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Intrapartum and obstetric emergencies > Labour pain and anaesthesia > Flashcards

Labour pain and anaesthesia Flashcards

1
Q

What type of pain predominates the first stage of labour?

A

Visceral pain caused by uterine contractions and cervical dilatation - distension of uterine mechanoreceptors and ischaemia of tissues.

Transmitted through T10 to L1 spinal nerves.

Poor localisation.

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2
Q

What type of pain predominates the second stage of labour?

A

Visceral AND somatic pain.

Somatic pain is caused by ligament stretching, ischaemia and injury of the pelvic floor, vagina and perineum.

Transmitted by:

  • Pudendal nerve and perineal br of the posterior cutaneous nerve of the thigh –> S2-4
  • Cutaneous br of ilioinguinal L1 and genitofemoral nerves to L1-2

Sharp and well localised.

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3
Q

Describe the pain pathway for visceral pain

A

Small unmyelinated ‘C’ fibres –> travel with sympathetic fibres –> uterine, cervical and hypogastric nerve plexuses –> main sympathetic chain –> white rami and into posterior nerve roots of T10 and L1 –> dorsal horn of spinal cord

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4
Q

Describe the pain pathway for somatic pain

A

Fine myelinated rapidly transmitting ‘A delta’ fibres –> S2-4 and L1-2 –> dorsal horn cells –> spino-thalamic tract –> brain

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5
Q

Outline management specific for LAST

A
  • Intralipid (20% lipid emulsion)
  • Benzodiazepines for seizures
  • Amiodarone for arrhythmias and manage cardiac arrest as per ACLS.
  • Cardiopulmomary bypass if doesn’t respond to lipid emulsion and ACLS
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6
Q

List the signs and symptoms of local anaesthetic systemic toxicity

A

CNS:

  • Tinnitus
  • Metallic taste
  • Agitation
  • Dysarthria
  • Circumoral tingling
  • Paraesthesia
  • Seizures
  • Loss of consciousness
  • Respiratory arrest

Cardiovascular:

  • Hypotension
  • Arrhythmias
  • Cardiac arrest
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7
Q

List indications for early epidural in labour

A
  • Twin pregnancy
  • Preeclampsia
  • Obesity BMI >40 or with OSA.
  • Difficult airway
  • Previous PPH
  • History of malignant hyperthermia
  • Maternal cardiac and respiratory disease
  • Intracranial disease (exclude raised ICP)
  • Breech
  • Intrauterine death
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8
Q

According to the Cochrane review 2012 on labour pain management:

What methods of pain relief are shown to be EFFECTIVE?

A

Pharmacological:

  • Epidural
  • CSE
  • entonox

Non-pharmacological:
- Continuous 1:1 support and care provider

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9
Q

According to the Cochrane review 2012 on labour pain management:

What methods of pain relief MAY BE EFFECTIVE?

A

Pharmacological:

  • Local anaesthetic nerve blocks
  • non-opioid medication

Non-pharmacological:

  • immersion in water
  • relaxation
  • acupuncture
  • massage.
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10
Q

According to the Cochrane review 2012 on labour pain management:

What methods of pain relief have INSUFFICIENT EVIDENCE to show effectiveness?

A

Pharmacological:
- Parenteral Opioids

Non-pharmacological:

  • Hypnobirthing and hypnosis
  • Aromatherapy
  • TENS
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11
Q

What are the adverse obstetric outcomes associated with epidural (Cochrane 2018)?

A

Adverse obstetric outcomes:

  • Fetal distress
  • Maternal hypotension
  • Prolonged first and second stage
  • Increased use of syntocin
  • Increased ventouse/forceps delivery (studies prior to 2005)
  • Increased CS for fetal distress BUT no increase in CS overall
  • Increased urinary retention post-delivery
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12
Q

What are contraindications for a neuraxial block?

A
  • Coagulopathy: Plt <80, INR >1.4
  • Maternal refusal
  • Local and untreated systemic infection
  • Uncontrolled hypovolaemia or haemorrhage
  • Expectation of significant haemorrhage
  • Certain spinal surgery and abnormalities
  • Lack of trained staff to provide safe care.
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13
Q

List the side effects of a neuraxial block

A
  • Failure 1:10
  • Hypotension 1:50
  • Pruritis
  • Nausea and vomiting
  • Urinary retention
  • Shivering
  • High block: inadvertent epidural dose given into subarachnoid or sudural space OR overdose of spinal anaesthesia
  • Local anaesthetic systemic toxicity
  • Dural puncture headache 1:100
  • Nerve damage very rare
  • Respiratory depression rare
  • Epidural abscess or meningitis <1:50,000
  • Dural haematoma 0.6:100,000
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14
Q

What are the main nerves that supply the pelvic organs?

A

Somatic:

Both motor and sensory the same

  • Pudendal
  • Ilio-inguial
  • Genital branch of genitofemoral nerve
  • Posterior cutaneous nerve of the thigh

Autonomic

Sympathetic: Sensory T10 - L1, Motor T5&6
Parasympathetic S2-S4

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15
Q

Nerve route of pudendal nerve

A

S2-S4

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16
Q

Nerve route of ilio-inguinal nerve

A

L1+2

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17
Q

Nerve route of Genital branch

A

L1+L2

18
Q

Describe the origin of pain in the first stage of labour

A

Mostly from the uterus + Cervix

Distension of uterine mechanoreceptors + ischaemia of uterine and cervical tissues
T10-L1 afferents

Referred Pain
Abdominal wall, lumbosacral, gluteal, thighs

Sensations are through A delta + C primary afferent fibres which pass through th einferior, middle and superior hypogastric plexus, the lumbar and lower thoracic sympathetic chain and end in rami communicantes associated with T10-L1 spinal nerves

19
Q

Describe pain in transition stage

A

Transition

Late first stage (7-10cm) to second stage
Greater nociceptive input: somatic pain from vaginal distension

20
Q

Describe pain in second stage

A

Somatic pain from vaginal, perineal and pelvic floor distension
Stretching of pelvic ligaments
Sacral afferents
S2-S4 (pudendal nerve)
More severe than first stage
Visceral pain form contractions and cervical stretching AND somatic pain
Rectal pressure as presenting part descends into pelvic outlet

Unlike visceral pain of first stage it is sharp and well localized, due mainly to less arborization and the faster conduction velocity in sacral pathways
Predominantly carried by A delta fibres.

21
Q

Labour pain:

Site of origin: Bladder

mechanism, pathway and site of action?

A

Mechanism: Overdistension

Pathway: Afferents which accompany sympathetic pathway T11-L1

Site of action? Suprapubic

22
Q

Adverse consequences of labour pain

A

Emotional distress and suffering

  • Postpartum psychological trauma contributes to PPD + PPA

Physiological effects on mother and fetus

  • Hyperventilation and alkalosis causes a left shift of oxyHb dissociation curve
  • Uterine vasoconstriction
  • Pain –> increased circulating catecholamines –>decreased uterine bloody flow –> fetal hypoxia + acidosis
23
Q

Pain coping strategies

A

Childbirth education
Relaxation and breathing
Birth environment
Continuous labour support
Maternal movement and positioning
Birth ball
Music and audioanalgesia
Biofeedback
Application of heat and cold
Water immersion
Sterile water injection
Touch and massage
Acupuncture and accupressure
Hypnosis
Aromatherapy
TENS

24
Q

Side effects of nitrous oxide

A

Nausea + vomiting
Affects recall

25
Q

How does the local anaesthetic in an epidural work?

A

Blocks voltage-gated sodium channels in nerves, preventing propagation of action potentials

Thus prevents transmission of nociceptive impulses in small diameter nerves entering the spinal canal

→Also affect the nerves leaving the spinal canal such as:

  • Sympathetic nerves innervating blood vessels: vasodilatation and hypotension
  • Motor nerves which innervate muscles, causing motor blockade

It is possible to use opioids and local anaesthetic drugs on their own for epidural analgesia, but combining the two drugs gives a synergistic effect with minimal side-effects.

26
Q

The effect of epidural on labour?

  • Duration of labour
A

2018 Cochrane review 40 trials, 11000 women.
- Secondary outcome (v opioid) (34 trials involving 10,440 women)

Both first and second stages of labour were shorter for the women who received opioids

First stage: MD 32.28 minutes,

Second stage: MD 15.38 minutes,

Heterogeneity high especially for the second stage

Secondary outcome (v placebo/no analgesia):

There was no clear difference between the groups for length of first stage of labour (minutes)

27
Q

The effect of epidural on labour?

  • Mode of birth
A

Caesarean section?

  • Opioids The caesarean section rate was no different between the groups
  • no analgesia/placebo: Fewer women in the epidural group underwent caesarean section compared to women in the placebo or no-treatment group

Operative Vaginal Birth

  • Opioids: The assisted vaginal birth rate was higher in the epidural group (RR1.44,).
  • no analgesia/placebo There was no clear difference in this outcome between the groups
28
Q

RANZCOG Q:

With respect to epidural anaesthesia in labour, discuss the impact of two interventions that could reduce this woman’s concern regarding the need for assisted vaginal birth:

A
  • Lower concentrations of local anaesthetic are associated with lower motor blockade
    1mg/mL bupivacaine
  • Although overall there appears to be an increase in assisted vaginal birth when women have epidural analgesia, a post hoc subgroup analysis shows that this effect is not seen in recent studies (after 2005), suggesting that modern approaches to epidural analgesia in labour do not affect this outcome.
29
Q

RANZCOG Q:

List the two (2) other adverse obstetric outcomes you should discuss, that are associated with epidural anaesthesia in labour, and are supported by randomized control trial evidence

A
  • Caesarean rate not higher but more Caesarean sections are done for fetal distress
  • Prolonged second stage
  • Urinary retention
    Opioid Group - More women in the epidural group had urinary retention compared with the opioid group
    Placebo: There was no clear difference in this outcome between the groups
30
Q

RANZCOG Q:

The woman has also heard that epidurals can cause fetal distress. Describe the pathophysiology of two (2) causes of fetal distress as a result of epidural anaesthesia and their associated abnormal fetal heart rate pattern/s. (2 marks)

A
  1. Hypotension: Spinal anesthesia blocks small, unmyelinated sympathetic fibers first. Sympathectomy from spinal or epidural analgesia ==> to a ↓ in blood pressure. ==> ↑ adrenaline ==>uterine artery constriction ==>↓ placental blood flow. ==> fetal bradycardia.

Both arteries and veins vasodilate, however the venous effect is more pronounced, leading to substantial decreases in preload

  1. Opioids:
    Intrathecal opioids ==> to a ↓ in sympathetic nervous system output + ↓ adrenaline levels. Adrenaline is in itself an effective tocolytic due to β2 activity. Therefore, the ↓ adrenaline levels ==> to unopposed noradrenaline activity, which ↑ uterine tone and ==> ↓ placental blood flow.
    If placental blood flow is ↓ enough ==> fetal bradycardia due to fetal compromise.
31
Q

RANZCOG Q:

This same woman is now in established spontaneous labour at 39 weeks gestation. Ten minutes ago an effective epidural was inserted for pain relief. The anaesthetist left promptly after inserting the block to attend a Code 1 caesarean section. You are called to review the woman urgently because her blood pressure is 70/40 and she has tingling in her arms.

(i) Identify the two (2) most likely epidural-related causes for these symptoms. (2 marks)

A

1) Local Anaesthetic Systemic Toxicity (LAST)
2) Total/high spinal blockade

32
Q

RANZCOG Q:

This same woman is now in established spontaneous labour at 39 weeks gestation. Ten minutes ago an effective epidural was inserted for pain relief. The anaesthetist left promptly after inserting the block to attend a Code 1 caesarean section. You are called to review the woman urgently because her blood pressure is 70/40 and she has tingling in her arms.

(ii) Outline six (6) steps for your immediate management. (6 marks)

A
  1. Send for help: Red Bell, including alerting the anaesthetist, senior obstetrician and neonatal provider
  2. Disconnect epidural
  3. Start Resuscitation 100% oxygen, woman on side, ensure 2 wide bore IV access and IV Fluids
    Continually reassess ABC
  4. Assess woman
    - Block height
    - Other symptoms
  5. Assess baby
    - Continuous CTG
  6. Definitive management
    - Definitive airway
    - ICU involvement / transfer
    - BP support - fluids +/- inotropes and vasopressors
    - Consider 20% Intralipid IV
    - Prepare for delivery if required to optimise maternal rescusitation
33
Q

Symptoms of total spinal blockade

A

Cardiorespiratory:

  • Hypotension
  • Bradycardia
  • Respiratory compromise / reduced respiratory effort
  • Reduced oxygen saturations
  • Difficulty speaking/coughing
  • Apnoea
  • Cardiac arrest (asystole)

Neurological:

  • Nausea + vomiting
  • Nausea and anxiety
  • Arm/hand paraesthesia or paralysis*
  • High sensory level block
  • Cranial nerve involvement
  • Loss of consciousness
34
Q

Why may a total spinal block occur?

A

Drug factors
a. Dose/concentration - Block height more dependent on dose than volume (higher dose gives higher risk)

b. Baricity – cephalad spread easier to control with hyperbaric solution
c. Prior drug administration – such as epidural local anaesthetic diffusion (unrecognised/sub-clinical block gives higher risk)

Patient factors
a. Body morphology – higher BMI or abdominal girth (including pregnancy) may reduce thecal volume and increase the risk of high block

b. Anatomical or pathological factors – compressed thecal sack (epidural fluid & dilated vessels), spinal canal abnormality can give higher risk
3. Technique factors
a. Higher lumbar insertion may increase final block height
b. Position at and following injection – sitting may minimise cephalad spread
c. Spinal needle – finer gauge and cephalad direction of needle hole may increase risk of higher block

35
Q

Symptoms and management of a total spinal

A
  • Bradycardia: Vagolytics e.g. atropine
    Sympathomimetics e.g. ephedrine, adrenaline
  • Hypotension: Vasopressors e.g. metaraminol, phenylephrine
    Fluid bolus
    Leg elevation
  • Respiratory dysfunction: Oxygenation, definitive airway, NIV/ventilation
  • Loss of consciousness: Secure airway
    Supportive measures
36
Q

Symptoms of LAST

A

Cardiovascular:

  • Initial Phase: Hypertension + tachycardia
  • Intermediate Phase: bradycardia + hypotension
  • Terminal phase: severe hypotension, arrhythmias e.g. sinus bradycardia, ventricular tachyarrhythmias, respiratory depression / apnoea, cardiac arrest / asystole.

Neurological:

  • Excitatory phase: Perioral tingling, tinnitus, slurred speech, lightheadedness, tremor. May progress to generalized convulsions
  • Depressive phase: Coma + respiratory depression

NB. cardiovascular collapse can occur before ANY neurological symptoms occur

37
Q

Maximum doses of the following drugs with/without adrenaline:

Lidocaine
Bupivocaine
Rupivocaine
Prilocaine

A

In ml/kg:

Lidocaine: 3, Adr: 7
Bupivocaine: 2 Adr: 2
Rupivocaine: 3 Adr: 3
Prilocaine: 6 Adr: -

38
Q

Risk factors for LAST

A

Patient factors:

  • Severe renal impairment: reduced clearance
  • Liver disease: reduced clearance
  • Severe cardiac failure: susceptible to LA induced myocardial depression and arrhythmias.
  • Pregnancy: a low α1-acid glycoprotein (AAG) titre results in a higher concentration of free LA
39
Q

Fetal risks of general anaesthesia in pregnancy?

A
  • Miscarriage risk 5-10% (highest in first trimester and if peritonitis)
  • LBW
  • preterm labour
  • stillbirth

No convincing evidence of teratogenicity anaesthetic agents - large scale trials do not show increased rates of birth defects above baseline 3%.

NB. Benzodiazepines may increase cleft palate and cardiac abnormalities.

40
Q

Maternal risks of general anaesthesia in pregnancy?

A

Cardiovascular:

Uterine perfusion not autoregulated
Decreased SVR/PVR - Hypotension common under RA + GA
Aortocaval compression requires LLT

Respiratory:

Increased minute ventilation = Faster inhalation induction
Increased oxygen consumption, V/Q mismatch - Potential hypoxaemia, rapid desaturation

Upward displacement of diaphragm - difficult ventilation
Mucosal oedema - Difficult laryngoscopy + intubation

Gastrointestinal:

Reduced cardiac sphincter tone and delayed gastric emptying - ↑ Aspiration risk
→ Antacid prophylaxis, RSI after 18/40

Intrapartum and obstetric emergencies (18 decks)

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