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Intensive Care Medicine Oct 2022In critically ill patients, fluid infusion is aimed at increasing cardiac output and tissue perfusion. However, it may contribute to fluid overload which may be harmful.... (Review)
Review
In critically ill patients, fluid infusion is aimed at increasing cardiac output and tissue perfusion. However, it may contribute to fluid overload which may be harmful. Thus, volume status, risks and potential efficacy of fluid administration and/or removal should be carefully evaluated, and monitoring techniques help for this purpose. Central venous pressure is a marker of right ventricular preload. Very low values indicate hypovolemia, while extremely high values suggest fluid harmfulness. The pulmonary artery catheter enables a comprehensive assessment of the hemodynamic profile and is particularly useful for indicating the risk of pulmonary oedema through the pulmonary artery occlusion pressure. Besides cardiac output and preload, transpulmonary thermodilution measures extravascular lung water, which reflects the extent of lung flooding and assesses the risk of fluid infusion. Echocardiography estimates the volume status through intravascular volumes and pressures. Finally, lung ultrasound estimates lung edema. Guided by these variables, the decision to infuse fluid should first consider specific triggers, such as signs of tissue hypoperfusion. Second, benefits and risks of fluid infusion should be weighted. Thereafter, fluid responsiveness should be assessed. Monitoring techniques help for this purpose, especially by providing real time and precise measurements of cardiac output. When decided, fluid resuscitation should be performed through fluid challenges, the effects of which should be assessed through critical endpoints including cardiac output. This comprehensive evaluation of the risk, benefits and efficacy of fluid infusion helps to individualize fluid management, which should be preferred over a fixed restrictive or liberal strategy.
Topics: Cardiac Output; Critical Illness; Fluid Therapy; Hemodynamics; Humans; Pulmonary Edema; Thermodilution
PubMed: 35945344
DOI: 10.1007/s00134-022-06808-9 -
Frontiers in Veterinary Science 2021Fluid overload (FO) is characterized by hypervolemia, edema, or both. In clinical practice it is usually suspected when a patient shows evidence of pulmonary edema,... (Review)
Review
Fluid overload (FO) is characterized by hypervolemia, edema, or both. In clinical practice it is usually suspected when a patient shows evidence of pulmonary edema, peripheral edema, or body cavity effusion. FO may be a consequence of spontaneous disease, or may be a complication of intravenous fluid therapy. Most clinical studies of the association of FO with fluid therapy and risk of harm define it in terms of an increase in body weight of at least 5-10%, or a positive fluid balance of the same magnitude when fluid intake and urine output are measured. Numerous observational clinical studies in humans have demonstrated an association between FO, adverse events, and mortality, as have two retrospective observational studies in dogs and cats. The risk of FO may be minimized by limiting resuscitation fluid to the smallest amount needed to optimize cardiac output and then limiting maintenance fluid to the amount needed to replace ongoing normal and pathological losses of water and sodium.
PubMed: 34268347
DOI: 10.3389/fvets.2021.668688 -
Journal of Thrombosis and Haemostasis :... Feb 2019The vascular endothelial surface is coated by the glycocalyx, a ubiquitous gel-like layer composed of a membrane-binding domain that contains proteoglycans,... (Review)
Review
The vascular endothelial surface is coated by the glycocalyx, a ubiquitous gel-like layer composed of a membrane-binding domain that contains proteoglycans, glycosaminoglycan side-chains, and plasma proteins such as albumin and antithrombin. The endothelial glycocalyx plays a critical role in maintaining vascular homeostasis. However, this component is highly vulnerable to damage and is also difficult to examine. Recent advances in analytical techniques have enabled biochemical, visual and computational investigation of this vascular component. The glycocalyx modulates leukocyte-endothelial interactions, thrombus formation and other processes that lead to microcirculatory dysfunction and critical organ injury in sepsis. It also acts as a regulator of vascular permeability and contains mechanosensors as well as receptors for growth factors and anticoagulants. During the initial onset of sepsis, the glycocalyx is damaged and circulating levels of glycocalyx components, including syndecans, heparan sulfate and hyaluronic acid, can be measured and are reportedly useful as biomarkers for sepsis. Also, a new methodology using side-stream dark-field imaging is now clinically available for assessing the glycocalyx. Multiple factors including hypervolemia and hyperglycemia are toxic to the glycocalyx, and several agents have been proposed as therapeutic modalities, although no single treatment has been proven to be clinically effective. In this article, we review the derangement of the glycocalyx in sepsis. Despite the accumulated knowledge regarding the important roles of the glycocalyx, the relationship between derangement of the endothelial glycocalyx and severity of sepsis or disseminated intravascular coagulation has not been adequately elucidated and further work is needed.
Topics: Animals; Blood Coagulation; Capillary Permeability; Cell Adhesion; Endothelial Cells; Glycocalyx; Humans; Sepsis; Signal Transduction
PubMed: 30582882
DOI: 10.1111/jth.14371 -
World Journal of Nephrology Sep 2022Acute post-streptococcal glomerulonephritis (APSGN) is the major cause of acute glomerulonephritis among children, especially in low- and middle-income countries. APSGN... (Review)
Review
Acute post-streptococcal glomerulonephritis (APSGN) is the major cause of acute glomerulonephritis among children, especially in low- and middle-income countries. APSGN commonly occurs following pharyngitis due to the activation of antibodies and complements proteins against streptococcal antigens through the immune-complex-mediated mechanism. APSGN can be presented as acute nephritic syndrome, nephrotic syndrome, and rapidly progressive glomerulonephritis, or it may be subclinical. The management of APSGN is mainly supportive in nature with fluid restriction, anti-hypertensives, diuretics, and renal replacement therapy with dialysis, when necessary, as the disease is self-limiting. Congestive heart failure, pulmonary edema, and severe hypertension-induced encephalopathy might occur during the acute phase of APSGN due to hypervolemia. APSGN generally has a favorable prognosis with only a small percentage of patients with persistent urinary abnormalities, persistent hypertension, and chronic kidney disease after the acute episode of APSGN. Decreased complement levels, increased C-reactive protein, and hypoalbuminemia are associated with disease severity. Crescent formations on renal biopsy and renal insufficiency on presentation may be the predictors of disease severity and poor outcomes in APSGN in children.
PubMed: 36187464
DOI: 10.5527/wjn.v11.i5.139 -
American Family Physician Mar 2015Hyponatremia and hypernatremia are common findings in the inpatient and outpatient settings. Sodium disorders are associated with an increased risk of morbidity and...
Hyponatremia and hypernatremia are common findings in the inpatient and outpatient settings. Sodium disorders are associated with an increased risk of morbidity and mortality. Plasma osmolality plays a critical role in the pathophysiology and treatment of sodium disorders. Hyponatremia and hypernatremia are classified based on volume status (hypovolemia, euvolemia, and hypervolemia). Sodium disorders are diagnosed by findings from the history, physical examination, laboratory studies, and evaluation of volume status. Treatment is based on symptoms and underlying causes. In general, hyponatremia is treated with fluid restriction (in the setting of euvolemia), isotonic saline (in hypovolemia), and diuresis (in hypervolemia). A combination of these therapies may be needed based on the presentation. Hypertonic saline is used to treat severe symptomatic hyponatremia. Medications such as vaptans may have a role in the treatment of euvolemic and hypervolemic hyponatremia. The treatment of hypernatremia involves correcting the underlying cause and correcting the free water deficit.
Topics: Diagnosis, Differential; Diuresis; Fluid Therapy; Humans; Hypernatremia; Hyponatremia; Isotonic Solutions; Saline Solution, Hypertonic; Sodium
PubMed: 25822386
DOI: No ID Found -
International Journal of Molecular... Jul 2020In Chronic Kidney Disease (CKD) patients, elevated blood pressure (BP) is a frequent finding and is traditionally considered a direct consequence of their sodium... (Review)
Review
In Chronic Kidney Disease (CKD) patients, elevated blood pressure (BP) is a frequent finding and is traditionally considered a direct consequence of their sodium sensitivity. Indeed, sodium and fluid retention, causing hypervolemia, leads to the development of hypertension in CKD. On the other hand, in non-dialysis CKD patients, salt restriction reduces BP levels and enhances anti-proteinuric effect of renin-angiotensin-aldosterone system inhibitors in non-dialysis CKD patients. However, studies on the long-term effect of low salt diet (LSD) on cardio-renal prognosis showed controversial findings. The negative results might be the consequence of measurement bias (spot urine and/or single measurement), reverse epidemiology, as well as poor adherence to diet. In end-stage kidney disease (ESKD), dialysis remains the only effective means to remove dietary sodium intake. The mismatch between intake and removal of sodium leads to fluid overload, hypertension and left ventricular hypertrophy, therefore worsening the prognosis of ESKD patients. This imposes the implementation of a LSD in these patients, irrespective of the lack of trials proving the efficacy of this measure in these patients. LSD is, therefore, a rational and basic tool to correct fluid overload and hypertension in all CKD stages. The implementation of LSD should be personalized, similarly to diuretic treatment, keeping into account the volume status and true burden of hypertension evaluated by ambulatory BP monitoring.
Topics: Blood Pressure; Diet, Sodium-Restricted; Humans; Hypertension; Hypertrophy, Left Ventricular; Kidney Failure, Chronic; Prognosis; Renal Dialysis; Renal Insufficiency, Chronic; Renin-Angiotensin System; Sodium Chloride, Dietary; Water-Electrolyte Imbalance
PubMed: 32635265
DOI: 10.3390/ijms21134744 -
Kidney360 Aug 2021The management of complex fluid and electrolyte disorders is central to the practice of nephrologists. The sensitivity of physical examination alone to determine fluid... (Review)
Review
The management of complex fluid and electrolyte disorders is central to the practice of nephrologists. The sensitivity of physical examination alone to determine fluid status is limited, precluding accurate clinical decision making. Point-of-care ultrasonography (POCUS) is emerging as a valuable, noninvasive, bedside diagnostic tool for objective evaluation of physiologic and hemodynamic parameters related to fluid status, tolerance, and responsiveness. Rapid bedside sonographic evaluation can obtain qualitative data on cardiac function and quantitative data on pulmonary congestion. Advanced POCUS, including goal-directed Doppler echocardiography, provides additional quantitative information, including flow velocities and pressures across the cardiac structures. Recently, abnormal Doppler flow patterns in abdominal organs secondary to increased right atrial pressure have been linked to congestive organ damage, adding another component to the hemodynamic assessment. Integrating POCUS findings with clinical and laboratory data can further elucidate a patient's hemodynamic status. This drives decisions regarding crystalloid administration or, conversely, diuresis or ultrafiltration and allows tailored therapy for individual patients. In this article, we provide an overview of the focused assessment of cardiovascular function and pulmonary and venous congestion using POCUS and review relevant literature.
Topics: Humans; Nephrologists; Point-of-Care Systems; Ultrasonography; Ultrasonography, Doppler; Water-Electrolyte Imbalance
PubMed: 35369665
DOI: 10.34067/KID.0006482020 -
Annals of Hepatology 2002The mechanism by which ascites develops in cirrhosis is multifactorial Severe sinusoidal portal hypertension and hepatic insufficiency are the initial factors. They lead... (Review)
Review
The mechanism by which ascites develops in cirrhosis is multifactorial Severe sinusoidal portal hypertension and hepatic insufficiency are the initial factors. They lead to a circulatory dysfunction characterized by arterial vasodilation, arterial hypotension, high cardiac output and hypervolemia and to renal sodium and water retention. There are evidences that arterial vasodilation in cirrhosis occurs in the splanchnic circulation and is related to an increased synthesis of local vasodilators. Vascular resistance is normal or increased in the remaining major vascular territories (kidney, muscle and skin and brain). Splanchnic arterial vasodilation not only impairs systemic hemodynamics and renal function but also alters hemodynamics in the splanchnic microcirculation. The rapid and high inflow of arterial blood into the splanchnic microcirculation is the main factor increasing hydrostatic pressure in the splanchnic capillaries leading to an excessive production of splanchnic lymph over lymphatic return. Lymph leakage from the liver and other splanchnic organs is the mechanism of fluid accumulation in the abdominal cavity. Continuous renal sodium and water retention perpetuates ascites formation. Large volume paracentesis associated with albumin infusion is the treatment of choice of tense ascites because it is very effective and rapid and is associated with fewer complications that the traditional treatment (sodium restriction and diuretics). However, diuretic should be given after paracentesis to prevent reaccumulation of ascites. In patients with moderate ascites diuretics should be preferred as initial therapy. Patients with refractory ascites could be treated by paracentesis or percutaneous transjugular portacaval shunt (TIPS). TIPS is more effective in the long term control of ascites but may impair hepatic function and induce chronic hepatic encephalopathy.
Topics: Ascites; Diuretics; Hepatorenal Syndrome; Humans; Liver Cirrhosis; Liver Function Tests; Liver Transplantation; Paracentesis; Peritoneovenous Shunt; Prognosis; Spironolactone; Splanchnic Circulation
PubMed: 15115971
DOI: No ID Found -
Critical Care (London, England) Jan 2019The glycocalyx is a gel-like layer covering the luminal surface of vascular endothelial cells. It is comprised of membrane-attached proteoglycans, glycosaminoglycan... (Review)
Review
The glycocalyx is a gel-like layer covering the luminal surface of vascular endothelial cells. It is comprised of membrane-attached proteoglycans, glycosaminoglycan chains, glycoproteins, and adherent plasma proteins. The glycocalyx maintains homeostasis of the vasculature, including controlling vascular permeability and microvascular tone, preventing microvascular thrombosis, and regulating leukocyte adhesion.During sepsis, the glycocalyx is degraded via inflammatory mechanisms such as metalloproteinases, heparanase, and hyaluronidase. These sheddases are activated by reactive oxygen species and pro-inflammatory cytokines such as tumor necrosis factor alpha and interleukin-1beta. Inflammation-mediated glycocalyx degradation leads to vascular hyper-permeability, unregulated vasodilation, microvessel thrombosis, and augmented leukocyte adhesion. Clinical studies have demonstrated the correlation between blood levels of glycocalyx components with organ dysfunction, severity, and mortality in sepsis.Fluid resuscitation therapy is an essential part of sepsis treatment, but overaggressive fluid therapy practices (leading to hypervolemia) may augment glycocalyx degradation. Conversely, fresh frozen plasma and albumin administration may attenuate glycocalyx degradation. The beneficial and harmful effects of fluid and plasma infusion on glycocalyx integrity in sepsis are not well understood; future studies are warranted.In this review, we first analyze the underlying mechanisms of glycocalyx degradation in sepsis. Second, we demonstrate how the blood and urine levels of glycocalyx components are associated with patient outcomes. Third, we show beneficial and harmful effects of fluid therapy on the glycocalyx status during sepsis. Finally, we address the concept of glycocalyx degradation as a therapeutic target.
Topics: Biomarkers; Endothelial Cells; Fluid Therapy; Glycocalyx; Heparin; Humans; Resuscitation; Sepsis; Syndecan-1
PubMed: 30654825
DOI: 10.1186/s13054-018-2292-6