Glyphosate poisoning - a case report.

Glyphosate is the most commonly used broad-spectrum, non-selective herbicide in the world. The toxicity is supposed to be due to uncoupling of oxidative phosphorylation and the surfactant polyoxyethylene amine (POEA)- mediated cardiotoxicity. Clinical features of this herbicide poisoning are varied, ranging from asymptomatic to even death. There is no antidote and aggressive supportive therapy is the mainstay of treatment for glyphosate poisoning. We present a 69-year-old female patient with suicidal consumption of around 500 ml of Glycel®. Initially, gastric lavage was done and intravenous fluids were given. Within two hours of presentation, the patient developed respiratory distress needing intubation, hypotension needing vasopressor support, and severe lactic acidosis. She also developed acute respiratory distress syndrome, hypokalemia, hypernatremia, and aspiration pneumonia. Our patient was critically ill with multiple poor prognostic factors, but with timely aggressive supportive management, the patient gradually recovered.

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.

The role of urea-induced osmotic diuresis and hypernatremia in a critically ill patient: case report and literature review.

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.

[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.

Use of a constant rate infusion of insulin for the treatment of hyperglycemic, hypernatremic, hyperosmolar syndrome in an alpaca cria.

CASE DESCRIPTION: A 3-day-old 9.5-kg (21-lb) female alpaca cria was examined because of lethargy and anorexia. CLINICAL FINDINGS: Physical examination revealed hyperthermia, muscle fasciculations, and tremors of the head. Seizures were also observed, which indicated CNS dysfunction. Hyperosmolar syndrome (HOS) was diagnosed on the basis of hyperglycemia, hypernatremia, azotemia, high plasma osmolarity, and metabolic acidosis. TREATMENT AND OUTCOME: A constant rate infusion of regular insulin was administered with hypo-osmolar fluids to treat HOS, and blood glucose and sodium concentrations were successfully lowered. Neurologic deficits resolved with treatment, and the cria was discharged 11 days after admission. CLINICAL RELEVANCE: Administration of insulin as a bolus in addition to hypo-osmolar fluids has been advocated in the management of neonatal camelids with HOS. Administration of regular insulin via a constant rate IV infusion was used to successfully manage a neonatal camelid with HOS. This form of insulin administration may allow more control of glucose kinetics in these patients.

Diagnosis and management of electrolyte emergencies.

Electrolyte and fluid imbalances are disorders frequently observed in critical care patients. In many instances patients are asymptomatic, but they may also present with neurological alterations, severe muscle weakness, nausea and vomiting or cardiovascular emergencies. Therefore, a pathophysiological understanding of these disorders is necessary for initiating an appropriate therapy. After a precise history-including drug prescriptions-has been obtained from the patient or his/her relatives, determination of the hydration status of the patient and measurement of acid-base status, plasma and urine osmolality and electrolytes are the first steps in the assessment of the disease. Once a diagnosis has been established, great attention has to be paid to the rate at which the disorder is corrected because this-if inappropriate-may cause more severe damage to the patient than the disease itself. This chapter addresses the initial diagnostic and therapeutic steps of the most common electrolyte emergencies.

Incidence of seizures that follow rehydration of hypernatremic rabbits with intravenous glucose or fructose solutions.

Hypernatremic dehydration was induced in rabbits during a 3- to 5-day period resulting in mean plasma sodium concentrations of 187 meq/liter. The animals were then rehydrated during a 4-h period by intravenous administration of a 2.5% glucose or fructose solution. The water content of four regions of brain sample showed a significant (P less than 0.05) increase in brain water content above normal in the rehydrated groups. Brain water content was significantly (P less than 0.01) greater in those animals with seizures compared with those without seizures, suggesting the importance of water intoxication in the pathogenesis of seizure activity. Changes in muscle Na, K, Cl, and water content were not similar to those of brain, indicating that muscle content of these substances was not an accurate reflection of the brain content specific time. The incidence of seizures was significantly (P less than 0.05) greater when glucose solution was used for rehydration (49%) compared with the use of fructose solution (25%). The mechanism(s) by which fructose resulted in a lower incidence of seizures is not known. The frequency of seizure activity was directly proportional to the rate of administration of intravenous solutions utilized to correct hypernatremia. In addition, the specific carbohydrate of the solution appeared to play an important role in the pathophysiology of the development of seizures.

Essential hypernatraemia, antidiuretic hormone and neurophysin secretion: response to chlorpropamide.

An adolescent boy with essential hypernatremia, absent corpus callosum, mental retardation, hypodipsia, and partial diabetes insipidus with "inappropriate" ADH regulation and secretion was studied regarding factors controlling ADH and neurophysin release. Persistent hyperosmolality was noted while on 100 mEq sodium intake daily. Endogenous vasopressin activity was demonstrated after prolonged water deprivation. Hypertonic saline infusion produced increased volumes but dilute urine. Aqueous pitressin increased urinary osmolality, decreased serum osmolality, urine flow rate, and free water clearance. Stable water diuresis was induced by water loading and on normal saline infusion. Nicotine-stimulated neurophysin remained unexpectedly low and below the level of detectability when sampled during the physiologic studies, whereas oestrogen-stimulated neurophysin was elevated during oestrogen stimulation, water loading, and orthostasis procedures. Plasma vasopressin was suppressed with water loading but remained suppressed 90 min after tilt table testing. These data indicate impairment of the osmoreceptor mechanism: however, since the patient had a normal response of oestrogen-stimulated neurophysin, that part of the neurohypophysis appears intact. Chlorpropamide was effective in alleviating the hyperosmolar state acutely and maintained normal osmolar concentrations during two years of therapy.