Hypoxic hepatitis. Prospective, clinical and hemodynamic study of 45 cases

The authors report 45 episodes of centrilobular liver cell necrosis, called ischemic hepatitis, in 43 cardiac patients. In 75 percent of the episodes, centrilobular liver cell necrosis was preceded by a period of progressive deterioration of myocardiac function. In 100 percent of the episodes, liver cell necrosis occurred after an acute clinical event inducing a transient fall of cardiac output. Shock was observed in only 47 percent of the episodes. The biological hallmarks of this centrilobular liver cell necrosis were a massive increase in serum aminotransferase levels and in 85 percent of the episodes, a decrease in the prothrombine time below 50 percent of control level. The mortality rate, 15 days after admission, was 42 percent. Prognosis was mainly related to cardiac function. The hemodynamic comparison between the 45 episodes of centrilobular liver cell necrosis and 22 cases of cardiogenic shock without liver cell necrosis showed that, besides hepatic ischemia, passive venous congestion of the liver and arterial hypoxemia were also involved in the onset of liver cell necrosis in these cardiac patients. Among these 45 episodes of liver cell necrosis of cardiac origin, a unique case of hepatic necrosis secondary to major hypoxemia and passive venous congestion, despite an high cardiac output was observed and is reported in detail. Accordingly, the appellation "hypoxic hepatitis" seems to be more appropriate than "ischemic hepatitis".     

The liver in heart failure

Severe congestive heart failure is associated with two distinct forms of liver dysfunction: jaundice that is related to passive congestion and acute hepatocellular necrosis that is caused by impaired perfusion. Cardiac cirrhosis (fibrosis) may result from prolonged recurrent congestive heart failure. Ischemic hepatitis (shock liver) usually manifests as asymptomatic elevation of the serum aminotransferase levels after an episode of hypotension, although the clinical presentation may mimic that of acute viral hepatitis. In most cases, ischemic hepatitis is of little clinical consequence and is self-limited. Acute liver failure may occur in patients with preexisting cirrhosis, severe chronic heart failure, or sustained hepatic ischemia.     

Pulmonary complications of acute myocardial infarct. Therapeutic orientation]

The heart and the lung make up an inseparable anatomic and functional unit. The changes in one affect the other and vice versa. In acute myocardial infarction a heart failure syndrome develops. This syndrome is characterized by passive pulmonary congestion, which leads to hypoxemia. This hypoxemia indicate the functional disturbance of the lung, and the hemodinamic evolution of the disease. Arterial gases determination is the best way to assess the sickness progression. A certain paralelism exists among the central venous saturation, cardiac insufficiency and the degree of pulmonary disfunction. Such a procedure is not very appreciable and does not substitute the direct analysis of the arterial PO2. The pulmonary complications in the myocardial infarction shock are directly responsable of death in 50% of the patients. To heart failure and shock, hipperfusion and hypoxia are added. Many vessels close due to the decrease in the pulmonary flow. This brings about the release of substances that are toxic to the vessel causing an inflammatory vascular reaction. The decrease in the flow harms the lung cell and for this reason atelectasia or alveolar colapse occur; besides inducing the formation of shunts. Under these conditions the lung compliance decreases. The areas that are badly ventilated and hypoperfused can easily become infected and pneumonitis and abscesses cause even more harm to the tissue. The decrease in the speed of circulation and hematologic changes of shock, induce a diseminated intravascular coagulation. What was stated before leads to an important reduction of the lung as a depurating organ and makes the shock irreversible. As far as therapy is concerned in the prevention of vascular colaps and the improvement of the oxemia, oxygen is very useful when there is a venous congestion (clinically, X rays, and oxemia). When the concentration of O2 is lower than 50% in the cases with slight cardiac failure; do not use oxygen in higher concentrations unless the hypoxia is associated to acute pulmonary edema and shock. Mechanic ventilators, and intermitent possitive pressure are recommended even though they have a posenous effect on the cardiac output. Always keep the air ways permeable: changing position, breathing exercises, humidifications, aspiration of secretions, intubation, or traqueostomy depending upon the various cases.     

Ischemic hepatitis: clinical presentation and pathogenesis

BACKGROUND: The pathophysiology of ischemic hepatitis, otherwise known as "shock liver," is poorly understood, although it is believed to be the result of a reduction in systemic blood flow as typically occurs in shock. The aim of this study was to investigate the importance of this phenomenon as well as other clinical features in patients with ischemic hepatitis.METHODS: We identified a cohort of 31 patients (case group) who met the most commonly accepted definition of ischemic hepatitis (an acute reversible elevation in either the serum alanine or aspartate aminotransferase level of at least 20 times the upper limit of normal, excluding known causes of acute hepatitis or hepatocellular injury, in an appropriate clinical setting). We also evaluated the clinical features and serum aminotransferase levels in a cohort (the control group) of 31 previously healthy patients who sustained major nonhepatic trauma at San Francisco General Hospital, a major trauma center. Both groups of patients had documented systolic blood pressures <75 mm Hg for at least 15 minutes. Clinical and hemodynamic (invasive and noninvasive) data were recorded.RESULTS: Despite the marked reduction in blood pressure, no patient in the control group developed ischemic hepatitis. The mean (+/- SD) peak serum aspartate aminotransferase level in the control group was only 78 +/- 72 IU, in contrast with a mean peak of 2,088 +/- 2,165 IU in the case group. All 31 patients with ischemic hepatitis had evidence of underlying organic heart disease, 29 (94%) of whom had right-sided heart failure.CONCLUSIONS: Systemic hypotension or shock alone did not lead to ischemic hepatitis in any patient. The vast majority of patients with ischemic hepatitis had severe underlying cardiac disease that had often led to passive congestion of the liver. These data lead us to propose that right-sided heart failure, with resultant hepatic venous congestion, may predispose the liver to hepatic injury induced by a hypotensive event.     

Risk and Prognosis of Acute Liver Injury Among Hospitalized Patients with Hemodynamic Instability: A Nationwide Analysis

Introduction and aim. Critically ill patients in states of circulatory failure are at risk of acute liver injury, from mild elevations in aminotransferases to substantial rises consistent with hypoxic hepatitis or “shock liver”. The present study aims to quantify the national prevalence of acute liver injury in patients with hemodynamic instability, identify risk factors for its development, and determine predictors of mortality.Material and methods. The 2009-2010 Nationwide Inpatient Sample was interrogated using ICD-9-CM codes for hospital admissions involving states of hemodynamic lability. Multivariable logistic regression was used to evaluate the risks of acute liver injury and death in patients with baseline liver disease, congestive heart failure, malnutrition, and HIV.Results. Of the 2,865,446 patients identified in shock, 4.60% were found to have acute liver injury. A significantly greater proportion of patients with underlying liver disease experienced acute liver injury (22.03%) and death (28.47%) as compared to those without liver disease (3.18% and 18.82%, respectively). The odds of developing acute liver injury were increased in all baseline liver diseases studied, including all-cause cirrhosis, hepatitis B, hepatitis C, alcoholic liver disease, and non-alcoholic fatty liver disease, as well as in congestive heart failure and malnutrition. All-cause cirrhosis and alcoholic liver disease, however, conferred the greatest risk. Similar trends were seen with mortality. HIV was not a predictor for acute liver injury.Conclusion. Liver injury is a major concern among patients with protracted circulatory instability, especially those suffering from underlying liver disease, heart failure, or malnutrition.     

Hypoxic hepatitis

Hypoxic hepatitis (HH), an acute liver injury also known as 'ischaemic hepatitis' or 'shock liver', is frequently observed in intensive care units. HH is heralded by a massive but transient rise in serum aminotransferase activities caused by anoxic necrosis of centrilobular liver cells. Cardiac failure, respiratory failure and toxic-septic shock are the main underlying conditions accounting for more than 90% of cases, but HH may also occur in other circumstances. Until recently, liver ischaemia, i.e. a drop in hepatic blood flow, was considered the leading, and even the sole, hemodynamic mechanism responsible for HH, and it was generally held that a shock state was required. In reality, other hemodynamic mechanisms of hypoxia, such as passive congestion of the liver, arterial hypoxaemia and dysoxia, play an important role while a shock state is observed in only 50% of cases. Accordingly, 'ischaemic hepatitis' and 'shock liver' are misnomers. Therapy of HH depends primarily on the nature of the underlying condition. The prognosis is poor, with more than half of patients dying during the hospital stay.     

A case of fulminant hepatic failure secondary to congestive heart failure

It has been generally accepted that congestive heart failure does not lead to fulminant hepatic failure, unless it is associated with cardiac shock or low cardiac output. Only three cases have been reported, in which liver congestion is followed by fulminant hepatic failure without a history of shock or low cardiac output. Here we present a case of a 48-year-old man with dilated cardiomyopathy and pulmonary infarction, who developed fulminant hepatic failure from congestion. When he was admitted for the control of diabetes mellitus, hepatomegaly of 3-finger breadth and marked cardiomegaly without pulmonary congestion was noted. Diabetes was controlled using insulin. But 3 weeks after admission, he sometimes complained of back dullness because of pulmonary infarction. His heart gradually increased in size, and Jugular venous dilatation and pretibial pitting edema also worsened. Jaundice was noted and serum GOT and GPT increased. A large liver of 6-finger breath below the right costal margin was able to be felt. But within one week, the size of the liver markedly decreased and the signs of hepatic failure such as jaundice, hepatic encephalopathy and numerous petechiae appeared. Blood pressure was maintained and no hypotension or cardiac shock was noted. The patient died of fulminant hepatic failure on the 20th days after onset of the hepatic failure. The autopsy revealed liver atrophy with severe central lobular necrosis, and thrombus in the right main pulmonary artery which caused severe pulmonary infarction. The mechanism of fulminant hepatic failure not accompanied with low cardiac output is discussed.     

入院老年感染性休克患者容量管理的特点与救治体会

目的：针对老年感染性休克血流动力学变化特点,实施容量管理,个体化液体复苏和治疗,达到改善微循环、纠正组织细胞低氧血症和恢复器官功能,提高抢救成功率.方法：通过临床评估和动态血流动力学监测,结合老年人自身生理特点,实施容量管理,一方面个体化液体复苏,纠正有效循环血容量不足,改善微循环,减少组织细胞缺血缺氧性损害,使患者度过危重期;另一方面避免输入液体过多,造成组织水肿,加重损害,延误患者抢救时机.结果：依据老年患者病理生理特点,实施容量管理,防止器官灌注不足或高灌注,改善微循环,纠正低氧血症,减少细胞损害,降低休克患者并发症发生率和病死率.结论：老年感染性休克患者,依据自身状况实施容量管理,个体化液体复苏和治疗,能够提高休克患者抢救成功率.     

Practical considerations in the management of shock complicating acute myocardial infarction A summary of current practice

Practical considerations in the bedside management of the patient with shock as a complication of acute myocardial infarction are reviewed. Routine monitoring techniques include the electrocardiogram, measurements of arterial and central venous pressure, measurements of skin temperature and arterial blood gas analyses. The mainstays of treatment are the relief of pain and anxiety, prevention of hypoxia, fluid repletion and the conservative and selective use of vasoactive drugs based on assessment of the patient's hemodynamic status. Digitalis glycoside is used for treatment of congestive heart failure. Arrhythmias are controlled by electrical conversion, adrenergic drugs, by the selective use of lidocaine and atropine, or by electrical pacing. Mechanical techniques of circulatory support and most surgical procedures are not yet sufficiently perfected for routine clinical application.     

Sleep apnea-hypopnea syndrome and the heart

Cardiovascular and cerebrovascular diseases are the most common diseases in industrialized societies. The main objectives of this article were to summarize the physiological effects of sleep apnea on the circulatory system and to review how treatment of this condition influences cardiovascular disease. Acute sleep apnea has a number of hemodynamic consequences, such as pulmonary and systemic hypertension, increased ventricular afterload and reduced cardiac output, all of which result from sympathetic stimulation, arousal, alterations in intrathoracic pressure, hypoxia and hypercapnia. When chronic, sleep apnea-hypopnea syndrome is associated with systemic hypertension, ischemic heart disease, congestive heart failure, and Cheyne-Stokes respiration in patients with congestive heart failure. Nocturnal treatment with continuous positive airway pressure decreases both the number of central apneic episodes and blood pressure in patients with sleep apnea-hypopnea syndrome and arterial hypertension.     

体外循环心脏术后急性肝功能损害的危险因素分析

目的：通过分析体外循环心脏手术后肝功能损害的危险因素，认识心脏手术后肝功能损害的发生规律及特点。方法：对397例体外循环心脏手术后发生肝功能损害的相关因素进行单因素和多因素分析。结果：单因素分析显示：高龄、风湿性心脏病、慢性病毒性肝炎、术前右心衰、肝淤血、黄疸、腹水、术后严重感染、乳酸酸中毒、低心排血量及低氧血症等因素可能会导致术后急性肝功能损害的发生；多因素分析显示：术前就有肝功能损害、手术中体外循环时间长（超过2h）、手术出血多导致血制品输入量超过1000ml、术后低心排血量以及低氧血症是术后急性肝功能损害发生的独立危险因素。结论：体外循环心脏手术后肝功能损害是多种因素共同作用的结果，应提高对围术期肝功能损害危险因素的认识，正确指导临床治疗，从而避免术后急性肝功能衰竭的发生。     

Hypoxic hepatitis: the point of view of the clinician

Hypoxic hepatitis better known under the terms of ischemic hepatitis or shock liver is the clinical manifestation of an acute liver cell necrosis consecutive to liver hypoxia. The clinical syndrome is defined as a massive but rapidly resolutive increase in serum aminotransferase activities (AT) occurring in a clinical setting of hemodynamic failure. Actually, when confronted to a case of massive increase in serum AT in the setting of cardiac or respiratory failure, the diagnosis of HH may be assumed without liver biopsy if another cause of hepatocyte necrosis such as viral hepatitis or drug induced hepatitis may be excluded. To our opinion, in these patients often aged and in poor general condition, it is particularly important to exclude herpes simplex virus infection and paracetamol intoxication. In case of doubt, a mere ultrasonography of the liver will be helpful. Indeed the majority of these patients will have a dilation of hepatic veins due to passive congestion of the liver. There is no specific liver therapy and the prognosis is poor depending on the severity of the underlying condition. In this point of view, we report what could be of interest for the hospital clinician.     

Disorders of hemodynamics and pulmonary gas exchange in the acute period of myocardial infarct

In 40 patients with massive myocardial infarction, the central hemodynamics was examined by probing the right-sided chambers of the heart and the pulmonary artery. The cardiac output was measured by thermodilution. The gas exchange (respiratory minute volume, capnography, gas analysis of arterial and mixed venous blood) was explored. Arterial hypoxemia was found to be associated with increased intrapulmonary blood shunting in patients with acute myocardial infarction complicated by congestive heart failure. Deterioration of arterial hypoxemia was promoted by a combination of increased overall pulmonary shunting and decreased residual venous oxygenation. Abnormalities in the ventilation-perfusion relations are of great importance.     

Relation between hemodynamic and ventilatory responses in determining exercise capacity in severe congestive heart failure

The cause of exercise intolerance in congestive heart failure is unclear. Hemodynamic and ventilatory responses were measured during symptomatic maximal upright bicycle exercise in 28 patients with chronic severe left ventricular failure who achieved a maximal oxygen uptake of only 12 +/- 4 ml/min/kg (+/- standard deviation). All patients reached anaerobic metabolism as the respiratory exchange ratio rose and arterial pH fell significantly. Pulmonary capillary wedge pressure increased from 20 +/- 10 mm Hg at rest to 38 +/- 9 mm Hg at peak exercise and cardiac index increased from 2.51 +/- 0.73 to 4.54 +/- 1.65 liters/min/m2 (both p less than 0.001). Systemic vascular resistance decreased, but pulmonary vascular resistance did not change during exercise. Despite the marked pulmonary venous hypertension at peak exercise, blood gases were unchanged (PaO2, 96 +/- 15 mm Hg; PaCO2, 35 +/- 7 mm Hg). Systemic arterial oxygen content increased from 16 +/- 2 to 17 +/- 2 vol% (p less than 0.01). Changes in pulmonary capillary wedge pressure did not correlate with changes in arterial oxygen content. Results were similar whether patients were limited by dyspnea or fatigue. Thus, exercise intolerance in patients with severe left ventricular failure is associated with marked elevation of pulmonary capillary wedge pressure and anaerobic metabolism without hypoxemia or altered carbon dioxide tension. These findings suggest that exercise ability in congestive heart failure is more dependent on cardiac output than on ventilatory consequences of pulmonary congestion.     

Severe sleep apnea syndrome diagnosed with acute myocardial infarction

A 55-year-old man with acute myocardial infarction and no heart failure, had episodes of severe oxygen desaturation and apnea, while his hemodynamic parameters were stable. Sleep recordings revealed severe sleep apnea, and pulmonary function tests showed bronchial obstruction. Apnea and desaturation resolved on bi-level positive airway pressure. Patients with acute myocardial infarction who have apnea and hypoxemia without evident heart failure should be evaluated for sleep disorders.     

Congestive heart failure as cause of fulminant hepatic failure

In this patient with long-standing cardiomyopathy and congestive heart failure the syndrome of fulminant hepatic failure developed on two occasions; he recovered both times. There was no evidence of viral or toxic hepatitis as a cause of his liver failure. We conclude that in this case, aggravation of long-standing congestive heart failure may have led to severe hepatocellular necrosis with signs of encephalopathy not commonly observed.     

Organ-specific responses to circulatory disturbances in heart failure: new insights

Recent studies have provided new insights into the pathophysiology of congestive heart failure. Organ-specific responses to circulatory disturbances may differ via a hypoperfusion state and a venous congestion state. The liver and the kidneys serve as a good example of a differential injury pattern based on the predominant circulatory insult. Cardiorenal syndrome appears to be a kidney-specific response to predominantly right-sided backward heart failure ("congestive state"), rather than forward heart failure. Despite significant progress in our understanding of cardiorenal interactions, there is no specific therapy for the cardiorenal syndrome, which is a marker of the severity of the heart failure state.     

中心静脉氧饱和度的监测及其应用

通过中心静脉导管监测中心静脉氧饱和度(ScVO2)是一个方便、可靠的方法,它能快速反映危重患者全身氧的供需平衡的瞬时变化,能早期发现组织缺氧,且优于其它传统的血流动力学参数,是评估组织氧合充分与否的有用的间接指标,也是评估危重患者院内病死率及预后的重要指标;用ScVO2、平均动脉压和中心静脉压来指导早期目标指导性治疗,可提高严重脓毒血症或感染性休克患者的存活率.因此,ScVO2的监测对危重患者的评估和管理是非常重要和有用的.     

Acute liver injury in COVID-19 patients hospitalized in the intensive care unit: Narrative review

In recent years, humanity has been confronted with a global pandemic due to coronavirus disease 2019 (COVID-19), which has caused an unprecedented health and economic crisis worldwide. Apart from the respiratory symptoms, which are considered the principal manifestations of COVID-19, it has been recognized that COVID-19 constitutes a systemic inflammatory process affecting multiple organ systems. Across the spectrum of organ involvement in COVID-19, acute liver injury (ALI) has been gradually gaining increasing attention by the international scientific community. COVID-19 associated liver impairment can affect a considerable proportion of COVID-19 patients and seems to correlate with the severity of the disease course. Indeed, COVID-19 patients hospitalized in the intensive care unit (ICU) run a greater risk of developing ALI due to the severity of their clinical condition and in the context of multi-organ failure. The putative pathophysiological mechanisms of COVID-19 induced ALI in ICU patients remain poorly understood and appear to be multifactorial in nature. Several theories have been proposed to explain the occurrence of ALI in the ICU setting, such as hypoperfusion and ischemia due to hemodynamic instability, passive liver congestion as a result of congestive heart failure, ischemia-reperfusion injury, hypoxia due to respiratory failure, mechanical ventilation itself, sepsis and septic shock, cytokine storm, endotheliitis with concomitant coagulopathy, drug-induced liver injury, parenteral nutrition and direct cytopathic viral effect. It should be noted that no specific therapy for COVID-19 induced ALI exists. Therefore, the therapeutic approach lies in preventive measures and is exclusively supportive once ALI ensues. The aim of the current review is to scrutinize the existing evidence on COVID-19 associated ALI in ICU patients, explore its clinical implications, shed light on the underlying pathophysiological mechanisms and propose potential therapeutic approaches. Ongoing research on the particular scientific field will further elucidate the pathophysiology behind ALI and address unresolved issues, in the hope of mitigating the tremendous health consequences imposed by COVID-19 on ICU patients.     

Morphometric study of the spleen in chronic Chagas' disease

There is frequently an increase in spleen size in infectious systemic and chronic venous congestion. The aim of this report was to perform a comparative study of the spleen tissue of chagasic or nonchagasic autopsied patients with or without congestive heart failure. Evaluations were made of 111 cases. Connective tissue intensity, follicular density and area, and follicular arterioles wall area were determined through the morphometric study. The connective tissue was similar in all groups. The density of the lymphoid follicles was significantly less among the chagasic cases (P = 0.032). The follicular area was larger among the chagasic cases and in the chagasic group with congestive heart failure. The chagasic group without congestive heart failure presented a greater area of follicular arteriole walls. Therefore, the spleen modifications in chronic Chagas' disease could be a consequence not only of the heart failure but also of the Chagas infection itself.