BACKGROUND: Therapeutic plasma exchange (TPE) is an effective and practical treatment for separation and removal of harmful antibodies or pathogenic substances from the blood. The volume of plasma removed must be replaced by a replacement fluid such as 4~5% albumin solution or Fresh frozen plasma (FFP). We conducted a study of coagulopathy using albumin solution and checked the chemical composition of fresh frozen plasma. METHODS: We measured pre- and post-TPE PT/aPTT for evaluation of the effect of albumin replacement on coagulation from 192 TPE sessions of 19 patients. We also investigated routine chemistry test items including glucose and electrolytes from 10 randomly selected FFP. RESULTS: The post PT and aPTT within four hours after TPE were prolonged due to a transient decrease in coagulation factors, but were normalized within 2 days after TPE. All coagulation time was corrected to the level of the pre-TPE status within four hours before the next TPE except the patients who received TPE 6 times or more. FFP showed higher level in glucose, sodium and inorganic phosphate. CONCLUSION: Albumin exchange produces temporary coagulation factor deficiency. However, this transient factor deficiency rarely causes clinical problems and the factors are rapidly corrected by redistribution and resynthesis. We should be careful about hypocalcemia, hyperglycemia, and hypernatremia when using FFP replacement.
Antibodies ; Blood Coagulation Factors ; Chemistry ; Electrolytes ; Glucose ; Humans ; Hyperglycemia ; Hypernatremia ; Hypocalcemia ; Plasma ; Plasma Exchange* ; Sodium

Hypernatremic dehydration is an important cause of intracranial hemorrhage. A possible association of intraventricular hemorrhage (IVH) with hypernatremia and/or high sodium intake has been suggested in preterm infants. To investigate the associations of early fluid and sodium intake or serum sodium concentrations with severe intraventricular hemorrhage (IVH) in extremely low birth weight (ELBW) infants, we reviewed the medical records of 169 inborn ELBW infants. Daily fluid and sodium intake, urine output, weight loss and serum sodium concentration during the first 4 days of life were obtained. Patients were divided into the severe IVH (grade 3/4) and the control (no or grade 1/2 IVH) group. The maximum serum sodium concentration and the incidence of hypernatremia did not differ between the two groups. Related to the fluid balance and sodium intake, the risk for severe IVH was strongly associated with total fluid and sodium intake during the initial four days of life. With respect to the fluids other than transfusion, severe IVH can be discriminated only by sodium intake but not by fluid intake. Large randomized controlled trials are required to clarify the causal relationship between the early sodium intake and severe IVH in ELBW infants.
Birth Weight ; Dehydration ; Drinking ; Heart Ventricles/*pathology ; Hemorrhage/mortality/*pathology ; Humans ; Hypernatremia/*blood ; Infant ; Infant Mortality ; Infant, Extremely Low Birth Weight/*blood ; Infant, Newborn ; Infant, Premature ; Infant, Premature, Diseases/epidemiology ; Retrospective Studies ; Sodium/*blood ; Sodium, Dietary

Hypernatremic dehydration is an important cause of intracranial hemorrhage. A possible association of intraventricular hemorrhage (IVH) with hypernatremia and/or high sodium intake has been suggested in preterm infants. To investigate the associations of early fluid and sodium intake or serum sodium concentrations with severe intraventricular hemorrhage (IVH) in extremely low birth weight (ELBW) infants, we reviewed the medical records of 169 inborn ELBW infants. Daily fluid and sodium intake, urine output, weight loss and serum sodium concentration during the first 4 days of life were obtained. Patients were divided into the severe IVH (grade 3/4) and the control (no or grade 1/2 IVH) group. The maximum serum sodium concentration and the incidence of hypernatremia did not differ between the two groups. Related to the fluid balance and sodium intake, the risk for severe IVH was strongly associated with total fluid and sodium intake during the initial four days of life. With respect to the fluids other than transfusion, severe IVH can be discriminated only by sodium intake but not by fluid intake. Large randomized controlled trials are required to clarify the causal relationship between the early sodium intake and severe IVH in ELBW infants.
Birth Weight ; Dehydration ; Drinking ; Heart Ventricles/*pathology ; Hemorrhage/mortality/*pathology ; Humans ; Hypernatremia/*blood ; Infant ; Infant Mortality ; Infant, Extremely Low Birth Weight/*blood ; Infant, Newborn ; Infant, Premature ; Infant, Premature, Diseases/epidemiology ; Retrospective Studies ; Sodium/*blood ; Sodium, Dietary

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 > or =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.
Blood Urea Nitrogen ; Creatinine ; Female ; Glucose ; Humans ; Hypernatremia ; Osmolar Concentration ; Renal Dialysis ; Sodium ; Specific Gravity ; Uremia ; Water

Type 1 myotonic dystrophy (DM1) is an autosomal-dominant inherited disorder with a multisystem involvement, caused by an abnormal expansion of the CTG sequence of the dystrophic myotonia protein kinase (DMPK) gene. DM1 is a variable multisystem disorder with muscular and nonmuscular abnormalities. Increasingly, endocrine abnormalities, such as gonadal, pancreatic, and adrenal dysfunction are being reported. But, Electrolytes imbalance is a very rare condition in patients with DM1 yet. Herein we present a 42-yr-old Korean male of DM1 with abnormally elevated serum sodium and potassium. The patient had minimum volume of maximally concentrated urine without water loss. It was only cured by normal saline hydration. The cause of hypernatremia was considered by primary hypodipsia. Hyperkalemic conditions such as renal failure, pseudohyperkalemia, cortisol deficiency and hyperkalemic periodic paralysis were excluded. Further endocrine evaluation suggested selective hyperreninemic hypoaldosteronism as a cause of hyperkalemia.
Adult ; Humans ; Hyperkalemia/complications/*diagnosis ; Hypernatremia/complications/*diagnosis ; Hypoaldosteronism/complications/diagnosis ; Kidney Concentrating Ability ; Male ; Myotonic Dystrophy/complications/*diagnosis/*genetics ; Potassium/blood ; Protein-Serine-Threonine Kinases/*genetics ; Sodium/blood

Hyperosmolar hyperglycemic syndrome (HHS) or hyperglycemic hyperosmolar nonketotic coma, an acute complication of type 2 diabetes mellitus, is commonly associated with hypernatremia. According to the treatment guideline of HHS and hypernatremia, plasma glucose and sodium concentration should be lowered at the recommended correction rate to prevent cerebral edema and, rarely, central pontine myelinolysis (CPM) or extrapontine myelinolysis (EPM). Recently we experienced a case of HHS with initial corrected serum sodium concentration of 198.5 mEq/L. The hypernatremia was corrected too rapidly on the first and second hospital days and the patient showed recent memory disturbance and difficulty in communication on the third hospital day. Brain MRI revealed abnormal signal intensities in the extrapontine areas, in favor of a diagnosis of EPM. We concluded that EPM of this case was induced by the rapid correction of hypernatremia.
Blood Glucose ; Brain ; Brain Edema ; Diabetes Mellitus, Type 2 ; Diagnosis ; Humans ; Hyperglycemic Hyperosmolar Nonketotic Coma ; Hypernatremia ; Magnetic Resonance Imaging ; Memory ; Myelinolysis, Central Pontine* ; Sodium

OBJECTIVETo explore the pathogenesis and the management of hypernatremia in burn patients.

METHODSTwenty eight burn patients with hypernatremia were enrolled in the study and were divided into infection and non-infection groups. The pathogenesis, clinical features, biochemical indices in blood, the therapeutic results and the prognosis were compared between the two groups.

RESULTSIn non-infection group, the hypernatremia was mainly induced by improper fluid resuscitation and occurred on the 3.1 postburn day (PBD), while that in the infected group, on 7.2 PBD. The patients in non-infected group exhibited much more excited and the blood levels of glucose and urea nitrogen (BUN) were obviously decreased when compared with those in the infected group (P < 0.01). The survival rate in non-infected and infected group were 94.12% and 9.09%, respectively.

CONCLUSIONThe mortality rate of the patients with hypernatremia could be lowered by means of taking optimal measures according to the different patterns of hypernatremia.

Adult ; Blood Glucose ; metabolism ; Blood Urea Nitrogen ; Burns ; blood ; complications ; mortality ; Female ; Humans ; Hypernatremia ; etiology ; mortality ; therapy ; Infection ; complications ; Male ; Middle Aged ; Survival Rate ; Treatment Outcome

Hypernatremia developing in nonhospitalized adults is predominantly a disease of the elderly and mentally handicapped patients, possibly revealing inadequate nursing care of these patients. It has long been claimed that the duration of hypernatremia and its rate of correction are correlated with improvement in patients' neurologic status. Since there are only a handful of cases with serum sodium levels greater than 200 mEq/L until recently, it is not clear at what rate plasma sodium concentration can be safely normalized in severe hypernatremic patients. We report a case of severe hypernatremia with survival. This patient underwent rapid correction of serum sodium concentration during the management of this metabolic derangement using isotonic solution.
Journal Article ; Female ; Human ; Hypernatremia/therapy* ; Hypernatremia/physiopathology ; Hypernatremia/blood ; Middle Age ; Sodium/blood* ; Treatment Outcome

BACKGROUND: Marked derangements in acid-base status are frequently seen during orthotopic liver transplantaton. To prevent the progression of metabolic acidosis, treatment with sodium bicarbonate has been recommended. However, sodium bicarbonate may exacerbate intracellular acidosis, increase plasma lactate, contribute to hypernatremia. The value of giving bicarbonate has been questioned. Accordingly, we reviewed the intraoperative the acid-base status of patients who underwent orthotopic liver transplatation. METHODS: We reviewed ten patients showed severe metabolic acidosis (7.2 < pH < 7.30 and base deficit (BD) > or = 10). Despite of BD > or = 10, sodium bicarbonate was not given to all. Intraoperative pH and BD were analyzed retrospectively. RESULTS: At the anhepatic and immediate post-reperfusion periods, the pH was decreased (P < 0.05) and BD was increased (P < 0.05), but both were normalized at the end of surgery. The mean blood pressure transiently decreased at the immediate post-reperfusion periods (P < 0.05), but that was acceptable. CONCLUSIONS: This study showed that a severe metabolic acidosis is tolerated by the patients undergoing orthotopic liver transplantation without administration of sodium bicarbonate.
Acidosis ; Blood Pressure ; Humans ; Hydrogen-Ion Concentration ; Hypernatremia ; Lactic Acid ; Liver Transplantation* ; Liver* ; Plasma ; Retrospective Studies ; Sodium Bicarbonate* ; Sodium*

BACKGROUND: Marked derangements in acid-base status are frequently seen during orthotopic liver transplantaton. To prevent the progression of metabolic acidosis, treatment with sodium bicarbonate has been recommended. However, sodium bicarbonate may exacerbate intracellular acidosis, increase plasma lactate, contribute to hypernatremia. The value of giving bicarbonate has been questioned. Accordingly, we reviewed the intraoperative the acid-base status of patients who underwent orthotopic liver transplatation. METHODS: We reviewed ten patients showed severe metabolic acidosis (7.2 < pH < 7.30 and base deficit (BD) > or = 10). Despite of BD > or = 10, sodium bicarbonate was not given to all. Intraoperative pH and BD were analyzed retrospectively. RESULTS: At the anhepatic and immediate post-reperfusion periods, the pH was decreased (P < 0.05) and BD was increased (P < 0.05), but both were normalized at the end of surgery. The mean blood pressure transiently decreased at the immediate post-reperfusion periods (P < 0.05), but that was acceptable. CONCLUSIONS: This study showed that a severe metabolic acidosis is tolerated by the patients undergoing orthotopic liver transplantation without administration of sodium bicarbonate.
Acidosis ; Blood Pressure ; Humans ; Hydrogen-Ion Concentration ; Hypernatremia ; Lactic Acid ; Liver Transplantation* ; Liver* ; Plasma ; Retrospective Studies ; Sodium Bicarbonate* ; Sodium*