Relationship of blood lead in women and children to domestic water lead.
Explore the source record for details and available documents.
Child↗
SEARCH · Search PubMed
Results for “Water Intoxication”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Desmopressin (DDAVP) in bleeding disorders of childhood.
As in adults, desmopressin (DDAVP) can be used in children for prophylaxis of bleeding and to stop bleeding in many hereditary and acquired bleeding disorders. DDAVP is the treatment of choice in children with mild hemophilia and type 1 von Willebrand's disease (vWD). It is effective in some variants of vWD and in many patients with platelet function defects. It reduces the bleeding diathesis of children with uremia and drug-induced bleeding complications. In any case, a test dose of DDAVP has to be given to the patient to predict the hemostatic effect before relying on this drug for treatment. The response can be measured by shortening of the bleeding time (BT) and of partial thromboplastin time (PTT), indicating a rise of Factor (F) VIII or von Willebrand factor (vWF). Side effects such as facial flushing, transient headache, increased pulse rate, and drop in systolic blood pressure are mild and transient. They can be minimized when the dose is not exceeding 0.3 microg/kg body weight, and the infusion lasts at least 20 to 30 minutes. The strong antidiuretic action of DDAVP has some potential problems that are negligible in adults and older children when water intake is restricted. In infants and small children under the age of 18 months, however, DDAVP should be used with caution and with close surveillance in order to prevent water intoxication and electrolyte imbalance. The danger is increased when the patients receive parenteral fluid substitution. The advantages of DDAVP include the reduction in the use of plasma factor concentrates, thereby minimizing the danger of immunological or infectious complications, as well as the considerable reduction of costs realized by treatment with this form of medication. Fortunately, it can be applied successfully in the most frequent hereditary bleeding disorder, namely vWD type 1.
Blood Coagulation Disorders↗
Evaluation of freezing point depression osmolality for classifying random urine specimens defined as substituted under HHS/DOT criteria.
This study evaluates the analytical performance characteristics of freezing point depression osmolality in urine and osmolality as a suitable analytical indicator for determining the concentration of urine specimens submitted for workplace drug testing. Specifically, this study attempted to determine the utility of urine osmolality to serve as an indicator of substitution as defined by HHS/SAMHSA criteria. Urine osmolality was validated by determining the accuracy, precision, analytical sensitivity, reportable range, and reference interval for the method. Osmolality was measured in workplace urine specimens (n = 66) with creatinine concentrations < or = 5.0 mg/dL. Comparing the results with the lower limit of the random urine reference intervals for specific gravity (1.002) and osmolality (50 mOsm/kg), 62% had specific gravities < or = 1.001, 52% had osmolalities < 50 mOsm/kg, and 47% had both a creatinine < or = 5.0 mg/dL, specific gravity < or = 1.001 and an osmolality < 50 mOsm/kg. Urine specimens (n = 311) were collected from 35 volunteers enrolled in a controlled water loading study in which at least 80 oz (2370 mL) of fluid was ingested over a 6-h period. The lowest achieved osmolality was 28 mOsm/kg. Polyuria disorders have produced abnormally low urine osmolalities (lowest reported 18 mOsm/kg) but osmolalities < or = 23 mOsm/kg have resulted in death from water intoxication. An osmolality substitution cut-off to delineate a specimen as inconsistent with normal human urine can be set at some value < 50 mOsm/kg, when used in a population of individuals with urine creatinine concentrations < or = 5.0 mg/dL.
Adult↗
The "ecstasy" hangover: hyponatremia due to 3,4-methylenedioxymethamphetamine.
3,4-Methylenedioxymethamphetamine (MDMA, or "ecstasy") has gained an undeserved reputation as a "safe" drug among its users. However, hyperthermia, rhabdomyolysis, hepatotoxicity, disseminated intravascular coagulation, long-term serotonergic neurotoxicity, and death are all associated with MDMA use. Hyponatremia is also reported, and its manifestations are frequently delayed several hours after the drug is ingested. The etiology of this hyponatremia is unclear; both the syndrome of inappropriate antidiuretic hormone release (SIADH) and free-water intoxication are advanced as explanations. We describe a 19-year-old female who presented to the emergency department with altered mental status 1 day after using MDMA. Her initial serum sodium was 121 mmol/L, and computerized tomography (CT) of her head demonstrated cerebral edema. She was treated with hypertonic saline and fluid restriction, and her serum sodium increased to 132 mmol/L over the next 24 hours. She regained consciousness completely within 48 hours of presentation and recovered uneventfully. MDMA toxicity, particularly the pathophysiology and treatment of MDMA-induced hyponatremia, are discussed.
Adult↗
Solute loss plays a major role in polydipsia-related hyponatraemia of both water drinkers and beer drinkers.
BACKGROUND: Polydipsia-related hyponatraemia is generally considered an acute dilutional state. AIM: To determine whether solute loss plays a role in the pathogenesis of polydipsia-related hyponatraemia. DESIGN: Prospective uncontrolled study. METHODS: We studied routine biochemical volume-related parameters before and after 2 l isotonic saline infusion over 24 h, in 10 consecutive hyponatraemic polydipsia patients (mean age 55 +/- 11 years; 6 beer drinkers and 4 compulsive water drinkers) with initial urinary osmolality <220 mosm/kg H(2)O. In five of these patients, we measured balance data over 24 h. RESULTS: Mean initial plasma protein concentration in the 10 studied polydipsia patients was 7 +/- 0.7 g/dl, unexpectedly high for an acute dilutional state. Mean plasma sodium concentration increased from 126 +/- 5 mmol/l before saline, to 135 +/- 5 mmol/l after infusion of 2 l isotonic saline (p < 0.01). Balance data in five polydipsia patients showed a mean decrease of 1.6 kg of their initial body weight and a mean salt retention of 406 mosm. DISCUSSION: Polydipsia-related hyponatraemia is a mixed disorder, in which about half of sodium decrease is due to solute loss. This explains the apparent paradox of a normal plasma protein concentration, despite the increase in body weight due to water intoxication.
Adult↗
MacConkey and glutamate media in the bacteriological examination of seawater.
Explore the source record for details and available documents.
Bacteria↗
Practical aspects of oxcarbazepine treatment.
In patients with refractory seizures, substitution of oxcarbazepine (OCBZ) for carbamazepine (CBZ) may be associated with reduced seizure frequency and an improved mental state. The recommended dosage of OCBZ as monotherapy for adults with epilepsy is 600-1,200 mg orally per day but may be higher in patients with refractory seizures and in patients requiring combination therapy. When OCBZ is substituted for ongoing CBZ therapy, it is possible to change the dosage immediately so that the patient finishes treatment with CBZ on one day and starts with a full dosage of OCBZ on the next day, even when the full dosage is 50% greater in milligrams than the corresponding CBZ dosage. Allergic skin reactions are rare, and crossreactivity is seen in about 25% of patients hypersensitive to CBZ. Hyponatremia after the use of OCBZ is usually benign, as long as the acute water intoxication is effectively treated. Because of its pharmacokinetic advantages and efficacy, we believe OCBZ is better than CBZ. We therefore consider OCBZ as the drug of first choice for conditions in which CBZ is currently indicated.
Adult↗
Effect of torasemide on intracranial pressure, mean systemic arterial pressure and cerebral perfusion pressure in experimental brain edema of the rat.
The study was performed to establish whether a lipophilic loop diuretic, torasemide could modify intracranial pressure and cytotoxic brain edema. Brain edema was induced by water intoxication in nephrectomized rats. Following intravenous injection of 100 mg torasemide/kg body weight at 50, 60, 70, 90 and 120 min, a significant decrease of intracranial pressure was observed.
Animals↗
The nephrotoxicity of Isotropis forrestii in sheep.
Sheep were drenched with a single toxic dose of dried and milled Isotropis forrestii in water. Intoxication resulted in early onset of glycosuria, enzymuria and proteinuria. Terminal gross lesions included pale kidneys and perirenal oedema. Histologically and ultrastructurally the renal lesions were typical of primary nephrotoxicosis, with extensive proximal tubular epithelial necrosis. The tubular damage was sufficient to cause acute primary renal failure, characterised by oliguria, azotemia and failure of urinary concentrating mechanisms.
Animals↗
Lipopolysaccharide-induced acute renal failure in conscious rats: effects of specific phosphodiesterase type 3 and 4 inhibition.
In conscious, chronically instrumented rats we examined 1) renal tubular functional changes involved in lipopolysaccharide (LPS)-induced acute renal failure; 2) the effects of LPS on the expression of selected renal tubular water and sodium transporters; and 3) effects of milrinone, a phosphodiesterase type 3 (PDE3) inhibitor, and Ro-20-1724, a PDE4 inhibitor, on LPS-induced changes in renal function. Intravenous infusion of LPS (4 mg/kg b.wt. over 1 h) caused an immediate decrease in glomerular filtration rate (GFR) and proximal tubular outflow without changes in mean arterial pressure (MAP). LPS-induced fall in GFR and proximal tubular outflow were sustained on day 2. Furthermore, LPS-treated rats showed a marked increase in fractional distal water excretion, despite significantly elevated levels of plasma vasopressin (AVP). Semiquantitative immunoblotting showed that LPS increased the expression of the Na(+),K(+),2Cl(-)-cotransporter (BSC1) in the thick ascending limb, whereas the expression of the AVP-regulated water channel aquaporin-2 in the collecting duct (CD) was unchanged. Pretreatment with milrinone or Ro-20-1724 enhanced LPS-induced increases in plasma tumor necrosis factor-alpha and lactate, inhibited the LPS-induced tachycardia, and exacerbated the acute LPS-induced fall in GFR. Furthermore, Ro-20-1724-treated rats were unable to maintain MAP. We conclude 1) PDE3 or PDE4 inhibition exacerbates LPS-induced renal failure in conscious rats; and 2) LPS treated rats develop an escape from AVP in the CDs, which could be aimed to protect against water intoxication in septic conditions associated with decreased GFR and high levels of AVP.
3',5'-Cyclic-AMP Phosphodiesterases↗
Hyponatraemic convulsion secondary to desmopressin treatment for primary enuresis.
The case of a 6 year old child who presented with convulsions and coma after unsupervised self administration of intranasal desmopressin (DDAVP) for nocturnal enuresis is presented. Children with enuresis can be embarassed by their condition and may believe that multiple doses of their nasal spray may bring about a rapid resolution. Water intoxication is an uncommon but serious adverse effect of treatment with intranasal DDAVP. These patients may present with seizure, mental state changes, or both. Basic management consists of stopping the drug, fluid restriction, and suppressive treatment for seizures. Recovery is usually rapid and complete. Administration of the nasal spray in children should be supervised by parents to prevent highly motivated children from accidental overdose. The risks of high fluid intake need to be carefully explained to both parents and children.
Child↗
Pathology of deaths associated with "ecstasy" and "eve" misuse.
AIMS: To study the postmortem pathology associated with ring substituted amphetamine (amphetamine derivatives) misuse. METHODS: The postmortem findings in deaths associated with the ring substituted amphetamines 3,4-methylenedioxymethyl-amphetamine (MDMA, ecstasy) and 3,4-methylenedioxyethylamphetamine (MDEA, eve) were studied in seven young white men aged between 20 and 25 years. RESULTS: Striking changes were identified in the liver, which varied from foci of individual cell necrosis to centrilobular necrosis. In one case there was massive hepatic necrosis. Changes consistent with catecholamine induced myocardial damage were seen in five cases. In the brain perivascular haemorrhagic and hypoxic changes were identified in four cases. Overall, the changes in four cases were the same as those reported in heart stroke, although only two cases had a documented history of hyperthermia. Of these four cases, all had changes in their liver, three had changes in their brains, and three in their heart. Of the other three cases, one man died of fulminant liver failure, one of water intoxication and one probably from a cardiac arrhythmia associated with myocardial fibrosis. CONCLUSIONS: These data suggest that there is more than one mechanism of damage in ring substituted amphetamine misuse, injury being caused by hyperthermia in some cases, but with ring substituted amphetamines also possibly having a toxic effect on the liver and other organs in the absence of hyperthermia.
3,4-Methylenedioxyamphetamine↗
Long-term treatment of trigeminal neuralgia with carbamazepine.
The results of treating 143 patients with trigeminal neuralgia with carbamazepine (CBZ) over a 16-year period have been reviewed. The drug was effective initially with few mild side effects in 99 patients (69%). Of these, 19 developed resistance later, i.e. between 2 months and 10 years after commencing treatment, and required alternative measures. Of the remaining 80 (56%), the drug was effective in 49 for 1-4 years and in 31 for 5-16 years. Thirty-six patients (25%) failed to respond to CBZ initially and required alternative measures, as did 8 (6%) who were intolerant of the drug. One patient developed CBZ-induced water intoxication with hyponatraemia. Subsequently hyponatraemia was excluded in 17 patients who had been taking CBZ for between 4 months and 7 years. This study has thus confirmed the efficacy of CBZ in the treatment of trigeminal neuralgia and shown that it may continue to be effective for many years.
Aged↗
Response to 1-deamino-8-D-arginine vasopressin in von Willebrand disease.
The synthetic agent, 1-deamino-8-D-arginine vasopressin (DDAVP), is generally regarded to be the treatment of choice for persons with type I von Willebrand disease (vWD), and may be useful in type IIA vWD as well. Several formulations of the drug are available, including a highly concentrated intranasal spray formulation which is ideal for home use. The degree of F VIII and vWF response to DDAVP varies among individuals, but is generally consistent in individual patients over time. Some have tachyphylaxis while others do not. While side effects are uncommon, DDAVP is a potent antidiuretic agent. Thus one should be aware of the possibility of hyponatremia and water intoxication if certain precautions are not observed.
Administration, Intranasal↗
Efficacy, safety, and dosing of desmopressin for nocturnal enuresis in Europe.
Desmopressin is a potent antidiuretic for nocturnal enuresis with few and mostly insignificant adverse reactions. Almost 80 years ago, the antidiuretic effects of extracts of the posterior pituitary were first reported. The molecular structure of the peptide vasopressin arginine vasopressin (AVP) became known in 1956, and by 1967, a synthesized modification of AVP, known as DDAVP, or desmopressin, was introduced. Toxicity studies performed on experimental animals support the conclusion that desmopressin is considerably more potent as an antidiuretic than AVP and has an exceptional safety margin. Further, clinical experience reveals that from 1974 to June 1992 only 21 patients using desmopressin had serious adverse reactions (water intoxication), and no fatalities occurred. Seven of 10 children with nocturnal enuresis who receive desmopressin stop their bedwetting completely or reduce it significantly, with best results noted in children over 10 years of age. Given these results, the preferred treatment in Europe for children with nocturnal enuresis is the sequential combination of desmopressin and the enuresis alarm.
Adolescent↗
Carbamazepine-induced thrombocytopenia, rash, and hepatic dysfunction.
Carbamazepine is an anticonvulsant agent that has been found clinically useful in the treatment of refractory seizure disorders. Its mechanism of action is not well understood. The drug also has been associated with several serious side-effects. These include bone marrow suppression, liver and renal dysfunction, water intoxication, and ocular lens opacities. A 33-year-old white female developed elevated liver enzymes, a rash, and thrombocytopenia following the short-term use of carbamazepine for temporal lobe seizures. All of these findings are consistent with literature reports. Other etiologic factors also are discussed. This case is presented to illustrate the importance of monitoring blood counts and liver function tests when carbamazepine is part of a particular treatment regimen. Clinicians must be aware that a variety of hematological disorders can occur with this drug. Liver dysfunction is usually first noted, with an elevation of liver function tests. When thrombocytopenia is noted, prompt withdrawal of the drug is required. The platelet count should return to normal within a few days.
Adult↗
The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in small-cell lung cancer.
Review of clinical data from 350 patients with small-cell lung cancer (SCLC) revealed hyponatremia (sodium less than 130 mEq/L) attributable to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in 40 patients (11%). Although hyponatremia was severe in most instances (median, sodium 117 mEq/L), symptoms attributable to water intoxication were identified in only 27% of hyponatremic episodes. Development of SIADH showed no correlation with clinical stage, distribution of metastatic sites, sex, or histologic subtype of small-cell carcinoma. SIADH occurred most often with initial presentation (33 of 40), and resolved promptly (less than 3 weeks) with initiation of combination chemotherapy in 80% of evaluable patients. The presence of SIADH did not influence response to chemotherapy or overall survival as an independent variable. However, in five patients profound hyponatremia developed immediately following primary cytotoxic therapy (range, one to five days). Despite initial control of SIADH, dilutional hyponatremia recurred in 70% of patients with tumor progression. Our findings suggest that development of clinically demonstrable SIADH in patients with SCLC is dependent on functional properties of the neoplastic cells, rather than tumor burden or metastatic site. The potential for development of clinically significant hyponatremia early in the course of cytotoxic therapy emphasizes the need to closely monitor patients, particularly those receiving chemotherapy regimens requiring substantial intravenous hydration.
Antineoplastic Combined Chemotherapy Protocols↗
Carbamazepine diminishes the sensitivity of the plasma arginine vasopressin response to osmotic stimulation.
Carbamazepine, a drug used to treat manic-depressive illness, has been reported to possess antidiuretic properties, but its effects on arginine vasopressin (AVP) secretion are controversial. Consequently, we examined plasma AVP secretion during hypertonic (5%) saline infusion in seven manic-depressive patients while on placebo and after 3-5 weeks of carbamazepine treatment. We also measured carbamazepine's effects on basal levels of the hormone in cerebrospinal fluid. Carbamazepine significantly reduced the sensitivity of the plasma AVP response to osmotic stimulation without affecting the osmotic threshold for AVP secretion. Moreover, carbamazepine did not affect baseline weight, plasma osmolality, plasma sodium, urine output, plasma AVP, or cerebrospinal fluid AVP. Although the functional significance of these findings remain to be fully determined, the fact that carbamazepine significantly reduced AVP secretion without inducing diuresis supports previous suggestions that carbamazepine enhances renal responsivity to available AVP. In addition, since carbamazepine failed to affect the osmotic threshold, the reported cases of carbamazepine-induced inappropriate AVP secretion and water intoxication must be very uncommon and probably represent idiosyncratic responses.
Arginine Vasopressin↗