Acute Hepatic Encephalopathy: Diffusion-Weighted and Fluid-Attenuated Inversion Recovery Findings, and Correlation with Plasma Ammonia Level and Clinical Outcome

McKinney, Alexander M.; Lohman, Brandon D.; Sarıkaya, Başar; Uhlmann, E.; Spanbauer, J.; Singewald, Timothy; Brace, Jeffrey R.

doi:10.3174/ajnr.a2112

Cited by 80 publications

(56 citation statements)

References 29 publications

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“…In the September 2010 issue of AJNR, we used a similar term of "acute hepatic encephalopathy" (most of the patients had hyperammonemia), and the terms could perhaps be considered interchangeable (notably, both would result in the acronym AHE). 2 We thank them for describing their findings, which are similar to the cases we described that, in our opinion, lie at the severe end of the spectrum of AHE. Of particular note is that 2 of their 4 patients died.…”

supporting

confidence: 56%

“…Indeed, our study did not find a significant correlation between plasma ammonia levels and the initial clinical severity of AHE, though we found that the initial clinical severity, the plasma ammonia level, and the extent of FLAIR and DWI abnormalities on MR imaging all significantly correlated with patient outcome. 2 Thus, while ammonia is inextricably linked to the pathogenesis of AHE, it may be a bit misleading to use the term "hyperammonemic encephalopathy," because ammonia is but 1 (albeit quite important) precursor to the development of encephalopathy. Both our study and that of U-King-Im et al 1 would suggest that prospective monitoring of serum ammonia levels and MR imaging findings, along with other clinical and laboratory tests, could further delineate the pathogenesis of this potentially reversible disorder.…”

mentioning

confidence: 99%

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Acute Hepatic (or Hyperammonemic) Encephalopathy: Diffuse Cortical Injury and the Significance of Ammonia

McKinney¹,

Sarıkaya²,

Spanbauer³

et al. 2011

AJNR Am J Neuroradiol

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We read with great interest the description by U-King-Im et al 1 in the February issue of the American Journal of Neuroradiology (AJNR) of 4 patients with "acute hyperammonemic encephalopathy" on diffusion-weighted imaging (DWI). In the September 2010 issue of AJNR, we used a similar term of "acute hepatic encephalopathy" (most of the patients had hyperammonemia), and the terms could perhaps be considered interchangeable (notably, both would result in the acronym AHE). 2 We thank them for describing their findings, which are similar to the cases we described that, in our opinion, lie at the severe end of the spectrum of AHE. Of particular note is that 2 of their 4 patients died. In our study, 3 of 5 patients died; they had a similar distribution on DWI, which we termed "diffuse cortical involvement." U-King-Im et al 1 limited this description to the cingulate and insular gyri, but review of their available images demonstrates the abnormalities to be more extensive than those 2 regions. We do not point this out for the purpose of criticism; rather, we agree that these findings should alert the radiologist to the possibility of AHE. Thus, the combination of these 2 studies would indeed suggest (though preliminarily) that "diffuse cortical involvement" or alternatively "cingulate and insular involvement" may portend a poor outcome, though AHE is potentially reversible with therapy (such as lactulose).They also similarly noted thalamic brain stem involvement in 1 patient, which we noted in most of our 20 patients. Hence, it would be of interest to us whether subtle involvement of the thalami or dorsal brain stem existed on further review of fluid-attenuated inversion recovery (FLAIR) or DWI in these 4 patients or if they may have other patients who may have been eventually excluded from their study or not included due to stringent criteria, for example due to confounding diagnoses with preliminarily negative findings on MR imaging (we have noted that such situations uncommonly occur). Such confirmation of milder cases limited to the thalami, for example, would help solidify our findings that AHE occurs along a spectrum, with multifocal diffuse cortical findings being at the severe end.We proposed the terminology "acute hepatic encephalopathy" rather than "acute hyperammonemic encephalopathy" for several reasons: 1) Although some correlation likely exists, the degree of correlation between serum ammonia levels and AHE severity (the "ammonia hypothesis") is still controversial. 2) Ammonia levels may be mildly elevated in patients with chronic cirrhosis without symptoms of AHE. 3) Severely encephalopathic patients may have normal ammonia levels. 4) Serum ammonia has been shown to be a poor predictor as a single test for the presence of AHE.3,4 More recent evidence suggests rather that there is a synergistic effect between ammonia and various other inflammatory cytokines that results in excess glutamine within astrocytes, leading to osmotic swelling of the astrocytes and the subsequent brain edema as well as other neuro...

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supporting

confidence: 56%

mentioning

confidence: 99%

Acute Hepatic (or Hyperammonemic) Encephalopathy: Diffuse Cortical Injury and the Significance of Ammonia

McKinney¹,

Sarıkaya²,

Spanbauer³

et al. 2011

AJNR Am J Neuroradiol

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“…Plasma ammonia levels have been shown to correspond to the extent of MRI abnormality. 4,9 It is unclear why the insular and cingulate cortices are particularly susceptible to toxic effects of ammonia. Ammonia crosses the blood-brain barrier through passive diffusion and cation channels.…”

Section: Discussionmentioning

confidence: 99%

Diffusion-Weighted Imaging in Acute Hyperammonemic Encephalopathy

Rosario

McMahon

Finelli

2013

The Neurohospitalist

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Magnetic resonance imaging (MRI) findings associated with chronic liver disease are characterized by cerebral atrophy and bilateral, symmetric hyperintensities of the globus pallidus on T1-weighted images without corresponding signal intensities in T2-weighted images. Recently, distinct MRI changes of acute hepatic encephalopathy have been described which may be misinterpreted given their resemblance to hypoxic-ischemic injury imaging changes as well as their limited description in the neurologic literature. We describe 3 cases of acute hyperammonemic encephalopathy primarily characterized by restricted diffusion involving the insular and cingulate cortices and thalamus bilaterally.

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“…Based on a study by McKinney et al (8) , five anatomical areas were identified-posterior limb of internal capsule, thalamus, insular cortex, periventricular white matter and diffuse cortical involvement. Each of these sites were evaluated for all patients and the extent of involvement on magnetic resonance imaging and correlated with initial clinical severity.…”

Section: Discussionmentioning

confidence: 99%

Magnetic Resonance Imaging in Acute Hepatic Encephalopathy

C¹,

Perumpalath²,

Rajendran³

et al. 2016

jemds

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AIMS AND OBJECTIVESTo study the pattern of brain involvement in acute hepatic encephalopathy in patients with chronic liver disease and correlate the extent of involvement on magnetic resonance imaging with serum ammonia and clinical severity. MATERIALS AND METHODSThirty patients with clinical or radiological evidence of chronic liver disease who presented with acute onset neuropsychiatric symptoms with a clinical diagnosis of acute hepatic encephalopathy. A detailed history was taken. Status of chronic liver disease confirmed, serum ammonia values estimated and magnetic resonance imaging done within 7 days of admission. The anatomic pattern of involvement in FLAIR and DWI (comparison with ADC maps) noted. The initial clinical severity (assessed by West Haven grade) and serum ammonia values were recorded and correlated with extent of involvement in magnetic resonance imaging. The patients were followed up for 21 days from the day of MRI to get an idea about inpatient or outpatient status; however, no clinical or radiological end points were evaluated. OBSERVATION AND RESULTSOn FLAIR and DWI, there were abnormalities in PLIC (73.3%, 60%), thalamus (63.3%, 53.3%), PVWM (26.7%, 16.7%) and IC (36.7%, 23.3%). There was significant correlation (P<0.05) for PVWM (P=0.001, 0.002) and IC (P=0.005, 0.009) involvement with clinical severity on FLAIR and DWI. There was no significant correlation for PLIC (P=0.371, 0.162) and thalamic (P=0.252, 0.92) involvement. All the patients showed elevated serum ammonia values and a period of inpatient stay >21 days. CONCLUSIONThe constellation of anatomic involvement in the appropriate clinical setting is suggestive of acute hepatic encephalopathy. Involvement of PVWM and IC indicated a higher grade of initial clinical severity.

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Acute Hepatic Encephalopathy: Diffusion-Weighted and Fluid-Attenuated Inversion Recovery Findings, and Correlation with Plasma Ammonia Level and Clinical Outcome

Cited by 80 publications

References 29 publications

Acute Hepatic (or Hyperammonemic) Encephalopathy: Diffuse Cortical Injury and the Significance of Ammonia

Acute Hepatic (or Hyperammonemic) Encephalopathy: Diffuse Cortical Injury and the Significance of Ammonia

Diffusion-Weighted Imaging in Acute Hyperammonemic Encephalopathy

Magnetic Resonance Imaging in Acute Hepatic Encephalopathy

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