

insulin-Dependent (Type 2) diabetes mellitus

Characteristics Type 1 Type 2

(Insulin Dependent) (Noninsulin Dependent)

Genetic locus HLA-D Chromosome 6 Chromosome 11 (?)

Age at onset Young (<40) Older (>40)

Habitus Normal to wasted Obese

Plasma insulin Low to absent Normal to high

Plasma glucagon High, suppressible High, resistant

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Characteristics Type 1 Type 2

(Insulin Dependent) (Noninsulin Dependent)

Acute complication Ketoacidosis Hyperosmolar coma

Concordance in <50% 100%

monozygotic twins

Insulin therapy
Responsive Responsive to resistant
Sulfonylurea therapy
Unresponsive Responsive

Diagnosis of Overt Diabetes during Pregnancy

 Glucosuria - Reducing substances - lactose - are commonly found in the urine of

pregnant women and glucosuria in pregnancy most often does not reflect
impaired glucose tolerance, but rather augmented glomerular filtration
 Ketoacidosis
 Random plasma glucose level > 11.1mmol/L plus classical signs and symptoms
such as;
- Polydipsia

- Polyuria

- Weight loss

Complications

The likelihood of successful outcomes for the fetus-infant and the overtly diabetic
mother are related somewhat to the degree of diabetes control, but more
importantly, to the intensity of any underlying maternal cardiovascular or renal
disease.

Effects on the Fetus

 Congenital malformations- Increased severe malformations are the
consequence of poorly controlled diabetes both preconceptionally as well as early
in pregnancy. Women with lower glycosylated hemoglobin values at
conception have less anomalous fetuses compared with women with abnormally
high values.

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FETAL ANOMALIES CORRELATED WITH DIABETIC VASCULOPATHY WITH
DURATION OF DISEASE > 10 YEARS.

Skeletal and Caudal regression syndrome

CNS
Neural tube defects excluding anencephaly

Anencephaly with/without herniation of neural elements

Microcephaly

Cardiac TGA with/without VSD

VSD

Coarctation of the aorta with/without VSD or PDA

Cardiomegaly

Renal anomalies Hydronephrosis

Renal agenesis

Ureteral duplication

Gastrointestinal Duodenal atresia

Anorectal atresia

Small left colon syndrome

Other Single umbilical artery

Situs inversus

 "Unexplained" Fetal Demise - Stillbirths without identifiable cause are a

phenomenon unique to pregnancies complicated by overt diabetes. They are
declared "unexplained" because no factors such as obvious placental
insufficiency, abruption, fetal growth restriction, or oligohydramnios are
apparent. These infants are typically large for age and die before labor, usually
at about 35 weeks or later
 Spontaneous abortion is associated with poor glycemic control during the
first trimester; type 1 diabetic women with initial glycohemoglobin A1
concentrations > 12% or persistent pre-prandial glucose concentrations >
6.7mmol/L were at increased risk for abortion.
 Macrosomia - The incidence of macrosomia rises significantly when mean
maternal blood glucose concentrations exceed 6.7mmol/L and appears to

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accrue primarily during the third trimester, although some macrosomic fetuses
can be recognized before 24 weeks.
 Diabetic pregnancies are often complicated by hydramnios
 Hyperglycemia-mediated chronic aberrations in transport of oxygen and fetal
metabolites leads to decreased fetal pH, and increased pCO2, lactate, and
erythropoietin in diabetic pregnancies

Neonatal complications
 Preterm births are associated with advanced diabetes and superimposed
preeclampsia associated with nephropathy
 Respiratory distress mostly due to gestational age, rather than overt diabetes
 Hypoglycemia - A rapid decrease in plasma glucose concentration after delivery
attributed to hyperplasia of the fetal -islet cell induced by chronic maternal
 Hypocalcaemia -  7 mg/dL - May be due to magnesium-calcium economy
unique to diabetic pregnancy, asphyxia, prematurity, and preeclampsia
 Hyperbilirubinemia - Factors implicated - prematurity and polycythemia (also
implicated in Renal vein thrombosis) with hemolysis
 Hypertrophic cardiomyopathy that occasionally progresses to congestive heart
failure - These infants are typically macrosomic and fetal hyperinsulinemia has
been implicated in the pathogenesis.

Effects on the Mother

 Mortality is increased 10-fold, most often as a result of;
- Ketoacidosis

- Underlying hypertension

- Preeclampsia

- Pyelonephritis

- Coronary artery disease (class H)

 Diabetic Nephropathy (Class F)

 The leading cause of end-stage renal disease (Class T). Subclinical diabetic
nephropathy increases abruptly when hemoglobin A1 values exceed 10%. The
natural history of clinically detectable nephropathy in type 1 disease begins with
microalbuminuria (30 - 300 mg of albumin per 24 hours), which may occur
as early as 5 years after the onset of diabetes. After another 10-15 years,
overt proteinuria (> 300 mg of albumin per 24 hours) develops in patients
destined to have end-stage renal disease. Hypertension invariably develops
during this period, and end-stage renal disease ensues typically 20-25 years
after the onset of diabetes

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 Preeclampsia - Women in the more advanced classes of overt diabetes
increasingly developed preeclampsia and indicated preterm delivery especially
women with diabetic nephropathy (class F). Hypertension induced or
exacerbated by pregnancy is the major complication that most often forces
preterm delivery in diabetic women. Special risk factors for preeclampsia
include any vascular complications, preexisting proteinuria, and/or chronic
hypertension: but is not related to glucose control. Plasma creatinine
values of ≥1.5 mg/dL and protein excretion of ≥3 g /24 hours before 20
weeks' gestation were predictive for preeclampsia
 Diabetic Retinopathy
- Background or nonproliferative retinopathy - small microaneurysms
form followed by blot hemorrhages when erythrocytes escape from the
aneurysms. These areas leak serous fluid that forms hard exudates.

- Preproliferative retinopathy (Class D) - With increasingly severe

retinopathy, the abnormal vessels of "background" eye disease become
occluded, leading to retinal ischemia with infarctions that appear as cotton
wool exudates.

Laser photocoagulation and good glycemic control during pregnancy minimizes

the potential for deleterious effects of pregnancy

 Diabetic Neuropathy - Although uncommon, some pregnant women will

demonstrate peripheral symmetrical sensorimotor neuropathy due to
diabetes. Another form, diabetic gastropathy, is very troublesome in pregnancy
because it causes nausea and vomiting, nutritional problems, and difficulty with
glucose control.
 Diabetic ketoacidosis may occur as a result of;
- Hyperemesis gravidarum

- Use of -sympathomimetic drugs for tocolysis

- Infections

- Use of corticosteroids to induce fetal lung maturation

 Infections - Sites of these infections include the genital tract (e.g., antepartum
candida vaginitis or pelvic puerperal infection) and the respiratory tract.

Management
Preconception

 Particular emphasis should be placed on normalizing blood glucose levels before

conception and during early pregnancy to reduce the risks of major birth
defects. Hemoglobin A1 or A1c measurement, which expresses an average of
circulating glucose for the past 4 to 6 weeks, is useful to assess early

19
metabolic control. The most significant risk for malformations is with levels
>10%
 Folate, 400 g/day, given periconceptually and during early pregnancy,
decreases the risk of neural-tube defects

First Trimester

Maternal glycemic control can usually be achieved with multiple daily insulin
injections and adjustment of dietary intake. Oral hypoglycemic agents are not
used because they may cause fetal hyperinsulinemia and congenital
malformations

The goals of self-monitored capillary blood glucose control recommended during

pregnancy

Specimen Blood Glucose (mmol/L)

Fasting 3.3-5.0

Premeal 3.3-5.8

Postprandial 1 hr 5.5-6.7

0200-0600 3.3-6.7

Diabetes tends to be unstable in the first trimester, followed by a stable

period, and then by an increase in insulin requirement from about 24 weeks
(3rd trimester) due to the increased production of pregnancy hormones,
which are insulin-antagonists

Second Trimester

Maternal serum alpha-fetoprotein concentration at 16 to 20 weeks is used in

association with targeted ultrasound at 18 to 20 weeks in an attempt to detect
neural-tube defects and other anomalies

Third Trimester

A weekly visit to monitor glucose control and to evaluate for preeclampsia is

a typical recommendation. Serial ultrasonography at 3 to 4 week intervals is
performed to evaluate both excessive and insufficient fetal growth as well as
amnionic fluid volume.

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Delivery

Ideally, delivery of the diabetic woman should be accomplished near term - after
37 completed weeks. Typically the lecithin-sphingomyelin ratio is measured
at about 37 weeks and, if ≥2.0, delivery is effected.

Indications for CS to avoid traumatic delivery of a large infant at or near term;

 If severe hypertension develops even though the lecithin-sphingomyelin ratio is

< 2.0.
 In the overtly diabetic woman within B or C White classification or with
vascular disease
If preterm labor occurs, tocolytic therapy with -sympathomimetic drugs is best
avoided in women with diabetes. These medications may significantly worsen
maternal glucose control, causing ketoacidosis.

Caution is advised in the use of corticosteroids to promote lung maturation.

It is important to considerably reduce or delete the dose of long-acting insulin

given on the day of delivery. Regular insulin should be used to meet most or all
of the insulin needs of the mother at this time, because insulin requirements
typically drop markedly after delivery.

During and after either cesarean section or labor and delivery, the mother should
be hydrated adequately intravenously as well as given glucose in sufficient amounts
to maintain normoglycemia.

Infection must be detected quickly and treated promptly.

Contraception

 Diabetes carries a risk of vascular disease, and the estrogens in oral

contraceptives statistically increase the risk of thromboembolus, stroke, and
myocardial infarction.
 Use of low-dose oral contraceptives should probably be restricted to women
without vasculopathy or additional risk factors such as a strong history of
ischemic heart disease.
 Progestin-only oral or parenteral contraceptives may be used because of
minimal effects on carbohydrate metabolism.
 Intrauterine devices in diabetic women are associated a possible increased risk of
pelvic infections

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B) GESTATIONAL DIABETES - DIAGNOSED DURING PREGNANCY
Carbohydrate intolerance of variable severity with onset or first recognition
during pregnancy regardless of whether or not insulin is used for treatment

Gestational diabetes is maturity-onset/type 2 diabetes unmasked or

discovered during pregnancy

Importantly, more than half of women with gestational diabetes ultimately

develop overt diabetes in the ensuing 20 years.

Carbohydrate Metabolism in pregnancy

Normal pregnancy is diabetogenic as characterized by;

 mild fasting hypoglycemia due to

 hyperinsulinemia secondary to β-cell hypertrophy, hyperplasia, and
hypersecretion probably mediated by estrogen, progesterone, and human
placental lactogen
 postprandial hyperglycemia
After an oral glucose meal, to ensure a sustained or maintained postprandial supply
of glucose to the fetus, there is;

 prolonged hyperglycemia
 -cell sensitivity to a glucose challenge is increased but that the -cell
sensitivity to a glucose stimulus is unaltered leading to;
- Hyperinsulinemia

- Suppression of glucagon

Pregnancy-induces a state of peripheral resistance to insulin, which is

suggested by;

 increased insulin response to glucose (increased plasma level and duration)

 reduced peripheral uptake of glucose (increased plasma level and duration)
 suppressed glucagon response
Accelerated starvation - pregnancy-induced switch in fuels from glucose to lipids;
The pregnant woman, changes rapidly from a postprandial state characterized by
elevated and sustained glucose levels to a fasting state characterized by decreased
plasma glucose and amino acids such as alanine and higher plasma concentrations
of free fatty acids, triglycerides, and cholesterol.

Predisposing factors of Gestational Diabetes

 familial history of diabetes (1st degree relative)
 demonstrate persistent glucosuria on at least 2 tests
 age > 30yrs

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 a prior macrosomic (> 4.5 Kg), malformed (renal tube defects), or stillborn
infant
 obesity - > 85Kg/BMI ≥ 30
 hypertension

Detection of Gestational Diabetes

Gestational diabetes is typically a disorder of late gestation, hyperglycemia during
the first trimester usually means overt diabetes.

Screening
All pregnant women should be screened using a Mini-GTT - 50-g oral glucose
tolerance test between 24 and 28 weeks without regard to time of day or last
meal, and that a plasma value at 1 hour > 7.8mmol/L be used as the cutoff for
performing the diagnostic 100-g 3-hour oral glucose tolerance test performed
after an overnight fast

Adverse fetal consequences of gestational diabetes

 Macrosomia - Insulin secreted by fetal pancreatic -cells (fetal
hyperinsulinemia) primarily during the second half of gestation resulting from
maternal hyperglycemia, is believed to stimulate excessive somatic growth
(except for the brain) and adiposity. This may result in birth trauma due to
shoulder dystocia. Similarly, hyperinsulinemia in the infant may provoke
hypoglycemia within minutes of birth.
 Class A2, has been associated with unexplained stillbirth
 long-range complications - obesity and diabetes in the offspring

Management
The goals of therapy are;

- To provide the necessary nutrients for the mother and fetus

- To control glucose levels

- To prevent starvation ketosis

 Women without persistent fasting hyperglycemia (class A1), are usually treated
by diet alone. They are typically seen at 1- to 2-week intervals, and fasting
and/or postprandial plasma glucose levels are measured to insure that the
glucose thresholds for insulin therapy have not been exceeded.
 Insulin therapy is usually recommended when standard dietary management does
not consistently maintain the fasting plasma glucose at < 5.8mmol/L or the 2-
hour postprandial plasma glucose at < 6.7mmol/L - Class A2. A total dose of 20
to 30 units given once daily, before breakfast, is commonly used to initiate

23
therapy. The total dose is usually divided into 2/3 intermediate-acting insulin
(NPH or Lente) and 1/3 short-acting insulin (regular).
 A liberal exercise program
 A woman diagnosed to have gestational diabetes should undergo a 2-hour 75-g
oral glucose tolerance at the first postpartum checkup 6 to 8 weeks after
delivery, or shortly after she stops breast feeding. This recommendation is based
on the 50% likelihood of women with gestational diabetes developing overt
diabetes within 20 years of delivery. If fasting hyperglycemia develops
during pregnancy - Class A2 - diabetes is more likely to persist postpartum.
Postpartum Evaluation for glucose intolerance in women with gestational
diabetes

2-hr 75-g Oral Glucose Tolerance Test

Plasma Glucose (mmol/L)

Time Impaired Glucose

Tested No Diabetes Tolerance Diabetes

Fasting < 6.2 < 7.8 ≥ 7.8*

½, 1, 1½ hr All < 11.1 1 value ≥ 11.1 1 value ≥ 11.1

2 hr < 7.8 7.8 - 11.1 ≥ 11.1

*Fasting plasma glucose determination of ≥ 7.8 on 2 occasions establish the

diagnosis.

 Dietary management and specifically, weight reduction in obese women can

significantly reduce the risk of subsequent overt diabetes.

4. raHYDRAMNIOS

Introduction:

 Minor to moderate degrees of hydramnios-2 to 3 L-are rather common.

 Because of the difficulty of complete collection and measurement of fluid, the diagnosis is
usually clinical and confirmed by sonographic estimation

Incidence:

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 Hydramnios is identified in around 1 percent of all pregnancies.
 Most clinical studies define hydramnios as an amnionic fluid index of greater than 24 to 25
cm-corresponding to greater than either the 95th or 97.5th percentiles
 Mild hydramnios: defined as pockets measuring 8 to 11 cm in vertical dimension-was
present in 80 percent of cases with excessive fluid.
 Moderate hydramnios: defined as a pocket containing only small parts and measured 12 to
15 cm deep-was found in 15 percent.
 Only 5 percent had severe hydramnios defined by a free-floating fetus found in pockets of
fluid of 16 cm or greater.
 Although two thirds of all cases were idiopathic, the other third were associated with fetal
anomalies, maternal diabetes, or multifetal gestation

Causes of hydramnios

 The degree of hydramnios, as well as its prognosis, is related to the cause.

 Obvious pathological hydramnios is frequently associated with fetal malformations,
especially of the central nervous system or gastrointestinal tract.
 For example, hydramnios accompanies about half of cases of anencephaly and esophageal
atresia.

Pathogenesis

 Early in pregnancy, the amnionic cavity is filled with fluid very similar in composition to
extracellular fluid.
 During the first half of pregnancy, transfer of water and other small molecules takes place not
only across the amnion but through the fetal skin.
 During the second trimester, the fetus begins to urinate, swallow, and inspire amnionic fluid
 These processes almost certainly have a significant modulating role in the control of fluid
volume.
 The major source of amnionic fluid in hydramnios has most often been assumed to be the
amnionic epithelium
 Because the fetus normally swallows amnionic fluid, it has been assumed that this
mechanism is one of the ways by which the volume is controlled.
 The theory gains validity by the nearly constant presence of hydramnios when swallowing is
inhibited, as in cases of esophageal atresia.
 Fetal swallowing is by no means the only mechanism for preventing hydramnios.
 In cases of anencephaly and spina bifida, increased transudation of fluid from the exposed
meninges into the amnionic cavity may be an etiological factor.

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 Another possible explanation in anencephaly, when swallowing is not impaired, is excessive
urination caused either by stimulation of cerebrospinal centers deprived of their protective
coverings, or lack of antidiuretic effect because of impaired arginine vasopressin secretion.
 The converse is well established-that fetal defects that cause anuria are nearly always
associated with oligohydramnios.
 In hydramnios associated with monozygotic twin pregnancy, the hypothesis has been
advanced that one fetus usurps (seizes)the greater part of the circulation common to both
twins and develops cardiac hypertrophy, which in turn results in increased urine output
 Increased fetal urine production is responsible for hydramnios
 Hydramnios that rather commonly develops with maternal diabetes during the third trimester
remains unexplained.
 One explanation is that maternal hyperglycemia causes fetal hyperglycemia that results in
osmotic diuresis

Symptoms

 Major symptoms accompanying hydramnios arise from purely mechanical causes and result
principally from pressure exerted within and around the overdistended uterus upon adjacent
organs.
 When distention is excessive, the mother may suffer from severe dyspnea and, in extreme
cases, she may be able to breathe only when upright.
 Edema, the consequence of compression of major venous systems by the very large uterus, is
common, especially in the lower extremities, the vulva, and the abdominal wall.
 Rarely, severe oliguria may result from ureteral obstruction by the very large uterus
 With chronic hydramnios, the accumulation of fluid takes place gradually and the woman
may tolerate the excessive abdominal distention with relatively little discomfort.
 In acute hydramnios, however, distention may lead to disturbances sufficiently serious to be
threatening.
 Acute hydramnios tends to develop earlier in pregnancy than does the chronic form-often as
early as 16 to 20 weeks-and it may rapidly expand the hypertonic uterus to enormous size.
 As a rule, acute hydramnios leads to labor before 28 weeks, or the symptoms become so
severe that intervention is mandatory.
 In the majority of cases of chronic hydramnios, and thus differing from acute hydramnios,
the amnionic fluid pressure is not appreciably higher than in normal pregnancy.

Diagnosis

 The primary clinical finding with hydramnios is uterine enlargement in association with
difficulty in palpating fetal small parts and in hearing fetal heart tones.
 In severe cases, the uterine wall may be so tense that it is impossible to palpate any fetal parts

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Pregnancy outcome

 In general, the more severe the degree of hydramnios, the higher the perinatal mortality rate.
 The outlook for the infant in pregnancies with marked hydramnios is poor.
 Perinatal mortality is increased further by preterm delivery, even with a normal fetus
 Erythroblastosis, difficulties encountered by infants of diabetic mothers, prolapse of the
umbilical cord when the membranes rupture, and placental abruption as the uterus rapidly
decreases in size, adds still further to bad outcomes.
 The most frequent maternal complications associated with hydramnios are placental
abruption, uterine dysfunction, and postpartum hemorrhage.
 Extensive premature separation of the placenta sometimes follows escape of massive
quantities of amnionic fluid because of the decrease in the area of the emptying uterus
beneath the placenta
 Uterine dysfunction and postpartum hemorrhage result from uterine atony consequent to
overdistention.
 Abnormal fetal presentations and operative intervention are also more common.

Management

 Minor degrees of hydramnios rarely require treatment.

 Even moderate degrees with some discomfort can usually be managed without intervention
until labor ensues or until the membranes rupture spontaneously.
 If there is dyspnea or abdominal pain, or if ambulation is difficult, hospitalization becomes
necessary.
 Bed rest rarely has any effect, and diuretics and water and salt restriction are likewise
ineffective.
 Recently, indomethacin therapy has been used for symptomatic hydramnios.

Amniocentesis

 The principal purpose of amniocentesis is to relieve maternal distress, and to that end it is
transiently successful.
 Therapeutic amniocentesis appears at times to initiate labor even though only a part of the
fluid is removed
 Common causes included twin-twin transfusion (38 percent), idiopathic (26 percent), fetal or
chromosomal anomalies (17 percent), and diabetes (12 percent).

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Amniotomy

 The disadvantages inherent in rupture of the membranes through the cervix are the
possibility of cord prolapse and especially of placental abruption.
 Slow removal of the fluid by amniocentesis helps to obviate these dangers.

Indomethacin therapy

 In their review of several studies, concluded that indomethacin impairs lung liquid
production or enhances absorption, decreases fetal urine production, and increases fluid
movement across fetal membranes.
 Doses employed by most investigators range from 1.5 to 3 mg/kg per day.
 A major concern for the use of indomethacin is the potential for closure of the fetal ductus
arteriosus

ANTEPARTUM HEMORRHAGE

Any bleeding that occurs from the genital tract after the stage of foetal viability (28wks) but
before the birth of the child. It may be caused by: -

 Placental site bleeding

 Abruptio placenta
 Placenta previa
 Vasa previa – rupture of the marginal sinuses
 Extra placental site bleeding
 Local causes – vulva vein varicosities, cervical erosions, cervical polyps,
cervical carcinoma, and trauma
 Other causes – excess show, coagulopathies, uterine rupture, and
idiopathic bleeding
 Unclassified (bleeding of unknown origin).

PLACENTAL ABRUPTION

Abruptio placentae is defined as the premature separation of the normally implanted placenta
from the uterus. Patients with abruptio placentae typically present with bleeding, uterine
contractions, and fetal distress. Abruptio placentae must be entertained as a diagnosis whenever
third-trimester bleeding is encountered.

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Pathophysiology: Hemorrhage into the decidua basalis occurs as the placenta separates from the
uterus. Vaginal bleeding usually follows, although the presence of a concealed hemorrhage in
which the blood pools behind the placenta is possible. If the bleeding continues, fetal and
maternal distress may develop. Fetal and maternal death may occur if appropriate interventions
are not undertaken. The primary cause of placental abruption is usually unknown, but multiple
risk factors have been identified.

Currently, placental abruption is responsible for approximately 6% of maternal deaths. Maternal

and fetal complications include issues related to (1) cesarean delivery, (2)
hemorrhage/coagulopathy, and (3) prematurity, described as follows:

 Cesarean delivery: Cesarean delivery is often necessary if the patient is far from her
delivery date or if significant fetal compromise develops. If significant placental
separation is present, the fetal heart rate tracing typically shows evidence of fetal
decelerations and even persistent fetal bradycardia. A cesarean delivery may be
complicated by infection, additional hemorrhage, the need for transfusion of blood
products, injury of the maternal bowel or bladder, and/or hysterectomy for uncontrollable
hemorrhage. In rare cases, death occurs.

 Hemorrhage/coagulopathy: Disseminated intravascular coagulation (DIC) may occur as a

sequela of placental abruption. Patients with a placental abruption are at higher risk of
developing a coagulopathic state than those with placental previa. The coagulopathy must
be corrected to ensure adequate hemostasis in the case of a cesarean delivery.

 Prematurity: Delivery is required in cases of severe abruption or when significant fetal or

maternal distress occurs, even in the setting of profound prematurity. In some cases,
immediate delivery is the only option, even before the administration of corticosteroid
therapy in these premature infants. All other problems and complications associated with
a premature infant are also possible.

Age: An increased risk of placental abruption has been demonstrated in patients younger than 20
years and those older than 35 years.

History: Symptoms may include vaginal bleeding, contractions, abdominal tenderness, and
decreased fetal movement. Eliciting any history of trauma, such as assault, abuse, or motor
vehicle accident, is important. A quick review of the patient's prenatal course, such as a known
history of placenta previa, may help lead to the correct diagnosis. The patient should also be
asked if she has had a placental abruption in a previous pregnancy. Questioning the patient about
cocaine abuse, hypertension, or tobacco abuse is also crucial.

 Vaginal bleeding: Vaginal bleeding is present in 80% of patients diagnosed with

placental abruptions. Bleeding may be significant enough to jeopardize both fetal and
maternal health in a relatively short period. Remember that 20% of abruptions are

29
associated with a concealed hemorrhage and the absence of vaginal bleeding does not
exclude a diagnosis of abruptio placentae.

 Contractions/uterine tenderness: Contractions and uterine hypertonus are part of the

classic triad observed with placental abruption. Uterine activity is a sensitive marker of
abruption and, in the absence of vaginal bleeding, should suggest the possibility of an
abruption, especially after some form of trauma or in a patient with multiple risk factors.

 Decreased fetal movement: This may be the presenting complaint. Decreased fetal
movement may be due to fetal jeopardy or death.

Physical: The physical examination of a patient who is bleeding must be targeted at determining
the origin of the hemorrhage. Simultaneously, the patient must be stabilized quickly. With
placental abruption, a relatively stable patient may rapidly progress to a state of hypovolemic
shock.

 Vaginal bleeding: Bleeding may be profuse and come in “waves” as the patient's uterus
contracts. A fluid the color of port wine may be observed when the membranes are
ruptured.

 Contractions/uterine tenderness: Uterine contractions are a common finding with

placental abruption. Contractions progress as the abruption expands, and uterine
hypertonus may be noted. Contractions are painful and palpable. Uterine
hyperstimulation may occur with little or no break in uterine activity between
contractions.

 Shock: Patients may present with hypovolemic shock, with or without vaginal bleeding,
because a concealed hemorrhage may be present. As with any hypovolemic condition,
blood pressure drops as the pulse increases, urine output falls, and the patient progresses
from an alert to an obtunded state as the condition worsens.

 Absence of fetal heart sounds: This occurs when the abruption progresses to the point that
the fetus dies.

 Signs of possible fetal jeopardy

o Fetal bradycardia is prolonged.
o Repetitive, late decelerations are present.
o Short-term variability is decreased.

 Fundal height: This may increase rapidly because of an expanding intrauterine

hematoma.

 Important note: Do not perform a digital examination on a pregnant patient with

vaginal bleeding without first ascertaining the location of the placenta. Before a pelvic
examination can be safely performed, an ultrasonographic examination should be
performed to exclude placenta previa. If placenta previa is present, a pelvic

30
examination, either with a speculum or with bimanual examination, may initiate
profuse bleeding.

Causes: While multiple risk factors are associated with abruptio placentae, only a few events
have been closely linked to this condition, including the following:

 Cigarette smoking/tobacco abuse

 Cocaine (powder or crack) abuse - The hypertension and increased levels of
catecholamines caused by cocaine abuse are thought to be responsible for a
vasospasm in the uterine blood vessels that causes placental separation and
abruption. However, this hypothesis has not been definitively proven.

 Trauma: Abdominal trauma is a major risk factor for placental abruption.

 Thrombophilia - Some literature supports the association of specific thrombophilias, such
as factor V Leiden mutation, and antithrombin III deficiency. The presence of a
thrombophilia may also influence the severity of the abruption.
 Other notable risk factors include the following:
o Previous placental abruption
o Chorioamnionitis
o Prolonged rupture of membranes (24 h or longer)
o Preeclampsia
o Hypertension
o Maternal age of 35 years or older
o Male fetal sex
o Low socioeconomic status

Differentials:

 Placenta Previa;
 Preterm Labor
 Labor with bloody show
 Vasa previa
 Vaginal trauma
 Malignancy (rare)

Lab Studies:

 There are no specific studies

 CBC count – indicates current hemodynamic state of patient
 Fibrinogen: Pregnancy is associated with hyperfibrinogenemia; therefore, modestly
depressed fibrinogen levels may represent significant coagulopathy. A fibrinogen level of
less than 200 mg/dL suggests that the patient has a severe abruption. The goal should be
to keep the fibrinogen level above 100 mg/dL, which can be accomplished via transfusion
of fresh frozen plasma or cryoprecipitate, as necessary.

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 Prothrombin time/activated partial thromboplastin time: Some form of DIC is present in
up to 20% of patients with severe abruptions. Because many of these patients may require
cesarean delivery, knowing a patient's coagulation status is imperative.
 Blood urea nitrogen/creatinine: The hypovolemic condition brought on by a significant
abruption also affects renal function. The condition usually self-corrects without
significant residual dysfunction if fluid resuscitation is timely and adequate.
 Kleihauer-Betke test:
o Findings help detect fetal red blood cells in the maternal circulation.
o If the abruption is significant, inadvertent transfusion of fetal blood into the
maternal circulation may occur. In women who are Rh-negative, this fetal-to-
maternal transfusion may lead to isoimmunization of the mother to Rh factor.
Kleihauer-Betke test findings help determine the volume of fetal blood transfused
into the maternal circulation.

 Blood type: for transfusion

 Rh type: Rh-negative require Rh immune globulin in order to prevent isoimmunization,
which could affect future pregnancies.

Imaging Studies:

 Ultrasonography.

o Placental abruption shows as a retroplacental clot on an ultrasound image, but not

all abruptions are ultrasonographically detectable.
o In the acute phase, a hemorrhage is generally hyperechoic, or even isoechoic,
compared with the placenta; a hemorrhage does not become hypoechoic for
nearly a week.
o Ultrasonography can help exclude other causes of third-trimester bleeding.
Possible findings consistent with an abruption include (1) retroplacental clot (ie,
hyperechoic to isoechoic in the acute phase, changing to hypoechoic within a wk),
(2) concealed hemorrhage, or (3) expanding hemorrhage.

Other Tests:

 Nonstress test

o External fetal monitors often reveal fetal distress, as evidenced by late

decelerations, fetal bradycardia, or decreased beat-to-beat variability.
o An increase in the uterine resting tone may also be noticed, along with frequent
contractions that may progress to uterine hyperstimulation.

 Biophysical profile
o A biophysical profile (BPP) can be used to help evaluate patients with chronic
abruptions who are being managed conservatively.A BPP score less than 6
(maximum of 10) may be an early sign of fetal compromise. A modified BPP

32
(nonstress test with amniotic fluid index) is sometimes used for monitoring in this
situation.

Histologic Findings: After delivery of the placenta, a retroplacental clot may be noted. Another
possible finding involves extravasation of blood into the myometrium, which produces a purple
discoloration of the uterine serosa. This phenomenon is known as a Couvelaire uterus.

33
Medical Care: Inpatient admission is required if abruptio placentae is considered likely.

 Procedures
o Obtain intravenous access using 2 large-bore intravenous lines.
o Institute crystalloid fluid resuscitation for the patient.
o Type and crossmatch blood.
o Begin a transfusion if the patient is hemodynamically unstable after fluid
resuscitation.
o Correct coagulopathy, if present.
o Administer Rh immune globulin if the patient is Rh-negative.

 Vaginal delivery
o This is the preferred method of delivery for a fetus that has died secondary to
placental abruption. The ability of the patient to undergo vaginal delivery depends
on her remaining hemodynamically stable. Delivery is usually rapid in these
patients secondary to increased uterine tone and contractions.

Surgical Care:

 Cesarean delivery
o Cesarean delivery is often necessary for both fetal and maternal stabilization.
o While cesarean delivery facilitates rapid delivery and direct access to the uterus
and its vasculature, it can be complicated by the patient's coagulation status.
Because of this, a vertical skin incision, which has been associated with less blood
loss, is often used when the patient appears to have DIC.
o The type of uterine incision is dictated by the gestational age of the fetus, with a
vertical or classic uterine incision often being necessary in the preterm patient.
o If hemorrhage cannot be controlled after delivery, a cesarean hysterectomy may
be required to save the patient's life.
o Before proceeding to hysterectomy, other procedures, including correction of
coagulopathy, ligation of the uterine artery, administration of uterotonics (if atony
is present), packing of the uterus, and other techniques to control hemorrhage,
may be attempted.

 ICU: If the patient is hemodynamically unstable, either before or after delivery, invasive
monitoring in an ICU may be required.

Consultations: Maternal-fetal medicine specialist, Pediatricians and Neonatologists

Diet: NPO if emergent delivery is a possibility

34
PLACENTA PREVIA

Def: In placenta previa, the placenta is located over or very near the internal os. Four degrees of
this abnormality have been recognized:

a) Total placenta previa. The internal cervical os is covered completely by placenta

b) Partial placenta previa. The internal os is partially covered by placenta
c) Marginal placenta previa. The edge of the placenta is at the margin of the internal os.
d) Low-lying placenta. The placenta is implanted in the lower uterine segment such that
the placenta edge actually does not reach the internal os but is in close proximity (2-3cm)
to it.

Another condition, termed vasa previa, is where the fetal vessels course through membranes
and present at the cervical os. This is an uncommon cause of antepartum hemorrhage and is
associated with a high rate of fetal death. Prenatal diagnosis by ultrasonography improves
perinatal salvage.

The degree of placenta previa will depend in large measure on the cervical dilatation at the time
of examination. Digital palpation to try to ascertain these changing relations between the
edge of the placenta and the internal os as the cervix dilates can incite severe hemorrhage!

Pathophysiology: Placenta previa is initiated by implantation of the embryo (embryonic plate)

in the lower (caudad) uterus. With placental attachment and growth, the developing placenta
may cover the cervical os. A defective decidual vascularization occurs, possibly secondary to
inflammatory or atrophic changes. When the decidua basalis is absent and incomplete
development of the fibrinoid layer occurs, the placenta can attach directly to the myometrium
(accreta), invade the myometrium (increta), or penetrate the myometrium (percreta). In
general, placenta accreta occurs in approximately 1 in 2500 deliveries. The rate increases to
10% in women with placenta previa. Maternal age and any uterine surgery (including
previous cesarean delivery) increase the risk for placenta accreta. The risk for placenta
accreta with placenta previa increases from 4% for those with no surgeries to 65% for those
with a history of multiple cesarean deliveries. Two of 3 patients with placenta accreta require
cesarean hysterectomy.

History:

 The classic presentation of placenta previa is painless vaginal bleeding.

35
 Nearly two thirds of symptomatic patients present before 36 weeks' gestation, with half
of these patients presenting before 30 weeks' gestation.
 Occasionally, this hemorrhage stops spontaneously and then recurs with labor.

Physical:

 Any pregnant patient beyond the first trimester who presents with vaginal bleeding
requires a speculum examination followed by diagnostic ultrasound, unless previous
documentation confirms no placenta previa.
 Because of the risk of provoking life-threatening hemorrhage, a digital examination is
absolutely contraindicated until placenta previa is excluded.
 Uterine activity monitoring reveals that approximately 20% of patients have concurrent
contractions with their bleeding.

Causes:

 Bleeding is thought to occur secondary to the thinning of the lower uterine segment in
preparation for the onset of labor. The placental attachments become disrupted or tear
with this thinning process and cervical dilatation.
 When this bleeding occurs at the implantation site in the lower uterus, the uterus is unable
to contract adequately and stop the flow of blood from the open vessels. This is not an
issue with placental implantation in the upper uterus, secondary to a larger volume of
myometrial tissue able to contract and constrict bleeding vessels.
 Other causes of hemorrhage in the setting of placenta previa include digital examination
and sexual intercourse.

DDx

 Abruptio Placentae
 Cervicitis
 Premature Rupture of Membranes
 Preterm Labor
 Vaginitis
 Vulvovaginitis

Lab Studies:

 Although coagulopathy is a rare occurrence, a baseline CBC count with a platelet count is
useful.
 A disseminated intravascular coagulopathy profile with prothrombin time, activated
partial thromboplastin time, fibrinogen, and fibrin split products may also be helpful
because retroplacental bleeding has been associated with consumptive coagulopathy.
 If the patient's alpha-fetoprotein screening study result is elevated, she may be at
increased risk for bleeding and preterm birth.

36
Imaging Studies: The most useful and least expensive study is ultrasonography. Transvaginal
ultrasound is 100% diagnostic.

Note: The phenomenon termed placental migration is when placenta previa is identified early in
pregnancy and resolves as the pregnancy proceeds.

Medical Care:

 If placenta previa is discovered incidentally (ie, after an ultrasonogram ordered for some
other reason), continue expectant management until bleeding occurs.
 Preterm labor can manifest as painless vaginal bleeding with placenta previa; Magnesium
sulfate is the tocolytic of choice. A 6-g loading dose followed by 3 g/h or more is
required to reduce uterine irritation.

 If bleeding is minimal and fetal reassurance is noted, consider expectant management to

allow for fetal maturity. For patients who are preterm (24-36 wk), expectant management
is the treatment of choice. Volume replacement, blood transfusion (if necessary), and
hematocrit maintenance between 30-35% is the goal. If the patient is at term (37 wk) with
good dating, perform delivery.
 Vaginal delivery may be considered in patients with marginal or partial placenta previa
who present in labor with minimal bleeding or in patients with previable gestations or
intrauterine fetal demise. In this setting, perform a thorough evaluation of maternal vital
signs and a semiquantitative evaluation of blood loss. If bleeding persists, proceed with
an immediate cesarean delivery rather than a double setup examination in the operating
room. (The double setup with full preparation implies having both pediatric and
anesthesia personnel in the operating room and having the patient prepared and draped to
proceed with emergent cesarean delivery if necessary. Only consider this option if a
prompt vaginal delivery is considered to be highly likely).

Surgical Care:

 Cesarean delivery is the safest mode of delivery for patients with complete placenta
previa or significant hemodynamic compromise.

5. SEEVERE PREECLAMPSIA AND

ECLAMPSIA

37
 Pregnancy Induced Hypertension or Preeclampsia is a potentially life-threatening
complication of pregnancy
 It causes mild to severe hypertension in a previously normotensive pregnant woman
 It also significantly affects the placental blood supply to the fetus
 It is a multisystem disease process that may affect the mother's liver, kidney, and brain
function. Women with severe preeclampsia can develop life-threatening seizures
(eclampsia).

DEFINATIONS

 Chronic hypertension is hypertension that is

present at the booking visit or before 20 weeks or
if the woman is already taking antihypertensive
medication when referred to maternity services. It
can be primary or secondary in aetiology.
 Eclampsia is a convulsive condition associated
with pre-eclampsia.
 HELLP syndrome is haemolysis, elevated liver
enzymes and low platelet count.
 Gestational hypertension is new hypertension
presenting after 20 weeks without significant
proteinuria.
 Pre-eclampsia is new hypertension presenting
after 20 weeks with significant proteinuria.
 Severe pre-eclampsia is pre-eclampsia with
severe hypertension and/or with symptoms,
and/or biochemical and/or haematological
impairment.
HYPERTENSION IN PREG

38
 Systolic blood pressure > 140 mmHg and/or diastolic > 90 mmHg
 Rise in systolic pressure 30 mmHg and /or diastolic 15 mmHg

PATHOPHYSIOLOGY

Genetic susceptibility

Inadequate trophoblastic invasion

Placental ischaemia

Endothelial cell damage

Vasoconstriction & platelet activation

Clinical syndrome of pre-eclampsia

RISK FACTORS

o Mother under 18 or over 35 years old

o First pregnancy
o Multifetal gestations

39
o Preeclampsia in a previous pregnancy (30% recurrence)
o Chronic hypertension
o Diabetes
o Kidney problems
o Obesity
o Molar pregnancy

CLASSFICATION

 Mild Preeclampsia
 Severe Preeclampsia
 Eclampsia

SEVERE PRE ECLAMPSIA

 Pre-eclampsia with severe hypertension and/or with symptoms, and/or biochemical

and/or haematological impairment.
 Systolic blood pressure > 160 mmHg and/or diastolic > 110 mmHg
 End organ involvement
 renal
 hepatic
 neurological
 haematological
 Cardiac
 fetoplacental

SYMPTOMS

• Rapid Swelling of hands and face

• Severe Headaches
• Visual disturbances (scotoma, blurred vision, flashing lights)
• Decreased urine output
• Nausea and vomiting
• Epigastric pain Proteinuria ≥ 5 gm/24 hr
• Oliguria < 500 cc/24 hr
• Cerebral or visual symptoms
• Pulmonary edema or cyanosis
• Low platelets
• Elevated liver function tests
• Fetal growth restriction

40
•

MATERNAL RISK

 Central nervous system manifestations, including seizures and stroke

 Disseminated intravascular coagulation (DIC) and its complications

 Increased likelihood of cesarean delivery

 Renal failure

 Hepatic failure or rupture

 Pulmonary oedema

41
 Maternal Death

 Eclampsia is a major cause of maternal mortality.

FOETAL RISK

 Oligohydramnios

 Uteroplacental insufficiency and Placental infarction

 Growth restriction

 Placental abruption

 Consequences of prematurity (when maternal disease necessitates delivery

remote from term)

 Fetal death

INVESTIGATIONS

o Urinalysis – proteinuria – Dip stick or 24hr Urine protein

o FBC – Anaemia, Pletelet level

o Renal functions – urea, creatinine, uric acid

o Liver function test – Raised transaminases

o Obstetric ultrasound to assess the fetal wellbeing – Amniotic fluid , growth-

BPP, Umbilical artery and Mid cerebral artery Resistive Index

MANAGEMENT

42
 The main objective of the management of preeclampsia must always be first
the safety of the mother and then the fetus.

 Although delivery is always appropriate for the mother, it might not be best
for a premature fetus.

 The decision between delivery and expectant treatment depends on fetal

gestational age, fetal status, and severity of maternal condition at the time of
assessment.

GOALS OF MANAGEMENT

 Control of Hypertension

 Prevention of Convulsions

 Preventing significant Maternal and Fetal morbidities.

 Timing of Delivery

ANTHYPERTENSIVES

 Treat women with severe hypertension who are in critical care during
pregnancy or after birth immediately with one or more of the following:

 Labetalol (oral or intravenous)

 Hydralazine (intravenous)

 Nifedipine (oral).

 Methyl Dopa

In women with severe hypertension who are in critical care, aim to keep systolic
blood pressure below 150 mmHg and diastolic blood pressure between 80 and
100 mmHg.

LABETALOL

43
 Hypertension

 100 mg PO q12hr initially; increased by 100 mg q12hr every 2-3 days

 Usual dosage range: 200-400 mg PO q12hr; not to exceed 2400 mg/day

 Hypertensive Emergency

 20 mg IV over 2 minutes initially, then 40-80 mg IV q10min; total dose not

to exceed 300 mg

 Alternative: 1-2 mg/min by continuous IV infusion; total dose of 300 mg has

been used

OTHER DRUGS

 Hydralazine – 5 -10 mg repeated after an hour with aim of Maintaining

Diastolic Bp at 90mmHg

 Nifedipine 20mg – 30mg bd

 Methyl Dopa 250mg – 500mg bd

ANTCONVASANTS

 If a woman in a critical care setting who has severe hypertension or severe

pre-eclampsia has or previously had an eclamptic fit, give intravenous
magnesium sulphate.

 Consider giving intravenous magnesium sulphate to women with severe pre-

eclampsia who are in a critical care setting if birth is planned within
24 hours.

DOSAGE

 Use the Collaborative Eclampsia Trial regimen for administration of

magnesium sulphate:

44
 Loading dose of 4 g should be given intravenously over 5 minutes, followed
by an infusion of 1 g/hour maintained for 24 hours

 Recurrent seizures should be treated with a further dose of 2–4 g given over
5 minutes.

 Be aware of toxicity effects – Respiratory, Renal and Tendon reflexes .

Antidote – Calcium gluconate

 Avoid use diazepam, phenytoin or lytic cocktail as an alternative to

magnesium sulphat in women with eclampsia

TIMING OF BIRTH

 Generally - Manage pregnancy in women with pre-eclampsia

conservatively until 34 weeks.

 Offer birth to women with pre-eclampsia before 34 weeks, after discussion

with neonatal and anaesthetic teams and a course of corticosteroids has been
given if:

 severe hypertension develops refractory to treatment

 maternal or fetal indications develop

 Recommend birth for women who have pre-eclampsia with severe

hypertension after 34 weeks when their blood pressure has been
controlled and a course of corticosteroids has been completed.

 Offer birth to women who have pre-eclampsia with mild or moderate

hypertension at 34+0 to 36+6 weeks depending on maternal and fetal
condition, risk factors and availability of neonatal intensive care.

 Recommend birth if on first contact within 24–48 hours for women

who have pre-eclampsia with mild or moderate hypertension after
37+0 weeks.

45
If birth is considered likely within 7 days in women with pre-
eclampsia:

 Give two doses of betamethasone/ Dexamethazone 12 mg intramuscularly

24 hours apart in women between 24 and 34 weeks

 Consider giving two doses of betamethasone/ Dexamethazone 12 mg

intramuscularly 24 hours apart in women between 35 and 36 weeks.

MODE OF DELIVERY

 Caesarean section versus induction of labour

 Choose mode of birth for women with severe hypertension, severe pre-
eclampsia or eclampsia according to the Clinical Indications /circumstances
and the woman's preference.

COMPLICATIONS

o Renal failure, acute

o Cerebral vascular accident

o Disseminated intra vascular coagulopathy

o Pulmonary edema

o HELLP

ECLAMPSIA

 Eclampsia is the clinical diagnosis given to obstetric patients who have

seizure activity due to preeclampsia.

 Eclampsia is considered one of the most severe forms of preeclampsia, and

delivery must be undertaken after a seizure.
46
CAUSES OF ZEISURE

The cause of the seizures is not clear, although some processes are
thought to be responsible in their development.

o Areas of cerebral vasospasm may be severe enough to cause focal ischemia,

which may in turn lead to seizures

o Pathologic alterations in cerebral blood flow and tissue edema induced by

vasospasm may result in headaches, visual disturbances, and hypertensive
encephalopathy, resulting in a seizure.

INVESTIGATIONS

o Complete blood cell count

o Platelet count

o 24 hr urine for protein/ creatinine

o Electrolytes

o Liver function tests

o Uric acid

o Serum glucose

o CT scan especially for cerebral vascular accidents

o A CT scan of the head, with or without contrast, may be indicated to exclude

cerebral venous thrombosis, intra cranial hemorrhage and central nervous
system lesions.

o Consider CT scan of the head in patients who

o have been involved in trauma

o are refractory to magnesium sulfate therapy

o have seizures >24hrs after delivery

47
o MRI where available, is most recommended as is more superior for
defining intra cranial anatomy and pathophysiology.

o Angiography may show widespread arterial vasoconstriction of the

intracranial vessels.

o Other tests such as EEG and cerebral spinal fluid studies may be used but
rarely if epilepsy or meningitis is considered in the diagnosis.

MANAGEMENT

Goals of therapy include:

o Control of seizures

o Prevention of maternal injury

o Correction of hypoxia and acidosis

o Control of severe hypertension

o Initiation of Delivery within 12 hours

o Magnesium sulphate is the treatment of choice for eclamptic seizures as

prevents seizure recurrence .

o Duration of therapy is 24 hrs post delivery or after a postpartum seizure .

o Given as 4g magnesium sulphate in 150 mls Normal saline/ Ringers lactate

if possible in a solucet and to run for 10-15 mins.

o After which 1g in 70-80mls of Normal saline/Ringers lactate hourly for 24

hrs.

o Give 2g stat after every repeat of a seizure and continue there after with the
maintenance dose of 1g hrly

48
o If convulsions are persistent/recurrent / status eclampticus/ toxicity to
Mgso4;- Phenytoin may be used at dose of 500mg IV slowly over 15
minutes then 250mg every 6 hrs

o Role of Diazepam *** Best in the set up of respiratory support.

o Discontinue magnesium sulphate immediately if signs of toxicity is noted

o Management should be based on clinical diagnosis

o Airway and oxygenation should be maintained; mechanical ventilation may

be necessary

o A pulse oxymetry if available should be used to monitor ventilation and

oxygenation

o Administer calcium gluconate 1g IV over at least 3 minutes

o Diuretic agents such as furosemide and mannitol may be administered

Hydrallazine hydrochloride IV, is the drug of choice for acute BP control
as it does not reduce the uteroplacental blood flow.

o IV hydrallazine hydrochloride should begin; 5mg in 25 mls Normal

saline/Ringers lactate in a solucet or as a slow bolus dose over a period of 2-
3 minutes or via a syringe pump where available

o Subsequent doses are repeated every 20-30 minutes if DBP is greater or

equal to 110mmHg in the same manner described above

o The aim is to maintain the BP at 90-100 mmhg

o Labetalol - Used as an alternative to hydralazine in eclampsia.

o 20-30 mg IV initially; 40-60 mg IV q10-20 min; not to exceed 300 mg

o Avoid its use in cardiogenic shock; pulmonary edema; bradycardia;

atrioventricular block; uncompensated congestive heart failure

o Nifedipine ( Adalat) produces calcium channel blockade, causing arteriolar

vasodilation

49
o Since it is only available in oral preparation, a patient with eclampsia should
only be given when out of acute phase and can take orally

o Should be given as 20mg twice daily.

o Methyl dopa-Aldomet also given orally, should be administered only when

the patient is out of the acute phase and is able to swallow orally

o Can be taken with adalat concurrently, though care should be taken in

monitoring the BP readings

o Can be given as 250mg or 500mg and frequency depends on severity of

disease

o patient must not be left unattended at all times

o Bed rails should be elevated and padded

o All IV access routes should be well secured, rings, bangles, and other
ornaments /traditional accessories removed

o All tight clothing removed

o Medical waste generated while managing the patient should be disposed off
appropriately as some are a source of injury especially the sharps

o Obtain arterial blood gases where possible

o Administer oxygen by mask or endotracheal tube as necessary

o Anticipate, diagnose and treat aspiration pneumonia

o Correct the relevant electrolyte imbalances as established

o No conservative management, patient should be delivered irrespective of

gestational age. Preferably deliver within 12 hours.

o Delivery to be undertaken after stabilization of patient status

o Vaginal delivery is mostly favorable for eclampsia in the absence of other

maternal or fetal complications

50
o When emergency cesarean delivery is indicated, there would be need to be
aware of anaesthetic risks and DIC.

NB: READ AND MAKE YOUR OWN NOTES ON

PHYLONEPHRITIS AND HIV IN PREGNANCY.

ABNORMAL LABOUR AND

DELIVERY
ABNORMALITIES AND COMPLICATIONS OF LABOR AND DELIVERY

INDUCTION OR STIMULATION OF LABOR

When induction of labor is indicated because of obstetric or medical disease, the disease
process should be under control; reasons for the induction should be precise and should be
recorded. The most successful and safest method for induction is giving dilute oxytocin IV, using
an infusion pump for precise control. Labor usually starts at a flow of 0.5 to 2 mU/min; if
contractions are inadequate, the dose is increased by 0.5 to 2 mU at 15- to 30-min intervals. A
rate of 40 mU/min should not be exceeded or maintained for > 30 min, because at that point,
water retention becomes a hazard. Rarely is > 10 to 12 mU/min needed.
External fetal monitoring is essential. Internal monitoring should be instituted as soon as the
membranes can be safely ruptured.
NB. READ FURTHER ON INDICATIONS AND CONTRAINDICATIONS OF
INDUCTION OF LABOUR

Stimulation or augmentation of labor with oxytocin is indicated when contractions occur in an

unsatisfactory pattern; before stimulation is attempted, the diagnosis must be reasonably precise.
If the patient is in the latent phase of labor (i.e., has little effacement, minimal dilation, and
irregular contractions), resting, walking, or support is preferable to using oxytocin. After true
labor has begun (4-cm dilation with nearly complete effacement), the cervix should dilate > 1
cm/h. If true labor does not occur, the patient is considered to have hypotonic uterine
dysfunction. The best treatment is dilute oxytocin stimulation until the pattern of contractions
becomes more normal.
An occasional patient has hypertonic dysfunctional labor, in which contractions are too strong,
too close together, or both. This contraction pattern is difficult to control.
Administration of any oxytocic drug should be discontinued promptly. Repositioning the patient
and administering an analgesic may help. A tocolytic drug, such as ritodrine, may be effective.

PRETERM LABOR
Onset of labor with effacement and dilation of the cervix before 37 wk gestation.

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Patients with preterm labor should be evaluated for infectious causes (e.g., chorioamnionitis) and
other known causes of preterm labor (e.g., uterine overdistention). Preterm labor associated with
vaginal bleeding or rupture of the membranes is difficult to stop. Bed rest helps occasionally, but
if dilation and effacement of the cervix begin, labor usually progresses to delivery. Preterm labor
not associated with bleeding or leaking amniotic fluid can be stopped in 50% of patients with bed
rest and hydration. Ethyl alcohol and barbiturates should not be used because of their adverse
effects on mother and fetus.
Magnesium sulfate infusion (similar to that used for preeclampsia) is the drug of choice.
Tolerance is good. Ritodrine, a β-adrenergic sympathomimetic drug, has a 70 to
80% success rate; however, because of its adverse effects (including maternal tachycardia and
hypotension and fetal tachycardia), it is relatively contraindicated. Terbutaline (0.25 mg sc q 30
to 60 min until contractions cease; maximum, 1 mg/4 h) has a similar success rate but fewer
adverse effects; the mother should be monitored for tachycardia. Maintenance with oral
terbutaline is not effective. If preterm labor is arrested, treating the mother with
betamethasone sodium phosphate and betamethasone acetate suspension 12 mg IM q 24 h for 2
doses/wk (or dexamethasone 5 mg IM q 12 h for 4 doses/wk), repeated weekly until 34 wk if the
mother is still threatening to deliver, appears to accelerate maturation of the fetal lungs and
decreases the incidence of neonatal respiratory distress syndrome. Other problems to which
preterm infants are predisposed.

PREMATURE RUPTURE OF MEMBRANES (PROM)

Rupture of the membranes >= 1 h before onset of labor.
Prompt delivery after premature rupture of the membranes (PROM) because of risk of neonatal
infection is no longer performed unless the pregnancy is at term. A digital examination of the
cervix is not performed, because it may initiate intrauterine infection (due to pathogens
ascending from the vagina). Rather, examination with a clean speculum is performed to verify
rupture, estimate dilation, and collect fluid for maturity studies and culture. Diagnosis of PROM
is confirmed when fluid is seen escaping from the cervix or when fetal vernix or meconium is
observed; other less reliable tests are determination of pH with Nitrazine paper (amniotic fluid is
alkaline, turning it blue) and microscopic examination for ferning in fluid dried on a glass slide.
If the L/S ratio or other tests performed on the amniotic fluid indicate that the fetal lungs are not
mature and if the mother and fetus are healthy, an attempt should be made to delay delivery until
maturity. Bed rest is effective for some patients; many need magnesium sulfate. If no digital
examination is performed and speculum examination is not repeated, the risk of infection is
minimal. The patient should be kept on bed rest, and her temperature and pulse should be
recorded at least twice daily.
Delivery should be accomplished if infection is suspected or when amniotic fluid studies indicate
maturity.

PROLAPSE OF THE UMBILICAL CORD

This rare complication can be occult or overt. Occult prolapse occurs with intact membranes
when the cord is expelled before the presenting part or is trapped in front of a shoulder. A
specific pattern on the electronic fetal monitoring tracing is generally diagnostic. Changing the
patient's position or elevating the fetus relieves pressure on the cord. Occasionally, cesarean
section is necessary.

52
Overt prolapse occurs with ruptured membranes when the cord is in front of the presenting part.
It most commonly occurs spontaneously with breech presentation but also occurs with vertex
presentation, particularly when membranes are ruptured and the presenting part is not engaged.
The cause may be iatrogenic--which is one reason that membranes should not be artificially
ruptured unless the head is well engaged in the pelvis. Treatment is immediate delivery, usually
by cesarean section, to avoid fetal damage. An attendant or the obstetrician must hold the
presenting part up off the prolapsed cord to prevent further, prolonged compression of the cord.
The cord should be kept in the vagina to prevent drying.

AMNIOTIC FLUID EMBOLISM

Amniotic fluid embolism, an extremely rare event, can occur at any gestational age, usually with
tumultuous labor and ruptured membranes, but it may occur during a cesarean section.
Amniotic fluid embolizes to the pulmonary circulation, and the patient responds with collapse,
shock, tachycardia, cardiac irregularity and arrest, and usually death. Autopsy reveals fetal
squamous cells and hair in the pulmonary circulation. If the patient survives, disseminated
intravascular coagulation is a common complication

POSTDATISM AND POSTMATURITY

Postdatism: Pregnancy continuing after 42 wk. Postmaturity: An uncommon syndrome of
failing placental function and fetal jeopardy that occurs after 42 wk.
Because calculation of the estimated delivery date is subject to error, the diagnosis of
postdatism may be uncertain. If the woman's menstrual cycles were >= 35 days, delivery may be
late by definition although the fetus is really only at term.
Signs of postmaturity are a reduction in uterine size and decrease in fetal motion in a pregnancy
that is > 42 wk gestation. Postmaturity can be confirmed by finding yellow fluid during
amniocentesis, caused by meconium staining of the amniotic fluid. Frequently, however, the
amount of amniotic fluid is markedly decreased in postmature pregnancies, and amniocentesis
may be difficult.
Postdatism can be treated expectantly, as long as no signs of postmaturity occur. If the
pregnancy continues past 42 wk, a nonstress test with amniotic fluid assessment or a contraction
stress test should be performed to help evaluate the fetus' condition. Some physicians
recommend starting testing at 41 wk and including a biophysical profile (e.g., amniotic fluid
volume, fetal movement, fetal breathing, fetal heart sounds). If results are abnormal, delivery
should be accomplished. If the cervix is not ripe, cesarean section should be performed.

PROBLEMS IN THE FIRST AND SECOND STAGES OF LABOR

Most of the problems that occur during delivery can and should be anticipated. Failure to
diagnose potential problems at the initial examination threatens mother and fetus. Signs of
danger during the 1st stage of labor include vaginal bleeding and abnormal fetal heart rate. Other
problems include abnormal fetal presentation and position. All of these problems must be
accurately diagnosed early in the 1st stage of labor so that appropriate treatment can be started.
The primary event in the 2nd stage of labor is descent of the presenting part into the pelvis.
In general, both cervical dilation and descent of the head into the pelvis should proceed by at
least 1 cm/h; if they do not, cephalopelvic disproportion is likely. cephalopelvic disproportion
requires delivery by forceps, vacuum extractor, or cesarean section. When an attempt at forceps
delivery proves too difficult, the obstetrician should perform a cesarean section.

53
If fetus and pelvic size are not disproportionate and labor does not progress normally with good
descent of the fetus, oxytocin should be administered IV. If oxytocin is unsuccessful, a cesarean
section should be performed. Fetal heart rate must be monitored; any significant abnormality of
heart rate requires immediate delivery by forceps or cesarean section.
Occasionally, for various reasons, an infant is born apneic although no problems existed before
delivery. Appropriate resuscitative measures must be started immediately. Thus, in addition to
the obstetrician, persons trained in resuscitation, who can be freed from providing anesthetics or
tending to maternal problems, should be present during delivery if possible.

Abnormal Presentations
When the fetal occiput is posterior in the pelvis (the most common abnormal presentation)
rather than anterior, the fetal neck is usually deflexed to some extent and a larger diameter of the
head is presented for passage through the maternal pelvis. Any degree of disproportion may
prolong labor and make delivery difficult. The obstetrician must evaluate this problem and
decide between forceps delivery and cesarean section. In face presentation, the head is
hyperextended, and the chin presents; if the chin is posterior and remains so, vaginal delivery is
not possible. Brow presentation rarely persists, but if it does, vaginal delivery at term is not
possible.
In breech presentation, the next most common abnormality, the buttocks present rather than the
head. There are several varieties of breech presentation: In a frank breech presentation, the fetal
hips are flexed but the knees are extended. In a complete breech presentation, the fetus seems to
be sitting with hips and knees flexed. Single or double footling presentation occurs when one or
both legs are completely extended and present before the breech. The primary problem with
breech presentation is that the presenting part is a poor dilating wedge, making delivery of the
head difficult. Thus, fetopelvic disproportion is encountered after the body has been delivered
and the head is trapped.
Consequently, the infant may be seriously injured or die. The perinatal death rate for breech
presentation is four times that for cephalic presentations; prematurity and congenital anomalies
are major contributing factors. The possibility of nerve damage due to stretching of the brachial
plexus or spinal cord and of brain damage due to anoxia is increased in breech presentation.
When the fetal umbilicus is visible at the introitus, the cord is being compressed by the fetal head
against the inlet of the pelvis so that little O2 exchange occurs, resulting in hypoxia. These
problems seem to be compounded in primigravidas because the pelvic tissues have not been
dilated by previous deliveries. Complications can be prevented only by diagnosing and
correcting the breech presentation before delivery (e.g., the fetus can be moved to vertex
presentation by external version before labor, usually at 37 or
38 wk, or a cesarean section can be scheduled). Many obstetricians advocate cesarean section for
most breech presentations in primigravidas and for all preterm breech presentations.
Other abnormal presentations may occur. Occasionally, presentation is shoulder-first with a
transverse lie in which the long axis is oblique or perpendicular rather than parallel to the
mother's long axis. These infants, unless a second twin, should be delivered by cesarean section.
Twins occur in 1 of 70 to 80 deliveries and can be diagnosed before delivery by
ultrasonography, x-ray, or the recording of two distinct heart-rate patterns on the fetal ECG.
Twins present in various ways, and abnormal presentations may complicate delivery.
Morbidity and mortality are higher for the second twin because the uterus may contract after
delivery of the first twin, shearing away the placenta of the second twin. Twins are often small

54
and premature because an overdistended uterus tends to go into labor before term. In some cases,
the overdistended uterus does not contract well after delivery, causing maternal hemorrhage.
Cesarean section is performed for the usual indications.

Shoulder Dystocia
An uncommon occurrence in which the anterior shoulder in vertex presentation impinges on the
symphysis pubis.
The head, after delivery, appears to be pulled back tightly against the vulva. The infant is unable
to breathe because the chest is compressed by the vaginal canal and the mouth is kept shut by
pressure against the vulva, preventing the obstetrician from inserting any kind of tube. Oxygen
deficit occurs within 4 to 5 min. This condition is most common with normal birth-weight to
large infants; the only consistent predictor is the need to perform midforceps delivery.
When shoulder dystocia occurs, all available personnel should be summoned to the room, and
then the mother's thighs are hyperflexed to increase the diameter of the pelvic outlet.
Suprapubic pressure is used to rotate the anterior shoulder. Fundal pressure should be avoided
because it may worsen the condition or cause uterine rupture. If this maneuver fails, a hand
should be inserted into the posterior part of the vagina and pressure placed on the anterior or
posterior part of the posterior shoulder to rotate the infant in whichever direction he will go
easily. With rotation, the anterior shoulder should disengage.
If neither attempt works, the posterior shoulder is pushed up into the hollow of the sacrum, the
obstetrician's hand is inserted to the fetal elbow, the fetal elbow is flexed, and the fetal hand is
grasped and pulled outside to deliver the entire fetal arm. The arm is then used (like a crank) to
turn the entire infant and disengage the anterior shoulder. When all maneuvers fail, the infant's
head is flexed and pushed back into the vagina; the infant is then delivered by cesarean section.

Forceps Delivery
Forceps delivery is elective when used to ease delivery or to provide greater control of the head;
it is indicated when problems of fetal distress or fetal position exist or to shorten the
2nd stage of labor when no complications are present but lengthy vaginal delivery is anticipated.
The 2nd stage occasionally does not progress when epidural anesthesia prevents the patient from
bearing down adequately. The decision to use forceps must be made by an obstetrician, because
cesarean section may be a better alternative.
Contraindications to vaginal forceps delivery include fetopelvic disproportion, incomplete
dilation of the cervix, failure of engagement, indeterminate presentation or position, and
insufficient skill of the operator. An alternative to forceps delivery is vacuum extraction.
Major complications that occur with forceps or vacuum extraction are injury to the fetus and
mother. Only specific training, skillful use, and experience can prevent these complications.

Cesarean Section
Surgical delivery by incision into the uterus.
Cesarean section should be performed when it is safer for the mother or fetus than vaginal
delivery. About 15 to 25% of deliveries are by cesarean section, depending on the institution and
the population served. Many centers are working to lower this rate. The decision and procedure
require an obstetrician, and management of anesthesia and resuscitation of newborns require an
anesthesiologist and neonatologist or someone skilled in neonatal resuscitation. The procedure is
safe because of current-day anesthesia, IV therapy, antibiotics, blood transfusions, and early

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ambulation. However, it is less safe than vaginal delivery, with a morbidity and mortality rate
that is several times higher.
Two types of uterine incision are used: classic and lower segment. A classic incision is
longitudinal in the anterior wall of the uterus, ascending to the fundus. This incision is usually
reserved for patients with placenta previa or a transverse lie of the fetus. The uterine wall is more
vascular in this area, so blood loss is greater than that with a lower segment incision, but the scar
is not as prominent in subsequent pregnancies. A lower segment incision is made transversely or
longitudinally in the thinned, elongated lower portion of the uterine body behind the bladder
reflection. Longitudinal incision is reserved for most abnormal presentations and for excessively
large infants to avoid lateral extension of a transverse incision into the uterine arteries, which
causes greater blood loss. Transverse incisions are easier to cover with the bladder flap, but
longitudinal incisions that extend into the upper segment for 1 to 2 cm can also be covered easily
and have no greater risk than transverse incisions. Vaginal birth after cesarean section has a
success rate approaching 75% and should be offered to all women who have had a cesarean
section with a lower segment incision. The best treatment for repeat cesarean section is correct
management of the previous labor.

PROBLEMS IN THE THIRD STAGE OF LABOR

Maternal hemorrhage must be prevented during the 3rd stage, when the placenta is delivered.
Ordinarily, 400 to 500 mL of blood is lost during delivery; if the loss is greater, the reasons must
be sought. Possible sources of bleeding include uterine atony, vaginal or cervical lacerations, or
retained portions of the placenta. If the uterus does not contract, hemorrhage will occur, because
the primary mechanism for hemostasis within the uterus is contraction of myometrium.
During the 3rd stage of labor, the patient must be observed by a trained staff member, preferably
an anesthesiologist; BP, heart rate, respirations, and alertness must be monitored.
When the placenta has dropped into the lower uterine segment and presents at the cervix, the
corpus may be depressed toward the pelvis to help push the placenta into the vagina.
However, the uterus can be inverted if this procedure is performed incorrectly, especially if
traction is applied on the cord before the placenta is completely separated.

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57
ABNORMAL PEUPERIUM

Breast engorgement, blocked ducts, breast cysts;

Breast engorgement

Swelling and fullness occurring from 3-7 days after delivery in all lactating women as breasts prepare for
milk production.

Pathophysiology

It is caused by venous congestion due to increased vascularity in breasts. Later on the problem is
compounded by pressure of accumulating milk. Extra blood and lymph fluids go into the breasts to
prepare milk and the formed milk itself causes this swelling. This happens due to increased
progesterone, estrogen and prolactin synthesis.

Risk factors /causes

a) Baby feeding ineffectively, leading to retention of excess milk in breasts.

b) Use of intravenous fluids in labor before birth.
c) Insufficient pumping of milk for mothers who do not breastfeed directly.
d) Sudden weaning too early.
e) Mothers who have had an intra-uterine fetal death (IUFD)
f) Mothers who have had recent breast surgery.
Diagnosis

This involves history taking from the mother so as to get full information concerning present condition
and breastfeeding status.

In addition physical examination of the mothers breasts will reveal; full hard (tender), warm, taut and
shiny breasts that may be painful to palpation.

Clinical manifestation

 Swelling of breasts, due to milk accumulation

 Tenderness of breasts

 Skin that is taut, shiny or transparent

 Throbbing low grade favor

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 Breasts are warm

 Anorexia, fatigue, weakness and chills

Management (general)

a) Apply hot moist towels to breasts for 2-5 months or take a hot shower before breast feeding to
enable proper latching of baby onto breasts and enable efficient breastfeeding.
b) Hand press some milk before breast feeding to soften areola
c) Use gentle breast massage before and during breastfeeding
d) Apply cold compress to the breasts after feeding to relieve discomfort
e) When a baby will take milk from only one breast, a breast pump should be used to extract milk
from the other breast during engorgement period
f) Use breast pump when the baby cannot latch onto breasts because they are too full

g) Take anti-inflammatory drugs and pain relievers i.e. Advil after feeds

Goals to be met n management

Enabling the baby to feed

Relieve edema and congestion

Promote flow of milk

Eliminate the cause of engorgement

Complications

Feeding problems or slow weight gain if baby is unable to latch onto the engorged breast

Sore nipples to the mother when the baby is fumbling with the engorged breast

Increased risk of mastitis due to pressure in the breast and inadequate milk flow

Damage to milk production cells that may cause decreased milk production leading to premature
weaning leading to malnutrition and retarded growth of baby

Heath education

Mother is encouraged to breastfeeding the baby 8-12 times in 24 hours to prevent discomfort and
mastitis

Mother is advised to avoid supplements such as formula for the first 3-4 days to exclusively breastfeed
the infant

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Mother advised to hand press milk in case of missed feeding

Mother encouraged to gradually weaning the baby

Mum encouraged to wear a good fitting supportive bra

Mother is advised to seek medical help if;

 Chills and fever(temp. greater than 38.5 ‘c)

 Feeling achy, tired or flu like symptoms

 A tender red swollen or warm area in her breast

 Red cracked bruised or bleeding nipples

 Engorgement doesn’t get better after following the care plan for 48 hours

Follow up care

Mother is given a return date for evaluation of all interventions instituted during the 1 st visit

Mother is advised to report to a health center if engorgement continues after management

Care plan is revaluated if symptoms don’t begin to resolve in 2-3 days

1. Blocked / plugged ducts

An area of breast when milk flow is obstructed. The nipple may be further back in the ductal system. It
comes on gradually and usually affects one breast

Pathogenesis

Increased milk production filling and causing back flow of milk into the tissues of the breast. This causes
swelling and inflammation, turning affected area red, warm, lumpy and painful.

If traces of milk enter the blood stream, flu like feeling and elated body temperature is triggered as the
body mistakenly sees the breast milk as foreign, triggering an immune response.

Causes/risk factors

Happens when the breasts are not completely drained of their milk on a regular basis. This may be due
to;

 Baby may be having difficulty in feeding i.e. improper latching or not feeding frequently enough

 Abrupt weaning

 A breast pump that is too powerful

 Illness

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Pressure against milk ducts may be caused by;

 Putting a diaper bag on mums chest

 Wearing a very tight bra

 Sleeping on the stomach

 Car seat belts

Untreated engorgement

Stress lowers oxytocin production that causes a reduction in milk let down reflex

Surgery

Inflammation

Diagnosis

This can be done mainly from;

 Patients history

 Physical examination of breasts

 Mammograms/mammographs

Clinical manifestation

Initially it may be a small, hard lump that is sore to touch or a very tender spot on the breast

Some women may also notice some redness in the area of the breast

Area may feel hot and swollen but feel better after breast feeding

Sometimes when you feel achy and fluirish this may be a sign of the clog getting infected

Distended glandular tissue due to engorgement

Management

Therapeutic;

Goals are;

 Improving milk removal through improved attachment and possibly milk expression

 Treat accompanying pain and inflammation

Massaging is contraindicated as it induces inflow of milk to the surrounding areas

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Management

Hand express milk to increase comfort and reduce inflammation

If it’s not too painful nurse the side with the clogged duct first as it may be dislodged when the baby
sucks

Vary the nursing position e.g. cradle, football, side lying

Promote a lot of rest for mother’s recovery

Balanced nutrition and hydration

To avoid future clogging, avoid long stretches between feeding and also ensure the mothers bras are
fitting and not compressing the milk ducts

Complication

If left untreated it may result into mastitis

Feeding problems for the baby leading to slow weight gain

Development of sore nipples

Health education

Education on reducing pressure on milk ducts by;

 Avoiding prone positions when sleeping

 Avoiding tight seat belts

 Avoiding tight bras

Seeking treatment for engorgement promptly

Completely draining milk or hand expressing milk occasionally

Not weaning the baby early

Follow up care

If the mother continues to feel pain after trying resting, frequenting nursing for more than 24 hours she
is advised to go to a health facility

She is also advised to call immediately after developing a fever as this may be a sign of infection

Relevant treatment plan. If symptoms do not resolve in 2-3 days, consider possibility of thrush if sore
nipples begin.

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2. Breast cysts

a lump on the breast that may thought to be breast cancer but is generally benign(a closed sac having
distinct membrane and elevation on nearby breast tissue that feels like a soft grape) water filled and
firm and may be painful

Pathogenesis

Breast cysts develop when an overgrowth of glands and connecting tissue (fibrocystic changes) blocked
milk ducts causing them to widen (dilate and fill with fluid)

Types of cysts;

Majorly grouped according to size and content;

 Simple/micro cysts ;

These are fluid filled cysts only with no solid content

 Complex/macro cysts ;

Mixture of fluid and solid matter that needs to be drained

Causes

These remain unknown. Some evidence however suggests that excess estrogen in the body can
stimulate breast tissue, therefore plays a role in cysts development

It’s also possible that cysts develop from an infection or inflammation

Diagnosis

Clinically as a movable lump as shown on screening sonogram or mammogram

Clinical manifestation

Tenderness in area of lump

Presence of a smooth, small circular mass

Sometimes the mother may feel pain

Affected area is usually tense and hard

Management

Gross palpable breast cysts and simple cysts are usually not associated with any breast carcinomas so
tend to be left alone with routine follow up; if bothersome it may be drained via needle aspiration

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Complicated and complex cysts are drained; smaller internal cysts are drained with ultra sound guidance
for the needle

The follow up interval for a complex cyst will typically be shorter around 6 months

Health education

Mother is taught on breast examination (self) to be able to identify any changes and return to a health
facility for a clinical exam

Complication

Breast feeding problems, especially if the cyst is large and around the nipple as latching is made difficult
and if not addressed early may result to inadequate baby nutrition

Follow up care

Mother is advised to visit the clinic on a regular basis for check up

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Assessment Nursing Planning and Intervention Rationale Evaluation
diagnosis E/O
Assess pain Pain and At the end of Administer Reducing After 48 hours
and mother’s discomfort therapy analgesic/ inflammation of therapy the
discomfort related to mother will Anti- pain and mother was
inflammation express inflammatory discomfort able to express
Onset, as evidenced comfort and medication to related to comfort during
location and by reduced pain be taken 20- engorgement breastfeeding
how mother verbalization before, during 30 minutes or blocked
relieves of pain and and after before feeding ducts
discomfort discomfort by breastfeeding
mother before (24-48 hours For comfort It helps
Assess breast feeds of therapy) mother release or let
for redness, applies cold or down of milk
warmth warm
compress to
her breast
Assess the Ineffective The mother Initiate To completely After 24 hours
baby’s ability breast feeding will; breastfeeding drain milk by of therapy
to latch onto related to -Express within 1st hour baby Mother was
breast mothers physical and after birth To avoid able to fully
discomfort emotional Keep infant skipped feeds express breast
Assess and the baby’s comfort in with mother feeding as
frequency o f inability to breastfeeding Discuss and To enable evidenced by
baby’s feeding latch as -Show demonstrate baby to breast safety of baby
evidenced by decreased breast feeding feeding and arrest of
Assess low weight anxiety and aids e.g. Infant comfortably engorgement
mothers gain by baby apprehension sling, nursing and efficiently
knowledge of State at least footstool,
breastfeeding one reason for Breast pumps
breastfeeding
Evidence of Breast feeding
inadequate Infant will; positions
intake -Feed
successfully on
Unsatisfactory both breasts
breastfeeding and be
process satisfied
-Grow and
thrive
Assess the Deficient Immediately Demonstrate Ensure Goals fully
mothers basic knowledge after therapy proper mothers achieved at
breast feeding related to (6 hours) breastfeeding participation the end of the
knowledge inadequate technique in care for care evidenced
Assess postpartum Mother will infant by mother
mothers teaching on express Provide expressing
beliefs and breastfeeding understanding information as Ensure that understanding
values on as evidenced on proper needed about mother is and proper

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breastfeeding by breastfeeding early infant properly demonstration
according to verbalization techniques as feeding equipped with and reduced
culture of lack of evidenced by Monitor necessary anxiety
Assess knowledge mothers effectiveness skills for confusion
availability of participation of current proper
breastfeeding in care breastfeeding lactation of
support provision efforts infant
services e.g. Verbalization Be able to
attending of point out
seminars understanding mistakes in
and reduced breastfeeding
anxiety
Assess breasts Risk for Mother will be Encourage To promote Goals fully met
for development free of sore mother to effective baby as mother is
development of sore nipples nipples and massage latch on kept out of
of cracked and mastitis mastitis before feeds breast risks
nipples, relating to throughout Encourage throughout
redness improper the mother to therapy
tender swollen latching and breastfeeding change
bleeding unaddressed period positions
nipples engorgement during feed

Monitor vitals
esp. temp for
fever

Assess feeling
of tiredness,
flu like
symptoms

Puerperal pyrexia and sepsis;

Puerperal sepsis.

This is an infection of the genital tract occurring any time between rapture of membranes or labor and
six weeks after delivery or abortion.

It can be caused by endogenous organisms like streptococcus fecali and clostridium which reside within
the vagina.

It can also be caused by exogenous organisms that come from sources outside the patient for instance
the doctor or midwife.

There are 3 types of puerperal sepsis; mild, moderate and severe.

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Mild infection

The infection is usually localized to tissues around the area such as the vagina, cervix or uterus. The
temperature is gradually stepped up but rarely goes beyond 38’c. The mother may have no other
complications or symptoms. With prompt treatment with antibiotics the infection can go away within 3-
4 days.

Moderate infection

When endometritis develops it manifests in about 48-72 hours after delivery. The mother complains
about loss of appetite, headache, backache and general discomfort. The pulse rate ranges between 100-
120 beats/minute. The uterus is bulky and tender to touch. Lochia discharge may increase in amount
and is brownish in color with a foul smell. In cases of hemolytic streptococcus, the lochia may be
odorless initially. If the infection is contained in the endometrium, it clears within 7-1-0 of treatment.

Severe infection

The virulent strain of hemolytic streptococcus rapidly infects the peritoneal cavity and causes septicemia
and hemolytic anemia by gaining access to the circulatory system through the placental site. The mother
will have a persistent fever of above 39’c. Rigors are common and the pulse rate ranges from 140-160
beats/min. the uterus is subinvoluted and tender to touch. Pallor is marked and there is persistent
vomiting and at times diarrhea. Mother is weak and complains of insomnia.

The sites of infection include;

 Episiotomy incision

 Caesarean incision

 Uterus

 Urinary tract

 Breast

General signs and symptoms

Fever which occurs within 24 hours

Increased pulse rate

Subinvoluted uterus

Foul smelling vaginal discharge

Headache, insomnia, anorexia

In severe sepsis the following are symptoms;

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Constant pelvic pain

Collection of pus in the pouch

Risk factors

Caesarean delivery

Trauma; provides access point to bacteria

Premature rapture of membranes, allows access of organisms into the interior uterus

Catherization; introduces organisms to urinary tract causing UTI

Excessive vaginal exam

Retained plasma fragments; provide growth medium to bacteria

Hemorrhage; leads to decreased immunity due to loss of WBC

Poor hygiene; provides conducive environment for organisms

Medical conditions especially diabetes

Diagnostic examination

The following should be followed when conducting a diagnostic examination;

 Head to toe exam

 Check uterus for pallor, throat for infection, abdominal tenderness and swollen glands

 Check uterus for sub involution, the perineum for signs of infection from episiotomy or tears

 Inspect legs for inflammation

When carrying out investigations, the following steps should be done;

 Take a high vaginal swab, perineal and endo cervical swabs for culture and sensitivity

 Sample blood fro haemogram, WBC total and differential

 Blood culture and sensitivity

 Ultrasound scan of pelvis

 Serum electrolytes

Medical treatment

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Broad spectrum antibiotics like amphicilin, gentamycin and canamycin should be admin

An analgesic given to reduce pain and ensure good sleep

Mother should be placed on iron supplements

If Hb is below 7.4 dl, packed cell transfusion is recommended

Fluids and electrolyte balances should be maintained. In cas4e of imbalances, 59 glucose infusions with
added vitamins and potassium chloride is given

In case of infected perineal wound, the stitch should be clipped to allow drainage of pus

Localized infection is treated with hydrogen peroxide and antibiotic spray

It may be necessary at times to incise and drain a pelvic abscess through posterior vaginal fornix or
rectum

Nursing care

Isolate her until cause has been identified, antibiotic started and temperature stable

Unless the mother is severely ill the baby stays with her and the midwife will help take care of the baby

Give the mother rest to prevent exhaustion

Nurse the mother in a propped up position with a pillow to encourage uterine drainage of lochia

Encourage the mother to eat a light nutritious diet with plenty of fluids

Saline baths 3 times daily

Monitor vital signs 4 hourly

Daily head to toe examination to assess her condition

Frequent change of vaginal pads

Patients in septic shock or having evidence of severe sepsis should be resuscitated without delay. Give
oxygen to patient via oxygen mask and transfuse blood

Prevention

 Hand hygiene; delivery assistants should wash their hands before the delivery.

 Equipment and delivery kits should be sterilized and cleaned prior to storage for infection
control.
 Training and education of traditional attendants on the need to maintain high standards of
hygiene

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 Vaginal antisepsis; use of chlorhexidine as a vaginal or perineal solution to decrease maternal
sepsis
 The mother should be advised to eat a well balanced diet before, during and after pregnancy to
prevent anemia which has been linked to puerperal sepsis and underweight mothers should be
given vitamin A or beta-carotene supplements
 Routine antibiotic prophylaxis during caesarean section decreases endometritis by at least 2/3

 Restricting VES to minimize PROM and PPROM

 Early diagnosis and treatment of vaginal infections and UTI

 Proper management of 1st, 2nd and 3rd stage of labor

 Encourage voiding during labor to avoid unnecessary catheterization

 Avoid unnecessary episiotomy

Puerperal pyrexia

This is a febrile condition presented by temperatures of 38’c and above 10-21 days after childbirth or
abortion.

It is a serious case of septicemia.

Causes

Genital tract infection

UTI

Breast disorders such as mastitis, breast engorgement or abscess

Thrombophlebitis

Respiratory tract infections

Other causes of pyrexia such as malaria

Vesico vaginal fistula

Recto vaginal fistula

Pyrexia of unknown origin

Puerperal sepsis

After separation of the placenta, a superficial wound is left on the uterine wall. Other wounds may be
present in the birth canal depending on the type of delivery. These wounds may be minor bruises or
deep tears of the cervix, vagina or perineum. If not properly managed puerperal pyrexia ensues.

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Bacteriology

Bacterial organisms are classified in 2 groups, endogenous and exogenous organisms.

 Endogenous; these are harmless organisms present in the lower intestinal tract, on the
perineum and in the vagina. They have a role to play in the ecology of the body. Eschoria coli
inhabit the bowel and the vagina. Streptococcus faecalis reside in the lower intestine and anus.
Anaerobic streptococci and clostridium welchii are found in the vagina.
 Exogenous; these are imported into the birth canal from other sources such as the hands of the
birth assistants or airborne infections from other patients or visitors. The organisms are
harbored in dust and in the throat. Staphylococcus aureus is the main cause of breast infection
found in dust and has developed resistance to antibiotics in recent years.

Pathology

When the organisms enter the tissues, the whole process depends on;

 Virulence of the organism

 The body’s ability to resist infection

 Trauma inflicted to tissues

 Effectiveness of the antibiotic and the time of commencement

Signs and symptoms

High fever

Headache

Vomiting

Rising pulse rate

Dyspanea

Unusual vaginal discharge

Complications

Puerperal pyrexia

Toxic shock syndrome

Multi organ failure

Death

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Urinary tract infections (UTI)
Urinary tract infection in pregnancy

UTI is an inflammation of the urinary epithelium in response to colonization by a pathogen. UTI refers to
infections affecting the urine pathway from the kidney to the urethral meatus and they are divided into
upper and lower UTI.

During pregnancy the bladder undergoes changes in size and muscle tone. During the 1 st trimester the
uterus begins to expand within the pelvic cavity applying pressure to the bladder causing the woman to
experience increased frequency and urge to urinate. During the 2 nd trimester the uterus extends into the
abdominal cavity and the urge to urinate decreases making her susceptible to UTI.

Etiology

 Bacterial

 Trauma; during delivery the bladder and uterus are traumatized by pressure of the descending
fetus which increases chances of a bacterial infection.
 Urinary stasis provides a good environment for bacteria to multiply and increase in number

 Women with a bacterial infection during childbirth are at high risk of developing UTI

 Vesicouteral reflux from bladder to urethra and back to the kidney during micturation causes
bacteria to ascend causing infection
 Instrumental insertion like catheters and endoscopies without using an aseptic technique

 Increased nutrients in urine i.e. glucose and amino acids provides a good environment for
bacteria to thrive

Epidemiology

It occurs in 2-4 % of post part women thus is the 2 nd most common postpartum infection

Pathophysiology

The post-partal woman is at an increased risk of developing UTI because of the normal post partal
dieresis, decreased bladder capacity, and decreased bladder sensitivity from stretching or trauma.

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Emptying of the bladder is vital, that unable to void cauterization is necessary. Retention of urine,
bacterial introduction during catherisation and traumatized bladder during childbirth combined provide
an excellent environment for development of bacteria and pyelonepliritis.

There are 2 types of UTI;

 Cystitis; Escherichia coli is the most common causative agent. Infection ascends to the kidney
because of vesicouteretal reflux. Symptoms of cystitis usually occur 2-3 days after delivery
 Pyelonepliritis; it is an infection of the renal pelvis and the interstitial. It has a sudden onset that
is accompanied by chills, high fever, vomiting, malaise, decreased urine output, dehydration,
and decreased creatinine clearance. In most cases infection ascends from the lower urinary tract
and if left untreated, renal cortex may be damaged and kidney function impaired.

Diagnostic studies

1. Urine dipstick may read positive for blood, WBCs and nitrates indicating infection.

2. Urine microscopy shows RBCs and many WBCs per field without epithelial cells.

3. Urine culture is used to detect bacteria and for antimicrobial sensitivity testing

4. Tender bladder base during palpation of pelvis. It is assessed by palpation of anterior vaginal
wall.
5. Renal ultrasound to evaluate for urinary tract obstruction

Clinical manifestations

Dysuria, frequency, urgency and nocturia

Suprapubic pain and discomfort

Microscopic or gross hematuria

Abdominal tenderness

Nausea and vomiting

Chills, fever, tachycardia and dehydration

Complications

Renal failure

Bacteremia

Glomerulonephritis

Pyelonephritis

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Exacerbation of baby blues

Treatment

Hospitalization and administration of IV antibiotics such as carbenicillin, cephalosporin

Nursing assessment

Determine whether the woman had UTI in childhood or previous pregnancy

Evaluate the voiding habits, personal hygiene practices and contraceptive use

Examine for Suprapubic tenderness as well as abdominal tenderness, guarding and rebound.

Assess for pain using the 1-10 scale to determine whether it increases during voiding.

Obtain clean catch urine sample for lab studies

Nursing diagnosis

Acute pain is related to inflammation of the bladder mucosa as evidenced by dysuria

Impaired urinary elimination related to dysuria as evidenced by urine infection

Increased risk of altered parenting related to the disease process as evidenced by generalized weakness

Knowledge deficit related to lack of information about self care measures to help prevent recurrence of
UTI

Goals

 To keep the mother free from infection during the post partal period.

 To educate the mother on prevention of infection and signs of infection.

Plans and implementation

 Encourage the intake of plenty of fluids in order to flush out the bacteria from the urinary tract.

 Encourage the mother to take perineal analgesics.

 Teach the mother how to self administer antibiotics

 Assess the vital signs 4 hourly, a temp above 38’c or tachycardia is suggestive of a bacterial
infection.
 Monitor bladder distention and empty 2 hourly to prevent over filling

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 Most bacteria enter the urethra from the anal area. The nurse should ensure the woman is
aware of good hygiene practices and provide information on other ways to avoid cystitis.
 Rapid treatment with antibiotics to avoid spread of bacterial infection.

 Dietary modification to avoid triggers such as tomatoes, citrus, chocolate and spicy food.

Evaluation

The woman implements self care measures to prevent cystitis as a routine.

The woman can identify signs and symptoms of UTI.

The infection is cured.

The woman completes the prescribed course of antibiotic therapy.

Family and patient education

Instruct the mother to void frequently and empty bladder because this enhances bacterial clearance,
reduces urine stasis and prevents reinfection.

Provide information on foods and fluids known to be bladder irritants.

Emphasize the importance of reporting signs and symptoms of UTI

Teach the importance of taking call medication even if signs and symptoms abate.

Hygiene information i.e. the woman should wipe from front to back and avoid douching while bathing.

Puerperal depression
This is a severe form of depression occurring in the 1 st few weeks after the baby is born. Postpartum
illness was initially conceptualized as a group of disorders specifically linked to pregnancy and child birth
and was considered distinct from other types of psychiatric illnesses.

It develops in about 8-26 % of post partum women. Although it may occur during the 1 st year
postpartum, the greatest risks occur within the 4 th week, just prior to initiation of menses and upon
weaning.

Etiology and predisposing factors

The cause is unknown but the predisposing factors are believed to be;

 Previous puerperal depression or depression during pregnancy

 Hormonal fluctuation

 Medical problems such as pre-eclampsia, pre existing diabetes mellitus, anemia or thymus
dysfunction during and after pregnancy

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 History of depression, mental illness or alcoholism either in the woman or in the family

 Immaturity or low self-esteem

 Marital dysfunction or difficult relationship with significant others

 Anger about the pregnancy

 Feeling of isolation or lack of social support

 Fatigue, sleep deprivation, financial worries

 Birth of an infant with abnormalities or illness

 Multifetal pregnancy

 Primiparity

 Residual pain

 Conflict in responsibility of looking after a newborn

 Woman dissatisfaction with self, including body image problems and eating disorders

 Lack of stable relationship with partner and parents

Signs and symptoms

Loss of interest in surrounding

Loss of usual emotional response to her family

Intense feeling of unworthiness, guilt and shame

Generalized fatigue irritability, difficulty in concentrating

Anorexia and sleep disturbances

Tense irritable appearance

Panic attacks and obsessive thoughts

Caring for the infant in a loving manner but not feeling any love or pleasure

Sadness and frequent crying

Persistent anxiety makes the woman to feel out of control

Obsessive feeling of inadequacy as a person and parent

Nursing assessment

 Assess for lack of concentration

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 Assess for lack of interest e.g. lack of previous interest in goals
 Assess for feelings of loneliness e.g. feeling uncomfortable around other people and isolating
oneself
 Assess for feelings of insecurity
 Assess for obsessive thinking
 Assess emotions e.g. feelings of emptiness, joy or love when caring for infant
 Assess for loss of self e.g. feeling that you are not the same person you used to be
 Assess for anxiety attacks e.g. palpitations, chest pains, sweating, tingling hands
 Assess for feelings of guilt e.g. feeling guilty due to belief that you’re not giving the infant
enough attention and love.
 Assess for any feeling of contemplating death e.g. feeling so low that the thought of leaving the
world is appealing to the mother

Nursing diagnosis

Ineffective individual coping related to post partum depression.

Risk for altered parenting related to post partum depression.

Alteration in bonding related to child neglect secondary to the depression.

Interventions

Assess all women for depression during pregnancy and after childbirth.

Nurses should alert the mother, partner and other family members to the possibility of postpartum
depression in the early days after birth and reassure them the short term nature of the condition

Symptoms of postpartum depression should be described and the mother encouraged to call her
healthcare provider if the symptoms become severe, fail to subside quickly or if at any time she feels
unable to function.

Allow ample time to convey a caring attitude

Recommend that the woman acknowledge her feelings and insist that others acknowledge them too

Emphasize to continued communication with the partner

Encourage continued contact with other adults

Explain the importance of good nutrition and adequate rest

Help the mother increase sensitivity to infant cries

Include family members in discussion

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Help mother identify and contact appropriate support groups

Evaluation

Expected outcome of nursing care includes;

 Signs of potential postpartum disorders are detected quickly and therapy is implemented
 The newborn is cared for effectively by the father and other support groups until the mother is
able to do so
 Mother shows love when caring for newborn
 Mother has no feelings of isolation from other people
 Mother shows no signs of anxiety
 Family members help in caring for the baby
 Mother shows increased sensitivity to infant cries

Medical management

Differential diagnosis

Clinician has to differentiate against the following disorders which need to be ruled out to establish a
precise diagnosis

 Baby blues; sometimes around third day or so the happy period ends abruptly and for 60% of
women or more ‘baby blues’ are experienced
 Pinks; during the first 3 days or so after birth most women experience a high where they feel
happy, excited, thrilled with the baby and may also experience difficulty in sleeping.
 Postnatal depression; begins some week after the baby is born. Women affected mostly
describe feeling of tiredness, irritability and anxiety.

Treatment

In the past electroconvulsive therapy was mostly used.

 Pharmacotherapy; it is continued for 6-12 months. Drugs include Amitriptyline (Elovil),

Desipramine (Norpramin), Imipramin pamoate, Fluoxetine (Prazal), Sertaline
 Counseling and psychotherapy;
Electroconvulsive therapy
Interpersonal therapy
Couples therapy

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Breast complications; Mastitis

Nipple discharge

Breast abscess
Mastitis

Inflammation of the breast.

It usually involves the glands and lactiferous tissue.

It normally occurs in the 2nd and 3rd week after birth although it may occur at any time during breast
feeding.

It’s most common in mother’s breastfeeding for the first time and it is preventable.

Causes

1. Non-infectious mastitis

It is caused by milk stasis.

Causes of milk stasis include;

- Baby not attaching to the breast properly during feeding

- Difficulties in sucking milk

- Breastfeeding infrequently

- Pressure on the breast by tight clothing

Milk stasis leads to blockage of the milk duct, breast tissue becomes inflamed because of cytokines in
the milk that the immune system uses and are passed to the baby.

The mother’s immune system attacks the cytokines mistakenly thinking they are micro-organisms.

Inflammation of the breast tissue occurs in order to stop the spreading of the supposed infection.

2. Infectious mastitis

The most common etiological organism is staphylococcus aureus. E.coli has also been thought to cause
the same.

If the milk ducts are blocked and milk stagnates there is a high likelihood of infection.

The normal flora that exists on the surface of the skin then enters the breast through cracks in the skin.

Bacteria from the baby’s mouth can also enter the breast when breastfeeding.

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Pathophysiology

With improper latching on the breast during feeding some sores and openings may develop in the
areola. The organisms which are carried on the mother’s hands, breast kin or baby’s mouth may enter
the breast through these sores and cracks.

Infection can also be caused by overgrowth of bacteria, the normal flora within the milk duct.
Overgrowth can occur if stagnant milk collects in the blocked milk ducts.

Incomplete emptying of the breasts will result in the breast being overly full and subsequent blockage of
milk ducts. There is usually engorgement and stasis of milk predisposing infection.

Constriction of the breast from bras that is too tight, interfering with normal emptying of duct.

Risk factors

Fatigue and stress lower the mother’s immune system

Primiparity

Sore and cracked nipples

Skin infection

Increased maternal age

Breast abnormalities

Failure to empty breast adequately

Wearing tight fitting bra, restrict milk flow

Diagnosis

Physical exam

Signs and symptoms

Ultrasound

Culture to examine the type of organism and type of antibiotic to give

Mammogram or breast biopsy

Signs and symptoms

Symptoms usually occur 2-4 weeks postpartum

Initial symptoms are flulike with fatigue and aching muscles

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Other symptoms include;

- Tender breast that’s warm to touch

- Chills, fever

- Tachycardia

- Malaise

- Headache

- Tension and engorgement caused by closed milk ducts

- Swelling of breasts

- Pain or burning sensation continuously when breast feeding

- Skin redness, inflamed v-shape area is seen

- Affected breast appears lumpy

- Purulent discharge may be present

Complications

Recurrence esp. in cases of delayed or inadequate treatment

Untreated mastitis may result in breast abscess

Milk stasis

Management

Antibiotic therapy

Continued decompression of the breast

Supportive measures including application of cold or ice compresses provides much relief

If mother can continue breastfeeding she should do so from both breasts or use a breast pump

The breast should be completely emptied at each feeding to prevent stasis

Massage over the affected area before, during and after feeding to ensure emptying

Mother should avoid formula supplements and avoid pressure on breast from baby carriers

Or tight bras

Encouragement sand reassurance

Health education

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The nurse should teach the mother on practices to avoid which put pressure on breast such as;

- Sleeping on stomach

- Gripping breast firmly when breast feeding

- Resting infant on breast when supine

- Pressing infants nose away from breast when feeding

- Stopping milk flow by pressing areola

Teach on clothing i.e. good fitting bras

Nursing care plan

 Assessment; right breast reddened and edematous, tender and warm to touch

 Nursing diagnosis; pain related to effects of mastitis

 Outcome identification; client will confirm she has increasing comfort

 Intervention;

Apply warm compress, instruct client in ways to apply warm moist heat with shower or at home

Urge client to breastfeed or drain breast every 1.5-2 hours

Encourage breastfeeding. Advice client to completely empty the breast each feeding

 Rationale

This promotes comfort and increasers circulation to the area thus decreasing inflammation and edema

Frequent emptying promotes lactation, aids in comfort and prevents infection

Milk is a good medium for bacteria growth. Complete emptying prevents stasis and engorgement
reducing the risk of infection and pain

 Outcome evaluation

Client states pain is reducing with treatment

Demonstrate measures to promote comfort

Right breast swelling, redness and tenderness decreasing

Breast abscess

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This is a condition whereby the breasts have pus-filled lumps which are painful and develop under the
skin of the breast

Causes

Complication of mastitis

Bacterial infection

Bacteria usually enter the breast through sores cracked nipples or breaks in the skin which can develop
during breastfeeding

Infection can also be caused by overgrowth of bacteria esp. if stagnant milk collects in the milk ducts

Pathophysiology

When bacteria enter the body, the immune system responds by sending WBCs to the area. As WBCs
fight bacteria some tissue on site die and create a hollow pocket

This pocket fills with pus from dead tissue, WBCs and bacteria, forming an abscess

As infection progresses the abscess may become bigger and more painful

Diagnosis

Physical exam

Signs and symptoms

Ultra sound to confirm if it’s an abscess or tumor

Culture for appropriate antibiotic

Signs and symptoms

Painful breast abscess

Swollen lumps that may be red

Feeling hot

Swelling of breast

Fever

Tender breast

Management

Broad spectrum antibiotics

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Mother can breastfeed with the unaffected breast and discontinued on the affected breast which is
pump-drained

For large abscess a small incision is made to drain the pus

Pump/nurse the affected breast while incision is healing to prevent engorgement, relieve pressure on
incision and to prevent mastitis

Health education

Teach on antiseptic technique when cleaning incision site

Assessment diagnosis planning Expected Nursing evaluation

outcome interventions
Reddened, Pain related to Instruct the Patient has to Analgesics Mother more
edematous the patient on how be Instruction on comfortable
warm and inflammation to apply warm comfortable how to apply and pain free
painful of breast as compresses in and pain free moist heat with
evidenced by the shower as within 24 compresses treatment
client it promotes hours
complaining of comfort and State of pain
pain decreases reduces with
inflammation treatment
Pain at nipple Ineffective Give analgesic Patient will Mother urged Mother
site, engorged breast feeding and encourage comfortably to breastfeed comfortable in
breast related to pain mother to breastfeed or empty breastfeeding
on site empty breast within the breasts within with time
every 1.5-2 first 24 hours 1.5-2 hours
hours of treatment
Weight loss, Altered Antibiotics Mother and Antibiotics Mother and
tachycardia nutrition less prescription baby recover given baby should
and than the body Continue lost weight as Decompression regain weight
engorgement requirement decompressing treatment of breast after
of the blocked related to breast when progresses Baby well fed treatment
milk ducts poor sucking feeding by mother at
response in Ensure an interval of
new born newborn is 2-3 hours
well fed Balanced diet
given to
mother

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Nipple discharge

Fluid that seeps out of the breast can either be normal or abnormal.

 Abnormal discharge

Bloody

From one breast

Spontaneous discharge without touch, stimulation or irritation to breast

Consistency varies from thick to milky thin

 Normal discharge

Released when the nipple is compressed or squeezed

Causes of normal discharge

Pregnancy; usually clear in early stage

In later stages it may turn milky

Stopping breastfeeding

Stimulation

May also occur when nipples are repeatedly chaffed by bra during physical exercise

Causes of abnormal discharge

 Fibrocystic breast changes

Fibrocystic is the presence of fibrous tissue and a cyst on the breast

This may cause lumps or thickening in the breast tissue, pain and itching

At times causes secretion of clear, white, yellow or green discharge

 Intraductal papilloma

These are non cancerous growths in the ducts of breasts

It’s the common cause of abnormal discharge when the growths become inflamed which is bloody or
sticky

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 Infections

The discharge contains pus and indicates infectious mastitis

It can occur in lactating and non lactating mothers

 Galactorrhea

This is a condition where the mother secretes a milky discharge even though she is not breastfeeding

Causes include;

- Certain medications

- Some herbs

- Hypothyroidism

- Illegal drugs

 Mammary duct ectasia

This is mostly seen in women approaching menopause

Condition results in inflammation and possible blockage of ducts located underneath the nipple

When it occurs infection may develop resulting in a thick greenish discharge

 Other causes include;

- Contraceptive pills

- Stimulation of nipple

- A type of non cancerous brain tumor called prolactinoma which increases level of prolactin

Diagnosis

Blood test

Mammogram and ultra-sound

Brain scan

Surgical excision and analysis of more ducts

Treatment

Abnormal findings from mammogram readings are often biopsied and removed

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For women with abnormal discharge they should follow a mammogram and physical exam for 1-2 years

Steroid, antifungal and antibiotic creams may be used to treat skin changes around the nipple

Teach client on breast care when breastfeeding

Removing of the blocked ducts is done right after period of examination

Puerperal psychosis
It refers to a mental disorder occurring in child birth characterized by deep depression, delusions of
infant’s death and homicidal feelings towards child.

It affects 2-3 women per 1000 births leading to psychiatric admission.

Etiology

Etiology is idiopathic.

Most women experiencing puerperal psychosis will be experiencing mental illness for the 1 st time.

 Hereditary/genetics; family history of manic depressive/bipolar disorder.

 Research shows psychosis is more related to biochemical changes more than stress factors

 Previous post partum psychosis

 Pre natal stressors e.g. lack of social support

 Ante natal and post natal factors-demands of the baby

-anxieties about parenting abilities
- Responsibilities of looking after baby
 Most common in primigravida

Pathophysiology

Onset is very sudden, commonly occurring within the 1 st post natal week and rarely before the 3rd post
partum day. Majority presenting before the 11 th day.

Symptoms are florid, presenting dramatically and very early tending to change very rapidly, altering
from day to day during the acute phase of the illness.

There are changes of mood states; irrational behavior and agitation, fear and perplexity as woman
quickly loses touch with reality.

Signs and symptoms

 Restlessness

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 Agitation

 Confusion

 Suspicion

 Insomnia

 Episodes of mania making the woman hyper active

 Talking rapidly and incessantly

 Being overactive and elated

 Neglect of basic needs

 Profound depressive mood

 Loss of memory and concentration

 Mood swings sometimes with inappropriate emotion

 Difficulties with lactation

 Reduced sexual response

 Thought process is disordered and chaotic. She is likely to hallucinate and become delusional

Diagnosis

Clinical diagnosis based on signs and symptoms by careful observation of woman’s behavior.

Encourage the mother to express her feelings about the baby’s arrival. This is a screening tool to identify
the coping ability of the mother.

Assess history of manic behavior.

Nursing management

During assessment, document any past history of psychiatric disturbances stating onset, duration and
treatment given.

Refer to mental health team.

Do not admit the mother in the general psychiatric ward for safety of both mother and baby.

Woman should be admitted in a specialist mother and baby unit with an out of area referral if necessary.

For women with a past history of psychiatric illness management begins pre conception and throughout
antenatal period

Hospitalization enables the woman to develop effective relationship with her infant and skills necessary
to be an able mother.

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The woman will eventually be assessed for her ability to take care of her baby and her needs to continue
this care back in the community.

Family education

Family counseling may be needed to enable family members understand more about the illness and
required care.

Family advised to contact physician immediately symptoms recur. They are told to monitor mother for
signs e.g. neglect of baby.

Family advised to offer emotional support, assist with house chores and care of baby.

Family teaching on importance of compliance with the medication and some of the expected side
effects.

Medical management

Pharmacotherapy

Medical options include use of atypical antipsychotic agents and mood stabilizers or anti-manic agents
e.g. lithium on anti-epileptic drugs.

Although monotherapy is preferable, some need more than one drug to achieve a desirable level of
symptom control and illness remission.

Neuroleptics

Important as initial part of treatment.

They will achieve sedation, reduced perplexity, fear, distress within 2 days.

The drug of choice is lithium bicarbonate.

 Lithium; very useful in the manic phase.

Used in treatment as well as prophylaxis.

Before admin, renal and thyroid functions are assessed 5 days before starting treatment.

Drug levels checked every 6-12 months after stabilizing.

Monitor for side effects

Monitor for lithium toxicity. To avoid this correct sodium and fluid level imbalances in the body patients
to avoid thiazides and non steroidal anti inflammatory drugs.

Normally the mother is advised to use alternative method of feeding the infant e.g. formula milk as the
drug is secreted in milk and can accumulate to toxic levels in the baby.

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For mothers who cannot afford formula or who insist on breastfeeding signs of lithium toxicity are to be
monitored in the baby.

In cases of relapse lithium carbonate or another mood stabilizers will be used for 6-12 months post
partially and up to 2 years prophilactically if a woman presents with post partum manic depressive
disorder.

 Anti depressants

Takes about 2 weeks for effectiveness hence not good for immediate management.

Medication continued to 6 months to avoid relapse.

 Electroconvulsive therapy (ECT)

It is used to induce convulsions using electric current.

Especially efficient in risk of suicide.

 Psychotherapy

This is done preferably by the psychiatrist.

Supportive psychotherapy that begins prior to hospital discharge may incorporate parenting skills and
infant interventions to address maternal infant bonding and infant development.

Other psychotherapy options e.g. family focused therapy, cognitive behavioral therapy or interpersonal
therapy

Complications

1) Suicide—majority of post partal maternal suicides were the sequel of puerperal psychosis and
severe depressive illness.
2) Infanticide—mother may kill the baby due to disturbed mental function

Follow up

Careful discharge plan is developed before the patient leaves the hospital.

Referral to intensive outpatient therapy along with closely spaced outpatient follow up visits is advisable
for first several weeks after discharge.

Prognosis

Post partum psychotherapy responds well to psychological interventions.

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Most women recover from puerperal psychosis. However there is risk of mental illness with subsequent
pregnancies.

Improvement is seen in 95% of women within 2-3 months.

There is 10-25% recurrence in subsequent pregnancies.

Risk of recurrence is highest if the woman has another baby within 2 years of recovery.

Prevention

Prompt detection

Appropriate referral

Early intervention

Effective and vigorous management

ADITIONAL NOTES FOR YOUR READING.

Amniocentesis
It is also referred to as amniotic fluid test or AFT.

It is a medical procedure involving aspiration of a small amount of amniotic fluid containing fetal tissues
sampled from the amnion or amniotic sac surrounding a developing fetus and fetal DNA is examined for
genetic abnormalities.

The fluid extracted contains tissue cells from the amnion and fetal skin, lungs and urinary tract.

The cells are grown in culture media allowing chromosomal, genetic, biochemical and molecular
biological analysis.

It is an invasive procedure posing risk to both mother and fetus.

Amniocentesis is usually done when a woman is about 12 weeks pregnant as there is sufficient fluid
around the baby and there is also sufficient amniotic fluid pressure.

The use of ultra sound has greatly reduced the risk associated with amniocentesis.

Indications for amniocentesis

Advanced maternal age i.e. above 35 years

Previous child with;

- Neural tube defects

- Chromosomal abnormalities e.g. down’s syndrome

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- Birth defect

Positive antenatal screening tests such as;

- Fetal ultra sound findings

- Raised maternal serum alpha fetoprotein

A history of;

- Parent carrying balanced chromosomal translocation

- Risk of recessively inherited metabolic disorder

- Mother carrying X- linked disorder

- Mother exposed to certain drugs or infections that cause fetal malformations

Analysis to detect specific conditions from;

- DNA e.g. fragile X syndrome, sickle cell disease

- Enzymatic activity in amniocytes

Procedure

Explain the procedure to the mother to allay any anxiety and ensure informed consent statement

Ask the mother to empty bladder by urinating

Ask her to maintain supine position

Drape the mother leaving only the abdomen and ask her to assume the left lateral position to prevent
supine hypotension and move the uterus off the IVC

Attach fetal heart monitors and uterine contraction monitors and take maternal BP and fetal heart rate
as baseline values

Do an ultrasound to locate fetus and placenta and to identify the largest pocket of amniotic fluid

Using an antiseptic solution wash the abdomen while observing aseptic technique

Local anesthesia is then administered

A 20-22 gauge needle is used and slight pressure on needle

Amniotic fluid is then withdrawn, the needle is removed and the woman rests quietly for about 30
minutes. 10-20 ml of fluid is then aspirated or approx. 1 ml per week of gestation.

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If the mother has Rh negative blood, an injection of anti-D immunoglobin is given to avoid Rh disease

Procedure in mid-trimester amniocentesis

Normally performed in the 2nd trimester from 14-16 weeks gestation

There is relatively more amniotic fluid enough for reliable cell culture about 20 mls

There is still time to terminate the pregnancy if the results indicate this to be advisable

Procedure in early amniocentesis

This has been conducted at 9-14 weeks

Less fluid is removed and ultrasound guidance is essential

Carries a higher risk of loss of pregnancy

Preferred over CVS where CVS is unreliable in twin pregnancies

Diagnostic testing of amniotic fluid

Amniocentesis usually reveals the following;

1) Genetic problems

Early in pregnancy, amniocentesis can be used to diagnose genetic and chromosomal disorders.

Rapid testing which reveals results in 24-72 hours is done to identify;

- Down’s syndrome

- Edward’s syndrome

- Patau’s syndrome

- Turner’s syndrome

- Klinefelter’s syndrome

- Sex chromosome abnormalities

2) Fetal lung maturity

In pregnancies greater than 30 weeks, the fetal lung maturity may be tested by sampling the amount of
surfactant in the amniotic fluid.

These tests include;

I. Lecithin sphingomyelin ratio

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These are protein components of lung enzyme surfactant that the alveoli begin to form within the 22 nd
and 24th week of pregnancy.

After amniocentesis L/S ratio is taken.

L/S ratio of 2:1 is acceptable as lung maturity.

L/S ratio of less than 2:1 indicates that the fetal lungs maybe surfactant deficient.

However, the results may be less reliable with maternal diabetes as the fetus tends to develop lecithin
pathways early but immature overall.

II. Phosphatidylglycerol PG presence

These are additional phospholipids in surfactant.

Their pathways mature at 35-36 weeks gestation.

Their presence indicates fetal lung maturity.

3) Alpha fetoprotein and acetyl cholinesterase

These tests for neural tube defects

Normal source is fetal urine if fetus has open body defects

Acetyl cholinesterase usually increases if neural tube defects are present

4) Direct DNA analysis

Techniques used to detect Tay Sachs disease phenylketonuria Duchene’s muscular dystrophy and cystic
fibrosis

5) Enzyme analysis

Mainly used for detecting inborn errors of metabolism

6) Bilirubin levels

The amount of bilirubin in amniotic fluid indicates amount of fetal RBC destruction which can be used to
detect isoimmune hemolysis and also analyze blood incompatibility.

7) Color of amniotic fluid

Amniotic fluid is the color of water. In late pregnancy, it may have a slight yellow tinge.

Strong yellow color indicates Rh incompatibility related to bilirubin secondary to RBC hemolysis.

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Green color suggests meconium staining and therefore assess for fetal distress

Risks and complications of amniocentesis

Maternal complications

 Amnionitis; infection of amniotic fluid

 Anxiety, caused by delay in diagnosis

 Amniotic fluid leakage

 Uterine bleeding

 Uterine cramping

 Hemorrhage from penetration of placenta

 Damage to intestines or bladder

 amniotic fluid embolism

 preterm labor

 miscarriage

 Rh disease of mother

Fetal complications

 Fetal trauma

 Hemorrhage

 Clubfoot

 Inconclusive results

Nursing and patient considerations

Reduce anxiety related to the procedure by;

- Explaining the procedure

- Informed consent

Reduce pain and discomfort related to the procedure by;

- Asking the mother to lie comfortably on her back with hand and a pillow on her head

- Allowing adequate time between infiltration of local anesthesia and introduction of needle in
amniotic sac

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Avoid potential traumatic injury to fetus, placenta and mother by;

- Have the woman empty bladder if fetus is above 20 weeks

- Locate the placenta using ultra sound

- Obtain maternal vital signs after 20 minutes. Fetal heart rate are also taken to serve as a
baseline data to evaluate possible complications
- Monitor the woman during and after the procedure for signs of premature labor

- Inform the woman to report signs of bleeding, unusual fetal activity or abdominal pain,
cramping or fever while at home

Caesarean delivery
Caesarean section is an operative procedure that is carried out under anesthesia whereby the fetus,
placenta and membranes are delivered through an incision in the abdominal wall and uterus.

This is usually done after viability has been reached that is 24 weeks of gestation onwards

Types of caesarean section

1. Elective caesarean section

This is whereby the woman is booked around term at a time convenient for mother and surgeon. It can
also be scheduled caesarean sections when it becomes clear that early delivery is required but there is
no immediate compromise to mother or fetus.

Definitive indications

Cephalopelvic disproportion

Major degree of placenta praevia

High order multiple pregnancies

Possible indications

Breech presentation

Moderate to severe pre-eclampsia

Medical condition that warrants the exclusion of maternal effort

Diabetes mellitus

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Intrauterine growth restriction

Ante partum hemorrhage certain fetal abnormalities e.g. hydrocephalus

2. Emergency caesarean section

This is carried out when adverse conditions develops during pregnancy or labor.

Indications

 Ante partum hemorrhage

 Cord prolapse
 Cephalopelvic disproportion
 rupture (dramatic / scar dehiscence)
 fulminating pre-eclampsia
 eclampsia
 failure to progress in the 1st and 2nd stage of labor and fetal compromise if delivery is not
imminent

Types of incisions

1. Uterine incisions

a) Low segment transverse incision made transversely in the lower segment of the uterus;

 Incision is made in the thinnest portion so blood loss is minimal and easier to open

 Lower segment is the area of least uterine activity

 Post operative convalesce is more comfortable

 Possibility of later rapture is lessened

 Incidence of post operative adhesion and danger of intestinal obstruction is lessened

 It is the incision of choice

b) Classic vertical incision is made directly into the wall of the body of the uterus usually done in
emergency situations only.
 Useful when bladder and lower segment are involved in extensive adhesion

 Selected in anterior placenta praevia or emergency situation

 Useful when fetus is in a transverse lie

 Increased blood loss with classic CS

 Increased risk of uterine rapture in subsequent

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c) T-extension (low transverse with vertical incision made in the middle of the horizontal incision)

 It may be extended upwards in a classical incision if extra room is needed in delivery

 Commonly used in preterm deliveries

2. Abdominal incisions

a) A horizontal incision right above the pelvic hairline.

 Cosmetic advantage of not being seen because pubic hair covers the incision

 Decreased chance of dehidence or hernia formation

b) A vertical incision made in the midline of the abdomen below the umbiliens to the pubis.
 Quicker procedure to perform
 Provides better uterine visualizations
 Cosmetically less appealing
 Greater chance of wound dehidence and hernia formation
Management

 NPO except possible ice chips during labor

 A blood sample should be typed and screened and should be made available to be cross
matched if needed, a complete blood count is obtained
 Anesthesia, regional or general depends on the indication for surgery

 Permit is signed and witnessed; informal consent observed

 A large bore IV is established and Foley catheter is inserted

 An antacid is administered to reduce gastric acidity and risk of aspiration pneumonia

 Antibiotics may be given prophilactically

 An abdominal prep is done and a grounding pad for elecrocautery is applied

Complications

 Increase in morbidity and mortality compared to vaginal birth

 Hemorrhage, endometritis
 Paralytic ileuses, intestinal obstruction
 Pulmonary embolism, thrombophlebitis
 Anesthesia accidents
 Bowel or bladder injury
 Anaphylactic syndrome of pregnancy

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 Respiratory depression of infant from anesthetic drugs
 Possible delay in mother infant bonding

Nursing assessment

Before delivery;

 Assess knowledge of procedure

 Perform admission assessment comparable to those used for labor and delivery admission(if not
already admitted i.e. elective or routine)
 Obtain 20-30 minute fetal tracing strip to access fetal and uterine status if needed

 Ensure informed consent is obtained, permits signed and witnessed

 Monitor maternal and fetal vital signs

 Determine maternal blood type and Rh

 Determine last time woman ate or drank

 Identify drug allergies or any other allergies

During delivery;

 Continue fetal assessment until abdominal preparation has been initiated. The FHR can still be
assessed during sterile technique and a doptone (place in sterile glove) if the start of the surgery
is delayed beyond 5 mins (high-risk) and 15 mins (low-risk) after abdominal preparation is
completed. If fetal spiral electrode is in place continue abdominal prep is completed(it should be
removed before birth but this is not required)
 Monitor and record maternal vital signs, FHR, condition of skin before incision and woman’s
emotional status.
 Maintain an awareness of how the support person is doing and assist as needed.

 Monitor and document maternal neonatal status before transport to recovery room and help
with transfer as needed

After delivery;

 Assess maternal vital signs every 15 mins the 1 st hour, every 30 mins the 2nd hour and then
hourly she is transferred to the post partum/labor and delivery unit or per year facility protocol.
a. Respiratory; airway patency, oxygen needs, rate/quality/depth of respirations,
auscultation of breath sounds, oxygen saturation readings.
b. Circulation; BP, pulse, ECG, color

c. LOC; orientation and response to verbal/tactile/painful stimulation.

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 Assess postpartum status at the same intervals ; fundal positions and contractions, condition of
incision and abdominal dressing , maternal-neonate attachment, lochia(color, amount), neonate
condition
 Assess hourly intake and output (IV, urine output) and bowel sounds

 Perform pain assessment; evaluate level of anesthesia, medications given (amount, time/
results)

Nursing diagnosis

Anxiety related to caesarean delivery

Acute pain and discomfort related to traumatized tissue

Risk for infection related to traumatized tissue

Risk for ineffective parent/infant attachment related to interruption in benching process.

Nursing interventions

Relieving anxiety;

Explain the reason for the CS delivery.

Answer any question the woman or her support may have about the CS delivery.

Allow the support to attend the birth.

Explain that a sensation of pressure will be experienced during the delivery and little pain will occur and
any pain should be reported to the nurse.

Explain the procedures before doing them for instance;

a. Insert Foley catheter, note amount and color of urine. If epidural anesthesia is being used delay
this until after it is administered.
b. Administer preparative medication according to the primary care providers’ orders.

c. Position the woman on the surgical table with a wedge in place

d. Prepare abdomen in accordance with facility policy

e. Apply grounding device

f. Ensure availability of neonatal team as well as availability and proper working order of
resuscitation equipment
g. Perform duties of circulating nurse in accordance with facility policy

h. Assist with post operative preparation of patient for transport to recovery room.

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Promoting comfort

a. Encourage use of relaxation techniques after pain medication is given

b. Monitor for respiratory depression up to 24 hours after epidural oploid admin

c. Use of backrub and a quiet environment to promote effectiveness of medication

d. Support and splint abdominal incision when coughing or deep breathing

e. Encourage frequent rest periods and place “DO NOT DISTURB” sign on door during rest and
sleep
f. To reduce pain caused by gas, encourage ambulation, use of rocking chair and lying on stomach
as much as possible

Preventing infection

a. If skin prep involves shaving, it should be done carefully to prevent nicks in skin and careful
surgical skin prep
b. Post operatively, use aseptic technique when changing wound dressing

c. Provide perineal care as well along with vital signs every 4 hours

d. Provide post operative care measures to prevent urinary or pulmonary infections

Promoting effective bonding

a. Encourage woman an support to talk about their feelings before and after delivery

b. When talking about the birth refer to it as caesarean delivery or birth rather than a surgical
procedure implying that it’s just another birth method
c. Encourage mother child bonding as soon as possible

d. Emphasize that adjustment to parenting under any circumstances are necessary and normal

Expected outcome/evaluation

a. Verbalizes an understanding of the caesarean procedure and post delivery care

b. Report relief of pain

c. Participates in care of self and infant

d. Has no signs of infection

Patient and family education;

Teach the woman the football hold for breastfeeding so the infant is not lying on its stomach.

101
Teach the woman to observe signs of infection;

a. Foul smelling lochia

b. Elevated temperature

c. Increased pain

d. Redness

e. Edema at incision site

And to report immediately

Assist woman in planning for the assistance of family, friends or hired help at home during period
immediately after discharge.

102
103