Short Answer Questions Anaesthesia

Short Answer Questions
Anaesthesia
& Intensive Care
For FCAI, FRCA & EDAIC
Modified by
AYMAN EDAROUS
Part: 5 – Obstetric Anaesthesia
Anaesthesia, Pain & Intensive Care Secrets Academy [APICSA]

‫بسم الله الرحمن الرحيم‬
For Original Materials and Editors, Please refer to:
North Ireland School of Anaesthesia Website

http://www.nischoolofanaesthesia-finalfrca.org.uk/SAQs/obstetric/
MODIFIED BY AYMAN EDAROUS OBSTETRIC ANESTHESIA 2
1- The Airway in the Pregnant Patient
a) What factors may contribute to difficulties encountered when securing the airway under general
anaesthesia in the pregnant patient? (9 marks)
b) What measures can be taken to reduce airway related morbidity and mortality associated with
general anaesthesia in a pregnant woman? (8 marks)
c) What are the recommendations in the 4th National Audit Project (Major Complications of Airway
Management in the UK, NAP 4) regarding airway management in the pregnant woman? (3 marks)
 The factors may contribute to difficulties encountered when securing the airway
under general anaesthesia in the pregnant patient:
 The measures can be taken to reduce airway related morbidity and mortality
associated with general anaesthesia in a pregnant woman:
Training/Guidelines
* Regular training of obstetric anaesthetists in airway skills, including failed incubation
drills
* Training in how to deal with failed/inadequate regional techniques
* Training of non-anaesthetic obstetric staff
* OAA/DAS Guideline on Obstetric GA and Failed intubation
Patient Measures
* Antacid prophylaxis/Sodium citrate
* Airway Examination: assessing for difficult intubation/ventilation/front of neck access

Theatre Measures
* Proper positioning of patient: ramped/Oxford pillow
* Ensuring adequate Pre-oxygenation
* Skilled anaesthetic assistant
* Specialist equipment available: e.g. video-laryngoscope
* Possibility of waking patient up if failure to secure airway and mother’f life not
immediately in danger
 The recommendations in the 4th National Audit Project (Major Complications of

Airway Management in the UK, NAP 4) regarding airway management in the pregnant
woman:
* Obstetric anaesthetists need to maintain their airway skills including strategies to

manage difficult intubation, failed intubation and CICV
* Obstetric anaesthetists should be familiar and skilled with supra-glottic airway devices
for rescuing the airway
* Anaesthetic departments should provide a service where the skills and equipment are
available to deliver awake fiberoptic intubation whenever indicated
* All staff working in recovery area of a delivery suite must be competency trained.

2- Mitral Stenosis in Pregnancy
A 27-year-old woman is 13 weeks pregnant. In the antenatal clinic she is found to have an
asymptomatic heart murmur. A subsequent Echo shows moderate to severe MS.
(a) List the causes of mitral stenosis. (15%)
(b) How do the cardiovascular changes in pregnancy exacerbate the pathophysiology of MS? (45%)
(c) Outline the specific management issues when she presents in established labour. (40%)
 Causes of Mitral Stenosis:

Infection: Rheumatic Fever, Infective Endocarditis with large vegetations, Whipple Dis.
Autoimmune: Systematic Lupus Erythematosus, Rheumatoid Arthritis, Sarcoidosis
Genetic: Congenital MS, Muco-polysaccharidoses of Hunter Hurler Phenotype, Fabry Dis.
Malignant: Malignant Carcinoid Syndrome.
Iatrogenic: Radiotherapy, Methysergide Therapy.
 Cardiovascular changes in Pregnancy exacerbate the pathophysiology of MS:

In normal pregnancy cardiac output increased by approximately 50%. However in a patient
with MS, they will have a fixed cardiac output state, which results in worsening pressure
through the pulmonary circulation and into the right heart. The risk of decompensation
depends on the severity of MS.
When the mitral valve area of 4-6 cm2 is reduced to 2 cm2 the symptoms of MS start to
appear. MS prevents emptying of the left Atrium and subsequent filling of the left
Ventricle, resulting in decreased Stroke Volume and thus, decreased cardiac output. As the
stenosis worsens the left Atrium dilates and left Atrial pressure rises. A pressure gradient
develops between the left Atrium and the left Ventricle. This back pressure leads to
pulmonary congestion, which can lead to Pulmonary Oedema. Long standing pulmonary
venous congestion leads to chronic Pulmonary Hypertension.
Women with severe MS cannot tolerate the CVS demands of Pregnancy. The increasing
volume load and tachycardia together with the Fixed Cardiac Output of MS cause a
progressive deterioration resulting in cardiac failure.
The increased HR limits the time for LV filling, resulting in increased Left Atrial and
Pulmonary Pressures. When the pulmonary capillary pressure exceeds the blood oncotic
pressure, Pulmonary Oedema develops. Atrial fibrillation worsens this further, and there is
a High Risk of Systemic Emboli.

 Specific Management issues when she presents in established labour:
 The risk of maternal death is greatest during labour and during the immediate post-
partum period.
 Haemodynamic goals for established labour are:
Afterload maintenance.
Heart Rate and Rhythm Control.
Careful Fluid Balance.
 Neuraxial blockade (Epidural) is often placed early to block tachycardia due to
sympathetic stimulation. A block should be achieved slowly and hypotension managed
with Alpha agonists. Epidurals can be titrated and Opioids utilised providing analgesia and
fewer haemodynamic effects.
 Delivery is often assisted, to limit labour duration and valsalva. If, despite maximal
medical treatment, pulmonary hypertension or NYHA III/IV are present, then Caesarean
section should be considered.
 Post delivery, patients are at risk of _lash Pulmonary Oedema, which occurs due to the
resultant decompression of the inferior vena cava along with auto-transfusion due to
uterine compression causing a sudden increase in preload.
This can be managed with head up positioning, increased FiO2 and if unstable intubation
and ventilation with adequate PEEP.
 Drugs; If Oxytocin is used, it should be administered cautiously due to its vasodilating
effects on the systemic circulation and its ability to increase pulmonary vascular resistance
(PVR). Ergometrine should not be used due to its pulmonary vasoconstriction effects.

3- Management of Pre-Eclampsia
A 25 year-old woman who is 37 weeks pregnant and known to have pre-eclampsia is
admitted to your labour ward with a BP of 160/110 mmHg on several readings.
(a) What is the definition of pre-eclampsia (1 mark) and which related symptoms should pregnant
women be told to report immediately? (2 marks)
(b) How should this patient be managed following admission to your labour ward? (12 marks)
(c) What changes would you make to your usual general anaesthetic technique for a pregnant woman,
if this woman needed a general anaesthetic for caesarean section? (5 marks)
 Pre-eclampsia: Hypertension (>140/90 on two occasions or 4 hours apart) presenting

after 20 weeks of Pregnancy with significant Proteinuria (Urinary Protein: Creatinine ratio
> 30 mg/mmol or 24hr urine collection with > 300mg protein).
Women should be told to Report Immediately:
 Severe Headache
 Visual Disturbance
 Abdominal/ Subcostal Pain
 Reduced Fetal Movement
 Management:
• If symptomatic, this would be defined as severe pre-eclampsia (BP >160/100).
MDT approach with involvement of senior members of Midwifery, OBGYN, Neonatology
and Anaesthetics teams is essential.
• Continuous fetal monitoring with CTG.
• Bloods should be checked 6 hourly at a minimum - U+E (Kidney function), FBP (Platelet
count), Coagulation studies and LFT’s (Liver Enzymes) are required.
• Patient should be catheterised with hourly Urine Output Monitoring.
• Fluid restriction to < 80 ml/hr (unless on-going losses).
• Invasive Arterial Blood Pressure Monitoring and continuous monitoring in an HDU.
• BP Control: initially with PO Labetalol (or Nifedipine); aiming for BP<150/80-100mmHg
reducing at around 1-2mmHg/min. If inadequate
reduction, IV Labetalol and/or Hydralazine should be used.
• Good Analgesia is imperative. If no contraindications, Epidural Analgesia is

recommended. Bloods should be checked within 2 hours prior to regional anaesthesia,
checking for Thrombocytopenia, rapidly falling platelets or DIC.

• Seizure Prophylaxis or Treatment is with Magnesium sulphate. Initially a 4-5g bolus is
given over 5 minutes, followed by an infusion of 1g/ hour for 24 hours. Further seizures to
be treated with 2g boluses. Seizures should be treated as an emergency in ABCD.
• Delivery is the only definitive treatment, and in the presence of severe symptoms this
may be operative.
 General Anaesthetic Technique:

• Ensure treatment for hypertension is on-going, and BP maintained <150/100mmHg
• In addition to the standard, invasive arterial BP monitoring is recommended.
• The hypertensive response to laryngoscopy must be avoided. This may be achieved with
a number of agents, including IV Alfentanil, Remifentanil, Esmolol, Labetalol, topical
Lidocaine or a combination of the above.
• Airway may be particularly difficult and plans should be made to deal with this. Upper
airway oedema should be expected, and a smaller than predicted ETT may be required.
• Non-depolarising muscle relaxants are potentiated by Magnesium. Therefore smaller
does than usual may be used and careful monitoring of adequate reversal is required.
• Care should be taken to not exceed fluid restrictions.
• Be prepared for potential coagulopathy, significant blood loss and DIC. Large bore IV
access is essential.
• Patient will be at a higher risk of PPH. If PPH occurs, Ergometrine should be avoided.
• Good post-operative analgesia is required. TAP blocks may be possible if coagulation and
platelets are within normal limits.
• Close post-operative monitoring is essential; this may be in HDU setting. Hypertension
may be persistent, and pulmonary oedema may occur.

4- Testing Spinal Block in Obstetrics
(a) Which methods of testing may be used to confirm the adequacy of a spinal block for elective CS?
(b) Describe the actions you could take if your spinal block proves inadequate on testing prior to
starting surgery for an elective (category 4) Caesarean section. (3 marks)
(c) What are the early symptoms and signs of a spinal block that is ascending too high? (5 marks)
 The methods of testing that may be used to confirm adequacy of spinal block can be
divided roughly into three categories corresponding with the Afferent, Efferent, and
Autonomic Nervous Systems.
Afferent (sensory Aδ, C & Aβ) function can be assessed by:-
· Pinprick
· Cold
· Touch
· Skin pinch
· Pressure
· Vibration
· Proprioception
· Tetanic stimuli – (correlates well to surgical anaesthesia area in research)
The upper end of the block may demonstrate a wide zone of differentiation of different
testing modalities. This can be over up to 6 dermatomes with the block to cold being
higher than pinprick which is higher than tough. Block to touch at T5 is associated with a
low incidence of intra-operative pain. Cold sensation is routinely used clinically, thus it is
appropriate to aim for 2-3 dermatomal segments above that required for surgical
anaesthesia to be insensitive to cold testing.
Efferent (Motor) function can be assessed using Bromage Scale

· 0 = No motor block
· 1 = Inability to straight leg raise but able to move knee and feet
· 2 = Inability to straight leg raise or move knee, able to move feet
· 3 = Complete motor block
This is a crude testing method although Bromage 3 indicates that the spinal block has
reached the high lumber segments
Autonomic features; are associated with spinal anaesthesia but are unreliable in
determining the extent/ adequacy of block. The features include:
· Hypotension - Bradycardia - Colour changes - Temperature changes.

 First of all I would require to determine if it was a complete or partial failure of the
block.If after 20 mins there was complete block failure then this is usually due to a
technical failure. I would seek senior advice but this situation is likely to require a repeat
attempt at the spinal anaesthesia.
More likely testing will reveal a partial

block failure. This may be due to:
 Drug factors.
 Technical factors.
 Patient factors.
 Inadequate dose of LA.
 Inadequate Baricity of LA.
 Needle displacement.
 Aberrant anatomical features.
If the block is developing, and particularly if hyperbaric solution used, positioning of the
patient in the first 20 minutes can help achieve block development as spread up to the
thoracic curve is required to achieve T5 block. The exact positioning will depend on the
pattern discovered during testing but could include
· Supine with wedge under right hip
· Supine with >15° lateral tilt
· Full lateral position
· Oxford position (left lateral tilt with slight head down and pillows under shoulders
and head to raise thoracic and cervical spine)
If the block is fully developed but remains inadequate this raises a dilemma and I would
seek senior advice. Repetition of the spinal is a possibility but using too much local
anaesthetic increases risk of a high spinal while using too little may result in ongoing
inadequacy of the block. Perhaps the safest option may be placement of an epidural with
titration of local anaesthetic to effect to achieve desired level of blockade.
As this is an elective (category 4) caesarean section discussion with the patient is also
important. Close monitoring to ensure maternal and foetal stability throughout is vitally
important. Assuming stability, and in discussion with the patient and obstetric team, a final
option would be postponement of the caesarean section with view to reassessment.
Should there may clinical concern the option of general anaesthesia with senior
anaesthetic support is likely to be the most appropriate.

 Early Symptoms and Signs of a High Spinal Block:
A spinal block at a level high enough to cause inadequate ventilation and cardiovascular
instability is too high and called a high or complete spinal.
The signs and symptoms are associated with depression of brainstem activity either due to
direct anaesthesia of brainstem or 2ry to ischaemia due to profound hypotension
associated with cervical spinal block.
The early symptoms and signs include bradycardia and hypotension which are not specific
to a high spinal.
Early Symptoms include:
· Nausea & Vomiting.
· Shortness of breath.
· Upper limb weakness including inability to grip.
· Upper limb altered sensation.
· Paraesthesia (tingling) upper limbs.
Early Signs include:
· Rapid spread of analgesia.
· Profound rapid motor block.
· Foetal heart rate decelerations.
· Severe hypotension.
· Recurrent hypotension despite treatment.
· Bradycardia.
· Weak phonation.
· Hyper to hypoventilation or apnoea.
· Loss of consciousness.

5- Post Dural Puncture Headache (PDPH)
The obstetric team tell you about a patient who is 2 days post-partum with what they
suspect is a post-dural puncture headache (PDPH).
(a) What is the differential diagnosis of post-partum headache? (8 marks)
(b) What features, in this patient, would lead you to consider a serious underlying cause? (7 marks)
(c) You diagnose a PDPH and arrange treatment by epidural blood patch (EBP). What are the described
risks of EBP? (5 marks)
 Differential diagnosis of post-partum headache:

 Non-specific/tension headache.
 Migraine.
 Pregnancy related: Pregnancy induced hypertension, Pre-eclampsia/Eclampsia.
 Iatrogenic: Post-dural puncture headache
 Infective: Meningitis, encephalitis, sinusitis
 Vascular: Subarachnoid haemorrhage, cerebral infarction, cortical vein thrombosis.
 Space occupying lesion: cerebral tumour.
 Posterior reversible Leucoencephalopathy Syndrome.
 Serious Underlying Cause:

 Associated hypertension.
 Deranged liver function tests and low platelets indicative of HELLP syndrome.
 Seizure activity.
 Reduced level of consciousness.
 Fever in keeping with infective cause.
 Petechial rash.
 Unilateral headache.
 Focal neurological signs particularly motor deficits.
 Risks of Epidural Blood Patch (EBP):

 Temporary and permanent nerve damage including paralysis
 Subdural haematoma
 Meningitis/arachnoiditis
Specific to EBP:
 Further dural tap and worsening of headache
 Recurrence of headache
 Failure/requirement for repeat procedure
 Backache  Radicular pain
 Bradycardia  Seizures.

5- Jehovah’s Witnesses and Caesarean Section
You are asked to review a woman in the anaesthetic antenatal clinic. She is 30 weeks
pregnant and a Jehovah’s Witness. She requires an elective caesarean section at 39 weeks
due to a low-lying placenta and a fibroid uterus.
a) What specific issues should be discussed with this patient based on the history outlined above?(10 marks)
b) Give the advantages and disadvantages of using intra-operative cell salvage during CS ? (10 marks)
 Anaesthetic Plan:
General Anaesthetic due to increased Risk of Major Bleeding.
 Post-op analgesia, will be more difficult to manage than for regional technique.
 Consent for TAP blocks.
 Partner will not be present in theatre for birth.
 Need for invasive monitoring - Arterial Line, consider Central Line.
Is she taking any medication that will impair clotting? Can these be stopped?
What blood products will she accept and refuse?
Would intra-operative cell salvage with a closed loop be accepted?
Can we Optimise Haemoglobin Pre-op?

- Oral or Intravenous Iron, Erythropoietin
Can consider pre-op placement of internal jugular balloons to reduce bleeding.
 Senior clinicians from Obstetrics and Anaesthetics will be present during the operation.
 Increased risk of major haemorrhage - low lying placenta.
 Further increase in risk due to limitations on blood products that Jehovah’s witness will
accept Increased risk of:
*Emergency Hysterectomy.
*Critical Care Stay Post-Op.
*Death.
Does she have an Advanced Directive?
Has she discussed the issues of  Risk of Bleeding and Blood Products with her Religious Leader?
Will need to fill in a specific Trust consent form for Jehovah’s Witness patients.
We will respect her wishes.

 Advantages and Disadvantages of using Intra-operative Cell Salvage during CS:
Advantages
 Reduced use of allogenic blood transfusion (valuable resource)
 Therefore reduced risk of:
 ABO incompatibility.
 Infection.
 Haemolytic Transfusion Reactions.
 Anaphylaxis.
 Transfused Autologous Blood has normal levels of 2,3-DPG.
 Transfused Autologous blood has longer intravascular lifespan than Allogenic blood.
 No pre-operative preparation of patient needed.
 Only >500ml of blood needed for processing - blood loss in CS often higher than this.
Disadvantages
 Costof set up and disposables
 Need for trained personnel to operate equipment
 Risk of:
 Infection in processed blood.
 Air Embolism.
 Amniotic Fluid Embolism (should be prevented with leukocyte depletion filter)
 Haemolysis and free Haemoglobin in transfused blood leading to Nephrotoxicity.
 Microaggregates —> Microembolism
 Cell Salvage Syndrome:
Dilution of blood in saline can produce cellular aggregates that activate clotting and
increase vascular permeability.
 Electrolyte Imbalance
 Leukocyte activation —> lung damage
 Autologous blood transfusion does not contain Platelets or Clotting factors -
- Additional blood products will be required in major Haemorrhage time delay from
collection to transfusion due to processing.

6- Non-Obstetric Surgery in Pregnancy
A 28 year-old woman presents for acute Appendicectomy - she is 22 weeks pregnant.
a) List the risks to the fetus during anaesthesia for the mother. (5 marks)
b) How can the risks to the fetus be minimised? (10 marks)
c) What additional pre and intra-op. steps would you take to ensure foetal safety if she was 27 weeks?
 The Risks to the Fetus during Anaesthesia for the Mother:

Spontaneous Abortion/preterm labour
IUGR
Placental ischaemia
Fetal hypoxia
Fetal acidosis/ion trapping
 How can the Risks to the fetus be Minimised?
Pre-operatively
 Confirm the diagnosis.
 Manage conservatively/delay surgery until 6 weeks post-partum where possible.
 Optimisation with Fluids/Antibiotics/Analgesia.
 Avoid premedication.
 Involve obstetric/midwifery team.
 Consider prophylactic Tocolytics.
Intra-operatively
 Experienced surgeon to minimise anaesthetic and operative times.
 Senior anaesthetist.
 Left lateral tilt.
 Adequate pre-oxygenation.
 Anticipate increased difficult airway.
 Ranitidine/Sodium Citrate/Metoclopramide.
 Modified RSI to prevent aspiration.
Reduce anaesthetic agent doses.
 Use drugs known to be safe in pregnancy
 Avoid drugs that cross the placenta/cause vasoconstriction/increased uterine tone.
 Consider prophylactic Antibiotics.
 Maintain adequate BP to maintain placental perfusion and normal pO 2, pCO2 ~ 4 …etc
 Consider FHR monitoring/Tocodynamometer with personnel capable of interpretation.
 If laparoscopic ensure minimal pressures (<15mmHg) and care with trocar placement.

Post-operatively
 Nurse on appropriate ward.
 Joint care between General surgeons and Obstetricians/Midwife.
 Consider FHR monitoring, Tocodynamometer (CTG).
 Adequate post-operative Pain relief to Avoid Vasoconstriction.
 Avoid NSAIDs (PDA closure).
 VTE prophylaxis.
 Additional pre and intraoperative steps would you take to ensure foetal safety if she
was 27 weeks pregnant:
Pre-operatively:
 Involvement of Obstetric team including plan for preterm labour and delivery.
 Involvement of paediatricians/PICU.
 Consider Steroids for lung maturation.
Intraoperatively:
 Be aware that physiological effects of pregnancy may be more pronounced.
 FHR and FHR variability monitoring/Tocodynamometer.
 Presence of Obstetricians/midwife in theatre.

7- Intra-uterine Death (IUFD) and Puerperal Sepsis
(a) What are the implications of a woman labouring with a known intrauterine death?
(b) How do the physiological changes of pregnancy complicate diagnosis, presentation and
management of sepsis and septic shock?
(c) What are the common organisms/causes for (i) Genital tract. (ii) Outside the Genital tract Sepsis?
(d) What are the risk factors for puerperal sepsis?
(e) Describe the principles of management of sepsis in the pregnant or postpartum patient.
 The Anesthetic implications of a Woman Labouring with a known intrauterine death:

 General care to help with psychological distress.
 Care provided in a quiet room, isolated from normal labour ward activity.
 One-to-one midwifery care.
 Free access of family members to support woman.
Obstetric Management  Method of Delivery:

 Previously women with IUFD were managed expectantly – approx 90% began
spontaneous labour within 3 weeks fetal death.
 Current practice: induce labour earlier given psychological distress of carrying fetus
and possibility of Coagulopathies/Sepsis.
 May require delivery by Caesarian section.
 Mandatory level 1 care (MEOWS) and possible transfer to level 2 care.
 Exclude Possible Causes :
-Antepartum: Congenital Malformation, Congenital Infection, Antepartum
Haemorrhage, Pre-eclampsia, Maternal Diabetes Mellitus.
-Intrapartum: Placental Abruption, Severe Maternal Or Foetal Infection, Cord
Prolapse, Uterine Rupture, Idiopathic Hypoxia-Acidosis.
Anaesthetic Management
 Should be offered to see duty anaesthetist at induction/in spontaneous labour to
discuss analgesic options (? Epidural)
 Assess for possibility of Coagulopathy +/- Sepsis
 Check FBP, Biochemistry inc CRP, Coag- screen
 Provide effective Analgesia: all usual modalities should be available. Particularly
important for IUFD given psychological stress
 Entonox
 Parenteral opioids: Diamorphine IM preferred over Pethidine, Morphine/
Fentanyl/ Remifentanil PCA according to protocol
 Supplementary regular IV paracetamol
 Regional Anaesthesia with Epidural PCEA – if not contraindicated

 Assessment for DIC/Coagulopathy and/or Sepsis should be undertaken before
performing Regional Anaesthesia.
 Maternal Sepsis can result in Epidural Abscess formation, Coagulopathy increases risk of
Spinal/Epidural haematoma
 Consider sedation
 Physiological changes of Pregnancy complicate diagnosis, presentation and

Management of Sepsis and Septic Shock:
Cardiovascular System Changes
Vascular changes
 SVR falls - due to vasodilatory effect of Progesterone, occurs as early as 8wks gestation
 Cardiac output increases hyperdynamic circulation – CO increases steadily due to
increased HR + SV to peak 30-50% above pre-pregnant values by 30wks gestation
 SV increase secondary to increased pre-load & end-diastolic volume (EDV) due to
increased blood volume (40% increase) overall increase of up to 2000ml blood volume
 C.O. increases by approx. 40% by end of 1st trimester
 Reduced blood pressure generally falls despite increased C.O. due to lower SVR
diastolic falls more than systolic
 Reduction in serum Albumin affects colloid osmotic pressure making women more
vulnerable to Pulmonary Oedema should Cardiac Failure occur.
 Implication for Sepsis:

Heart may be considered to be under ever increasing stress as a pregnancy progresses,
if Sepsis develops, this stress on her Heart will be further compounded by Sepsis-induced:
 Reduction in SVR.
 Vasodilation.
 Myocardial Depression, which may result in rapid haemodynamic collapse.
Respiratory System
 Oxygen requirements  & CO2 production  by 60% during pregnancy Anatomical &
Physiological changes occur to meet Metabolic demands.
 Increased Minute Ventilation; upto 45% by 2nd trimester mainly from  TV, minimal
increase in RR progesterone lowers CO2 response threshold of respiratory centre.
 Decreased FRC; by 20% upright, 30% supine position as uterus expands, diaphragm
pushed cephalad.
 Decreased PaCO2 – 4kPa at term compensatory increase in renal bicarbonate excretion

 Increased O2 consumption/decreased FRC means parturients become hypoxaemic
quickly during Apnoea (despite careful preoxygenation)
 Implication for Sepsis: factors

will reduce a woman’s ability to compensate for any
acidosis that develops as part of sepsis and septic shock, particularly if there is associated
respiratory failure.
Renal system
 Ureteric dilatation, caused by smooth muscle relaxation, and compression of the ureters
by the gravid uterus as they pass over the pelvic rim
 Implication for Sepsis: increases the risk of Pyuria and Pyelonephritis.
Haematological system
 Leucocytosis may complicate initial diagnosis as baseline WCC elevated in pregnancy.
 The Common Organisms/Causes for:

(i) Genital Tract Related Sepsis
Potential sources
- Chorioamnionitis.
- Endometritis.
- Septic Abortion.
Common pathogens
- Group A Streptococcal (GAS) – 13/29 sepsis related deaths in 2006-08 CMACE report.
- Others: E.coli, Clostridium, Staph aureus, Coliforms, ESBL.
(ii)Sepsis Outside the Genital Tract:
 Mastitis
-May lead to Breast Abscesses, Necrotizing Fasciitis and Toxic Shock Syndrome (TSS).
-During 2005–2008, two women died of mastitis-related sepsis, one with necrotizing
mastitis attributable to GAS and the other with S.aureus.
 Urinary tract infection
-Gram-negative bacterial infections are particularly associated with the urinary tract.
-Acute pyelonephritis should be treated aggressively
 Pneumonia
-Severe haemoptysis and low peripheral white cell count suggest PVL-associated
staphylococcal necrotising pneumonia, which has a mortality rate >70%.

 Skin and soft-tissue infection
-Intravenous cannulae/injection sites and caesarean or episiotomy wounds
-Skin and soft-tissue infections are particularly associated with toxic shock syndromes.
-Recurrent abscess formation, including labial abscesses, is a feature of PVL-producing
staphylococci.
-Septicaemic seeding of streptococci from a uterine focus may give rise to a
secondary focus in a limb, simulating a venous thrombosis.
-Women with suspected thrombosis who are systemically unwell with any features of
sepsis should be examined very carefully. Presence of shock or other organ
dysfunction mandates rapid referral to critical care.
 Gastroenteritis
-Salmonella and Campylobacter rarely cause severe systemic infection and should be
managed symptomatically unless features of bacteraemia are present.
-Diarrhoea and vomiting may be features of Toxic Shock Syndrome together with
features of profound sepsis. C. difficile is rare but
increasingly found in obstetric patients.
 Pharyngitis
-Most viral, but approx 10% of cases in adults are attributable to GAS.
 Infection related to regional anaesthesia
-Spinal abscess is a very rare complication after regional anaesthesia in obstetrics.
-The usual organism responsible is S. aureus, with streptococci, Gram-negative rods
and sterile specimens accounting for 15% each.
 The Risk Factors for Puerperal Sepsis:

* Obesity
* Impaired glucose tolerance / diabetes
* Impaired immunity / immunosuppressant medication
* Anaemia
* Vaginal discharge
* History of pelvic infection
* Amniocentesis and other invasive procedures
* Cervical cerclage
* Prolonged spontaneous rupture of membranes
* Vaginal trauma, caesarean section, wound haematoma
* Retained products of conception
* GAS infection in close contacts / family members
* Black or minority ethnic group origin.
 The Principles of Management of Sepsis in the Pregnant or Postpartum Patient:
Protocolised approach to the Early Resuscitation of the patient with Treatment directed
towards achieving the following goals within the First six hours after diagnosis of sepsis.
Resuscitation Goals:
* Central venous pressure (CVP): 8 - 12 mmHg.
* Mean arterial pressure (MAP) ≥ 65 mmHg.
* Urine output ≥ 0.5 ml/kg/h.
* Central venous (superior vena cava) 70% or mixed SvO2 ≥ 65%.
Fluid Therapy
* In the event of hypotension and/or a serum Lactate greater than 4 mmol/L: initial
minimum 20 ml/kg of crystalloid or an equivalent.
* Larger volumes may be required in septic shock but this must be done with careful
monitoring - myocardial suppression caused by sepsis and the existing strain of pregnancy
may make the patient more susceptible to fluid overload.
* Central Venous Pressure (CVP) monitoring may help guide effective Fluid therapy (but
should not delay resuscitation) - can also be used for Vasopressor and Inotrope infusion
and for sampling central venous blood to monitor tissue oxygenation.
* Other methods of monitoring cardiac output, e.g. ODM may be used to guide and
optimise fluid resuscitation if they are available.
Antimicrobial Therapy
* Intravenous Broad-Spectrum Antibiotics should be started as early as possible, always
within the First hour of recognising severe sepsis.
* The choice of antibiotics may be refined once a microbiological diagnosis has been made
and should be reviewed daily to optimise efficacy, prevent resistance, avoid toxicity and
minimize costs.
* Appropriate Cultures should be obtained if this does not cause a significant delay in
commencing antibiotic therapy. At least two sets of blood cultures are advised, of which
one should be taken though a fresh venous puncture.
* If any vascular access devices have been in place for more than 48 hours, a blood culture
sample should be taken from each of these. Other sites should be cultured as clinically
indicated including:
-Swabs from throat, Vagina, Baby (if infection suspected during labour and/or delivery)
mid-stream Urine
-Other relevant samples including: Sputum, Breast Milk, Stool if indicated
Blood Product Administration
- Common for patients with severe sepsis to develop Coagulopathy & Thrombocytopenia.
- If the patient is not actively bleeding and no invasive procedures are planned it may be
possible to tolerate the abnormal laboratory clotting results.
- If the platelet count falls to 5 x 109/L, platelets should be given regardless of bleeding.
- If there is significant Risk Of Bleeding or if Surgery or Invasive Procedures are planned,
platelets will be required to maintain the count above 50 x 109/L.
- Transfuse if Hb less than 7.0 g/dl with the aim of achieving a target Hb of 7–9 g/dl.
Vasopressors
- Aim to achieve and maintain MAP > 65 mmHg within the First six hours following
diagnosis of severe sepsis - Noradrenaline infusion if required.
Corticosteroids
- High-dose corticosteroid therapy is No Longer Recommended in sepsis management.
- Low-dose (< 300mg Hydrocortisone/day) may be used in adult septic shock when
hypotension remains poorly responsive to adequate fluid resuscitation and vasopressors.
Glucose control
- Intravenous insulin infusions are used to control hyperglycaemia in patients with severe
sepsis: Aim to Maintain < 10 mmol/L.
Other Treatments in Critical Care

 Stress ulcer/DVT prophylaxis
 Mechanical ventilation +/- CRRT if required
 Removing the source of sepsis
-Focus of infection should be identified as a priority and if surgery is necessary to
remove the source of sepsis, it should be considered early.
-If the uterus is the primary focus of infection, retained products should be excluded
by ultrasound examination and exploration of the uterine cavity considered.
 Hysterectomy should be considered if the woman is critically ill and may be life
saving.

8- Placenta Praevia
(a) What is Placenta Praevia? How is it classified?
(b) What is Placenta Accreta? (ii) Placenta Increta (iii) Placenta Percreta?
(c) What precautions would you take prior to anaesthetizing CS patient with ant. Placenta Praevia?
(d) What are the changes of Pregnancy with regard to Coagulation?
(e) What is Disseminated Intravascular Coagulopathy (DIC)? How is it managed?
 Placenta Praevia and its classification:

- Placenta praevia is a condition where a low lying placenta covers the internal cervical os
- Incidence = 1 in 200 deliveries
Risk factors:
*Muliparty.
*Previous Caesarean section / other uterine surgery.
*Advanced maternal age.
*Uterine trauma.
*Previous placenta praevia.
Classified by amount of OS covered:

*Marginal: minimal placental coverage of os.
*Partial: incomplete coverage of cervical os.
*Complete (Centralis): placenta covers entire internal cervical os, preventing vaginal delivery
of foetus.

 Placenta Accreta: refers to a placenta that is abnormally adhered to the Myometrium
but has not invaded it.
- Placenta Incretata denotes a placenta that has invaded the Myometrium
- Placenta Percreta is invasion through the serosa.
**Massive haemorrhage can occur when attempts are made at removing the placenta
after delivery
The Precautions would you take prior to providing Anaesthetic for

Placenta Praevia:
- Consideration as to whether Elective or Emergency procedure.
- Likely to be Significant Blood Loss.
- 2x large bore IV access.
- Fluid resuscitation if bleeding / haemodynamically unstable.
- Baseline FBC & Clotting studies.
- Ensure group and cross-matched and blood available.
- Prime rapid infuser.
- Have senior anaesthetist & obstetrician present.
- Will Require General Anaesthetic; prepare for this.
- Consider Cell Salvage.
- Invasive Arterial Monitoring.
- Make patient aware may need blood transfusion.
- Discuss need for HDU / ICU post-op in case of massive haemorrhage.

 The changes of Pregnancy with regard to Coagulation:
- Relatively Hypercoagulable state.
-  activity of Clotting Factors (I, VII, VIII, IX, X, XII).
- Decreased activity of physiologic Anticoagulants (including significant  in
Protein-S activity & Acquired Activated Protein-C Resistance).
-  levels of Fibrinogen.
- Enhanced fibrinogen catabolism by Thrombin.
- Procoagulant changes balanced by:

- Significant activation of fibrinolytic system.
- Deactivation of natural anti-fibrinolytics via  in activity of factors XI & XIII. This
causes decreased polymerisation of fibrin monomers into fibrin & diminishes cross
links of α2-antiplasmin to fibrin which makes fibrin less resistant to degradation.
- Platelet count can be low or normal.
- Dramatic short term  in Co-agulability immediately after delivery due to:
* Increase in factor V and VIII activity.
* Decrease in fibrinogen levels.
* Decrease in partial thrombophlebitis time (PTT).
* Fibrinogen Factor XIII Factor XI.
* Factor V Platelet count Anti-thrombin III.
* Factor VII PT Anti-factor Xa.
* Factor VIII PTT Platelet count.
* Factor IX.
* Factor X.
* Factor XII.
* Fibrin split products.
* Von Willebrand factor.
 Management of Disseminated Intravascular Coagulopathy (DIC): Consumptive Coagulopathy

 Aberrant activation of Clotting Cascade  Fibrin Deposition in Small Vessels.
 Combined with activation of Fibrinolytic Mechanisms Bleeding.
- Is a common final haemostatic disorder caused by other conditions eg; Sepsis

- Coagulation proteins and platelets can become depleted as consumed by ongoing
prothrombotic & fibrinolytic processes leading to bleeding
 Thrombosis and Haemorrhage can occur Simultaneously

Management of DIC
 Treat underlying disorder (eg; Sepsis).
 Supportive therapy.
 Evaluate Platelets, PT, APTT, D-dimer,Fibrinogen every 4-6 hrs or as clinically indicated
 Assess for bleeding or risk of bleeding.
 Blood products to be given if DIC with significant bleeding or elevated risk of bleeding:
 Transfuse Platelets to > 20 x 109/L (or > 50 x109/L if life-threatening Haemorrhage).
 Cryoprecipitate should be given to keep Fibrinogen > 1g/L.
 Transfuse FFP to keep PT & APTT < 1.5 times normal range.
 If symptomatic Anaemia or Hb < 8g/dL, PRC should be transfused.
 Reassess Patient and Lab Values:
 If bleeding improved & high bleeding risk no longer present, check bloods 8-12 hrly
until DIC resolved
 If bleeding improved but persistent high risk of bleeding, check bloods 6-8 hrly and
continue to administer blood products as above.
 If bleeding not improved / thrombosis present, aim for platelets > 50 x109/L.
 Consider heparin if persistent bleeding or thrombosis (not if major / life-threatening
haemorrhage).

9- Post dural Puncture Headache (PDPH) and Blood Patches
(a) How may a post dural puncture headache be prevented?
(b) What are the differential diagnoses for a headache in a post partum patient?
(c) What is the pathophysiology of post dural puncture headache
(d) What are the options for management of a PDPH
(e) Describe the process of performing a blood patch
(f) What are the complications of a PDPH and the complications of a blood patch?
 Prevention of Post-Dural Puncture Headache (PDPH) secondary to Spinal:

- Needle type: use of non-cutting spinal needle e.g. Whitacre, Sprotte is associated with 
incidence of PDPH as dural fibres are separated rather than cut.
- Needle size: smaller needle size thought to cause fewer PDPH however too small a
needle is associated with increased rate of spinal failure; optimal size
thought to be 25G or 27G.
Prevention of Post-Dural Puncture Headache (PDPH) secondary to Epidural:

- Using loss of resistance to Saline Technique may  incidence of PDPH by; continuously
anteriorly displacing dura with saline as needle tip approaches.
- If dural puncture occurs, inserting the catheter intrathecally at time of puncture and
leaving in situ for 24hours  incidence of PDPH (thought to  amount of CSF lost)
- Prophylactic intrathecal Morphine both at time of dural puncture and when removing
catheter 24hours later although NB associated with severe itch & delayed respiratory 
- Prophylactic blood patch can be done at time of dural puncture although not thought to
be effective

 The differential diagnoses for a headache in a post-partum patient:
- Pregnancy Related: PIH, pre-eclampsia/eclampsia, lactation headache.
- Infective: meningitis, encephalitis.
- Vascular: aneurysmal SAH, cerebral infarction, cortical vein thrombosis.
- Iatrogenic: PDPH.
- Space occupying lesion: Cerebral Tumour.
- Non-specific: Migraine, Tension Headache, Dehydration, Exhaustion.
 The Pathophysiology of post dural puncture headache:

CSF leaks out through dural puncture site leading to intracranial hypotension this
causes Pain by 2 Mechanisms:
- Traction on cerebral structures such as dura/meninges/veins.
- Compensatory Vaso- & Venodilation (secondary to activation of Adenosine receptors in
response to decreased intracranial volume) the vasodilation is worsened on standing/
sitting upright leading to increased pain in these positions.
 Management of a PDPH:
- Conservative: bed rest and ensuring patient is: Adequately Hydrated, Avoiding any
stooping or heavy lifting, or Constipation.
- Pharmacological:
* Simple analgesics such as NSAIDs and Paracetamol should be used regularly
* Caffeine: potent cerebral stimulant (therefore beware risk of seizures in pre-
eclamptic patient); is also a cerebral vasoconstrictor therefore thought to reduce
pain associated with cerebral vasodilation (although limited evidence available).
- Can be given in IV/tablet form or patient can be encouraged to drink highly
caffeinated drinks
* 5-HT3 antagonist e.g. Sumatriptan, used in treatment of Migraine, thought to act as
cerebral vasoconstrictor synthetic ACTH thought to increase retention of CSF
although not commonly used in clinical practice.
- Invasive:
- Epidural Blood Patch (EBP) involved autologous injection of 10-30ml of blood into
the epidural space. It is thought to tamponade the puncture site, increasing
intracranial pressure, relieving the headache. Subsequent clot formation may
prevent further leak of CSF epidural patching using saline or Dextran solutions have
also been described however are not as popular as EBP.

 Performing a Blood Patch:
- Typically done 24-72 hours following dural puncture.
- Written informed consent must be gained from patient.
- Requires 2 trained staff (at least one Anaesthetist
competent at performing epidurals) +/- an assistant
- Strict Aseptic Technique must be used by both parties.
- Routine Monitoring should be attached.
- Ideally patient should lie in lateral decubitus position for comfort.
- The epidural is performed at the same level of puncture or the site below ; once epidural
space is identified, the second operator withdraws 10-30ml blood from peripheral vein.
- This is then passed to the anaesthetist who injects 10-20ml SLOWLY epidurally.
- If any back or radicular pain is experienced, injection is stopped
- The patient is advised to lie flat for 1-2 hours following procedure & avoid any heavy lifting
for a number of days following the procedure
 Complications of a PDPH and the Complications of a Blood Patch:
PDPH complications:
- Persistant pain preventing patient from carrying out new mother duties.
- Tinnitus.
- Hearing Loss.
- Rarely traction on intracranial structures can lead to Abducens Nerve Palsy.
EBP complications:
- Failure to relieve headache.
- Further dural puncture and worsening headache.
- Transient Bradycardia.
- Localised back pain and radicular pain.
- Infection (Meningitis).
- Subdural Haematoma.
- Arachnoiditis.

10- Uterine Inversion and Haemorrhage
(a) What is uterine inversion? What is the difference between complete and incomplete inversion?
(b) What are the potential risk factors for uterine inversion?
(c) What are the signs and symptoms of a patient who is experiencing an uterine inversion?
(d) Describe the (i) Pharmacological and (ii) Non-pharmacological options for management of
haemorrhage accompanying inversion
(e) Describe the specific surgical and anaesthetic management of uterine inversion.
 Uterine Inversion and the difference between complete and incomplete inversion:
- Serious, infrequent complication of childbirth
- Displacement of the uterine fundus, usually during the 3rd stage of labour.
- Complete inversion is when fundus passes through the cervix whereas incomplete if it
remains above this level.
- Can be classified according to anatomical severity:
Stage 1: inversion is intrauterine / fundus remains within cavity.
Stage 2: complete inversion through fibromuscular cervix.
Stage 3: total inversion: fundus protrudes through vulva.
Stage 4: vagina also involved with complete inversion.
Or by timing:
Acute: within 24hrs delivery)
Subacute: >24 hours postpartum).
Chronic: >1month postpartum).
 A life-threatening obstetric emergency due to associated blood loss and CVS instability.
 Blood Loss may be rapid / frequently underestimated.
 Mortality rate approach 15%.
 The potential Risk Factors for Uterine Inversion:

- Underlying causes not completely understood: 50% spontaneously in young Primparous.
- Occurs with vigerous fundal pressure and inappropriate umbilical cord traction during
3rd stage of labour in the presence of an atonic uterus.
- Associated Factors:
*Maternal: uterine structural anomaly / connective tissue disorder.
*Placental: fundal placenta/ placenta praevia / abnormal adherence.
*Umbilical cord: short.
*Fetus: Macrosomia.
*Labour: Precipitate labour / uterine atony.
*Iatrogenic: Antepartum tocolysis eg; MgSO4 / poor management 3rd Stage.
*Idiopathic

 Signs and Symptoms of a patient who is experiencing Uterine Inversion:
- Usual presentation of Major Haemorrhage and Abdominal Pain / Can vary depending on
degree / severity
- Displaced uterus while delivering the placenta; fundus cannot be palpated and uterus
may fill the vault or protrude from vagina.
- Usually associated with profuse, continued post-partum haemorrhage and shock out of
proportion to blood loss – thought to be neurogenic – Parasympathetic effect of traction
on the ligaments supporting the uterus +/- associated Bradycardia / probable under-
estimation of blood loss
- Exaggerated bleeding from placental site due to restricted venous outflow – loss related
to duration of inversion
- Shock in 40% cases with EBL of 2L
 Management of Haemorrhage accompanying Uterine Inversion:

Management has 2 important Components:
- Tx haemorrhagic shock – start immediately.
- Replacement of uterus: chance of immediate reduction 20-40% : if fails further attempts
should be delayed until haemodynamically stable. If possible leave placenta in place to
minimize blood loss
- Subsequent contraction of the cervix may require relaxation by Tocolysis or General
Anesthesia/Laparotomy in severe cases (Regional A.. doesn’t provide uterine relaxation)
- GA recommended to relax uterus / exposes mother to risk of GA (Aspiration /Hypoxic
brain injury / Death) and CV depression at a time of haemodynamic instability.
Pharmacological:
 IV Fluid Resuscitation +/- Blood Products.
 Tocolytic drugs: promote myometrial relaxation
 B2-agonists eg; Terbutaline 0.25mg - Generally considered drug of choice with a success
rate of 63% - readily available on labour ward / familiarity of use.
 GTN: small IV dose 50 - 200ug (rapid < 1 min / reliable/ short duration / little
haemodynamic disturbance
 Magnesium sulphate: 4g – takes at least 10 min to be effective.
 GA: treatment of choice if reduction remains difficult or severe haemodynamic
compromise.
Non-pharmacological:
 Manual external pressure on inverted uterus ‘Johnson Maneuver’ attempts to replace
uterus digitally – manual repositioning should be attempted without removing the
placenta if separation has not occurred.

 Hydrostatic replacement: O’Sullivan’s Hydrostatic Technique: done in theatre with patient
in lithtomy position. Warmed fluid infused into vagina – the created pressure used to
achieve reduction.
 Modified technique using 6cm Ventouse Cup.
 Specific Surgical and Anaesthetic Management of Uterine Inversion:

Surgical Management:
Laparotomy: various techniques including:
*The Huntington’s technique: the cup of inversion is identified and Allis forcep placed and
upward traction exerted
*The Haultain technique is where a longitudinal incision is made in the posterior uterine
wall and cervical ring releasing pressure and facilitating replacement.
*Use of a Ailastic cup.
Laparoscopic technique: has been described
Trans-vaginal approach: anterior and posterior transections of cervix used.
Anaesthetic Management
- Time critical factor in ttt (profuse haemorrhage will continue from exposed uterus)
- Hypovolemia: aggressive Resuscitaion of circulating volume and stability: Wide-bore IV
access x2 / consider invasive BP monitoring +/- CVP. Rapid IV fluids /
blood / vassopressors may be required.
- Blood products: may warrant massive transfusion (Request early): Goals to Maintain:
*Hct > 0.3
*Platelets >100
*Fibrinogen > 2
*Ionised Calcium > 1
*Temperaure > 36oC.
- Pain Control: often in severe pain: choice RA vs GA: regional risky in light of inadequate
vascular volume / GA will relax uterus but requires higher than usual concentrations with
associated CV depression.
- Pharmacological intervention may be needed to rapidly relax uterus to allow reinsertion
- Warraning use of GTN / Volatile agents in a hypovolaemic patient
- GA is often required to facilitate uterine reduction: rapid / focused anaesthetic history
and airway assessment must be performed along with immediate resuscitation. RSI
indicated.
- Consider post-operative care? HDU /ICU care depending of stability.

11- Intra-uterine Resuscitation
(a) What abnormalities on Cardiotocogram (CTG) might suggest fetal distress during Labour?
(b) Describe the principles of intrauterine foetal resuscitation during preparation for an emergency CS.
(c) What factors during labour & delivery impair a neonates ability to breathe spontaneously once born?
(d) Describe physiological changes occur when switching from a foetal circulation to a neonatal one.
 Abnormalities on Cardio-tocogram (CTG) might suggest fetal distress during Labour:

- Foetal Heart Rate (normal ranging from 110-160 bpm).
*Bradycardia (<110 bpm) can be indicative of foetal distress due to cord compression
and foetal hypoxia.
*Tachycardia can be due to foetal infection or chronic hypoxia, but may also be due to
maternal factors (stress, pyrexia) or excessive foetal movement and uterine stimulation.
- Variability in Foetal Heart Rate: normal variability is 5-15 bpm.
In foetal distress could be increased (>15 bpm), decreased (<5 bpm) or absent (<2 bpm)
- Decelerations:
*Late Decelerations:
- Commence more than 15s after the peak of uterine contraction.
- Associated with Decreased Uterine Blood Flow
*Variable Decelerations:
- Variable in timing and size.
- Caused by cord compression and Reflect Foetal Hypoxia.
*Prolonged Decelerations:
- Reduction in foetal HR >30 bpm for greater than 2 minutes.
- Caused by reduced foetal oxygen transfer, eg;
*Maternal Hypotension.
*Cord Compression.
*Uterine Hypertonia.
 Principles of intrauterine foetal resuscitation during preparation for emergency CS:
The aim of intrauterine foetal resuscitation is to  oxygen delivery to the placenta and
umbilical blood flow to reverse foetal hypoxia and Acidaemia. These measures can be
employed to ‘buy time’ when preparing for an emergency section:
 Stop Syntocinon Infusion to  uterine contractility & improve placental blood flow
 Position: move to Left Lateral to Reduce Aorto-Caval Compression and improve maternal
cardiac output OR Knee-Elbow Position in case of umbilical cord compression.
 Oxygen: to help improve maternal saturations and oxygen delivery.
 Intravenous fluids: increases cardiac output, reduces blood viscosity and has a

temporary tocolytic effect, increasing placental and umbilical blood flow.
 Low BP: Intravenous Vasopressor may be required
 Tocolysis: Terbutaline 250mcg is the first line choice.
 GTN sublingual spray (2 puffs up to 3 times) can also
be used. Caution should be noted for maternal
hypotension & increased risk of haemorrhage from a
relaxed uterus.
 Factors during labour and delivery may impair a neonates ability to breathe
spontaneously once born:
 Neonatal:
- Surfactant production begins at 24 weeks gestation.
- Premature delivery is associated with reduction surfactant production.
- More negative pressures required to overcome surface tension in the immature alveoli
during the first initial breaths of extra-uterine life.
 Maternal:
- Onset of labour initiates catecholamine surge, which leads to reabsorption of lung fluid
reducing viscosity of fluid in neonatal lungs and therefore subsequent work of breathing.
This normal response can be lost in situations where labour has not commenced, eg;
Elective Caesarean Sections.
- Surgical delivery also impairs normal physiological stimulus to co-ordinate 1st breath
such as auditory stimulation, temperature changes and touch associated with vaginal
delivery.
 Anaesthetic:
- Use of systemic Opioids and Volatile anaesthetics can blunt normal respiratory drive to
hypercarbia and hypoxia.
 Physiological changes which occur when switching from a Foetal Circulation to a

Neonatal one at birth:
- The transition from foetal to neonatal circulation requires:

 Increased Pulmonary Blood Flow.
 Removal of the Placenta.
 Closure of the Foramen Ovale, Ductus Arteriosus (PDA) and Ductus Venosus.

Closure of Ductus Venosus is achieved by:
- Closure of umbilical vessels at delivery due to increased O2 content.
- Clamping of umbilical vessels and removal of low resistance placenta.
- Passive closing of ductus venosus between days 3-7 of life.
Functional Closure of Foramen Ovale:
- Lung expansion and increased alveolar O2 content  Pulmonary Vascular Resistance.
- Marked increase in blood return to left atrium
- Reduction in Right Atrial pressure and subsequent increase in Left Atrial pressure
- Functional closure of Foramen Ovale with initial breaths post-delivery.
- Completely closed in 50% by 5 years; remains patent in 30% of adults.
Closure of Ductus Arteriosus (PDA) is achieved by:
- Decrease in pulmonary artery pressure and  in SVR reverses flow across PDA.
- Loss of Prostaglandin E2, produced in the placenta, leads to Vasoconstriction.
- Functional closure occurs by 60 hours in 93% of neonates.
- Permanent structural closure occurs by endothelial destruction and subintimal
proliferation over 4-8 weeks.

12- Amniotic Fluid Embolism (AFE)
(a) What is amniotic fluid embolism (AFE)?
(b) What risk factors have been associated with AFE?
(c) How does it present clinically?
(d) Describe the diagnostic criteria for AFE.
(e) What is the differential diagnoses?
(f) Describe briefly the principles of management.
 Amniotic Fluid Embolism (AFE):

-A rare, potentially fatal, syndrome that is unique to Pregnancy.
-It usually presents in the intra- or immediate post partum period.
-Initially thought to be caused by a mechanical obstruction in the maternal circulation
caused by Amniotic Fluid.
-Now believed it is caused by Fetal Antigens contained within Amniotic Fluid, which
stimulate a cascade of endogenous mediators (Anaphylaxis).
 Risk factors have been associated with AFE:

-There is limited evidence proving risk factors, however, the following appear to be
associated with a higher incidence of AFE.
 Maternal age over 35 years.
 Placental Abnormalities: Placenta Previa and Placental Abruption.
 Caesarean section or instrumental delivery.
 Pre-eclampsia and Eclampsia.
 Fetal Distress.
 Induction and augmentation of labour.
 Multiparity.
 Meconium stained liquor.
 Chorio-amnionitis.
 Uterine rupture.
 Microsomia. 
 Polyhydramnios.
 Clinical Presentation:
-Timing: most present intra-partum or in the immediate post-partum period.
-Maternal collapse associated with: Dyspnoea, Cyanosis, headache, Dysrythmia,
Bleeding and development of DIC, Uterine Atony and Bronchospasm.
-May also present with Seizures and Cardiac Arrest.

 The Diagnostic Criteria:
The UK Obstetric Surveillance System
criteria for defining a case of AFE is used in
the UK.
Either (in the absence of another clear

cause) one of more of: Acute Fetal
Compromise, Cardiac Arrest, Coagulopathy,
Convulsion, Hypotension, Maternal
Haemorrhage, Shortness of Breath and
Premonitory Sytmptoms (eg: restlessness
or agitation).
OR
It may be diagnosed at post mortem by
finding fetal squames or hair in the lungs
 The Differential Diagnosis:

Pregnancy specific:
Acute Haemorrhage, uterine rupture, Eclampsia and peripartum Cardiomyopathy
Anaesthetic specific: high regional block or Local Anaesthetic Toxicity (LAST).
Others: pulmonary embolism, air embolism, anaphylaxis, sepsis, cardiac ischaemia,

anaemia, asthma, chest infection, arrythmia or transfusion reaction
 The principles of Management:

-Treatment is largely supportive
-Early recognition and resuscitation is vital to maternal and neonatal survival.
-Senior obstetric, anaesthetic and intensive care staff should be involved early.
-The fetus should be delivered by the quickest and safest route.
-If CPR is ongoing: airway should be secured rapidly with a cuffed endotracheal tube,
peri-mortem section should be started by 4 minutes of CPR and there should be left
lateral tilt employed.
-Rapid IV fluids, vasopressors and inotropes may be necessary to improve cardiac output.
-Uterine tone should be maintained as per local policy.
-Majority of women will have evidence of coagulopathy and consultation with
haematology should guide therapy. Recombinant factor VII has been used.

13- Physiological Changes in Pregnancy
(a) Describe the hormonal changes of pregnancy
(b) Describe the physiological changes of pregnancy in:
(i) the cardiovascular system
(ii) the respiratory system
(iii) the haematological system
(c) What factors make a pregnant patient more prone to (i) a difficult airway (ii) aspiration?
 The Hormonal Changes of Pregnancy:

- Principle hormone of Pregnancy is Progesterone.
- After fertilisation, developing Placenta produces human Chorionic Gonadotropin (hCG).
- Sustains Corpus Luteum until 6-8th wk of pregnancy enabling it to produce Progesterone.
- After this placenta takes over as the main source of Progesterone
- Placenta also produces human Placental Lactogen;
* Effects are similar to growth hormone.
* May cause maternal insulin resistance & may also result in anatomical changes
similar to Acromegaly that are occasionally seen during pregnancy
- Thyroid gland hypertrophies during pregnancy, can increase in size by 20%
increased production of Thyroxine and Triiodothyronine are normally balanced by
increased production of thyroid binding globulin so the levels of the free hormones
remain the same
- Parathyroid hormone tend to fall during pregnancy as does the level of serum Calcium,
although the level of ionized Calcium remains constant due to the changes in the
serum Albumin concentration
- Pregnancy is diabetogenic state; relative insulin resistance & compensatory increased
insulin synthesis and secretion
 The Physiological Changes of Pregnancy in:
(I) The Cardiovascular System

- Overall hyperdynamic circulation.
- Vascular changes:
*SVR falls, due to vasodilatory effect of Progesterone, occurs as early as 8wks gestation.
*Blood flow to uterus increases to approx. 700ml/min at term.
*Increased blood flow to skin/kidneys but brain & liver unaltered.

- Cardiac Output : if arterial pressure is to be maintained (essential for effective utero-
placental functioning), cardiac output must increase initially by increasing SV, but
eventually plateaus then HR increases.
-SV increase secondary to increased pre-load & end-diastolic volume (EDV) due to
increased blood volume
- Overall increase of up to 2000ml blood volume.
- C.O. increases by approx. 40% by end of 1st trimester.
- Structural changes heart displaced upward & to left by gravid uterus.
- LV hypertrophy and dilatation flow murmurs quite common due to increased plasma
volume & cardiac output regurgitant murmurs due to cardiac dilatation.
- ECG changes:
*left axis deviation.
*ST segment depression.
*T-wave flattening.
- Reduced blood pressure generally falls despite increased C.O. due to lower SVR
diastolic falls more than systolic
- Aorto-caval compression: gravid uterus can compress both IVC and descending aorta in
supine position  Venous Return & therefore  CO as uteroplacental circulation
possesses no autoregulation – can lead to reduced placental perfusion
(ii) The Respiratory System:

- Oxygen requirements & CO2 production increase 60% during pregnancy anatomical &
physiological changes occur to meet metabolic demands:
-  minute ventilation (MV) – up to 45% by 2nd trimester mainly from increased TV,
minimal increase in RR progesterone lowers CO2 response threshold of respiratory centre
-  FRC; by 20% upright, 30% in supine as uterus expands, diaphragm pushed cephalad.
- PaCO2 : 4kPa at term with compensatory increase in renal Bicarbonate Excretion
-  O2 consumption/decreased FRC means parturients become hypoxaemic quickly
during apnoea (despite careful Pre-oxygenation)
(iii) The Haematological System:

- Physiological Anaemia of pregnancy  plasma volume 40-50% (from 6-8wks to
maximum at 32-34wks) but increased Red Cell Mass only 20%  dilutional anaemia.
- Hypercoagulable state to facilitate clotting at time of placental separation & prevent
bleeding during pregnancy 10-fold increased tisk of VTE / 25-fold increase post-partum
All clotting factors except XI and XIII increase decrease in natural anticoagulants
- Thrombocytopenia platelet production increases but platelet count decreases due to
increased destruction & haemodilution risk of pre-eclampsia and HELLP syndrome
- Leucocytosis
 (i) Factors make a pregnant patient more prone to A Difficult Airway:
- Hormonal changes to mucosal vasculature of respiratory tract - cause capillary

engorgement & oedema of upper airway
- Can be exacerbated by fluid overload/oedema assoc. with PIH/pre-eclampsia
- Can lead to upper airway obstruction
- May make BMV and tracheal intubation more difficult
- Smaller diameter ET tube may be required
- Increased BMI/chest diameter/larger breasts can make laryngoscopy more difficult.
(ii) Factors make a pregnant patient more prone to Aspiration:

- Gravid uterus displaces stomach upwards as pregnancy progresses   Gastric Pressure
- Decreased oesophageal sphincter tone
- Both contribute to cephalad passage of acidic gastric content
- In labouring, anxiety, pain of labour and opioid use (by any route) delay gastric emptying.

14- Thromboembolism and Pregnancy
(a) What are the physiological changes with regard to haematology and coagulation during pregnancy?
(b) Classify and list the disorders of coagulation encountered in pregnancy (20%)
(c) What are the risk factors for venous thromboembolism in pregnancy? (20%)
(d) Summarise the RCOG guidelines for thromboprophylaxis in pregnancy according to risk (20%)
(e) What is the management of a life threatening PE developing during the 2nd trimester of pregnancy?
 Haematological and Coagulation changes which occur during Pregnancy:

 Hematological changes begin as early as 4 weeks and are progressive.
 Increases in Progesterone and Oestrogen cause the kidneys to activate the Renin
Angiotensin System to retain Sodium and  total body water.
 Red Cell Mass  20% due to an  in EPO production. This increase is less than the
 in Plasma volume therefore Hb .
 White Cell Count  throughout pregnancy and peaks after delivery.
Changes occur to affect the Coagulation and Fibrinolytic System.

 Many of the Clottng Factors  and Anticoagulation Factors  causing Augmented
Coagulation and  Fibrinolysis.
 All Clottng Factors except XI and XIII gradually .
 Though there is an  in platelet production the overall count  because of

increased platelet activity and consumption.
 An increase in fibrinolysis in reflected in increase Anti-thrombin III, Plasminogen and
Fibrin Degradation Products (FDP).
 Disorders of Coagulation encountered in Pregnancy Classification:

(A) Clotting Factor Abnormalities (B) Platelet Abnormalities
Congenital coagulopathies: Quantitative abnormalities:
-Von Willebrands disease -Gestational thrombocytopenia
-Haemophilia A and B - Idiopathic/immunological thrombocytopenic purpura
-Anti-thrombin deficiency - HELLP syndrome
Acquired coagulopathies - DIC
-Pregnancy induced hypertension Qualitative Disorders:
-Placental abruption -
-Retain dead foetus -
-Amniotic fluid embolus -
-Liver disease
-Anticoagulants: Aspirin and Heparin

 Risk factors for Venous Thrombo-embolism in Pregnancy:
Pregnancy itself is a risk factor for VTE. The other risk factors in pregnancy for VTE
contribute to Virchow’s triad the components of which are changes in blood flow, altered
vessel wall and hypercoagulopathy. It is well known that the presence of Virchow’s triad
markedly increases the chances of a VTE forming.
Physiological Risk Factors: Maternal Risk Factors:
 Circulatory Stasis by Gravid uterus:  Age >35 years.
which obstructs venous return. This  Obesity.
with venous dilatation  venous stasis.  Smoking.
 Hyper-coagulable state: in pregnancy  Family history of VTE.
there is an increase in several pro-  Previous VTE: one of the most important
coagulant factors and a  in risks. Risk of recurrence is highest in
anticoagulants. unprovoked VTE
 Vascular wall injury: can occur during  Varicose Veins.
delivery.  Immobility.
Pregnancy Specific Risk Factors: Delivery and Post-Partum Risk Factors:
 Multiple pregnancies  Planned and emergency caesarean section:
 Pre-eclampsia. risk greater with emergency CS.
 Hyperemesis.  Placental Abruption.
 Multiparity.  Post-partum Infection.
 Assisted reproduction techniques(IVF)  Post-partum Haemorrhage.

 The RCOG guidelines for thrombo-prophylaxis in pregnancy according to Risk:
The guidelines recommend that:
 All women should undergo a documented assessment of risk factors for VTE in early
pregnancy.
 This assessment should be repeated if the women develops any antenatal problems or is
admitted to hospital.
 The patient can then be classed as Low, Intermediate and High Risk for developing VTE.
The following should be assessed:

o Age >35 years.
o Obesity (BMI > 30).
o Parity >3.
o Smoker.
o Gross varicose veins.
o Current infection.
o Immobility.
o Pre-eclampsia.
o Dehydration/hyperemesis.
o Multiple Pregnancy.
 If
less than three of these risk factors are present, the patient is deemed Low Risk and
mobilisation and avoidance of dehydration is advised in the antenatal period.
 If
three or more risk factors (2 or more if admitted to hospital) then they are deemed
Intermediate Risk and management changes (See below). If any of the following are present:
o Single previous VTE (no fhx or thrombophilia).
o Thrombophilia + no VTE.
o Medical co-morbidities e.g. SLE/cancer/inflammatory conditions.
o Surgical procedure eg; Appendictomy.
Then the patient is considered Intermediate Risk and antenatal prophylaxis with LMWH
should be considered and trust expert advice sought.
 If
any of the following are present:
o Single previous VTE +
o Thrombophilia or fhx
o Unprovoked/oestrogen-related
o Previous recurrent VTE >1
Then the patient is deemed High Risk and requires antenatal prophylaxis with LMWH.
The patient should also be referred to a specialist dealing with thrombosis in pregnancy.

 Management of a life threatening PE developing during the 2nd trimester:
 The priority here is maternal wellbeing as this is turn will affect the foetus.
 The management of any life threatening medical emergency is obviously with an ABCDE
approach however, specific management for pulmonary embolism is paramount.
 If the patient is haemodynamically unstable (Shocked/Hypotensive) , as would be
suggested with a life threatening PE a number of things must occur at once:
 Airway should be secured and protected, ideally with ETT whilst full monitoring as per
AAGBI guidelines is instigated.
 IV access should be obtained whilst Blood Pressure is supported with Fluids and
Inotropes if needed.
 If circulatory collapse has occurred then CPR should be initiated immediately as per ALS
guidelines, remembering Left Lateral Tilt throughout.
 Senior HELP should be sought and a decision made for:
 Anti-coagulant therapy.
Thrombolytic therapy.
Thoracotomy
Surgical Embolectomy on a case by case basis.
 All of this management is pointless if the underlying cause is not identified. Other causes
of maternal collapse must be ruled out and if suspicion of a PE is high then management
for this should commence immediately.
 An urgent CTPA or portable echo within 1 hour of presentation should be arranged.
However if the patient is in extremis then Immediate Thrombolysis should be considered
prior to confirmation.
 If a massive PE is present with cardiovascular compromise the RCOG guideline
recommends the initiation of IV un-fractionated heparin. An example of a regimen is a
loading does of 80units/kg followed by a continuous IV infusion of 18units/kg/hr.
 However the RCOG guideline admits that there is a case for immediate thrombolytic
therapy with massive PE and haemodynamic compromise as anti-coagulant therapy will
not reduce the obstruction of the pulmonary circulation.
 In the case of a life threatening PE, especially if there is haemodynamic collapse then
thrombolytic therapy should be initiated as soon as possible. During the delivery of
thrombolytic treatment full resuscitation should be on-going. If the woman is unsuitable
for thrombolysis or moribund then the case should be discussed with the cardiothoracic
surgeons with a view to urgent Thoracotomy.
 There are obviously concerns regarding maternal bleeding and adverse foetal effects
with thrombolytic treatment. The foetus is potentially viable if late in the second trimester.
 A number of case reports have been published on the use of thrombolytic therapy in
pregnancy. Problems reported included non-fatal maternal bleeding, three foetal deaths
and a risk of premature delivery.
 The commonly used thrombolytic agents are large molecules that do not cross placenta.
 Surgical intervention also carries the risk of morbidity and mortality to the foetus. The
risk to the baby for any treatment must be weighed against the risk of harm to the mother
and treatment should not be delayed which life is saving for the mother.

15- Epidural Space and Failed Regional Anaesthesia
(a) Describe the anatomical boundaries of the epidural space
(b) What types of pathology may affect epidural space location catheterisation?
(c) Describe the reasons behind failed spinal anaesthesia and how they may be prevented
(d) List the patterns in which failed regional block may occur
(e) Describe management of an elective CS under spinal during which the patient complains of pain.
 Anatomical Boundaries of the Epidural Space:

Superiorly:Fusion of the spinal and periosteal
layers of the dura at foramen magnum.
Inferiorly: Sacrococcygeal membrane
Anterior: Posterior longitudinal ligament,
vertebral bodies and discs.
Lateral: Pedicles and intervertebral foraminae.
Posterior: Ligamentum flavum, capsule of
facet joints and Laminae.
 Types of pathology may affect Epidural

space location Catheterisation:
Congenital
Achondroplasia, Congenital Adolescent
Scoliosis and Spina Bifida.(epidural
contraindicated)
Acquired
Ligamentum Flavum Hypertrophy, contributing to Spinal Stenosis, Foraminal Stenosis and
Disc Prolapse
 The Reasons behind failed Spinal Anaesthesia:
Failed spinal - due to the extent, quality, or duration of local anaesthetic action
Patient factors:
*Anxiety and Pain.
*Explanation (before and during the procedure) and gentle, unhurried patient handling
*Light anxiolytic premedication if anxiety.
*Local anaestheic infiltration SC and intradermal.
Operator
*failure to locate space
*Lack of careful attention to detail whilst performing spinal

Poor Clinical Technique
*Inexperience.
Equipment
*Inability to obtain CSF 'Dry Tap' due spinal lumen of needle blocked - ensure equipment
checked before use and never advance needle without stylet.
*Poor positioning of the patient due anatomical abnormalities of the spine (kyphosis,
scoliosis, calcification of ligaments, osteoporosis), obesity, and patient anxiety.
*Improve by patient on hard surface, flex whole spine, hips and knees. Avoid rotation.
Sitting> lying. Use assistant to position pt. Longer spinal needle if obesity.
*Incorrect needle insertion - good knowledge of spinal anatomy
-Midline and angle of needle important
-Ultrasound to locate depth of space and midline,
-Use Paramedian approach
*Pseudo-successful lumbar puncture: clear fluid but may be epidural fluid if previously had
*Glucose not definitely mean CSF
Inadequate Dose of Local:

*LAs volume/ concentration / baricity adequate for block required. adjunct opioid,
clonidine, ketamine. Combined spinal epidural technique.
*Loss of injectate: The connection between syringe and needle not attached tightly
*Misplaced injection- avoid displacement when attaching syringe to needle
*Fluid aspiration should confirm free flow- the dorsum of one hand should be anchored
firmly against the patient’s back and the fingers used to immobilize the needle, while the
other hand is used to manipulate the syringe.
 Patterns in which Failed Regional Block may Occur:

 Complete failure.
 Missed segments.
 One sided.
 Inadequate height.
 Sacral sparing.
 Management of CS under Spinal During which the Patient Complains of Pain:
 Ask nature of pain. Is it discomfort/pulling/pressure?

 Is there an element of anxiety?
 Is it sharp pain which would be more suggestive of inadequate regional.

Management:
 If anxiety is issue, offer Midazolam explaining amnesic effect.
 Stop operating.
 Test block again, maybe inadequate time to allow block to work.
 Manipulation of the patient’s posture to encourage wider spread of the injected LA.
 Repeat spinal in lateral position with drapes still applied.
 IV opioid such as Fentanyl/ Alfentanil
 N2O/O2 face mask
 LA infiltrate by surgeon
 Ask the surgeons to avoid precipitating factors such as uterine exteriorisation and
large paracolic surgical packs if possible as will cause discomfort and often unnecessary.
 Offer GA – RSI.
 Discuss with patient fully and document timing of offer and agreed action
 Follow patient up after delivery.
 Discuss events concerns and implications for future pregnancies.

16- CEMACH report 2006-8
(a) What is definition of maternal death according to the CEMACH report 2006-8? How is it classified?
(b) Discuss the categories of death in which anaesthetics may/was thought to have contributed? (20%)
(c) Summarise the recommendations that emerged from the 2006-8 report (20%)
(d) How do the physiological changes of pregnancy exacerbate sepsis and septic shock? (20%)
(e) List potential signs and symptoms of maternal sepsis (20%).
 CEMACH: The Confidential Enquiry into Maternal and Child Health, started in April 2003
Maternal Death: death occurring while pregnant OR within 42 days of termination of
pregnancy, from any cause related to or aggravated by the pregnancy but not from
accidental or incidental causes.
Classified as:
 Direct (eg; APH, Ectopic).
 Indirect (eg; PE, Heart Disease).
 Late (between 42 days and 1 year post-pregnancy).
 The Categories of Death:

 Failure to ventilate (repeated attempts at intubation during GA and tracheostomy
dislodgement).
 Post-operative complications:
- Opioid toxicity with PCA.
- Possible transfusion reaction.
- Cardiac arrest in substance abuser possibly related to Ergometrine.
- Aspiration on emergence from GA.
 Other: rare reaction to spinal empyema causing Disseminated Encephalomyelities.
 The recommendations that emerged from the 2006-8 report:

 Antepartum counselling.
 Interpreting service.
 Communication and specialist referrals.
 Early appropriate multidisciplinary referral.
 Regular updates in clinical skills.
 Identifying and managing sick women – use of MEOWS.
 Urgent treatment of systolic hypertension (>150)
 Education of patients and staff in early signs of sepsis &
aggressive treatment.
 Better reporting of incidents and deaths.
 Improved autopsy service.

 Normal Pregnancy Effect:
CVS:
 Hyperdynamic circ. masks early signs of sepsis (tachycardia, warm peripheries)
 Vasodilation more rapid & sudden hypotension & haemodynamic collapse
 Anaemia further reduced O2 delivery to tissues
 Lower albumin low oncotic pressure and increased risk pulmonary oedema
Resp:
 Reduced tidal volume/ Masks early signs
 Increased RR/increased MV Reduced compensatory methods
Renal:
Ureteric dilatation and external Increased risk compression of kidneys pyelonephritis
 Glycosuria Increased incidence UTI
 Reduced concentrating ability More profound dehydraion
Other: Failure to investigate radiologically and delayed diagnosis
 Signs and Symptoms of Maternal Sepsis:
- Pyrexia.
- Hypothermia (if severe).
- Tachycardia >100.
- Tachypnoea >20 (sensitive marker).
- Leucopenia <4.
- Diarrhoea or vomiting.
- Lower abdominal pain.
- Abnormal or absent foetal heart.
http://www.frca.co.uk/article.aspx?articleid=101045

17- Labour Pain Pathways and Inhalational Anaesthesia
(a) What are the causes and pathways of labour pain in the first and second stages? (20%)
(b) What are the potential benefits of labour pain? (20%)
(c) What are the adverse consequences of labour pain? (20%)
(d) List the non-neuraxial methods of pain relief in labour (20%)
(e) What are the advantages and disadvantages of inhalational analgesics in labour? (20%).
 Causes and Pathways of Labour pain in the first and second stages
1st Stage
- Uterine contraction and cervical dilatation.
- Pain transmitted by T10 to L1 Sympathetic Nerves.
- Displacement of other intra-abdominal structure by
gravid uterus can cause pain transmitted by the coeliac
plexus and from the diaphragm by the phrenic nerve.
2nd Stage
- Perineal pain
- Pain transmitted by Pudental Nerve (S2-4), Para-
sympathetic.
- Genitofemoral Nerve plays a role also.
- Foetal position may cause compression on adjacent
structures - most commonly back pain transmitted by L5-
S1.
 Potential Benefits of Labour Pain:

- Reassurance that labour is progressing
- Abnormal pains indicate complications such; Uterine Rupture and Placental Abruption.
- Positive psychological effect!.
 The Adverse Consequences of Labour Pain:

- Psychological distress.
- Increasing sympathetic activity  increased CO and SVR may lead to complications in
patients with pre-eclampsia and cardiac disease
- Increased Catecholamines & Vasoconstriction can cause  uteroplacental blood flow.
- Delayed gastric emptying

 The Non-neuraxial Methods of Pain Relief in Labour:
Non-pharmacological
- Psychological preparation and support.
- TENS.
- Water baths.
- Hypnosis.
- Acupuncture.
- Aromatherapy.
- Reflexology
- Sterile water injections in the sacrum.
Pharmacological
- Parenteral opioids administered by midwife- Pethidine or Diamorphine or rarely
Morphine and fentanyl given IM or IV.
- Patient controlled Analgesia: Remifentanil PCA or Fentanyl (declining in
use due to accumulation with prolonged use).
- Inhaled Analgesics- Entonox (N2O with O2) or Inhalational Anaesthetic (Isoflurane)
 Advantages and Disadvantages of Inhalational Analgesics in Labour:

Advantages
- Paient feels in control of her Analgesia.
- Patient will stop using the drug if she becomes very sedated (safety feedback mechanism).
- Reversible Effects.
- No Accumulation.
- Minimal Metabolism.
Disadvantages
- Sedative.
- Emetic.
- Increased respiratory depression when used in combination with Opioids.
- Scavenging is rarely available in delivery suites so potential risk to staff of gas exposure.
- Difficulties with delivery of volatile agents - need for draw over vaporizers.

18- Maternal Cardiac Arrest and Peri-mortem Caesarean Section
(a) Classify the potential causes of maternal cardiac arrest (20%)
(b) What physiological/anatomical changes hinder resuscitation in pregnancy? (20%)
(c) What modifications are necessary to the standard resuscitation procedures in a pregnant woman?
(d) What is the rationale for peri-mortem Caesarean section after 4-5 minutes? (20%)
(e) What factors influence the decision for a peri-mortem Caesarean section during resuscitation?
 Causes of Maternal Cardiac Arrest:

- Can be classified according to traditional ALS teaching in to 4H & 4T or into those that are
pregnancy or procedure specific.

- Thromboembolism, haemorrhage, AFE, eclampsia, toxins (either from self-poisoning or
iatrogenic such as magnesium or local anaesthetic), sepsis, cardiac failure (secondary to
congenital or acquired pathology) are all specific causes of cardiac arrest in pregnancy.
 Physiological / Anatomical changes hinder Resuscitation in Pregnancy:

Airway: large breasts & laryngeal oedema can hamper intubation attempts but there is
an increased Risk of Aspiration from increased volume and reduce pH of gastric contents
with reduced barrier pressure.
Breathing: reduction of FRC reduces time to desaturation with Apnoea.
Circulation: blood volume is around 100ml/kg therefore signs of massive haemorrhage
may late and or masked. After 20 weeks gestation the gravid uterus causes Aortocaval
compression and impairs Cardiac Output.
Other: changes in protein binding alter the pharmacokinetic profile of Local Anaesthetics
and pregnancy hormones reduce sensitivity to LA.
 Modifications are necessary to Resuscitation procedures in a Pregnant Woman:

- Early Cricoid Pressure should be applied if the air way is at
risk in an obtunded patient.
- Early intubation and ventilation is there indicated.
- Either Left Lateral Tilt or Manual Displacement of the
uterus should be used to ameliorate the effects of
aortocaval compression.
- In cardiac arrest Perimortem Caesarean Section should be
considered if ROSC is not obtained in 4minutes.
 Peri-mortem Caesarean section after 4-5 minutes:

 Facilitate mother resuscitation by emptying the uterus & relieve aortocaval compression.
 After 24 weeks this will also allow resuscitation of the neonate.
 Factors influence the decision for a Peri-mortem CS during Resuscitation:

 Gestational age: < 20 weeks not indicated 20 – 23 weeks foetal survival not probable, 24
or more weeks potential foetal survival.
 Features of Cardiac Arrest: duration of arrest, pre-arrest decline of mother with hypoxia,
foetal distress prearrest.
 Professional setting: staff equipment and resources to carry out perimortem hysterotomy
and NICU to continue neonatal care if needed.
19- Pre-eclampsia: Risk Factors and Magnesium (MgSO4)
(a) What are the criteria for the diagnosis of pre-eclampsia? (20%)
(b) What are the risk factors for pre-eclampsia (20%)
(c) Describe the classes of drugs available to treat hypertension associated with pre-eclampsia.
(d) Describe the symptoms and signs of magnesium toxicity (10%)
(e) How may hyper-magnesaemia be treated? (20%).
 The Criteria for the Diagnosis of Pre-eclampsia:

HTN after 20 weeks Gestation Systolic >140, Diastolic >90, with >0.3g Protein in urine in 24hrs/ 2+ on
dipstick. Considered severe if one or more of the following criteria are present:
 BP is ≥160 mmHg systolic and/or ≥110 mmHg diastolic (on 2 occasions at least 6 hr apart)
 Proteinuria of ≥5 g/24 hours or ≥3+ (on 2 random urine samples, collected at least 4 hr apart)
 Oliguria <500 mL/24 hours
 Cerebral or visual disturbances
 Pulmonary oedema or cyanosis
 Epigastric or right upper quadrant pain
 Impaired liver function
 Thrombocytopenia
 Fetal growth restriction.
 The risk factors for pre-eclampsia:

*Previous pre-eclampsia.
*Multiple pregnancy.
*Hypertensive disease.
*Nulliparity.
*Obesity.
*Diabetes.
*Anti-phospholipid syndrome.
 Classes of drugs available to treat hypertension associated with pre-eclampsia:

 Beta Blockers: Labetalol alpha & beta antagonist (1:7); SVR & HR 200mg PO or 50mg IV.
 Calcium Channel Blockers: Nifedipine 10mg causes vasodilation.
 Vasodilators e.g. hydralazine 5mg direct on vascular smooth muscle mostly arterial
 Centrally acting e.g. Methyldopa inhibits DOPA decarboxylase therefore reducing amount
dopamine (a pre-cursor for noradrenaline)

 Symptoms and Signs of Magnesium Toxicity:
 Nausea and Vomiting
 Respiratory muscle weakness.
 Cardiovascular depression.
 Reduced reflexes (patellar first sign).
 Drowsiness, double vision and flushing.
 Hyper-magnesaemia Treatment:
 10ml 10% calcium Gluconate.
 Supportive management for respiratory/CV system in ICU environment.
 Stop Mg infusion.

20- Remifentanil and Labour Analgesia
(a) Describe pharmacokinetics of Remifentanil & how these influence its suitability as labour analgesic
(b) What are the potential indications for a Remifentanil PCA? (20%)
(c) What are the potential contraindications for a Remifentanil PCA? (20%)
(d) List the maternal and foetal side-effects of Remifentanil (20%)
(e) What the main safety points you would include in a protocol for Remifentanil PCAs in labour ward?
 Pharmacokinetics of Remifentanil:
 Rapid onset of effect of around 1 minute.
 Peak effect at approximately 2.5minutes.
 Rapid metabolism by non-specific tissue and plasma esterases to inactive metabolites
 Clearance of 40ml/kg/min.
 Context sensitive half-life of 3 minutes after 3 hour infusion - no accumulation even after
prolonged administration.
 No accumulation in renal failure.
 Therefore suitable for the cyclical pain of uterine contractions – with PCA administration
and 2-3 minute lock out peak effect would coincide with second or subsequent
contractions.
 Provides modest analgesia with high maternal satisfaction.
 Side effects in mother and foetus/baby short lived due to rapid metabolism.
 Indications for a Remifentanil PCA:

-Analgesia for first stage of Labour.
-Alternative to those who cannot have an epidural.
-Analgesia for second/third stage – less reduction in pain scores.
-Analgesia for obstetric procedures – perineal repair, removal placenta.
-For Anaesthesia interventions eg; Epidural placement.
 Contraindications of a Remifentanil PCA:
-Allergy to Opioid drugs.
-Multiple pregnancy.
-Pre-eclampsia.
-IUGR.
-Drug dependency.
-Previous Pethidine within 4 hours.
-Previous Diamorphine within 12 hours.
Special Precautions:
-BMI >40
-Diabetes (on Insulin infusion)
 The Maternal and Foetal side-effects of Remifentanil:
Maternal side effects:
-Respiratory Depression.
-Oxygen Desaturation.
-Sedation.
-Dizziness.
-Nausea/vomiting.
-Itch.
-Bradycardia, Hypotension – uncommon.
Foetal side effects:

No study has confirmed an increase in non-reassuring CTG/in low Apgar scores/naloxone
requirement at birth – confirming rapid metabolism in the foetus
However potential for respiratory depression and oxygen desaturation.
 The main Safety points:

-Criteria for Remifentanil analgesia for established labour; gestation over 37 weeks.
-Contraindications.
-Informed Consent required.
-Administration: Dedicated cannula, patient shown how to use PCA and told to press the
button just before or at the start of a contraction, no other drugs via this cannula, only
patient to press PCA button, cannula to be removed when no longer needed
-Monitoring: Continuous SpO2, presence of midwife throughout
-Observations: specific Remifentanil PCA observation sheet, Sedation Score every 30 min.
-Indications for contacting an anaesthetist:
*Patient does not respond to voice.
*Respiratory rate <8 bpm.
*SpO2 remaining <95% despite Oxygen via nasal specs
Ideal Intravenous Opiate:

- Onset and offset matching time course of uterine contractions.
- Preserves uterine contractility.
- Reassuring CTG.
- Good analgesia.
- Little respiratory depression.
- Minimal neonatal effects so administration can be continued up to and during delivery.
- Gastric emptying should not be delayed should (or in case general anesthesia is require).

21- Pre-eclampsia
(a) Describe the pathophysiology of pre-eclampsia (20%)
(b) What are the features that support the diagnosis of pre-eclampsia? (20%)
(c) What is HELLP syndrome? (20%)
(d) Describe pre-anaesthetic assessment of a patient with HELLP syndrome prior to a Category II CS.
(e) Describe the management of an eclamptic seizure (20%).
 Pathophysiology of Pre-eclampsia:
- Precise aetiology unknown
- Genetic predisposition likely
- Autoimmune reaction against placenta may be involved
- Deficient placental implantaton and platelet aggregation within placental bed result in
placental ischaemia
- Vasoactive substances released by the ischaemic placenta lead to widespread endothelial
damage and vasospasm
- Endothelial dysfunction leads to increased vascular permeability
- Disordered prostaglandin metabolism: increase in thromboxane and decrease in
prostacyclin – leads to platelet dysfunction and further vasoconstriction
 Diagnosis of Pre-eclampsia:
Hypertension (SBP ≥ 140 mmHg, DBP ≥ 90 mmHg) and proteinuria (≥ 300mg in 24 hours) occurring
after 20 weeks gestation
Features of severe pre-eclampsia: (after 20 weeks gestation)
- Systolic BP: ≥ 160 mmHg
- Diastolic BP: ≥ 110 mmHg
- Proteinuria levels: ≥ 5 g in 24 hours
- Oliguria: < 500 mls in 24 hours
- CNS signs: headache, blurred vision, decreased
conscious level
- Pulmonary Oedema
- Epigastric/RUQ pain
 HELLP syndrome:
- Severe complication of Pre-eclampsia
- Haemolysis, Elevated Liver enzymes and
Low Platelet syndrome.
- Combination of micro-angiopathic haemolytic
anaemia, thrombocytopenia and hepatic ischaemia
with periportal haemorrhage and necrosis.

 Pre-anaesthetic assessment of a patient with HELLP syndrome prior to a Cat II CS
- History (AMPLE):
Allergies, Medical, Obstetric, Anaesthetic History, Medications, Fasting status.
- Examination:
Airway Assessment, also assess for haemodynamic instability, other features associated
with pre-eclampsia such as: Pulmonary Oedema, Hypertension,  level of conscious
and Oliguria.
- Investigations:
Check bloods for FBC, U&Es, LFTs, Coag, CRP, Magnesium and Calcium.
- Cross match 6 units of RBCs; as high risk of bleeding.
- May require Blood/Platelets/Cryo prior to C-section depending on blood results
- As high risk of bleeding, be prepared with level 1 transfuser and Cell Salvage.
- Insert wide bore IV access.
- Insert Arterial Blood Pressure Monitoring
- Not be suitable for Regional Technique due to low Platelets/Coag derangements.
- Antacid prophylaxis: IV Ranitidine 50 mg, IV Metoclopramide 10 mg, oral 0.3M Sodium
Citrate 30 ml.
- Consent patient for GA section, possible requirement for blood transfusion, cell salvage
- Discuss with consultant Anaesthetist and also Haematology for advice.
 Management of an Eclamptic Seizure:

- Left Lateral Tilt if ante or intra-partum.
- ABC, high flow Oxygen and obtain IV Access.
- Magnesium Sulphate, 4 g IV over 5 mins.
- Continue Magnesium as infusion at 1g/hr until 24hr post delivery or 24hr post seizure.
- Treat recurrent seizures with 2g IV Magnesium Sulphate bolus.
- If antenatal, decision has to be made regarding delivery.
- If seizures not terminated by magnesium sulphate consider Benzodiazpines/Phenytoin
and prepare for intubation and ventilation.

22- Adjuvant Opioids in Epidural Anaesthesia
(a) Describe the clinical effects of Epidural block according to level of blockade (20%)
(b) What are advantages of adding adjuvant Opioids to Labour Epidurals/Regional Anaesthesia for CS?
(c) How do intrathecally and epidurally administered opioids exert their actions? (20%)
(d) Compare and contrast Fentanyl, Morphine and Diamorphine (20%)
(e) What are the side-effects of Regional Opioids? How may these be minimised or treated? (20%).
 The clinical effects of epidural block according to level of blockade:

The effects of epidural blockade can be subdivided into sensory, motor and sympathetic.
Commonly, the sympathetic block will be two spinal segments higher than the sensory
block, and the motor blockade two below the sensory block
Effects will vary depending on the height of the epidural block and these again can be
subdivided into 1. Lumbosacral, 2.Mid/low thoracic, 3. High thoracic, as follows;
1. Lumbo –Sacral (L1-S5):

Sensory block involves pelvic visceral organs, perineum, lower limbs and buttocks. Motor
block involves Hip, knee and ankle flexors/extensors. Generally minimal sympathetic out
flow at this level so minimal sympathetic signs
2. Mid/Low Thoracic(T6-12):
Sensory involves abdominal organs and overlying skin. Motor block includes abdominal
muscles and lower intercostals/chest muscles. Blockade of the sympathetic chain at this
level results in vasodilation, hypotension, compensatory tachycardia, loss of sweating,
warm vasodilated peripheries
3. High Thoracic (T1-5):

Sensory includes chest wall and thoracic viscera and possibly medial aspect of upper arm.
Motor blockade includes the intercostals and arm weakness.
Sympathetic blockade includes the cardiac accelerator fibres, causing unopposed
parasympathetic, or vagal tone, with resultant bradycardia, hypotension and
cardiovascular instability
 Advantages of adding adjuvant Opioids to Labour Epidurals/Regional Anaesthesia:

- The advantages of adjuvant opioids are numerous
- They increase the efficiency and potency of the blockade
- Opioids do this by improving the depth of the blockade, reducing the latency, prolonging
the duration of the blockade

- They reduce the dose of local anaesthetic required, therefore, reducing any potential
local anaesthetic side effects or toxicity
- Opioids augment analgesia in the distribution of sensory blockade (they also exert a small
systemic effect as explained later).
- They increase the rapidity of onset of the block, which is of use particularly in the
emergency setting i.e. emergency caesarean section.
- They increase the duration, which is of use intra-operatively, reducing the likelihood of
pain intra-operatively.
- Opioids can be used in infusions, e.g. in continuous epidural infusions in labour safely.
Lesser doses of local anaesthetics are required; the advantage being that local anaesthetic
toxicity is LESS likely, which is of importance when being infused over longer periods
 Mechanism of Action of Opioids:

There are three main mechanisms.
- Opioid receptors (mu, kappa, delta and nociceptin) are found throughout the nervous
system, including various areas in the cerebral cortex, thalamus and hypothalamus, the
dorsal root of the spinal cord, and peripherally in non neural tissues. In neuroaxial
anaesthesia the vast majority of action is in the dorsal root of the spinal cord
- The local anaesthetic diffuses across neuronal tissue (either from the CSF in intrathecal
injection, or across the dura into the CSF then the SC in epidural injection) and the opioid
or ligand binds directly with the receptors in the dorsal horn. The rapidity and amount
amount of opioid that does this depends on its lipid solubility
- The second most common mode of analgesia is by convectional flow, along with the CSF
centrally to the brainstem, where the opioid binds with central opioid receptors
To a lesser degree again, the third mechanism is by systemic absorption, particularly in the
epidural space where the venous plexi mean that the opioids are absorbed into the
systemic blood and the opioids can therefore exert their effects centrally
 Fentanyl, Diamorphine and Morphine are all opioids which used as Neuroaxial Adjuvant
- Fentanyl is a synthetic phenypiperidine derivative, diamorphine is semisynthetic and
morphine naturally occurring
- Fentanyl and diamorphine are lipophilic (particularly fentanyl) and morphine is
hydrophilic
- Because of this fentanyl has the most rapid onset (5 minutes intrathecally,10 minutes
epidurally), followed by diamorphine, followed by the slowest onset with morphine 15
minutes intrathecally, 30 minutes epidurally)
- Fentanyl is 100 times more potent than morphine, diamorphine is 2 imes more potent
than morphine

- Fentanyl being very lipophilic is absorbed rapidly from the CSF and binds to the receptors
in the dorsal horn. Therefore it gives a “narrow band” of segmental analgesia. Very little is
carried by convection to the CSF centrally.
- As a result of its lipid solubility, Fentanyl is more likely to cause EARLY respiratory
depression if administered Epidurally due to rapid systemic absorption
- Morphine, being the least lipophilic, remains more so in the CSF. Therefore it binds less
rapidly to the receptors in the DH.
- Its longer duration stems from this slower diffusion across the neurones.
- It may also give a wider area of analgesia because it moves up the column of CSF by
diffusion
- Problematically, morphine is more likely to cause LATE respiratory depression and nausea
and vomiting secondary to central spread through the CSF
- Its other side effects are more pronounced than with the other two agents; urinary
retention and pruritus
- Diamorphine has a longer duration than Fentanyl but slightly less than Morphine (around
10-20 hours)
- As it is almost as lipophilic as Fentanyl rapid onset is usual and delayed respiratory
depression uncommon
- Pruritus is common with Diamorphine. It is a pro drug which is metabolised to active
metabolites Morphine and 6 Mono-acetylmorphine
 The Side Effects of Regional Opioids:

 If administered Intrathecally, the side effects may be more likely due to cephalad
spread secondary to upward CSF convection
 If administered Epidurally, the side effects may be more likely from systemic absorption
 Common side effects include Pruritus. This is best treated with Anti-histamines.
 Nausea and vomiting are common (20-50%) especially in females and when
administered intrathecally. Using an agent with minimal central CSF spread (ie; not
Morphine) will  the risk. Dopaminergic (D2) and 5HT3 stimulation in the CTZ which
causes this. Therefore use of anti-emetics such as Ondansatron can prevent or treat this
 Sedation and Respiratory Depression are concerning side effects. Close monitoring of
these patients up to 24 hr is required, with well labelled notes to ensure avoidance of
further opioid use and recognition that these patients are at risk. Supplemental Oxygen
may be of use. Naloxone can be used in an emergency to antagonise the opioid.
 Urinary retention, more common with Morphine. Standard practice to catheterize.
 Other less common: CNS excitation and thermoregulatory dysfunction.
 Using safe doses will keep these side effects to a minimum.

23- Massive Obstetric Haemorrhage and Uterotonics
(a) Define the term massive obstetric haemorrhage (10%)
(b) What are the risk factors for obstetric haemorrhage (20%)
(c) What are the pharmacological methods - and mechanisms of action - for treating uterine atony?
(d) Describe the anaesthetic management of obstetric haemorrhage (35%).
(e) What surgical/radiological techniques exist to aid haemostasis? (15%).
 Massive Obstetric Haemorrhage:

Blood loss in a parturient > 24/40 gestation up to 6 weeks postpartum >1500 ml
or > one circulating blood volume
or drop in Hb >4g/dl
or requiring 4 units of PRBC
 The risk factors for Obstetric Haemorrhage:
Antepartum Postpartum
 Placenta praevia.  Vaginal/ Cervical tears.
 Placenta abruption.  Invereted Uterus.
 Uterine rupture.
 Trauma. Tissue
 Tone-uterine atony.  Retained Placenta
 Prolonged Labour.  Thrombin
 Mutiple Gestation.  Inherited or Acquired Coagulopathy
 High parity.
 Prolonged Oxytocin use.
 Macrosomia.
 Polyhydroamnios.
 Trauma.
 Pharmacological Methods & Mechanisms of Action for treating Uterine Atony:

Syntocinon- oxytocin analogue, mimics action of uterine contraction via oxytocin receptor
on the uterus. 5- 10 iU bolus. Side effects, hypotension, tachycardia
Ergometrine-ergot alkaloid causes uterine and vascular smooth muscle contraction. IM
250-500 micg . Side effect coronary spasm, chest pain, palpitations, hypertension,
bradycardia, GI symptoms, nausea,vomiting,diarrhoea
Syntometrine-Combination: of syntocinon and ergometrine
Carboprost Promethamine (Hemabate-15 methyl PGF2 alpha)- Binds to PGF2 receptor
causing myometrial contraction. 250 micg repeated up to 2 mg. Side effects vomiting

diarrhoea, GI spasm, hives, flushing, bronchospasm, tacycardia, increase cardiac output
Prostaglandin (Misoprostol)- PGE1 analog, binds to prostaglandin receptors on uterus
causing myometrial contraction. 800 micg, does not require refrigeration. Side effects
diarrhoea, abdo pain.
 Anaesthetic Management of Obstetric Haemorrhage:

Initial
Two large-bore i.v. cannulae
Commence rapid saline infusion
Full left lateral if APH – head down, feet up
Oxygen 100% via facemask
Send blood for:
 Crossmatch 6 units.
 Full blood count.
 Coagulation screen.
 Call for senior help.
 Alert haematologist, mobilize portering service.
 Transfuse red cells as soon as possible.
Until then:
 Crystalloid,maximum 2 litre
 Colloid, maximum 1.5 litre
 Use group specific or O RH negative blood
 Warm resuscitation fluids
 Restore normovolaemia, monitor haematocrit and haemoglobin
 If massive bleeding continues, give FFP 1 litre, Cryo 10 units while awaiting lab results.
 Use coagulation screens to guide and monitor use of blood products
 Monitor pulse rate, blood pressure, blood gases and urine output
 Consider invasive monitoring to guide therapy,intraarterial BP.
 Avoid: Hypothermia, Cogulopathy, Acidosis
Definitive:
 Assess patient for Anaesthesia.
 Airway.
 Last Meal.
 Allergies.
 Coexisting medical condition.

 In haemodinamically unstable, GA, RSI.
 Ketamine 1.5mg/kg or Etomidate or cautious
Thiopentone/Propofol
 Regional contraindicated if , haemodynamic instability,
coagulopathy, spinal haematoma, surgery maybe lengthy,
risk of further deterioration.
 Uterotonics as per obstetrician request if post op.
 Be prepared to go to interventional radiology.
 Post op care on HDU/ITU.
 Surgical / Radiological techniques exist to aid Haemostasis:

 Bimanual compression.
 Manual removal of placenta.
 Uterine packing.
 Intrauterine tamponade baloon (Rusch/Bakri).
 Ligation of uterine and hypogastric vessels.
 Uterine brace suture (B-Lynch).
 Hysterectomy consideration.
 Selective embolization of pelvic vessels.
 Interventional radiology balloon angiography to internal
illiac artery.

Transfusion Management of Massive Haemorrhage in Adults
Patient
Patient bleeding
bleeding // collapses
collapses
Insert
Insert local
local arrangements:
arrangements:
Activation Ongoing
Ongoing severe
severe bleeding
bleeding eg:
eg: 150
150 mls/min
mls/min and
and Clinical
Clinical shock
shock
Activation Tel
Tel Number(s)
Number(s)
Administer
Administer Tranexamic
Tranexamic Acid
Acid –– esp
esp in
in trauma
trauma and
and ideally
ideally within
within 11 hour
hour
(1g
(1g bolus
bolus followed
followed by
by 1g
1g infusion
infusion over
over 88 hours)
hours)
•Emergency
•Emergency O O red
red cells
cells
-- location
location of
of supply:
supply:
Activate Massive Haemorrhage Pathway
** Time
Time to
to receive
receive at
at this
this clinical
clinical Call for help
area:
area: ‘Massive
‘Massive Haemorrhage,
Haemorrhage, Location,
Location, Specialty’
Specialty’
•Group
•Group specific
specific red
red cells
cells Alert
Alert emergency
emergency response
response team
team (including
(including RESUSCITATE
•• XM
XM red
red cells
cells
blood
blood transfusion
transfusion laboratory,
laboratory, portering/
portering/ Airway
transport
transport staff)
staff)
Consultant
Breathing
Consultant involvement
involvement essential
essential
Circulation
Transfusion lab 
Transfusion lab 
Take
Take bloods
bloods andand send
send to
to lab
lab:: Continuous
Continuous cardiac
cardiac
Consultant Haematologist 
Consultant Haematologist  XM,
XM, FBC,
FBC, PT,
PT, APTT,
APTT, fibrinogen,
fibrinogen, U+E, Ca2+
U+E, Ca 2+
monitoring
monitoring
NPT:
NPT: ABG,
ABG, TEG
TEG // ROTEM
ROTEM ifif available
available
and
and Prevent
Prevent Hypothermia
Hypothermia
Order
Order Massive
Massive Haemorrhage
Haemorrhage Pack
Pack 11 Use
Use fluid
fluid warming
warming device
device
Red
Red cells*
cells* 44 units
units
STOP THE FFP
FFP 44 units
units
Used
Used forced
blanket
blanket
forced air
air warming
warming
BLEEDING (*Emergency
(*Emergency O
XM
XM blood
O blood,
blood, group
blood depending
group specific
depending on
specific blood,
blood,
on availability)
availability) Consider
Consider 10
10 mls
mls Calcium
Calcium
chloride
chloride 10%
10% over
over 10
10 mins
mins
Give
Give MHP
MHP 11 22 packs
packs cryoprecipitate
cryoprecipitate ifif
Haemorrhage
Haemorrhage Control
Control fibrinogen
fibrinogen << 1.5g/L
1.5g/L or
or as
as guided
guided
Direct
Direct pressure
pressure // tourniquet
tourniquet ifif by
by TEG
TEG // ROTEM
ROTEM (< (< 2g/L
2g/L for
for
appropriate
appropriate Reassess
Stabilise
Reassess obstetric
obstetric haemorrhage)
haemorrhage)
Stabilise fractures
fractures Suspected
Suspected continuing
continuing haemorrhage
haemorrhage
Surgical
Surgical intervention
intervention –– consider
consider requiring
requiring further
further transfusion
transfusion
damage
damage control
control surgery
surgery Take Aims
Aims for
for therapy
therapy
Interventional
Interventional radiology
radiology Take bloods
bloods andand send
send to to lab
lab:: Aim
FBC,
FBC, PT,
PT, APTT,
APTT, fibrinogen,
fibrinogen, U+E, Ca2+
U+E, Ca 2+ Aim for:
for:
Endoscopic
Endoscopic techniques
techniques Hb 80-100g/L
NPT:
NPT: ABG,
ABG, TEG
TEG // ROTEM
available Hb 80-100g/L
Platelets
Platelets >75 1099/L
>75 xx 10 /L
PT ratio
PT ratio < 1.5
< 1.5
Haemostatic
Haemostatic Drugs
Drugs Order
Order Massive
Massive Haemorrhage
Haemorrhage Pack
Pack 22 APTT
APTT ratio
ratio <1.5
<1.5
Red
Red cells
cells 44 units
units Fibrinogen >1.5g/L
Fibrinogen >1.5g/L
Vit
Vit KK and
and Prothrombin
Prothrombin complex
complex FFP
FFP 44 units
units Ca2+
Ca 2+ >1
>1 mmol/L
mmol/L
concentrate
concentrate for
for warfarinised
warfarinised Platelets
Platelets 11 dose
dose (ATD)
(ATD) Temp
Temp 36ooCC
>> 36
patients
patients and
and and
and subsequently
subsequently pH
pH >> 7.35
7.35 (on
(on ABG)
ABG)
Other
Other haemostatic
haemostatic agents
agents and
and request
request Cryoprecipitate
Cryoprecipitate 22 packs
packs
reversal Monitor
Monitor forfor hyperkalaemia
hyperkalaemia
reversal of
of new
new anticoagulants:
anticoagulants: ifif fibrinogen
fibrinogen <1.5g/l
<1.5g/l or
or according
according toto TEG
TEG //
discuss
discuss with
with Consultant
Consultant ROTEM
ROTEM (<2g/l(<2g/l for
for obstetric
obstetric haemorrhage)
haemorrhage)
Haematologist
Haematologist STAND DOWN
Give
Give MHP
MHP 22 Inform lab
Cell
Cell salvage
salvage ifif available
available and
and Return unused
appropriate
appropriate components
Consider
Consider ratios
ratios of
of other
other Once
Once MHP
MHP 22 administered,
administered, repeat
repeat bloods:
bloods:
components:
components: FBC,
FBC, PT,
PT, APTT,
APTT, fibrinogen,
fibrinogen, U+E,
U+E, Complete
11 unit
unit of
of red
red cells
cells == c.250
c.250 mls
mls NPT:
NPT: ABG,
ABG, TEG
TEG // ROTEM
available documentation
salvaged
salvaged blood
blood To
To inform
inform further
further blood
blood component
component Including audit
requesting
requesting proforma
Thromboprophylaxis should be considered when patient stable
ABG – Arterial Blood
MODIFIED Gas
BY AYMAN APTT – Activated partial thromboplastin time
EDAROUSMHP ATD- Adult Therapeutic
OBSTETRIC Dose
ANESTHESIA 87
FFP- Fresh Frozen plasma – Massive Haemorrhage Pack NPT – Near Patient Testing
PT- Prothrombin Time TEG/ROTEM- Thromboelastography XM - Crossmatch V3 2013
Laboratory Management of Massive Haemorrhage
Massive Haemorrhage Pathway Activated
Transfusion
Transfusion receives
receives Call
Call
‘Massive
‘Massive Haemorrhage,
Haemorrhage, Location,
Location, Specialty’
Specialty’
On
On standby
standby
Receive
Receive call
call from
from designated
designated communication
communication lead
lead in
in clinical
clinical area:
area:
‘This
‘This relates
relates to
to massive
massive haemorrhage
haemorrhage situation’
situation’
The
The caller
caller will
will state:
state:
•Communication
•Communication lead’s lead’s name
name and and contact
contact telephone
telephone number,
number, namename ofof consultant
consultant responsible,
responsible, andand
the
the name
name and
and grade
grade of
of the
the person
person activating
activating the
the protocol
protocol
•Patient’s
•Patient’s ID
ID (surname,
(surname, forename,
forename, hospital
hospital number,
number, DOB
DOB oror minimum
minimum acceptable
acceptable patient
patient
identifiers
identifiers ifif unknown)
unknown)
•Requirements:
•Requirements:
•• Whether
Whether OO Neg Neg isis to
to be/has
be/has been
been used
used
•• Order
Order massive
massive haemorrhage
haemorrhage pack pack 11
•• Clarify
Clarify urgency
urgency ofof requirements
requirements to to decide
decide on
on need
need for
for further
further emergency
emergency groupgroup OO,,oror time
time
to
to wait
wait forfor group
group specific
specific oror crossmatched
crossmatched red red cells
cells (issue
(issue as
as part
part of
of pack
pack 1)
1)
•• U+E,
U+E, FBC,
FBC, PT,
PT, APTT,
APTT, Fibrinogen,
Fibrinogen, ABG*,
ABG*, Calcium*,
Calcium*, lactate*
lactate* **may may be
benear
near patient
patient test
test
Receive
Receive samples
samples and
and request
request forms
forms
Haematology
Haematology Transfusion
Transfusion
Perform
Perform FBC,
FBC, PT,
PT, APTT,
APTT, Fibrinogen
Fibrinogen Perform
Perform Group,
Group, antibody
antibody screen
screen and
and
crossmatch
crossmatch
Prepare
Prepare MHP
MHP 11
Ring
Ring results
results to
to communication
communication Red
Red cells*
cells* 44 units
units
lead
lead when
when available
available (*emergency
(*emergency group O blood, group
group O blood, group specific
specific
blood,
blood, XM’d
XM’d blood
blood depending
depending on on urgency)
urgency)
FFP
FFP (group
(group specific)
specific) 44 units
units
Platelets:
Platelets: ensure that 22 ATD
ensure that ATD areare available
available in
in
Receive
Receive further
further calls
calls from
from stock, or order from blood centre
stock, or order from blood centre
communication
communication lead
lead in
in clinical
clinical
area:
area: Ring
Repeat
Repeat investigations
investigations
Ring clinical
clinical area
area
Order
Order for
for MHP
MHP 22 (communication
(communication lead)
lead) when
when
Liaise
Liaise with
with on
on call
call haematologist
haematologist blood
blood // components
components ready
ready
(consultant
(consultant // SpR)
SpR)
Order
Order for
for further
further components
components
dependent
dependent on on ongoing
ongoing results
results
Prepare
Prepare MHP
MHP 22
Stand Red
Red cells
cells 44 units
units
Stand down
down
FFP
FFP 44 units
units
Platelets
Platelets 11 ATD
ATD
Cryoprecipitate
Cryoprecipitate 22 packs
packs ifif requested
requested
Restock
Restock Emergency
Emergency Group
Group OO blood
blood in
in satellite
satellite fridges
fridges
Complete traceability audit trail
Complete traceability audit trail
v2 2011

Guidelines For Management Of Bleeding With Dabigatran , Rivaroxaban and Apixaban
Initiate standard resuscitation measures
STOP Dabigatran / Rivaroxaban/ Apixaban
Consider stopping any antiplatelet therapy Contact Haematologist
Request: 1. Coagulation screen to include APTT, prothrombin time, fibrinogen and request plasma levels of drug if available- discuss results with
haematologist
2. Full blood count, urea and electrolytes, group and save. Indicate time of last dose of anticoagulant, if known
There is currently NO specific reversal agent for Dabigatran, Rivaroxaban or Apixaban and vitamin K will have no effect on their anticoagulant effect
Consider oral charcoal for ingestion of Dabigatran< 2 hours ago or Apixaban <6 hours ago
Minor Bleeding Major Bleeding Life Threatening Bleeding or urgent reversal for life saving surgery
Initiate Trust Major Haemorrhage Pathway as appropriate
 Mechanical compression  Maintain blood pressure and urine output

 Control haemorrhage
 Delay next anticoagulant  As for major bleeding
o Mechanical compression
dose or discontinue o Surgical/radiological intervention  Discuss the use of haemostatic
treatment as appropriate o Wound packing agents with haematologist on call*
 Tranexamic acid 1g bolus over 10 mins, followed Insert Local Trust Guidance here:
by 1g IV infusion over 8 hours
 Blood component support
If bleeding continues o Aim Hb> 80g/L
o Aim Plt > 75 x 109/L or Consider
o If CNS bleed aim Plt > 100 x 109/L
o Fibrinogen > 1.5g/L Haemodialysis for Dabigatran – may
 Discuss the use of haemostatic agents with take 6-8 hours to clear
haematologist on call*
Major bleed: reduction in Hb >20g/L, transfusion of>2 units of red blood cells or symptomatic bleeding in critical area ( i.e. intraocular, intracranial, intraspinal, intramuscular with compartment
syndrome (be aware of concealed bleeding), retroperitoneal, intraarticular or pericardial bleeding
Life threatening bleed: Symptomatic intracranial bleed, reduction in Hb > 5g/dl, transfusion of > 4 units of red cells, hypotension requiring inotropic agents or bleeding requiring surgical intervention
*
The choice of haemostatic agent is currently based on limited published evidence and will depend on availability as well as advice from the haematologist

GOOD LUCK FOR ALL
Ayman Edarous, 2018

Anaesthesia, Pain & Intensive Care Secrets Academy [APICSA]
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Short Answer Questions Anaesthesia

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Anaesthesia, Pain & Intensive Care Secrets Academy [APICSA]

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MODIFIED BY AYMAN EDAROUS OBSTETRIC ANESTHESIA 3

 The recommendations in the 4th National Audit Project (Major Complications of

* Obstetric anaesthetists need to maintain their airway skills including strategies to

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 Causes of Mitral Stenosis:

 Cardiovascular changes in Pregnancy exacerbate the pathophysiology of MS:

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 Pre-eclampsia: Hypertension (>140/90 on two occasions or 4 hours apart) presenting

• Good Analgesia is imperative. If no contraindications, Epidural Analgesia is

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 General Anaesthetic Technique:

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Efferent (Motor) function can be assessed using Bromage Scale

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More likely testing will reveal a partial

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 Differential diagnosis of post-partum headache:

 Serious Underlying Cause:

 Risks of Epidural Blood Patch (EBP):

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Can we Optimise Haemoglobin Pre-op?

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 The Risks to the Fetus during Anaesthesia for the Mother:

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 The Anesthetic implications of a Woman Labouring with a known intrauterine death:

Obstetric Management  Method of Delivery:

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 Physiological changes of Pregnancy complicate diagnosis, presentation and

 Implication for Sepsis:

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 Implication for Sepsis: factors

 The Common Organisms/Causes for:

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 The Risk Factors for Puerperal Sepsis:

Other Treatments in Critical Care

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 Placenta Praevia and its classification:

Classified by amount of OS covered:

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The Precautions would you take prior to providing Anaesthetic for

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- Procoagulant changes balanced by:

 Management of Disseminated Intravascular Coagulopathy (DIC): Consumptive Coagulopathy

- Is a common final haemostatic disorder caused by other conditions eg; Sepsis

 Thrombosis and Haemorrhage can occur Simultaneously

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 Prevention of Post-Dural Puncture Headache (PDPH) secondary to Spinal:

Prevention of Post-Dural Puncture Headache (PDPH) secondary to Epidural:

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 The Pathophysiology of post dural puncture headache:

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 Complications of a PDPH and the Complications of a Blood Patch:

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 The potential Risk Factors for Uterine Inversion: