Rapid Correction Of Severe Hyponatremia Research Articles

Osmotic demyelination syndrome: revisiting the diagnostic criteria through two fatal cases

BackgroundOsmotic Demyelination Syndrome (ODS) encompasses Central Pontine Myelinolysis and Extrapontine Myelinolysis, both of which are serious neurological conditions linked to the overly rapid correction of hyponatremia. Despite growing evidence, the exact etiology of ODS remains incompletely understood. The present paper describes two case studies, aiming to provide a comprehensive overview of the pathological findings and clinical outcomes associated with ODS.Case presentationCase #1. A 74-year-old woman was admitted to the emergency department following a head trauma caused by a loss of consciousness. Initial laboratory tests revealed severe hyponatremia (sodium level of 101 mmol/L) and hypokalemia (potassium level of 2.9 mmol/L). The patient underwent corrective therapy with saline and potassium chloride. Despite the correction of electrolyte imbalances, the patient developed a hyperintense lesion in the median portion of the pons on T2-fluid-attenuated inversion recovery (FLAIR) MRI sequence 14 days post-treatment, consistent with ODS. The patient’s condition deteriorated, leading to irreversible coma and status epilepticus, culminating in death 32 days after admission. Case #2. An 81-year-old woman with a medical history of hypothyroidism, hypertension, major depression, and stage 3 chronic kidney disease presented with mild gait disturbances. Subsequent testing revealed severe hyponatremia (sodium level of 100 mmol/L). Following an initial clinical improvement due to sodium correction, the patient’s condition worsened, with symptoms progressing to confusion, lethargy, and eventually, ODS. Dermatological manifestations, including blistering lesions and facial edema, appeared as the condition advanced. The patient succumbed to irreversible coma 47 days after admission.ConclusionODS traditionally carried a poor prognosis, with high mortality rates and diagnoses often made postmortem. However, recent advances in understanding the pathophysiology, along with improvements in diagnostic techniques such as MRI and intensive care treatments, have led to earlier identification, treatment, and recognition of milder forms of the syndrome. Despite these advancements, ODS remains a critical condition with significant risks, particularly following the rapid correction of severe hyponatremia.

A Case of Intra- and Extra-Pontic Myelinolysis Complicating the Rapid Correction of Severe Hyponatremia

A Case of Intra- and Extra-Pontic Myelinolysis Complicating the Rapid Correction of Severe Hyponatremia

Rapid correction of severe hyponatremia and control of subsequent overcorrection in operative hysteroscopy intravascular absorption syndrome: A case report

Operative hysteroscopy intravascular absorption syndrome (OHIAS) results from systemic absorption of hypotonic solution during hysteroscopy, which may induce severe hyponatremia within hours. Depending on the serum sodium (Na+) level, this can be life-threatening and requires prompt and careful remedial treatment. A 53-year-old woman underwent hysteroscopic myomectomy for submucosal leiomyoma. Approximately 3 hours postoperatively, the serum Na+ level decreased to 82 mM/L, accompanied by pulmonary edema and lactic acidosis. The patient was strongly suspicious of OHIAS. A rapid correction was made using 3% NaCl to prevent brain edema as an initial response. After the serum Na+ level reached 120 mM/L, gradual correction was performed considering osmotic demyelination syndrome, and desmopressin was administered to prevent overcorrection caused by excessive water diuresis. Serum Na+ level normalized in 4 days and the patient recovered without any specific sequelae. The detection of OHIAS may be delayed under general anesthesia, and prior vigilance is important if the operation time is prolonged. In severe hyponatremia with an apparently rapid onset, such as OHIAS, a two-step correction process may be safe and useful: rapid correction followed by more gradual correction.

Hyponatremia, osmotic demyelination syndrome, and the importance of the patient’s history

Central pontine myelinolysis (CPM), first described in 1959, is a symmetrical non-inflammatory demyelinating disease with loss of oligodendrocytes that occurs most often following a rapid correction of severe hyponatremia (i.e., <120 mmol/L). It presents as a biphasic disease with initial seizure or encephalopathy, followed by clinical improvement and subsequent rapid deterioration with bulbar dysfunction, oculomotor dysfunction, various degree of paresis, and even locked in syndrome. Its occurrence is rare (≈0.6% of severe hyponatremia), it is diagnosed clinically and confirmed with brain imaging, ideally with magnetic resonance image, and it is reversible in approximately half the patients. Lesions are classically identified in the pons but extra pontine lesions (in basal ganglia, cerebellar white matter, thalamus, and hippocampus) have also been identified. The most commonly accepted molecular mechanism involves brain cell volume regulation with a rapid shift of osmole following brain edema which establishes during the chronic hyponatremic phase. For these reasons, osmotic demyelination syndrome (ODS) is a better term. The most identified risk factor is severe hyponatremia, but other electrolyte abnormalities can contribute, in particular, if the patient is an alcoholic or malnourished. This diagnosis should also be suspected in post-op patients with nausea and headache non-responsive to antiemetic and analgesic drugs. An essential step is an appropriate medical history, a list of medications, physical examination, and basic initial lab tests with the goal of identifying possible easily reversible causes of hyponatremia. Correction of severe hyponatremia with neurological symptoms should be done using rapid boluses of hypertonic saline solution in rapid succession with goals of increasing serum sodium by 5-6 mEq/L in the first two hours, which should be stopped if the level has risen by 10 mEq/L in the first five hours, and with the overall correction goal not to exceed 15-20 mEq/L in 48 hrs. This method has been shown safe in all hospital settings studied. Serial measurements of electrolyte levels and neurological examinations are recommended, as are correction of all electrolyte abnormalities, in
 particular magnesium and potassium. Thiamine should be given to all patients with chronic alcohol use who present with hyponatremia and encephalopathy.

Mielinólise pontina: relato de caso

Introdução: A mielinólise pontina central (MPC) e a mielinólise extrapontina (MEP) são agrupadas dentro do contexto de síndromes de desmielinização osmótica as quais são caracterizadas pela dissolução das bainhas de mielina, preservando os axônios. O objetivo deste relato de caso é descrever o relato de caso de paciente com quadro de MPC e realizar a revisão na literatura médica. Detalhamento de caso: Trata-se de uma paciente do sexo feminino, 57 anos, que desenvolveu MPC após rápida correção da hiponatremia secundária a vômitos persistentes. Evolui com síndrome pseudobulbar, tetraparesia, disartria, rebaixamento do nível de consciência e disfagia. Após cinco meses de internação para tratamento sintomático e das complicações inerentes ao seu quadro clínico evoluiu com melhora parcial dos sintomas motores. Discussão: A etiologia da MPC e MEP é multifatorial, com incidência desconhecida e prevalência igual em ambos os sexos, podendo ser encontrada em todas as idades, com elevadas taxas de morbimortalidade. Embora seu principal fator desencadeante seja a correção excessivamente rápida da hiponatremia grave, alguns pacientes podem desenvolvê-la com concentrações séricas de sódio mais elevadas e com menores taxas de correção. O diagnóstico é essencialmente clínico, porém a ressonância magnética é o exame complementar de eleição para confirmação. Os pacientes podem apresentar desde recuperação completa até sequelas neurológicas irreversíveis, não existindo tratamento específico.

Risk Factors and Outcomes of Rapid Correction of Severe Hyponatremia.

Rapid correction of severe hyponatremia can result in serious neurologic complications, including osmotic demyelination. Few data exist on incidence and risk factors of rapid correction or osmotic demyelination. In a retrospective cohort of 1490 patients admitted with serum sodium <120 mEq/L to seven hospitals in the Geisinger Health System from 2001 to 2017, we examined the incidence and risk factors of rapid correction and osmotic demyelination. Rapid correction was defined as serum sodium increase of >8 mEq/L at 24 hours. Osmotic demyelination was determined by manual chart review of all available brain magnetic resonance imaging reports. Mean age was 66 years old (SD=15), 55% were women, and 67% had prior hyponatremia (last outpatient sodium <135 mEq/L). Median change in serum sodium at 24 hours was 6.8 mEq/L (interquartile range, 3.4-10.2), and 606 patients (41%) had rapid correction at 24 hours. Younger age, being a woman, schizophrenia, lower Charlson comorbidity index, lower presentation serum sodium, and urine sodium <30 mEq/L were associated with greater risk of rapid correction. Prior hyponatremia, outpatient aldosterone antagonist use, and treatment at an academic center were associated with lower risk of rapid correction. A total of 295 (20%) patients underwent brain magnetic resonance imaging on or after admission, with nine (0.6%) patients showing radiologic evidence of osmotic demyelination. Eight (0.5%) patients had incident osmotic demyelination, of whom five (63%) had beer potomania, five (63%) had hypokalemia, and seven (88%) had sodium increase >8 mEq/L over a 24-hour period before magnetic resonance imaging. Five patients with osmotic demyelination had apparent neurologic recovery. Among patients presenting with severe hyponatremia, rapid correction occurred in 41%; nearly all patients with incident osmotic demyelination had a documented episode of rapid correction. This article contains a podcast at https://www.asn-online.org/media/podcast/CJASN/2018_06_05_CJASNPodcast_18_7_G.mp3.

Plasma exchange successfully treats central pontine myelinolysis after acute hypernatremia from intravenous sodium bicarbonate therapy

BackgroundOsmotic demyelination syndrome (ODS) primarily occurs after rapid correction of severe hyponatremia. There are no proven effective therapies for ODS, but we describe the first case showing the successful treatment of central pontine myelinolysis (CPM) by plasma exchange, which occurred after rapid development of hypernatremia from intravenous sodium bicarbonate therapy.Case presentationA 40-year-old woman presented with general weakness, hypokalemia, and metabolic acidosis. The patient was treated with oral and intravenous potassium chloride, along with intravenous sodium bicarbonate. Although her bicarbonate deficit was 365 mEq, we treated her with an overdose of intravenous sodium bicarbonate, 480 mEq for 24 hours, due to the severity of her acidemia and her altered mental status. The next day, she developed hypernatremia with serum sodium levels rising from 142.8 mEq/L to 172.8 mEq/L. Six days after developing hypernatremia, she exhibited tetraparesis, drooling, difficulty swallowing, and dysarthria, and a brain MRI revealed high signal intensity in the central pons with sparing of the peripheral portion, suggesting CPM. We diagnosed her with CPM associated with the rapid development of hypernatremia after intravenous sodium bicarbonate therapy and treated her with plasma exchange. After two consecutive plasma exchange sessions, her neurologic symptoms were markedly improved except for mild diplopia. After the plasma exchange sessions, we examined the patient to determine the reason for her symptoms upon presentation to the hospital. She had normal anion gap metabolic acidosis, low blood bicarbonate levels, a urine pH of 6.5, and a calyceal stone in her left kidney. We performed a sodium bicarbonate loading test and diagnosed distal renal tubular acidosis (RTA). We also found that she had Sjögren’s syndrome after a positive screen for anti-Lo, anti-Ra, and after the results of Schirmer’s test and a lower lip biopsy. She was discharged and treated as an outpatient with oral sodium bicarbonate and potassium chloride.ConclusionThis case indicates that serum sodium concentrations should be carefully monitored in patients with distal RTA receiving intravenous sodium bicarbonate therapy. We should keep in mind that acute hypernatremia and CPM can be associated with intravenous sodium bicarbonate therapy, and that CPM due to acute hypernatremia may be effectively treated with plasma exchange.

A Case of Central Pontine Myelinolysis in a Type 2 Diabetic Patient without Electrolyte Changes

Received: 26 October 2010, Accepted: 11 January 2011 Corresponding author: Ji Hye Suk Department of Internal Medicine, Maryknoll Medical Center, 4-12 Daecheong-dong, Jung-gu, Busan 600-730, Korea Tel: +82-51-461-2693, Fax: +82-51-465-7470, E-mail: Jihyesuk@gmail.com Central pontine myelinolysis (CPM) by complicating rapid correction of severe hyponatremia has been widely reported. Additionally, CPM was occasionally reported among patients with post-liver transplantation, burns, chronic renal failure with dialysis, or other diseases associated with or not associated with other electrolyte changes or hyperosmolarity. However, there have been a few reports of CPM occurring in diabetic patients without documented electrolyte changes. This report is, to the best of our knowledge, the first report of CPM in type 2 diabetic patients without electrolyte changes in Korea. A 40-year-old man with type 2 diabetes mellitus with abruptly developed dysarthria and ataxia was admitted to our facility. He suffered from poor glucose control and multiple diabetic complications. Brain magnetic resonance imaging (MRI) revealed a well-defined bilateral symmetric hyperintense lesion in the central portion of the pons on T2and diffusion-weighted images, which was consistent with CPM. After the patient’s blood glucose and blood pressure normalized, his dysarthria and ataxia improved. Six months after discharge, follow-up MRI showed a persistent, but greatly reduced symmetric lesion in the central pons. It is certainly possible for CPM to be overlooked clinically in diabetic patients, but more cases could be diagnosed if careful attention was paid to this syndrome. (Endocrinol Metab 26:263-267, 2011)

Comments on “Wernicke’s Encephalopathy after Laparoscopic Roux-en-Y Gastric Bypass: A Misdiagnosed Complication”

In a recent issue of Obesity Surgery, Iannelli and colleagues reported a case of a 27-year-old woman that developed diplopia, weakness in both upper and lower extremities, urinary incontinence, and memory loss to recent events 10 months after laparoscopic Roux-en-Y gastric bypass for morbid obesity. They established the diagnosis of Wernicke’s encephalopathy (WE) based on clinical manifestations as well as a 12-month follow-up [1]. This case is interesting because it provided general surgeons an insight into the overlooked diagnosis of WE after obesity surgery. However, we have some concerns about the differential diagnoses of this case. WE is defined as the combination of ataxia, ophthalmoplegia, nystagmus, and mental confusion resulting from vitamin B1 deficiency [2]. In their report, the authors did not detect the level of vitamin B1 in the serum. As a result, differential diagnoses should be distinguished from the diagnosis they proposed, i.e. WE. The patient was admitted at a peripheral hospital with severe dehydration and a history of persistent vomiting. We would like to know whether electrolyte disorders exist at that time. Electrolyte disorders such as hypopotassaemia and hyponatremia may present as quadriplegia, absent deep tendon reflexes, and disturbance of consciousness. We agree that thiamine plays a role in carbohydrate metabolism and the administration of glucose and other carbohydrates without thiamine can be dangerous for patients with thiamine deficiency, while extrapontine myelinolysis (EPM) due to rapid correction of severe hyponatremia should also be taken into account since the patient manifested diplopia, weakness in both upper and lower extremities, urinary incontinence, and memory loss to recent events after she was admitted by the authors [3]. Lesions in extrapontine myelinolysis have been increasingly documented, including cerebellum, lateral geniculate body, external and extreme capsules, hippocampus, putamen, cerebral cortex/subcortex, thalamus, and caudate nucleus. Unusual sites for EPM include spinal cord, mamillary bodies, amygdala, columns of the fornix, anterior commissure, optic tract, subthalamic nucleus, etc. The clinical manifestations, as a consequence, vary according to different lesions [4–8]. In WE, MRI may show a symmetrically increased T2 signal in the paraventricular regions of the thalamus, hypothalamus, mamillary bodies, and/or midline cerebellum [9]. However, MRI of this case showed only multiple ranges of subcortical edema in the occipital regions, which not only support the diagnosis of WE but also EPM. In addition, polyneuropathy is not uncommon in patients with vitamin B1 deficiency [10]. The patient was reported to have quadriplegia and absent deep tendon reflexes in knee and ankle joints bilaterally, whereas pathological signs, which are important in differentiating peripheral paralysis from central paralysis, were not reported. In particular, urinary incontinence that the patient presented with may be indicative of spinal cord involvement. K.-J. Zhang :D. Zhang Department of Plastic Surgery, The First Hospital of Jilin University, Changchun, China

Central pontine and extrapontine myelinolysis: from epileptic and other manifestations to cognitive prognosis

The objective of this study is to review the presentation, outcome and aetiology of central pontine and extrapontine myelinolysis (CPEPM) in a tertiary hospital center. The study method is a case series and included identification of patients from University of Montreal Health Centre archives database (1995-2007). All diagnoses were confirmed by neuroimaging or brain autopsy. Twelve individuals (25-66 years old) presented heterogeneous manifestations. Co-morbidities included diabetes insipidus (n = 2), haemodialysis (n = 1), cirrhosis (n = 3), gastroenteritis (n = 2) and potomania (n = 1). Aetiologies included rapid correction of severe hyponatremia (n = 6)/acute hypernatremia (n = 1); immediate (n = 2) or remote (n = 1 with recurrent cirrhosis) orthotopic liver transplantation (OLT) with tacrolimus-induced immunosuppression (n = 3); and chronic alcoholism (n = 4, two with hyponatremia). Four individuals died acutely. Two were lost to follow-up. Six had good motor or cerebellar recovery. Neuropsychological evaluations (n = 5/6) revealed a subcortical/frontal dysfunction. Cognitive impairment represented the major remaining lasting sequel (n = 4). Three salient clinical syndromes were observed: (1) predominant cerebellar presentation in individuals with alcoholism (n = 4); (2) significant alteration of consciousness at presentation (n = 4), all resulting in death (OLT, n = 3); (3) seizures persisting after natremia correction (n = 2). Clinical presentation of CPEPM is heterogeneous and can even include seizures. Cognitive impairment should be screened as it is a significant factor limiting return to normal life.

Ocular Motor and Imaging Abnormalities of Midbrain Dysfunction in Osmotic Demyelination Syndrome

After rapid correction of severe hyponatremia, a 36-year-old man developed osmotic demyelination syndrome (ODS), manifested neurologically by impaired cognition, extremity weakness, bilateral third cranial nerve palsies, and gaze-evoked upbeat and rotary nystagmus. Brain MRI showed restricted diffusion in the rostral midbrain and temporal and parietal lobes but not in the pons. Over several weeks, all neurologic and imaging deficits resolved. This is the first report to document ocular motor abnormalities associated with midbrain dysfunction in ODS.

Extrapontine myelinolysis after correction of hyponatremia presenting as generalized tonic seizures

Central pontine myelinolysis and extrapontine myelinolysis are rare complications of rapid correction of chronic hyponatremia. Central pontine myelinolysis is more common and more predictable in presentation. Extrapontine myelinolysis' presenting symptoms vary and may be as general as lethargy or altered mood. We report experience with a patient who developed only extrapontine myelinolysis after rapid correction of severe hyponatremia associated with gastroenteritis. His presenting sign, generalized seizures, has not been previously reported. We summarize risk factors for myelinolysis, which may be more common than previously thought, as well as steps to minimize risk while managing vulnerable patients.

Klüver Bucy syndrome, unusual consequence of excessively rapid correction of severe hyponatremia

Features of Klüver-Bucy syndrome (KBS) include hypersexuality, hyperorality, placidity, visual agnosia, amnesia, hypermetamorphosis, and emotional and nutritional behavior changes. It is a clinical presentation of bitemporal disorders with limbic system abnormalities. The most common cause of KBS is herpes encephalitis. An otherwise healthy 61-year-old woman presented with mental status changes (MMSE-0) after 6 days of severe vomiting. Extracellular dehydration, hyponatremia (107 mmol/L), low levels of natriuresis, and mild hypokalemia were noted. The initial computed tomography (CT) of the brain was normal. Over 36 hours of hospitalization in a district hospital she developed unusual neuropsychiatric disorders: hypersexuality, hyperorality, absence, visual agnosia, sensory aphasia, amnesia, and depression typical of KBS. She was then transferred to a neurology department. Clear improvement was visible 3 months later: MMSE-22, moderation of hypersexuality and hyperorality, partial correction of amnesia and aphasia, regression of visual agnosia. But the prosopagnosia (face blindness) persisted, and the patient remained unable to differentiate positive and negative facial expressions. Intracranial mass, epilepsy, neuromeningeal infection and head trauma were all ruled out. Antiepileptic and antiherpetic agents were tested without success. There was no evidence of adrenal insufficiency or inappropriate vasopressin secretion. Only severe vomiting, corrected by water intake, could explain the hyponatremia. The first MRI showed bitemporal edema; 3 months later it showed large bitemporal lesions, both internal and external, with atrophy of the hippocampus and limbic system. These MRI findings are characteristic of KBS. To our knowledge, this is the only the second case of KBS with bitemporal myelinolysis reported related to excessively rapid correction of hyponatremia (increase of 30 mmol/L over 36 h), which leads more usually to central pontine myelinolysis.

Rapid Correction of Severe Hyponatremia After Computed Tomography With Intravenous Contrast

To the Editor: Overly rapid correction of hyponatremia is a major concern in severely hyponatremic patients because of the potential development of osmotic demyelination. Numerous factors can contribute to overly rapid correction of hyponatremia (Table 1).1Pham P-CT Pham P-MT Miller J et al.Treatment of chronic hyponatremia.Proc UCLA Healthcare. Fall 2002; 6: 32-36Google Scholar We report a case in which a patient developed osmotic diuresis after contrast dye injection that rapidly self-corrected the severe hyponatremia.TABLE 1Potential Causes of Overly Rapid Correction of HyponatremiaAdapted from Proceedings of UCLA HealthCare,1Pham P-CT Pham P-MT Miller J et al.Treatment of chronic hyponatremia.Proc UCLA Healthcare. Fall 2002; 6: 32-36Google Scholar with permission. Unawareness of the recommended rate of correction for hyponatremiaMiscalculationsUnrecognized sources of sodium Exogenous Sodium administration at another site before transfer to the current unitAddition of excess salt to patient's diet by patient's family or facility staff membersEndogenous Potassium supplementation with resultant extracellular sodium shiftExcess free water loss Water deprivation in primary polydipsiaWithdrawal of thiazide diuretics during treatment of hyponatremiaGlucocorticoid replacement in a cortisol-deficient patientRecovery from acute respiratory failureExcessive gastrointestinal, pulmonary, or skin hypotonic fluid lossSevere hyponatremia with subsequent cerebral edema and pituitary infarctionNonelectrolyte osmotic diuresis: urea, glucose, mannitol, contrast dye, total parenteral nutritionIntracellular free water shift SeizuresRhabdomyolysisCorrection of hyperglycemiaPotassium supplementation Open table in a new tab Report of a Case. A 59-year-old woman with diabetes mellitus and hypertension presented with a 1-week history of slow mentation, fatigue, nausea, vomiting, abdominal pain, and subjective left hemiparesthesia. A dietary history revealed that she routinely ate only fruits and cereals and drank only water. Her medications included hydrochlorothiazide, fosinopril, atenolol, metformin, and aspirin. Physical examination revealed dry oral mucosa, slow mentation, and generalized sluggish deep tendon reflexes. On initial evaluation, the serum sodium concentration was 115 mEq/L, and urinary studies revealed an osmolality of 526 mosm/kg, a sodium level of 130 mEq/L, and a chloride level of less than 10 mEq/L. The patient was given two 500-mL boluses of normal saline during the first 12 hours of hospitalization. In the interim, she underwentcomputed tomography of the head and abdomen with intravenous contrast (iohexol). Despite correction of the hypovolemia, the patient had no improvement in her symptoms or serum sodium concentration during the first 24 hours. However, approximately 24 to 26 hours after presentation, she developed progressive polyuria (up to 150-175 mL/h). During the polyuric phase, the urine osmolality ranged from 217 to 393 mosm/kg. During the subsequent few hours, the patient's mentation noticeably improved in association with a spontaneous rapid increase in serum sodium concentration (8 mEq/L over 6 hours). In fact, hypotonic saline had to be administered to halt the rapid self-correction of the hyponatremia. Given the patient's history of poor dietary nutrition, use of hydrochlorothiazide, and current pain and vomiting, we suspected that the hyponatremia resulted from ongoing water intake concurrent with the patient's inability to excrete free water maximally because of a reduced dietary solute load and syndrome of inappropriate secretion of antidiuretic hormone-induced enhanced free water reabsorption.2Fichman MP Vorherr H Kleeman CR Telfer N Diuretic-induced hyponatremia.Ann Intern Med. 1971; 75: 853-863Crossref PubMed Scopus (239) Google Scholar, 3Thaler SM Teitelbaum I Berl T “Beer potomania” in non-beer drinkers: effect of low dietary solute intake.Am J Kidney Dis. 1998; 31: 1028-1031Abstract Full Text Full Text PDF PubMed Scopus (89) Google Scholar Despite saline infusion, the patient's serum sodium concentration remained at 115 mEq/L 12 to 18 hours after presentation, presumably a reflection of the sustained syndrome of inappropriate secretion of antidiuretic hormone caused by her nausea and pain. However, by 24 hours after presentation, the patient had a rapid increase in urinary output as well as serum sodium concentration despite the discontinuation of all intravenous fluids at least 6 hours previously. At that point, the patient possibly had adequate volume reexpansion, reduced proximal tubular reabsorption of salt and water, and resultant increased distal delivery for excretion. In addition, the control of nausea and pain and the volume reexpansion may have inhibited antidiuretic hormone secretion sufficiently to result in the aquaretic phase. However, subsequent urinary electrolyte studies revealed high osmolality (217-393 mosm/kg) relative to serum osmolality (240-264 mosm/kg), which suggested that she had osmotic diuresis, not aquaresis. Further analysis of her urine by ultraviolet spectrophotometry revealed that the predominant source of the urine osmolality during the polyuric phase was the contrast dye iohexol. The findings in this case are important because computed tomography with intravenous contrast is performed routinely for the evaluation of nonspecific complaints in severely hyponatremic patients.

Severe Hyponatremia - Is Rapid Correction Safe?

In view of the continuous controversy about the treatment of hyponatremia (rapid or slow correction), we retrospectively studied 40 patients with severe hyponatremia (serum level of 120 mmol/L and less). Thirteen cases were acute, the remainder (27) were chronic. The mean rate of correction calculated from the rise of serum sodium over the initial 12 hours in both acute and chronic patients, and over the initial 24 hours in the acute and in the majority of the chronic patients was consistent with the definition of rapid correction (increase of serum sodium of >/=0.5 mmol/L/hr). Six of the acute and three of the chronic patients died during follow-up of six months. All deaths were caused by the underlying diseases or by complications not related to the hyponatremia or its treatment. None of the patients (alive or deceased) developed any clinical features of central pontine and extrapontine myelinolysis (CPM). In some of the studies of rapid correction of hyponatremia, chronic alcoholism was felt to be one of the risk factors in the development of CPM. As our patient population, due to religious reasons, abstained from alcohol intake, our results would suggest that in the absence of chronic alcoholism and its attendant malnutrition, rapid correction of severe hyponatremia is probably safe.

Rapid correction of severe hyponatremia results in myelinolysis, brain protein oxidation, and altered blood chemistries

Rapid correction of severe hyponatremia results in myelinolysis, brain protein oxidation, and altered blood chemistries

Diuretic Abuse and Central Pontine Myelinolysis

Patients with eating disorders often use diuretics to eliminate fluid to achieve lower body weight. Diuretic abuse can lead to severe hyponatremia. Central pontine myelinolysis, a disruption of the myelinated neurons of the pons, has been associated with rapid correction of severe hyponatremia. A case is presented of a 35-year-old woman who was brought to the emergency service by ambulance complaining of vomiting for 7 days and that she could not hear well because she was 'worn out'. Initial laboratory values included serum Na 91 mEq/l, K 1.6, Cl 46, bicarbonate 33, BUN 4 mg/dl, glucose 306 mg/dl. After 32 h of intravenous fluids, the serum Na was 126, K 4.0, Cl 89, bicarbonate 25, glucose 118 mg/dl. On the 3rd hospital day the serum Na was 139. On the 4th hospital day she was alert and appropriate. On the 5th hospital day, however, she was confabulating and chatty. The serum Na was 139. She progressed to develop a spastic quadriparesis, speech and swallowing difficulties. A magnetic resonance imaging scan showed central pontine myelinolysis. She acknowledged taking 400 mg daily of furosemide and drinking much water. She had a past history of anorexia nervosa. She had a residual weight phobia and strove to keep her weight below 106 lb. Her height was 5 feet, 6 inches. As illustrated by this case, diuretic abuse can cause severe hyponatremia and the subsequent risk of central pontine myelinolysis. In patients with severe chronic or subacute hyponatremia, a safe restoration rate for serum Na has been less than 0.55 mEq/l/h. Serum Na should be below 135 within the first 48 h and hypernatremia should be avoided.

Rapid correction of severe hyponatremia in the rat: histopathological changes in the brain.

The purpose of the present studies was to examine the effects of rapid correction of severe hyponatremia (serum sodium less than 120 meq/liter) either to mildly hyponatremic levels (serum sodium = 130 meq/liter) or to normonatremic levels (serum sodium = 150 meq/liter) on the brain histology of rats. In group I, 13% of the rats revealed brain lesions following correction to mildly hyponatremic levels by the administration of 855 mM NaCl. All the rats (100%) in group II had brain lesions following correction to normonatremic levels by 24 h of water restriction. Similarly, all the rats in group III showed brain lesions following correction to normonatremic levels by the administration of 855 mM NaCl. Severe hyponatremia by itself did not cause any brain lesions in another group. We conclude that rapid correction of severe hyponatremia to mildly hyponatremic levels by the administration of 855 mM NaCl does not cause significant brain lesions. On the other hand, rapid correction to normonatremic levels either by water restriction or by the administration of 855 mM NaCl results in significant brain lesions.

Rapid correction of severe hyponatremia with intravenous hypertonic saline solution

Severe hyponatremia with hypoosmolality carries a high morbidity and mortality and constitutes a life-threatening emergency. We report seven cases of severe hyponatremia (serum sodium concentration 99.7 ± 3.0 meq/liter) (mean ± SEM) with hypoosmolality (212 ± 8 mOsm/kg water) that presented with severe neurologic complications. Serum sodium concentration was corrected in 13.3 ± 2.2 hours to mildly hyponatremic levels (serum sodium concentration 128.3 ± 1.6 meq/liter). The rate of correction of serum sodium concentration was 2.4 ± 0.5 meq/liter/hr. This was achieved by the intravenous administration of 3 percent hypertonic saline solution (687 ± 43 meq sodium chloride) and furosemide or by hemodialysis where indicated. No complications occurred from treatment and all of our patients recovered without neurologic sequelae. Early diagnosis and rapid correction of serum sodium concentration appear to reduce the significant morbidity and mortality of severe hyponatremia.

Rapid correction of severe hyponatremia with intravenous hypertonic saline solution: Ayus JC, Olivero JJ, Frommer JP: Am J Med 1982; 72: 43–48

Rapid correction of severe hyponatremia with intravenous hypertonic saline solution: Ayus JC, Olivero JJ, Frommer JP: Am J Med 1982; 72: 43–48