KALPESH DIXIT
AIMS
 CASE DETAILS
 DISCUSSION ON THOUGHT PROCESSES
AND REPORT
 FURTHER ISSUES
 OUTCOME OF CASE
 FUTURE PROBLEMS
 FINAL DIAGNOSIS
 CONCLUSIONS AND LEARNING
CASE
 BA, 8 months.
 Visit Royal Oldham, August,
 Trivial fall in July and then August
 Swelling left side of head- increasing
 Referral to RMCH- neurosurgery
 CT – previous craniotomy, burr hole, subdural
hematomas bilateral L > R, dual attenuation of
subdurals, hematoma under scalp left parietal
region. Acute bleed and cranial swelling hyperdense
but equal in density
Case
 MR SCAN- acute on chronic subdural collection with
more recent bleed, bilateral extending into the
posterior inter-hemispheric fissures.
 Dating of subdural collections about 3 weeks before
scan, intensity of acute subdural collection and scalp
hematoma – same
 Increased intensity ? Due to sedimentation ? Acute
bleed.
 Left temporal and parietal atrophy compared to right
CP medical
 Dad unaware of fall
 Previous history in Pakistan about 3 months ago.
 D & V- pale, low Hb, fits followed by Rt sided
weakness. Glasgow coma scale -4/15
 CT- left large extradural hematoma with no fractureevacuation- improvement
 History of fall??. Skeletal survey normal.
 First cousins, close family ties.
Case CP medical
Findings normal apart from left parietal
swelling. Normal neurology. No other bruises.
Opinion
 Facts: Extradural hematoma with no
history and Ix done in Pakistan
Trivial falls
Boggy increasing swelling
CT and MR reports acute on
chronic bleeds?
 NAI or other?
Discussion
 Consideration of NAI in view of MR scan
report
 Discussion with Neurosurgeon in Pakistan
 Correspondence obtained
 Reports
 Bloods normal, Coagulation normal.
 Case conference – in foster care
Subsequent events
 Parents denied causation
 Further opinions
 Further presentations with bruises
 Further discussions with hematologists
 Normal clotting, normal factor 8 and VW
factor. Platelet assay normal.
 Meetings at solicitors with evidence base.
Multiprofessionals meeting
 Note previous neurosurgery
 Subdurals common
 1st event in july trivial fall could have caused
bleed
 2nd event from settee further injury and scalp
bleed
 Thus acute on chronic appearances
 However why bilateral appearances
 Literature evidence revisited.
Literature
 Intentional: Shaken baby +/-impact
 Non-intentional: RTA
Neurosurgery
Perinatal events and traumatic birth
Cranial malformations-arachnoid cystsminor trauma can cause SDH
Infections
Coagulation disorders (factor 8, VWD, DIC,
sickle, Leukemia, ITP, HDN)
Metabolic- Glutaric aciduria, Galactosuria
Hypernatremia- salt poisoning.
Evidence
 Americal Journal of Paediatrics: Fatal abusive head
injuries in infants and children: rebleeding
spontaneous should not be offered as explanation in
absence of previous injury and re injury which may
be trivial.
 Paediatric chronic subdural hematoma: a
retrospective analysis; Paediatric Neurosurgery 1992
Waxing and waning during course and so re bleeding
with trivial trauma/impact.
Literature
 Trial of Randall Alexander -Georgia v Brady:
during organisation of subdurals- blood
vessels which are forming are still fragile and
with minor bump one can get a fresh
bleeding. Re bleeds are venous and gradual
so often there may not be symptoms.
Classic thinking
 “Sometimes identification of a chronic and acute SDH
makes the well-paid ‘prosecution experts’ jump to the
conclusion that his finding must mean recurrent
abuse when in fact the opposite conclusion may be
more appropriate. The simple fact that the baby was
well-cared for and had no visible external injuries
when seen repeatedly for routing paediatric care ,
while having a subdural haemorrhage, is strong
evidence against inflicted trauma”- Shaken or not:
that is the question- Edward Yazbak
Final answer
 Repeat and extensive hematology tests
 Factor 13 deficiency detected.
 Note no previous bleed
 Explanation more easy
 Child back with parents
Factor 13 deficiency
 Factor 13 responsible for crosslinking of fibrin clot.
 Hence instability of clot and delayed haemorrhage.
 Typically D 1 trauma- bleeding after 12-36
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hours(pathognomonic of Factor 13 deficiency)
Often mild bruising seen
Delayed separation of cord with bleeding
Poor wound healing.
CNS haemorrhage is frequent and occurs spontaneously after
trivial trauma(25-30%)
Soft tissue bleeding and bruising very common. Bleeding oral
and gums during teething.
Ix- normal INR and aPTT. clot stable for 24 hours if no
deficiency. Factor assay.
Rx-FFP, cryoppt, Factor 13 concentrate.
Learning
 Detailed history of bleeding tendencies
needed
 Acute on chronic subdurals report may not
always mean multiple insults
 There are many causes of subdural effusion
or bleed and one needs to consider them
when writing a report.
 Mixture of CSF with blood causing mixed
effects.
When and what to do in an extended
hematology screen
 History if suspicious of a disorder
 Bruising or hematoma which is delayed in
appearance after injury.
 What tests are to be done:
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FBC + Film
PT, APTT, Fibrinogen
PFA-100
Factor VIII, von Willebrand Antigen and Activity
Urea Clot Lysis screen and a Factor XIII assay.
‘Injustice anywhere is a threat to
justice everywhere’
Martin Luther King Jr