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Journal of Radiology Case Reports

White Matter Microsusceptibility Changes in Patients With Hepatic Encephalopathy

Case Report

Adina F. Achiriloaie1*, Daniel Kido1, Dan Wycliffe1, J. Paul Jacobson1

Radiology Case. 2011 Aug; 5(8):1-7 :: DOI: 10.3941/jrcr.v5i8.393

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1. Department of Radiology, Loma Linda University Medical Center, Loma Linda, California, USA

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  ABSTRACT
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We report a new radiological finding in two patients with hepatic encephalopathy. A new susceptibility-weighted (SWI) magnetic resonance imaging sequence revealed multiple bilateral microsusceptibility changes in the corpus callosum and white matter, while the conventional T1 and T2 weighted images were unremarkable. We postulate that the etiology of the microsusceptibility changes may be related to hepatic coagulopathy and other factors, such as impaired cerebral blood flow and brain edema.








  INTRODUCTION
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Hepatic encephalopathy is a serious clinical complication of acute liver failure and end-stage liver disease, as well as an important prognostic factor in the course of the disease. Previously described cerebral abnormalities associated with hepatic encephalopathy include edema and impaired cerebral blood flow. Brain edema may result from hyperammonemia and can be detected by CT (1). MRI studies in patients with hepatic encephalopathy have also shown signs of edema in the white matter and cortico-spinal tracts (2). The resultant intracranial hypertension is the main cause of mortality in patients with fulminant hepatic failure. The pathophysiology of brain edema may be linked to increased uptake of ammonia by the brain, which leads to osmotic disturbance in the astrocytes (3) and also alterations in cerebral blood flow (CBF). Impaired CBF may result from defective metabolism and dilation of cerebral arterioles (4). Another common radiological finding in hepatic encephalopathy is hyperintense signals in the globus pallidi, putamen and internal capsules on MRI T1-weighted images and this may result from increase manganese and copper deposition (5). Hepatic coagulopathy, which relates to our study, is mainly due to decreased liver production of coagulation proteins. In advanced cases, this can result in consumption coagulopathy and disseminated intravascular coagulopathy, which can lead to petechial hemorrhages in various organs in the body.

In this case-report study we present a new MRI finding in two different patients with hepatic encephalopathy, one who recovered and one who didn`t. The conventional T1 and T2 weighted images were unremarkable, but a new high resolution susceptibility-weighted (SWI) magnetic resonance imaging sequence revealed multiple microsusceptibility (1-2 mm) foci in the corpus callosum and white matter (Fig. 1 Preview this figure

Figure 1: Magnetic Resonance Imaging
Case 1: 72 year-old female with end-stage liver disease and hepatic encephalopathy. Comparison of FLAIR (1.5 Tesla, TR: 9999, TE: 110) and SWI (1.5 Tesla, TR: 57, TE: 40) sequences. A, The FLAIR sequence shows diffuse edema in the peripheral portion of the white matter and in the corpus callosum. B, on a lower slice through the ventricles, the FLAIR sequence shows edema in the splenium of the corpus callosum (arrow). C, FLAIR shows hyperintensity in the red nuclei (arrows). D, SWI, which corresponds to A and shows microsusceptibility changes in the corpus callosum (thick arrows) and in the peripheral white matter (thin arrows). E, SWI corresponds to B and shows multiple microsusceptibility changes in the splenium of corpus callosum (arrow). F, SWI corresponds to C and demonstrates no microsusceptibility changes in the red nuclei (arrows).
, Fig. 3 Preview this figure
Figure 3: Magnetic Resonance Imaging
Case 2: 40 year-old female with cirrhosis and likely hepatic encephalopathy. Comparison of FLAIR (1.5 Tesla, TR: 9999, TE: 110) and SWI (1.5 Tesla, TR: 57, TE: 40) sequences. A, A FLAIR image shows normal findings. B, SWI, which corresponds to A, shows multiple microsusceptibility changes in the splenium of corpus callosum (arrow). C, SWI close to the vertex shows microsusceptibility changes in the body of the corpus callosum (arrow).
). We are postulating that white matter microsusceptibility change may be due to either intravascular coagulopathy or microhemorrhages. We are also proposing that its etiology might be associated with hepatic coagulopathy, as well cellular changes in brain edema and alterations in cerebral blood flow.

  CASE REPORT
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CASE REPORT 1
A 72 y/o female was transferred to our institution after a fall due to severe lower extremity edema secondary to long-standing cryptogenic cirrhosis. In addition, she developed altered level of consciousness after aggressive dehydration. At the time of admission, the patient was lethargic and confused, with a GCS of 11 (eyes: 4, vision: 2, motor: 5). She had asterixis and 2+ peripheral edema. Four years ago, she had a history of esophageal variceal hemorrhage and TIPS placement.

The patient`s laboratory results included increased PT (35.8 sec, normal 9-12 sec), PTT (49.0 sec, normal 20-36 sec), and INR (3.97, normal 0.9-1.2) increased D-dimer (3.5 ug/mL, normal < 0.2 ug/mL), decreased fibrinogen (100 mg/dL, normal 200-400 mg/dL) as well as thrombocytopenia (72 bil/L, normal 100-450 bil/L) and macrocytic anemia. She also had decreased total protein (5.5 g/dL, normal 6.0 - 8.5 g/dL) and albumin (2.7 g/dL, normal 3.2 -5.0 g/dL) , and markedly increased total bilirubin (4.9 mg/dL, normal 0.1 - 1.2 mg/dl). Towards the end of her hospitalization, the coagulopathy worsened, with platelets in the 40-60 bil/L range. On the day of her death, her platelets dropped to 19 bil/L. Other terminal values included D-dimer of >20 ug/mL and fibrinogen of 80 mg/dL.

On day 2 of hospitalization, the patient had a MRI scan of the head, as well as an MRA and MRS. Her brain MRI showed T2 hyperintensities in the superficial portion of the white matter and in the corpus callosum. (Fig. 1 Preview this figure

Figure 1: Magnetic Resonance Imaging
Case 1: 72 year-old female with end-stage liver disease and hepatic encephalopathy. Comparison of FLAIR (1.5 Tesla, TR: 9999, TE: 110) and SWI (1.5 Tesla, TR: 57, TE: 40) sequences. A, The FLAIR sequence shows diffuse edema in the peripheral portion of the white matter and in the corpus callosum. B, on a lower slice through the ventricles, the FLAIR sequence shows edema in the splenium of the corpus callosum (arrow). C, FLAIR shows hyperintensity in the red nuclei (arrows). D, SWI, which corresponds to A and shows microsusceptibility changes in the corpus callosum (thick arrows) and in the peripheral white matter (thin arrows). E, SWI corresponds to B and shows multiple microsusceptibility changes in the splenium of corpus callosum (arrow). F, SWI corresponds to C and demonstrates no microsusceptibility changes in the red nuclei (arrows).
, A-C, Fig. 2 Preview this figure
Figure 2: Magnetic Resonance Imaging
Case 1: 72 year-old female with end-stage liver disease and hepatic encephalopathy. A, axial T1 weighted image (1.5 Tesla, TR: 770, TE: 14) shows increased signal in the basal ganglia bilaterally (arrows). B, axial T2 weighted images (1.5 Tesla, TR: 4000, TE: 120) show increased signal in the peripheral white matter corresponding to Fig.1, FLAIR images A and B. C, MR spectroscopy in the left occipital white matter corresponding to image B shows markedly decreased myo-Inositol peak and large lactate peak, likely due to increased glycolysis, consistent with hepatic encephalopathy.
, B) The SWI sequences showed multiple microsusceptibility changes in the corpus callosum and throughout the superficial portion of the white matter. (Fig. 1 Preview this figure
Figure 1: Magnetic Resonance Imaging
Case 1: 72 year-old female with end-stage liver disease and hepatic encephalopathy. Comparison of FLAIR (1.5 Tesla, TR: 9999, TE: 110) and SWI (1.5 Tesla, TR: 57, TE: 40) sequences. A, The FLAIR sequence shows diffuse edema in the peripheral portion of the white matter and in the corpus callosum. B, on a lower slice through the ventricles, the FLAIR sequence shows edema in the splenium of the corpus callosum (arrow). C, FLAIR shows hyperintensity in the red nuclei (arrows). D, SWI, which corresponds to A and shows microsusceptibility changes in the corpus callosum (thick arrows) and in the peripheral white matter (thin arrows). E, SWI corresponds to B and shows multiple microsusceptibility changes in the splenium of corpus callosum (arrow). F, SWI corresponds to C and demonstrates no microsusceptibility changes in the red nuclei (arrows).
, D-E) The MRA study showed normal cerebral vessels. MR spectroscopy showed markedly decreased myo-Inositol peak and large lactate peak, likely due to increased glycolysis. These findings were consistent with hepatic encephalopathy (Fig. 2 Preview this figure
Figure 2: Magnetic Resonance Imaging
Case 1: 72 year-old female with end-stage liver disease and hepatic encephalopathy. A, axial T1 weighted image (1.5 Tesla, TR: 770, TE: 14) shows increased signal in the basal ganglia bilaterally (arrows). B, axial T2 weighted images (1.5 Tesla, TR: 4000, TE: 120) show increased signal in the peripheral white matter corresponding to Fig.1, FLAIR images A and B. C, MR spectroscopy in the left occipital white matter corresponding to image B shows markedly decreased myo-Inositol peak and large lactate peak, likely due to increased glycolysis, consistent with hepatic encephalopathy.
, C).

The patient`s mental status continued to deteriorate, despite aggressive medical management and two attempts to close the TIPS. On day 22 of admission, she could no longer follow commands. Two days later, she became comatose and unresponsive and expired on day 37 of hospitalization.



CASE REPORT 2
A 40 y/o woman presented to the emergency room with altered level of consciousness and right-sided facial droop, as well as multiple bruises secondary to a fall. On physical exam, the patient was sleepy, not oriented to time and had amnesia of recent events. She had lower extremity clonus and hyper-reflexia. Her abdominal exam was remarkable for right upper quadrant pain on palpation.

The patient`s blood studies were positive for microcytic anemia (Hb: 8.3 g/dL, normal > 12 g/dL ; Hct: 27.4%, normal > 36%), increased liver enzymes (AST: 556 IU/L, normal 0-20 IU/L; ALT: 397 IU/L, normal 0-35 IU/L), decreased albumin (3.4g/dL, normal 3.2 -5.0 g/dL) and abnormal coagulation markers (PT: 17.3sec, PTT 38.8sec, INR 1.29, D-dimer: 3.8 ug/mL). Platelets were normal at 384 bil/L. A hepatitis panel revealed reactive HBsAg and negative HBsAb.

A CT of the head was ordered for cerebral hemorrhage, but it was normal. MRI of the head revealed multiple punctate foci of decreased intensity in the corpus callosum on the SWI sequence. (Fig. 3 Preview this figure
Figure 3: Magnetic Resonance Imaging
Case 2: 40 year-old female with cirrhosis and likely hepatic encephalopathy. Comparison of FLAIR (1.5 Tesla, TR: 9999, TE: 110) and SWI (1.5 Tesla, TR: 57, TE: 40) sequences. A, A FLAIR image shows normal findings. B, SWI, which corresponds to A, shows multiple microsusceptibility changes in the splenium of corpus callosum (arrow). C, SWI close to the vertex shows microsusceptibility changes in the body of the corpus callosum (arrow).
) The conventional T1- and T2-weighted images showed no abnormalities. An abdominal ultrasound study showed hepatomegaly and splenomegaly, enlargement of portal vein and diffuse gall bladder wall thickening consistent with portal hypertension.
The patient`s level of consciousness and facial droop improved by day 5 of hospitalization and the patient was discharged. Her clinical findings were believed to be due to a minor stroke secondary to hypovolemia combined with hepatic encephalopathy.

  DISCUSSION
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Hepatic encephalopathy has several brain findings. Some of them, like cerebral edema and hyperintense T1 signal in the globus pallidi have been extensively studied. In our first case report, the conventional MRI sequences showed T2 hyperintensities in the superficial portion of the white matter and in the corpus callosum, as has been previously shown. In the second case report, the T1- and T2-weighted images showed no abnormalities. However, a new MRI technique, SWI, detected microsusceptibility changes in corpus callosum and peripheral white matter.

SW imaging was originally developed to enhance the detection of deoxyhemoglobin within vessels. More recently, this technique has been used for better detection of extravascular deoxyhemoglobin and methemoglobin present in areas of hemorrhage in patients with diffuse axonal injury (6). It is a relatively new technique and is the only technique that images phase changes. The SW images are created by amplifying the phase images by a factor of four and then combining them with appropriate magnitude images. Therefore, the SWI technique is approximately five times more sensitive to susceptibility changes in the brain compared to conventional gradient echo. Please refer to the articles by Tong et al. and Reichenbach et al., which have more detailed description of the technique (6,7).

The etiology of these white matter microsusceptibility changes is currently unknown, but may be associated with the accompanying hepatic coagulopathy. Both patients presented in this study had coagulopathy and DIC. Previous clinical studies in patients with DIC have described similar MRI findings of white matter microhemorrhages. Lesions consistent with multiple cerebral infarctions have been found in the paraventricular white matter in a patient with blue-rubber-bleb-nevus syndrome and chronic DIC (8) and in the pons region in a patient with DIC due to obstetric complication (9). It is likely then that the white matter hemorrhages described in our study were produced through a similar process generated by the systemic coagulopathy.

Our two cases and other studies show lesions in specific areas of the brain, mainly the white matter and sometimes the basal ganglia and pons. These are the areas supplied by small perforating blood vessels and are often associated with hypertensive disease or other angiopathies. In hepatic encephalopathy, these small cerebral blood vessels may be preferentially affected. Susceptibility changes were especially prominent in the corpus callosum, which may be due to the fact that the callosal white matter fibers are closely packed together, so that the penetrating vessels have even smaller diameters and less compliance, therefore may be at increased risk of developing intravascular thrombi or microhemorrhages. There is also alteration in cerebral blood flow, which may also be responsible in part for brain hyperemia, resulting in cerebral edema. The lack of autoregulation of CBF in liver failure patients is believed to be due to brain hyperammonemia, in combination with dilation of cerebral arterioles and cerebral vasoparalysis. (4) These changes in microvasculature could also be the reason that small arterioles are more susceptible to injury and create the hypointensities which can be detected by SWI.

  TEACHING POINT
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This article describes a new finding of white matter and corpus callosum microsusceptibility changes by using a new MRI technique, susceptibility-weighted imaging (SWI) in two patients with hepatic encephalopathy. The etiology of these lesions is probably related to the presence of hepatic coagulopathy, but other factors, such as impaired cerebral blood flow and brain edema may also play a role.








  FIGURES
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Display figure 1 in original size

Figure 1: Case 1: 72 year-old female with end-stage liver disease and hepatic encephalopathy. Comparison of FLAIR (1.5 Tesla, TR: 9999, TE: 110) and SWI (1.5 Tesla, TR: 57, TE: 40) sequences. A, The FLAIR sequence shows diffuse edema in the peripheral portion of the white matter and in the corpus callosum. B, on a lower slice through the ventricles, the FLAIR sequence shows edema in the splenium of the corpus callosum (arrow). C, FLAIR shows hyperintensity in the red nuclei (arrows). D, SWI, which corresponds to A and shows microsusceptibility changes in the corpus callosum (thick arrows) and in the peripheral white matter (thin arrows). E, SWI corresponds to B and shows multiple microsusceptibility changes in the splenium of corpus callosum (arrow). F, SWI corresponds to C and demonstrates no microsusceptibility changes in the red nuclei (arrows).

Figure 1: Magnetic Resonance Imaging (Open in original size)
Case 1: 72 year-old female with end-stage liver disease and hepatic encephalopathy. Comparison of FLAIR (1.5 Tesla, TR: 9999, TE: 110) and SWI (1.5 Tesla, TR: 57, TE: 40) sequences. A, The FLAIR sequence shows diffuse edema in the peripheral portion of the white matter and in the corpus callosum. B, on a lower slice through the ventricles, the FLAIR sequence shows edema in the splenium of the corpus callosum (arrow). C, FLAIR shows hyperintensity in the red nuclei (arrows). D, SWI, which corresponds to A and shows microsusceptibility changes in the corpus callosum (thick arrows) and in the peripheral white matter (thin arrows). E, SWI corresponds to B and shows multiple microsusceptibility changes in the splenium of corpus callosum (arrow). F, SWI corresponds to C and demonstrates no microsusceptibility changes in the red nuclei (arrows).

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Display figure 2 in original size
Figure 2: Case 1: 72 year-old female with end-stage liver disease and hepatic encephalopathy. A, axial T1 weighted image (1.5 Tesla, TR: 770, TE: 14) shows increased signal in the basal ganglia bilaterally (arrows). B, axial T2 weighted images (1.5 Tesla, TR: 4000, TE: 120) show increased signal in the peripheral white matter corresponding to Fig.1, FLAIR images A and B. C, MR spectroscopy in the left occipital white matter corresponding to image B shows markedly decreased myo-Inositol peak and large lactate peak, likely due to increased glycolysis, consistent with hepatic encephalopathy.

Figure 2: Magnetic Resonance Imaging (Open in original size)
Case 1: 72 year-old female with end-stage liver disease and hepatic encephalopathy. A, axial T1 weighted image (1.5 Tesla, TR: 770, TE: 14) shows increased signal in the basal ganglia bilaterally (arrows). B, axial T2 weighted images (1.5 Tesla, TR: 4000, TE: 120) show increased signal in the peripheral white matter corresponding to Fig.1, FLAIR images A and B. C, MR spectroscopy in the left occipital white matter corresponding to image B shows markedly decreased myo-Inositol peak and large lactate peak, likely due to increased glycolysis, consistent with hepatic encephalopathy.

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Display figure 3 in original size
Figure 3: Case 2: 40 year-old female with cirrhosis and likely hepatic encephalopathy. Comparison of FLAIR (1.5 Tesla, TR: 9999, TE: 110) and SWI (1.5 Tesla, TR: 57, TE: 40) sequences. A, A FLAIR image shows normal findings. B, SWI, which corresponds to A, shows multiple microsusceptibility changes in the splenium of corpus callosum (arrow). C, SWI close to the vertex shows microsusceptibility changes in the body of the corpus callosum (arrow).

Figure 3: Magnetic Resonance Imaging (Open in original size)
Case 2: 40 year-old female with cirrhosis and likely hepatic encephalopathy. Comparison of FLAIR (1.5 Tesla, TR: 9999, TE: 110) and SWI (1.5 Tesla, TR: 57, TE: 40) sequences. A, A FLAIR image shows normal findings. B, SWI, which corresponds to A, shows multiple microsusceptibility changes in the splenium of corpus callosum (arrow). C, SWI close to the vertex shows microsusceptibility changes in the body of the corpus callosum (arrow).

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Figure 4: Summary table for hepatic encephalopathy

Figure 4: Table (Open in original size)
Summary table for hepatic encephalopathy

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Figure 5: Differential diagnoses for hepatic encephalopathy

Figure 5: Table (Open in original size)
Differential diagnoses for hepatic encephalopathy

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  REFERENCES
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1. Wijdicks EF, Plevak DJ, Rakela J, Wiesner RH. Clinical and radiologic features of cerebral edema in fulminant hepatic failure. Mayo Clin Proc 1995 Feb;70(2):195-6 Get full text
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2. Rovira A, Cordoba J, Raguer N, Alonso J. Magnetic resonance imaging measurement of brain edema in patients with liver disease: resolution after transplantation. Curr Opin Neurol 2002 Dec;15(6):731-7 Get full text
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3. Ahl B, Weissenborn K, van den Hoff J, Fischer-Wasels D, Kostler H, Hecker H, Burchert W. Regional differences in cerebral blood flow and cerebral ammonia metabolism in patients with cirrhosis. Hepatology 2004 Jul;40(1):73-9 Get full text
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4. Larsen FS. Cerebral blood flow in hyperammonemia: heterogeneity and starling forces in capillaries. Metab Brain Dis 2002 Dec;17(4):229-35 Get full text
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5. Miranda M, Caballero L. Chronic hepatic encephalopathy: the role of high serum manganese levels and its relation with basal ganglia lesions in nuclear magnetic resonance of the brain. Rev Med Chil 2001 Sep;129(9):1051-5 Get full text
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6. Tong KA, Ashwal S, Holshouser BA, Shutter LA, Herigault G, Haacke EM, Kido DK. Hemorrhagic shearing lesions in children and adolescents with posttraumatic diffuse axonal injury: improved detection and initial results. Radiology 2003; 227: 332-339 Get full text
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7. Reichenbach JR, Venkatesan, R, Schillinger, DJ, Kido, DK, Haake, EM. Small vessels in the human brain: MR venography with deoxyhemoglobin as an intrinsic contrast agent. Radiology 1997; 204: 272-277 Get full text
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8. Hashimoto Y, Eto K, Uyama E, Uchino M, Araki S. Blue-rubber-bleb-nevus syndrome presented vascular dementia and chronic DIC. Rinsho Shinkeigaku 1989 Feb;29(2):202-8 Get full text
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9. Ishizuka T, Suzuki K, Hara M, Nakajima S, Hirose T, Harigai M, Hidaka T, Kawaguchi S, Kawagoe M, Nakamura H. A case of pregnant woman with lupus anticoagulant positive systemic lupus erythematosus complicated with intrauterine fetal death, eclampsia, and brainstem vascular damage. Ryumachi 1991 Apr;31(2):184-93 Get full text
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  ABBREVIATIONS
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ALT - alanine transaminase
AST - aspartate transaminase
CBF - cerebral blood flow
GCS- Glasgow comma scale
MRA - magnetic resonance angiogram
MRI - magnetic resonance imaging
MRS - magnetic resonance spectroscopy
NAA - N-acetyl aspartate
SWI - susceptibility-weighted imaging.









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