Severe Hypernatremia During Hydatid Cyst Surgery: An Anusual Cause Of Acute Abdomen.

Treatment of liver hydatid cysts is still in most cases surgical. To avoid the recurrence of hydatid cysts injection of scolicidal products inside the cystic cavity is an important step in the surgical procedure. Many scolicidal solutions are used. Hypertonic Saline Solution (HSS) is widely used by surgeons; however, there is a risk of hypertonic saline resorption and acute hypernatremia. Iatrogenic hypernatremia can be life-threatening. We report three cases of hypernatremia secondary to HSS injection for hydatid cyst disease treatment. The objective of this study was to discuss the clinical features, and treatment of this rare complication.

Management of Central Diabetes Insipidus in Disabled Children with Diluted Oral Desmopressin Lyophilisate Formulation Administered Through Nasogastric Tube: A Retrospective Case Series.

BACKGROUND: Experience with nasogastric administration of oral DDAVP [desamino-D-arginine-8-vasopressin] lyophilisate (ODL) for central diabetes insipidus (CDI) in disabled children with swallowing coordination difficulties is limited. OBJECTIVE: We aimed to assess the safety and efficacy of nasogastric use of ODL in disabled children with CDI. Time to serum sodium normalisation was compared with that of children with normal intellect and CDI treated with sublingual DDAVP. METHODS: Clinical, laboratory and neuroimaging characteristics were evaluated for 12 disabled children with CDI treated with ODL through nasogastric tube at Dr Behcet Uz Children's Hospital, Turkey, between 2012 and 2022. RESULTS: Six boys and six girls with a mean (±SD) age of 43 (± 40) months were evaluated. These children (mean [±SD] weight standard deviation score [SDS] - 1.2 ± 1.7; mean [±SD] height SDS - 1.3 ± 1.4) presented with failure to thrive, irritability, prolonged fever, polyuria and hypernatraemia (mean serum sodium 162 [±3.6] mEq/L). At diagnosis, mean serum and urine osmolality were 321 (± 14) mOsm/kg and 105 (± 7.8) mOsm/kg, respectively. Arginine vasopressin (AVP) levels were undetectable (< 0.5 pmol/L) at diagnosis in all patients. Nasogastric tube administration of DDAVP lyophilisate (120 µg/tablet) dissolved in water (10 mL) was commenced at a dose of 1-5 µg/kg/day in two divided doses together with controlled water intake to avoid hyponatraemia. The frequency and dose of DDAVP were titrated based on urine output and serum sodium concentration. Serum sodium declined at a rate of 0.11 ± 0.03 mEq/L/h and reached normal range in a mean duration of 174 ± 46.5 h. Serum sodium declined faster in children with normal intellect and CDI treated with sublingual DDAVP (1.28 ± 0.39 mEq/L/h; p = 0.0003). Three disabled children needed rehospitalisation because of hypernatraemia due to unintentional DDAVP omission by caregivers. No episode of hyponatraemia was observed. Weight gain and growth were normal during the median (± interquartile range) follow-up duration of 32 ± 67 months. CONCLUSIONS: Nasogastric administration of oral DDAVP lyophilised formulation was safe and effective in the treatment of CDI in disabled children in this small retrospective series.

The role of urea-induced osmotic diuresis and hypernatremia in a critically ill patient: case report and literature review / O papel da diurese osmótica induzida por ureia na geração de hipernatremia no paciente crítico: relato de caso e revisão da literatura

Abstract Hypernatremia is a common electrolyte problem at the intensive care setting, with a prevalence that can reach up to 25%. It is associated with a longer hospital stay and is an independent risk factor for mortality. We report a case of hypernatremia of multifactorial origin in the intensive care setting, emphasizing the role of osmotic diuresis due to excessive urea generation, an underdiagnosed and a not well-known cause of hypernatremia. This scenario may occur in patients using high doses of corticosteroids, with gastrointestinal bleeding, under diets and hyperprotein supplements, and with hypercatabolism, especially during the recovery phase of renal injury. Through the present teaching case, we discuss a clinical approach to the diagnosis of urea-induced osmotic diuresis and hypernatremia, highlighting the utility of the electrolyte-free water clearance concept in understanding the development of hypernatremia.

Resumo A hipernatremia é um distúrbio eletrolítico comum no ambiente de terapia intensiva, com uma prevalência que pode chegar a 25%. Está associada a maior tempo de internação hospitalar e é um fator de risco independente para a mortalidade. Este relato ilustra um caso de hipernatremia de origem multifatorial no ambiente de terapia intensiva. Destacaremos o papel da diurese osmótica por geração excessiva de ureia, uma causa de hipernatremia pouco conhecida e subdiagnosticada. Este cenário pode estar presente em pacientes em uso de elevadas doses de corticoides, com sangramento gastrointestinal, em uso de dietas e suplementos hiperproteicos e estado de hipercatabolismo, especialmente durante a fase de recuperação de injúria renal. A seguir, discutiremos uma abordagem clínica para o diagnóstico da hipernatremia secundária à diurese osmótica induzida por ureia, destacando a importância do conceito de clearance de água livre de eletrólitos nesse contexto.

Effects of pneumoperitoneum on severe hypernatremia in an adult patient who underwent laparoscopic surgery of hydatid cysts.

We describe the first case of severe hypernatremia associated to laparoscopic surgery for hydatid cyst in an adult patient after the use of hypertonic saline solution with complete resolution. Severe hypernatremia is an unusual fact at the immediate postoperative period but may have fatal consequences for the patient and need immediate action. The patient reached a serum sodium concentration of 179 mmol/L without adverse effects after 6 days of treatment. Laparoscopy could play a crucial role in Na+ absorption due to high intraabdominal pressure caused by the pneumoperitoneum and its limitations to avoid peritoneal absorption of hypertonic saline solution. The relation between this surgical technique and the severe complication is discussed. More experience is needed in terms of safety for the patient.

[MODERN APPROACHES TO CORRECTION OF HYPERNATREMIA IN NEUROSURGICAL PATIENTS].

The article presents the analysis of the intensive therapy through the correction of persistent hypernatremia in neurosurgical patients after removal of brain tumors. The aim of this work was to evaluate the effectiveness of Sterofundin in the framework of complex therapy of hypernatremia in neurosurgical patients after removal of brain tumors. We analyzed the dynamics of the concentrations of sodium, potassium, chorus of the plasma, anion gap and buffer bases in the postoperative period of these patients. For obtaining reliable results, the patients were divided into groups according to the nature of the treatment: Sterofundin and symptomatic correction of hypotonic solution of sodium chloride, saluretic and Verospiron respectively. In a comparison between the groups, a distinct difference in the speed of regression of hypernatremia and durability of the achieved effect was observed. In case of treatment with Sterofundin there was a significant decrease of hypernatremia by the end of the second day of the postoperative period without tendency to re-raise. The prevalence of hypotonic solutions of sodium chloride and potassium-sparing saluretics in intensive care allowed reducing the sodium concentration non-persistently to the fourth day on the background of significant fluctuations in its concentration. The use of Sterofundin in complex therapy of electrolyte disturbances, particularly of hypernatremia in neurosurgical patients after removal of brain tumors, is reflected in the form of significant regression of increased sodium concentration in plasma compared with the method of use "hypotonic" hemodilution, saluretics and potassium-sparing diuretics.

The Impact of a Standardized Sodium Protocol on Incidence and Outcome of Dysnatremias in Neurocritical Care.

BACKGROUND: Dysnatremias are common and prognostically serious in neurocritical care. We studied whether a standardized sodium protocol would improve our neurocritical care of dysnatremias. METHODS: A 5-year prospective study of a standardized sodium protocol for 1,560 patients admitted with various brain diseases in an adult neurologic-neurosurgical intensive care unit (NNICU) was compared with a 5-year retrospective analysis of 1,440 patients without the sodium protocol. Hyponatremia was defined as serum sodium (SNa(+)) < 135 mmol/L and hypernatremia SNa(+ )> 150 mmol/L. The sodium protocol involved measuring SNa(+), serum, and urine osmolality, measured and calculated renal function parameters, fluid intake 40 mL/kg weight/day without hypotonic saline, thiazide, and desmopressin acetate in all normonatremic NNICU patients. RESULTS: In the protocol study, hyponatremia occurred slightly less often (15.7 versus 16.3% of patients; p = 0.684), hypernatremia was significantly higher (respectively 8.5% versus 5.2% of patients; p < 0.001), and no differences were noted in hypo/hypernatremia (p = 0.483). There were no differences in the incidence of hypo-osmolal hyponatremia (respectively 3.5% versus 3.5% of patients; p = 0.987), cerebral salt wasting (CSW; respectively 1.7% versus 1.7% of patients; p = 0.883), syndrome of inappropriate secretion of antidiuretic hormone (SIADH; respectively 0.1% versus 0.3% of patients; p = 0.152), central diabetes insipidus (CDI; respectively 1.0% versus 0.6% of patients; p = 0.149). In hyponatremia there were no differences in the Glasgow Coma Scale (GCS) score upon onset of hyponatremia (p = 0.294), NNICU mortality (respectively 1.0% versus 0.4% patients; p = 0.074), and bad outcome upon discharge from NNICU (respectively 5.1% versus 6.5% of patients; p = 0.101), but in hypernatremia GCS score upon onset (p < 0.001), mortality (respectively 2.8% versus 1.0%; p < 0.001), and bad outcome from NNICU (respectively 6.7% versus 2.7% patients; p < 0.001) were significantly higher. Multivariate logistic regression analysis showed that hypernatremia, compared with hyponatremia, was a significant predictor of mortality during NNICU stay (respectively odds ratio [OR]: 1.14; p = 0.003 versus OR; 5.3; p = 0.002). CONCLUSIONS: The standard sodium protocol lowered the frequency of SIADH, which was encountered in only one patient over 5 years. However, it did not significantly reduce the incidence and improve the outcome of hyponatremia. Hypernatremia occurred more often and had a higher mortality and worse outcome than hyponatremia, but these patients were neurologically worse upon its onset. The prospective study confirmed that CSW, SIADH, and CDI were not common in our neurocritical care.

[A case of hypernatremia treated with human atrial natriuretic peptide].

We describe a case of 65-year-old obese female patient with pulmonary embolism and life-threatening hypernatremia after removal of craniopharyngioma. On the 18th day after neurosurgical procedure, pulmonary embolism developed abruptly. Immediately after placement of inferior vena cava filter, surgical removal of the pulmonary thrombus was performed under cardiopulmonary bypass. Although mechanical ventilatory support and infusion of noradrenaline were required postoperatively, the trachea was extubated on the 10th postoperative day. Meanwhile, daily serum Na level increased gradually and reached 178 mEq x l(-1). We suspected that dehydration and pituitary dysfunction were mainly responsible for the hypernatremia. Human atrial natriuretic peptide (hANP) was infused from the 2nd to the 4th postoperative day, and her urinary Na excretion became increased and serum Na level became normal. After discontinuation of hANP, urinary Na excretion became decreased again and serum Na levels increased transiently. However, her consciousness level and cardiopulmonary condition improved and she was discharged from the ICU after twelve days of ICU stay. HANP may be useful for treatment of life-threatening hypernatremia.

Survival with serum sodium level of 180 mEq/L: permanent disorientation to place and time.

A 41-year-old woman who had undergone transfrontal craniotomy for a pituitary tumor 4 months before presentation was admitted with confusion and orientation only to self. She had a fever of 40 degrees C. Serum sodium and chloride levels on admission were 180 and 139 mEq/L, respectively. Measured serum osmolality was 380 mOsmol/L with a urine osmolality of 360 mOsmol/L. Magnetic resonance imaging revealed a 1.5-cm mass in the sella turcica, which was nonfunctioning on endocrine evaluation. The "bright spot" of a normal posterior pituitary was absent. Central diabetes insipidus was confirmed by a 300% increase in urine osmolality with desmopressin. The patient survived her severe hypernatremia, which has 70% mortality with a serum sodium level of 160 mEq/L or above. However, she developed permanent (6 months) disorientation to time and place even when hypernatremia was corrected, which has not been described previously.

Idiopathic hypothalamic dysfunction with precocious puberty and adipsic hypernatremia first presenting in adolescence.

BACKGROUND: Idiopathic hypothalamic dysfunction is a rare syndrome that has been described in young children. This syndrome is characterized by a disturbance of thirst regulation with hypernatremia, hyperosmolarity, and altered hypothalamic function. PATIENT REPORT: At age 6 years the reported patients presented with precocious puberty, by age 12 years she had hypernatremia presumed secondary to central diabetes insipidus and was treated with DDAVP, and at age 14 was identified to have hyperprolactinemia. At age 19 she presented with serum sodium of 185 mg/dl during an episode of illness associated with dehydration. After hydration, her sodium remained elevated. Arginine vasopressin was measurable but inappropriate to serum sodium, while urinary cyclic AMP response to vasopressin was appropriate. CONCLUSIONS: This is the first case of precocious puberty identified in association with the more classic features of idiopathic hypothalamic dysfunction, including later-onset hypernatremia, poor thermoregulatory function, obesity, and hyperprolactinemia.

Correção dos desvios da concentração de sódio e potássio na infância / Treatment of the sodium and potassium disturbances in childhood

Este artigo tem por objetivo abordar os aspectos mais relevantes da correção das alterações da concentração de sódio e potássio na infância. Sao abordados inicialmente os distúrbios do sódio, hipernatremia e hiponatremia. A hipernatremia é considerada clinicamente relevante se a concentração de sódio exceder a 160 mEq/I e a hiponatremia rio caso de ser inferior a 120 mEq/1. Para a correção dos distúrbios do sódio devem ser levados em conta a volemia do paciente, o tempo de instalação do distúrbio e a intensidade do mesmo. É importante evitar as complicações decorrentes da correção inadequada dos desvios da concentração de sódio que são o edema cerebral, no caso da hipernatremia, e a mielinólise pontina central, em relação à hiponatremia. Os distúrbios do potássio são abordados na segunda parte do texto. Tanto na hiperpotassemia quanto na hipopotassemia é importante avaliar a distribuição do potássio entre os compartimentos intra e extracelular, a capacidade do rim em excretar esse ion e o conteúdo de potássio corporal total. As manifestações clínicas mais graves decorrentes dos desvios da concentração de potássio dizem respeito a seus efeitos sobre o miocárdio e outros tecidos excitáveis. A correção desses desvios deve priorizar a reversão dos efeitos eletrofisiológicos tanto da hiper quanto da hipopotassemia e, posteriorrnente, a normalização dos níveis séricos deste íon.

The aim of this paper is to establish some guidelines for the treatment of sodium and potassium disturbances in childhood. First, sodium disorders, such as hypernatremia and hyponatremia, are discussed. The hypernatremia is considered clinically relevant if the sodium concentration is above 160 mEq/1. Regarding hyponatremia, the inferior limit for sodium concentration is 120 mEq/1. The patient's extracellular fluid volume, the duration of the disturbance and the magnitude of the alteration in sodium levels must be taken into account in order to correct the hydroelectrolyte imbalance. It is important to avoid the complications due to an inadequate correction of sodium disarrangement such as brain edema in hypernatremia and central pontine myelinolysis in hyponatremia. The disorders of potassium metabolism are discussed in the second part of this article. For the appropriate treatment of hyperkalemia and also hypokalemia, it is important to evaluate the distribution of potassium between extra and intracellular fluid, its renal excretion and the total amount of this ion in the body. The most severe clinical features are due to the effect of potassium disorders on the cell membranes. The treatment of potassium disarrangement must emphasize the correction of electrophysiological effects of the hyperkalemia and also hypokalemia. The normalization of potassium levels should be obtained afterward.

Treatment of sodium disorders after surgery of craniopharyngioma.

OBJECTIVE: To study the treatment of the patients with blood sodium disorder after craniopharyngioma surgery. METHOD: The blood sodium in 44 patients with craniopharyngiomas was daily examined from operative to post-operative days. Hypernatremia is defined as [Na] > 145 mmol/l, and hyponatremia as [Na] < 135 mml/L. RESULTS: Of the 44 patients, 36 developed sodium disorder. Among them, simple hyponatremia was 16 patients, simple hypernatremia was 9 patients, and alternative sodium disorder was 11 patients. CONCLUSION: The blood sodium disorder in patients with craniopharyngiomas after surgery appears to present complicated changes. Three types of blood sodium disorder could be determined as simple hyponatremia, simple hypernatremia, and alternative sodium disorder. Treatment of the sodium disorder in patients with after surgery could be carried in accordance with the above three types.

Hypercalcemia accompanied by hypothalamic hypopituitarism, central diabetes inspidus and hyperthyroidism.

We present here a case of prominent hypercalcemia accompanied by hypothalamic tumor and Graves' disease. A 24-year-old man with hypothalamic tumor showed hypopituitarism, central diabetes inspidus (DI) and hyperthyroidism. Nausea, loss of thirst and appetite, and general fatigue were found with the unveiling of hypercalcemia and hypernatremia. Parathyroid hormone (PTH) and 1alpha-dihydroxyvitamin D levels were suppressed with a normal range of PTH-related protein values. One-desamino-(8-D-arginine)-vasopressin (DDAVP) and half-saline administration normalized hypernatremia, while hypercalcemia was still sustained. Administration of cortisone acetate and thiamazole reduced the elevated serum Ca level. In the present case, concurrent hyperthyroidism was assumed to accelerate skeletal mobilization of calcium into the circulation. Hypocortisolism and central DI was also considered to contribute, to some extent, to the hypercalcemia through renal handling of Ca.

Hipernatremia grave em paciente portadora de provável meningite asséptica / Acute hypernatremia in patient with probable asseptic meningitis

Nós descrevemos o caso de uma paciente que desenvolveu níveis séricos de sódio de 196 meq/L na véspera do óbito, e 202 meq/L nas amostras de sangue colhidas na manhä do óbito.

Diabetes insipidus. Current treatment recommendations.

Cranial diabetes insipidus (DI) arises when release of arginine vasopressin (AVP, antidiuretic hormone) in response to osmotic stimuli is inadequate. The correct diagnosis and management of cranial DI is particularly important when it arises as an acute complication of surgery, trauma or in subjects who lack thirst sensation. Desmopressin (1-desamino-8-D-arginine-vasopressin, DDAVP) provides an effective and convenient replacement therapy when given by the intranasal route. However, nasal administration is difficult for some patients, and in the future oral or transcutaneous desmopressin formulations may prove to be satisfactory alternatives. By contrast, treatments for nephrogenic DI, where there is failure of the antidiuretic response to endogenous or exogenous vasopressin, have been disappointing and water replacement remains the mainstay of therapy. An understanding of the physiology and pathophysiology of water homeostasis and correct interpretation of water balance and electrolyte data are essential for correct diagnosis and management of all cases of DI.

[Renal protection in acute neurosurgical diseases--effect of a low dose dopamine with reference to acute renal failure and hypernatremia in patients with dehydration].

The authors reviewed the effect of low dose dopamine administration (1-5 micrograms/kg/min) in neurosurgical patients with acute renal failure (5 cases) or hypernatremia (7 cases) in whom cerebral dehydration therapy for intracranial hypertension was thought to be causative of these disorders. Cases with hypernatremia (serum sodium over 155 mEq/l) were considered in the stage of impending acute renal failure as in the majority of cases serum creatinine levels were mildly elevated while urinary sodium was markedly diminished. Associated with systemic hypovolemia, in cases with acute renal failure (with serum creatinine over 3.5 mg/dl and urinary output of less than 20 ml/hr for more than 4 hour duration) the urinary sodium levels were less than 20 mEq/l. In all the cases treated by low dose dopamine, urinary output and sodium increased within 6 hours and in the following 24 hours stabilized urinary output with its elevated sodium (some 100 mEq/l) was obtained. As the result, elevated urea-nitrogen or serum sodium was rather easily washed out and the patients were kept adequately hydrated afterwards. Any complications such as aggravation of cerebral edema or convulsive disorder were not associated with this regime. The authors, therefore, would emphasize that low dose dopamine administration resulting in sodium diuresis and increase in renal blood flow is a practical way of method in treating patients with hypernatremia or acute renal failure caused by hyperosmolar agent infusion in their acute stage.

The clinical physiology of water metabolism. Part III: The water depletion (hyperosmolar) and water excess (hyposmolar) syndromes.

Hyperosmolality occurs when there are defects in the two major homeostatic mechanisms required for water balance-thirst and arginine vasopressin (AVP) release. In this situation hypotonic fluids are lost in substantial quantities causing depletion of both intracellular and extracellular fluid compartments. Patients with essential hypernatremia have defective osmotically stimulated AVP release and thirst but may have intact mechanisms for AVP release following hypovolemia. Hyperosmolality can also be seen in circumstances in which impermeable solutes are present in excessive quantities in extracellular fluid. Under these conditions there is cellular dehydration and the serum sodium may actually be reduced by water drawn out of cells along an osmotic gradient. Hyposmolality and hyponatremia may be seen in a variety of clinical conditions. Salt depletion, states in which edema occurs and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) may all produce severe dilution of body fluids resulting in serious neurologic disturbances. The differential diagnosis of these states is greatly facilitated by careful clinical assessment of extracellular fluid volume and by determination of urine sodium concentration. Treatment of the hyposmolar syndromes is contingent on the pathophysiology of the underlying disorder; hyponatremia due to salt depletion is treated with infusions of isotonic saline whereas mild hyponatremia in cirrhosis and ascites is best treated with water restriction. Severe symptomatic hyponatremia due to SIADH is treated with hypertonic saline therapy, sometimes in association with intravenous administration of furosemide. Less severe, chronic cases may be treated with dichlormethyltetracycline which blocks the action of AVP on the collecting duct.

Hypothalamic hypernatremia due to volume--dependent ADH release, and its treatment with carbamazepine and clofibrate.

A 23-year-old man, diagnosed as having a pituitary adenoma at the age of 17 and received an operation 1 month ago showed a fluctuating hypernatremia and hypodipsia. The water deprivation, water load and hypertonic saline infusion tests were carried out. After a 14-hr water deprivation test, plasma osmolality was 310 mOsm/kg, plasma ADH was 1.5 microunits/ml, and urine osmolality was 591 mOsm/kg. On the water load test subsequently performed, the plasma osmolality decreased to 297 mOsm/kg, but the urine was still hypertonic. Infusion of 2.5% saline solution elicited paradoxically a marked diuresis and dilution of urine despite the elevàtion of plasma osmolality. On the treatment with carbamazepine and clofibrate, the urinary osmolality increased, the hypernatremia was normalized, and a marked natriuresis was elicited with a gain in body weight. These results suggested that the secretion of ADH is regulated by changes in blood volume rather than by the plasma osmolality in this patient. The hypernatremia may be explained as a disturbance or lack of osmoreceptor function for ADH release and the loss of thirst sensation, though the volume receptor still remains functioning for ADH secretion. Depletion of the extracellular fluid volume may be another contributing factor to the elevation of serum sodium level by enhancing the reabsorption of sodium from renal tubules.