Complicated Childbirth Notes PDF

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Complicated Childbirth NotesPairman et al., Chapter 40: Life threatening emergencies. Pg 1094 - 1155As time progresses, more and more women are considered to be ‘high risk’ when pregnant. This is thought to be because of the technology that allows women who would not become pregnant ‘naturally’ to c...

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Complicated Childbirth Notes Pairman et al., Chapter 40: Life threatening emergencies. Pg 1094 - 1155 As time progresses, more and more women are considered to be ‘high risk’ when pregnant. This is thought to be because of the technology that allows women who would not become pregnant ‘naturally’ to conceive and carry. Despite these figures however, the maternal mortality rate has lowered over the past 20 years with NZ having 17.8 deaths per 100,000. Prevention of life-threatening complications - Pre-pregnancy counselling - Professional interpretation services. - Communication and referrals - Multidisciplinary specialist care for those who have pre-existing conditions - Clinical skills and training - Specialist clinical care: identifying sick women - Women with systolic hypertension requires immediate treatment - Treatment for genital tract infections (sepsis)

Cord Prolapse: Rare and unpredictable. Not bad for the woman but life-threatening for the fetus. Interventions used to save the baby can put the mother at-risk. Cord presentation: “The umbilical cord is interposed between the leading part of the fetus and the internal os of the uterine cervix but the amniotic membranes remain intact” FHR with deep decels can be an early sign of this complication. Cord prolapse: Decent of the cord into the cervix, with (occult) or without (overt) the accompanying presenting part. Occurs in the presence of oligohydramnios or an ARM has been performed. On FHR: severe and variable deceleration with profound fetal bradycardia. Can cause fetal hypoxia, brain damage and death. Would indicate immediate VE to assess presenting part. Risk factors: - Multiparity - LBW - Prematurity - Congenital anomalies - Breech (flexed or footling most risky) - Transverse or unstable lie - Twin #2 - Polyhydramnios - Low lying placenta - ARM - Manipulation of fetal presentation (ECV)

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Exposure of the cord to air irritates and cools the cord leading to vasospasm, causing severe fetal hypoxia and acidosis. Perinatal asphyxia can lead to hypoxic-ishaemic encephalopathy and cerebral palsy. Delays in implementing management is associated with perinatal morbidity and mortality. First level management: - Change mothers position – Sims : hips elevated on pillows OR left lateral - Note time, confirm diagnosis - CTG monitoring - Minimise compression of the cord between presenting part and pelvis: on VE insert and keep two fingers in the vagina to push away presenting part. If the cord is out of the introitus gently push it back into the vagina or cover in saline soaked swabs. - Administer 100% O2 6-8L/min - Obtain IV access - Explain briefly to mother and whanau - Prepare women for OT If the fetus is dead or is very preterm nature should take its course and proceed with a vaginal birth. Fetal death can be confirmed only with USS. If at home or a primary unit: a foley catheter should be inserted into the bladder where 500750mls of saline is injected to prevent the fetal presenting part from engaging

Shoulder dystocia One of the most dramatic and severe obstetric emergencies. High physical and psychological trauma for the mother and neonate. Causes severe morbidity for mother and neonate. Occurs when the fetal head is birthed but the body/shoulders cannot be due to the anterior shoulder being impacted by the symphysis pubis (can be posterior or both shoulders although rarer). No pressure on the fetal head or episiotomy will relieve this. Common for obese women to have ‘tight’ shoulders however not a true dystocia as often comes without turtling of the neck (more incidence of just large baby rather than impacted shoulders). Whilst there are risk factors for a dystocia, beause it is a mechanical event it can occur in any birth – even SGA babies. Risk factors: - AMA - BMI > 35 - Abnormal pelvis - GDM - Prolonged pregnancy - Previous shoulder dystocia - Short stature - Macrosomia 2

- Asymmetric accelerated growth - Epidural - Precipitous second stage - Protracted/ prolonged 1st or 2nd stage NON preventable Warning sings: Bobbing of the head Prolonged second stage Head remains tight around the vulva Failed restitution Failure of shoulders to descend into pelvis Normal manoeuvres to birth baby fail. Management Emergency manoeuvres need to do one of three things - Increase functional size of pelvis - Decrease biosacromial diameter - Change the relationship of the biosacromial diameter Mc Roberts applies to the first After a shoulder dystocia blood gases should be taken. NORMAL: pH > 7.25 and lactates < 4.1mmol/L BORDERLINE: pH 7.25-7.20 and lactates 4.1-4.7 INDICITIVE OF FETAL ACIDEMIA NEEDING INTERVENTION: pH 7.20 – 7.00 and lactates >4.7 PATHOLOGICAL FETAL ACIDEMIA: pH 5.8 After 6 min in a shoulder dystocia there is increased risk of neonatal mortality and morbidity H call for help E evaluate need for episiotomy L legs (McRoberts) P Subpubic pressure E Enter manoeuvres (internal) R remove posterior arm R roll women onto all fours (Gaskin) Last resort - Purposeful dislocation of fetal clavicle - Zavanelli: EMLSCS - GA: can help relax all muscles - Symphysiotomy: intentional division of symphysis pubis (very risky for mothers) Complications of shoulder dystocia: Baby: Brachial plexus injury 3

Broken clavicle Death Hypoxia Fractured humorous Mother: PPH Rectovaginal fistula Symphysial separation or diastasis Third- or fourth-degree tear Uterine rupture

Uterine inversion Occurs when the fundus folds into the uterine cavity. Happens in various degrees during third stage or postpartum. Survival rate 85%. Causes PPH and shock. Minimised by prompt recognition and management. Requires surgery and sometimes a hysterectomy. Several risk factors: most common is mismanagement of third stage or traction on cord when placenta hasn’t separated. - Short umbilical cord - Multiparity - Sudden increase in abdominal pressure - Placenta acreta, previa, percreta - Chronic endometriosis - Macrosomia - MgSO4 - VBAC - Precipitous birth - Tocolysis 1st degree: fundus reaches internal os 2nd degree: body of uterus in internal os 3rd degree: the cervix, uterus and vagina are inverted and visible Call for help. Obstetric assistance required Hold of giving uterotonic Do not try and remove placenta 100% O2

Amniotic fluid embolism Leading cause of maternal death in NZ. Unpreventable, unpredictable and rapidly progressive. Leads to cardiac arrest, adult RDS, haemorrhage, seizures, encephalopathy and maternal infant mortality. Requires ICU admission. Occurs when amniotic fluid and contents enter maternal circulation. 4

50% of women will experience DIC Risk factors: - Multiparty - Physiologically intense contractions - Synto infusion - Age >30 - C/S - Cervical tear - Premature placental separation - Intrauterine fetal death - Abdominal trauma - 80% occur in labour - 20% before or after birth

DIC Disseminated intravascular coagulation. Occurs when blood is activated systemically to clot, resulting in multiple organ dysfunction syndrome. Consumption and exhaustion of clotting factors can lead to severe and uncontrollable haemorrhage. Management is always individualised treated to the underlying disorder. However, replacement bloods and fluids + administration of anticoagulants may be used. Risk: Placental abruption, previa. PET Eclampsia HELLP Retained fetus Infection Mortality rate is 40-80% ALWAYS AN UNDERLYING CONDITION

HELLP Is associated with severe preeclampsia. Is a rare but life-threatening liver disorder. Haemolysis Elevated Liver enzymes Low Platelet count Symptoms: - Oedema - Hypertension - Proteinuria - Liver tenderness (radiating pain from ribs) - Raised bilirubin, AST, ALT, ALP. 5

ONLY TREATMENT IS DELIVERY OF BABY Complications: - Liver rupture - Haemolytic disorders: DIC, haemorrhage, haematoma - Cardiac arrest, myocardial ischemia - Pulmonary oedema and failure, pulmonary embolism and RDS - Cerebral haemorrhage and stroke - Renal failure

Eclampsia Is a convulsive condition associated with severe pre-eclampsia. Most often occurs after 20 weeks or in the PN period. Can occur in the absence of hypertension of proteinuria. Characterised by hypercoagulability and vasoconstriction. Seizure lasts form 60-75 seconds, respiration stops for the duration of the seizure. Imminent symptoms: - Severe frontal headache - Hyperreflexia (overresponsive reflexes) - Low urinary output - Visual disturbances - Epigastric pain (liver pain) - Vomiting and nausea - Oedema - Altered mental status - Changes in vital signs Management: - Tx to a tertiary hospital - Magnesium sulphate is best choice for first line management/prevention During a seizure: - DR ABCD - Call for help - Position woman on left side for open airway - Protect woman from injury - Administer 100% O2 - Apply ECG - Apply CTG - After seizure take bloods and perform neurological exam ONLY TREATMENT IS DELIVERY OF BABY With PET or eclampsia, it is important to control BP. Not to drop it dramatically however as this can have severe impacts on the placental perfusion. 160/110 requires immediate treatment. Aim is to reduce systolic pressure by 20-30 and diastolic by 10-15. Hydralazine is good at treating severe PET/ eclampsia. Has many side effects. Labetalol is another good first line treatment. 6

Diazoxide should only be used if a woman is in intensive care. If using MgSO4 and urinary output is less than 100mls in 4 hours, it needs to be stopped. Fluid balance should be monitored closely, and fluid overload should be watched out for. Birth can be via C/S or NVD. IOL should be considered where possible. Corticosteroids should be administered if preterm. Magnesium sulphate treatment should persist for 24 hours after birth. Monitoring maternal SPO2 is important after birth as women are at risk due of eclampsia and hypertension to fluid overload during labour. Complications: - DIC - Neurological damage - Fetal changes: IUGR, oligohydramnios, placental abruption - Hepatic damage - Increased risk of PET with subsequent pregnancies - Neonatal or maternal death

Ruptured uterus Occurs when there is a tear that opens the uterus up into the abdominal cavity. Onset is marked by severe fetal bradycardia. Variable or late decels can be a sign of impending rupture. Bleeding, abdominal pain, tenderness and high presenting part, no progress in labour, rapid pulse, distention of abdomen, chest pain, shortness of breath, changes in uterine shape – are also associated with uterine rupture. Treatment needs to be prompt to prevent maternal and neonatal mortality. Rupture during labour is most severe due to the risk of infection and shock. Ruptured uterus can be ‘complete’ or ‘incomplete’. Complete is caused by a full thickness tear – can occur with a previous C/S. Incomplete results in windows of separation – results in maternal and neonatal complications. Although associated with previous c/s, the lower segment scar significantly reduces the risk of uterine rupture compared to previous alternate methods. Risks: 7

Scarred uterus: surgery or c/s Prior uterine rupture Previous vaginal birth (grandmultip) Teen

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AMA High or low BMI Short stature Short space between births. Trauma TOP Malpresentation Forceps IOL Cocaine use

Treatment: DRABCDE Resuscitate the mother whilst arranging transport to OT for c/s // laparotomy Monitor vital signs Insert 2x large bore cannulas. Administer rapid IV fluids and blood where available. Hysterectomy may be required.

Trauma & Cardiac arrest Family violence most common. Automobile crashes. All women over 20 weeks involved in trauma especially to the abdomen should undergo CTG monitoring for 4 hours prior to hospital discharge. In the presence of trauma, a Keilhauer should be performed. An abdominal ultrasound should also occur. Complications of trauma: - Rupture of membranes leading to chorioamnionitis, preterm labour or cord prolapse. - Retroperitoneal haemorrhage Check for before d/c - PV loss - No FMH - Normal USS normal uterine activity - Given AntiD if needed Perimortem C/S is rare where resus on the mother is unsuccessful. The fetus must be delivered within 4-5min. CPR is to continue throughout the procedure until the baby is delivered. Maternal and fetal survival from CPR is rare. 30 compressions to 2 breaths. Displace the uterus in pregnant women over 30 weeks gestation.

PPH Women at risk of a PPH should be treated AN to minimise likelihood. 8

Anemia should be identified and treated in pregnancy. Consultation with an obstetrician should occur for women at high risk. Make a plan with the women for an actively managed third stage. Risk factors: - APH - Previous PPH - Placenta acreta - Multiple pregnancy - Coagulopathies - Anaemia - Nulliparity - PET - Macrosomia - Obesity - LSCS - Precipitous labour - Oxytocin infusion for IOL - Prolonged labour - Pyrexia - Shoulder dystocia - Episiotomy - Placental retention Assess 4 Ts Mild shock is proceeded by tachycardia and a fallen BP Treatment: - Keep the mother warm - Lie flat - Address concerns - Call for help - Uterotonics: 1st and 2nd line if necessary - Apply O2 mask - Assess and treat the 4 Ts: repair trauma, check for retained products, fundal massage etc.. - IV access: two large bore cannulas and take bloods and start infusion of fluids/bloods. - Bimanual compression - IDC into bladder - Transfer to OT Women whom decline blood products administer vitamin K, discussion should occur AN, inform OB team. Respect choice.

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GESTATIONAL DIABETES MELLITUS (GDM) • •

GDM is a carbohydrate intolerance of variable severity, with onset or first recognition of hyperglycaemia during pregnancy Gestational diabetes is a condition in which women without previously diagnosed diabetes exhibit high blood glucose levels during pregnancy (especially in the third trimester)

Rates of diabetes is increasing in the general population and that during pregnancy. In general, diabetes in the adult population diagnosed and undiagnosed is 7% Prediabetics are at 18.6% Highest among pacific (6.4%), Maori (2.2%), European and others (1.5%) Higher among those with obesity (4.1%) compared those with normal (0.5%), or overweight (0.6%). Pregnancies in NZ with GDM have gone from 1.3% in 2001 to 2% in 2006 to now 4.9% in 2012 – an increase of 13.9% annually. Rates vary by ethnicity: - Asian 8.1% - Pacific 7.2% - Middle eastern/ African / latin American 7.5% - Maori 3.3% (could be a reflection of low screening rates/attendance rather than just a low rate of GDM When discussing diabetes make sure to be specific: type 1, type 2, GDM? Probable undiagnosed diabetes – Diabetes (type 1 or type 2) that is first detected in pregnancy and that has often been referred to as gestational diabetes. However, blood glucose levels do not return to normal ranges following the birth and diabetes is confirmed following postpartum screening (HbA1c value of ≥ 50 mmol/mol). Prediabetes – A state in which some but not all of the criteria are met for a diagnosis of diabetes (type 1 or type 2). It is often termed ‘borderline diabetes’ (HbA1c value of 41–49 mmol/mol). Abnormal glucose levels are likely to continue after pregnancy. Borderline gestational diabetes – A state first identified in pregnancy in which some but not all of the criteria are met for a diagnosis of gestational diabetes. Blood sugar levels are likely to be controlled by diet and lifestyle alone and usually return to within normal ranges after birth. Hyperglycaemia/glucose intolerance – ‘Glucose intolerance’ is used as an umbrella term for metabolic conditions resulting in higher than normal blood glucose levels – hyperglycaemia. Types of diabetes: • 10

Type 1 diabetes

• •

Type 2 diabetes Gestational diabetes

N.B. some women may be Type 2 before becoming pregnant, can identify now if HbA1c done before 20 weeks otherwise confirm diagnosis post-partum Type 1 diabetes – diagnosed in childhood but can develop in adulthood, autoimmune condition, body is unable to make insulin (or very little) and requires treatment with insulin. Type 2 diabetes – diagnosed in adulthood, insufficient insulin being made by the body, treatment can include diet alone or in combination with oral hypoglycaemic drugs and/or insulin. Gestational diabetes – Diabetes that is first detected in pregnancy and resolves following the birth of the baby. Pathophysiology of GDM Carbohydrate Metabolism • Food is broken down to provide the glucose essential to all the cells in the body. • The glucose metabolism is mainly controlled by insulin. • The insulin is secreted by pancreatic βcell. Secreted Insulin unlocks the body’s cells to allow glucose to enter. • The insulin therefore promotes the glucose metabolism in tissues throughout the body. • As the blood glucose is utilized, the blood glucose levels would be lowered.

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It is estimated that insulin sensitivity is decreased by 40% in the 3rd trimester Mechanisms • • •

The decreased insulin sensitivity & insufficient insulin secretion by the βcells is the key for the mechanism of GDM (These result in blood glucose being elevated). Elevated/uncontrolled glucose in the blood results in an inflammatory response (this causes the damage to blood vessels, eyes, renal etc) For GDM, there are no placental hormones after delivery of placenta, so the insulin sensitivity and the blood glucose levels would be restored to the normal.

The role of insulin • facilitates the uptake of glucose by facilitating its movement from the blood into target cells (liver, skeletal and muscle) • stimulates formation and storage of lipids and glycogen • lowers circulating blood glucose. It does this by: • increasing glucose transport by target cells • accelerating glucose utilisation (target cells) and enhanced ATP production • stimulating glycogen synthesis (skeletal, muscle and liver cells) • decreasing glucogenesis (production of glucose). Role of the opposing glucagon: • mobilizes energy reserves and promotes glucose • synthesis and glycogen breakdown • elevates blood glucose concentrations It does this by: • stimulating the breakdown of glycogen in skeletal, • muscle and liver cells • stimulating the breakdown of triglycerides in • adipose tissues stimulating the production of glucose • in the liver. Risk factors associated with GDM: • • • • • • • • •

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Advancing age: ≥ 35 years for Māori, Indo-Asian and Pacific peoples; ≥ 45 years for other ethnicity Family history of diabetes in first-degree relative High-risk ethnic group (Indo-Asian, Māori, Pacific peoples, Middle Eastern) Elevated body mass index: ≥ 27 kg/m2 in Indo-Asian, ≥ 30 kg/m2 in other ethnicities Previous macrosomic infant (> 4500 g) Previous history of gestational diabetes mellitus Previous history of impaired fasting glucose or impaired glucose tolerance Women with polycystic ovary syndrome Known cardiovascular disease, persistent hypertension (> 135/80 mmHg), elevated triglycerides/cholesterol

• • • •

Acanthosis nigricans – dark patches of skin Long-term use of steroids/antipsychotic medication Physical inactivity/sedentary lifestyle Previous stillbirth

Screening HbA1c • • • •

(glycated haemoglobin) – tested on whole blood HbA1c indicates the average blood glucose levels over the previous six to eight weeks. It is a reliable method of detecting probable undiagnosed diabetes in the first 20 weeks of pregnancy. Do not offer an HbA1c as a diagnostic test for gestational diabetes as it is not sensitive enough to detect gestational diabetes.

HbA1c screening (threshold ≥ 34.4 mmol/mol) was superior to risk factor screening. Risk factor screening alone would have missed 18% of all subjects and a third of Europeans who had an HbA1c ≥ 8% (64mmol/mol) Results • All women with HbA1c /=

7.0

5.1

5.3

5.1

5.5

2 Hours >/=

7.8

8.5

8.6

8.5

9.0

Notes

One abnormal value required

Two abnormal value required