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Obstetrics Flashcards

1
Q

What is eclampsia?

A

It is defined as the occurence of more than or equal to 1 convulsion in a pre eclamptic woman

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2
Q

What are the clinical features of eclampsia?

A

Tonic clonic seizure lasting 60-75 seconds with a variable lasting post ictal phase

Headache

Hyperreflexia

Epigastric/RUQ Pain

Oedema

Visual disturbance

N+V

Jaundice

Convulsions may cause foetal distress andbradycardia

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3
Q

What investigations would you do for eclampsia?

A 
FBC- low HB, low platelets 
U and Es- raised urea, creatinine, urate 
LFTs- raised ALT, AST and bilirubin 
Blood glucose 
Clotting studies

US- ? Placental abruption

CTG- foetal distress and bradycardia

CT/MRI head - if querying seizures

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4
Q

What is the management of eclampsia?

A

Resucitation:
A to E assessment
Lie patients in a left lateral positon with a secured airway and oxygen therapy

Seizure cessation with magnesium sulfate once decision to deliver is made

IV bolus of 4g over 5-10mins then 1g/hr and treat further fits with a 2g bolus

Blood pressure control- IV labetalol/hydralazine aiming for BP <120mmHg

Delivery once mother is stable (c section)

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5
Q

What ate the complications of Eclampsia?

A

For mother- HELLP syndrome, DIC, cerebrovascular haemorrhage, AKI, ARDS

Foetal- IUGR, prematurity, RDS, placental abruption, intra uterine death

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6
Q

What are the risk factors for shoulder dystocia?

A 
Pre labour: 
Previous shoulder dystochia 
Macrosomia
Maternal diabetes
Maernal BMI>30 and IOL

Intrapartum: prolonged labour, oxytocin, assisted vaginal delivery

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7
Q

How would you manage shoulder dystocia?

A

Advise mum to stop pushing
Apply axial traction
Consider epiostomy

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8
Q

What are the manouevers used for shoulder dystocia?

A 
Mcroberts manoeuvre (hyperflex and abduct the maternal hips and tell the mum to stop pushing) 
Suprapubic pressure

If this doesnt work then posterior arm removal or internal rotation

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9
Q

What are the complications of shoulder dystocia?

A

For mother- PPH, tears, pelvic floor weakness, temporary nerve damage

For foetus- humerus/clavicle fracture, brachial plexus injury, hypoxic brain injury (umbilical cord compressed in pelvic inlet)

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10
Q

What is a umbilical cord prolapse?

A

This is where the umbilical cord descends through the cervix with/before the presenting part of the foetus
There are a few types; occult, ovet, and cord presentation

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11
Q

What are the risk factors for chord prolapse?

A 
Breech 
Unstable lie
Artificial ROM with foetal staton 
Polyhydramnios 
Prematurity 
Multiple pregnancy
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12
Q

How should you manage someone with cord prolapsion?

A

Keep cord warm and moist and avoid handling
Manually elevate the presenting part off the cord by DV exam
Re position the mother to relieve the pressure on cord from presenting part…

  • knee position on all fours
  • left lateral lie

Consider tocolysis (this relaxes the uterus and stops comtractions and therefore relieves pressure of the cord)

Delivery is by emergency c section and instrumental delivery if the cervix is fully dilated and presenting part is low

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13
Q

What are the causes for foetal asphyxia in cord prolapse?

A

Occlusion by presenting part of foetus pressing on the umbilical cord

Arterial vasospasm- exposure of the umbilical cord to the cold atmosphere results in umbilical arterial vasospasm, reducing blood flow to the foetus

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14
Q

What is PPPH defined as?

A

PV blood loss within 24 hours of delivery

Minor PPH: 500-1000ml blood loss
Major PPH: >1L blood loss

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15
Q

What causes PPPH?

A

Tone- uterine atony (most common) where the uterus fails to contract adequately

Tissue- retention of placental tissue

Trauma- damage sustained during delivery

Thrombin- coagulopaghies and vascular abnormalities

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16
Q

What are the risk factors for PPPH?

A

Mother: >40, BMI >25, asian, previous PPH
Uterine overdistension: multiple pregnancy, polyhydramnios, macrosomia
Placental problems- placenta praevia, placenta accreta, placental abruption, pre eclampsia
Labour- IOL, prolonged >12 hours
Delivery- precipitate delivery, shoulder dystocia, instrumental, episiotomy, C section

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17
Q

What are investigations and management needed for PPPH?

A 
FBC 
G+S and X match 4-6 units of blood 
Coagulation progile 
U and Es 
LFTs 
Examine placenta 
Immediate management; 
15L 100% O2 via. NRBM 
Insert two 14G cannulas 
Give cross matched blood 
Until then give 2L warmed crystalloid, 1-2L warmed colloid, O negative blood or uncross matched group specific blood

Catheterise

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18
Q

What is the definitive management of PPPH?

A 
Stopping PPH: 
Uterine massage 
Bimanual compression 
Tranexamic acid 
Massive obstetric haemorrhage call

Fluds and blood
Crystallid- up to 2L hartmanns
Colloid- up to 1.5L until blood arrives
Blood should he given when available, O neg, group specific or cross matched depending on urgency
Fresh frozen plasma: 4 units FFP to every 4 units blood or if clotting prolonged

Platelets are given if PLT <75 and bleeding is ongoing

Cryoprecipitate if fibrinogen <2

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19
Q

Give two examples of uretotonic drugs?

A

Oxytocin

Misoprostol

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20
Q

What is secondary PPH associated with?

A

Endometritis
Or retained products of conception

Mothers may need abx +/- surgical evacuation of retained products

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21
Q

What investigations would you want for SPPH?

A

Bloods- FBC, G+S, X match, coagulation (may need FFP), u and Es, cultures

Pelvic USS- can diagnose retained placental tissue

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22
Q

What is the treatment of secondary PPH?

A

Abx- ampicillin and metronidazole
Gentamicin added if endometritis or overt sepsis
Uterotonics- oxytocin, sytrometrine, carboprost, misoprostal)
Intrauterine balloon tamponade if excessive bleeding

Massive SPPh may be managed the same as PPPH

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23
Q

What is an amniotic fluid embolism caused by?

A

Either strong contractions (IOL)
Polyhydramnios (more amniotic fluid to move)
Disruption of the vessels supplying the uterus

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24
Q

What are the clinical features of amniotic fluid embolism?

A 
Dyspnoea 
Tachycardia 
Hypotension 
Hypoxia 
Cyanosis 
Seizures
Arrythmias 
Cardiac arrest
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25
Q

What happens to people who experience an amniotic fluid embolism?

A

If they survive, 30 minutes later they may develop DIC and then ARDs

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26
Q

What are the differentials for Amniotic fluid embolism?

A 
PE
Anaphylaxis
Sepsis
Eclampsia
MI
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27
Q

What investigations and management is used for amniotic fluid embolism?

A

There are no diagnostic tests but can do…
Bloods- FBC, UEs, ABG, vlotting studies, calcium and magnesium

ECG (ischaemic changes)

CXR (pulmonary oedema)

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28
Q

How do you treat amniotic fluid embolism?

A

Resucitate via A to E approach

Treat DIC

If the mother is stable then continous goetal monitoring with a view to delivery imminently

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29
Q

What are the three types of breech?

A

Complete breech
Frank breech
Footling breech

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30
Q

What are the risk factors for breech?

A

Uterine- multiparity, uterine malformations, fibroids, placenta praevia

Foetal- prematurity, macrosomia, polyhydramnios, oligohydramnos, multiple pregnancies

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31
Q

How should you treat breech?

A

External cephalic version
Casarean section
Vaginal breech birth

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32
Q

When can external cephalic version be offered?

A

ECV should be offered from 36 weeks in nulliparous women and 37 weeks in multiparous women

It involes manipulation of the foetus to a cephalic presentation through the maternal abdomen to enable a vaginal delivery

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33
Q

When is ECV contraindicated and what should you do instead?

A 
APH within last 7 days
Abnormal CTG 
Major uterine  anomaly 
Ruptured membranes
Multiple pregnancy 
Placenta praevia

C sectoon!
Foetal abnormalities
Pre eclampsia
Hypertension

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34
Q

What are the contraindications to vaginal breech birth.

A

Footling or kneeling breech
Large or small foetus
Previous c section
Hyper extended foetal neck

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35
Q

What is oligohydramnios?

A

Amniotic fluid which is below the 5th centile for the gestational age

Amniotic flis increases steadily intil 33 weeks, then plateus at 33-38 and then declines
Amniotic fluid at term is 500ml

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36
Q

What is PPROM?

A

A pregnancy complication where the sac (amniotic membrane) surrounding the baby breaks (ruptures) before week 37 of pregnancy

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37
Q

What causes oligohydramnios?

A

PPROM
Placental insufficiency (blood flow is redistributed to the brain rather than abdo and kidneys- causing poor urine output)
Renal agenesis (potters syndrome- a complete absence of one or both kidneys)
Non functioning foetal kidneys
Obstructive uropathy
Gentic/ chrosomal abnormalities
Viral infections (may also cause polyhydramnios)

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38
Q

What are the Ix for amniotic fluid volume?

A

USS to either measure max pool depth or amniotic fluid index

Once oligohydramnios is diagnosed it is essential to identify the cause…

Symphysis- fundal height to look for IUGR
Speculum to look for PPROM
USS to look for structural abnormalities

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39
Q

What is the prognosis of a foetus with oligohydramnios?

A

It is associated with prematurity
Also amniotic fluid allows the foetus to move limbs in utero and therefore without it the foetus can develop severe muscle contractures leading to disability

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40
Q

What is polyhydramnios?

A

An amniotic fluid index that is above the 95th centile for the gestational age

41
Q

What are the causes of polyhydramnios?

A

Idiopathic in most cases
Any condition that prevents the foetus from swallowing- oesophageal atresia, CNS abnormalities, muscular dystrophies, congenital diaphragmatic hernia (obstructs oesophagus)

Duodenal atresia (DOUBLE BUBBLE)

Anaemia

Twin to twin transfusion

Viral infection

Maternak diabetes

Maternal ingestion of lithium

Macrosomia

42
Q

How do you investigate polyhydramnios?

A

USS
Once polhydramnios is diagnosed it is essential to identify the cause…

USS- foetal size, structural abnormalities, doppler (to assess anaemia) 
Maternal glucose tolerance test 
Karyotyping 
TORCH 
T= toxoplasmosis
Other= parvovirus
R= rubella 
C= CMV 
H= hepatitis
43
Q

What are the risks with polyhydramnios?

A

Pre term labour due to over distension of uterus

Underlying congenital abnormality

Malpresentation

Cord prolapse

44
Q

What is placenta abruption?

A

Partial or complete seperation of the placebta from the uterus prior to delivery

45
Q

What are the causes of APH?

A

Vasa praevia
Placental abruption
Placental praevia

Or may just be due to local reasons like trauma or cervical pathology

46
Q

What are the risk factors for placental abruption?

A 
Previous PA 
Low lying placenta
Multiple pregnancy 
Polyhydramnios 
Cocine
Smoking
IUGR 
Pre eclampsia
47
Q

What are the risk factors for placenta praevia?

A

Placenta praevia can be minor/partial or major/complete

Previous c section 
Previous TOP
Age >40 
Multiparity 
Smoking
Multiple pregnancy
48
Q

What happens if placenta is low at 20 weeks?

A

It often is therefore you need to repeat the scan at 32 weeks, if the placenta covers the internal os or is within 2cm then you need to do a c section

49
Q

What is placenta praevia associated with?

A

Previous C sections!!!

50
Q

How should you manage vasa praevia?

A

Elective C section at 35-37 weeks

51
Q

What is the typical history od vasa praevia?

A

Bleeding from spontaneous rupture of membranes, it is fetal not maternal blood that is lost

52
Q

How is severity of APH determined?

A

Minor=<50mls and stopped

Major= 50-1000mls, no signs of shock

Massive= >1000mls or signs of shock

53
Q

What questions do you want to ask with APH?

A 
When 
What
Associated with waters breaking?
Quantity?
Provoked by sexual intercourse?
Abdo pain?
54
Q

What examination components are important with APH?

A

Basic observations- look for features of shock…

Abdo palpation- is the uterus stony hard suggesting abruption?

Speculum- can you see the bleeding

Do not perform vaginal exam if known placenta praevia (USS)

55
Q

How do you manage APH?

A

The following steps are critical to the management of any APH.

ABCDE approach
Fluid resuscitation
Blood products (as needed)
Escalate to multidisciplinary seniors (obstetrics, anaesthetics, midwifery, neonatal).
Mother and baby stable - discuss with a consultant, consider induction of labour
Induction of labour is by artificial rupture of membranes & syntocinon
The aim should be for a vaginal delivery if possible
The same management is considered if the mother is stable with intrauterine death (IUD)
Mother and baby unstable - discuss with consultant, emergency C-section
Anticipate post-partum haemorrhage

56
Q

What is the management of APH in long term?

A

When the mother has mild spotting only and the baby is deemed okay, they can be considered for discharge. Mothers with bleeding heavier than spotting need to be admitted and monitored for a minimum of 24 hours following the bleed and until it stops.

If there is an unexplained minor APH, but settles, mothers can be discharged with a plan for serial growth ultrasound to assess for the following:

Oligohydramnios
Pre-term pre-labour rupture of membranes (PPROM)
Intra-uterine growth restriction (IUGR)
Premature delivery
Need for C-Section
In the presence of an APH, steroids should be considered for fetal lung maturation if at 24-34+6/40. If the mother is > 37/40 with minor or major APH, and both mother and baby are well, then the recommendation is for induction of labour (IOL). Confirmation that there is no placenta praevia is essential prior to IOL.

57
Q

What are the complications of APH?

A

The complications of an APH can be divided into either maternal or foetal/neonatal.
Maternal

Need for emergency caesarean section
Anaemia
Need for blood transfusion
Disseminated intravascular coagulation (DIC)
Organ failure
Death
Foetal/Neonatal
Premature delivery
Hypoxic injury
Anaemia
Intra-uterine death
Neonatal death
58
Q

What is pre eclampsia?

A

Complication of pregnancy characterised by hypertension and proteinuria with or without oedema

59
Q

What can severe cases of pre eclampsia cause?

A

Seizures (eclampsia)
Multi organ failure (in particular liver and kidneys)
Significant coagulopathy

60
Q

What is gestational hypertension?

A

New onset hypertension after 20 weeks gestation

61
Q

What are the risk factors for pre eclampsia?

A

History of hypertensive disease during previous pregnancy

Chronic kidney disease

Autoimmune disease (SLe/antiphospholipid)

Type 1 or type 2 diabetes

Chronic hypertension

First preg

> 40

BMI >35

FHx

Multiple pregnancy

62
Q

What can you use to prevent pre eclampsia?

A

Aspirin 75-150mg OD from 12 weeks until birth

63
Q

When is onset of pre eclampsia normally?

A

Onset is after 34 weeks

When its before 34 weeks it classified as early onset

64
Q

What are the symptoms, signs of pre eclampsia?

A

Symptoms

Headaches
Abdo pain
Vision changes
Vomiting

Signs 
Altered mental status
Dyspnoea 
Clonus 
Oedema
65
Q

What are the investigations of pre eclampsia?

A

Combination of hypertension (after 20 weeks) and proteinuria

Bedside

  • blood pressure
  • vital signs
  • urine dipstick and culture
  • albumin: creatinine ratio (if high- theres more proteinuria)

Blood tests
FBC (falling platelet counts may indicate HELLP)

Renal function- serum creatinine should be monitored for signs of developing AKI

LFTs- become elevated in HELLP

Clotting screen- coagulopathy may develop

USS or CT if headache and concerns of acute intracranial event

66
Q

Whatis the management of pre eclampsia?

A 
Admit
Labetalol
BP monitor
Get senior 
Blood tests twice a week
USS and CTG and repeat USS every 2 weeks
67
Q

What are the complications of Pre eclampsia?

A

HELLP syndrome (haemolysis, elevated liver enzymes, low platelets)

DIC

Life-threatening coagulopathy where wide-spread activation of the clotting system leads to micro-thrombi formation and consumption of clotting factors. It can lead to haemorrhage and multi-organ failure.

68
Q

When is hyperemesis gravidarum likely to be resolved by?

A

20 weeks

69
Q

What id the triad of hyperemesis gravidarum?

A

> 5% pre pregnancy weight loss
Dehydration
Electrolyte imbalance

70
Q

What contributes to the development of hyperemesis gravidarum?

A

Beta hCG high levels

71
Q

What electrolyte abnormality would you get with hyperemsis gravidarum?

A

Hypokalaemia causing weakness, malaise, arrythmias

72
Q

What are the differentials for hyperemesis gravidarum?

A 
Gastroenteritis
Acute pancreatitis
PUD
Gastritis
H.pylori infection
Cholecystitis
Urinary tract infections
Metabolic conditions (e.g. DKA)
Drug-induced nausea & vomiting
73
Q

What scoring system can be used for hyperemesis gravidarum?

A

PUQE-24

74
Q

What is associated with hyperemesis gravidarum?

A

Molar pregnancy

75
Q

What are the investigations of hyperemesis gravidarum?

A

The investigations ordered depend on the severity of symptoms; checking electrolytes, monitoring blood sugar and assessing for starvation ketosis may all be indicated.
Bedside

Vital signs
Blood sugar
Urine dipstick (in particular ketones)
MSU
Bloods

FBC
Urea and electrolytes
In refractory cases or for patients with previous admissions:

Liver function tests
Amylase
Thyroid profile
Bone profile (for calcium & phosphate)
Magnesium
ABG/VBG
Ultrasound

An USS is used to confirm a viable intrauterine pregnancy. It can also identify multiple pregnancies or trophoblastic disease (e.g. molar pregnancy).

76
Q

What is the management of hyperemesis gravidarum?

A

Management involves supportive measures including antiemetics and appropriate fluid rehydration.
The management is dependent on the severity of symptoms and follows the guidelines set out by RCOG. The options include outpatient care, ambulatory care and inpatient management (see below). Antiemetics are central to the management of nausea and vomiting in pregnancy and hyperemesis:

First-line options: cyclizine, prochlorperazine, promethazine, chlorpromazine
Second-line options: metoclopramide, domperidone
Third-line options: corticosteroids (initially hydrocortisone IV converted to prednisolone orally when able)
Fluid replacement and maintaining good hydration is important. In those managed as an inpatient or via ambulatory care, IV replacement can be given. The fluid of choice is normal saline with potassium supplementation as appropriate. Dextrose should not be given without first administering (and giving further doses of) Pabrinex to avoid precipitating a Wernicke’s encephalopathy.

In more severe cases ongoing monitoring of electrolytes with appropriate replacement is indicated.

77
Q

What is gestational diabetes

What are the complications

A

Diabetes triggered by pregnancy
Caused by reduced insulin sensitivity during pregnancy, resolves after birth

Most significant immediate complication is macrosomia and large for dates baby
This causes shoulder dystocia

78
Q

What are the risk factors for gestational diabetes?

A

Previous gestational diabetes
Previous macrosomic baby (≥ 4.5kg)
BMI > 30
Ethnic origin (black Caribbean, Middle Eastern and South Asian)
Family history of diabetes (first-degree relative)

79
Q

What is the screening test for gestational diabetes?

A

OGTT
Used when there are risk factors or features suggesting gestational diabetes- large for dates fetus, polyhydramnios (increased amniotic fluid), glucose on urine dipstick

80
Q

What are the normal results for fasting glucose?

A

Fasting: < 5.6 mmol/l
At 2 hours: < 7.8 mmol/l
Results higher than these values are used to diagnose gestational diabetes.

81
Q

What is the management of gestational diabetes?

A

Patients with gestational diabetes are managed in joint diabetes and antenatal clinics, with input from a dietician. Women need careful explanation about the condition, and to learn how to monitor and track their blood sugar levels. They need four weekly ultrasound scans to monitor the fetal growth and amniotic fluid volume from 28 to 36 weeks gestation.

The initial management suggested by the NICE guidelines (2015) is:

Fasting glucose less than 7 mmol/l: trial of diet and exercise for 1-2 weeks, followed by metformin, then insulin
Fasting glucose above 7 mmol/l: start insulin ± metformin
Fasting glucose above 6 mmol/l plus macrosomia (or other complications): start insulin ± metformin

Glibenclamide (a sulfonylurea) is suggested as an option for women who decline insulin or cannot tolerate metformin.

82
Q

How do you manage pre existing diabetes in a pregnant woman?

A

Before becoming pregnant, women with existing diabetes should aim for good glucose control. They should take 5mg folic acid from preconception until 12 weeks gestation.

Women with existing type 1 and type 2 diabetes should aim for the same target insulin levels as with gestational diabetes. Women with type 2 diabetes are managed using metformin and insulin, and other oral diabetic medications should be stopped.

Retinopathy screening should be performed shortly after booking and at 28 weeks gestation. This involves referral to an ophthalmologist to check for diabetic retinopathy. Diabetes carries a risk of rapid progression of retinopathy, and interventions may be required.

NICE (2015) advise a planned delivery between 37 and 38 + 6 weeks for women with pre-existing diabetes. (Women with gestational diabetes can give birth up to 40 + 6).

A sliding-scale insulin regime is considered during labour for women with type 1 diabetes. A dextrose and insulin infusion is titrated to blood sugar levels, according to the local protocol. This is also considered for women with poorly controlled blood sugars with gestational or type 2 diabetes.

83
Q

What is the postnatal care for women wirh diabetes?

A

Diabetes improves immediately after birth. Women with gestational diabetes can stop their diabetic medications immediately after birth. They need follow up to test their fasting glucose after at least six weeks.

Women with existing diabetes should lower their insulin doses and be wary of hypoglycaemia in the postnatal period. The insulin sensitivity will increase after birth and with breastfeeding.

Babies of mothers with diabetes are at risk of:

Neonatal hypoglycaemia
Polycythaemia (raised haemoglobin)
Jaundice (raised bilirubin)
Congenital heart disease
Cardiomyopathy

Babies need close monitoring for neonatal hypoglycaemia, with regular blood glucose checks and frequent feeds. The aim is to maintain their blood sugar above 2 mmol/l, and if it falls below this, they may need IV dextrose of nasogastric feeding.

TOM TIP: If you remember two complications of gestational diabetes, remember macrosomia and neonatal hypoglycaemia. Babies become accustomed to a large supply of glucose during the pregnancy, and after birth they struggle to maintain the supply they are used to with oral feeding alone.

84
Q

What is intrahepatic cholestasis of pregnancy?

A

Liver disease unique to liver disease unique to pregnancy that is characterised by pruritus and elevated bile acids

85
Q

Why is ICP important to recognise?

A

It is associated with increased risk of fetal demise and stillbirth
Particularly when the bile acid concentration is >100micromol/L

86
Q

What are the pregnancy associated liver disease?

A

Intrahepatic cholestasis of pregnancy (ICP)
HELLP syndrome (haemolytic anaemia, elevated liver function tests, low platelets)
Acute fatty liver of pregnancy (AFLP)
Liver dysfunction in pre-eclampsia
Liver dysfunction in hyperemesis gravidarum

87
Q

What Ix are done for obstetric cholestasis?

A

Bile acids
LFTS
Bilirubin
Imaging (liver US)

88
Q

What is the principal treatment of ICP?

A

Ursodeoxycholic acid
The American College of Obstetricians and Gynaecologists and authors of Uptodate generally recommend active management (i.e. induction of labour) based on bile acid levels.

Bile acids ≥ 100 micromol/L: consider delivery at 36 weeks gestations. Certain situations may warrant even earlier delivery (e.g. excruciating/unremitting maternal pruritus)
Bile acids < 100 micromol/L: consider delivery at 36-39+0 weeks gestation. Consider delivery at diagnosis if diagnosed >39+0 weeks.

CTG continously should be used in labour

89
Q

When will the pruritis go with intrahepatic cholestasis of pregnancy?

A

A few days after delivery

90
Q

What are the medical indications for C section?

A

Breech presentation
Multiple pregnancy
Tranmission of bloodborne viruses (HIV)
Placenta praevia

91
Q

What are the emergency indicators of C section?

A

The decision to conduct an emergency caesarean section should be made by a senior obstetrician.
Clear communication with the mother and family is essential as is with all members of the MDT to ensure a timely and safe birth. Indications include:

Cord prolapse
Antepartum haemorrhage
Foetal distress
Failure to progress

92
Q

What are the considerations for c section?

A

Pre operative considerations….

Blood tests: all patients require a full blood count to identify anaemia pre-operatively. Haemorrhage is a complication of caesarean section with blood loss > 1000ml occurring in around 4-8% of cases. According to NICE, patients who are otherwise well do not require group and saves or clotting screens pre-operatively.

Urinary catheter: a urinary catheter should be placed, particularly in patients undergoing regional anaesthesia.

93
Q

What are the risks of c section?

A 
Bladder/ureteric injury 
VTE 
Need for further surgery 
Need for emergency hysterectomy 
Death 
Abdo and wound discomfort l
Infection
Haemorrhage
Abdo/wound discomfort
94
Q

What is a risk of Vaginal birth after casarean?

A

Uterine rupture

95
Q

What does Agpar stand for?

A

Its calculated at one and fuve mins after cleanjng and drying the baby in warm towel

Activity
Grimace
Pulse
Appearance
Resp effort
96
Q

What are the two types of postpartum haemorrhage?

A 
Postpartum haemorrhage (PPH) can be classified as either primary or secondary.
Primary PPH: is defined as vaginal bleeding that occurs from delivery of baby to 24 hrs postpartum.
Secondary PPH: is defined as vaginal bleeding from 24 hrs postpartum to 12 weeks postpartum.
97
Q

How can PPH be graded?

A

Minor: 500-1000mls
Moderate: 1000-2000mls
Severe: > 2000mls.

98
Q

What are the causes for PPH?

A

The aetiology of PPH can be remembered as the ‘four T’s’.
The four T’s include Tone, Trauma, Tissue and Thrombin and refer in particular to primary PPH:

Tone (most common): reduction in uterine tone, typically the result of prolonged labour, macrosomia, twins, uterine anomalies or polyhydraminos. ‘Active’ management of the third stage reduces the risk.
Trauma: usually due to episiotomy, extensive perineal tears or uterine rupture.
Tissue: refers to retained placenta and placenta accreta.
Thrombin: refers to either pre-existing or newly developed coagulopathies. Coagulopathies may also result from significant APH or PPH!

99
Q

What are the risk factors for edtopic pregnancy?

A

Previous EP
Endometriosis
Tubal ligation
Salpingitis

Finals (24 decks)

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