Head & neck imagingCase Type
Alfredo José Páez Carpio, Christian Zwanzger Medina, Gemma Isus Olive, Laura Oleaga Zufiría
Hospital Clínic de Barcelona, Barcelona, SpainPatient
24 years, male
A 24-year-old male patient with a sudden loss of consciousness. At admission, the Glasgow coma scale was <8, and ventricular fibrillation was demonstrated. CT was performed.
Brain non-contrast CT: Effacement of cerebral sulci, and decrease in size of the ventricles with preserved grey matter to white matter differentiation. No signs of intra-axial or subarachnoid haemorrhage were observed.
Brain MRI: Bilateral grey matter involvement, increase of signal on diffusion-weighted, T2-weighted and FLAIR images in the cerebral cortex, hippocampi, connecting fibres between globus pallidus and substantia nigra, white matter, splenium of corpus callosum, caudate and lenticular nuclei.
Background: Hypoxic encephalopathy is a syndrome produced by a decreased oxygen supply or sustained reduction of cerebral blood flow. It can be caused by systemic hypoxaemia, an oxygen transport alteration or a global reduction of cerebral blood flow, with a cardiorespiratory arrest being the most common cause in adults .
Coma is commonly observed in the first several hours to days and about half of these patients die. Up to 200 people per one million inhabitants are saved after cardiac arrest in developed countries; however, half of these survivors suffer severe neurological sequelae. Therefore, an effective diagnosis approach is mandatory .
Clinical Perspective: Neuroimaging is an essential part of the work-up of patients after a cardiac arrest. Imaging findings are useful in the prediction of neurologic recovery. CT has a limited value in most cases. MRI due to its sensitivity is the technique of choice to assess the extent and severity of the injured brain.
Imaging Perspective: Severe hypoxic encephalopathy affects the cerebral cortex, basal ganglia and hippocampi. The thalamus and cerebellum may also be affected; the brainstem and cerebral white matter are usually spared. Brain CT is the initial imaging modality performed when brain anoxic-ischaemic cerebral injury is suspected after a cardiac arrest.
The main finding on CT images is cerebral oedema with loss of grey matter to white matter differentiation (reversal sign) (Fig. 1), decreased bilateral basal ganglia attenuation (Fig. 2), decreased attenuation of the cerebral hemispheres in comparison to the cerebellum (white cerebellum sign)  and effacement of the CSF-containing spaces. Hyperattenuation of the sulci and/or basal cisterns on non-contrast-enhanced CT (pseudo-subarachnoid haemorrhage), can be demonstrated in patients with severe brain oedema. The swelling of the brain narrows the subarachnoid spaces and displaces the cerebrospinal fluid .
MRI has a better sensitivity to detect cerebral oedema [4, 5]. From week two after the arrest, hyperintense cortical lesions can be observed on T2W, FLAIR and diffusion-weighted sequences (Fig. 3, 4, 5, 6). Cortical laminar necrosis can also be visualised as serpiginous high-signal intensity in the cortex on T1W images . Diffusion-weighted images are more sensitive to demonstrate affected areas at early stages [7, 8].
Differential diagnosis includes subarachnoid haemorrhage; in these cases there is hyperattenuation of the subarachnoid space, but the grey-white matter differentiation is preserved. Drug abuse and toxic poisoning must be taken into account, patients usually present with acute cognitive impairment after the exposure. The diagnosis is usually established with toxicology and laboratory tests. Arterial ischaemic infarcts follow a characteristic distribution and patients present clinically with focal neurological deficits.
Outcome: Hypoxic encephalopathy poses a difficult diagnostic from a neuroimaging point of view. Imaging patterns are highly variable and depend on the severity, duration, type of injury and timing of imaging studies. CT images are relatively insensitive in the early phases of injury. CT findings are most often normal when performed early after cardiac arrest. Loss of grey-white matter differentiation and the presence of the pseudo-subarachnoid haemorrhage sign is an indication of poor neurologic outcome. Diffusion-weighted MR imaging is the most sensitive technique in the acute stage. ADC reduction on MRI is a strong prognosticator of poor outcome.
Take-Home Message: MRI images can determine the extent of brain injury after a cardiac arrest and represent a good predictor of clinical outcome. Diffusion MR is the most sensitive sequence when evaluating hypoxic encephalopathy.
Written patient consent for this case was waived by the Editorial Board. Patient data may have been modified to ensure patient anonymity.
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