C is an eight-and-a-half-year-old girl who suffers from a right sided hemiplegic cerebral palsy associated with developmental delay affecting her motor and cognitive function. The cause of her condition is a perinatal arterial ischaemic stroke affecting the left basal ganglia region of her brain… [1]
The claim on breach of duty raises two main points for my determination: the first [on 22 November 2010] is whether a finding of a retroplacental haematoma at 16+ weeks gestation is a significant finding mandating senior obstetric review, consultant-led antenatal care and serial growth scans throughout the pregnancy; the second [on 24 February 2011, 30+2] concerns the interpretation of cardiotocograph traces (“CTG traces”) of the pre-term fetal heart as opposed to the term fetus. [2]
[22 November 2010] …. an ultrasound scan which confirmed the presence of a singleton pregnancy, a foetal heart and foetal movements… also recorded… a “small area of retroplacental hypoechogenicity at the fundus highly suggestive of a haematoma.”…[7]
The pregnancy resumed its uneventful course… an anomaly scan at 20 weeks’ gestation on 17 December 2010… all of the structures which were visualised appeared to be normal including the placenta.[9]
on 24 February 2011… 30 weeks plus 2 days gestation. This is the second occasion upon which it is alleged that the antenatal care was negligent…. episodic right sided abdominal pain and pins and needles affecting her arms. [10]
…an abdominal examination…was soft and non-tender with no palpable tightenings… a normal neurological examination and the absence of clinical evidence of a DVT. [13]
…the repeat CTG had been reviewed and was reassuring [14]
…seen again at regular intervals at the antenatal clinic. The pregnancy appeared to be progressing well. The pregnancy was allowed to continue post term (her due date was 2 May 2011). [15]
At 06.00 on 16 May 2011 (at 42 weeks’ gestation)… admitted to hospital with contractions. CTG monitoring… suspicious with reduced beat to beat variability and some early decelerations. fetal blood sample showed a mild metabolic acidosis and at 13.12 a decision was made that C should be delivered by emergency caesarean section. [16]
C was delivered at 13.23 on 16 May 2011. The placenta was noted to be gritty and calcified but was not sent for histology. A large amount of meconium was present. C appeared flat with no spontaneous breaths and a slow heart rate. C… APGAR scores were 5 at one minute, 6 at 5 minutes and 10 at 10 minutes. Her birthweight was 2535 g on the 0.4th centile… head circumference was on the 2nd centile. Her length was on the 50th centile… very small for gestational age… admitted to the neonatal ward. [17]
[C noted on 16 May 2011 to be in respiratory distress, tachypnoeia, have episodes of desaturation; on 17 May 2011 episodes of desaturation]
[18 May 2011] At 06.00, the following concerns were noted: “has had two episodes of profound desaturations, hypertonia, deviation of eyes. Dropping to 40s to 60s associated with increased heart rate, mouthing, starey look, deviation of eyes to one side and hypertonic. Also noted to be cyanosed with one episode. Desaturations not related to feeds, 1st episode lasted for a few seconds, 2nd episode for approximately 5 minutes, not improved with tactile stimulation, needed facial oxygen. After the episodes, baby was noted to be hypertonic by nurses”. [23]
[18 May 2011] cranial ultrasound was performed “with difficult views”, but on subsequent review… (on 24 May 2011)… no abnormality could be seen. [25]
Neuroimaging of C’s brain (on 13 March 2012) at 10 months of age demonstrated a range of findings which were all considered to be secondary to destruction to the left basal ganglia region of the brain and associated white matter destruction. [26]
C’s case that, having suffered one placental abruption on 22 November 2010, she went on to suffer a further abruption on 24 February 2011 and that this explains the abnormalities in the fetal heart trace on that occasion: the reduction in beat to beat variability, the fetal tachycardia, the absence of any accelerations and the presence of decelerations. Given the fact of the earlier abruption and those abnormalities on the trace, this was a second opportunity to refer for consultant-led antenatal care. The failure to do so was negligent. [30]
The pregnancy would not have been permitted to continue to term and labour would have been induced at or around 38 weeks. [31]
Delivery at 38 weeks would have avoided the stroke…the stroke was caused by a small fragment of blood clot or debris from the calcified and gritty placenta which crossed through into the fetal circulation and lodged in the left middle cerebral artery causing occlusion and death (or infarct) of the area of the brain served by that vessel. C’s case is that the stroke occurred (or at least the embolisation of the placental debris had occurred) before the umbilical cord was cut. [32]
D denies breach of duty and both factual and medical causation:
(a) denies that the finding of the retroplacental clot in November 2010 was a significant finding.
(b) denies that the CTG trace in February 2011 demonstrated abnormal features…would not have organised serial growth scans
(c) D takes issue with C’s case on the causation of the stroke ..likely that the stroke was suffered in the neonatal period and not pre-delivery relying in part upon C’s condition at delivery and the timing of the C’s abnormal neurology at around 31 hours of age.
(d) D’s admission that, had C’s intrauterine growth retardation been diagnosed, then early, preterm, delivery would have been indicated. It is also admitted that, if the medical cause of the stroke is proven to be embolisation of placental debris, then delivery at 38 weeks would probably have avoided the stroke. All other elements of the Claimant’s case (on breach and causation) remain in issue. [34]
C has not made out her case on breach of duty on either of the occasions: November 2010 or February 2011. The management of the clinicians at the Trust was reasonable. [82]
it remains possible that the stroke was due to a placental embolus. But equally on the scientific evidence it could have been due to any one of a huge range of other factors… [94]
This claim fails on both breach of duty and causation. [100]
medicalnegligencenow.com 