Severe Hypernatremia Research Articles

An unusual case of central diabetes insipidus & hyperglycemic hyperosmolar state following cardiorespiratory arrest

BackgroundWe are describing an unusual case of severe hyperglycemia and hypernatremia, resistant to treatment.Case presentationA thirty year old female with adenocarcinoma of rectum was admitted with increasing lethargy, headache and drowsiness. She deteriorated rapidly and had cardiac arrest, following which she remained comatose. Her initial serum glucose and sodium were normal, but after receiving dexamethasone and mannitol, the serum glucose progressively increased to 54.7 mmol/L and sodium to 175 mmol/L, despite receiving very high dose of intravenous (IV) insulin infusion. She was evaluated for diabetes insipidus because of continued polyuria even after correction of hyperglycemia. Her serum osmolality was 337 mmol/kg, and urine osmolality was 141 mmol/kg which rose to 382 mmol/kg, after receiving 4 mcg of IV Desmopressin.ConclusionOur patient developed central diabetes insipidus post cardiac arrest and severe dehydration because of diabetes insipidus. Stress of critical illness, dehydration, dexamethasone and IV dextrose infusion were likely responsible for this degree of severe and resistant to treatment hyperglycemia.

RETRACTED

Squirrel monkeys (Saimiri spp) are one of the most consistently used New World primates in biomedical research and are increasingly being used in neuroscience research, including models of drug abuse and addiction. Spontaneous neurologic disease in the squirrel monkey is uncommonly reported but includes various infectious diseases as well as cerebral amyloidosis. Hypernatremia is an extremely serious condition of hyperosmolarity that occurs as a result of water loss, adipsia, or excess sodium intake. Neurologic effects of hypernatremia reflect the cellular dehydration produced by the shift of water from the intracellular fluid space into the hypertonic extracellular fluid space. Severe hypernatremia may result in cerebrocortical laminar necrosis (polioencephalomalacia) in human patients as well as in a number of domestic species, including pigs, poultry, and ruminants. We report the clinical, histopathologic, and immunohistochemical findings of polioencephalomalacia in 13 squirrel monkeys. Polioencephalomalacia in these animals was associated with hypernatremia that was confirmed by serum levels of sodium greater than 180 mmol/L (reference range, 134.0-154.0 mmol/L [mEq/L]). All animals had concurrent diseases or experimental manipulation that predisposed to adipsia. Immunohistochemical investigation using antibodies to neuronal nuclei (NeuN), CNPase, Iba-1, and CD31 revealed necrosis of predominantly cerebral cortical layers 3, 4, and 5 characterized by neuronal degeneration and loss, oligodendrocytic loss, microglial proliferation, and vascular reactivity. The squirrel monkey is exquisitely sensitive to hyperosmolar metabolic disruption and it is associated with laminar cortical necrosis.

Survival of Acute Hypernatremia Due to Massive Soy Sauce Ingestion

BackgroundIntentional massive sodium chloride ingestions are rare occurrences and are often fatal. ObjectivesThere are a variety of treatment recommendations for hypernatremia, ranging from dialysis to varying rates of correction. We report a case of acute severe hypernatremia corrected with rapid free-water infusions that, to our knowledge, has not been previously reported. Case ReportA 19-year-old man presented to the Emergency Department in a comatose state with seizure-like activity 2 hours after ingesting a quart of soy sauce. He was administered 6 L of free water over 30 min and survived neurologically intact without clinical sequelae. Corrected for hyperglycemia, the patient's peak serum sodium was 196 mmol/L, which, to our knowledge, is the highest documented level in an adult patient to survive an acute sodium ingestion without neurologic deficits. ConclusionEmergency physicians should consider rapidly lowering serum sodium with hypotonic intravenous fluids as a potential management strategy for acute severe hypernatremia secondary to massive salt ingestion.

Acute kidney injury after acute gastroenteritis in an infant with hereditary hypouricemia

Hereditary hypouricemia is a rare disorder characterized by extremely low serum uric acid levels caused by excessive urinary excretion due to an inherited tubular defect in urate handling. Exercise-induced acute kidney injury (AKI) is the main complication of this disorder, though AKI may also be induced by other factors. A 7-month-old boy with hereditary hypouricemia developed AKI associated with severe dehydration caused by rotavirus gastroenteritis. He also showed severe hypernatremia and metabolic acidosis and received continuous renal replacement therapy for 3 days. He showed no signs of hydronephrosis or urolithiasis. However, hypouricemia was noted when his renal function recovered (serum uric acid <0.6 mg/dl). Analysis of the urate transporter 1 gene revealed a homozygous nonsense mutation in exon 4 (c.774G > A, p.W258X). Both parents were heterozygous for the mutation and his younger brother was later determined to have severe hypouricemia (0.6 mg/dl). Uric acid is an essential factor for scavenging oxidative stressors. In this patient, severe dehydration may have directly caused pre-renal AKI, but susceptibility to oxidative stressors under severe dehydration, as well as exercise, may also contribute to AKI. Careful attention should be paid to dehydration, especially in young children, to avoid the development of AKI in patients with hereditary hypouricemia.

Severe hypernatremia and hyperchloremia in an elderly patient with IgG-kappa-type multiple myeloma

A 77-year-old male was admitted to hospital after suffering a pelvic bone fracture in a road traffic accident and was incidentally found to have IgG-kappa-type multiple myeloma with hypercalcemia. The patient was also noted to be hypokalemic and had low HCO3−, with possible damage to the distal tubules in the kidneys. When the treatment was begun with bortezomib/dexamethasone/elcatonin and sodium bicarbonate (NaHCO3) in normal saline (equivalent to a daily sodium dose of 200 millimoles per liter [mmol/L]), the patient was in a state of poor oral fluid intake. The patient developed hypernatremia and hyperchloremia, with a peak serum sodium and chloride levels of 183 mmol/L and 153 mmol/L, respectively, at the sixth day after the start of treatment. Following the switch of the intravenous infusions from normal saline to soldem 1 and soldem 3 solutions, these high-electrolyte levels gradually returned to normal over the next 7 days. Although the patient showed disturbed consciousness (Japan Coma Scale = JCS-I-3) during the period of electrolyte abnormality, he eventually fully recovered without sequelae. In this patient, we successfully managed the severe hypernatremia/hyperchloremia, caused by the combined effects of intravenous saline burden in a state of poor oral fluid intake, during the treatment for IgG-kappa type multiple myeloma.

A Case of Severe Hypernatremic Myopathy by Primary Hypodipsia, Hyperglycemic Hypertonic State in a 17-Year-Old Patient With Mental Retardation

Although severe hypernatremia, defined as a sodium concentration > 180 mEq / L, is associated with a high mortality rate, particularly in adults, little is known about severe hypernatremia in patients with diabetic ketoacidosis (DKA). Hypernatremic myopathy has been reported in patients with severe dehydration, acute kidney injury, and rhabdomyolysis. Dehydration in a diabetic patient with mental retardation may be caused by osmotic diuresis and exacerbated by hypodipsia, which requires the patient to be educated about regular oral hydration. Here, we describe a 17-year-old patient with reversible severe hypernatremia (serum corrected sodium, 180 mEq / L) and primary hypodipsia, but without DKA. The patient visited the emergency room due to agitation and weakness in both lower extremities. Initial laboratory tests showed hyperglycemia, acute kidney injury, acute hepatitis, and myopathy. Following rehydration with one-quarter isotonic saline and intensive insulin therapy, the patient ’ s symptoms (including leg weaknesses) and laboratory findings improved. doi: http://dx.doi.org/10.4021/jmc1136w

Salt Poisoning as a Cause of Morbidity and Mortality in Neonatal Dairy Calves

Salt Poisoning as a Cause of Morbidity and Mortality in Neonatal Dairy Calves

Severe neonatal hypernatraemia: a population based study

AimsTo describe incidence, presentation, treatment and short term outcomes of severe neonatal hypernatraemia (SNH, sodium ≥160 mmol/l).MethodsProspective, population based surveillance study over 13 months using the British Paediatric Surveillance Unit....

Severe Hypernatremia From a Urea-Induced Diuresis due to Body Protein Wasting in an Insulin-Resistant Type 2 Diabetic Patient

Hypernatremia is encountered after pituitary or hypothalamic surgery and typically is secondary to vasopressin deficiency resulting in increased free water clearance with inadequate water replacement. We report a type 2 diabetic patient with severe hypernatremia (Na⁺ = 161 mEq/L) after hypothalamic surgery. Unexpectedly, this was accompanied by persistent urinary hypertonicity and negative total but positive electrolyte free water clearance. Measurement of urinary electrolytes and urea revealed that an osmotic diuresis induced by urea derived principally by breakdown of endogenous protein was causative. Body protein losses over 48 hours were estimated to exceed 2 kg of lean mass. High-dose glucocorticoid, insulin resistance, and a postsurgical catabolic stress likely contributed. In surgically severely stressed individuals, proteolysis of endogenous protein can strongly impact body water metabolism and contribute to severe hypernatremia.

Radiological remission and recovery of thirst appreciation after infliximab therapy in adipsic diabetes insipidus secondary to neurosarcoidosis

Neurosarcoidosis is a rare and aggressive variant of systemic sarcoidosis which may result in hypothalamic-pituitary dysfunction. We report a case of hypothalamic hypopituitarism secondary to neurosarcoidosis complicated by adipsic diabetes insipidus (ADI). Initiation of anti-tumour necrosis factor-α (TNF-α) therapy resulted in both radiological disease remission and recovery of osmoregulated thirst appreciation after 3 months. A 22-year-old man was referred to the endocrinology service with profound weight gain, polyuria and lethargy. Biochemical testing confirmed anterior hypopituitarism while posterior pituitary failure was confirmed by hypotonic polyuria responding to desmopressin. Magnetic resonance imaging (MRI) demonstrated extensive hypothalamic infiltration; neurosarcoidosis was confirmed histologically after excisional cervical lymph node biopsy. Osmoregulated thirst appreciation was normal early in the disease course despite severe hypotonic polyuria. However, subsequent subjective loss of thirst appreciation and development of severe hypernatraemia in the setting of normal cognitive function indicated onset of ADI. Clinical management involved daily weighing, regular plasma sodium measurement, fixed daily fluid intake and oral desmopressin. We initiated immunosuppressive therapy with pulsed intravenous anti-TNF-α therapy (infliximab) after multidisciplinary team consultation. Infliximab therapy resulted in successful radiological disease remission and complete recovery of osmoregulated thirst appreciation. This was confirmed by subjective return of thirst response and maintenance of plasma sodium in the normal range in the absence of close biochemical monitoring.

Hypernatremia Is Associated with Increased Risk of Mortality in Pediatric Severe Traumatic Brain Injury

Acquired hypernatremia in hospitalized patients is often associated with poorer outcomes. Our aim was to evaluate the relationship between acquired hypernatremia and outcome in children with severe traumatic brain injury (sTBI). We performed a retrospective cohort study of all severely injured trauma patients (Injury Severity Score ≥12) with sTBI (Glasgow Coma Scale [GCS] ≤8 and Maximum Abbreviated Injury Scale [MAIS] ≥4) admitted to a Pediatric Critical Care Unit ([PCCU]; 2000-2009). In a cohort of 165 patients, 76% had normonatremia (135-150 mmol/L), 18% had hypernatremia (151-160 mmol/L), and 6% had severe hypernatremia (>160 mmol/L). The groups were similar except for lower GCS (p=0.002) and increased incidence of fixed pupil(s) on admission in both hypernatremia groups (p<0.001). Mortality rate was four-fold and six-fold greater with hypernatremia and severe hypernatremia, respectively (p<0.001), and mortality rates were unchanged when patients with fixed pupils or those with central diabetes insipidus were excluded (p<0.001). Hypernatremic patients had fewer ventilator-free days (p<0.001). Survivors with hypernatremia had greater PCCU (p=0.001) and hospital (p=0.031) lengths of stays and were less frequently discharged home (p=0.008). Logistic regression analyses of patient characteristics and sTBI interventions demonstrated that hypernatremia was independently associated with the presence of fixed pupil(s) on admission (odds ratio [OR] 5.38; p=0.003); administration of thiopental (OR 8.64; p=0.014), and development of central diabetes insipidus (OR 5.66; p=0.005). Additional logistic regression analyses demonstrated a significant association between hypernatremia and mortality (OR 6.660; p=0.034). In summary, acquired hypernatremia appears to signal higher risk of mortality in pediatric sTBI and is associated with a higher discharge level of care in sTBI survivors.

Intraoperative hypernatremia and polyuric syndrome induced by dexmedetomidine

Hypernatremia and polyuria are the main symptoms of diabetes insipidus. Polyuria is characterized by a 24-h urine volume in excess of 40-50 ml/kg in adults. Dexmedetomidine, a highly selective, short-acting intravenous alpha-2 agonist, is used as a component of anesthesia, and has been suspected to induce polyuric syndrome. We report a patient who presented with severe hypernatremia and polyuria after intravenous infusion of dexmedetomidine.

Rotavirus Disease in Germany—A Prospective Survey of Very Severe Cases

Rotavirus (RV) gastroenteritis is a notifiable disease in Germany. The reports to the authorities contain few data concerning the severity of disease. The aims of this study were to determine incidence and outcome of very severe cases of RV disease. Cases of very severe RV disease were collected by the German Paediatric Surveillance Unit for rare diseases (Erhebungseinheit für seltene pädiatrische Erkrankungen in Deutschland) using anonymous questionnaires based on hospitalized patients between April 2009 and March 2011. Inclusion criteria were detection of RV antigen in feces, patient aged 0-16 years and 1 or more of the following criteria: intensive care treatment, hypernatremia or hyponatremia (>155 mmol/L or <125 mmol/L), clinical signs of encephalopathy (somnolence, seizures, apnea) and RV-associated death. During 2 years, 130 cases of very severe RV disease were reported, 101 of 130 were verified. Seventeen patients had nosocomial infection, of whom 14 were neonates in intensive care. Among those, 12 infants had verified or suspected necrotizing enterocolitis. Eighty-four community-acquired cases were reported, median age was 10.5 months (0-108 months). The median hospital stay was 6 days, and 48 patients needed intensive care treatment. Among children less than 5 years of age, the yearly incidence of community-acquired very severe RV disease was 1.2 of 100,000 (95% confidence interval: 0.9-1.4/100,000). A total of 26 of 84 and 10 of 84 patients had severe hypernatremia or hyponatremia, respectively, and 58 of 84 patients had signs of encephalopathy. Three deaths were reported (1 nosocomial and 2 community acquired). RV infection in Germany can have a life-threatening course. A substantial number are nosocomial infections.

Severe Hypernatremia by Excessive Bamboo Salt Ingestion in Healthy Young Woman

Severe hypernatremia is an important electrolyte disorder that has serious effects. The patient had no medical history. A. 20-year-old ingested bamboo salt for digestion and weight reduction according to the folk remedies posted on an internet website. She presented with vomiting and diarrhea over ten times per day. Her initial serum sodium concentration was 174mEq/L. Her symptoms improved rapidly with hypotonic saline infusion. She recovered completely without any sequelae in three days. Severe hypernatremia in a normal young adult with clear consciousness and normal renal function has not been reported in Korea yet. So we report a case of severe hypernatremia by excessive bamboo salt ingestion in healthy young woman.

Paranoid Adipsia-induced Severe Hypernatremia and Uremia treated with Hemodialysis

We describe a patient with severe hypernatremia and uremia caused by paranoid adipsia who was treated successfully with hydration and hemodialysis. A previously healthy 40-year-old woman developed the paranoid idea that her water was poisoned, so she refused to drink any water. On admission, her blood urea nitrogen was 208mg/dL, creatinine 4.90mg/dL, serum osmolality 452mOsm/L, serum sodium 172mEq/L, urine specific gravity ≥1.030, urine osmolality 698mOsm/L, and urine sodium/potassium/chloride 34/85.6/8mEq/L. We diagnosed her with uremic encephalopathy and started intravenous dextrose, but the sodium correction was incomplete. She underwent two sessions of hemodialysis to treat the uremic encephalopathy and hypernatremia, and recovered fully without neurological sequelae. Although the standard treatment for severe hypernatremia is hydration, hemodialysis can be an additional treatment in cases of combined uremic encephalopathy.

Prognostic consequences of borderline dysnatremia: pay attention to minimal serum sodium change

IntroductionTo assess the prevalence of dysnatremia, including borderline changes in serum sodium concentration, and to estimate the impact of these dysnatremia on mortality after adjustment for confounders.MethodsObservational study on a prospective database fed by 13 intensive care units (ICUs). Unselected patients with ICU stay longer than 48 h were enrolled over a 14-year period were included in this study. Mild to severe hyponatremia were defined as serum sodium concentration < 135, < 130, and < 125 mmol/L respectively. Mild to severe hypernatremia were defined as serum sodium concentration > 145, > 150, and > 155 mmol/L respectively. Borderline hyponatremia and hypernatremia were defined as serum sodium concentration between 135 and 137 mmol/L or 143 and 145 respectively.ResultsA total of 11,125 patients were included in this study. Among these patients, 3,047 (27.4%) had mild to severe hyponatremia at ICU admission, 2,258 (20.3%) had borderline hyponatremia at ICU admission, 1,078 (9.7%) had borderline hypernatremia and 877 (7.9%) had mild to severe hypernatremia. After adjustment for confounder, both moderate and severe hyponatremia (subdistribution hazard ratio (sHR) 1.82, 95% CI 1.002 to 1.395 and 1.27, 95% CI 1.01 to 1.60 respectively) were associated with day-30 mortality. Similarly, mild, moderate and severe hypernatremia (sHR 1.34, 95% CI 1.14 to 1.57; 1.51, 95% CI 1.15 to 1.99; and 2.64, 95% CI 2.00 to 3.81 respectively) were independently associated with day-30 mortality.ConclusionsOne-third of critically ill patients had a mild to moderate dysnatremia at ICU admission. Dysnatremia, including mild changes in serum sodium concentration, is an independent risk factor for hospital mortality and should not be neglected.

A Clinical Approach to the Treatment of Chronic Hypernatremia

Hypernatremia is a commonly encountered electrolyte disorder occurring in both the inpatient and outpatient settings. Community-acquired hypernatremia typically occurs at the extremes of age, whereas hospital-acquired hypernatremia affects patients of all age groups. Serum sodium concentration is linked to water homeostasis, which is dependent on the thirst mechanism, arginine vasopressin, and kidney function. Because both hypernatremia and the rate of correction of hypernatremia are associated with significant morbidity and mortality, prompt effective treatment is crucial. Chronic hypernatremia can be classified into 3 broad categories, hypovolemic, euvolemic, and hypervolemic forms, with each form having unique treatment considerations. In this teaching case, we provide a clinically based quantitative approach to the treatment of both hypervolemic and hypovolemic hypernatremia, which occurred in the same patient during the course of a prolonged illness.

Characteristics, Symptoms, and Outcome of Severe Dysnatremias Present on Hospital Admission

ObjectiveDysnatremias are common in critically ill patients and associated with adverse outcomes, but their incidence, nature, and treatment rarely have been studied systematically in the population presenting to the emergency department. We conducted a study in patients presenting to the emergency department of the University of Bern. MethodsIn this retrospective case series at a university hospital in Switzerland, 77,847 patients admitted to the emergency department between April 1, 2008, and March 31, 2011, were included. Serum sodium was measured in 43,911 of these patients. Severe hyponatremia was defined as less than 121 mmol/L, and severe hypernatremia was defined as less than 149 mmol/L. ResultsHypernatremia (sodium>145 mmol/L) was present in 2% of patients, and hyponatremia (sodium<135 mmol/L) was present in 10% of patients. A total of 74 patients had severe hypernatremia, and 168 patients had severe hyponatremia. Some 38% of patients with severe hypernatremia and 64% of patients with hyponatremia had neurologic symptoms. The occurrence of symptoms was related to the absolute elevation of serum sodium. Somnolence and disorientation were the leading symptoms in hypernatremic patients, and nausea, falls, and weakness were the leading symptoms in hyponatremic patients. The rate of correction did not differ between symptomatic and asymptomatic patients. Patients with symptomatic hypernatremia showed a further increase in serum sodium concentration during the first 24 hours after admission. Corrective measures were not taken in 18% of hypernatremic patients and 4% of hyponatremic patients. ConclusionsDysnatremias are common in the emergency department. Hyponatremia and hypernatremia have different symptoms. Contrary to recommendations, serum sodium is not corrected more rapidly in symptomatic patients.

Central diabetes insipidus and adipsia due to astrocytoma: diagnosis and management.

Adipsia and/or diabetes insipidus is rarely a direct complication of astrocytoma. We report a young man with recurrence of anaplastic astrocytoma who presented as severe hypernatremia. This case highlights key diagnostic and therapeutic challenges: (1) the interpretation of the response to exogenous vasopressin in a patient with steroid-induced hyperglycemia and (2) the potential risk of brain edema and herniation if excess water is prescribed along with vasopressin supplementation. The patient was successfully managed with prescribed fluid replacement, daily weights, and regular electrolyte monitoring but no exogenous vasopressin for 8months until he succumbed to his tumor.

Hypernatremia severity and the risk of death after traumatic brain injury

PurposeTo investigate the relationship between severity of hypernatremia and the risk of death for patients with traumatic brain injury (TBI) who have been admitted to the neurosurgical intensive care unit (NICU). MethodsA total of 1044 patients with TBI were admitted to our NICU from January 2005 to January 2010. Of these patients, 881 were included in this study. Based on blood serum sodium level in the NICU the 881 patients were divided into four groups: 614 had normal serum sodium (Na<150mmol/L), 34 had mild hypernatremia (Na 150–<155mmol/L), 66 had moderate hypernatremia (Na 155–160mmol/L) and 167 had severe hypernatremia (Na≥160mmol/L). ResultsThe mortality rates for the mild, moderate, and severe hypernatremia groups were 20.6%, 42.4%, and 86.8%, respectively; the mortality rate for the normal group was 2.0%. In multivariable analysis, mild, moderate, and severe hypernatremia were independent risk factors for mortality; compared with the normal group the odds ratios of mild, moderate, and severe hypernatremia were 9.50, 4.34, and 29.35, respectively. ConclusionsSevere hypernatremia is an independent risk factor with extremely high odds ratio for death in patients with TBI who are admitted to the NICU.