Central pontine and extrapontine myelinolysis after rapid correction of hyponatremia by hemodialysis in a uremic patient

Osmotic demyelination syndrome, a well-known entity, is characterized by demyelination in the pons and extrapontine areas. Rapid correction of chronic hyponatremia is its most important cause. This report presents a 52-year-old man with uremia and hyponatremia. Demyelination syndrome developed after the first hemodialysis session. Brain images showed central pontine myelinolysis and extrapontine myelinolysis. This case emphasizes the fact that demyelination syndrome can occur when hyponatremia is corrected too rapidly, even in uremic patients. Lowering dialysate sodium with multiple, short durations of hemodialysis at a low blood flow rate should be prescribed during hemodialysis in select hyponatremic patients.     

Central and extrapontine myelinolysis in a patient in spite of a careful correction of hyponatremia

We report the case of a 54-year-old alcoholic female patient who was hospitalized for neurologic alterations along with a severe hyponatremia (plasma Na+: 97 mEq/l). She suffered from potomania and was given, a few days before admission, a thiazide diuretic for hypertension. A careful correction of plasma Na+ levels was initiated over a 48-hour period (rate of correction < 10 mEq/l/24h) in order to avoid brain demyelination. After a 2-day period of clinical improvement, her neurologic condition started to deteriorate. By the 5th day of admission, she became tetraplegic, presented pseudobulbar palsy, ataxia, strabism, extrapyramidal stiffness and clouding of consciousness. Scintigraphic and MRI investigations demonstrated pontine and extrapontine lesions associated with Gayet-Wernicke encephalopathy. After correction of ionic disorders (hyponatremia, hypokaliemia) and vitamin B (thiamine) deficiency, the patient almost completely recovered without notable disabilities. This case illustrates that profound hyponatremia, in a paradigm of slow onset, can be compatible with life. It also demonstrates that demyelinating lesions, usually considered as a consequence of a too fast correction of hyponatremia, may occur despite the strict observance of recent guidelines. There is increasing evidence to suggest that pontine swelling and dysfunction may sometimes occur in alcoholic patients even in absence of disturbance in plasma Na+ levels. It is therefore of importance, while managing a hyponatremic alcoholic patient, to identify additional risk factors (hypokaliemia, hypophosphoremia, seizure-induced hypoxemia, malnutrition with vitamin B deficiency) for brain demyelination and to correct them appropriately.     

Brain dehydration and neurologic deterioration after rapid correction of hyponatremia

We made rats severely hyponatremic, varying the rate of onset and duration of the disturbance, and then compared rapid correction to slow correction. An acute fall in the plasma Na to 106 mEq/liter within seven hours caused seizures and coma, but these findings resolved and survival was 100% after either rapid or slow correction. A more gradual fall in plasma Na to 95 mEq/liter in three days caused neither seizures nor coma. Measurements of brain water and electrolytes showed that adaptive losses of brain Na and K (maximally depleted within seven hours) and slower losses of non-electrolyte solutes progressively reduced brain edema. After three days of hyponatremia, rapid correction to 119 mEq/liter with 1 M NaCl or to 129 mEq/liter by withdrawing DDAVP caused brain dehydration because lost brain K and non-electrolyte solutes were recovered slowly. This treatment was followed by a delayed onset of severe neurologic findings, demyelinating brain lesions and a mortality rate of over 40%. Slow correction (0.3 mEq/liter/hr) avoided these complications and permitted 100% survival. We conclude that the rat adapts quickly to hyponatremia and can survive with extremely low plasma sodium concentrations for prolonged periods. Although rapid correction is well tolerated when hyponatremia is of brief duration, it may cause brain damage in animals that have had time to more fully adapt to the disturbance.     

Severe hyponatremia occurring after surgical stress in a patient with mitochondrial disease

A 53-year-old man with mitochondrial disease underwent gastrectomy because of gastric cancer. Three days after the surgery, he developed severe hyponatremia (Na, 106 mmol·l^?1) together with hypovolemic shock and lactic acidosis. Despite the hyponatremia, his urine sodium concentration was high, suggesting renal salt wasting. Although mitochondrial diseases are not common and hyponatremia in patients with these diseases is not well known, clinicians should pay close attention to serum sodium levels and maintain them properly.     

Centropontine myelinolysis after correction of hyponatremia: role of associated hypokalemia

BACKGROUND: Patients with severe hyponatremia have a high risk for centropontine myelinolysis (CPM) during treatment, but the incidence rate and risk factors have not been well-assessed. METHODS: This study was conducted in a medical intensive care unit (ICU) of a university teaching hospital. All patients with a serum sodium concentration < 120 mmol/l and a serum osmolality level < 250 mosmol/kg upon ICU admission were enrolled in this prospective study and were included if they underwent a baseline brain computerized tomography scan (CT scan) and a follow-up brain magnetic resonance imaging 1 month after admission. The diagnosis of CPM was based on cerebral magnetic resonance imaging findings, i.e. T1-weighted images with T2-weighted images showing hyperintense signal in the corresponding areas which were not apparent on the initial cerebral CT scan. RESULTS. Of the 22 patients included, 12 were considered as having acute hyponatremia and 8 were chronic alcoholics. In 12 patients, the increase in serum sodium level was < 12 mmol/I in any 24-hour period. CPM was diagnosed in 7/22 patients (31.8%) and was asymptomatic in 4 of them. CPM was present in 4 patients with acute hyponatremia and in 4 chronic alcoholics. It was associated with a lower baseline potassium level (p = 0.05) and NaCl administration during the first 24 hours (p = 0.005). However, non-acute hyponatremia, chronic alcoholism and rapid correction of serum sodium did not appear as risk factors. CONCLUSION: The incidence rate of CPM following severe hyponatremia is high and can develop even when there is a slow correction of serum sodium level. Hypokalemia is a predisposing factor.     

Cerebral pathology and hyponatremia. Cerebral damage with central pontine myelinolysis after rapid correction

Hyponatremia is a state of relatively common observation among neurosurgical patients and it may determine or precipitate a condition of brain swelling in the head-injured. The quick reversal to normal values of serum sodium concentration may cause relevant neurological disturbances: they are related to peculiar neuropathological changes, the most representative of which is central pontine myelonilysis. Two cases (one in pediatric age) of head injured patients with brain damage resulting from rapid correction of a SIADH related hyponatremia are presented.     

DDAVP to prevent rapid correction in hyponatremia

Correction of hyponatremia can be complicated by brisk free water diuresis with a rise in the serum sodium (s-Na) in excess of the generally accepted rate of 10-15 mmol/l/24 hours. We describe this complication and its treatment with desmopressin (dD-AVP), in a 56-year-old female with severe hyponatremia secondary to polydipsia and antidiuretic (ADH) activity. The patient developed a large free water diuresis with a markedly dilute urine (urine osmolality 61 mmol/kg) and a rise in the serum sodium of 19 mmol/l in 19 hours despite the addition of large volumes of free water intravenously and orally. To reduce the free water excretion, desmopressin (dD-AVP) 8 microg was given intravenously. This resulted in a rise in the urinary osmolality, a reduction in the urine volume, and a 2 mmol/l reduction in the serum sodium. Thereafter, the serum sodium rose 4 mmol/l in 24 hours. There were no neurological sequellae. In cases of appropriate but rapid correction of hyponatremia secondary to rapid free water diuresis, dD-AVP can safely reduce the free water excretion, slow the rate of correction of the serum sodium and simplify the fluid therapy of the patient.     

Recurrent hyponatremia in a patient with chronic kidney disease

Hyponatremia, albeit common in chronic renal insufficiency, necessitates a detailed search of the underlying hidden causes. We report on a 67-year-old woman with chronic kidney disease (creatinine 230 micromol/L) and hypertension who suffered from general fatigue, dizziness, nausea, vomiting and abdominal fullness off and on for 6 months. Hyponatremia (plasma Na(+) 106-125 mmol/L) on 4 occasions during the past 6 months was noticed. Her extracellular volume status was apparently normal. Plasma Na(+) concentration 110 mmol/L was the most striking laboratory abnormality with mild metabolic acidosis (HCO(3)- 19.8 mmol/L). Her urine Na(+) concentration and osmolality were inappropriately high. Her hyponatremia was refractory to normal saline, hypertonic NaHCO(3) and 0.1-microg 9 alfa-fludrocortisone. Despite normal plasma cortisol and thyroid hormone concentrations, a provocation test with cosyntropin (250 microg) showed a blunted cortisol (<579 nmol/L) but intact aldosterone response. Magnetic resonance imaging of her brain displayed a normal pituitary gland and hypothalamus. A history of intermittent intravenous steroid therapy to treat her allergic rhinitis for 3 years was uncovered. Steroid supplements induced water diuresis and corrected hyponatremia to 135 mmol/L in 5 days. With nonspecific clinical symptoms, glucocorticoid insufficiency must be kept in mind as a cause of hyponatremia even in patients with impaired renal function and normal plasma cortisol concentration.     

Anesthetic management of a patient with severe hyponatremia

A 62-year-old woman was scheduled for an operation for ileus. Before the operation, we noticed severe hyponatremia (Na 117 mEq x l(-1)) probably due to dehydration. We corrected her hyponatremia slowly to avoid central pontine myelinolysis. Serum Na level increased to 131 mEq x l(-1) after surgery. She recovered from anesthesia without any neurologic problems.     

Isotonic hyponatremia and cerebrospinal fluid sodium during and after transurethral resection of the prostate

We examined the effects on the central nervous system of hyponatremia during transurethral resection of the prostate (TURP). Initially, a prospective study was done on 165 consecutively treated patients undergoing TURP, to evaluate symptoms related to the serum osmolality. There were ten patients with hyponatremia below 120 mEq·L⁻¹, and in whom the serum sodium decreased to 111.9±6.4 mEq·L⁻¹ (mean±SD) postoperatively, the measured serum osmolality remained near normal. The calculated osmolality decreased to 237.4±11.9 mOsm·kg⁻¹ and the estimated osmolar gap was 33.5±10.4 mOsm·kg⁻¹ due to absorption of the irrigating sorbitol. Neurological symptoms were mild and complications such as seizures or loss of consciousness nerver occurred. There were five other patients with hyponatremia (serum sodium 118.0±6.7 mEq·L⁻¹) from whom lumbar cerebrospinal fluid (CSF) was collected before and after TURP through a single puncture. CSF sodium did not decrease throughout 1.5 h after TURP, and there was a CSF-to-serum sodium gradient. Our study shows that in cases of acute dilution hyponatremia during and after TURP, symptoms are mild because the serum osmolality remains near normal and CSF sodium does not decrease despite severe postoperative hyponatremia.     

Anesthetic management of a patient with severe hyponatremia]

A 79 year old man, with left femoral neck fracture, was scheduled for an elective operation. After admission, severe hyponatremia probably due to diuretics developed. No neurological abnormalities were observed before surgery. He recovered from anesthesia with no problems. But on the 5th postoperative day he showed transient unresponsiveness. Grand mal seizures were also seen after the serum Na level had recovered to around 130 mEq.l-1. This case shows that in the management of severe hyponatremia, the discrimination between acute and chronic hyponatremia seems to be important.     

Changes in serum sodium concentration after transurethral procedures

The aim of this study is to evaluate the changes in serum sodium concentration and the degree of correlation with factors such as the amount of intravenous fluid intake, the kind and the amount of irrigating fluids and the duration of the procedure. In this framework, 98 male patients who underwent transurethral procedure were studied and the correlation between the magnitude of hyponatraemia and the above-mentioned parameters was evaluated. All procedures were performed under spinal anesthesia and a solution of either manitol–sorbitol or sterilized water was used as irrigation fluid. Serum sodium concentration was measured before and after the procedure, while the kind and amount of the irrigating fluids, the amount of fluid intake and the duration of the procedure were also recorded. The patients were divided into three groups according to the duration of the procedure (i) <30 min, (ii) 30–60 min, and (iii) >60 min. Significant reduction in serum sodium concentration was found postoperatively (P < 0.001) and this was more profound in procedures longer than 1 h. This reduction was strongly correlated only with the duration of the transurethral procedure (P < 0.01). In conclusion, in transurethral procedures the reduction in serum sodium is postoperatively related to the duration of the procedure, while the intravenous and irrigating fluids to play no role on it.