British Journal of Radiology (2006) 79, 449-451
© 2006 British Institute of Radiology
doi: 10.1259/bjr/24873219
A catastrophic complication
D R Vummidi, MRCP
R S Kasthuri, MRCS, FRCR
and
R W Bury, FRCR
Department of Radiology, Blackpool Victoria Hospital and University of Manchester, Manchester, Cheshire, UK
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Case
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A 61-year-old Caucasian male was admitted as an emergency with central abdominal pain. On examination he was in hypovolaemic shock, with a pulsatile lower abdominal mass. Based on a clinical diagnosis of ruptured abdominal aortic aneurysm, emergency surgical repair was undertaken. He was admitted to the intensive therapy unit following successful aneurysm repair. Renal dysfunction and gradual obtundation were features of a stormy post-operative period.
His biochemical profile was significantly deranged and included elevated serum amylase.
Worsening mentation was the immediate concern and a CT scan was organized to investigate this (
Figures 1 and 2
).
What are the abnormalities demonstrated on the CT images? What is the differential diagnosis of this appearance? What case specific diagnosis would be appropriate?
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Discussion
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The CT brain demonstrates marked attenuation of the grey/white matter differentiation. There is associated diffuse cerebral oedema with effacement of the sulci and basal cerebrospinal fluid (CSF) spaces. Furthermore, the magnified images also demonstrate multiple petechial haemorrhages (
Figures 2 and 3
). These are early findings of diffuse cerebral anoxia. There is often progression to a more diffusely low density brain, with possible "reversal" of the grey/white matter attenuation.
At this stage, the differential for this appearance includes profound and persistent hypotension, asphyxiation and carbon monoxide fume inhalation [1].
In the given scenario, cerebral hypoperfusion would be most appropriate from the above mentioned list of differential diagnosis. Multiple cerebral fat emboli can also result in generalized cerebral hypoperfusion and result in similar appearances [1].
The described patient unfortunately succumbed to his illness. The post mortem examination revealed multiple cerebral fat emboli (Figure 4
), secondary to acute necrotising pancreatitis.
Fat embolism syndrome is an uncommon but recognized complication of acute necrotising pancreatitis [2]. Pathophysiologically, the chylomicrons and VLDL from the pancreatic fat necrosis are propagated into the vascular system resulting in cerebrovascular occlusion and consequent infarction. Multiple such embolisation into the intracranial vasculature results in global cerebral hypoperfusion.
Cerebral CT scans demonstrate features as described above, but these are not specific to fat emboli. MRI is more sensitive in the neuroradiological diagnosis of intracranial fat embolism [3]. MRI findings include multiple intracranial infarcts, returning low signal on T1 weighted and relatively high signal on T2 weighted MRI. Similar areas are also seen to involve the corpus callosum and the basal ganglia. More diffuse grey and white matter abnormalities akin to CT imaging are demonstrated in the later stages. Diffusion weighted MRI has also been reported to have role in the diagnosis of cerebral fat emboli [4].
Whilst the cerebral imaging features are specific to diffuse cerebral hypoperfusion, the aetiology is broad. This case besides highlighting an unusual cause of cerebral anoxia emphasises the importance of clinical correlation of the radiological differential diagnosis.
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Acknowledgments
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The authors acknowledge Dr Patrick Shenjere, Specialist Registrar, Department of Histopathology, Blackpool Victoria Hospital, Blackpool, UK.
Received for publication April 6, 2005.
Revision received May 12, 2005.
Accepted for publication June 27, 2005.
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References
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