Coagulopathy related intracerebral hemorrhage on background of uremic encephalopathy

Case contributed by Mohamed Mahmoud Elthokapy
Diagnosis almost certain

Presentation

Known uremic patient on regular dialysis and oral anticoagulants presented to ER with decreased consciousness and acute onset of right hemiplegia No history of trauma. Not diabetic nor hypertensive.

Patient Data

Age: 60 years
Gender: Male

Marked left hemicerebral intra-axial recent hemorrhage involving mainly left frontoparietal white matter regions measures about 9.5 x 7.8 x 6 cm along its maximum AP, TV, and CC dimensions respectively, It presents well defined irregular margin, elicits non-homogeneous hyperdensity (average is 70 HU) with fluid-fluid level (hematocrit effect), mild surrounding hypodense edema exerting mass effect termed by effacement of overlying cortical sulci, compression of left lateral ventricle, significant midline shift (by about 20 mm), sub-falcine herniation and left uncal herniation.

Further intraventricular extension of blood smear along lateral ventricles, third ventricle, and fourth ventricle as well as basal cisterns.

Kinked foramen of Monro with slightly prominent right lateral ventricle mainly occipital and to less extent temporal horns.

Diffuse cerebral edema with exaggerated white matter hypodensities.

Bilateral basal ganglionic swelling and signal alteration mainly involving the lentiform nuclei with probable minor involvement of other gangliocapsular structures, elicit low signal in T1 and high signal in T2 with marginal thin linear hyperintensity in T2 and FLAIR. Diffusion restriction is seen in the DWI and ADC more evident at the globus pallidum. In the clinical context of chronic renal failure, the possibility of metabolic pathology especially uremic encephalopathy would be more reliable to be on the top of this long DD list. 

Left parietal white matter focal signal alteration elicits low signal in T1 and high signal in T2 and FLAIR with diffusion restriction consistent with a recent lacunar infarct.

Right lentiform nucleus small focal blooming in T2 GRE measures about 5mm suggestive of a microhemorrhage.

Bilateral cerebral hemispheric periventricular deep white matter pencil-thin lining as well as punctate foci of T2 and FLAIR hyperintensities with no surrounding edema or associated mass effect denoting chronic microangiopathy (Fazekas grade I).

Left hemi-pontine and thalamic foci of similar signal alteration with no diffusion restriction likely related to the chronic small vessel disease. 

Mild age-related cerebral involutional changes with mild ventricular and sulcal dilatation.

Case Discussion

The clinical scenario is a known uremic patient presented one week before with delirium, unsteadiness, and confusion. He was referred for an MRI brain study that revealed changes related to metabolic encephalopathy uremic encephalopathy, which was the result of the accumulation of urea, uric acid, and other metabolites in the blood that have affected the brain. During the investigation, it was found that the patient missed his dialysis session twice. The patient was managed at an outpatient clinic with medical treatment managing metabolic acidosis and anti-ischemic tablets.

One week later, the patient was brought to ER with lost consciousness (GCS 3) and acute hemiplegia, which prompted a CT study that revealed large intraparenchymal and intraventricular hemorrhage, later admitted to ICU for management and care.

Blood-blood levels in acute intracerebral hemorrhage are moderately sensitive to the presence of coagulopathy and highly specific for this condition. Thus, coagulopathy can prevent the formation or lysis of a blood clot, resulting in this appearance.

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