Hypoxic hepatitis in patients with cardiac failure: incidence in a coronary care unit and measurement of hepatic blood flow

Henrion, Jean; Descamps, Olivier; Luwaert, R.; Schapira, M.; Parfonry, Alex; Heller, F.

doi:10.1016/s0168-8278(94)80226-2

Cited by 120 publications

(108 citation statements)

References 16 publications

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“…By contrast, in the setting of unstable CHF, we showed in prior studies that HH was the result of an acute fall in CO (and thus in liver blood flow) arising on a liver sensitized to hypoxia by the chronic action of passive congestion. 3,13 Similarly, this study shows that, in patients with exacerbation of CRF, HH is the result of a bout of extreme hypoxemia arising on a liver sensitized by chronic passive congestion.…”

Section: Discussionsupporting

confidence: 52%

Hypoxic hepatitis caused by acute exacerbation of chronic respiratory failure: A case-controlled, hemodynamic study of 17 consecutive cases

et al. 1999

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Out of a prospective series of 142 consecutive episodes of hypoxic (ischemic) hepatitis (HH), we identified 17 episodes associated with an acute exacerbation of chronic respiratory failure (CRF) without left cardiac failure. In the aim to evaluate the role of arterial hypoxemia in the pathogenesis of HH associated with respiratory failure, these 17 episodes of HH (study group) were hemodynamically compared with a control group of 17 episodes of HH associated with congestive heart failure (CHF) (control group 1) and a group of 16 episodes of acute respiratory failure (ARF) not complicated by HH (control group 2). Arterial hypoxemia was significantly more severe in the study group (

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Section: Discussionsupporting

confidence: 52%

Hypoxic hepatitis caused by acute exacerbation of chronic respiratory failure: A case-controlled, hemodynamic study of 17 consecutive cases

et al. 1999

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“…Rather, the combination of elevated central venous pressures and decreased cardiac output appears to be critical. 106,107 A classic example of this combination is the single-ventricle anatomy palliated to Fontan circulation. Patients with repaired TOF with residual pulmonary regurgitation, Ebstein anomaly with severe tricuspid regurgitation, complete transposition of the great arteries with obstructed systemic venous baffles, and Eisenmenger syndrome can also be affected by this combination of hemodynamic disturbances (Table 1).…”

Section: -95mentioning

confidence: 99%

Diagnosis and Management of Noncardiac Complications in Adults With Congenital Heart Disease: A Scientific Statement From the American Heart Association

Lui¹,

Saïdi²,

Bhatt³

et al. 2017

Circulation

176

136

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ABSTRACT:Life expectancy and quality of life for those born with congenital heart disease (CHD) have greatly improved over the past 3 decades. While representing a great advance for these patients, who have been able to move from childhood to successful adult lives in increasing numbers, this development has resulted in an epidemiological shift and a generation of patients who are at risk of developing chronic multisystem disease in adulthood. Noncardiac complications significantly contribute to the morbidity and mortality of adults with CHD. Reduced survival has been documented in patients with CHD with renal dysfunction, restrictive lung disease, anemia, and cirrhosis. Furthermore, as this population ages, atherosclerotic cardiovascular disease and its risk factors are becoming increasingly prevalent. Disorders of psychosocial and cognitive development are key factors affecting the quality of life of these individuals. It is incumbent on physicians who care for patients with CHD to be mindful of the effects that disease of organs other than the heart may have on the well-being of adults with CHD. Further research is needed to understand how these noncardiac complications may affect the long-term outcome in these patients and what modifiable factors can be targeted for preventive intervention.

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“…These findings indicate that ischemic hepatitis is more likely a consequence of both hepatic congestion and a low cardiac output. 66 From a laboratory perspective, ischemic hepatitis is characterized by rapid increases in serum aminotransferases and lactate dehydrogenase, often to dramatic levels. The aminotransferases peak ≈1 to 3 days after the hemodynamic insult and can rise to 250 times the upper limit of normal.…”

Section: Clinical Manifestationsmentioning

confidence: 99%

Gastrointestinal and Liver Issues in Heart Failure

2016

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Abstract-Heart failure affects ≈23 million people worldwide and continues to have a high mortality despite advancements in modern pharmacotherapy and device therapy. HF is a complex clinical syndrome that can result in the impairment of endocrine, hematologic, musculoskeletal, renal, respiratory, peripheral vascular, hepatic, and gastrointestinal systems. Although gastrointestinal involvement and hepatic involvement are common in HF and are associated with increased morbidity and mortality, their bidirectional association with HF progression remains poorly fathomed. The current understanding of multiple mechanisms, including proinflammatory cytokine milieu, hormonal imbalance, and anabolic/ catabolic imbalance, has been used to explain the relationship between the gut and HF and has been the basis for many novel therapeutic strategies. However, the failure of these novel therapies such as anti-tumor necrosis factor-α has resulted in further complexity. Key Words: gastrointestinal tract ◼ heart failure H eart failure (HF) is a systemic disorder caused by the inability of the heart to accommodate the venous return and to maintain sufficient cardiac output to meet the body's metabolic needs.1 These hemodynamic perturbations result in a state of systemic inflammation with well-described and well-studied consequences in a variety of other organ systems, including the renal, cerebral, musculoskeletal, and immune systems. In contrast, the gastrointestinal and hepatic systems have received less attention, although gastrointestinal symptoms are common. With increasing clinical efforts to resuscitate the advanced HF patient, a greater appreciation and a better understanding of the gastrointestinal and hepatic manifestations of HF are needed. 2,3With some notable exceptions, gastrointestinal and hepatic involvement in heart disease has historically received little attention from cardiologists. 4 Mechanisms of gastrointestinal and hepatic dysfunction remain poorly understood despite the common presence of gastrointestinal-related symptoms and the increased morbidity and mortality associated with their presence. The specific involvement of the gastrointestinal system in HF results in a bidirectional relationship that has been called the cardiointestinal syndrome.5 For example, the systemic volume overload characteristic of HF is generally accompanied by concomitant gut edema, which can lead to bacterial translocation into the systemic circulation. Consequent monocyte activation and excessive cytokine release result in systemic inflammation, increased symptoms, and disease progression. In this review, we describe the current state of understanding of the gastrointestinal and hepatic systems in HF. Although nutritional status is also relevant in this discussion, we refer the reader to other excellent reviews of nutritional aspects of chronic disease. 7,8The Gut in HF Gastrointestinal System as a Venous ReservoirStudies of implantable hemodynamic monitors to manage HF patients document that acute decompensated HF was not associ...

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Hypoxic hepatitis in patients with cardiac failure: incidence in a coronary care unit and measurement of hepatic blood flow

Cited by 120 publications

References 16 publications

Hypoxic hepatitis caused by acute exacerbation of chronic respiratory failure: A case-controlled, hemodynamic study of 17 consecutive cases

Hypoxic hepatitis caused by acute exacerbation of chronic respiratory failure: A case-controlled, hemodynamic study of 17 consecutive cases

Diagnosis and Management of Noncardiac Complications in Adults With Congenital Heart Disease: A Scientific Statement From the American Heart Association

Gastrointestinal and Liver Issues in Heart Failure

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