Childbirth is the culmination of a human pregnancy or gestation period with the birth of one or more newborn infants from a woman’s uterus.  The process of normal childbirth is categorized in three stages of labour: the shortening and dilation of the cervix, descent and birth of the infant, and birth of the placenta.

Stage 1

Onset of regular painful contractions, effacement of the cervix and dilation of the cervical Os to full dilatation.

Latent phase - cervix dilates slowly for the first 3 cm – may take hours.

Active phase- average cervical contraction is 1cm/hr in nulliparous women and 2cm/hr in multiparous women.

Stage 2

From full dilatation of the Os to the birth of the baby.

Passive stage - full dilatation → head reaches the pelvic floor and women experience a desire to push.

Active stage – when mother is pushing, pressure of the head on the pelvic floor produces a desire to bear down and push with contractions.

Stage 3

From the birth of the baby to the expulsion of the placenta & membranes.

Takes around 15 minutes on average

Small amount of blood and the cord lengthens.

Uterine contractions compress blood vessels supporting the placenta which shears away from the wall.

It’s really important to be able to take an thorough obstetric history, because missing something could potentially have a huge impact on both mother and unborn child.  This particular history has a number of questions that are not part of the standard history taking format and therefore it’s important to be aware of just what information an obstetric history requires.

Presenting complaint

Give the patient time to explain the problem/symptoms they’ve been experiencing. 

You can then move on to more focused questioning.

Pregnancy history

Last Menstrual Period – first day
EDD – dates or scan (LMP + 9 months + 7 days)
Menstrual cycle

• Regularity
• Duration (normal 28 day cycle?)
• Flow? – heavy/light – can be useful to ask number of sanitary towels/tampons

Contraceptive use? – COCP, POP, Depot, Implant
How was pregnancy confirmed?
Any other scans or tests whilst been pregnant? – dating scan, anomaly scan

Symptoms of Pregnancy

Nausea / Vomiting - if severe known as hyperemesis gravidarum
Urinary frequency – pressure on the bladder causes this – rule out UTI
Tiredness
Breast Changes – increase in glandular tissue – lactation
Fetal Movements - usually felt at around 18-20 weeks gestation, earlier in multips
Cravings

Ideas, Concerns & Expectations…

Previous Obstetric History

Gravidity – number of times a woman has been pregnant, regardless of outcome

Parity –  X = (any live or still birth after 24 weeks) |    Y = (number lost before 24 weeks)

Details of each pregnancy:

• Date / Year
• Place of birth
• Gestation
• Mode of delivery

Baby – sex, weight, current health

Problems during antenatal, labour & postnatal

Miscarriages & Terminations

Past Gynae History

Last Cervical Smear – was the result normal? – CIN?

Any gynae surgery:

- Loop excision of transitional zone (LETZ) -↑ risk of cervical incompetence
- Previous C-sections - ↑ risk of uterine rupture / placenta accreta /adhesions

Gynae investigations & treatment for:

- Infertility
- Ectopic – ↑ risk of future ectopics
- PID - chlamydia is most common cause – ↑ risk of ectopic

Past Medical History

Any hospital admissions?- when, where & why?
Any operations – abdominal or gynae?

Thromboembolic disease – previous PE/DVT – high risk in following pregnancy
Diabetes – tight glycaemic control is essential – congenital defects, macrosomia 
Epilepsy – some medications are teratogenic - needs neurologist input
Hypothyroidism – TFT’s need close monitoring to keep them normal – Cretinism
Hypertension – patients BP may rise through pregnancy – PIH/Pre-eclampsia

Drug History

Pregnancy medication - folates, iron, anti-emetics, antacids

Teratogenic drugs – avoid at all costs - ACEi, Retinoids, Sodium Valproate, Methotrexate

OTC Drugs - make sure to ask patient about these, to ensure nothing unsafe

Recreational drug use – cocaine can cause placental abruption, alcohol causes FAS

ALLERGIES

Family History

Medical conditions - gestational diabetes
Inherited genetic conditions – CF
Pregnancy Loss - recurrent miscarriages in mother & sisters 
Pre-eclampsia - in mother or sister? – increased risk

Social History

Smoking – How many smoked and for how long? – strongly encourage to stop

Alcohol – Get specific! – How much?, How often?, Everyday? Type of alcohol?

Drug use- Recreational, IV

Living Situation – House or bungalow? Who lives with you? Is there support if needed?

Relationship Status – Married, Single

Activities of Daily Living - How are you coping at home?

Occupation - Maternity leave arranged, light duties?

Systemic Enquiry

Cardiovascular – Chest pain, PND, Orthopnoea, SOB, Cough, Ankle swelling, Palpitations, Cyanosis

Respiratory – Cough, Sputum, Haemoptysis, Chest Pain, SOB, Tachypnoea, Hoarseness, Wheezing

GI – Appetite, Diet, Nausea, Indigestion, Dysphagia, Pain,  Bowel habit, Haematemesis, Jaundice

Urinary – Frequency, Dysuria, Polyurea, Urgency, Hesitancy, Nocturia, Back pain, Incontinence

Nervous System – Visual/other senses, Headache, Fits/Faints, LOC, Weakness, Numbness

Musculoskeletal – Pain in muscles, bones & joints, swelling, gait

Dermatology - Skin changes, dryness, ulcers, rashes

Introduction

Introduce yourself

Wash Hands

Ask if patient has any pain anywhere before you begin

Explanation

Describe what you are going to do

Gain consent

Get a chaperone!!

Inspection

Position patient to the supine position

Expose abdomen from xiphisternum to the pubic symphysis

Inspect the abdomen

Asymmetry

Foetal Movements

Surgical Scars

Cutaneous Signs of Pregnancy:

• Linea Nigra
• Striae Gravidarum
• Striae Albicans

Palpation

Ask about tenderness before starting!

Measure symphyseal-fundal height

• Palpate using ulnar border of left hand moving from sternum downwards
• Locate the fundus of the uterus (firm feeling)
• Locate upper border of pubic symphysis
• Measure distance in cm
• The distance should correlate with gestational age (+/- 2cm)

Determine foetal lie

Fundal Palpation

Do this with both hands to identify which pole of foetus is at fundus

Lateral Palpation

Palpate either side of uterus, moving down to determine where the fetal back lies

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Pelvic Manoeuvre

Turn to face patients feet

Press down on either side of lower uterus to determine presenting part

The head will be ballotable (be gentle)

How many 5th’s palpable?

Foetal head is divided into fifths in the coronal plane

If you are able to feel the entire head in the abdomen it is 5/5th’s palpable (not engaged)

If you are not able to feel the head at all abdominally it is 0/5th’s palpable (fully engaged)

Auscultation

Use a Pinard’s stethoscope

You have already identified the fetuses back

Place over anterior fetal shoulder (scapulae)

To complete the examination

Re-cover patient - allow patient to re-dress in privacy

Thank Patient

Wash Hands

Summarise Findings - “fundal heigh is 36cm which is in keeping with the current gestation.  The foetus is in a longitudinal lie, with cephalic presentation, 2/5th’s palpatable with a regular heart rate”

What is the gonadal axis?

The gonadal axis comprises of the interaction between the hypothalamus, pituitary gland and the gonads.  The system works together to regulate development, reproduction, ageing and many other body processes.  It’s regulation relies upon a number of complex negative feedback loops which when lost result in disease.

How the male gonadal axis works

1. The hypothalamus secretes GnRH

• Testosterone is required for spermatogenesis and many other important biological processes

• ABG is a protein which binds to testosterone & keeps it within the seminiferous tubules
• Inhibin helps support spermatogenesis and inhibits production of FSH, LH and GnRH

8. ↑ levels of testosterone & inhibin cause -ve feedback on the pituitary & hypothalamus

9. This results in decreased production of LH & FSH

10. As a result production of testosterone & inhibin is also decreased

How the female gonadal axis works

1. The hypothalamus secretes GnRH

2. GnRH travels down to the anterior pituitary gland

3. It binds to receptors on the pituitary gland

4. This causes release of LH (luteinizing hormone) & FSH (follicle stimulating hormone)

5. LH & FSH travel in the blood stream to the ovaries

6. When LH & FSH bind to the ovaries they stimulate production of oestrogen & inhibin

• Oestrogen helps regulate the menstrual cycle & is essential in many body processes
• Inhibin causes inhibition of activin which is usually responsible for stimulating GnRH production

7. Increasing levels of oestrogen & inhibin cause -ve feedback on the pituitary & hypothalamus

8. This leads to decreased production of GnRH, LH & FSH

9. This in turn results in decreased production of oestrogen and inhibin

What is Pre-eclampsia?

Pre-eclampsia is a disease of pregnancy involving the development of both hypertension as well as proteinurea. The disease appears to be caused by release of various factors from the placenta which results in widespread endothelial cell dysfunction & organ damage. Pre-eclampsia can develop anytime from 20 weeks gestation until up to 6 weeks post-partum. The earlier pre-eclampsia develops the higher the risk of serious complications. The only way to cure pre-eclampsia is to deliver the baby & remove the placenta as this is central to the disease process. Pre-eclampsia is a major cause of poor pregnancy outcome for both mother & foetus and is associated with significant mortality, therefore early recognition & intensive management can make a huge difference.

What is the mechanism of Pre-eclampsia?

The most accepted theory currently suggests the following mechanism¹,²;

1. The placenta (trophoblast) does not implant adequately into the uterine wall

2. As a result the blood supply to the placenta is relatively poor

3. This results in under-perfusion of the placenta causing hypoxia of the placental tissue

4. The hypoxic placenta releases inflammatory factors triggering an exaggerated immune response

5. The immune attack results in further release of inflammatory mediators & substances causing vasoconstriction

6. As a result the mothers blood vessels endothelial lining is damaged & peripheral vascular resistance increases

7. Increased peripheral vascular resistance results in the development of hypertension

8. Hypertension causes further damage to blood vessels & major organs including the kidney’s, which leak protein as a result

Risk factors

Patient factors

Maternal age >40

Ethnicity - african american’s have increased risk³

Obesity – BMI > 35

Family history of pre-eclampsia – mother or sister

Pregnancy factors

Previous pre-eclampsia

First pregnancy

Multiple pregnancy

Change of partner

Assisted reproduction techniques

Pre-existing conditions

Obesity

Diabetes mellitus

Chronic hypertension

Chronic renal disease

Thombophillia – anti-phospholipid syndrome

Symptoms & Signs

Mild

Hypertension

Significant proteinurea (>0.3g in 24hrs)

Often women are not aware of any symptoms in the early stages

Severe

Severe headache – usually frontal

Epigastric pain

Vomiting

Severe oedema - face, hands, legs, feet

Papilloedema – flashing lights, reduced vision

Reduced foetal movements - foetal distress

Intrauterine Growth Restriction

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HELLP syndrome

HELLP syndrome can develop in severe pre-eclampsia

It is a serious disorder involving the liver & the clotting system

It’s main features are;

• Haemolysis
• Elevated Liver enzymes
• Low Platelets

Diagnosis

Both Hypertension & Proteinurea must be present for the diagnosis of Pre-eclampsia to be confirmed

Hypertension

A pregnant women may classed as having hypertension in a number of ways¹

These include;

• ≥140/90mmHg on 2 occasions more than 4 hours apart
• Systolic BP of 30mmHg above the booking systolic BP
• Diastolic BP of 15-25mmHg above booking diastolic BP

Proteinurea

>0.3g in 24-hrs

This approximates to 1+ or more on a urine dipstick

Investigations

Blood pressure monitoring

Urinalysis - protein, microscopy, culture & sensitivities

24 hour urine collection

FBC - monitor RBC for drops suggesting haemolysis

LFT – monitor liver enzymes for signs of HELLP syndrome

U&E – monitor renal function (hypertension can cause renal failure)

Clotting – if suspicious of HELLP

Management

Regular monitoring

Regular checking of;

• BP – hypertension
• Urine – proteinurea

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Admission to hospital

Women may need admitting to hospital if they display any of the following¹;

• If BP >170/110mmHg or 140/90mmHg with 2+ proteinurea
• Significant symptoms
• Abnormal biochemistry/ haematology
• Significant proteinurea
• Requires antihypertensive treatments
• Signs of foetal compromise

Antihypertensives

The aim is to reduce the diastolic BP to <100mmHg¹

• Labetalol – oral/IV
• Nifedipine – oral
• Hydralazine – IV

Avoid use of Atenolol, ACE Inhibitors or Angiotensin receptor blockers

.

Anti-seizure medication

Given if there is significant risk of eclampsia

• Magnesium sulphate - IV – Membrane stabiliser

It halves the risk of eclampsia!¹

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Fluid restriction

Vascular permeability is increased in pre-eclampsia

As a result fluid excess fluid spills into the extravascular compartments

If too much fluid is given it can result in pulmonary oedema

If too little fluid is given it can result in renal failure

Therefore controlling fluid intake reduces risk of fluid overload or depletion

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Delivery of baby

Delivery is the only cure for pre-eclampsia
However the woman needs to be stable before this can be done
If foetus is <34 weeks then steroids should be given
Delivery can be delayed only if pre-eclampsia is controlled – regular monitoring required
Delaying delivery may improve perinatal outcome but increases risk to the mother
A balance must be struck between foetal & maternal wellbeing

Eclampsia

Eclampsia is a life threatening complication of pregnancy which can occur if pre-eclampsia is not controlled & becomes severe. It is characterised by the appearance of tonic clonic seizures. Eclampsia can cause coma & death in a very short period of time, therefore immediate action should be taken³.

Symptoms

Tonic Clonic Seizure:

• Sudden loss of consciousness
• Tonic Phase - body becomes rigid & lasts for 15-20 seconds
• Clonic Phase - rapid contraction & relaxation of muscles causing forceful jerking of entire body

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Coma

Death - 1 in 50 women will die from eclampsia

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Effect’s on the foetus

Foetal distress

Bradycardia

Reduced variability on CTG

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Placental abruption

High risk of abruption in eclampsia

The foetus becomes hypoxic as a result

Death or serious brain damage can occur

Management

ABC

Place patient on left side – avoids aortocaval compression¹

Secure airway

Give high flow oxygen

.

Antihypertensives

Labetalol, Nifedipine, Hydralazine

Given at higher doses than in routine pre-eclampsia

The aim is to stabilise BP before delivering baby via C-section

.

Magnesium sulphate

Has membrane stabilising effects reducing neuronal excitability

It halves the risk of eclampsia

Also reduces maternal mortality

.

Delivery of baby

C-section is used as it is less demanding on the body & much quicker

Carried out as soon as women is stable

Even if foetus is very premature you have to deliver

Otherwise mother will undergo multiple organ failure & die

References

1. Drife JO, Magowan (eds). Clinical Obstetrics and Gynaecology, chapter 39, pp 367-370. ISBN 0-7020-1775-2.

2. Courtney Reynolds, MD, William C. Mabie, MD, & Baha M. Sibai, MD (2006). “Preeclampsia”. Pregnancy – Hypertensive Disorders. Armenian Medical Network. Retrieved 2006-11-23.

3. Douglas KA, Redman CW (November 1994). “Eclampsia in the United Kingdom”. BMJ 309 (6966): 1395–400. PMC 2541348.PMID 7819845.

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What is the menstrual cycle?

The menstrual cycle is a complex series of physiological changes occurring in women on a monthly basis.  It results in production of an ovum & thickening of the endometrium to allow for implantation if fertilisation should occur.  The menstrual cycle is orchestrated by the endocrine system through the complex interaction of the hypothalamus, pituitary and gonads.  The entire cycle lasts around 28 days, with the cycle beginning on the first day of menstruation & ovulation occurring around day 14.

How is it controlled?

1. The hypothalamus produces Gonadotrophin Releasing Hormone (GnRH)

2. This binds to the pituitary stimulating release of;

• Luteinizing hormone (LH)
• Follicle Stimulating Hormone (FSH)

.

3. FSH binds to the ovaries stimulating;

• Development of  ovarian follicles
• Secretion of oestrogen
• Secretion of inhibin

The follicle most sensitive to FSH becomes dominant & is known as the Graafian follicle

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4. LH binds to the ovaries causing;

• Production of oestrogen which is required for ovulation & thickening of the endometrium
• Conversion of the Graafian follicle into the progesterone producing corpus luteum
• Progesterone causes the endometrium to become receptive to implantation of a fertilised ovum

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5. Oestrogen, Progesterone & Inhibin all cause -ve feedback on the pituitary & hypothalamus

6. This results in reduction of GnRH, FSH & LH production

7. In pregnancy GnRH, FSH & LH all remain inhibited, causing cessation of menstruation

Phases of the menstrual cycle

Follicular Phase

1. At the start of the cycle levels of FSH rise causing stimulation of a few ovarian follicles

2. As follicles mature they compete with each other for dominance

3. The 1st follicle to become fully mature will produce large amounts of oestrogen

4. This inhibits the growth of the other competing follicles

5. The 1 follicle reaching full maturity is called the Graafian follicle (oocyte develops within this)

6. The Graafian follicle continues to secrete increasing amounts of oestrogen

.

7. Oestrogen causes;

• Endometrial thickening
• Thinning of cervical mucous to allow easier passage of sperm

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8. Oestrogen also initially inhibits LH production from the pituitary gland

9. However when the ovum is mature, oestrogen reaches a threshold level which conversely causes a sudden spike in LH around day 12

10. The high amounts of LH cause the membrane of the Graafian follicle to become thinner

11. Within 24-48 hours of the LH surge, the follicle ruptures releasing a secondary oocyte

12. The secondary oocyte quickly matures into an ootid & then into a mature ovum

13. The ovum is then released into the peritoneal space  & is taken into the Fallopian tube via fimbriae (finger like projections)

Luteal Phase

14. Once ovulation has occurred the hormones LH & FSH cause the remaining graffian follicle to develop into the corpus luteum
15. The corpus luteum then begins to produce the hormone progesterone

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16. Increased levels of progesterone result in;

• Endometrium becoming receptive to implantation of the blastocyst
• Increased production of oestrogen by the adrenal glands
• Negative feedback causing decreased LH & FSH (both needed to maintain the corpus luteum)
• Increase in the woman’s basal body temperature
  
  .

17. As the levels of FSH & LH fall, the corpus luteum degenerates

18. This results in progesterone no longer been produced

18. The falling level of progesterone triggers menstruation & the entire cycle starts again

19. However if an ovum is fertilised it produces hCG which is similar in function to LH

20. This prevents degeneration of the corpus luteum (continued production of progesterone)

21. Continued production of progesterone prevents menstruation

22. The placenta eventually takes over the role of the corpus luteum (from 8 weeks)

The Uterine Cycle

The uterus has it’s own cycle which is driven by the cyclical release of hormones by the ovaries which we’ve previously talked about.  The inside lining of the uterus is known as the endometrium. The endometrium is the part of the uterus most affected by these changes in hormone levels.

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It is composed of 2 layers;

• Functional layer – this grows thicker in response to oestrogen & is shed during menstruation
• Basal layer - this forms the foundation from which the functional layer develops – it is not shed

Phases of the uterine cycle

The uterine cycle has 3 phases known as the proliferative, secretory & menstrual phases

Proliferative phase

During the proliferative phase the endometrium is exposed to an increase in oestrogen levels caused by FSH & LH stimulating the ovaries. This oestrogen causes repair & growth of the functional endometrial layer allowing recovery from the recent menstruation & further proliferation of the endometrium.

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Continued exposure to increasing levels of oestrogen causes;

• Increased endometrial thickness
• Increased vascularity -spiral arteries grow into the functional endometrial layer
• Development of increased numbers of secretory glands

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Secretory phase

The secretory phase begins once ovulation has occurred

This phase is driven by progesterone produced by the corpus luteum

It results in the endometrial glands beginning to secrete various substances

These secretions make the uterus a more welcoming environment for an embryo to implant

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Menstrual phase

At the end of the luteal phase the corpus luteum degenerates (if no implantation occurs)

The loss of the corpus luteum results in decreased progesterone production

The decreasing levels of progesterone cause the spiral arteries in the functional endometrium to contract

The loss of blood supply causes the functional endometrium to become ischaemic & necrotic

As a result the functional endometrium is shed & exits out through the vagina

This is seen as the 3-5 day period of menstruation a woman experiences each month

Window of fertility

A woman’s most fertile period is between 5 days before ovulation until 1 to 2 days after

Women can therefore use knowledge of their cycle to improve chances of conception

Women may also monitor symptoms that suggest they are about to ovulate such as;

• Basal body temperature measuring – it spikes during the LH surge  24-48 hours before ovulation
• Thinning of cervical mucous

Symptoms experienced in the menstrual cycle

Abdominal pain & cramps

Heavy vaginal bleeding

Vaginal pain

Nausea

Diarrhoea

Sweating

Fatigue

Irritability

Dysphoria (unhappiness)

References

1. Uterine cycle image - http://legacy.owensboro.kctcs.edu/gcaplan/anat2/notes/Image719.gif

Ignore any Accelerations or Decelerations

A normal foetal heart rate is between 110-150 bpm¹

Foetal bradycardia is defined as a baseline heart rate less than 120 bpm.

Mild bradycardia of between 100-120bpm is common in the following situations:

• Post-date gestation
• Occiput posterior or transverse presentations

Severe prolonged bradycardia (< 80 bpm for > 3 minutes) indicates severe hypoxia

Causes of prolonged severe bradycardia are:¹

• Prolonged cord compression
• Cord prolapse
• Epidural & Spinal Anaesthesia
• Maternal seizures
• Rapid foetal descent

If the cause cannot be identified and corrected, immediate delivery is recommended

Variability

Baseline variability refers to the variation of foetal heart rate from one beat to the next

Variability occurs as a result of the interaction between the nervous system, chemoreceptors, barorecptors & cardiac responsiveness.

Therefore it is a good indicator of how healthy the foetus is at that moment in time.

This is because a healthy foetus will constantly be adapting it’s heart rate to respond to changes in it’s environment.

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Normal variability is between 10-25 bpm³

To calculate variability you look at how much the peaks & troughs of the heart rate deviate from the baseline rate (in bpm)

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Variability can be categorised as: ⁴

• Reassuring – ≥ 5 bpm
• Non-reassuring – < 5bpm for between 40-90 minutes
• Abnormal – < 5bpm for >90 minutes

..

Reduced variability can be caused by: ³

• Foetus sleeping - this should last no longer than 40 minutes – most common cause
• Foetal acidosis (due to hypoxia) – more likely if late decelerations also present
• Foetal tachycardia
• Drugs – opiates, benzodiazipine’s, methyldopa, magnesium sulphate
• Prematurity – variability is reduced at earlier gestation (<28 weeks)
• Congenital heart abnormalities

 .

Accelerations

Accelerations are an abrupt increase in baseline heart rate of >15 bpm for >15 seconds

The presence of accelerations is reassuring

Antenatally there should be at least 2 accelerations every 15 minutes¹

Accelerations occurring alongside uterine contractions is a sign of a healthy foetus

However the absence of accelerations with an otherwise normal CTG is of uncertain significance

Decelerations are an abrupt decrease in baseline heart rate of >15 bpm for >15 seconds

There are a number of different types of decelerations, each with varying significance

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Early deceleration

Early decelerations start when uterine contraction begins & recover when uterine contraction stops

This is due to increased foetal intracranial pressure causing increased vagal tone

It therefore quickly resolves once the uterine contraction ends & intracranial pressure reduces

This type of deceleration is therefore considered to be physiological & not pathological³

Variable deceleration

Variable decelerations are seen as a rapid fall in baseline rate with a variable recovery phase

They are variable in their duration & may not have any relationship to uterine contractions

They are most often seen during labour & in patients with reduced amniotic fluid volume

Variable decelerations are usually caused by umbilical cord compression¹

• The umbilical vein is often occluded first causing an acceleration in response
• Then the umbilical artery is occluded causing a subsequent rapid deceleration
• When pressure on the cord is reduced another acceleration occurs & then the baseline rate returns
• Accelerations before & after a variable deceleration are known as the “shoulders of deceleration”
• There presence indicates the foetus is not yet hypoxic & is adapting to the reduced blood flow.

Variable decelerations can sometimes resolve if the mother changes position

The presence of persistent variable decelerations indicates the need for close monitoring

Variable decelerations without the shoulders is more worrying as it suggests the foetus is hypoxic

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Late deceleration

Late decelerations begin at the peak of uterine contraction & recover after the contraction ends.

This type of deceleration indicates there is insufficient blood flow through the uterus & placenta

As a result blood flow to the foetus is significantly reduced causing foetal hypoxia & acidosis

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Reduced utero-placental blood flow can be caused by: ¹

• Maternal hypotension
• Pre-eclampsia
• Uterine hyper-stimulation

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The presence of late decelerations is taken seriously & foetal blood sampling for pH is indicated

If foetal blood pH is acidotic it indicates significant foetal hypoxia & the need for emergency C-section

 …

Prolonged deceleration

A deceleration that last more than 2 minutes

If it lasts between 2-3 minutes it is classed as Non-Reasurring

If it lasts longer than 3 minutes it is immediately classed as Abnormal

Action must be taken quickly – e.g. Foetal blood sampling / emergency C-section

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Sinusoidal Pattern

This type of pattern is rare, however if present it is very serious

It is associated with high rates of foetal morbidity & mortality ¹

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It is described as:

• A smooth, regular, wave-like pattern
• Frequency of around 2-5 cycles a minute
• Stable baseline rate around 120-160 bpm
• No beat to beat variability

A sinusoidal pattern indicates:

• Severe foetal hypoxia
• Severe foetal anaemia
• Foetal/Maternal Haemorrhage

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Immediate C-section is indicated for this kind of pattern.

Outcome is usually poor

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Overall impression

Once you have assessed all aspects of the CTG you need to give your overall impression

The overall impression can be described as either: ⁴

• Reassuring
• Suspicious
• Pathological

The overall impression is determined by how many of the CTG features were either reassuring, non-reassuring or abnormal. The NICE guideline below demonstrates how to decide which category a CTG falls into.⁴

References

Click to show

Primary Postpartum Haemorrhage

Primary postpartum haemorrhage (PPH) is defined as loss of more than 500ml of blood from the genital tract within 24 hours of delivery¹

PPH can be described as minor or major depending upon the level of blood loss;

• Minor PPH involves the loss of of anything up to 1000mls of blood
• Major PPH involves the loss of more than 1000mls of blood

Causes

Causes of postpartum haemorrhage include uterine atony, trauma, retained placenta, and coagulopathy. These causes are often referred to as the ”four Ts” Tone (uterine atony) Trauma (lacerations) Tissue (retained placenta)  Thrombin (coagulopathy)2

Uterine atony

Uterine atony is the most common cause of PPH account for around 70% of cases.² It occurs due to the uterus losing its muscle tone.  As a result it does not contract after delivery and therefore the uterine vessels are not clamped down on allowing large amounts of bleeding to occur.  The uterus can become atonic for a number of reasons such as prolonged labour (the uterus tires out) or multiple birth (the uterus is large & stretched making it less effective at contracting)

Retained placenta

Retained placenta accounts for around 10% of cases of PPH.² It results from either all or part of the placenta been retained within the uterus. This prevents the uterus from contracting fully and therefore the uterine vessels are not occluded & continue to bleed.

Vaginal or Vulval Lacerations

Vulval & vaginal lacerations account for most of the other 20% of PPH cases.² They occur due to the mechanics of birth and can be very severe.  They must be monitored for some time afterwards to ensure no infection develops and proper healing occurs.

Coagulopathy

Around 1% of PPH cases occur as a result of coagulapathy.² Common causes of coagulopathy include haemophilia A or B.   It’s important to rule out coagulopathy as it can result in the death of a patient if not identified early.

Risk factors

Pregnancy factors³

Placenta praevia (15 x risk)

Multiple pregnancy (5 x risk)

Pre-eclampsia (4 x risk)

Previous PPH (3 x risk)

Nulliparity (first childbirth) (3 x risk)

Placental abruption

Delivery factors³

Emergency caesarian section (9 x risk)

Retained placenta (5 x risk)

Elective caesarian section (4 x risk)

Mediolateral Episiotomy

Prolonged labour (>12 hours)

Big baby (>4kg)

Maternal factors³

Obesity – BMI >35 (2 x risk)

Asian ethnicity

Haemophilia (type A or B)

Anaemia (<9g/dl)

Age > 40 years

Symptoms & Signs

Symptoms³

Prolonged & worsening vaginal bleeding after delivery

Passing many large clots

Lower abdominal pain

Pelvic pain

Light headedness / Fainting

Shortness of breath

Signs

Pale skin

Tachycardia

Tachypnea

Hypotension

Tender abdomen

Fever

Decreased consciousness

Investigations³

Vaginal examination – determine source of bleeding

Abdominal examination – tender abdomen suggests uterine bleeding

FBC – sudden drop in Hb suggests acute blood loss

Clotting – prolonged PT & APTT suggest disseminated intravascular coagulation

Blood pressure – low BP indicates blood loss

Pulse rate – usually tachycardia present due to hypovolaemic shock

Oxygen saturation – may be decreased to decreased red blood cells & Hb

Hourly urine output - if decreased suggests blood volume loss

ECG

Complications

Hypovolaemic Shock 

HELLP – Haemolysis, Elevated Liver Enzymes, Low Platelets

Disseminated Intravascular Coagulation – due to consumption of clotting factors

Management ³

Minor PPH

If minor PPH with no clinical signs of shock;

• Contact obstetric doctor
• Get IV access with two 14 gauge cannula’s
• Crystalloid infusion
• Crossmatch 2 units of blood
• BP, Pulse & Oxygen Saturation
• FBC
• Clotting
• Regular clinical monitoring & observation

Major PPH

Contact senior clinical staff

Call Obstetric registrar & alert Consultant

Call Anaesthetic registrar & alert Consultant

Experienced Midwife

Alert consultant haematologist on call

Alert blood transfusion lab

Call porters to transfer specimens & blood products quickly

Airways & Breathing

Check airway - if compromised get anaesthetist to secure airway

Give Oxygen at 10/15 L/min

.

Circulation

Secure IV access with two 14 gauge cannula’s

Blood sample should be taken & sent for;

• FBC
• Coagulation
• U&E
• Crossmatch – 4 units
• Renal & Liver function tests

Resuscitation

Position patient in supine position

Keep patient warm - bear-hugger

Transfuse blood as soon as possible - give 4 units of fresh frozen plasma for every 6 units of blood

.

Until blood is available infuse;

• up to 3.5 litres of warmed crystalloid Hartmann’s solution
• and/or 1-2 litres of colloid as rapidly as required

.

Give platelets if PLT count <50 x 10⁹

Give cryoprecipitate if fibrinogen <1g/L

Stopping the bleeding

In uterine atony try each of the following measures in turn until bleeding stops;

• Bimanual uterine compression (rubbing up the fundus) – stimulates contractions
• Syntocinon - 5 units – slow IV injection
• Ergometrine – 0.5mg – slow IV injection
• Syntocinon infusion - 40 units in 500 ml Hartmann’s solution at 125 ml/hour
• Carboprost - 0.25 mg by intramuscular injection every 15 mins (max of 8 doses) 
• Carboprost - intramyometrial – 0.5mg
• Misoprostol - 1000mg rectally

If pharmacological measures fail, surgical treatment should be initiated in the following order;

• Intrauterine balloon tamponade – blood inside uterus to compress vessels
• Haemostatic brace suturing - large sutures around uterus to compress it
• Bilateral ligation of uterine arteries
• Bilateral ligation of internal iliac arteries
• If bleeding will not stop hysterectomy must be performed - do not hesitate with decision

Intensive monitoring

Prevention

Active management of the 3rd stage of labour reduces maternal blood loss & chances of PPH

Prophylactic oxytocics should be offered to all women as they reduce chances of PPH by 60%

• Low risk vaginal delivery – oxytocin – 5 or 10 IU’s – IM injection
• Caesarian section – oxytocin – 5 IU – slow intravenous infusion

 Secondary Postpartum Haemorrhage

Secondary PPH presents as abnormal bleeding from the genetical tract anytime from 24 hours after delivery until up to 6 weeks postpartum.

Causes

Infection (Endometritis) – 1-3% of spontaneous vaginal deliveries

Retained products of conception 

Examination

Tachycardia

Fever

Rigors

Tender abdomen (suprapubic)

Fundus may be elevated in cases of retained products

Investigations

FBC - low Hb may suggest significant blood loss

MSU - could give pain & haematuria which may be confused with PPH

High vaginal swab – can confirm presence of infection

USS -often can be normal despite retained products been present

Blood cultures – may show septicaemia

Management³

Speculum examination

Look for signs of inflammation

Rule out lacerations

Identify clots preventing closure of cervical OS

Clots can then be removed at the time

Antibiotics

If antibiotics are indicated combination of ampicillin and metronidazole is appropriate. 

If patient has endomyometritis (tender uterus) or sepsis, gentamicin should also be used

Surgery

Surgical measures should be undertaken if there is excessive or continuing bleeding

• Regardless of ultrasound findings
• Surgical evacuation of retained products of conception – consultant required

References

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