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Orthostatic hypertension, defined by an increase of systolic blood pressure (SBP) of ≥20 mmHg upon standing, harbors an increased cardiovascular risk. We pooled data from two rigorously conducted head-down tilt bedrest studies to test the hypothesis that cardiopulmonary deconditioning and hypovolemia predispose to orthostatic hypertension. With bedrest, peak VO 2 decreased by 6 ± 4 mlO 2 /min/kg (p < 0.0001) and plasma volume by 367 ± 348 ml (p < 0.0001). Supine SBP increased from 127 ± 9 mmHg before to 133 ± 10 mmHg after bedrest (p < 0.0001). In participants with stable hemodynamics following head-up tilt, the incidence of orthostatic hypertension was 2 out of 67 participants before bedrest and 2 out of 57 after bedrest. We conclude that in most healthy persons, cardiovascular deconditioning and volume loss associated with long-term bedrest are not sufficient to cause orthostatic hypertension., (© 2024. The Author(s).)

Objective: Hyperglycemia in patients with type 2 diabetes mellitus is frequently encountered in the hospital setting. The recent guidelines for the management of inpatient hyperglycemia have included the use of dipeptidyl peptidase 4 inhibitors as an alternative to standard insulin therapy in select patients. This raises the question of the inpatient use of sodium-glucose cotransporter 2 inhibitors (SGLT2i), which have gained increasing popularity in the outpatient setting because of beneficial cardiovascular and renal outcomes. This article describes the risks associated with the use of SGLT2i for the management of inpatient hyperglycemia., Methods: A literature review was performed using PubMed and Google Scholar for studies assessing the inpatient use of SGLT2i. Search terms included "SGLT2 inhibitors," "euglycemic DKA," "inpatient hyperglycemia," "DPP4 inhibitors," "hypovolemia," and "urinary tract infections." Studies not written in English were excluded. Forty-eight articles were included., Results: Review of the literature showed significant safety concerns with the use of SGLT2i for the inpatient management of hyperglycemia. Hospitalized patients treated with SGLT2i were at increased risk of diabetic ketoacidosis, euglycemic diabetic ketoacidosis, hypovolemia, and urinary tract infections. When compared head-to-head, SGLT2i were not more effective for inpatient glycemic control than dipeptidyl peptidase 4 inhibitors and did not reduce insulin requirements when used in combination with insulin. Although SGLT2i can be considered for the treatment of congestive heart failure, they should be started close to or at the time of discharge., Conclusion: Although SGLT2i are a preferred pharmacotherapy class for the outpatient management of type 2 diabetes mellitus, there are considerable safety concerns when using them in a hospital setting, and avoidance is recommended., Competing Interests: Disclosure Y.T.H. is an investigator on trials sponsored by Ionis Pharmaceuticals, Neurocrine Biosciences, and Novo Nordisk. The other authors have no conflicts of interest to disclose., (Copyright © 2023 AACE. Published by Elsevier Inc. All rights reserved.)

Hyponatremia and hypernatremia are electrolyte disorders that can be associated with poor outcomes. Hyponatremia is considered mild when the sodium concentration is 130 to 134 mEq per L, moderate when 125 to 129 mEq per L, and severe when less than 125 mEq per L. Mild symptoms include nausea, vomiting, weakness, headache, and mild neurocognitive deficits. Severe symptoms of hyponatremia include delirium, confusion, impaired consciousness, ataxia, seizures, and, rarely, brain herniation and death. Patients with a sodium concentration of less than 125 mEq per L and severe symptoms require emergency infusions with 3% hypertonic saline. Using calculators to guide fluid replacement helps avoid overly rapid correction of sodium concentration, which can cause osmotic demyelination syndrome. Physicians should identify the cause of a patient's hyponatremia, if possible; however, treatment should not be delayed while a diagnosis is pursued. Common causes include certain medications, excessive alcohol consumption, very low-salt diets, and excessive free water intake during exercise. Management to correct sodium concentration is based on whether the patient is hypovolemic, euvolemic, or hypervolemic. Hypovolemic hyponatremia is treated with normal saline infusions. Treating euvolemic hyponatremia includes restricting free water consumption or using salt tablets or intravenous vaptans. Hypervolemic hyponatremia is treated primarily by managing the underlying cause (e.g., heart failure, cirrhosis) and free water restriction. Hypernatremia is less common than hyponatremia. Mild hypernatremia is often caused by dehydration resulting from an impaired thirst mechanism or lack of access to water; however, other causes, such as diabetes insipidus, are possible. Treatment starts with addressing the underlying etiology and correcting the fluid deficit. When sodium is severely elevated, patients are symptomatic, or intravenous fluids are required, hypotonic fluid replacement is necessary.

Purpose: Early postoperative mobilization can be hindered by orthostatic intolerance (OI). Postoperative OI has multifactorial pathogenesis, possibly involving both postoperative hypovolemia and autonomic dysfunction. We aimed to investigate the effect of mild acute blood loss from blood donation simulating postoperative hypovolemia, on both autonomic function and OI, thus eliminating confounding perioperative factors such as inflammation, residual anesthesia, pain, and opioids., Methods: This prospective observational cohort study included 26 blood donors. Continuous electrocardiogram data were collected during mobilization and night sleep, both before and after blood donation. A Valsalva maneuver and a standardized mobilization procedure were performed immediately before and after blood donation, during which cardiovascular and tissue oxygenation variables were continuously measured by LiDCOrapid™ and Massimo Root™, respectively. The incidence of OI, hemodynamic responses during mobilization and Valsalva maneuver, as well as heart rate variability (HRV) responses during mobilization and sleep were compared before and 15 min after blood donation., Results: Prior to blood donation, no donors experienced OI during mobilization. After blood donation, 6/26 (23%; 95% CI, 9 to 44) donors experienced at least one OI symptom. Three out of 26 donors (12%; 95% CI, 2 to 30) terminated the mobilization procedure prematurely because of severe OI symptoms. Cardiovascular and cerebral tissue oxygenation responses were reduced in patients with severe OI. After blood loss, HRV indices of total autonomic power remained unchanged but increased sympathetic and decreased parasympathetic outflow was observed during mobilization, but also during sleep, indicating a prolonged autonomic effect of hypovolemia., Conclusion: We describe a specific hypovolemic component of postoperative OI, independent of postoperative autonomic dysfunction, inflammation, opioids, and pain., Study Registration: ClinicalTrials.gov (NCT04499664); registered 5 August 2020., (© 2023. The Author(s).)

On February 6, two major earthquakes with magnitudes of 7.8 and 7.7 on the Richter scale hit Turkey and Northern Syria causing more than 50,000 deaths. In the immediate aftermath of the earthquakes, our major tertiary medical referral center received dozens of cases of crush syndrome, presenting with a variety of imaging findings. Crush syndrome is characterized by hypovolemia, hyperkalemia, and myoglobinuria that can lead to rapid death of victims, despite their survival of staying under wreckage for days. The typical triad of crush syndrome consists of the acute tubular necrosis, paralytic ileus, and third-space edema. In this article, we focus primarily on characteristic imaging findings of earthquake-related crush syndrome and divided them into two distinct subsections: myonecrosis, rapid hypovolemia, excessive third-space edema, acute tubular necrosis, and paralytic ileus, which are directly related to crush syndrome, and typical accompanying findings of earthquake-related crush syndrome. Lower extremity compression in earthquake survivors results in the typical third-space edema. In addition to the lower extremities, other skeletal muscle regions are also affected, especially rotator muscles, trapezius, and pectoral muscles. Although it may be relatively easy to better detect myonecrosis with contrast-enhanced CT scans, changing the windowing of the images may be helpful., (© 2023. The Author(s), under exclusive licence to American Society of Emergency Radiology (ASER).)

Background: Cryptosporidium is recognized as a significant pathogen of diarrhea disease in immunocompromised hosts, and studies have shown that Cryptosporidium infection is high in solid organ transplantation (SOT) patients and often has serious consequences. Because of the lack of specificity of diarrheasymptoms cased by Cryptosporidium infection, it is rarely reported in patients undergoing liver transplantation (LT). It frequently delays diagnosis, coming with severe consequences. In clinical work, diagnosing Cryptosporidium infection in LT patients is also complex but single, and the corresponding anti-infective treatment regimen has not yet been standardized. A rare case of septic shock due to a delayed diagnosis of Cryptosporidium infection after LT and relevant literature are discussed in the passage., Case Presentation: A patient who had received LT for two years was admitted to the hospital with diarrhea more than 20 days after eating an unclean diet. After failing treatment at a local hospital, he was admitted to Intensive Care Unit after going into septic shock. The patient presented hypovolemia due to diarrhea, which progressed to septic shock. The patient's sepsis shock was controlled after receiving multiple antibiotic combinations and fluid resuscitation. However, the persistent diarrhea, as the culprit of the patient's electrolyte disturbance, hypovolemia, and malnutrition, was unsolved. The causative agent of diarrhea, Cryptosporidium infection, was identified by colonoscopy, faecal antacid staining, and blood high-throughput sequencing (NGS). The patient was treated by reducing immunosuppression and Nitazoxanide (NTZ), which proved effective in this case., Conclusion: When LT patients present with diarrhea, clinicians should consider the possibility of Cryptosporidium infection, in addition to screening for conventional pathogens. Tests such as colonoscopy, stool antacid staining and blood NGS sequencing can help diagnose and treat of Cryptosporidium infection early and avoid serious consequences of delayed diagnosis. In treating Cryptosporidium infection in LT patients, the focus should be on the patient's immunosuppressive therapy, striking a balance between anti-immunorejection and anti-infection should be sought. Based on practical experience, NTZ therapy in combination with controlled CD4 + T cells at 100-300/mm 3 was highly effective against Cryptosporidium without inducing immunorejection., (© 2023. The Author(s).)

Importance: Spontaneous hemoperitoneum in pregnancy (SHiP) is a rare life-threatening event previously associated with endometriosis. Although pregnancy is thought to improve the symptoms of endometriosis, abrupt intraperitoneal bleeding can occur, jeopardizing both maternal and fetal outcomes., Objective: The aim of this study was to review the published information regarding SHiP pathophysiology, presentation, diagnosis, and management in a flowchart approach., Evidence Acquisition: A descriptive review of published articles in the English-language was carried out., Results: SHiP most commonly presents in the second half of pregnancy with a combination of abdominal pain, hypovolemia, a decline in hemoglobin level, and fetal distress. Nonspecific gastrointestinal symptoms are not uncommon. Surgical management is suitable in most scenarios and avoids complications such as recurrent bleeding and infected hematoma. Maternal outcome has improved greatly, whereas perinatal mortality remained unchanged. In addition to physical strain, SHiP was reported to have a psychosocial sequela., Conclusions and Relevance: A high index of suspicion is required when patients present with acute abdominal pain and signs of hypovolemia. Early use of sonography contributes to narrowing down the diagnosis. Health care providers should be familiar with the SHiP diagnosis because early identification is crucial when attempting to safeguard maternal and fetal outcomes. Maternal and fetal requirements are often contradictory, creating a greater challenge in decision-making and treatment. A multidisciplinary team approach should coordinate the treatment, whenever a SHiP diagnosis is suspected.

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., (© 2022 The Authors. Diabetic Medicine published by John Wiley & Sons Ltd on behalf of Diabetes UK.)

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., (© 2023. The Author(s).)

Diabetic ketoacidosis (DKA), a frequent complication of type 1 diabetes (T1D), is characterized by hyperosmolar hypovolemia. The response of water-regulating hormones arginine vasopressin (AVP; antidiuretic hormone) and aldosterone to DKA treatment in children is not well understood, although they may have potential as future diagnostic, prognostic, and/or treatment monitoring markers in diabetic patients. We aimed to characterize the dynamics of the response in copeptin (marker for AVP) and aldosterone secretion to rehydration treatment in pediatric patients with DKA. Data originated from a prospective, observational, multicenter study including 28 pediatric T1D patients treated for DKA (median age, 11.5 years; weight, 35 kg). Serial measurements of hormone levels were obtained during 72 h following rehydration start. Semimechanistic pharmacometric modeling was used to analyze the kinetic/dynamic relationship of copeptin and aldosterone secretion in response to the correction of hyperosmolality and hypovolemia, respectively. Modeling revealed different sensitivities for osmolality-dependent copeptin secretion during the first 72 h of rehydration, possibly explained by an osmotic shift introduced by hypovolemia. Response in aldosterone secretion to the correction of hypovolemia seemed to be delayed, which was well described by an extra upstream turnover compartment, possibly representing chronic upregulation of aldosterone synthase (cytochrome P450 11B2). In conclusion, semimechanistic modeling provided novel physiological insights in hormonal water regulation in pediatric patients during DKA treatment, providing rationale to further evaluate the potential of monitoring copeptin, but not aldosterone due to its delayed response, for future optimization of rehydration treatment to reduce the risk of acute complications such as cerebral edema., (© 2022 The Authors. CPT: Pharmacometrics & Systems Pharmacology published by Wiley Periodicals LLC on behalf of American Society for Clinical Pharmacology and Therapeutics.)

Aims: SGLT2 inhibitors provide cardiovascular and renal protection in people with type 2 diabetes (T2DM). Real-world data on their effect on improving glucose and cardiovascular risk factors, and adverse effects in South Asians are limited., Methods: We retrospectively analyzed clinical, demographic, anthropometric and biochemical data among adults with T2DM, commenced on empagliflozin and followed up for at least one month in a diabetes clinic in Colombo., Results: Among 1523 participants (men 49.6 %, age 54.9 (± 10.8) years, diabetes duration 11.5 (± 7.6) years, body mass index 28.2 (± 4.5 kg/m 2 ), over a median follow up of 12 months (range: 1-24 months), reduction in HbA1c, weight, systolic blood pressure (SBP) and urine albumin-creatinine ratio were evident within the first month. Benefits sustained up to two-years (mean changes from baseline: HbA1c - 0.31 (± 1.49), weight - 1.14 (± 4.17), SBP - 3.44 (± 21.75), UACR - 19.84 (± 108.22) follow up. eGFR declined by the third month, returned to baseline by 12th and remained stable over 24 months. Higher baseline HbA1c, weight and SBP predicted greater decline in HbA1c, weight and SBP respectively. Weight reduction independently predicted the SBP reduction. Eighteen participants per 100 patient-years discontinued therapy due to adverse effects: genital mycotic infections and features of hypovolaemia were the commonest. We observed only two events of diabetic ketoacidosis., Conclusions: Empagliflozin effectively improves glucose, weight and SBP and retards progression of renal impairment in South Asians with T2D. Genital mycotic infections and hypovolaemia were the commonest reasons for discontinuation. Careful patient selection and advice can avoid other sinister complications., Competing Interests: Conflicts of interests The authors declare that they have no competing interests., (Copyright © 2022. Published by Elsevier Ltd.)

Purpose: To assess the frequency of hypovolemic shock complex (HSC) signs on CT in patients who presented to the emergency department (ED) with undifferentiated non-traumatic shock. Secondary aim was to assess the correlation between HSC signs and all-cause mortality., Methods: This retrospective, single-center study included 100 patients who underwent contrast-enhanced thoraco-abdominal CT in the ED to evaluate the etiology for non-traumatic undifferentiated shock. All patients were retrospectively assigned a shock subtype (i.e., distributive, cardiogenic, hypovolemic, obstructive, multifactorial, and unknown) based on medical records. Patients' demographics and time to all-cause mortality up to 90 days were collected. All CT studies were re-assessed for the presence of HSC signs. Correlation between HSC signs, mortality and shock subtype was assessed., Results: Overall, 58% (58/100) of all patients had at least one HSC sign. Flattened inferior vena cava and adrenal hyper-enhancement were the most common HSC signs (27.3%, 27/99; in both). Overall mortality was 59% (59/100). When evaluated separately, shock liver was the only HSC sign to significantly correlate with increased mortality (84.6% vs. 55.2%, p = .04). However, patients with at least two HSC signs had a significantly higher mortality rate compared to patients without any HSC signs (73.5% vs. 45.2%, p = .017)., Conclusion: Most patients with non-traumatic shock had at least one HSC sign. Mortality rates were significantly higher in patients with two or more HSC signs compared to patients without any signs. Patients with shock liver sign had significantly higher mortality rates., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Hypernatremia occurs when the plasma sodium concentration is greater than 145 mmol/L. Depending on the duration, hypernatremia can be differentiated into acute and chronic. According to severity: mild, moderate and threatening hypernatremia. Finally, depending on pathogenesis, hypernatremia can be defined as hypervolemic, hypovolemic, and euvolemic. Acute hypervolemic hypernatremia is often secondary to increased sodium intake (hypertonic NaCl and NaHCO 3 solutions). Instead, chronic hypervolemic hypernatremia may be an expression of primary hyperaldosteronism. Euvolemic hypernatremia occurs in diabetes insipidus: depending on the underlying pathogenesis, it can be classified into two basic types: neurogenic (or central) and nephrogenic. The neurogenic form may be triggered by traumatic, vascular or infectious events; the nephrogenic form may be due to pharmacological causes, such as lithium, or non-pharmacological ones, such as hypokalemia. For hypovolemic hypernatremia, possible explanations are renal or extrarenal losses. The main goal of treatment of hypernatremia is the restoration of plasma tonicity. In particular, if the imbalance has occurred acutely, rapid correction improves the prognosis by preventing the effects of cellular dehydration; if hypernatremia has developed slowly, over a period of days, a slow correction rate (no more than 0.4 mmol/L/h) is recommended., (© 2022 Walter de Gruyter GmbH, Berlin/Boston.)

Importance: Hyponatremia is the most common electrolyte disorder and it affects approximately 5% of adults and 35% of hospitalized patients. Hyponatremia is defined by a serum sodium level of less than 135 mEq/L and most commonly results from water retention. Even mild hyponatremia is associated with increased hospital stay and mortality., Observations: Symptoms and signs of hyponatremia range from mild and nonspecific (such as weakness or nausea) to severe and life-threatening (such as seizures or coma). Symptom severity depends on the rapidity of development, duration, and severity of hyponatremia. Mild chronic hyponatremia is associated with cognitive impairment, gait disturbances, and increased rates of falls and fractures. In a prospective study, patients with hyponatremia more frequently reported a history of falling compared with people with normal serum sodium levels (23.8% vs 16.4%, respectively; P < .01) and had a higher rate of new fractures over a mean follow-up of 7.4 years (23.3% vs 17.3%; P < .004). Hyponatremia is a secondary cause of osteoporosis. When evaluating patients, clinicians should categorize them according to their fluid volume status (hypovolemic hyponatremia, euvolemic hyponatremia, or hypervolemic hyponatremia). For most patients, the approach to managing hyponatremia should consist of treating the underlying cause. Urea and vaptans can be effective treatments for the syndrome of inappropriate antidiuresis and hyponatremia in patients with heart failure, but have adverse effects (eg, poor palatability and gastric intolerance with urea; and overly rapid correction of hyponatremia and increased thirst with vaptans). Severely symptomatic hyponatremia (with signs of somnolence, obtundation, coma, seizures, or cardiorespiratory distress) is a medical emergency. US and European guidelines recommend treating severely symptomatic hyponatremia with bolus hypertonic saline to reverse hyponatremic encephalopathy by increasing the serum sodium level by 4 mEq/L to 6 mEq/L within 1 to 2 hours but by no more than 10 mEq/L (correction limit) within the first 24 hours. This treatment approach exceeds the correction limit in about 4.5% to 28% of people. Overly rapid correction of chronic hyponatremia may cause osmotic demyelination, a rare but severe neurological condition, which can result in parkinsonism, quadriparesis, or even death., Conclusions and Relevance: Hyponatremia affects approximately 5% of adults and 35% of patients who are hospitalized. Most patients should be managed by treating their underlying disease and according to whether they have hypovolemic, euvolemic, or hypervolemic hyponatremia. Urea and vaptans can be effective in managing the syndrome of inappropriate antidiuresis and hyponatremia in patients with heart failure; hypertonic saline is reserved for patients with severely symptomatic hyponatremia.

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., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Background: In patients receiving total parenteral nutrition (TPN), the frequency of hyponatraemia is high. However, the causes of hyponatraemia in TPN have not been elucidated, although diagnosis is required for appropriate therapy. The aim of this study is to describe the aetiology of hyponatraemia in non-critical hospitalised patients receiving TPN., Methods: Prospective multicentre study in 19 Spanish hospitals. Non-critically hyponatraemic patients receiving TPN and presenting hyponatraemia over a 9-month period were studied. Data collected included sex, age, previous comorbidities, and serum sodium levels (SNa) before and following TPN initiation. Parameters for study of hyponatraemia were also included: clinical volaemia, the presence of pain, nausea, gastrointestinal losses, diuretic use, oedema, renal function, plasma and urine osmolality, urinary electrolytes, cortisolaemia, and thyroid stimulating hormone., Results: 162 patients were included, 53.7% males, age 66.4 (SD13.8) years. Volume status was evaluated in 142 (88%): 21 (14.8%) were hypovolaemic, 96 (67.6%) euvolaemic and 25 (17.6%) hypervolaemic. In 111/142 patients the analytical assessment of hyponatraemia was completed. Hypovolaemic hyponatraemia was secondary to GI losses in 10/111 (9%), and to diuretics in 3/111 (2.7%). Euvolaemic hyponatraemia was due to Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH) in 47/111 (42.4%), and to physiological stimuli of Arginine Vasopressin (AVP) secretion in 28/111 (25.2%). Hypervolaemic hyponatraemia was induced by heart failure in 19/111 (17.1%), cirrhosis of the liver in 4/111 (3.6%)., Conclusions: SIADH was the most frequent cause of hyponatraemia in patients receiving TPN. The second most frequent cause was physiological stimuli of AVP secretion induced by pain/nausea., (Copyright © 2021 SEEN and SED. Published by Elsevier España, S.L.U. All rights reserved.)

Background: Assessing intravascular hypovolemia due to hemorrhage remains a clinical challenge. Central venous pressure (CVP) remains a commonly used monitor in surgical and intensive care settings for evaluating blood loss, despite well-described pitfalls of static pressure measurements. The authors investigated an alternative to CVP, intravenous waveform analysis (IVA) as a method for detecting blood loss and examined its correlation with echocardiography., Methods: Seven anesthetized, spontaneously breathing male Sprague Dawley rats with right internal jugular central venous and femoral arterial catheters underwent hemorrhage. Mean arterial pressure (MAP), heart rate, CVP, and IVA were assessed and recorded. Hemorrhage was performed until each rat had 25% estimated blood volume removed. IVA was obtained using fast Fourier transform and the amplitude of the fundamental frequency (f1) was measured. Transthoracic echocardiography was performed utilizing a parasternal short axis image of the left ventricle during hemorrhage. MAP, CVP, and IVA were compared with blood removed and correlated with left ventricular end diastolic area (LVEDA)., Results: All 7 rats underwent successful hemorrhage. MAP and f1 peak amplitude obtained by IVA showed significant changes with hemorrhage. MAP and f1 peak amplitude also significantly correlated with LVEDA during hemorrhage (R = 0.82 and 0.77, respectively). CVP did not significantly change with hemorrhage, and there was no significant correlation between CVP and LVEDA., Conclusions: In this study, f1 peak amplitude obtained by IVA was superior to CVP for detecting acute, massive hemorrhage. In addition, f1 peak amplitude correlated well with LVEDA on echocardiography. Translated clinically, IVA might provide a viable alternative to CVP for detecting hemorrhage.

A 12-year-old neutered male German shepherd dog was evaluated after dying suddenly at home. A few hours prior to the unexpected death the dog displayed anorexia and lethargy. Post-mortem examination and histopathology led to a diagnosis of marked hemoabdomen and hypovolemia due to a single ruptured splenic hemangiosarcoma., (Copyright and/or publishing rights held by the Canadian Veterinary Medical Association.)

A fundamental tenet of heart failure (HF) pathophysiology hinges on a propensity for fluid retention leading to blood volume (BV) expansion and hemodilution. Whether this can be applied to heart failure patients with preserved ejection fraction (HFpEF) remains uncertain. The present study sought to determine BV status and key hormones regulating fluid homeostasis and erythropoiesis in HFpEF patients. BV and hemoglobin mass (Hb mass ) were determined with high-precision, automated carbon monoxide (CO) rebreathing in 20 stable HFpEF patients (71.5 ± 7.3 years, left ventricular ejection fraction = 55.7 ± 4.0%) and 15 healthy age- and sex-matched control individuals. Additional measurements comprised key circulating BV-regulating hormones such as pro-atrial natriuretic peptide (proANP), copeptin, aldosterone and erythropoietin (EPO), as well as central hemodynamics and arterial stiffness via carotid-femoral pulse wave velocity (PWV). Carotid-femoral PWV was increased (+20%) in HFpEF patients versus control individuals. With respect to hematological variables, plasma volume (PV) did not differ between groups, whereas BV was decreased (-14%) in HFpEF patients. In consonance with the hypovolemic status, Hb mass was reduced (-27%) in HFpEF patients, despite they presented more than a twofold elevation of circulating EPO (+119%). Plasma concentrations of BV-regulating hormones, including proANP (+106%), copeptin (+99%), and aldosterone (+62%), were substantially augmented in HFpEF patients. HFpEF patients may present with hypovolemia and markedly reduced Hb mass , underpinned by a generalized overactivation of endocrine systems regulating fluid homeostasis and erythropoiesis. These findings provide a novel perspective on the pathophysiological basis of the HFpEF condition., (© 2019 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.)

Postoperative acute kidney injury (AKI) is a common complication of surgery that is associated with significant adverse outcomes, including increased morbidity and mortality. The perioperative burden of AKI risk factors is complex and potentially large, including high-risk nephrotoxic medications, hypotension, hypovolemia, radiologic contrast, anemia, and surgery-specific factors. Understanding the pathogenesis, risk factors, and potential cumulative impact of perioperative nephrotoxic exposures is particularly important in the prevention and reduction of perioperative AKI. This review outlines the possible strategies to reduce perioperative nephrotoxicity and the development of postoperative AKI., (Crown Copyright © 2019. Published by Elsevier Inc. All rights reserved.)

Objective: Hyponatraemia is common in community-acquired pneumonia (CAP) and is associated with increased mortality. The mechanism of hyponatraemia in CAP is not completely understood and treatment is therefore ill-defined. We aimed to define the causation of hyponatraemia in CAP., Design: Prospective, single-centre, observational study of all patients with CAP and hyponatraemia (≤ 130 mmol/L) during a 9-month period., Patients: The prevalence of each subtype of hyponatraemia, and the associated mortality, was determined in 143 admissions with CAP (Study 1). A sub-cohort of patients with SIAD (n = 10) was prospectively followed, to document the natural history of SIAD associated with CAP (Study 2)., Measurements: In Study 2, blood and urine were collected on day 1, 3, 5 and 7 following admission for measurement of plasma vasopressin, sodium, osmolality and urine osmolality., Results: In study 1, 143/1723(8.3%) of CAP patients had hyponatraemia (≤130 mmol/L). About 66 had SIAD (46%), 60(42%) had hypovolaemic hyponatraemia (HON), 13(9%) had hypervolaemic hyponatraemia (HEN) and 4(3%) patients had hyponatraemia due to glucocorticoid hormone deficiency. Mortality was higher in the HEN than in the HON, SIAD or normonatraemic groups (P < 0.01). In Study 2, plasma sodium concentration normalized in 8/10 (80%) by day 7. Two patients with persistent hyponatraemia were discovered to have underlying bronchiectasis., Conclusions: Hyponatraemia in CAP is most commonly secondary to SIAD or hypovolaemia. HEN is less common, but has worse prognosis. Prospective observation demonstrates that in SIAD, plasma AVP and sodium concentrations normalize with antimicrobials; failure of reversal of suggests underlying lung disease, such as bronchiectasis., (© 2019 John Wiley & Sons Ltd.)

Hypotension and especially very low diastolic blood pressure could be an at-risk situation in very old and frail patients and in those with coronary heart disease. Chronic hypotension in people with heart failure is an indicator of poor prognosis and hinders the management of therapy. Orthostatic hypotension is a decrease in blood pressure>20mmHg for systolic and/or>10mmHg for diastolic within 3minutes after transition from supine to upright. Orthostatic hypotension may be symptomatic or not. The search for orthostatic hypotension is part of the clinical examination of elderly patients with hypertension, falling, diabetes and or polymedication. First intention treatment aims to correct modifiable modifying factors and to limit the circulatory consequences of orthostatism by elastic venous compression., (Copyright © 2018. Published by Elsevier Masson SAS.)

Hypovolemic patients can develop postintubation hypotension (PIH). Our objective is to review the literature regarding PIH and the association with mortality. We searched MEDLINE from inception to February 2018. A meta-analysis was performed to assess the effect of PIH on mortality. The results of the meta-analysis were reported in forest plots of the estimated effects of the included studies with a 95 per cent confidence interval. Heterogeneity was evaluated using the I ² test, which corresponded to low ( I ² < 25%), medium ( I ² = 25-75%), and high ( I ² > 75%) heterogeneity. We identified 243 records. Four studies were included in the meta-analysis. The studies reported 2044 patients with 36.8 per cent (n = 753) developing PIH. Data indirectly reflecting the hemodynamic status were available in three studies (n = 1117 patients). Overall mortality was 24.6 per cent (n = 503) and was significantly higher in patients that developed PIH [mortality, n (%): PIH = 250/753 (33.2%) vs 253/1291 (19.6%), P < 0.001]. Patients that develop PIH have an increased mortality. Considering a targeted resuscitation in hypovolemic patients is pivotal to minimize PIH.

The etiology of hyponatremia is often multifactorial. The most common causes include hypovolemia from gastrointestinal (GI) or other fluid losses, thiazide diuretics, and SIAD [1]. In this chapter, we will discuss hypovolemic hyponatremia, as well as the clinical parameters that help distinguish between hypovolemic and euvolemic states. These include not only the urine [Na+] concentration but also the fractional uric acid excretion, a parameter that can be employed even when diuretics have been prescribed [2,3,4,5,6,7]. Among the common causes of hypovolemic hyponatremia are GI fluid loss, a range of endocrinopathies [7], and thiazide-induced hyponatremia, which is best considered as a distinct entity, in particular because recent data suggest that it has a genetic predisposition. Also, the discontinuation of thiazide is a key step in treatment [2,7]. The management of hypovolemic hyponatremia starts with confirming its presence and determining the underlying cause. Correction focuses on the appropriate use of isotonic fluid to effect volume repletion while avoiding an overly rapid rise in serum [Na+] concentration., (© 2019 S. Karger AG, Basel.)

Introduction: Identifying reversible causes of cardiac arrest is challenging. The diagnosis of pulmonary embolism is often missed. Pulmonary embolism increases alveolar dead space resulting in low end-tidal CO 2 (EtCO 2 ) relative to arterial CO 2 (PaCO 2 ) tension. Thus, a low EtCO 2 /PaCO 2 ratio during resuscitation may be a sign of pulmonary embolism., Methods: Post hoc analysis of data from two porcine studies comparing ultrasonographic measurements of right ventricular diameter during resuscitation from cardiac arrest of different causes. Pigs were grouped according to cause of arrest (pulmonary embolism, hypovolemia, primary arrhythmia, hypoxia, or hyperkalaemia) and EtCO 2 /PaCO 2 ratios were compared., Results: Data from 54 pigs were analysed. EtCO 2 levels at the third rhythm analysis were significantly lower when cardiac arrest was caused by pulmonary embolism than by primary arrhythmia, hypoxia and hyperkalaemia, but there was no significant difference between pulmonary embolism and hypovolemia. In contrast, PaCO 2 levels were higher in cardiac arrest caused by pulmonary embolism than in the other causes of cardiac arrest. Consequently, the EtCO 2 /PaCO 2 ratio was lower in pulmonary embolism 0.2 (95%CI 0.1-0.4), than in hypovolaemia 0.5 (95%CI 0.3-0.6), primary arrhythmia 0.7 (95%CI 0.7-0.8), hypoxia 0.5 (95%CI 0.4-0.6), and hyperkalaemia 0.6 (95%CI 0.6-0.7)., Conclusion: A low EtCO 2 /PaCO 2 ratio during cardiopulmonary resuscitation suggests pulmonary embolism., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Assessment of the volume status by blood pressure (BP) monitoring is difficult, since baroreflex control of BP makes it insensitive to blood loss up to about one liter. We hypothesized that a machine learning model recognizes the progression of central hypovolemia toward presyncope by extracting information of the noninvasive blood pressure waveform parametrized through principal component analysis. This was tested in healthy volunteers exposed to simulated hemorrhage by lower body negative pressure (LBNP). Fifty-six healthy volunteers were subjected to progressive central hypovolemia. A support vector machine was trained on the blood pressure waveform. Three classes of progressive stages of hypovolemia were defined. The model was optimized for the number of principal components and regularization parameter for penalizing misclassification (cost): C. Model performance was expressed as accuracy, mean squared error (MSE), and kappa statistic (inter-rater agreement). Forty-six subjects developed presyncope of which 41 showed an increase in model classification severity from baseline to presyncope. In five of the remaining nine subjects (1 was excluded) it stagnated. Classification of samples during baseline and end-stage LBNP had the highest accuracy (95% and 50%, respectively). Baseline and first stage of LBNP demonstrated the lowest MSE (0.01 respectively 0.32). Model MSE and accuracy did not improve for C values exceeding 0.01. Adding more than five principal components did not further improve accuracy or MSE. Increment in kappa halted after 10 principal components had been added. Automated feature extraction of the blood pressure waveform allows modeling of progressive hypovolemia with a support vector machine. The model distinguishes classes between baseline and presyncope., (© 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.)

Volume resuscitation is of utmost importance in the treatment of shock. It is imperative that this resuscitation be guided using a reliable method of ascertaining volume status to avoid the ill-effects of hypovolemia while also avoiding those of over-resuscitation. There are numerous tools and methods available in this era to aid the bedside physician in guiding volume resuscitation, many of which will be described in this review of literature. The methods to assess preload responsiveness are broadly divided into static and dynamic measurements. Static measurements involve 'snapshot' estimations of preload. Dynamic measurements rely on fluctuations in heart-lung interactions or a simulated volume challenge to predict whether increasing preload by volume loading will be beneficial. Dynamic measurements are favored over static measurements, however the conditions to be met for most dynamic measurements to be valid leave these methods to be used reliably in a very discrete critically-ill population. This issue is overcome by utilizing maneuvers that have been developed to assess fluid responsiveness that liberalize the conditions required for most dynamic measurements, such as passive leg raising, end expiratory occlusion, and mini-fluid boluses. This review of literature highlights the differences between static and dynamic measurements of fluid responsiveness, and proposes a guide to choosing the most reliable methods of ascertaining volume responsiveness individualized to each patient., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Hypervolemic (dilutional) hyponatremia is the most common dysnatremia in cirrhosis, with a prevalence close to 50% in patients with ascites, while hypovolemic hyponatremia occurs in a minority of cases. Hyponatremia carries a poor prognosis, being associated with increased mortality and reduced survival after liver transplantation. Hypernatremia is rarer and is also associated with an adverse prognosis. Increased non-osmotic secretion of arginine vasopressin and altered renal tubular sodium handling due to impaired free water generation are the mechanisms leading to hypervolemic hyponatremia, while diuretic-induced fluid loss is the main cause of hypovolemic hyponatremia. Hypernatremia usually follows hypotonic fluid losses due to osmotic diuresis (glycosuria) or lactulose-induced diarrhea. The main clinical manifestations of dysnatremias are due to their effects on the central nervous system: astroglial cell hyperhydration follows hyponatremia-an abnormality that exacerbates ammonia neurotoxicity-while the opposite abnormality occurs with hypernatremia. Asymptomatic or mildly symptomatic hypervolemic hyponatremia is mainly managed by correcting of precipitating factors and non-osmotic fluid restriction. Severe, life-threatening hyponatremia requires hypertonic saline infusion, avoiding rapid and complete correction of serum sodium concentration to prevent neurological sequelae such as osmotic demyelination. V 2 receptor blockade by vaptans may be considered in patients with sustained hyponatremia waitlisted for liver transplantation. Diuretic withdrawal and plasma volume expansion are required in hypovolemic hypernatremia. Prompt recognition, removal of the precipitating factor(s) and non-osmotic fluid administration represent the mainstays of hypernatremia management. Rapid correction of long-standing hypernatremia can lead to cerebral edema and has to be avoided.

Acute kidney injury (AKI) is a common disorder worldwide that is associated with severe morbidity, mortality and cost. If managed adequately and in a timely manner, the majority of these cases are preventable, treatable and often reversible with simple measures. We conducted a two years prospective study of patients admitted to medical and surgical units of a tertiary care center in Central India to identify the causes of Hospital Acquired AKI (HAAKI) and its impact on patient outcomes. HAAKI occurred in 215 of 9,800 patients (2.1%). Sepsis (75; 34.88%), volume depletion and hypo perfusion (62; 28.83%), drugs (50; 23.25%), multifactorial (18; 8.37%) and radiocontrast agents (9; 4.2%) were the causes of HAAKI. Thirty-nine percent of patients had complete recovery and 9.3% had partial recovery of renal function. The overall inhospital mortality due to HAAKI was 41.86%. On multivariate analysis, oliguria, multi-organ failure, metabolic acidosis, anemia, and sepsis showed significant association with in-hospital mortality. The mortality and morbidity associated with HAAKI mandates the need for active measures to decrease its incidence. Knowledge of incidence and risk factors is crucial because it drives local and international efforts on detection and treatment. To the best of our knowledge, no epidemiological study has been conducted or published on HAAKI from the Central India., Competing Interests: None declared

Hypovolemia is frequent in patients with sepsis and may contribute to worse outcome. The management of these patients is impeded by the low quality of the evidence for many of the specific components of the care. In this paper, we discuss recent advances and controversies in this field and give expert statements for the management of hypovolemia in patients with sepsis including triggers and targets for fluid therapy and volumes and types of fluid to be given. Finally, we point to unanswered questions and suggest a roadmap for future research.

Objective: Compare the maximum concentration (Cmax), time to maximum concentration (Tmax), mean concentration, rate of return of spontaneous circulation (ROSC), time to ROSC, and odds of ROSC when epinephrine is administered by humerus intraosseous (HIO) compared to intravenous (IV) routes in both a hypovolemic and normovolemic cardiac arrest model., Design: Prospective, between subjects, randomized experimental study., Setting: TriService Facility., Subjects: Twenty-eight adult Yorkshire Swine were randomly assigned to four groups: HIO normovolemia; HIO hypovolemia; IV normovolemia; and IV hypovolemia., Intervention: Swine were anesthetized. The hypovolemic group was exsanguinated 31 percent of their blood volume. Subjects were placed into arrest. After 2 minutes, cardiopulmonary resuscitation (CPR) was initiated. After another 2 minutes, 1 mg epinephrine was given by IV or HIO routes; blood samples were collected over 4 minutes. Hypovolemic groups received 500 mL of 5 percent albumin following blood sampling. CPR continued until ROSC or for 30 minutes., Main Outcome Measures: ROSC, time to ROSC, Cmax, Tmax, mean concentrations over time, odds of ROSC., Results: Cmax was significantly higher, the Tmax, and the time to ROSC were significantly faster in the HIO normovolemic compared to the HIO hypovolemic group (p < 0.05). All seven in the HIO normovolemic group achieved ROSC compared to three of the HIO hypovolemic group. Odds of ROSC were 19.2 times greater in the HIO normovolemic compared the HIO hypovolemic group., Conclusion: The HIO is an effective route in a normovolemic model. However, the findings indicate that sufficient blood volume is essential for ROSC in a hypovolemic scenario.

Introduction: Although hypovolemia remains the most relevant problem during acute decompensated diabetes in its clinical manifestations (diabetic ketoacidosis, DKA, and hyperglycemic hyperosmolar state, HHS), the electrolyte derangements caused by the global hydroelectrolytic imbalance usually complicate the clinical picture at presentation and may be worsened by the treatment itself., Aim: This review article is focused on the management of dysnatremias during hyperglycemic hyperosmolar state with the aim of providing clinicians a useful tool to early identify the sodium derangement in order to address properly its treatment., Discussion: The plasma sodium concentration is modified by most of the therapeutic measures commonly required in such patients and the physician needs to consider these interactions when treating HHS. Moreover, an improper management of plasma sodium concentration (PNa+) and plasma osmolality during treatment has been associated with two rare potentially life-threatening complications (cerebral edema and osmotic demyelination syndrome). Identifying the correct composition of the fluids that need to be infused to restore volume losses is crucial to prevent complications., Conclusion: A quantitative approach based on the comparison between the measured PNa+ (PNa+ M) and the PNa+ expected in the presence of an exclusive water shift (PNa+ G) may provide more thorough information about the true hydroelectrolytic status of the patient and may therefore, guide the physician in the initial management of HHS. On the basis of data derived from our previous studies, we propose a 7-step algorithm to compute an accurate estimate of PNa+ G., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)

Hyponatremia is associated with bone demineralization. We hypothesized that, during hyponatremia, calciuria and calcium balance depend on volemic status. We evaluated calciuria in patients with hyponatremia, secondary to SIAD or hypovolemia. Patients with SIAD exhibited a volemic expansion that was associated with hypercalciuria. Calciuria was proportional to markers of volemia., Introduction: Chronic mild hyponatremia has been associated with bone demineralization of unknown mechanisms. During chronic hyponatremia, arginine-vasopressin secretion can result from hypovolemia or from syndrome of inappropriate anti-diuresis (SIAD) that leads to a slightly volemic expansion. Since volemia determines renal calcium excretion and balance, we evaluated calcium homeostasis in patients with chronic hyponatremia, related to SIAD or to hypovolemia., Methods: We retrospectively included all patients referred to our Department between May 2006 and May 2014 for hyponatremia, resulting from SIAD or chronic hypovolemia. None had edema, cirrhosis, cardiac, or renal insufficiency. Exploration included estimation of volemia, extracellular fluid volume (ECFV) measurement with inulin, and calcium homeostasis., Results: In total, the SIAD and hypovolemic groups included 22 and 7 patients, respectively. The SIAD group exhibited signs of increased volemia: higher glomerular filtration rate, higher fractional excretion of uric acid, and lower plasma renin. ECFV exceeded that of the hypovolemic group and was above usual values. There was no difference between the two groups regarding plasma calcium, PTH, and vitamin D. However, in the SIAD group, calciuria was higher than in the hypovolemic group, reaching levels of hypercalciuria. Furthermore, there was a positive correlation between calciuria and markers of volemia., Conclusions: Our results show that SIAD results in a volemic expansion tendency that is associated with a decrease in renal calcium reabsorption and thus hypercalciuria, whereas in the hypovolemic group, calciuria was not increased. Therefore, renal loss of calcium and bone demineralization in SIAD patients could be partly induced by volemic expansion.

Objectives: Dilation of the right ventricle during cardiac arrest and resuscitation may be inherent to cardiac arrest rather than being associated with certain causes of arrest such as pulmonary embolism. This study aimed to compare right ventricle diameter during resuscitation from cardiac arrest caused by hypovolemia, hyperkalemia, or primary arrhythmia (i.e., ventricular fibrillation)., Design: Thirty pigs were anesthetized and then randomized to cardiac arrest induced by three diffrent methods. Seven minutes of untreated arrest was followed by resuscitation. Cardiac ultrasonographic images were obtained during induction of cardiac arrest, untreated cardiac arrest, and resuscitation. The right ventricle diameter was measured. Primary endpoint was the right ventricular diameter at the third rhythm analysis., Setting: University hospital animal laboratory., Subjects: Female crossbred Landrace/Yorkshire/Duroc pigs (27-32 kg)., Interventions: Pigs were randomly assigned to cardiac arrest caused by either hypovolemia, hyperkalemia, or primary arrhythmia., Measurements and Main Results: At the third rhythm analysis during resuscitation, the right ventricle diameter was 32 mm (95% CI, 29-35) in the hypovolemia group, 29 mm (95% CI, 26-32) in the hyperkalemia group, and 25 mm (95% CI, 22-28) in the primary arrhythmia group. This was larger than baseline for all groups (p = 0.03). When comparing groups at the third rhythm analysis, the right ventricle was larger for hypovolemia than for primary arrhythmia (p < 0.001)., Conclusions: The right ventricle was dilated during resuscitation from cardiac arrest caused by hypovolemia, hyperkalemia, and primary arrhythmia. These findings indicate that right ventricle dilation may be inherent to cardiac arrest, rather than being associated with certain causes of arrest. This contradicts a widespread clinical assumption that in hypovolemic cardiac arrest, the ventricles are collapsed rather than dilated.

Sodium disorders (ie, hyponatremia, hypernatremia) are common electrolyte disturbances in clinical medicine and are associated with increased rates of morbidity and mortality. Etiologies of hyponatremia are classified into four categories. The first is pseudohyponatremia, in which the sodium level is low due to hyperproteinemia, hyperlipidemia, or hyperglycemia. The other three categories are based on overall patient fluid status and include hypovolemic (commonly due to fluid loss), hypervolemic (commonly due to fluid retention from heart failure, cirrhosis, or renal failure), and euvolemic (most often because of syndrome of inappropriate secretion of antidiuretic hormone). Hypovolemic hyponatremia is managed by rehydration with isotonic saline. Hypervolemic hyponatremia is managed by addressing the underlying cause. Euvolemic hyponatremia is managed by restricting free water intake, addressing the underlying cause, and occasionally with drugs (eg, vasopressin receptor antagonists). Patients with severe or acutely symptomatic hyponatremia (eg, altered mental status, seizures), including those with acute symptomatic exercise-induced hyponatremia, require urgent treatment. This should consist of hypertonic saline administration along with monitoring of sodium levels to avoid overly rapid correction. Hypernatremia most often occurs because of water loss or inadequate water intake. Depending on severity, management involves oral or intravenous hypotonic fluids and addressing the underlying cause., (Written permission from the American Academy of Family Physicians is required for reproduction of this material in whole or in part in any form or medium.)

We present the case of a 85-year-old patient admitted with palpitations and dyspnea. When assuming a recumbent position, we noticed a significant improvement in dyspnea, as well as a rise in arterial oxygen saturation. This is a typical presentation of platypnea-orthodeoxia syndrome (POS). The diagnosis was confirmed by serial analyses of the arterial oxygen saturation in different positions. In our patient, POS was caused by a cardiac right-left shunt through a patent foramen ovale, facilitated by an atrial septal aneurysm, a dilated aortic root and a large Eustachian valve. A low-volume state, caused by diarrhea and worsened by administration of diuretics in the emergency room, triggered the POS to become clinically apparent. We also noticed a rise in arterial oxygen saturation when the patient was in a hypertensive state. This has never been described before and underlines the influence of hemodynamic changes on the right-left shunt that underlies POS.

Orthostatic hypotension, defined by a drop in blood pressure of at least 20mmHg for systolic blood pressure and at least 10mmHg for diastolic blood pressure within 3minutes of standing up, is a frequent finding, particularly in elderly patients. It is associated with a significant increase in morbidity and mortality. Although it is often multifactorial, the first favoring factor is medications. Other etiologies are divided in neurogenic orthostatic hypotension, characterized by autonomic failure due to central or peripheral nervous system disorders, and non-neurogenic orthostatic hypotension, mainly favoured by hypovolemia. Treatment always requires education of the patient regarding triggering situations and physiological countermanoeuvers. Pharmacological treatment may sometimes be necessary and mainly relies on volume expansion by fludrocortisone and/or a vasopressor agents such as midodrine. There is no predefined blood pressure target, the goal of therapy being the relief of symptoms and fall prevention., (Copyright © 2017 Association Société de néphrologie. Published by Elsevier Masson SAS. All rights reserved.)

Background: Epidemiological data on Acute Kidney Injury (AKI) from low-income countries is sparse. The aim of this study was to establish the incidence, severity, aetiology, and outcomes of community-acquired AKI in Malawi., Methods: We conducted a prospective observational study of general medical admissions to a tertiary hospital in Blantyre between 27 th April and 17 th July 2015. All patients were screened on admission with a serum creatinine; those with creatinine above laboratory reference range were managed by the nephrology team. Hospital outcome was recorded in all patients., Results: Eight hundred ninety-two patients were included; 188 (21 · 1%) had kidney disease on admission, including 153 (17 · 2%) with AKI (median age 41 years; 58 · 8% HIV seropositive). 60 · 8% of AKI was stage 3. The primary causes of AKI were sepsis and hypovolaemia in 133 (86 · 9%) cases, most commonly gastroenteritis (n = 29; 19 · 0%) and tuberculosis (n = 18; 11 · 8%). AKI was multifactorial in 117 (76 · 5%) patients; nephrotoxins were implicated in 110 (71 · 9%). Inpatient mortality was 44 · 4% in patients with AKI and 13 · 9% if no kidney disease (p <0.0001). 63 · 2% of patients who recovered kidney function left hospital with persistent kidney injury., Conclusion: AKI incidence is 17 · 2% in medical admissions in Malawi, the majority is severe, and AKI leads to significantly increased in-hospital mortality. The predominant causes are infection and toxin related, both potentially avoidable and treatable relatively simply. Effective interventions are urgently required to reduce preventable young deaths from AKI in this part of the world.

Background: Abdominal compartment syndrome (ACS) sometimes occurs in critically ill patients following damage control surgery. The purpose of the present study was to develop a model of ACS and to evaluate its pathologic impact on liver, kidney, and lung morphology., Methods: Twenty Wistar rats (mass 300-350 g) were randomly divided into four groups: 1) intra-abdominal hypertension (IAH): a laparotomy was performed and the abdomen packed with cotton until an intra-abdominal pressure (IAP) of 15 mm Hg was reached; 2) hypovolemia (HYPO): blood was withdrawn until a mean arterial pressure ~60 mm Hg was reached; 3) IAH + HYPO (to resemble clinical ACS); and 4) sham surgery. After 3 hours of protective mechanical ventilation, the animals were euthanized and the liver, kidney and lungs removed to examine the degree of tissue damage., Results: IAH resulted in the following: oedema and neutrophil infiltration in the kidney; necrosis, congestion, and microsteatosis in the liver; and alveolar collapse, haemorrhage, interstitial oedema, and neutrophil infiltration in the lungs. Furthermore, IAH was associated with greater cell apoptosis in the kidney, liver and lungs compared to sham surgery. HYPO led to oedema and neutrophil infiltration in the kidney. The combination of IAH and HYPO resulted in all the aforementioned changes in lung, kidney and liver tissue, as well as exacerbation of the inflammatory process in the kidney and liver and kidney cell necrosis and apoptosis., Conclusions: Intra-abdominal hypertension by itself is associated with kidney, liver and lung damage; when combined with hypovolemia, it leads to further impairment and organ damage.

Although vasovagal syncope (VVS) is a common clinical condition, the underlying pathophysiology is not fully understood. A decrease in cardiac output has recently been suggested as a factor in orthostatic VVS. The aim was to investigate compensatory mechanisms to maintain central blood volume and venous return during hypovolemic stress in women with VVS. Fourteen VVS women (25.7 ± 5.0 yr) and 15 matched controls (22.8 ± 3.2 yr) were investigated. Single-step and graded lower body negative pressure (LBNP) to presyncope were used to create hypovolemic stress. Peripheral mobilization of venous blood from the arm (capacitance response and net capillary fluid absorption) and lower limb blood pooling (calf capacitance response) were evaluated using a volumetric technique. Cardiovascular responses and plasma norepinephrine (P-NE) were measured. Resting P-NE was elevated in VVS women (P < 0.01). Despite a similar hypovolemic stimulus, the increase in P-NE was blunted (P < 0.01) and the maximal percent increase in total peripheral resistance was reduced (P < 0.05) during graded LBNP in VVS women. The arm capacitance response was slower (P < 0.05) and reduced in VVS women at higher levels of LBNP (P < 0.05). Capillary fluid absorption from extra- to intravascular space was reduced by ∼40% in VVS women (P < 0.05). Accordingly, the reduction in cardiac output was more pronounced (P < 0.05). In conclusion, in VVS women, mobilization of peripheral venous blood and net fluid absorption from tissue to blood during hypovolemic stress were decreased partly as a result of an attenuated vasoconstrictor response. This may seriously impede maintenance of cardiac output during hypovolemic stress and could contribute to the pathogenesis of VVS., (Copyright © 2017 the American Physiological Society.)

Systolic anterior (septal) motion of the mitral valve (SAM) is a common secondary phenomenon in hypertrophic cardiomyopathy (HCM) in people and cats. In humans, it is increasingly recognized that SAM may be found in other cardiac and non-cardiac disease states. In small animal cardiology, SAM unassociated with HCM has been described in dogs with mitral valve dysplasia and right ventricular pressure overload. In this report, we describe two cases of dogs where transient SAM was caused by hypovolemia. When SAM was present both dogs showed pseudohypertrophy and tachycardia. Important factors in the genesis of SAM in this scenario are probably hypovolemia induced changes in left ventricular geometry affecting the orientation of the mitral valve apparatus combined with elevated catecholamine levels. SAM associated with increased wall thickness is not pathognomonic of HCM; this observation is of particular clinical importance when extrapolated to species where HCM is highly prevalent, e.g., cats. An echocardiographic diagnosis should always be evaluated together with full clinical assessment of history and physical examination., (Copyright © 2016. Published by Elsevier B.V.)

Aim: Sheehan's syndrome (SS) remains a frequent cause of hypopituitarism in undeveloped and developing countries, but due to improvements in obstetric care, it is rare in developed countries. We aimed to share the results of a retrospective study analyzing the demographic, clinical, imaging, and hormonal characteristics of a large group of patients with SS, and also increase awareness of this syndrome especially in developed countries., Methods: The medical records of 124 patients with SS patients who were followed up in the Endocrinology Department of Dicle University between 1995 and 2015 were assessed retrospectively., Results: The mean period of diagnostic delay was 20.37 ± 8.34 years on average. 5.7% of patients with SS were literate; 62% of patients delivered at home. Anemia was identified in 64.5% of SS patients. Mean blood sodium levels were 129.8 ± 11.3 mEq/L. The mean urine densities were 1013 ± 6.5. Osteoporosis and osteopenia were found in 44 (35.4%) and 71 (57.2%) patients, respectively, According to pituitary magnetic resonance imaging (MRI) analyses, 92 (74.2%) patients with SS had completely empty sella, 29 (23.3%) had partially empty sella, and 1 patient had microadenoma, and 2 had normal pituitary MRI results., Conclusions: Improved obstetric care and effective interventions for postpartum hemorrhage have limited the prevalence of SS in developed countries. However, in developing countries like Turkey, SS due to postpartum bleeding remains common. Thus, physician's awareness of the symptoms of SS is urgently required to avoid the associated morbidity and mortality.

Intact cerebral blood flow (CBF) is essential for cerebral metabolism and function, whereas hypoperfusion in relation to hypovolemia and hypocapnia can lead to severe cerebral damage. This study was designed to assess internal carotid artery blood flow (ICA-BF) during simulated hypovolemia and noninvasive positive pressure ventilation (PPV) in young healthy humans. Beat-by-beat blood velocity (ICA and aorta) were measured by Doppler ultrasound during normovolemia and simulated hypovolemia (lower body negative pressure), with or without PPV in 15 awake subjects. Heart rate, plethysmographic finger arterial pressure, respiratory frequency, and end-tidal CO 2 (ETCO 2 ) were also recorded. Cardiac index (CI) and ICA-BF were calculated beat-by-beat. Medians and 95% confidence intervals and Wilcoxon signed rank test for paired samples were used to test the difference between conditions. Effects on ICA-BF were modeled by linear mixed-effects regression analysis. During spontaneous breathing, ICA-BF was reduced from normovolemia (247, 202-284 mL/min) to hypovolemia (218, 194-271 mL/min). During combined PPV and hypovolemia, ICA-BF decreased by 15% (200, 152-231 mL/min, P = 0.001). Regression analysis attributed this fall to concurrent reductions in CI (β: 43.2, SE: 17.1, P = 0.013) and ETCO 2 (β: 32.8, SE: 9.3, P = 0.001). Mean arterial pressure was maintained and did not contribute to ICA-BF variance. In healthy awake subjects, ICA-BF was significantly reduced during simulated hypovolemia combined with noninvasive PPV Reductions in CI and ETCO 2 had additive effects on ICA-BF reduction. In hypovolemic patients, even low-pressure noninvasive ventilation may cause clinically relevant reductions in CBF, despite maintained arterial blood pressure., (© 2016 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.)

Background: The first government funded and sustainable dialysis unit was established in Ethiopia at Saint Paul's Hospital Millennium Medical College (SPHMMC). This has led to the development of a unique cohort of patients about which very little is known. This study was conducted to describe the clinical profile and outcome of adult Acute Kidney Injury (AKI) patients treated with intermittent haemodialysis at the dialysis center of SPHMMC., Methods: A retrospective review of clinical records of cases of AKI who required haemodialysis support during the time period from August 1, 2013 to February 1, 2015 was conducted., Results: A total of 151 cases AKI requiring dialysis were included for the study. Overall, the patients were generally younger with a mean age of 36.7 years and thus with few premorbid conditions. The most common causes of AKI were hypovolemia (22.5 %), acute glomerulonephritis (AGN) (21.9 %) and pregnancy related causes (18.5 %). Nearly a third (29.1 %) of patients succumbed to the AKI., Conclusion: Infections, AGN, obstetric causes and nephrotoxins were the primary causes of dialysis requiring AKI. Most of these causes can be prevented with simple interventions such as health education on oral rehydration, quality prenatal and emergency obstetric care, appropriate management of infections and taking appropriate precautions when prescribing potentially nephrotoxic medications.