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James' final FRCA SOE > Obstetric > Flashcards

Obstetric Flashcards

1
Q

What is acute fatty liver of pregnancy?

A

Acute fatty liver of pregnancy is a rare but serious condition of the 3rd trimester characterised by progressive lipid accumulation in hepatocytes leading to liver dysfunction and multiorgan failure

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2
Q

Describe management of acute fatty liver of pregnancy?

A

Specific vs Supportive

Specific
Expedited delivery

= Regional anaesthesia contraindicated generally due to coagulopathy
= High foetal mortality and liver/renal failure may worsen in 48hrs following delivery

Supportive
- IV access
- Careful IV fluid resuscitation (risk of peripartum cardiomyopathy and ARDS
- IV glucose if hypoglycaemic
- Correction of coagulopathy with blood products
- Intubation/vent if ARDS
- RRT

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3
Q

Differentials for maternal collapse?

A

Haemorrhagic
- Postpartum
- Antepartum (p. praevia/accreta, p. abruption, uterine rupture, ectopic)

Thromboembolic
- PE
- Amniotic F.E

Cardiac disease
- Myocardial infarction
- Cardiomyopathy
- Valve lesions
- Arrythmias

Neuro:
- Eclamptic fit
- SAH

Regional anaesthesia related:
- High block (high spinal)
- LAST

Immunological:
- Sepsis
- Anaphylaxis

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4
Q

Pathophysiology of AFE?

A

Amniotic fluid enters maternal circulation via ruptured uterine/cervical veins

Thought to be likely IMMUNE mediated rather than embolic

Phase 1
- Mast cell degranulation to foetal antigents, biochemical mediators
- PA vasospasm –> P. hypertension –> RV dysfunction,
- Hypoxaemia and hypotension

Phase 2
- LV failure and pulmonary oedema
- Endothelial activation and leakage
- DIC and uterine atony

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5
Q

Features of AFE?

A

Maternal cardiac arrest and neonatal distress

Cardiac - profound hypotension, collapse, arrhythmia
Resp - breathlessness, cyanosis
Haem - DIC

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6
Q

Risk factors of AFE?

A

Strong:
- Induction of L
- Oxytocin use
- Instrumental/c. section

Moderate
- Advanced mat. age
- Male foetus
- Multiple preg.
- Abruption
- IUFD

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7
Q

Management principles of AFE?

A

ABCDE assessment and mx.
Aim is to maintain organ perfusion and oxygenation
May include:
I+V, high FiO2
L Lat tilt (antepartum)
Peri-mortem C.section
Haemorrhage mx

Supportive therapies
- ECMO
- TEG
- PA catheter
- IABP
- Pulm vasodilators

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8
Q

Patient factors - maternal sepsis

A

Obesity
Diabetes
Immunosuppression
Low socioeconomic class
Black or Asian ethnicity
History of PID

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9
Q

Obstetric factors - maternal sepsis

A

Amniocentesis/cervical suture

Prolonged rupture of membranes
Prolonged trauma with repeated VEs
Vaginal trauma
Episiotomy
C. Section
Retained products

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10
Q

Causes of antepartum haemorrhage?

A

Placenta praevia (33%)
- Placenta encroaches or covers cervical os

Placental abruption (33%)
- Abnormal separation of placenta from uterus
- May have retroperitoneal clot

Uterine rupture

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11
Q

What is placenta accreta ?

A

Placenta attaches to myometrium (not just endometrium)

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12
Q

What is placenta increta?

A

Placenta invades into the myometrium

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13
Q

What is placenta percreta?

A

Placenta invades through the perimetrium

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14
Q

Mx of p. accreta spectrum

A

Screening those with risk factors to identify antenatally
- P. praevia with prev. scar
- Increased maternal age
- Multiparity

MDT planning, deliver at tertiary centre 34-36 weeks
Prompt resuscitation and mx postpartum haemorrhage

Neuraxial is ok

X-match preparation of blood

Access to TEG

IR availability
Balloon occlusion of internal iliac arteries

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15
Q

Classification of p. praevia

A

Complete vs. partial. vs. margina (marginal = placenta >2cm from os) - suitable for vaginal delivery

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16
Q

What % of deliveries affected by PPH?
What is it?

A

Affects 5% of deliveries in the UK

Defined as >500mls blood loss from the genital tract within 24hrs of delivery

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17
Q

How can PPH be classified

A

May be classified as MINOR (500-999mls) or MAJOR (>1000mls) blood loss

Major PPH
- Moderate MAJOR = 1000-1999mls
- Severe MAJOR = >2000mls

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18
Q

Causes of PPH

A

Four ‘T’s’

Tone (uterine atony, 70%)
Trauma (genital tract lacerations)
Tissue (retained placenta, placental fragments)
Thrombin (coagulopathy)

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19
Q
A
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20
Q

How would you manage PPH?

A

This is an emergency.

I would confirm the vital sign readings
Call for help
Scan the patient, surgical field and monitors and
Alert the surgeons to the issue

My priorities in this incidence are
1) resuscitation with crystalloid and blood products
2) specific treatments for the underlying cause of the PPH

Utilising additional resources I would lead this crisis and allocate tasks accordingly.

1)
I would give 100% O2, increase flows or put on NRB
Place patient flat or head down
Establish (if not already) IV access and sending blood for urgent x-match if not already sent
Activating the major haemorrhage protocol and communicating with blood bank for group-specific blood
Whilst waiting for blood administer boluses of crystalloid aiming for MAP >65 or titrating to clinical signs
Administer 1g of TXA
Consider additional monitoring e.g. art line if sufficient resources

2) Treat specific cause
If ATONY, uterotonics etc etc

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21
Q

Management of uterine atony

A

Non-pharmacological
- Bimanual uterine compression
- Emptying bladder

Pharmacological
1. TXA
- WOMAN study showed reduced mortality , 1g loading, 1 additional if bleeding >30mins or rebleed

  1. Syntocinon
    - 5units slow IV bolus
    - 10iu/hr infusion
    - SE = tachycardia
  2. Ergometrine (ergot alkaloid)
    - 0.5mg IM
    - SE = diarrhoea, nausea, vomiting, hypertension, contraindicated in pre-eclampsia + ischaemic HD
  3. Carboprost (prostaglandin)
    - 0.25mg IM or intramyometrial, up to 8 doses 15minute intervals
    - SE = bronchospasm, contraindicated in asthmatics
    5
    . Misoprostol 800mcg PR (prostaglandin E1 analogue)

Surgical
- Intrauterine balloon tamponade (Bakri balloon)
- Uterine compression sutures (B-lynch suture)
- Interventional Radiology, intra-arterial balloon occlusion/embolisation
- Pelvic vessel ligation (internal iliac, uterine, hypogastric, ovarian)
- Hysterectomy

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22
Q

What is inverted uterus?

A

A rare life-threatening complication of 3rd stage of labour - complete inversion where fundus passes through cervix

Haemorrhage may be profuse

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23
Q

How is inverted uterus managed?

A

Resuscitation
- Blood products
- Do not remove placenta

Replacement of uterus
- Manual attempts whilst resus attempts ongoing
- Wait until pt. haemodynamically stable
- GA likely required to provide relaxation of cervix
- Tocolytics may be required

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24
Q

What agents are tocolytics?

A

Magnesium Sulfate
GTN
B2 agonists
Calcium channel blockers

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25
What is massive transfusion
Transfusion of greater volume of blood than a patient's circulating volume in a 24hr period OR More than half a patient's circulating volume in a 4hr period
26
Complications of massive transfusion
1. Hypothermia 2. Dilutional coagulopathy 3. Hypocalcaemia 4. Hyperkalaemia 5. Acidosis
27
Anaesthetic management of cord prolapse
Due to the head-down knee-chest position and Category 1 CS a GA is required Sodium citrate through straw Pre-oxygenated in kneechest RSI with cricoid pressure
28
Risk factors for cord prolapse?
Most likely to occur within 5 minutes of SROM Factors that increase likelihood Fetal malpresentation Polyhydramnios Prematurity Multiple gestation Following obstetric procedures - artificial ROM, fetal scalp electrode placement, manual rotation of head
29
Categories of caesarian section
1. Immediate threat to life of woman or foetus Perform as quickly after making decision Aim for <30 mins decision to delivery 2. Maternal or foetal compromise not immediately life-threatening As soon as possible, 30-75 minutes of decision 3. No maternal or foetal compromise but needs early delivery 4. Delivery timed to suit woman or staff
30
What is intrauterine resuscitation
Applying specific measures to increase O2 delivery to placenta in order to reverse foetal hypoxia and acidosis Position - left lateral Infusion of crystalloid 500mls Maternal O2 Stop synto infusion Tocolysis e.g. terbutaline 250mcg iv or sc
31
What is risk of awareness from NAP 5 in C.sections
C.section most over-represented surgical procedure for AAGA Incidence of 1:670
32
What are NAP 5 recommendations for AAGA
Consent for possible AAGA Reduce risk of AAGA through - Increased induction agent dose - Rapid end-tidal volatile post induction - Use of nitrous - Use of opioids - Plan for difficult airway, have midaz drawn up - Seperate abx to avoid wrong-drug error
33
What are the considerations when doing anaesthesia for the parturient with non obstetric pathology
Key things to consider 1. Physiological changes of pregnancy and the impact on anaesthetic management 2. Providing safe anaesthesia to the mother whilst 3. Minimising risks to the developing foetus
34
Conduct of anaesthesia for lap chole in obstetric patient
Key things to mention: Monitoring: >24 weeks, continuous CTG, obstetrician available for delivery if distress <24 weeks, confirmation of foetal well being post op Left tilt >20 weeks gestation due to aortocaval compression Sodium citrate (non particulate antacid) Head up positioning to maximise FRC and alleviate GORD and displace breasts Pre-oxygenation 3 minutes tight fitting mask RSI with cricoid pressure (> first trimester)
35
What are the treatment options for MS
During acute attacks - corticosteroids Immunomodulators - alemtuzumab Symptomatic 1. Pain = gabapentin, carbamazepine 2. Spasticity = baclofen, dantrolene 3. Depression = antidepressants 4. Bladder/bowel dysfunction = anticholinergics
36
What are the clinical features of PDPH
Occurs within 24-72hrs of procedure Severe frontal or occipital headache Worse on sitting or standing (positional) Nausea in 60% Photophobia and neck stiffness may occur Hearing loss and tinnitus may occur Pressure of right hypogastrium, elevating epidural venous pressure, may alleviate symptoms
37
What causes the PDPH headache
Intracranial hypotension results in caudal brain displacement Meningeal vasodilation Traction on pain-sensitive meninges
38
Pospartum headache differential
Tension headache Migraine Cerebral venous thrombosis Pre-eclampsia headache SAH Space occupying lesion Meningitis Sinusitis PRES
39
PDPH incidence
Following spinal 1/300 Following epidural 1/100 If dural puncture noted during epidural then risk of PDPH is 50-80%
40
Treatment strategies for PDPH
Non-specific - Hydration with oral intake/IV fluid - Bed rest (relieves in first 48 hrs, VTE risk) - Simple analgesics Specific therapies - Caffeine 150-200mg /day (equiv to 4-5 coffees) - Epidural blood patch 60-90% cure rate, more effective >48hrs
41
Risks of not treating PDPH
Cranial nerve palsies especially 6th Subdural heamatoma Chronic headache Venous sinus thrombosis
42
Complications of EBP
Failure Backache - 35% discomfort at 48hrs, 16% backache at 28days Repeated dural puncture Neurological complications - seizure, CN palsy
43
What is peripartum cardiomyopathy
It is a diagnosis of exclusion PPCM is an idiopathic cardiomyopathy that causes heart failure 2ndary to left ventricular systolic dysfunction towards the end of pregnancy or in the months following pregnancy, in the abscence of other causes of heart failure
44
Risk factors for peripartum cardiomyopathy
Hypertensive disorders of pregnancy - gestational HTN, pre-eclampsia Maternal age >35 Genetics - FHx, African descent Multiple gestation
45
Clinical presentation of PPCM
Classic features of heartf ailure - Exertional dyspnoea - Dry cough - PND - Poor exercise tolerance - Ankle swelling - Chest pain - Palpitations 2/3 present post delivery 2/3 have severe disease EF <35% and NYHA >3
46
Meds for PPCM ?
Ace-i/ARBS are contra-indicated Therefore - Loop diuretic - Beta blocker e.g. metoprolol - Hydralazine if HTN - LMWH
47
Key points about management of PPCM
Early senior involvement Arterial line Early epidural to reduce sympathetic surge Post delivery represents a high risk for clinical deterioration Autotransfusion Reduced aortocaval compression Both may lead to acute decompensation Uterotonics have cardiovascular side effects - use with caution - Syntocinon = dec SVR, reflex tachy, increased PVR - Give SLOWLY
48
Physiological changes of multiple pregnancy
Exagerrated version of singleton Resp - FRC further reduced with higher O2 consumption therefore high risk of desaturation CVS - Higher blood volume than singleton by 40%, proportionally less red cells therefore greater physiological anaemia - CO 20% greater than singleton preg - More aorocaval compression - More blood loss at delivery - Manual removal twice as common - Pre-eclampsia twice as common CNS - Greater cephalad spread of local GI - Higher aspiration risk
49
What is pre-eclampsia
Pre-eclampsia is a potentially life-threatening multi-system disease of pregnancy and the postpartum period which complicates around 7% of pregnancies It is caused by abnormal placentation and characterised by hypertension and proteinuria
50
Diagnostic criteria of pre-eclampsia?
Systolic > 140 OR diastolic >90 on 2 occasions (>4 hrs apart) Occurring in parturients >20 weeks + One or more of: 1. Proteinuria, PCR >30mg/mmol , alb:creat >8mg/mmol, proteinuria +2 on dipstick 2. Neurological signs - headache, clonus, stroke, altered mental status, eclampsia, visual scotoma 3. Kidney - creat >90 4. Liver - ALT >70 5. Haem - Plt <150, DIC, haemolysis
51
Diagnostic criteria of pre-eclampsia with SEVERE features?
Severe HYPERtension, systolic >160, diastolic >110 that does not respond to treatment Ongoing or recurring severe headache Nausea/vomiting Epigastric pain Oliguria <500ml/24hrs Deterioration in prev. lab tests of organ dysfunction
52
What is the pathophysiology of pre-eclampsia?
Spiral arteries supply the uterine endometrium During normal pregnancy they undergo dilatational change in order to improve blood supply to foetus In pre-eclampsia, impaired trophoblastic invasion leads to failure of dilation of spiral arteries Leads to placental hypoperfusion and release of vasoactive cytokines and inflammatory mediators into maternal circulation which cause maternal endothelial cell dysfunction and IUGR to foetus
53
Risk factors for pre-eclampsia
Primigravida Previous hx of P-Eclamp FHx of P-Eclamp Advanced maternal age Multiparity Chronic hypertension CKD Obesity Autoimmune disease
54
Management strategy for pre-eclampsia
1. BP control - Labetalol, Nifedipine, Methyldopa, Hydralazine, Nitrates 2. Prevention of convulsions: Mag Sulp 3. Prevention of PreEclampsia with low dose aspirin 4. Delivery of foetus
55
Principles of fluid management in severe pre-eclampsia
Renal impairment is common Widespread vasoconstriction reduces circulating volume Fluid overload is easy to cause Practical tips: 4hrly UO rather than 1hrly Aim for total INPUT of 85mls/hr (remember to count infusion of antihypertensive) Careful fluid boluses
56
Anaesthetic implications of pre-eclampsia
Airway/breathing: Laryngeal and upper airway oedema common CVC Hypotensive response to central neuraxial blockade is absent/reduced Hypotension may be difficult to control due to increased vasopressor sensitivity Hypovovaemia and intravascular depletion common due to vasoconstricted circulation Fluid overload easy to precipitate Neuro: Hypertensive response to laryngoscopy may lead to stroke Pt. may have reduced GCS or altered mental status MgSO4 can potentiate neuromuscular blocking drugs Haem: Coagulopathy may complicate neuraxial blockade
57
GA things to remember for pre-eclampsia
Obtund sympathetic reponse to laryngoscopy with opioid e.g. 15mcg/kg around 1mg of alfentanil Manage perioperative hypotension predominantly by using IV vasopressors rather than IV fluid Prepare for difficult laryngoscopy with VL, have smaller tube available
58
Management of eclampsia
MgSo4 used for PROPHYLAXIS (in severe P.E) and TREATMENT of eclamptic seizures ABCDE approach MgSo4 4g loading IV over 5 minutes Maintanence 1g/hr for 24hrs 2g additional. bolus in repeat seizure
59
How to assess for Mg toxicity
Diminished reflexes RR (low) O2 sats (low) Treatment - stop infusion, Cal gluconate 10mls 10% over 10mins
60
How does magnesium work in pre-eclampsia?
Antagonist at calcium channels reducing systemic and cerebral vasospasm NMDA receptor antagonist - anticonvulsant action Increased endothelial prostacyclin may restore thromboxane-prostacyclin imbalance
61

James' final FRCA SOE (17 decks)

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