Obstetric Flashcards
Amniotic fluid embolism
A. can be associated with a mortality rate of 80%
B. has an incidence of 1 in 2000 pregnancies
C. is an uncommon cause of peripartum death
D. is associated with a small chance of complications in survivors
E. only presents during labour or caesarean section
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Finals Mcq O&g
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SF62 ANZCA version [2004-Aug] Q125, [2005-Apr] Q18, [Jul07]
Amniotic fluid embolism
A. can be associated with a mortality rate of 80%
B. has an incidence of 1 in 2000 pregnancies
C. is an uncommon cause of peripartum death
D. is associated with a small chance of complications in survivors
E. only presents during labour or caesarean section
ANSWER A
A - True - Mortality approaches 80%, 90% have cardiac arrest.
However, probably due improved vigilance, medical care and inclusion of less severe cases, mortality is now reported as 20-40%
B - False - 1:15,000 to 1:50,000 Live Births
C - False - 3rd most common in UK and most common cause of direct maternal deaths in Australia, check out http://www.npsu.unsw.edu.au/NPSUweb.nsf/page/md2 …………… or more recent [1] (http://www.npsu.unsw.edu.au/NPSUweb.nsf/page/md3)
D - False - neonate 20% mortality, 50% with neurological deficit
E - False - Usually occurs during labor but has occurred during abortion, abdominal trauma, and amnioinfusion.
What are the risk factors for Amniotic Fluid Embolism?
- Maternal age > 35 years, multiparity
- Placental abnormalities: placenta previa, placental abruption
- Caesarean delivery or forceps/vacuum assisted
- Eclampsia
- Fetal distress, meconium stained liquor
- Induction/augmentation of labour : strong frequent or tetanic uterine contractions
**<20yo appears to be protective
**HIstory of AFE is not a RF
Timing :
70% during labor
20% during LUSCS
10% following vaginal delviery
Can also occur during
early gestation
second trimester abortions
amniocentesis, amnioinfusion
abdominal trauma
What are the risk factors for Amniotic Fluid Embolism?
- Maternal age > 35 years, multiparity
- Placental abnormalities: placenta previa, placental abruption
- Caesarean delivery or forceps/vacuum assisted
- Eclampsia
- Fetal distress, meconium stained liquor
- Induction/augmentation of labour : strong frequent or tetanic uterine contractions
**<20yo appears to be protective
**HIstory of AFE is not a RF
Timing :
70% during labor
20% during LUSCS
10% following vaginal delviery
Can also occur during
early gestation
second trimester abortions
amniocentesis, amnioinfusion
abdominal trauma
What is the pathogenesis of Amniotic Fluid Embolism?
Unclear at this stage.
Amnoitic fluid, mucin, fetal cells and hair enter the maternal circulation down a pressure gradient from the uterus to veins. Mainly through small tears in the lower uterine segment and endocervix.
3 proposed theories
- Mechanical obstruction of materal vasculature by amniotic fluid but this does not explain coagulopathy
- CLark in 1995 suggested Humoral mechanism : amniotic fluid found to contain inflammatory mediators (bradykinin, prostaglandins, leukotrines, platelet activating factor) which could explain coagulopathy, increased vascular permeability, vasodilation and bronchoconstriction.
1 and 2 largely discarded following discovery that amniotic and fetal cells are common finding in the vasculature of preganant women with no evidence of AFE.
- Histamine mediated in susceptilbe women similar to septic and anaphylatic shock
What is the clinical presentation of Amniotic Fluid Embolism?
Typically presents during labor and delivery or the immediate postpartum period (5 minutes), but also after
a. blunt abdominal trauma
b. cervical suture removal
c. transabdominal amniocentesis.
Non specific early signs : vomiting, chills, breathlessness.
Classical presentation sudden collapse and catastrophic
a. cardiovascular collapse : increase in both SVR and PVR, causing a transient hypertension resulting in LVF and Pulmonay oedema. Increasing heart strain, myocardial depression by activated mediator, myocardial ischemia secondary to hypoxemia quickly lead to hypotension and shock.
b. respiratory distress : pulmonary vasospasm and LVF result in rapid and profound hypoxaemia, can lead to ARDS type picture
c. coaguloapathy : 4 hours post initial presentation, activation of consumputive coagulopathy, rise APTT and PT with fall in fibrinogen, leading to DIC
d. fetal compromise
What is the incidence of AFE? What is the morbidity and mortality?
Factors which do NOT contribute to the increased risk of aspiration pneumonitis during pregnancy include
A. increased gastrin production
B. a tendency for the stomach to be pushed up against the left diaphragm
C. increased acidity of gastric secretion
D. increased volume of gastric secretion
E. decreased secretion of the hormone motilin
ANSWER E
A - Gastrin is produced by placenta during pregancy. Causing hypersecretion of gastric acid. Nearly all parturients have gastric pH under 2.5, and over 60% have gastric volumes greater than 25 mL.
B : stomach is pushed anterior and superior against left hemidiaphragm
C : See A
D : See A
E : mixed reports in the literature, levels may or may not change, but they are not clearly associated with an increased risk of aspiration
SF What increases the risk of threading an epidural catheter into a blood vessel?
A. not doing a CSE
B. injecting saline prior to threading catheter
C. LOR to saline instead of air
D. paramedine instead of midline approach
E. sitting position instead of lateral
ANSWER E
A - it is thought that CSE decreases risk by ensuring catheter is midline, but no documented research.
B : LOR NS decreases risk by distenting epidural space. OR 0.45 LOR NS vs LOR air.
C : See B
D : no difference (only 1 RCT showing this, ?insufficient data)
E : epidural vein engorgement/ distention is greater when sitting instead of lateral position. Risk of epidural vein cannulation is higher in sitting position.
Metanalysis of 7 techniques in obstretric women
1. position : supine vs sittting OR 0.53 6 RCT
2. approach : paramedian vs midline no difference 1 RCT
3. touhy size : 16 vs 18 no difference 1 RCT
4. LOR technique : NS vs air, OR 0.45 8 RCT
5. oriface catheter : single vs multi OR 0.64 5 RCT
6. wire embbeded catheter 1 RCT
7. limiting catheter insertion to 6cm, >7cm OR 0.27 3 RCT
Outline your management of AFE.
IMMEDIATE MANAGEMENT
Key Factors
-early recognition
-prompt resuscitation
-delivery of fetus
-input of consultants : anaesthetist, obstetrician, hematologist, intensivist
Oxygenation
-maintain oxygenation
-due to high maternal oxygen consumption and reduced FRC, desaturation occurs rapidly with significant neurological morbidity to mother and baby.
-intubate early by experienced clinician due to potential difficult airway.
-assist ventilation with PEEP
Haemodynamic
-rapid IV filling
-direct acting vasopressors
-inotropes if required
-CPR with left uterine displacement
-bimanual compression if bleeding results until surgical intervention
-anticipate haemorrhage : insert large bore IVC, order blood products early
Uterine tone
-maintained using oxytocin, ergometrine and prostaglandins (misoprostol)
-bimanual or uterine packing if required
Coagulation
-consumptive coagulopathy should be anticipated
-consult haemotologist early
-plasma, cryo, platelets
-recombinant factor VII
Delivery of baby
-CPR, surgical delivey within 5 min for improved maternal outcome
ICU MANAGEMENT
-supportive
-steriods
-prostacyclin or nitric oxide to improve oxygenation with ARDS
-ballon pump to assist LVF
-plasma exchange/haemofiltration to removed amniotic fluid debris
-ECMO
Differential diagnosis for maternal collapse?
Pregnancy specific
-AFE
-acute haemorrhage
-Uterine rupture
-Eclampsia
-Peropartum cardiomyopathy
Anaesthetic Specific Diagnosis
-high regional block
-local anaesthetic toxicity
Non obstretic causes
-pulmonary emobolism
-air embolism
-anaphylaxis
-sepsis
-cardiac ischemia
-arrhythmia
-transfusion reaction
Best immediate treatment of severe post-partum haemorrhage after delivery of a complete placenta:
A. IV Ergometrine
B. Blood transfusion
C. Evacuation of uterus without blood transfusion
D. Bimanual compression of the uterus
E. Aortic compression
ANSWER A
All answers are correct, but the ‘best immediate treatment’
Maternal cardiac arrest. In making the diagnosis of amniotic fluid embolism, large amount of PMNs surrounding foetal squamous cells are
A. Pathonomonic
B. Supportive
C. Only found at postmortem
D. Irrelevant
E. Incidental
ANSWER B
No diagnostic test for AFE, it is diagnosis of exclusion.
Non specific tests
FBE : anaemia, thrombocytosis
Coag : consumptive coagulopathy
ABG : hypoxemia, low Pa02 to FiO2 ratio
CXR : early ARDS
ECG : strain, arrythmias
Diagnostic test
-cytological analysis of central venous blood and broncho-alveolar fluid
-Sialyl tn antigen test
-zinc coproporphyrin
-serum tryptase levels
all are non specific and only suggestive of AFE
Labour epidurals increase maternal and foetal temperature. This results in neonatal:
A. Increased sepsis
B. Increased investigations for sepsis
C. increased non shivering thermogenesis
D. Increased need for resuscitation
E. Cerebral palsy
ANSWER B
Chestnut’s Obstetric Anesthesia: Principles and Practice (4th Edn), Chestnut et al. 2009; p457.
Labour epidural analgesia is associated with an increase in maternal core body temperature, but also with an increased neonatal temperature and fetal heart rate. Several studies have shown that labour epidural analgesia is associated with increased neonatal neonatal sepsis evaluations, but no increase in neonatal sepsis.
Most common cause of maternal cardiac arrest
A. Pulmonary embolism
B. Amniotic fluid embolism
C. Haemorrhage
D. Preeclampsia
E. Cardiomyopathy
ANSWER B
CEMACH ???
SF84 [Apr07] Q112
Analgesic requirements during labour are reduced by each of the following except
A. Acupressure
B. Acupuncture
C. Hypnosis
D. One to one support by midwife
E. TENS
ANSWER A
AMPSE : “complementary and other methods of pain relief in labour”
Midwife/support person one on one- reduces analgesic use (level 1) hypnosis- decreased requirement for phar,acological analgesia (level 1) acupunture- decreased need for analgesics (level 1)
TENS- “evidence of a weak opioid sparing effect” (level 1) no mention of acupressure
‘Analgesia in labour: non-regional techniques’ Caroline Fortescue, Michael YK Wee BJA CEA CCP Volume 5 Number 1 2005 p9-13
- Acupuncture (Acupressure, laser acupuncture) - One RCT of 100 women in Sweden comparing acupuncture with no acupuncture suggested former group needed less analgesia, including epidurals
- Hypnosis - Cochrane review of three RCTs: one reported less anaesthesia and another less narcotic use, but overall meta-analysis showed no difference in the need for pain relief
- Continuous support - Cochrane review of 15 RCTs involving 12 791 women. Those with continuous support, as opposed to conventional care, were less likely to have intrapartum analgesia, operative birth or be dissatisfied with their experiences
- TENS - Systematic review of eight RCTs failed to demonstrate analgesic effect
38yo obese female with DM, other comorbidities, undergoing LSCS with spinal anaesthetic with a 27G Whitacre needle, having this and that, blah, blah. then two days later complains of numbness on a small patch on lateral aspect of mid-thigh. On full neuro exam - no other signs/symptoms.
A. conus medullaris injury
B. L2 nerve root compression
C. L3 root lesion
D. L4 root lesion
E. meralgia paraesthetica
ANSWER E
A : Conus medullaris ends at L1/L2
Sudden bilateral pain with dural puncture,
Reflex : knee jerk preserved, ankles affected
Radicular pain : minimal
Lumbargo : severe
Sensroy : saddle numbness, symmetrical and bilateral
Motor : symmetric, hyperreflexic distal paresis
Sphinter dysfunction
E: Meralgia Paresthetica
Mono neuropathy of lateral cutaneous nerve (purely sensory over anterolateral thigh, no motor)
Focal entrapment as it passes through inguinal ligament
Causes : DM, pregnancy, tight clothing, obesity, fetal position
Treatment is conservative, lignicaine + steriod injection if paraesthesia is bad.
A 25yo primipara with an uncomplicated pregnancy presents to delivery suite in labour at term. Her membranes spontaneously rupture soon after, and it is blood-stained. At the same time, a severe foetal bradycardia appears on the CTG. What is the most likely cause of this?
A. Placenta accreta
B. Placental abruption
C. Uterine rupture
D. Vasa praevia
E. True knot in the umbilical cord
ANSWER D
A : Placenta Accreta
-abnormally deep attachment of the placenta, through the endometrium and into the myometrium
-bleeding occurs when placenta removed post birth **Cause of PPH
-1:2,500 pregnancy
-very rarely recognized before birth, and is very difficult to diagnose
Placenta Increta - invasion past myoemtrium
Placenta Percreta - invasion through uterine serosa into neighbouring organs (bladder)
RF - uterine surgery, LUSCS, myomectomy
B : Placental Abruption
-abnormal separation of placenta from uterine wall 20 weeks after
-symptoms : pain, pallor, fetal distress, raising fundus (continued bleeding)
-in severe cases PV bleeding
-RF : maternal hypertension, abdominal trauma, short umbilical cord, prolonged ruptured of membranes, <20 >35, prev abruption
C : Uterine rupture
-usually during labor
-integrity of myometrium breached
-similar presentation to placental abruption, but pain and bleeding follow fetal distress
-RF : LUSCS, previous uterine surgery, induction, high parity
D : Vasa Praevia
The classic triad are membrane rupture followed immediately by painless vaginal bleeding and fetal bradycardia
E : True Knot
Painless
Fetal distress
Patient with placenta acreta. Surgical management MOST likely to save her life
A B lynch suture around the uterus for external tamponade
B Rusch balloon in the uterus for internal tamponade
C ligation of the internal iliac arteries
D ligation of the uterine arteries
E subtotal or total hysterectomy
ANSWER E
Tricky question.
A : B-Lynch Suture - Developed in 1997 by B Lynch. Heavy suture that envolopes and mechanically compress an atonic uterus in severe PPH, not yet used much in SE asia. No data so far to suggest usefulness in Placenta Acreta.
B : Rusch balloon
-used for atony or lower segment bleeding
C : Ligation of internal iliac arteries
-high rate of failure 50% as uterine arteries still bleeding
D : Ligation of uterine arteries
-high rate of failure 50% as internal iliac still bleeding
E : subtotal or total hysterectomy
-indicated if accreta is diagosed before delivery.
-hysterectomy is performed with placenta still intact
During laparoscopic surgery, pneumoperitoneum usually results in a fall in cardiac output when intra-abdominal pressure exceeds
A. 10 mmHg….
B. 20 mmHg
C. 30 mmHg
D. 40 mmHg
E. 50 mmHg
ANSWER B
Reference CEACCP 2004, V4,107:
IAP < 10 mm Hg: increases VR, increases CO
IAP 10–20 mm Hg decreases VR, decreases CO BUT increases SVR and therefore BP unchanged or increased
IAP > 20 mm Hg greater decrease VR, greater decrease CO, so decreases BP
True of False
- Regional anaesthesia is impossible with laboring women with scoliosis.
- Routine fluid loading is not required with low dose techniques as hypotension is uncommon.
- CSA is inferior to epidurals
- False
Thoraco-lumbar scoliosis if 4 times more common in females (incidence 2%)
Corrective surgery has improved recently, but older posterior approach obliterates or distorts epidural space with fibrous scar tissue, blood clot or metalwork crossing the midline.
Cephalo-pelvic disproportion is increased in scoliosis therefore instrumentation and LUSCS increased 2.5 fold
Disadvantages include technical difficulties identifying epidural space, patchy/poor analgesia, inadvertant subdural or intrathecal catheter placement and subsequent PDPH
Techniques to find epidural space
1. Gain access to epidural space below surgical scar
2. CSE
3. CSA
Case reports indicate successful placement in 50% of women with scoliosis
- TRUE
Level 1 evidence that hypotension is uncommon
Low dose is 25mg bupivacaine
Higher doses will require IV prelaoding as incidence of hypotension increases - False
CSA is associated with better early analgesia, less motor block, higher maternal satisfaction
However, pruitus is more common and technically more difficult, with higher failure rates.
