Diagnostic Adjunct Techniques in the Assessment of Hypovolemia: A Prospective Pilot Project.

INTRODUCTION: Measuring the hypovolemic resuscitation end point remains a critical care challenge. Our project compared clinical hypovolemia (CH) with three diagnostic adjuncts: 1) noninvasive cardiac output monitoring (NICOM), 2) ultrasound (US) static IVC collapsibility (US-IVC), and 3) US dynamic carotid upstroke velocity (US-C). We hypothesized US measures would correlate more closely to CH than NICOM. METHODS: Adult trauma/surgical intensive care unit patients were prospectively screened for suspected hypovolemia after acute resuscitation, excluding patients with burns, known heart failure, or severe liver/kidney disease. Adjunct measurements were assessed up to twice a day until clinical improvement. Hypovolemia was defined as: 1) NICOM: ≥10% stroke volume variation with passive leg raise, 2) US-IVC: <2.1 cm and >50% collapsibility (nonventilated) or >18% collapsibility (ventilated), 3) US-C: peak systolic velocity increase 15 cm/s with passive leg raise. Previously unknown cardiac dysfunction seen on US was noted. Observation-level data were analyzed with a Cohen's kappa (κ). RESULTS: 44 patients (62% male, median age 60) yielded 65 measures. Positive agreement with CH was 47% for NICOM, 37% for US-IVC and 10% for US-C. None of the three adjuncts correlated with CH (κ -0.045 to 0.029). After adjusting for previously unknown cardiac dysfunction present in 10 patients, no adjuncts correlated with CH (κ -0.036 to 0.031). No technique correlated with any other (κ -0.118 to 0.083). CONCLUSIONS: None of the adjunct measurements correlated with CH or each other, highlighting that fluid status assessment remains challenging in critical care. US should assess for right ventricular dysfunction prior to resuscitation.

Near-Infrared Spectroscopy Monitoring to Detect Changes in Cerebral and Renal Perfusion During Hypovolemic Shock, Volume Resuscitation, and Vasoconstriction.

INTRODUCTION: Rapidly changing hemodynamic conditions, such as uncontrolled hemorrhage and the resulting hypovolemic shock, are a common contributor to active duty military deaths. These conditions can cause cerebral desaturation, and outcomes may improve when regional cerebral oxygen saturation (CrSO2) is monitored using near-infrared spectroscopy (NIRS) and desaturation episodes are recognized and reversed. The purpose of this porcine study was to investigate the ability of NIRS monitoring to detect changes in regional cerebral and regional renal perfusion during hypovolemia, resuscitation by volume infusion, and vasoconstriction. MATERIALS AND METHODS: Hemorrhagic shock was induced by removing blood through a central venous catheter until mean arterial pressure (MAP) was <40 mmHg. Each blood removal step was followed by a 10-minute stabilization period, during which cardiac output, blood pressure, central venous pressure, blood oxygen saturation, and CrSO2 and regional renal oxygen saturation (RrSO2) were measured. Shock was reversed using blood infusion and vasoconstriction separately until MAP returned to normal. Statistical comparisons between groups were performed using the paired t-test or the Wilcoxon signed-rank test. RESULTS: Using volume resuscitation, both CrSO2 and RrSO2 returned to normal levels after hypovolemia. Blood pressure management with phenylephrine returned CrSO2 levels to normal, but RrSO2 levels remained significantly lower compared to the pre-hemorrhage values (P < .0001). Comparison of the percent CrSO2 as a function of MAP showed that CrSO2 levels approach baseline when a normal MAP is reached during volume resuscitation. In contrast, a significantly higher MAP was required to return to baseline CrSO2 during blood pressure management with phenylephrine (P < .0001). Evaluation of carotid blood flow and CrSO2 indicated that during induction of hypovolemia, the two measures are strongly correlated. In contrast, there was limited correlation between carotid blood flow and CrSO2 during blood infusion. CONCLUSIONS: This study demonstrated that it is possible to restore CrSO2 by manipulating MAP with vasoconstriction, even in profound hypotension. However, MAP manipulation may result in unintended consequences for other organs, such as the kidney, if the tissue is not reoxygenated sufficiently. The clinical implications of these results and how best to respond to hypovolemia in the pre-hospital and hospital settings should be elucidated by additional studies.

Fluid therapy in the acute brain injured patient.

Adequate fluid therapy in the acute brain injured (ABI) patient is essential for maintaining an adequate brain and systemic physiology and preventing intra- and extracranial complications. The target of euvolemia, implying avoidance of both hypovolemia and fluid overloading (or "hypervolemia," by definition associated with fluid extravasation leading to tissue edema) is of key importance. Primary brain injury can be aggravated by secondary brain injury and systemic deterioration through diverse pathways which can challenge appropriate fluid management, e.g. neuroendocrine and electrolyte disorders, stress cardiomyopathy (also known as cardiac stunning) and neurogenic pulmonary edema. This is an updated expert opinion aiming to provide a practical overview on fluid therapy in the ABI patient, partly based on more recent work and stressing the fact that intravenous fluids should be regarded as drugs, with their inherent potential for both benefit and (unintended) harm.

Volumetric evaluation of fluid responsiveness using a modified passive leg raise maneuver during experimental induction and correction of hypovolemia in anesthetized dogs.

OBJECTIVE: To demonstrate if modified passive leg raise (PLRM) maneuver can be used for volumetric evaluation of fluid responsiveness (FR) by inducing cardiac output (CO) changes during experimental induction and correction of hypovolemia in healthy anesthetized dogs. The effects of PLRM on plethysmographic variability index (PVI) and pulse pressure variation (PPV) were also investigated. STUDY DESIGN: Prospective, crossover study. ANIMALS: A total of six healthy anesthetized Beagle dogs. METHODS: Dogs were anesthetized with propofol and isoflurane. They were mechanically ventilated under neuromuscular blockade, and normothermia was maintained. After instrumentation, all dogs were subjected to four stages: 1, baseline; 2, removal of 27 mL kg-1 circulating blood volume; 3, after blood re-transfusion; and 4, after 20 mL kg-1 hetastarch infusion over 20 minutes. A 10 minute stabilization period was allowed after induction of each stage and before data collection. At each stage, CO via pulmonary artery thermodilution, PVI, PPV and cardiopulmonary variables were measured before, during and after the PLRM maneuver. Stages were sequential, not randomized. Statistical analysis included repeated measures anova and Tukey's post hoc test, considering p < 0.05 as significant. RESULTS: During stage 2, PLRM at a 30° angle significantly increased CO (mean ± standard deviation, 1.0 ± 0.1 to 1.3 ± 0.1 L minute-1; p < 0.001), with a simultaneous significant reduction in PVI (38 ± 4% to 21 ± 4%; p < 0.001) and PPV (27 ± 2% to 18 ± 2%; p < 0.001). The PLRM did not affect CO, PPV and PVI during stages 1, 3 and 4. CONCLUSIONS AND CLINICAL RELEVANCE: In anesthetized dogs, PLRM at a 30° angle successfully detected FR during hypovolemia, and identified fluid nonresponsiveness during normovolemia and hypervolemia. Also, in hypovolemic dogs, significant decreases in PVI and PPV occurred in response to PLRM maneuver.

[Fluid Management in Intensive Care Patients - New Strategies and optimal target?] / Steuerung der Volumentherapie von Intensivpatienten: Neue Strategien und optimale Zielparameter?

Adequate therapy with intravenous fluids is crucial in the initial treatment of critically ill patients. Both hypovolemia and hypervolemia are associated with organ dysfunction and adverse outcomes. A recent international randomized trial investigated a restrictive volume management in comparison with a standard volume regimen. 90-day-mortality was not significantly reduced in the group with restrictive fluid administration. Instead of using a fixed fluid strategy - either restrictive or liberal - fluid therapy should be individualised: Adequate fluid application optimizes cardiac preload and tissue perfusion and avoids the harms of abundant volume therapy. Early use of vasopressors may facilitate the achievement of mean arterial pressure targets and minimize the risk of volume overload. Appropriate volume management requires evaluation of fluid status, knowledge of hemodynamic parameters and accurate testing of fluid responsiveness. Regarding the absence of evidence-based criterias and treatment goals for volume management in shock patients, an individualised approach resorting to diverse monitoring tools should be considered. UItrasound-based assessment of IVC diameter and echocardiography are excellent non-invasive tools to evaluate volume status. Passive leg raising (PLR) test represents a valid method for the assessment of volume responsiveness.

Intraoperative hypovolemia as a possible precipitating factor for pituitary apoplexy: a case report.

BACKGROUND: Pituitary apoplexy is acute infarction with or without hemorrhage of the pituitary gland. It is a rare but potentially life-threatening emergency that most commonly occurs in the setting of pituitary adenoma. The mechanisms underlying pituitary apoplexy are not well understood, but are proposed to include factors of both hemodynamic supply and adenoma demand. In the case of patients with known pituitary macroadenomas undergoing major surgery for other indications, there is a theoretically increased risk of apoplexy in the setting of "surgical stress." However, risk stratification of patients with nonfunctioning pituitary adenomas prior to major surgery is challenging because the precipitating factors for pituitary apoplexy are not completely understood. Here we present a case in which intraoperative hypovolemia is a possible mechanistic precipitating factor for pituitary apoplexy. CASE PRESENTATION: A 76-year-old patient with a known hypofunctioning pituitary macroadenoma underwent nephrectomy for renal cell carcinoma, during which there was significant intraoperative blood loss. He became symptomatic with ophthalmoplegia on the second postoperative day, and was diagnosed with pituitary apoplexy. He was managed conservatively with cortisol replacement therapy, and underwent therapeutic anticoagulation 2 months after pituitary apoplexy for deep vein thrombosis. His ophthalmoplegia slowly resolved over months of follow-up. Pituitary apoplexy did not recur with therapeutic anticoagulation. CONCLUSIONS: When considering the risk of surgery in patients with a known pituitary macroadenoma, an operation with possible high-volume intraoperative blood loss may have increased risk of pituitary apoplexy because intraoperative hypovolemia may precipitate ischemia, infarction, and subsequent hemorrhage. This may be particularly relevant in the cases of elective surgery. Additionally, we found that we were able to therapeutically anticoagulate a patient 2 months after pituitary apoplexy for the management of deep vein thrombosis without recurrence of pituitary apoplexy.

Demystifying hyponatremia: A clinical guide to evaluation and management.

Hyponatremia (serum sodium <135 mEq/L) is a frequent electrolyte abnormality complicating the clinical care of hospitalized patients. Hyponatremia has been associated with an increased risk of mortality. Hyponatremia can be seen in patients with euvolemia, hypovolemia, or hypervolemia. Evaluation of hyponatremia relies on clinical assessment and estimation of serum sodium, urine electrolytes, and serum and urine osmolality in addition to other case-specific laboratory parameters. In addition, point-of-care ultrasonography is an important adjunct to physical assessment in estimation of volume status. Understanding the pathophysiology of the underlying process can lead to a timely diagnosis and appropriate management of hyponatremia.

The Intensivist's Perspective of Shock, Volume Management, and Hemodynamic Monitoring.

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.

Fluid therapy for severe malaria.

Fluid therapy is an important supportive measure for patients with severe malaria. Patients with severe malaria usually have normal cardiac index, vascular resistance, and blood pressure and a small degree of hypovolaemia due to dehydration. Cell hypoxia, reduced kidney function, and acidosis result from microcirculatory compromise and malarial anaemia, which reduce tissue oxygenation, not hypovolaemia. Hence, aggressive fluid loading does not correct acid-base status, enhance kidney function, or improve patient outcomes, and it risks complications such as pulmonary oedema. Individualised conservative fluid management is recommended in patients with severe malaria. Physical examination and physiological indices have limited reliability in guiding fluid therapy. Invasive measures can be more accurate than physical examination and physiological indices but are often unavailable in endemic areas, and non-invasive measures, such as ultrasound, are mostly unexplored. Research into reliable methods applicable in low-resource settings to measure fluid status and response is a priority. In this Review, we outline the current knowledge on fluid management in severe malaria and highlight research needed to optimise fluid therapy and improve survival in severe malaria.

The pathophysiology of uncontrolled hemorrhage in horses.

BACKGROUND: Hemorrhagic shock in horses may be classified in several ways. Hemorrhage may be considered internal versus external, controlled or uncontrolled, or described based on the severity of hypovolemic shock the patient is experiencing. Regardless of the cause, as the severity of hemorrhage worsens, homeostatic responses are stimulated to ameliorate the systemic and local effects of an oxygen debt. In mild to moderate cases of hemorrhage (<15% blood volume loss), physiological adaptations in the patient may not be clinically apparent. As hemorrhage worsens, often in the uncontrolled situation such as a vascular breach internally, the pathophysiological consequences are numerous. The patient mobilizes fluid and reserve blood volume, notably splenic stored and peripherally circulating erythrocytes, to preferentially supply oxygen to sensitive organs such as the brain and heart. When the global and local delivery of oxygen is insufficient to meet the metabolic needs of the tissues, a cascade of cellular, tissue, and organ dysfunction occurs. If left untreated, the patient dies of hemorrhagic anemic shock. CLINICAL IMPORTANCE: An understanding of the pathophysiological consequences of hemorrhagic shock in horses and their clinical manifestations may help the practitioner understand the severity of blood volume loss, the need for referral, the need for transfusion, and potential outcome. In cases of severe acute uncontrolled hemorrhage, it is essential to recognize the clinical manifestations quickly to best treat the patient, which may include humane euthanasia. KEY POINTS: Uncontrolled hemorrhage may be defined as the development of a vascular breach and hemorrhage that cannot be controlled by interventional hemostasis methods such as external pressure, tourniquet, or ligation. Causes of uncontrolled hemorrhage in horses may be due to non-surgical trauma, surgical trauma, invasive diagnostic procedures including percutaneous organ biopsy, coagulopathy, hypertension, cardiovascular anomaly, vascular damage, neoplasia such as hemangiosarcoma, toxicity, or idiopathic in nature. When a critical volume of blood is lost, the respondent changes in heart rate, splenic blood mobilization, and microcirculatory control can no longer compensate for decreasing oxygen delivery to the tissues In spite of organ-specific microvascular responses (eg, myogenic responses, local mediator modulation of microvasculature, etc), all organs experience decreases in blood flow during severe hypovolemia Acute, fatal hemorrhagic shock is characterized by progressive metabolic acidosis, coagulopathy, and hypothermia, often termed the "triad of death," followed by circulatory collapse.

Novel Method of Calculating Pulse Pressure Variation to Predict Fluid Responsiveness to Transfusion in Very Low Birth Weight Infants.

A novel technique was used to calculate pulse pressure variation. The algorithm reliably predicted fluid responsiveness to transfusion, with a receiver operating characteristic area under the curve of 0.89. This technique may assist clinicians in the management of fluids and vasoactive medications for premature infants.

Vancomycin prophylaxis for revision hip arthroplasty in penicillin and cephalosporin sensitive patients: Is dose adjustment necessary in accordance with blood loss and fluid replacement?

OBJECTIVE: The aims of this study were (1) to investigate the changes in the serum concentration of prophylactically administrated vancomycin in the perioperative period of revision hip arthroplasty in penicillin/cephalosporin-allergic patients, (2) to assess whether the postoperative re-administration of vancomycin is needed, and (3) to determine the relationships of vancomycin serum concentration with blood loss, body weight, and fluid replacement in such patients. METHODS: This study consisted of 29 patients (20 females, 9 males; mean age=63.3 years; age range=45-79 years) with a history of penicillin/cephalosporin allergy undergoing revision hip arthroplasty secondary to aseptic loosening or periprosthetic fractures. Serum vancomycin levels were measured (1) before administration of vancomycin, (2) at the time of skin incision, (3) every 1,5 hours thereafter until the end of the operation, (4) during the skin closure, and (5) after three and 12 hours from the initial dosage. Data regarding body weight, amounts of intraoperative blood loss, fluid and blood replacements and postoperative wound drainage were recorded. RESULTS: The average blood loss, fluid replacement, and drain volume were 1280.3±575.8 (500-2700) mL, 2922.6±768.8 (1700-4600) mL, and 480.2±163.7 (200-850) mL, respectively. The mean levels of serum vancomycin were 46.3±21.8 (14.1-80.7) mg/L at the time of skin incision, 17.9±4.7 (9.4-30.9) and 9.8±2.2 (4.3-13.8) mg/L after 1.5 and 3 hours from the beginning of the surgery and 5.1±1.1 (2.9-6.8)mg/L after 12th hour postoperatively. The measured vancomycin levels were below the effective serum concentrations (< 5 mg/L) for 18 patients at 12 hours the administration of the first dose. A moderate level negative correlation between the blood loss/body weight ratio and vancomycin levels was found (p=0.004, r=-0.493). Predictive ROC curve analysis resulted in determining a blood loss volume higher than 1150 ml and a blood loss/body weight ratio higher than 18,5 is significant to estimate the vancomycin level below the minimum effective serum level at 12th hour postoperatively (AUC=0.793±0.16, p=0.009, AUC=0.753) 26±0.12, p=0.025, respectively). CONCLUSION: Evidence from this study has indicated vancomycin concentration at 12th hour is below the effective level in most patients. Thus, earlier repetitive infusion of vancomycin seems to be necessary in penicillin/cephalosporin-allergic patients undergoing revision hip arthroplasty, especially in those with high blood loss. LEVEL OF EVIDENCE: Level III, Therapeutic Study.

Mechanisms and management of gastrointestinal symptoms in postural orthostatic tachycardia syndrome.

Postural orthostatic tachycardia syndrome (POTS) is a disorder of orthostatic intolerance associated with many GI manifestations that can be broadly classified into two different categories: those present all the time (non-positional) and those that occur with orthostatic position change. There are also many conditions that can co-exist with POTS such as mast cell activation syndrome and the hypermobile form of Ehlers-Danlos syndrome (hEDS) that are also oftentimes associated with GI symptoms. In the current issue of Neurogastroenterology and Motility, Tai et al. explored the relationship between functional GI disorders among hEDS patients with and without concomitant POTS and showed that the hEDS-POTS cohort was more likely to have more than one GI organ involved compared to the cohort with hEDS alone, and certain GI symptoms were also more common in the hEDS-POTS cohort. In this review article, we will briefly review the literature surrounding putative mechanisms responsible for GI symptoms in POTS with an emphasis on the contributory role of concomitant hEDS and then discuss management strategies for GI symptoms in POTS.

Phases of fluid management and the roles of human albumin solution in perioperative and critically ill patients.

OBJECTIVE: Positive fluid balance is common among critically ill patients and leads to worse outcomes, particularly in sepsis, acute respiratory distress syndrome, and acute kidney injury. Restrictive fluid infusion and active removal of accumulated fluid are being studied as approaches to prevent and treat fluid overload. Use of human albumin solutions has been investigated in different phases of restrictive fluid resuscitation, and this narrative literature review was undertaken to evaluate hypoalbuminemia and the roles of human serum albumin with respect to hypovolemia and its management. METHODS: PubMed/EMBASE search terms were: "resuscitation," "fluids," "fluid therapy," "fluid balance," "plasma volume," "colloids," "crystalloids," "albumin," "hypoalbuminemia," "starch," "saline," "balanced salt solution," "gelatin," "goal-directed therapy" (English-language, pre-January 2020). Additional papers were identified by manual searching of reference lists. RESULTS: Restrictive fluid administration, plus early vasopressor use, may reduce fluid balance, but in some cases fluid overload cannot be entirely avoided. Deresuscitation, with fluid actively removed through diuretics or ultrafiltration, reduces duration of mechanical ventilation and intensive care unit stay. Combining hyperoncotic human albumin solution with diuretics increases hemodynamic stability and diuresis. Hyperoncotic albumin corrects hypoalbuminemia and raises colloid osmotic pressure, limiting edema formation and potentially improving endothelial function. Serum levels of albumin relative to C-reactive protein and lactate may predict which patients will benefit most from albumin therapy. CONCLUSIONS: Hyperoncotic human albumin solution facilitates restrictive fluid therapy and the effectiveness of deresuscitative measures. Current evidence is mostly from observational studies, and more randomized trials are needed to better establish a personalized approach to fluid management.

An evidence-based approach to nonoperative management of traumatic hemorrhagic shock in the emergency department.

The management of traumatic hemorrhagic shock has evolved, with increasing emphasis on damage control resuscitation principles. Despite these advances, hemorrhage is still the leading preventable cause of death in trauma. This issue provides evidence-based recommendations for the assessment and treatment of traumatic hemorrhagic shock. Hemostatic techniques as well as correction of hemorrhagic hypovolemia and traumatic coagulopathy are presented. The safety and efficacy of practices such as resuscitative endovascular balloon occlusion of the aorta (REBOA), viscoelastic clot testing, and whole blood resuscitation are also reviewed.

Lessons learnt from an old foe.

Neurotuberculosis usually responds well to standard antitubercular therapy. Some; patients have prolonged course A 11 year old boy diagnosed TBM, an immunocompetent patient, had an unusual course of illness in the form of prolonged fever, persistent hyponatremia and CSF; pleocytosis despite adequate treatment. Clinical course in the management of TBM can be; protracted with complications despite adequate therapy.