Acute Hyponatremia Research Articles

Death from Acute Hyponatremia Following Uneventful Abdominal Hysterectomy: Lessons from a Case Report

Death from Acute Hyponatremia Following Uneventful Abdominal Hysterectomy: Lessons from a Case Report

Mysterious disease porphyria: challenge of diagnosis. Analysis of the clinical case of porphyric polyneuropathy

Brief overview represents the description of the relationship between the clinical picture of porphyria and the description of vampires in the literature. Porphyria is a group of hereditary diseases caused by disorders of heme synthesis, with an increase in the level of its precursors in the blood and urine. The most characteristic description of vampires in the literature are the clinical manifestations of congenital erythropoietic porphyria. The most frequent and severe form of porphyria is an acute intermittent porphyria. The triad of seizures, acute abdominal pain and hyponatremia in young women are clear evidence of the disease. During an acute attack most patients can experience various psychiatric disorders. The dangerous complication of porphyria is the development of motor axonal or axonal‑demyelinating polyneuropathy. A definite marker of acute porphyria attacks is the urine excretion of various shades of red color. The actual mechanisms of damage to nervous system tissue are poorly understood, focal lesion of the brain in porphyria is not specific. Laboratory confirmation of porphyria is elevated urinary excretion of aminolevulinic acid, porphobilinogen, uroporphyrin and coproporphyrin. In the article the clinical presentation of a patient with porphyric polyneuropathy is described with the following one‑year dynamic observation. Management of acute attack with intravenous heme, increased glucose supplementation in the acute period of the disease, followed by physical rehabilitation of the patient in the recovery period, will help restore lost functions. However, the main idea is to explain to a patient what drugs are porphyrinogenic and necessity to change his life style.

Plasma electrolyte imbalance in pediatric kidney transplant recipients.

In current practice, pediatric kidney transplant recipients receive large volumes of intravenous fluid intraoperatively to establish allograft perfusion, and further fluid to replace urinary and insensible losses postoperatively. Acute electrolyte imbalance can result, with potential for neurological sequelae. We aimed to determine the incidence and severity of postoperative plasma electrolyte imbalance in pediatric kidney transplant recipients managed with the current standard intravenous crystalloid regimen. A retrospective analysis of plasma electrolytes in the first 72hours post-kidney transplant in 76 children transplanted between January 1, 2015, and January 31, 2018, managed with a standard intravenous fluid strategy used in most UK pediatric transplant centers. Of 76 pediatric transplant recipients of median age 9.9 (range 2.2-17.9) years predominantly managed with 0.45% sodium chloride 5% glucose, 45 (59%) developed acute hyponatremia, 23 (30%) hyperkalemia, and 43 (57%) non-anion-gap acidosis in the postoperative period. Hyperglycemia occurred in 74 (97%) patients. Hyperkalemia was more prevalent in deceased than live donor recipients (P=0.003) and was significantly associated with non-anion-gap acidosis (P<0.001). Recipient weight was not associated with overt electrolyte imbalance. Postoperative plasma electrolyte imbalance is common in pediatric kidney transplant recipients. Current clinical care strategies mitigate the associated risks of neurological sequelae to some degree. Further studies to optimize intravenous fluid therapy and minimize electrolyte disturbance in this group of patients are needed.

A case of cocaine-induced acute symptomatic hyponatraemia

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Delirium in elderly patients undergoing chemotherapy for solid cancers and lymphoma

Introduction: Prevalence and risk factors for delirium in geriatric oncology patients is not well described. Aim: To determine the prevalence and factors associated with delirium in elderly patients undergoing chemotherapy for solid cancers. Methods: We reviewed medical records of patients with cancer aged ≥65 years who were admitted in 2015 with “delirium”, “encephalopathy”, “confusion”, or “altered mental status” within 30 days of chemotherapy for solid cancers and lymphoma. Descriptive and matched pair statistics were used to compare demographics, chemotherapy, medications, comorbidities, and laboratory data between the patients with clinical diagnosis of delirium and their controls matched by age, gender, and cancer diagnosis. Results: One hundred and twenty three patients were hospitalized in an academic comprehensive cancer center. Median (range) age was 71 (65 to 89). 60% were women. Most common cancers (%) were gastrointestinal (25), lymphoma (20), genitourinary (18), pulmonary (15) and breast (12). The most common admissions were for chemotherapy (22%) and infection (21%). 64% were treated with chemotherapy, 24% with chemo and immunotherapy, and 12% with immunotherapy only. A total of 43% received 2 anticancer agents, 32% one, and 18% three agents. Charted delirium prevalence was 7.3% (N=9/123). Five were men. Compared to matched controls, patients in whom delirium was recognized were more likely to have elevated BUNs, acute kidney injury (AKI) and hyponatremia. Conclusions: Delirium was infrequently documented in our cohort of elderly patients admitted for inpatient care following chemotherapy. Elevated BUN, AKI and hyponatremia were significantly associated with the clinical diagnosis and documentation of delirium.

Retracted: Marathon Runner with Acute Hyponatremia: A Neurological Disorder.

[This retracts the article DOI: 10.1155/2012/342760.].

Generalized Seizure Due To Acute Hyperosmolar Hyponatremıa Followıng Coronary Angıography: A Lesson Learned From A Case Report

Hyponatremia is a common electrolyte disorder, but symptomatic hyponatremia following coronary angiography is rare. Although patients with hyponatremia are generally asymptomatic, neurological manifestations may result in lethal complications. Here we presented a 69-year-old female, admitted for elective coronary angiography due to exertional chest pain. Seven hours later after coronary angiography, however, the patient had a headache, temporary mental confusion and her speech was slurring. A brain magnetic resonance imaging (MRI) test, arterial blood gas analysis, and the neurological examination were carried out. The neurological examination showed no focality and brain diffusion MRI was normal. Arterial blood gas analysis revealed sodium of 110 mmol/L and potassium of2.8 mmol/L. The patient was treated with hypertonic saline (3% NaCl) and vasopressin antagonist tolvaptan 15 mg at first and isotonic saline (0,09 NaCl) with a gradual normalization of electrolytes. Diagnosis of acute hyperosmolar hyponatremia should be considered in patients with developing mental or behavioral abnormalities following coronary angiography.

Higher Diuretic Requirements in Acute Heart Failure With Admission Hyponatraemia Versus Normonatraemia

BackgroundDiuretic requirements in patients with acute decompensated heart failure (ADHF) and hyponatraemia versus normonatraemia on admission has not been previously explored. MethodsThe Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) trial dataset was utilised to examine the characteristics and diuretic requirements of patients with ADHF with hyponatraemia or normonatraemia on admission. ResultsPatients with ADHF and admission hyponatraemia (n = 103, average Na 130.2 meq/L) had a higher degree of congestion evident in higher frequency of jugular venous distension (JVD) >12 cmH2O (p = 0.007), 2+ lower extremity oedema (p = 0.001), and higher right atrial pressure (p = 0.007), compared with normonatraemic patients (n = 327, average Na 138.6 meq/L). Despite a similar baseline furosemide dose in both groups (median 200 mg), the hyponatraemia group received higher in-hospital furosemide (280 vs. 200 mg, in both groups, respectively, p < 0.001) which represented a higher percentage of furosemide utilisation relative to baseline, compared with the normonatraemia group (33% vs 0%, in both groups respectively, p = 0.007). With in-hospital diuresis, the Na level of hyponatraemic subjects started significantly increasing at discharge and up to 6 months after randomisation—all relative to baseline. Hyponatraemic patients had significantly lower systolic blood pressure (SBP) longitudinally at multiple time points compared with normonataremic patients, but it did not further decrease despite the higher furosemide dose in the former group. ConclusionPatients with ADHF and hyponatraemia on admission had a higher degree of congestion and required higher doses of furosemide, compared with normonatraemic subjects. The lower Na and SBP in this instance should not lead to withholding or minimising diuretic dosage which should rather be dictated by volume status.

Hyponatremia in Neurosurgical Patients.

Hyponatremia is a frequent occurrence in patients with neurosurgical disorders. Acute onset hyponatremia is particularly common in patients who have any type of cerebral insult, including traumatic brain injury, subarachnoid hemorrhage, and brain tumors. Furthermore, it is a common complication of intracranial procedures. Acute hyponatremia creates an osmotic gradient between the brain and the plasma, which promotes the movement of water from the plasma into brain cells, causing cerebral edema and neurological compromise. It is therefore far more likely to be symptomatic, and to have adverse outcomes, than chronic hyponatremia. Uncorrected acute hyponatremia with consequent cerebral edema may manifest through impaired consciousness level, seizures, elevated intracranial pressure, and, potentially, death due to cerebral herniation. The majority of cases of hyponatremia due to neurosurgical pathology are caused by the syndrome of inappropriate antidiuresis, but acute glucocorticoid insufficiency is increasingly being recognized as an important contributing factor. In this chapter, we summarize the existing literature on the clinical features and differential diagnosis of hyponatremia in the neurosurgical patient, and briefly discuss the management options.

Severe Persistent Hyponatremia: A Rare Presentation of Biliary Fluid Loss

Hypotonic hyponatremia is caused by a serum sodium level of <135 mEq/L in the setting of excess solute loss accompanied by free water retention because of antidiuretic hormone release, subsequent to decreased effective arterial blood volume. Acute hyponatremia can have various neurological manifestations, including drowsiness, lethargy, coma, seizures, respiratory depression, and even death. In this article, we present a case of a 41-year-old man who presented with hyponatremia as a result of sodium containing biliary fluid loss and resultant renal free water retention in response to increased antidiuretic hormone secretion. He underwent placement of a cholecystostomy tube for acalculous cholecystitis and was found to be persistently hyponatremic despite repletion with sodium-containing fluids. Once the cholecystostomy tube was removed, the patient’s sodium levels improved, and his symptoms resolved. Our case highlights choleuresis as an unusual but significant cause of hyponatremia in patients who have external biliary drainage.

Hyponatremia: A clinician's perspective

Hyponatremia is a commonly encountered clinical problem by all physicians. It is classified according to volume status as hypovolemic, euvolemic, or hypervolemic hyponatremia. The clinical presentation depends on the type of hyponatremia and the speed of onset. Acute hyponatremias can result in altered sensorium, convulsions, and coma, making it a medical emergency. Chronic hyponatremias can be due to drugs and several systemic illnesses. The syndrome of inappropriate secretion of antidiuretic hormone is common and can occur in several diseases as euvolemic hyponatremia. Its onset can be deceptively slow but needs attention to prevent complications. Investigations of serum and urine, osmolality and sodium, help in classification of this condition. Apart from intravenous correction with hypertonic saline, which may be urgently needed in acute hyponatremia to prevent mortality, vaptans offer an oral option in chronic hyponatremia. Care must be taken to avoid rapid correction of serum sodium, to prevent osmotic demyelination syndrome.

Morbidity and Mortality of Hyponatremia.

In hypotonic hyponatremia, which is the most common form of hyponatremia, clinical manifestations are largely due to brain swelling caused by entry of water into the cells. In acute and severe hyponatremia, dramatic symptoms, such as seizures, acute psychosis, permanent brain damage, brain-stem herniation, leading to coma and death may occur. In chronic hyponatremia, symptoms are generally less dramatic and may include headache, nausea, vomiting, gait alterations, muscle cramps, restlessness, and disorientation. It has become evident in recent years that mild forms of chronic hyponatremia may also be associated with clinical signs, if carefully investigated. Several studies also reported an increased length of stay in the hospital of patients with hyponatremia in different clinical settings, leading to increased costs. Most important, this condition has been clearly associated with a significantly increased risk of death, even when serum [Na+] is slightly reduced. On the contrary, there is convincing evidence that the mortality risk is reduced when hyponatremia improves.

Safety and Efficacy of Venetoclax Combined with Rituximab, Ifosfamide, Carboplatin and Etoposide Chemoimmunotherapy (VICER) for Treatment of Relapsed Diffuse Large B Cell Lymphoma: Results from the Phase 1 Study

Safety and Efficacy of Venetoclax Combined with Rituximab, Ifosfamide, Carboplatin and Etoposide Chemoimmunotherapy (VICER) for Treatment of Relapsed Diffuse Large B Cell Lymphoma: Results from the Phase 1 Study

Successful Use of Fludrocortisone in a Child with Refractory Cerebral Salt Wasting Syndrome: A Case Report and Review of Literature

Hyponatremia post-neurosurgical intervention can be dangerous and potentially life-threatening. Two of its most common causes are cerebral salt wasting (CSW) and syndrome of inappropriate anti-diuretic hormone release (SIADH). CSW is proposed to be secondary not only to the elevated levels of circulating atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) but inhibition of steroidogenesis in the zona glomerulosa of the adrenal cortex, thus resulting in mineralocorticoid deficiency. We present a two-year-old male who had developed acute hyponatremia secondary to CSW on post-operative day two after a sub-total resection of a low-grade juvenile pilocytic astrocytoma (WHO grade I). Fludrocortisone was successfully used to manage the refractory hyponatremia and alleviated the need to use very large amounts of oral sodium supplementation.

A swine model of intracellular cerebral edema – Cerebral physiology and intracranial compliance

Cerebral edema leading to elevated intracranial pressure (ICP) is a fundamental concern after severe traumatic brain injury (TBI), stroke, and severe acute hyponatremia. We describe a swine model of water intoxication and its cerebral histological and physiological sequela. We studied female swine weighing 35–45 kg. Four serum sodium intervals were designated: baseline, mild, moderate, and severe hyponatremia attained by infusing hypotonic saline. Intracranial fluid injections were performed to assess intracranial compliance. At baseline and following water intoxication wedge biopsy was obtained for pathological examination and electron microscopy. We studied 8 swine and found an increase in ICP that was strongly related to the decrease in serum sodium level. Mean ICP rose from a baseline of 6 ± 2 to 28 ± 6 mm Hg during severe hyponatremia, while cerebral perfusion pressure (CPP) decreased from 72 ± 10 to 46 ± 11 mm Hg. Brain tissue oxygen tension (PbtO2) decreased from 18.4 ± 8.9 to 5.3 ± 3.0 mm Hg. Electron microscopy demonstrated intracellular edema and astrocytic foot process swelling following water intoxication. With severe hyponatremia, 2 cc intracranial fluid injection resulted in progressively greater ICP dose, indicating a worsening intracranial compliance. Our model leads to graded and sustained elevation of ICP, lower CPP, and decreased PbtO2, all of which cross clinically relevant thresholds. Intracranial compliance worsens with increased cerebral swelling. This model may serve as a platform to study which therapeutic interventions best improve the cerebral physiological profile in the face of severe brain edema.

Effects of gene polymorphisms on the risk of severe hyponatremia during DCF chemotherapy for patients with esophageal squamous cell carcinoma.

Combination chemotherapy using docetaxel, cisplatin and 5-fluorouracil (DCF) is a promising treatment option for patients with advanced esophageal squamous cell carcinoma (ESCC), although its clinical application is limited by severe systemic toxicities. There are no validated markers for predicting the adverse effects caused by this regimen. This pharmacogenetic study enrolled 57 patients with chemotherapy-naive advanced ESCC between July 2012 and March 2016 (UMIN000008462). All patients received at least one course of DCF chemotherapy (docetaxel, 60 mg/m2 on day 1; cisplatin, 70 mg/m2 on day 1; 5-fluorouracil, 600 mg/m2 on days 1-5). The associations between four gene polymorphisms (ERCC1 rs11615, GSTP1 rs1695, TYMS rs151264360 and XPD rs13181) and the development of grade 3/4 adverse events during the first course of chemotherapy were prospectively investigated. The patients had a median age of 66 years (range, 45-77 years) and the majority were male (51 males vs. 6 females). The treatment settings were neoadjuvant (47 patients), adjuvant (1 patient) and salvage (9 patients), with dose intensities of 100% (51 patients) or 80% (6 patients). The severe adverse events were leukopenia (70.2%), neutropenia (86.0%), febrile neutropenia (36.8%), acute kidney injury (29.1%) and hyponatremia (43.9%). Two polymorphisms were independently associated with the development of severe hyponatremia among patients carrying the minor allele (vs. patients with major homozygote genotype): TYMS 3'-UTR rs151264360 (odds ratio, 3.64; 95% confidence interval, 1.11-11.9) and XPD Lys751Gln rs13181 (odds ratio, 10.1; 95% confidence interval, 1.10-93.3). Therefore, the presence of the TYMS and XPD polymorphisms may aid in identifying patients with a high risk of developing severe hyponatremia during DCF chemotherapy.

NSAIDS related hyponatremia in brain injury patients: A silent factor for their deterioration

Hyponatremia is the most common disorder of electrolytes encountered in clinical practice, occurring in 22% of hospitalized patients. Acute severe hyponatremia can cause severe morbidity and mortality. Adverse outcomes are higher in hyponatremic patients with a wide range of underlying conditions. There are different causes of hyponatremia but NSAID's used commonly in brain injury patients for managing pain can result in hyponatremia leading to complications such as lethargy, confusion, dizziness, gait disturbances, muscle cramps, seizures, coma and even death. Too rapid correction of hyponatremia in these patients can also lead to life threatening complications. A case study was conducted on a brain injury inpatient who suffered from hyponatremia in our unit secondary from NSAID's which were started for her arthritis. Patient responded to the treatment initially very well but later on showed quick decline in her clinical status with varying signs and symptoms ranging from confusion, lethargy, speech and swallowing decline as well as seizures and gait disturbance. Her blood tests showed gradual hyponatremia and this was co-related exactly with the time of starting NSAID's. Patient responded slowly but very well with stopping NSAID's and treating with fluid restriction for a time being although the clinical decline remained there for sometime. Avoid the use of NSAID's in brain injury patients as their use can cause significant hyponatremia, which could result in life threatening complications. Even the rapid correction of this hyponatremia can be too dangerous or fatal. NSAIDs related Hyponatremia in Brain Injury patients has been proven as a silent factor for their deterioration and thus needs careful monitoring and treatment.

Histidine-Tryptophan-Ketoglutarate Solution versus Blood Cardioplegia in Cardiac Surgery: A Propensity-Score Matched Analysis.

Choosing a cardioplegic solution is a significant issue in modern cardiac surgery. Although different options are available, the optimal strategy for myocardial protection has not been established. The aim of this study was to compare intraoperative and postoperative effects of histidine-tryptophan-ketoglutarate (HTK) solution with those of standard blood cardioplegia with St Thomas No 2 solution. The study was conducted using a large cohort of adult patients undergoing complex cardiac surgery. This study was a single center retrospective review of prospectively collected data. Between January 2008 and December 2015, 4480 patients underwent cardiac surgery using cardiopulmonary bypass (CPB) and cardioplegic arrest. Patients were divided into a blood cardioplegia group (n = 3852) and an HTK solution group (n = 628). Propensity score matching was used to adjust for differences between the two groups, and 292 matched pairs were identified. The primary end point was Intensive Care Unit (ICU) length of stay (LOS). Secondary end points included intraoperative changes in serum sodium concentration, readmission to ICU, transfusion of blood products, 30-day hospital readmission, 30-day mortality, and the incidence of major postoperative complications.Results: No significant differences were found between the matched groups with regard to baseline characteristics. Aortic cross-clamp and CPB times were longer for the blood cardioplegia (147.4 versus 132.8 min; P < .001). Administration of HTK solution was associated with acute and transient hyponatremia (141 versus 130 mmol/L; P < .001). ICU LOS was comparable between the groups (5.4 versus 5.4 days; P = .585). No significant differences were noted in any other secondary end point. During complex cardiac surgery, both cardioplegia techniques were equivalent in terms of early clinical outcomes.

Acute hyponatraemia complicating therapy of acute hepatic porphyria need immediate correction before become symptomatic: a case report

Acute hyponatraemia complicating therapy of acute hepatic porphyria need immediate correction before become symptomatic: a case report

Iatrogenic Takotsubo Cardiomyopathy Secondary to Norepinephrine by Continuous Infusion for Shock.

Takotsubo cardiomyopathy is a condition characterized by transient left ventricular systolic and diastolic dysfunction, with a possible direct causal role of catecholamine in its pathophysiology. We present a case of a woman with shock and adrenal insufficiency in whom Takotsubo cardiomyopathy developed after treatment with norepinephrine. This case confirms the direct causal role of catecholamine in the pathophysiology of Takotsubo cardiomyopathy. An 82-year-old woman presented with asthenia, anorexia, nausea and abdominal pain. The patient had been on chronic corticosteroid therapy until 3 months before, when she underwent abdominal surgery and corticosteroids were stopped. She now presented with acute kidney injury, hyponatremia and hyperkalemia and shock. A norepinephrine continuous infusion was administered to maintain a mean arterial pressure over 65 mmHg. An echocardiogram showed severe hypokinesis in the apical segments and hyperdynamic basal segments, with an ejection fraction of 25%. Plasma cortisol level was 4.5 μg/dL (reference range 5–25). Corticosteroid therapy was begun and norepinephrine was tapered and stopped. A new echocardiogram showed normalization of cardiac wall motion and an ejection fraction of 70%. This case highlights the importance of the correction of the cause of shock, as well as the risks associated with the use of norepinephrine if hypotension is severe or if it persists despite fluid administration, as usually recommended. It also confirms the direct causal role of catecholamine in the pathophysiology of Takotsubo cardiomyopathy. To the best of our knowledge, this is the first report of stress-induced cardiomyopathy secondary to norepinephrine by continuous infusion for shock.LEARNING POINTSTakotsubo cardiomyopathy is a condition characterized by transient left ventricular dysfunction of the apex and midventricle in the absence of attributable coronary artery disease.In patients with shock and adrenal insufficiency, who can be erroneously interpreted as septic shock, Takotsubo cardiomyopathy can develop after treatment with norepinephrine.In the management of shock, there are risks associated with recommending the use of norepinephrine if hypotension is severe or if it persists despite fluid administration, when the cause of shock is other than septic shock and is not corrected.There is a direct causal role of catecholamine in the pathophysiology of Takotsubo cardiomyopathy.