Neuromuscular alterations in the critically ill patient: critical illness myopathy, critical illness neuropathy, or both?
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Critical Care↗
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[Polyneuropathy in the critically ill patient--critical illness polyneuropathy].
Polyneuropathy developing in critically ill patients ("critical illness polyneuropathy"--CIP) is diagnosed with increasing frequency in intensive care units. CIP is an axonal polyneuropathy leading to difficulties in weaning from artificial ventilation and symmetrical flaccid tetraparesis. Pathogenetically CIP is considered to be part of the multiple organ dysfunction syndrome (MODS) in the course of sepsis or systemic inflammatory response syndrome (SIRS). The incidence of CIP in septic patients with MODS ranges from 50% to 70%. Electroneurography (ENG) and electromyography (EMG) are essential diagnostic procedures. The mortality in patients with CIP is higher than in patients without CIP. Depending on the severity of CIP, recovery of neurological function in survivors is usually relatively good.
Critical Care↗
The role of erythropoietin therapy in the critically ill.
Critically ill patients receive an extraordinarily large number of blood transfusions. Between 40% and 50% of all patients admitted to intensive care units (ICUs) receive at least one allogeneic red blood cell (RBC) unit and average close to 5 U of RBCs during their ICU admission. RBC transfusion is not risk-free, and there is little evidence that "routine" transfusion of stored allogeneic RBCs is beneficial to critically ill patients. It is clear that most critically ill patients can tolerate hemoglobin levels as low as 7 g/dL, and therefore, a more conservative approach to RBC transfusion is warranted. Anemia of critical illness is a distinct clinical entity characterized by blunted erythropoietin (EPO) production and abnormalities in iron metabolism identical to what is commonly referred to as anemia of chronic disease. As such, the bone marrow in many of these patients responds to the administration of exogenous EPO, in spite of their underlying critical illness. The efficacy of perioperative recombinant human erythropoietin (rHuEPO) has been demonstrated in a variety of elective surgical settings. Similarly, in critically ill patients, rHuEPO therapy will also stimulate erythropoiesis. In randomized placebo-controlled trials, therapy with rHuEPO resulted in a significant reduction in allogeneic RBC transfusions. Strategies to increase the production of RBCs are complementary to other approaches to reduce blood loss in the ICU and decrease the transfusion threshold in the management of all critically ill patients.
Anemia↗
Risks and benefits of nutritional support during critical illness.
Critically ill patients who depend on intensive care for more than a few days reveal profound erosion of lean body mass, which is thought to contribute to high morbidity and mortality. Despite a shortfall of evidence that supplemental feeding actually alters clinical outcome of these life-threatening disease states, this observation evoked an almost universal, albeit often inappropriate, use of nutritional support (NS) in the critically ill, administered via the parenteral or the enteral route. Lack of knowledge and overenthusiasm subsequently resulted in complications associated with both parenteral nutrition (PN) and enteral nutrition (EN), which led to the standing controversy over which should be preferred. With time, however, it became clear that EN and PN are not mutually exclusive and that critically ill patients requiring NS should be fed according to the functional status of the gastrointestinal tract. In addition, tight blood glucose control with insulin is advised in fed critically ill patients because overall metabolic control appears to surpass any outcome benefit attributed to the route of feeding. Recently, various special nutritional formulas have been suggested to prevent or treat multiorgan failure in the critically ill, among other pathways via modulation of immune function. Although special nutritional formulas may be promising in a variety of clinical settings, based on currently available data, these cannot be recommended for routine use in critically ill patients.
Critical Care↗
Stress hyperglycemia and adrenal insufficiency in the critically ill.
Critical illness evoked by trauma, extensive surgery, or severe medical illnesses is the ultimate example of acute severe physical stress. The endocrine response in a critically injured and stressed patient is varied and complex. Although the acute and chronic phases of critical illness are characterized by distinct endocrine responses, the diagnosis of these disorders is controversial. The inability to define the endocrine change as either adaptation or pathology renders the issue of treatment even more controversial. In addition, patients may have preexisting endocrine diseases, either previously diagnosed or unknown, and hence endocrine evaluation in a critically ill patient poses a major challenge to the health care provider. This review provides a novel insight into the dynamic endocrine alterations that occur during evolution of stress hyperglycemia and adrenal insufficiency in the critically ill patient and the available evidence for the therapy of these disorders.
Adrenal Insufficiency↗
Anemia and red blood cell transfusion in the critically ill.
Critically ill patients are anemic early in their intensive care unit (ICU) course. As a consequence of this anemia they receive a large number of red blood cell (RBC) transfusions. There is little evidence that "routine" transfusion of stored allogeneic RBCs is beneficial to critically ill patients and may in fact be associated with worse clinical outcomes. It is clear that most critically ill patients can tolerate hemoglobin levels as low as 7 g/dl and therefore a more conservative approach to RBC transfusion is warranted. Strategies to minimize loss of blood and increase the production of RBCs are also important in the management of all critically ill patients.
Anemia↗
Insulin resistance and glucose-induced thermogenesis in critical illness.
Critical illness is associated with a marked increase in metabolic rate and progressive wasting, despite aggressive nutritional support. The metabolic events which are responsible for these phenomena are unclear, but are characterised by marked impairment of the anabolic effects of insulin on glucose metabolism and excessive activation of the sympathetic nervous system. It has been suggested that critical illness may be associated with impaired carbohydrate oxidation and a marked increase in the loss of heat energy associated with glucose administration (glucose-induced thermogenesis). This situation may result in impaired efficiency of nutrient assimilation. Studies employing combinations of nutrient infusions both at clinically-relevant rates and in association with euglycaemic hyperinsulinaemia have, however, demonstrated that nutrient-induced thermogenesis is unaffected in critical illness in human subjects, and that defective glucose utilization occurs as a consequence of impaired insulin-mediated glucose storage rather than oxidation. Although the cellular and molecular mechanisms underlying these changes are controversial, the recent validation of a human model of insulin resistance in critical illness should provide a means of studying this response in future, and allow the identification of therapeutic targets. This information should increase the efficacy of nutritional support in some of our most seriously-ill patients.
Animals↗
Endocrine aspects of acute and prolonged critical illness.
Critical illness is characterized by striking alterations in the hypothalamic-anterior-pituitary-peripheral-hormone axes, the severity of which is associated with a high risk of morbidity and mortality. Most attempts to correct hormone balance have been shown ineffective or even harmful because of a lack of pathophysiologic insight. There is a biphasic (neuro)endocrine response to critical illness. The acute phase is characterized by an actively secreting pituitary, but the concentrations of most peripheral effector hormones are low, partly due to the development of target-organ resistance. In contrast, in prolonged critical illness, uniform (predominantly hypothalamic) suppression of the (neuro)endocrine axes contributes to the low serum levels of the respective target-organ hormones. The adaptations in the acute phase are considered to be beneficial for short-term survival. In the chronic phase, however, the observed (neuro)endocrine alterations appear to contribute to the general wasting syndrome. With the exception of intensive insulin therapy, and perhaps hydrocortisone administration for a subgroup of patients, no hormonal intervention has proven to beneficially affect outcome. The combined administration of hypothalamic releasing factors does, however, hold promise as a safe therapy to reverse the (neuro)endocrine and metabolic abnormalities of prolonged critical illness by concomitant reactivation of the different anterior-pituitary axes.
Acute Disease↗
Cholescintigraphy in the critically ill.
Critical review of cholescintigraphy in critically ill patients suggests the examination will not conclusively prove or disprove the diagnosis of acute cholecystitis. Of 17 scans performed in critically ill patients with clinical evidence of acute cholecystitis, 7 were true-negative, 1 was false-negative, 6 were false-positive, and 3 were nondiagnostic. Cholestasis and hepatocyte dysfunction, common in the critically ill, result in abnormal clearance of hepatobiliary radionuclide imaging agents, decreasing the usefulness of cholescintigraphy in this patient population. Diagnosing acute cholecystitis in a critically ill patient remains difficult.
Acute Disease↗
Complications of sedation and critical illness.
Critically ill patients require sedation to reduce anxiety, agitation, and achieve therapeutic goals. Over-sedation in combination with multiple causes for extreme muscle weakness, however, interferes with recovery from critical illness. This article describes contributing factors and explores methods of preventing over-sedation and related sequelae.
Adult↗
Enteral nutrition and the critically ill.
Critically ill patients invariably require nutritional intervention. Traditionally, enteral nutrition has not been widely employed in this patient population. This is due in part to the success of present-day parenteral nutrition, and to difficulties encountered with enteral feeding. Recent evidence has demonstrated that enteral is preferable to parenteral nutrition in terms of cost, complications, gut mucosal maintenance, and metabolic and immune function. Enterally administered nutritional support can and should be utilised as the preferred route of nourishment for the critically ill. The appropriate choice of access and formula, as well as a rational strategy for implementation, should improve the likelihood of success. This article describes the unique features of critical illness as they pertain to nutritional support, the benefits of enteral nutrition, and the obstacles to success, and offers suggestions which may improve the ability to provide nutrients adequately via the intestinal tract.
Critical Care↗
The intestinal response to critical illness.
Critical illness is characterized by the presence of several factors that can cause marked alterations in the structure and function of multiple organ systems (1-2). These factors include injury, ischemia, sepsis, and starvation (Fig. 1). It is common for more than one of these problems to be present in the individual patient. Our current understanding of the effect of these various factors on intestinal structure and function has increased markedly during the past decade (3). Furthermore, the patterns of intestinal dysfunction that occur in response to these conditions have also been better characterized. Although malabsorption and motility disorders have long been recognized as clinical problems, more recently loss of intestinal barrier function and immune dysfunction have gained attention. This improved understanding of the response of the intestine to critical illness may lead to prevention of intestinal failure or permit more specific therapy when it occurs. The goals of this manuscript are to describe the response of the small intestine to critical illness and to identify potential therapeutic strategies for preventing and treating intestinal failure in this setting.
Critical Illness↗
Neuromuscular manifestations of critical illness.
Critical illness, more precisely defined as the systemic inflammatory response syndrome (SIRS), occurs in 20%-50% of patients who have been on mechanical ventilation for more than 1 week in an intensive care unit. Critical illness polyneuropathy (CIP) and myopathy (CIM), singly or in combination, occur commonly in these patients and present as limb weakness and difficulty in weaning from the ventilator. Critical illness myopathy can be subdivided into thick-filament (myosin) loss, cachectic myopathy, acute rhabdomyolysis, and acute necrotizing myopathy of intensive care. SIRS is the predominant underlying factor in CIP and is likely a factor in CIM even though the effects of neuromuscular blocking agents and steroids predominate in CIM. Identification and characterization of the polyneuropathy and myopathy depend upon neurological examination, electrophysiological studies, measurement of serum creatine kinase, and, if features suggest a myopathy, muscle biopsy. The information is valuable in deciding treatment and prognosis.
Humans↗
Continuous arteriovenous hemodialysis: an alternative therapy for acute renal failure associated with critical illness.
Critically ill patients often cannot tolerate conventional hemodialysis because of hemodynamic instability. Continuous arteriovenous hemofiltration provides control of fluid and electrolyte balance but is inefficient in the management of azotemia. Continuous arteriovenous hemodialysis (CAVHD) combines dialysis with hemofiltration. We performed 15 CAVHD treatments of 2 or more days' duration in 12 critically ill patients aged 23 to 85 (mean 64.4) years who had acute oliguric renal failure as a component of multiple organ system failure and who were unsuitable for conventional hemodialysis. The total treatment time was 106 days. The serum creatinine and urea levels were controlled in all the patients during CAVHD. The ultrafiltrate losses were sufficient to allow appropriate nutrition and fluid administration and still maintain a negative fluid balance. Renal function returned in five patients (42%), of whom four survived to be discharged home. CAVHD is an effective means of managing acute oliguric renal failure in critically ill patients.
Acute Kidney Injury↗
Long-term outcomes after critical illness.
Critical illness is a severe and generalized monophasic event, and it is likely that there will be evidence of compromised reserve in all end organs if one looks hard enough for it. The crucial issues are to understand which end organs are the most vulnerable to this insult, in which organ systems the incremental disability is of the most functional consequence, and how to design an effective intervention to ameliorate the dysfunction. The long-term morbidity in survivors of critical illness is likely multifactorial. Studies of survivors of acute respiratory distress syndrome (ARDS) have shown that there are both long-term physical and neuropsychological consequences of severe illness. We need to gain a better understanding of the specific determinants of patients' inability to resume their prior work/lifestyle so that an appropriate multidisciplinary intervention can be designed and tested.
Cognition↗
Objective, quantitative measurement of severity of illness in critically ill patients.
Severity of illness must be quantitated in critically ill patients if studies of outcome and therapeutic efficacy are to be meaningful. Objective physiologic indicators of critical illness, such as pertinent laboratory values, can be quantitated using the Therapeutic Intervention Scoring System--TISS. TISS data were obtained for 199 consecutive Class IV critically ill surgical ICU patients and compared to the same data obtained in less critically ill Class II and III ICU patients who served as the control group. For the physiologic indicators of critical illness, a wide range of normal values was established prospectively. The actual values generated by Class IV patients were compared to values of the same indicators as measured in Class II and III ICU patients. Of all objective indicators of critical illness, 55% were either outside the normal range or more than 2 SD away from the mean value of objective indicators for Class II and III ICU patients; 49% were beyond the normal range or more than 3 SD away. Of all TISS indicators, 73% were abnormal, and 36% of all physiologic indicators were still abnormal despite massive therapeutic support when compared to Class II or III ICU patients. Those patients who had more than 40% of their physiologic indicators abnormal were more likely to die. However, the percentage of abnormal TISS indicators did not discriminate between patients who died and those who lived, because almost all patients received massive support.(ABSTRACT TRUNCATED AT 250 WORDS)
Critical Care↗
Glutamine: essential for immune nutrition in the critically ill.
Critically ill patients on intensive care units are at an increased risk of sepsis, which is a major cause of mortality in these patients. Recent evidence suggests that impairment of the functioning of the immune system contributes to the development of sepsis in such patients. In particular, monocytes show reduced expression of HLA-DR antigen, associated with impaired antigen presenting capability and decreased phagocytic activity; lymphocytes show decreased proliferation in response to mitogens and T-helper cells show a shift in the Th1/Th2 ratio consistent with impaired immunity. The amino acid glutamine becomes conditionally essential in the critically ill, yet such patients frequently have a marked deficiency of glutamine; the reasons for this are still unclear. Glutamine is required by the cells of the immune system both as a primary fuel and as a carbon and nitrogen donor for nucleotide precursor synthesis. In vivo studies have demonstrated that glutamine is essential for optimal immune cell functioning for monocytes, lymphocytes and neutrophils. A number of trials of patients fed by the enteral or parenteral route have shown improved infectious morbidity when supplemented with glutamine. However, the exact mechanism of glutamine action in these patients remains to be determined.
Critical Illness↗
Clinical review: Emergency department overcrowding and the potential impact on the critically ill.
Critical care constitutes a significant and growing proportion of the practice of emergency medicine. Emergency department (ED) overcrowding in the USA represents an emerging threat to patient safety and could have a significant impact on the critically ill. This review describes the causes and effects of ED overcrowding; explores the potential impact that ED overcrowding has on care of the critically ill ED patient; and identifies possible solutions, focusing on ED based critical care.
Critical Care↗