Low Cerebral Oxygen Consumption and Blood Flow in Patients With Cirrhosis and an Acute Episode of Hepatic Encephalopathy

Iversen, Peter; Sørensen, Michael; Bak, Lasse K.; Waagepetersen, Helle S.; Vafaee, Manouchehr Seyedi; Borghammer, Per; Mouridsen, Kim; Jensen, Svend Borup; Vilstrup, Hendrik; Schousboe, Arne; Ott, Peter; Gjedde, Albert; Keiding, Susanne

doi:10.1053/j.gastro.2008.10.057

Cited by 97 publications

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“…4,5 In accordance with this, one study reported that reductions in CMRO 2 and CBF were restored when patients, treated with a dopamine agonist, recovered from HE.…”

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confidence: 50%

“…[7][8][9] In humans, cerebral metabolic rate of blood ammonia (CMRA) seems to be primarily determined by the arterial blood concentration of ammonia 10,11 ; in a cross-sectional positron emission tomography (PET) study of patients with cirrhosis with HE, patients with cirrhosis with no history of HE and healthy subjects, CMRO 2 and CBF correlated negatively to the arterial blood ammonia concentration. 5 The relationship between changes in blood ammonia levels and CMRO 2 and CBF has, to the best of our knowledge, not been investigated in the same individuals during and after recovery from an episode of HE.…”

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confidence: 99%

“…1 Studies have shown decreased cerebral oxygen consumption (CMRO 2 ) and blood flow (CBF) in patients with cirrhosis and HE when compared to patients with cirrhosis without HE or healthy subjects, whereas the latter two groups of subjects had similar values. [2][3][4][5] Cross-sectional studies point to the reductions being related to the HE condition and not to the liver disease itself. 4,5 In accordance with this, one study reported that reductions in CMRO 2 and CBF were restored when patients, treated with a dopamine agonist, recovered from HE.…”

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confidence: 99%

“…[2][3][4][5] Cross-sectional studies point to the reductions being related to the HE condition and not to the liver disease itself. 4,5 In accordance with this, one study reported that reductions in CMRO 2 and CBF were restored when patients, treated with a dopamine agonist, recovered from HE. 3 Another study, however, found decreased CMRO 2 but unchanged CBF in patients with a history of HE when compared to patients without a history of HE or healthy controls.…”

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Hepatic encephalopathy is associated with decreased cerebral oxygen metabolism and blood flow, not increased ammonia uptake

et al. 2013

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Studies have shown decreased cerebral oxygen metabolism (CMRO 2 ) and blood flow (CBF) in patients with cirrhosis with hepatic encephalopathy (HE). It remains unclear, however, whether these disturbances are associated with HE or with cirrhosis itself and how they may relate to arterial blood ammonia concentration and cerebral metabolic rate of blood ammonia (CMRA). We addressed these questions in a paired study design by investigating patients with cirrhosis during and after recovery from an acute episode of HE type C. CMRO 2 , CBF, and CMRA were measured by dynamic positron emission tomography (PET)/computed tomography (CT). Ten patients with cirrhosis were studied during an acute episode of HE; nine were reexamined after recovery. Nine patients with cirrhosis with no history of HE served as controls. Mean CMRO 2 increased from 0.73 lmol oxygen/mL brain tissue/min during HE to 0.91 lmol oxygen/mL brain tissue/min after recovery (paired t test; P < 0.05). Mean CBF increased from 0.28 mL blood/mL brain tissue/min during HE to 0.38 mL blood/mL brain tissue/min after recovery (P < 0.05). After recovery from HE, CMRO 2 and CBF were not significantly different from values in the control patients. Arterial blood ammonia concentration decreased 20% after recovery (P < 0.05) and CMRA was unchanged (P > 0.30); both values were higher than in the control patients (both P < 0.05). Conclusion: The low values of CMRO 2 and CBF observed during HE increased after recovery from HE and were thus associated with HE rather than the liver disease as such. The changes in CMRO 2 and CBF could not be linked to blood ammonia concentration or CMRA. (HEPATOLOGY 2013;57:258-265) B rain energy metabolism is believed to be disturbed in patients with cirrhosis with hepatic encephalopathy (HE).1 Studies have shown decreased cerebral oxygen consumption (CMRO 2 ) and blood flow (CBF) in patients with cirrhosis and HE when compared to patients with cirrhosis without HE or healthy subjects, whereas the latter two groups of subjects had similar values.2-5 Cross-sectional studies point to the reductions being related to the HE condition and not to the liver disease itself. 4,5 In accordance with this, one study reported that reductions in CMRO 2 and CBF were restored when patients, treated with a dopamine agonist, recovered from HE.3 Another study, however, found decreased CMRO 2 but unchanged CBF in patients with a history of HE when compared to patients without a history of HE or healthy controls.6 It thus remains an open question whether the reductions in CMRO 2 and CBF in patients with cirrhosis and HE normalize after recovery from HE, and in the present study we therefore measured CMRO 2 and CBF during and after recovery from an episode of HE in individual patients with cirrhosis.Another key question is how changes in CMRO 2 and CBF may relate to the blood concentration of ammonia. Patients with cirrhosis with HE usually have higher Abbreviations: CBF, cerebral blood flow; CMRA, cerebral metabolic rate of blood ammonia; CMRO 2 , cerebral o...

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“…4,5 In accordance with this, one study reported that reductions in CMRO 2 and CBF were restored when patients, treated with a dopamine agonist, recovered from HE.…”

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Hepatic encephalopathy is associated with decreased cerebral oxygen metabolism and blood flow, not increased ammonia uptake

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“…CBF could be a differentiating factor involved in the development of intracranial hypertension in ALF vs. CLD. A decrease in CBF has been documented in patients with CLD (Almdal et al, 1989, Burra et al, 2004, Dam et al, 1998, Iversen et al, 2009, Iwasa et al, 2000and Trzepacz et al, 1994, whereas an increase in CBF commonly occurs during ALF (Jalan et al, 2004a, Larsen et al, 1996, Strauss et al, 1997and Wendon et al, 1994. Given that blood accounts for 10% of brain volume, a rise in CBF could contribute to intracranial hypertension, as observed in ALF.…”

Section: Relationship Between Intracranial Pressure and Brain Edemamentioning

confidence: 99%

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Bosoi

Rose

2013

Neurochemistry International

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Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome that typically develops as a result of acute liver failure or chronic liver disease. Brain edema is a common feature associated with HE. In acute liver failure, brain edema contributes to an increase in intracranial pressure, which can fatally lead to brain stem herniation. In chronic liver disease, intracranial hypertension is rarely observed, even though brain edema may be present. This discrepancy in the development of intracranial hypertension in acute liver failure versus chronic liver disease suggests that brain edema plays a different role in relation to the onset of HE. Furthermore, the pathophysiological mechanisms involved in the development of brain edema in acute liver failure and chronic liver disease are dissimilar. This review explores the types of brain edema, the cells, and pathogenic factors involved in its development, while emphasizing the differences in acute liver failure versus chronic liver disease. The implications of brain edema developing as a neuropathological consequence of HE, or as a cause of HE, are also discussed. HighlightsBrain edema is a common feature in ALF and CLD. HE is inconsistently associated with the presence of brain edema. Fibrous and protoplasmic astrocytes are differentially implicated in the pathogenesis of HE. The pathogenesis of HE is multifactorial causing an array of neurological symptoms.

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Central Nervous System and Pulmonary Complications of End‐Stage Liver Disease

Bajaj

2015

Yamada' S Textbook of Gastroenterology

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Low Cerebral Oxygen Consumption and Blood Flow in Patients With Cirrhosis and an Acute Episode of Hepatic Encephalopathy

Cited by 97 publications

References 43 publications

Hepatic encephalopathy is associated with decreased cerebral oxygen metabolism and blood flow, not increased ammonia uptake

Hepatic encephalopathy is associated with decreased cerebral oxygen metabolism and blood flow, not increased ammonia uptake

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Central Nervous System and Pulmonary Complications of End‐Stage Liver Disease

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