Książki na temat „Intravascular volume”

Pyloric stenosis is one of the most common surgical conditions affecting neonates and young infants. Hypertrophy of the pyloric muscular layers results in gradual gastric outlet obstruction. Persistent episodic projectile vomiting and dehydration as well as hypochloremic, hypokalemic metabolic alkalosis are cardinal features. Definitive treatment is surgical pyloromyotomy, but it is not a surgical emergency. Emergency medical intervention is often required to correct intravascular volume depletion and electrolyte disturbances. Morbidity and mortality should be limited due to advancements in surgical and perioperative care. Morbidity can occur due to poor preoperative resuscitation, anesthetic management difficulties, or postoperative complications. The following manuscript is a review of current evidence-based perioperative care of infants with pyloric stenosis. It reviews the pathophysiology that results in metabolic disturbances and intravascular volume depletion. It focuses on preoperative assessment and correction of electrolyte abnormalities and anesthetic technique including airway management and postoperative analgesia.

Contrast-induced acute kidney injury (CI-AKI) occurs because all forms of intravascular contrast contain iodine and their biochemical structures induce immediate changes in systemic and renal vasoreactivity. In the kidneys, contrast induces a transient decrease in renal blood flow. This is more pronounced in patients with chronic kidney disease and diabetes mellitus. The reduction in blood flow allows slowed transit of contrast and reabsorption by the proximal tubular cells where contrast is directly toxic resulting in tubular cell dysfunction and death. When there is considerable damage, a transient rise in serum creatinine and reduction in urine output will be observed in the hours to days after contrast exposure. Principles to reduce CI-AKI include limiting the amount of contrast used, intravascular volume expansion to maximize renal blood flow and speed transit of contrast, and possibly agents to reduce the oxidative damage caused by the contrast agents themselves.

An understanding of the physiology of body fluids is essential when considering appropriate fluid resuscitation and fluid replacement therapy in critically-ill patients. In healthy humans, the body is composed of approximately 60% water, distributed between intracellular and an extracellular compartments. The extracellular compartment is divided into intravascular, interstitial and transcellular compartments. The movement of fluids between the intravascular and interstitial compartments, is classically described as being governed by Starling forces, leading to a small net efflux of fluid from the intravascular to the interstitial compartment. More recent evidence suggests that a model incorporating the effect of the endothelial glycoclayx layer, a web of glycoproteins and proteoglycans that are bound on the luminal side of the vascular endothelium, better explains the observed distribution of fluids. The movement of fluid to and from the intracellular compartment and the interstitial fluid compartment, is governed by the relative osmolarities of the two compartments. Body fluid status is governed by the difference between fluid inputs and outputs; fluid input is regulated by the thirst mechanism, with fluid outputs consisting of gastrointestinal, renal, and insensible losses. The regulation of intracellular fluid status is largely governed by the regulation of the interstitial fluid osmolarity, which is regulated by the secretion of antidiuretic hormone from the posterior pituitary gland. The regulation of extracellular volume status is regulated by a complex neuro-endocrine mechanism, designed to regulate sodium in the extracellular fluid.

Administration of intravenous fluids for maintenance and the more consequential fluid resuscitation are common therapeutic interventions in the neurosciences intensive care unit. Intravenous fluids are provided to ensure adequate hydration because acutely ill neurologic patients often cannot swallow safely. There is a reason to use certain types of fluids and certain measures to maintain an adequate fluid balance specifically in patients admitted to the neurosciences ICU. This chapter covers the regulation of fluid status and the effect of certain fluids on intravascular volume. Daily fluid requirements and the best methods of resuscitation are discussed. The chapter also outlines fluid solutions and the infusion rate associated with different techniques. The side effects of large-volume resuscitation are emphasized.

Perioperative clinicians caring for patients with diabetes should understand the underlying mechanisms, diagnosis, and treatment of hyperglycemic crises. Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) require prompt recognition and treatment. Disturbances such as these can create acute problems associated with intravascular volume and electrolyte abnormalities, as well as effect postoperative recovery and wound healing. Common precipitants, clinical manifestations, and basic treatment algorithms aimed at safely correcting the underlying cause, as well as the associated problems, are described in this chapter. Perioperative glycemic control is an area of recent intense investigation, and specific recommendations are provided herein.

Osmotic drugs are ubiquitously used in neurocritically ill patients. Mannitol and hypertonic saline are readily available in emergency departments and intensive care units to reduce intracranial pressure. Mannitol depletes and hypertonic saline expands the volume status. Hyperosmolar fluids increase the intravascular osmolality, draw water from the brain, reduce or temporize shift, and reduce globally increased intracranial pressure from any cause. These osmotic fluids change fluid compartments and cannot be used indiscriminately. Particularly when they are administered regularly, close monitoring is needed and target goals should be set. This chapter discusses triggers for the use of these osmotic agents, how to judge their effect, and how to dose adequately.

Vasopressors and inotropes are used in the neurosciences intensive care unit to treat hypotension and to augment blood pressure. Hypotension can be attributed to abnormal cardiac output, abnormal intravascular volume or abnormal systemic vascular resistance. Vasopressors are needed to manage hemodynamic augmentation in patients with severe cerebral vasospasm and aneurysmal subarachnoid hemorrhage, in patients with critical carotid or basilar artery stenosis producing marginal blood flow, or when patients are maintained in drug-induced comas. The main incentive is to maintain adequate perfusion pressure to the brain and vital organs, particularly the kidneys. This chapter provides the essentials of management of these complex drugs and how to avoid unintended side effects.

Hyponatraemia is the most common electrolyte disorder in hospitalized patients and is primarily a water balance disorder. Therefore, hyponatraemia is due to a relative excess of water in comparison with sodium in the extracellular fluid volume. Hyponatraemia is usually due to the release of vasopressin despite hypo-osmolality; this secretion is either ‘appropriate’ (i.e. due to a low intravascular volume) or ‘inappropriate’. The diagnostic approach to hyponatraemia relies on the assessment of the time of development, symptoms, and volume status, along with laboratory parameters such as urine sodium and urine osmolality. Complications are mainly neurological and usually depend on the rate of development and correction. If hyponatraemia develops acutely, treatment should be directed towards counteracting the water shift to or brain cells. Conversely, in more chronic cases of hyponatraemia, treatment should be directed at the underlying cause, while avoiding over-correction.

The left atrium (LA) plays an important role in cardiovascular performance, not only as a mechanical contributor, elastic reservoir, and a primer for left ventricular filling, but also as a participant in the regulation of intravascular volume through the production of atrial natriuretic peptide.Although LA diameter in the parasternal long-axis view has been routinely employed, LA volume is a more robust marker for predicting events than LA areas or diameters. The assessment of LA performance based on two-dimensional volumetrics, Doppler evaluation of mitral, pulmonary vein flow, and annular tissue Doppler, as well as deformation imaging techniques, may provide incremental information for prognostic purposes and for the evaluation of severity and duration of conditions associated with LA overload.The aims of this chapter are to explain the basics of LA function, and to describe the role of Doppler echocardiography techniques, and how to implement them, for the non-invasive evaluation of LA in clinical practice.

The mechanism by which loss of serum proteins into the urine causes expansion of extracellular fluid volume and oedema has become clearer. A key initiating abnormality is avid sodium retention by the kidney, leading to increased whole-body sodium and increased extracellular fluid volume. This appears to be driven primarily by overactivation of the amiloride-sensitive epithelial sodium channel (ENaC) in the collecting duct, activated proteolytically through abnormal filtration of plasminogen, and its activation to plasmin in the nephron. Conventional explanations for nephrotic oedema focused on low colloid osmotic pressure as a consequence of loss of serum proteins, leading to egress of extracellular fluid from the intravascular compartment. It was hypothesized that this led to underfilling of the circulation and a drive to sodium retention. While low osmotic pressure may play a part in the clinical picture of nephrotic syndrome, a variety of observations suggest that underfilling is not a common feature except in the most severe nephrotic syndrome. Furthermore the gradient in colloid osmotic pressure between serum and interstitium tends to be preserved in nephrotic syndrome. The distribution of excess extracellular fluid is markedly different in patients with nephrotic syndrome from that seen in patients who have reduced glomerular filtration rate as the cause of sodium retention. This is not fully understood but hypotheses centre on capillary permeability and colloid osmotic pressure effects.

‘Crystalloid’ refers to solutions of crystalline substances that can pass through a semipermeable membrane and are distributed widely in body fluid compartments. The conventional Starling model predicts transvascular exchange based on the net balance of opposing hydrostatic and oncotic forces. Based on this model, colloids might be considered superior resuscitative fluids. However, observations of fluid behaviour during critical illness are not consistent with such predictions. Large randomized controlled studies have consistently found that colloids offer no survival advantage relative to crystalloids in critically-ill patients. A revised Starling model describes a central role for the endothelial glycocalyx in determining fluid disposition. This model supports crystalloid utilization in most critical care settings where the endothelial surface layer is disrupted and lower capillary pressures (hypovolaemia) make volume expansion with crystalloids effective, since transvascular filtration decreases, intravascular retention increases and clearance is significantly reduced. There are important negative consequences of both inadequate and excessive crystalloid resuscitation. Precise dosing may be titrated based on functional measures of preload responsiveness like pulse pressure variation or responses to manoeuvres such as passive leg raising. Crystalloids have variable electrolyte concentrations, volumes of distribution, and, consequently variable effects on plasma pH. Choosing balanced crystalloid solutions for resuscitation may be potentially advantageous versus ‘normal’ (isotonic, 0.9%) saline solutions. When used as the primary fluid for resuscitation, saline solutions may have adverse effects in critically-ill patients secondary to a reduction in the strong ion difference and hyperchloraemic, metabolic acidosis. Significant negative effects on immune and renal function may result as well.

Oliguria and acute kidney injury (AKI) are common in critically-ill patients with studies reporting AKI affecting more than 50% of critically-ill patients. AKI is independently associated with increased mortality and is a potentially modifiable aspect of critical illness. The pathogenesis of AKI is complex and varies according to aetiology. The most common trigger in ICU patients is sepsis—the pathophysiology of septic AKI is poorly understood and probably involves intrarenal haemodynamic and inflammatory processes. In the setting of septic AKI, the classic acute tubular necrosis described in experimental models does not occur and histological changes are only minor. Activation of neurohormonal mechanisms is also important, particularly in the hepatorenal syndrome, where activation of the remain-angiotensin system appears to play a major role. The treatment of oliguria and AKI in ICU patients has traditionally relied on the administration of intravenous fluids. While such therapy is warranted in patients with a clear history, and physical examination suggestive of intravascular and extravascular volume depletion, its usefulness in other patients (e.g. septic patients) remains controversial. Removal of nephrotoxins, rapid treatment of the triggering factors, and attention to cardiac output and mean arterial pressure remain the cornerstones of the prevention and treatment of AKI in ICU.

The term ‘polytrauma’ refers to blunt (or crush) trauma that involves multiple body regions or cavities, and compromises physiology to potentially cause dysfunction of uninjured organs. Polytrauma frequently affects muscles resulting in rhabdomyolysis. In daily life, it mostly occurs after motor vehicle accidents, influencing a limited number of patients; after mass disasters, however, thousands of polytrauma victims may present at once with only surgical features or with additional medical complications (crush syndrome). Among the medical complications, acute kidney injury (AKI) deserves special mention, since it is frequent and has a substantial impact on the ultimate outcome.Several factors play a role in the pathogenesis of polytrauma (or crush)-induced AKI: (1) hypoperfusion of the kidneys, (2) myoglobin-induced direct nephrotoxicity, and intratubular obstruction, and also (3) several other mechanisms (i.e. iron and free radical-induced damage, disseminated intravascular coagulation, and ischaemia reperfusion injury). Crush-related AKI is prerenal at the beginning; however, acute tubular necrosis may develop eventually. In patients with crush syndrome, apart from findings of trauma, clinical features may include (but are not limited to) hypotension, oliguria, brownish discoloration of urine, and other symptoms and findings, such as sepsis, acute respiratory distress syndrome, disseminated intravascular coagulation, bleeding, cardiac failure, arrhythmias, electrolyte disturbances, and also psychological trauma.In the biochemical evaluation, life-threatening hyperkalaemia, retention of uraemic toxins, high anion gap metabolic acidosis, elevated serum levels of myoglobin, and muscle enzymes are noted; creatine phosphokinase is very useful for diagnosing rhabdomyolysis.Early fluid administration is vital to prevent crush-related AKI; the rate of initial fluid volume should be 1000 mL/hour. Overall, 3–6 L are administered within a 6-hour period considering environmental, demographic and clinical features, and urinary response to fluids. In disaster circumstances, the preferred fluid formulation is isotonic saline because of its ready availability. Alkaline (bicarbonate-added) hypotonic saline may be more useful, especially in isolated cases not related to disaster, as it may prevent intratubular myoglobin, and uric acid plugs, metabolic acidosis, and also life-threatening hyperkalaemia.In the case of established acute tubular necrosis, dialysis support is life-saving. Although all types of dialysis techniques may be used, intermittent haemodialysis is the preferred modality because of medical and logistic advantages. Close follow-up and appropriate treatment improve mortality rates, which may be as low as 15–20% even in disaster circumstances. Polytrauma victims after mass disasters deserve special mention, because crush syndrome is the second most frequent cause of death after trauma. Chaos, overwhelming number of patients, and logistical drawbacks often result in delayed, and sometimes incorrect treatment. Medical and logistical disaster preparedness is useful to improve the ultimate outcome of disaster victims.

Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 5-10% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as sepsis). Acute kidney injury replaced the previously used term ‘acute renal failure’ and comprises the entire spectrum of the disease, from small changes in function to the requirement of renal replacement therapy. Not only failure, but also minor and less severe decreases, in kidney function are of clinical significance both in the short and long-term. The most recent definition for acute kidney injury is proposed by the Kidney Disease: Improving Global Outcomes clinical practice guidelines workgroup. This definition is a modification of the RIFLE and AKIN definitions and staging criteria, and it stages patients according to changes in the urine output and serum creatinine (see Tables 68.1 and 68.2). Acute kidney injury is a heterogeneous syndrome with different and multiple aetiologies, often with several insults occurring in the same individual. The underlying processes include nephrotoxicity, and neurohormonal, haemodynamic, autoimmune, and inflammatory abnormalities. The most frequent cause for acute kidney injury in intensive cardiac care patients are low cardiac output with an impaired kidney perfusion (cardiogenic shock) and/or a marked increase in venous pressure (acute decompensated heart failure). Predictors for acute kidney injury in these patients include: baseline renal dysfunction, diabetes, anaemia, and hypertension, as well as the administration of high doses of diuretics. In the intensive cardiac care unit, attention must be paid to the prevention of acute kidney injury: monitoring of high-risk patients, prompt resuscitation, maintenance of an adequate mean arterial pressure, cardiac output, and intravascular volume (avoidance of both fluid overload and hypovolaemia), as well as the avoidance or protection against nephrotoxic agents. The treatment of acute kidney injury focuses on the treatment of the underlying aetiology, supportive care, and avoiding further injury from nephrotoxic agents. More specific therapies have not yet demonstrated efficacy. Renal replacement therapy is indicated in life-threatening changes in fluid, electrolyte, and acid-base balance, but there are also arguments for more early initiation.

Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 5-10% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as sepsis). Acute kidney injury replaced the previously used term ‘acute renal failure’ and comprises the entire spectrum of the disease, from small changes in function to the requirement of renal replacement therapy. Not only failure, but also minor and less severe decreases, in kidney function are of clinical significance both in the short and long-term. The most recent definition for acute kidney injury is proposed by the Kidney Disease: Improving Global Outcomes clinical practice guidelines workgroup. This definition is a modification of the RIFLE and AKIN definitions and staging criteria, and it stages patients according to changes in the urine output and serum creatinine (see Tables 68.1 and 68.2). Acute kidney injury is a heterogeneous syndrome with different and multiple aetiologies, often with several insults occurring in the same individual. The underlying processes include nephrotoxicity, and neurohormonal, haemodynamic, autoimmune, and inflammatory abnormalities. The most frequent cause for acute kidney injury in intensive cardiac care patients are low cardiac output with an impaired kidney perfusion (cardiogenic shock) and/or a marked increase in venous pressure (acute decompensated heart failure). Predictors for acute kidney injury in these patients include: baseline renal dysfunction, diabetes, anaemia, and hypertension, as well as the administration of high doses of diuretics. In the intensive cardiac care unit, attention must be paid to the prevention of acute kidney injury: monitoring of high-risk patients, prompt resuscitation, maintenance of an adequate mean arterial pressure, cardiac output, and intravascular volume (avoidance of both fluid overload and hypovolaemia), as well as the avoidance or protection against nephrotoxic agents. The treatment of acute kidney injury focuses on the treatment of the underlying aetiology, supportive care, and avoiding further injury from nephrotoxic agents. More specific therapies have not yet demonstrated efficacy. Renal replacement therapy is indicated in life-threatening changes in fluid, electrolyte, and acid-base balance, but there are also arguments for more early initiation.