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Clinical Journal of the American... May 2022One of the primary reasons for intensive care admission is shock. Identifying the underlying cause of shock (hypovolemic, distributive, cardiogenic, and obstructive) may... (Review)
Review
One of the primary reasons for intensive care admission is shock. Identifying the underlying cause of shock (hypovolemic, distributive, cardiogenic, and obstructive) may lead to entirely different clinical pathways for management. Among patients with hypovolemic and distributive shock, fluid therapy is one of the leading management strategies. Although an appropriate amount of fluid administration might save a patient's life, inadequate (or excessive) fluid use could lead to more complications, including organ failure and mortality due to either hypovolemia or volume overload. Currently, intensivists have access to a wide variety of information sources and tools to monitor the underlying hemodynamic status, including medical history, physical examination, and specific hemodynamic monitoring devices. Although appropriate and timely assessment and interpretation of this information can promote adequate fluid resuscitation, misinterpretation of these data can also lead to additional mortality and morbidity. This article provides a narrative review of the most commonly used hemodynamic monitoring approaches to assessing fluid responsiveness and fluid tolerance. In addition, we describe the benefits and disadvantages of these tools.
Topics: Critical Care; Fluid Therapy; Hemodynamic Monitoring; Hemodynamics; Humans; Hypovolemia; Shock
PubMed: 35379765
DOI: 10.2215/CJN.14191021 -
American Family Physician Mar 2020Upper gastrointestinal (GI) bleeding is defined as hemorrhage from the mouth to the ligament of Treitz. Common risk factors for upper GI bleeding include prior upper GI... (Review)
Review
Upper gastrointestinal (GI) bleeding is defined as hemorrhage from the mouth to the ligament of Treitz. Common risk factors for upper GI bleeding include prior upper GI bleeding, anticoagulant use, high-dose nonsteroidal anti-inflammatory drug use, and older age. Causes of upper GI bleeding include peptic ulcer bleeding, gastritis, esophagitis, variceal bleeding, Mallory-Weiss syndrome, and cancer. Signs and symptoms of upper GI bleeding may include abdominal pain, lightheadedness, dizziness, syncope, hematemesis, and melena. Physical examination includes assessment of hemodynamic stability, presence of abdominal pain or rebound tenderness, and examination of stool color. Laboratory tests should include a complete blood count, basic metabolic panel, coagulation panel, liver tests, and type and crossmatch. A bolus of normal saline or lactated Ringer solution should be rapidly infused to correct hypovolemia and to maintain blood pressure, and blood should be transfused when hemoglobin is less than 7 g per dL. Clinical prediction guides (e.g., Glasgow-Blatchford bleeding score) are necessary for upper GI bleeding risk stratification and to determine therapy. Patients with hemodynamic instability and signs of upper GI bleeding should be offered urgent endoscopy, performed within 24 hours of presentation. A common strategy in patients with failed endoscopic hemostasis is to attempt transcatheter arterial embolization, then proceed to surgery if hemostasis is not obtained. Proton pump inhibitors should be initiated upon presentation with upper GI bleeding. Guidelines recommend high-dose proton pump inhibitor treatment for the first 72 hours post-endoscopy because this is when rebleeding risk is highest. Deciding when to restart antithrombotic therapy after upper GI bleeding is difficult because of lack of sufficient data.
Topics: Adult; Anti-Bacterial Agents; Anti-Inflammatory Agents, Non-Steroidal; Anticoagulants; Blood Transfusion; Endoscopy, Gastrointestinal; Fibrinolytic Agents; Gastroenteritis; Gastrointestinal Hemorrhage; Helicobacter Infections; Humans; Mallory-Weiss Syndrome; Peptic Ulcer; Platelet Aggregation Inhibitors; Proton Pump Inhibitors; Risk Factors; Selective Serotonin Reuptake Inhibitors
PubMed: 32109037
DOI: No ID Found -
Kidney International Jul 2019Fluid therapy, which is provided to restore and maintain tissue perfusion, is part of routine management for almost all critically ill patients. However, because either... (Review)
Review
Fluid therapy, which is provided to restore and maintain tissue perfusion, is part of routine management for almost all critically ill patients. However, because either too much or too little fluid can have a negative impact on patient outcomes, fluid administration must be titrated carefully for each patient. The "salvage, optimization, stabilization, de-escalation" (SOSD) mnemonic should be used as a general guide to fluid resuscitation, and fluid administration should be adapted according to the course of the disease. In the initial salvage phase, lifesaving fluid should be administered generously. Once hemodynamic monitoring is available, fluid administration should be optimized by determining the patient's fluid status and the need for further fluid. This determination can be difficult, however; clinical indicators of hypovolemia, such as heart rate, blood pressure, and urine output, may not detect early hypovolemia, and edema is a late sign of fluid overload. Dynamic tests of fluid responsiveness such as pulse pressure or stroke volume variation can be used in only a small percentage of critically ill patients, and thus a fluid challenge technique is most frequently used to assess ongoing fluid requirements. Once a patient has been stabilized, efforts should start to concentrate on removing excess fluid. Which fluid should be used remains a matter of some debate. Crystalloid solutions are cheaper than colloid solutions, but colloid solutions remain in the intravascular space for a longer period, making edema less likely. Thus crystalloids and colloids should be used together, especially in patients likely to require large fluid volumes. Human albumin is a natural colloid and may have beneficial effects in patients with sepsis in addition to its volume effects. Fluids should be prescribed as are other medications, taking into account individual patient factors, disease processes, and other treatments.
Topics: Colloids; Critical Illness; Fluid Therapy; Humans; Hypovolemia; Isotonic Solutions; Monitoring, Physiologic; Plasma Substitutes; Resuscitation; Treatment Outcome
PubMed: 30926137
DOI: 10.1016/j.kint.2018.11.047 -
Revista Da Associacao Medica Brasileira... Jan 2020Acute kidney injury is a very common diagnosis, present in up to 60% of critical patients, and its third main cause is drug toxicity. Nephrotoxicity can be defined as... (Review)
Review
Acute kidney injury is a very common diagnosis, present in up to 60% of critical patients, and its third main cause is drug toxicity. Nephrotoxicity can be defined as any renal injury caused directly or indirectly by medications, with acute renal failure, tubulopathies, and glomerulopathies as common clinical presentations. Some examples of drugs commonly associated with the acute reduction of glomerular filtration rate are anti-inflammatories, antibiotics, such as vancomycin and aminoglycosides, and chemotherapeutic agents, such as cisplatin and methotrexate. Cases of tubulopathy are very common with amphotericin B, polymyxins, and tenofovir, and cases of glomerulopathies are common with VEGF inhibitors, bisphosphonates, and immunotherapy, and it is also common to have more than one clinical presentation related to a single agent. Early diagnosis is essential for the good evolution of the patient, with a reduction of renal exposure to the toxic agent, which requires knowing the risk factors and biomarkers. General measures such as correcting hydroelectrolytic disorders and hypovolemia, monitoring the serum level, avoiding combinations with the synergy of renal injury, and looking for similar options that are less toxic are the foundations for the treatment of complications that are still common and often preventable.
Topics: Acute Kidney Injury; Drug-Related Side Effects and Adverse Reactions; Humans; Nephrotic Syndrome; Risk Factors
PubMed: 31939540
DOI: 10.1590/1806-9282.66.S1.82 -
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 -
Critical Care (London, England) Mar 2023During septic shock, fluid therapy is aimed at increasing cardiac output and improving tissue oxygenation, but it poses two problems: it has inconsistent and transient... (Review)
Review
During septic shock, fluid therapy is aimed at increasing cardiac output and improving tissue oxygenation, but it poses two problems: it has inconsistent and transient efficacy, and it has many well-documented deleterious effects. We suggest that there is a place for its personalization according to the patient characteristics and the clinical situation, at all stages of circulatory failure. Regarding the choice of fluid for volume expansion, isotonic saline induces hyperchloremic acidosis, but only for very large volumes administered. We suggest that balanced solutions should be reserved for patients who have already received large volumes and in whom the chloremia is rising. The initial volume expansion, intended to compensate for the constant hypovolaemia in the initial phase of septic shock, cannot be adapted to the patient's weight only, as suggested by the Surviving Sepsis Campaign, but should also consider potential absolute hypovolemia induced by fluid losses. After the initial fluid infusion, preload responsiveness may rapidly disappear, and it should be assessed. The choice between tests used for this purpose depends on the presence or absence of mechanical ventilation, the monitoring in place and the risk of fluid accumulation. In non-intubated patients, the passive leg raising test and the mini-fluid challenge are suitable. In patients without cardiac output monitoring, tests like the tidal volume challenge, the passive leg raising test and the mini-fluid challenge can be used as they can be performed by measuring changes in pulse pressure variation, assessed through an arterial line. The mini-fluid challenge should not be repeated in patients who already received large volumes of fluids. The variables to assess fluid accumulation depend on the clinical condition. In acute respiratory distress syndrome, pulmonary arterial occlusion pressure, extravascular lung water and pulmonary vascular permeability index assess the risk of worsening alveolar oedema better than arterial oxygenation. In case of abdominal problems, the intra-abdominal pressure should be taken into account. Finally, fluid depletion in the de-escalation phase is considered in patients with significant fluid accumulation. Fluid removal can be guided by preload responsiveness testing, since haemodynamic deterioration is likely to occur in patients with a preload dependent state.
Topics: Humans; Shock, Septic; Sepsis; Blood Pressure; Shock; Fluid Therapy; Hemodynamics; Cardiac Output
PubMed: 36964573
DOI: 10.1186/s13054-023-04363-3 -
Critical Care (London, England) May 2023Fluid normally exchanges freely between the plasma and interstitial space and is returned primarily via the lymphatic system. This balance can be disturbed by diseases... (Review)
Review
Fluid normally exchanges freely between the plasma and interstitial space and is returned primarily via the lymphatic system. This balance can be disturbed by diseases and medications. In inflammatory disease states, such as sepsis, the return flow of fluid from the interstitial space to the plasma seems to be very slow, which promotes the well-known triad of hypovolemia, hypoalbuminemia, and peripheral edema. Similarly, general anesthesia, for example, even without mechanical ventilation, increases accumulation of infused crystalloid fluid in a slowly equilibrating fraction of the extravascular compartment. Herein, we have combined data from fluid kinetic trials with previously unconnected mechanisms of inflammation, interstitial fluid physiology and lymphatic pathology to synthesize a novel explanation for common and clinically relevant examples of circulatory dysregulation. Experimental studies suggest that two key mechanisms contribute to the combination of hypovolemia, hypoalbuminemia and edema; (1) acute lowering of the interstitial pressure by inflammatory mediators such as TNFα, IL-1β, and IL-6 and, (2) nitric oxide-induced inhibition of intrinsic lymphatic pumping.
Topics: Humans; Hypovolemia; Hypoalbuminemia; Edema; Respiration, Artificial; Crystalloid Solutions
PubMed: 37245039
DOI: 10.1186/s13054-023-04496-5 -
Diabetic Medicine : a Journal of the... Mar 2023Hyperosmolar Hyperglycaemic State (HHS) is a medical emergency associated with high mortality. It occurs less frequently than diabetic ketoacidosis (DKA), affects those... (Review)
Review
Hyperosmolar Hyperglycaemic State (HHS) is a medical emergency associated with high mortality. It occurs less frequently than diabetic ketoacidosis (DKA), affects those with pre-existing/new type 2 diabetes mellitus and increasingly affecting children/younger adults. Mixed DKA/HHS may occur. The JBDS HHS care pathway consists of 3 themes (clinical assessment and monitoring, interventions, assessments and prevention of harm) and 5 phases of therapy (0-60 min, 1-6, 6-12, 12-24 and 24-72 h). Clinical features of HHS include marked hypovolaemia, osmolality ≥320 mOsm/kg using [(2×Na ) + glucose+urea], marked hyperglycaemia ≥30 mmol/L, without significant ketonaemia (≤3.0 mmol/L), without significant acidosis (pH >7.3) and bicarbonate ≥15 mmol/L. Aims of the therapy are to improve clinical status/replace fluid losses by 24 h, gradual decline in osmolality (3.0-8.0 mOsm/kg/h to minimise the risk of neurological complications), blood glucose 10-15 mmol/L in the first 24 h, prevent hypoglycaemia/hypokalaemia and prevent harm (VTE, osmotic demyelination, fluid overload, foot ulceration). Underlying precipitants must be identified and treated. Interventions include: (1) intravenous (IV) 0.9% sodium chloride to restore circulating volume (fluid losses 100-220 ml/kg, caution in elderly), (2) fixed rate intravenous insulin infusion (FRIII) should be commenced once osmolality stops falling with fluid replacement unless there is ketonaemia (FRIII should be commenced at the same time as IV fluids). (3) glucose infusion (5% or 10%) should be started once glucose <14 mmol/L and (4) potassium replacement according to potassium levels. HHS resolution criteria are: osmolality <300 mOsm/kg, hypovolaemia corrected (urine output ≥0.5 ml/kg/h), cognitive status returned to pre-morbid state and blood glucose <15 mmol/L.
Topics: Child; Adult; Humans; Aged; Hyperglycemic Hyperosmolar Nonketotic Coma; Diabetes Mellitus, Type 2; Hyperglycemia; Blood Glucose; Hypovolemia; Inpatients; Diabetic Ketoacidosis; Insulin; Dehydration; Glucose; Potassium
PubMed: 36370077
DOI: 10.1111/dme.15005 -
Clinical Journal of the American... Jul 2019Acute pancreatitis is a common disorder of the pancreas. It is the most frequent gastrointestinal cause for hospitalization and one of the leading causes of in-hospital... (Review)
Review
Acute pancreatitis is a common disorder of the pancreas. It is the most frequent gastrointestinal cause for hospitalization and one of the leading causes of in-hospital deaths. Its severity ranges from mild self-limited disease to severe acute necrotizing pancreatitis characterized by systemic complications and multiorgan failure. Severe acute pancreatitis develops in about 20% of patients with acute pancreatitis and may be associated with multiorgan failure (respiratory, cardiovascular, and kidney). AKI is a frequent complication of severe acute pancreatitis and develops late in the course of the disease, usually after the failure of other organs. It carries a very poor prognosis, particularly if kidney replacement therapy is required, with mortality rates exceeding 75%. The exact pathophysiology of AKI in acute pancreatitis remains unclear but appears to result from initial volume depletion followed by complex vascular and humoral factors. Here, we provide an overview of the epidemiology, pathogenesis, causes, and management of AKI in patients with severe acute pancreatitis.
Topics: Acute Kidney Injury; Fluid Therapy; Humans; Pancreatitis; Renal Replacement Therapy
PubMed: 31118209
DOI: 10.2215/CJN.13191118 -
International Journal of Molecular... Jul 2021Anaphylaxis is a severe, acute, life-threatening multisystem allergic reaction resulting from the release of a plethora of mediators from mast cells culminating in... (Review)
Review
Anaphylaxis is a severe, acute, life-threatening multisystem allergic reaction resulting from the release of a plethora of mediators from mast cells culminating in serious respiratory, cardiovascular and mucocutaneous manifestations that can be fatal. Medications, foods, latex, exercise, hormones (progesterone), and clonal mast cell disorders may be responsible. More recently, novel syndromes such as delayed reactions to red meat and hereditary alpha tryptasemia have been described. Anaphylaxis manifests as sudden onset urticaria, pruritus, flushing, erythema, angioedema (lips, tongue, airways, periphery), myocardial dysfunction (hypovolemia, distributive or mixed shock and arrhythmias), rhinitis, wheezing and stridor. Vomiting, diarrhea, scrotal edema, uterine cramps, vaginal bleeding, urinary incontinence, dizziness, seizures, confusion, and syncope may occur. The traditional (or classical) pathway is mediated via T cells, Th2 cytokines (such as IL-4 and 5), B cell production of IgE and subsequent crosslinking of the high affinity IgE receptor (FcεRI) on mast cells and basophils by IgE-antigen complexes, culminating in mast cell and basophil degranulation. Degranulation results in the release of preformed mediators (histamine, heparin, tryptase, chymase, carboxypeptidase, cathepsin G and tumor necrosis factor alpha (TNF-α), and of de novo synthesized ones such as lipid mediators (cysteinyl leukotrienes), platelet activating factor (PAF), cytokines and growth factors such as vascular endothelial growth factor (VEGF). Of these, histamine, tryptase, cathepsin G, TNF-α, LTC, PAF and VEGF can increase vascular permeability. Recent data suggest that mast cell-derived histamine and PAF can activate nitric oxide production from endothelium and set into motion a signaling cascade that leads to dilatation of blood vessels and dysfunction of the endothelial barrier. The latter, characterized by the opening of adherens junctions, leads to increased capillary permeability and fluid extravasation. These changes contribute to airway edema, hypovolemia, and distributive shock, with potentially fatal consequences. In this review, besides mechanisms (endotypes) underlying IgE-mediated anaphylaxis, we also provide a brief overview of IgG-, complement-, contact system-, cytokine- and mast cell-mediated reactions that can result in phenotypes resembling IgE-mediated anaphylaxis. Such classifications can lead the way to precision medicine approaches to the management of this complex disease.
Topics: Anaphylaxis; Animals; Capillary Permeability; Endothelium, Vascular; Gap Junctions; Humans; Inflammation
PubMed: 34360549
DOI: 10.3390/ijms22157785