scholarly journals Life threatening water intoxication

2020 ◽  
Vol 44 (2) ◽  
pp. 71-77
Author(s):  
Shahad W. Ahmed
Keyword(s):  
Water Intake ◽  
Water Movement ◽  
Fatal Outcome ◽  
Plasma Osmolality ◽  
Water Intoxication ◽  
Osmotic Gradient ◽  
Psychogenic Polydipsia ◽  
Military Population ◽  
Initial Symptoms ◽  
Life Threatening

Water intoxication is a fatal disorder associated with disturbance in brain function, known as hypo-osmolar syndrome which resulting from an excessive water intake, with dilutional hypernatremia leads to a potentially fatal outcome. A change in the electrolyte equilibrium such as this sudden drop in serum sodium level and then subsequent mortality. With hyponatremia, the plasma osmolality decreased leading to water movement into the brain according to the osmotic gradient, resulting in hyponatremic encephalopathy and cerebral oedema. Increased water intake such as in Psychogenic polydipsia is followed by urination of high amount of diluted urine (polyuria) which are the main initial symptoms of water intoxication with headache, blurred vision, nausea, tremor, and deterioration in psychosis. Other serious symptoms involve muscle spasms, Early detection of seizures and coma are more serious outcomes, Untreated cases may lead to death, Risk factor for water intoxication are Marathon runners, military population and athletes and due to this endurance events, these behaviors encouraging heavy sweating that result in heat exhaustion and consume large volumes of fluid, then hyponatremia developed as a result of excessive fluid substitution. Child abuse is other pediatric clinical cases reported with water intoxication. Psychogenic polydipsia which is psychiatric disorder with obsessive water drinking leading to a serious self-induced water intoxication (SIWI), water is normally metabolized and excreted by different means and it is mainly by kidneys in urine, evaporation through the skin, by respiratory system through the respired water vapor and little quantity of water was lost from the gastrointestinal tract (GI).The LD50 of water is > 90 ml/kg orally in rats. The current review illustrates the Life threatening effects of water when it is aggressively consumed.

OSMOTIC INHIBITION OF THE NATRIFERIC RESPONSE OF THE TOAD URINARY BLADDER TO VASOPRESSIN

1975 ◽  
Vol 67 (1) ◽  
pp. 119-125
Author(s):  
P. J. BENTLEY
Keyword(s):  
Urinary Bladder ◽  
Water Movement ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Toad Bladder ◽  
Toad Urinary Bladder ◽  
Electrical Potential Difference ◽  
Osmotic Gradient

SUMMARY The electrical potential difference and short-circuit current (scc, reflecting active transmural sodium transport) across the toad urinary bladder in vitro was unaffected by the presence of hypo-osmotic solutions bathing the mucosal (urinary) surface, providing that the transmural flow of water was small. Vasopressin increased the scc across the toad bladder (the natriferic response), but this stimulation was considerably reduced in the presence of a hypo-osmotic solution on the mucosal side, conditions under which water transfer across the membrane was also increased. This inhibition of the natriferic response did not depend on the direction of the water movement, for if the osmotic gradient was the opposite way to that which normally occurs, the response to vasopressin was still reduced. The natriferic response to cyclic AMP was also inhibited in the presence of an osmotic gradient. Aldosterone increased the scc and Na+ transport across the toad bladder but this response was not changed when an osmotic gradient was present. The physiological implications of these observations and the possible mechanisms involved are discussed.

scholarly journals Urine and Plasma Osmolality in Patients with Autosomal Dominant Polycystic Kidney Disease: Reliable Indicators of Vasopressin Activity and Disease Prognosis?

2015 ◽  
Vol 41 (3) ◽  
pp. 248-256 ◽  
Author(s):  
Niek F. Casteleijn ◽  
Debbie Zittema ◽  
Stephan J.L. Bakker ◽  
Wendy E. Boertien ◽  
Carlo A. Gaillard ◽  
...  
Keyword(s):  
Water Intake ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Kidney Volume ◽  
Polycystic Kidney ◽  
Estimated Gfr ◽  
Total Kidney Volume ◽  
Autosomal Dominant Polycystic Kidney ◽  
Crude Analysis

Background: Vasopressin plays an essential role in osmoregulation, but has deleterious effects in patients with ADPKD. Increased water intake to suppress vasopressin activity has been suggested as a potential renoprotective strategy. This study investigated whether urine and plasma osmolality can be used as reflection of vasopressin activity in ADPKD patients. Methods: We measured urine and plasma osmolality, plasma copeptin concentration, total kidney volume (TKV, by MRI) and GFR (125I-iothalamate). In addition, change in estimated GFR (eGFR) during follow-up was assessed. Results: Ninety-four patients with ADPKD were included (56 males, age 40 ± 10, mGFR 77 ± 32 ml/min/1.73 m2, TKV 1.55 (0.99-2.40) l. Urine osmolality, plasma osmolality and copeptin concentration were 420 ± 195, 289 ± 7 mOsmol/l and 7.3 (3.2-14.6) pmol/l, respectively. Plasma osmolality was associated with copeptin concentration (R = 0.54, p < 0.001), whereas urine osmolality was not (p = 0.4). In addition, urine osmolality was not associated with TKV (p = 0.3), in contrast to plasma osmolality (R = 0.52, p < 0.001) and copeptin concentration (R = 0.61, p < 0.001). Fifty-five patients were followed for 2.8 ± 0.8 years. Baseline plasma and urine osmolality were not associated with change in eGFR (p = 0.6 and p = 0.3, respectively), whereas baseline copeptin concentration did show an association with change in eGFR, in a crude analysis (St. β = -0.41, p = 0.003) and also after adjustment for age, sex and TKV (St. β = -0.23, p = 0.05). Conclusions: These data suggest that neither urine nor plasma osmolality are valid measures to identify ADPKD patients that may benefit from increasing water intake. Copeptin appears a better alternative for this purpose.

scholarly journals Survival from paraquat induced renal impairment in a 17 years old male

2021 ◽  
Vol 8 (2) ◽  
pp. 300
Author(s):  
Medo M. Kuotsu ◽  
N. Biplab Singh ◽  
Nyamnyei Konyak ◽  
Vikie-o Khruomo ◽  
Senjele Kath ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Treatment Options ◽  
Fatal Outcome ◽  
Radical Scavenging ◽  
Case Fatality ◽  
Kidney Injury ◽  
Organ Damage ◽  
Paraquat Poisoning ◽  
Adequate Hydration ◽  
Life Threatening

N, N’-dimethyl-4, 4’-bipyridinium dichloride (paraquat) is a herbicide commonly used in India that leads to fatal outcome on ingestion. Paraquat interferes in the intracellular electron transfer systems inhibiting the reduction of NADP to NADPH resulting in accumulation of superoxide radical causing lipid cell membranes destruction leading to various organ damage. Life threatening effects such as acute kidney injury as paraquat elimination is mainly by kidney, acute respiratory distress syndrome and multi-organ failure are the causes of mortality in paraquat poisoning. There is no specific antidotes for paraquat poisoning so prevention and aggressive decontamination remains the mainstay of management in case of exposure or ingestion. Paraquat poisoning presentation may vary in cases depending on the amount of paraquat consumed and thus the outcome. Here we report a case of a 17 years old male who presented with acute kidney injury following ingestion of paraquat in a suicidal attempt. In our case, induced vomiting of the stomach content readily after ingestion of the poison, early haemodialysis, use of immunosuppression such as methylprednisolone, cyclophosphamide and antioxidants such as acetylcysteine, Vitamin C and Vitamin E as free radical scavenging agent , supportive measures such as adequate hydration and antibiotics might have helped in the patient’s survival. The case fatality remains very high in paraquat poisoning till date owing to lack of effective treatment options.

scholarly journals Endoscopic stent insertion for anastomotic leakage following oesophagectomy

2013 ◽  
Vol 95 (1) ◽  
pp. 43-47 ◽  
Author(s):  
M Schweigert ◽  
N Solymosi ◽  
A Dubecz ◽  
RJ Stadlhuber ◽  
H Muschweck ◽  
...  
Keyword(s):  
Anastomotic Leakage ◽  
Stent Implantation ◽  
Fatal Outcome ◽  
Invasive Procedure ◽  
High Volume ◽  
Primary Treatment ◽  
Stent Insertion ◽  
Endoscopic Stent ◽  
Life Threatening ◽  
Life Threatening Complication

Introduction Intrathoracic anastomotic leakage following oesophagectomy is a crushing condition. Until recently, surgical re-exploration was the preferred way of dealing with this life threatening complication. However, mortality remained significant. We therefore adopted endoscopic stent implantation as the primary treatment option. The aim of this study was to investigate the feasibility and results of endoscopic stent implantation as well as potential hazards and pitfalls. Methods Between January 2004 and December 2011, 292 consecutive patients who underwent an oesophagectomy at a single high volume centre dedicated to oesophageal surgery were included in this retrospective study. Overall, 38 cases with anastomotic leakage were identified and analysed. Results A total of 22 patients received endoscopic stent implantation as primary treatment whereas a rethoracotomy was mandatory in 15 cases. There were no significant differences in age, frequency of neoadjuvant therapy or ASA grade between cases with and without a leak. However, patients with a leak were five times more likely to have a fatal outcome (odds ratio: 5.10, 95% confidence interval: 2.06–12.33, p<0.001). Stent migration occurred but endoscopic reintervention was feasible. In 17 patients (77%) definite closure and healing of the leak was achieved, and the stent was removed subsequently. Two patients died owing to severe sepsis despite sufficient stent placement. Moreover, stent related aortic erosion with consecutive fatal haemorrhage occurred in three cases. Conclusions Stent implantation for intrathoracic oesophageal anastomotic leaks is feasible and compares favourably with surgical re-exploration. It is an easily available, minimally invasive procedure that may reduce leak related mortality. However, it puts the already well-known risk of stent-related vascular erosion on the spot. Awareness of this life threatening complication is therefore mandatory.

SYMPTOMATIC HYPONATREMIA IN ACUTE INFECTIONS OF THE CENTRAL NERVOUS SYSTEM

PEDIATRICS ◽  
1956 ◽  
Vol 18 (4) ◽  
pp. 604-613
Author(s):  
William L. Nyhan ◽  
Robert E. Cooke
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Hypertonic Saline ◽  
Water Intake ◽  
Extracellular Fluid ◽  
Water Intoxication ◽  
Extracellular Fluid Volume ◽  
Acute Infections ◽  
The Central Nervous System ◽  
Acute Hyponatremia

Acute hyponatremia has been noted on seven occasions in five patients with acute infections of the central nervous system. Symptoms were those of water intoxication and the response to the administration of hypertonic saline was prompt and dramatic. The hyponatremia appears to be due to acute expansion of the extracellular fluid volume in association with antidiuresis. Frequent determinations of the concentrations of electrolytes in the serum and prophylactic limitation of water intake are recommended as possible means of reducing mortality in disease of the central nervous system.

Volume influences on thirst and vasopressin secretion in dehydrated sheep

1986 ◽  
Vol 251 (3) ◽  
pp. R621-R626
Author(s):  
R. G. Park ◽  
M. Congiu ◽  
D. A. Denton ◽  
M. J. McKinley
Keyword(s):  
Water Intake ◽  
Water Consumption ◽  
Interstitial Fluid ◽  
Extracellular Fluid ◽  
Plasma Osmolality ◽  
Fluid Volume ◽  
Experimental Protocol ◽  
Vasopressin Secretion ◽  
Total Body ◽  
Reduced Water

The contribution of extracellular fluid volume (ECFV) to water consumption and plasma vasopressin concentration (PAVP) after water deprivation for 52 h was examined in sheep. Intravenous infusion of isotonic NaCl, equivalent to either estimated ECFV loss or total body water loss, significantly reduced water intake by 37% when water was offered 3 h after infusion but not when water was offered 1 h after infusion. Plasma osmolality (POsm) was reduced after 3 h. Infusion of 200 mM NaCl, which maintained POsm, decreased water consumption by the same degree as isotonic NaCl infusion. Thus large decreases in POsm had no effect on water intake in this experimental protocol. Lack of inhibition of drinking 1 h after infusion suggests that the decrease observed after 3 h may have been mediated by receptors in the interstitial fluid (ISF) compartment and not the intravascular compartment. PAVP was reduced 3 h after infusion of NaCl but not at 1 or 2 h after infusion. POsm was also decreased at 3 h. Thus reduction of PAVP by NaCl infusion may have been caused by either ISF or intracellular fluid volume expansion.

Influence of steady-state PaCO2 on escape from ADH-induced water retention in the dog

1978 ◽  
Vol 234 (4) ◽  
pp. F291-F296
Author(s):  
W. D. Kaehny ◽  
A. Gougoux ◽  
J. J. Cohen
Keyword(s):  
Steady State ◽  
Water Intake ◽  
Water Deprivation ◽  
Water Retention ◽  
Plasma Osmolality ◽  
Similar Extent ◽  
Water Excretion ◽  
Average Value ◽  
Marked Disparity ◽  
Per Se

The influence of the prevailing PaCO2 on the water-retaining effects of sustained elevations in ADH was assessed by administering vasopressin (5 U in oil, twice daily) and a fixed water intake to dogs with eucapnia (n, 7), chronic hypercapnia (n, 6), and chronic hypocapnia (n, 8). Although water excretion initially fell to a similar extent in all three groups, cumulative water retention by day 4 of vasopressin administration was 77 mg/kg in the hypocapnic group, 46 ml/kg in the eucapnic group, and only 14 ml/kg in the hypercapnic group. These differences were reflected in a marked disparity in the degree of hyposmolality of body fluids, plasma osmolality falling by day 4 to an average value of 223, 237, and 268 mosmol/kg in the hypocapnic, eucapnic, and hypercapnic animals, respectively. In a separate group of dogs, water deprivation and water loading studies revealed that sustained hypercapnia does not affect the maximal concentrating or diluting ability of the kidney. We conclude, therefore, that the striking influence of the prevailing PaCO2 on the water-retaining effects of administered vasopressin cannot be ascribed to an altered responsiveness of the nephron per se, but that this influence reflects an alteration in the ease with which the kidney can escape from the antidiuretic effects of this substance.

scholarly journals The Vasopressin System in the Risk of Diabetes and Cardiorenal Disease, and Hydration as a Potential Lifestyle Intervention

2018 ◽  
Vol 72 (Suppl. 2) ◽  
pp. 21-27 ◽  
Author(s):  
Sofia Enhörning ◽  
Olle Melander
Keyword(s):  
Type 2 Diabetes ◽  
Water Intake ◽  
Kidney Diseases ◽  
Urine Volume ◽  
Plasma Osmolality ◽  
Premature Mortality ◽  
Urine Osmolality ◽  
High Plasma ◽  
Effective Prevention

Background: Type 2 diabetes, chronic kidney disease (CKD) and its cardiovascular complications are increasing as health problems worldwide. These diseases are interrelated with overlapping occurrence and once diabetes is established, the risk of cardiorenal disease is dramatically elevated. Thus, a search for unifying modifiable risk factors is key for effective prevention. Summary: Elevated fasting plasma concentration of vasopressin, measured with the marker copeptin, predicts new onset type 2 diabetes as well as renal function decline. Furthermore, we recently showed that increased plasma copeptin concentration independently predicts the development of both CKD and other specified kidney diseases. In consequence, high copeptin is an independent risk factor for cardiovascular disease and premature mortality in both diabetes patients and in the general population. Vasopressin is released when plasma osmolality is high, and the easiest way to lower plasma vasopressin and copeptin concentration is to increase water intake. In a human water intervention experiment with 1 week of 3 L/day increased water intake, the one third of the participants with the greatest copeptin reduction (water responders) were those with a phenotype of low water intake (high habitual plasma copeptin and urine osmolality, and low urine volume). The water-responders had a copeptin reduction of 41% after 1 week of increased water intake compared to a control week; in contrast, a 3% reduction occurred in the other two thirds of the study participants. Among water responders, increased water intake also induced a reduction in fasting glucagon concentration. Key Messages: Elevated copeptin, a measure of vasopressin, is a risk marker of metabolic and cardiorenal diseases and may assist in the detection of individuals at higher risk for these diseases. Furthermore, individuals with high copeptin and other signs of low water intake may experience beneficial glucometabolic effects of increased water intake. Future randomized control trials investigating effects of hydration on glucometabolic and renal outcomes should focus on individuals with signs of low water intake including high plasma copeptin concentration.

scholarly journals Retroperitoneal Hematoma Following Enoxaparin Treatment in an Elderly Woman - A Case Report

1970 ◽  
Vol 3 (1) ◽  
pp. 94-97 ◽  
Author(s):  
MM Haq ◽  
SDM Taimur ◽  
SR Khan ◽  
MA Rahman
Keyword(s):  
Acute Coronary Syndrome ◽  
Fatal Outcome ◽  
Anticoagulation Therapy ◽  
Retroperitoneal Hematoma ◽  
Low Molecular Weight ◽  
Retroperitoneal Hemorrhage ◽  
Coronary Syndrome ◽  
Anticoagulation Treatment ◽  
Life Threatening ◽  
Arterial Aneurysms

Retroperitoneal hematoma may occur as a result of trauma, rupture of arterial aneurysms (aortic or iliac), surgical complications, tumors and anticoagulation therapy. A life threatening retroperitoneal hemorrhage or hematoma is an infrequent complication of anticoagulation treatment. Enoxaparin is a low-molecular-weight heparin (LMWH) with several advantages over unfractionated heparin. Nevertheless, enoxaparin use is not without risk and severe retroperitoneal bleeding may occur following its use with a potentially fatal outcome. We report a case of sixty six years old female patient who develops a fatal retroperitoneal hematoma two days after enoxaparin treatment for acute coronary syndrome. Keywords: Retroperitoneal hematoma; Enoxaparin; Acute coronary syndrome. DOI: 10.3329/cardio.v3i1.6434Cardiovasc. j. 2010; 3(1): 94-97

Reduced osmotic water permeability of the peritoneal barrier in aquaporin-1 knockout mice

1999 ◽  
Vol 276 (1) ◽  
pp. C76-C81 ◽  
Author(s):  
Baoxue Yang ◽  
Hans G. Folkesson ◽  
Jian Yang ◽  
Michael A. Matthay ◽  
Tonghui Ma ◽  
...  
Keyword(s):  
Water Transport ◽  
Peritoneal Cavity ◽  
Knockout Mice ◽  
Fluid Transport ◽  
Water Movement ◽  
Osmotic Gradient ◽  
Half Time ◽  
Aquaporin 1 ◽  
Osmotic Water ◽  
Major Route

Aquaporin-1 (AQP1) water channels are expressed widely in epithelia and capillary endothelia involved in fluid transport. To test whether AQP1 facilitates water movement from capillaries into the peritoneal cavity, osmotically induced water transport rates were compared in AQP1 knockout [(−/−)], heterozygous [(+/−)], and wild-type [(+/+)] mice. In (+/+) mice, RT-PCR showed detectable transcripts for AQP1, AQP3, AQP4, AQP7, and AQP8. Immunofluorescence showed AQP1 protein in capillary endothelia and mesangium near the peritoneal surface and AQP4 in adherent muscle plasmalemma. For measurement of water transport, 2 ml of saline containing 300 mM sucrose (600 mosM) were infused rapidly into the peritoneal cavity via a catheter. Serial fluid samples (50 μl) were withdrawn over 60 min, with albumin as a volume marker. The albumin dilution data showed significantly decreased initial volume influx in AQP1 (−/−) mice: 101 ± 8, 107 ± 5, and 42 ± 4 (SE) μl/min in (+/+), (+/−), and (−/−) mice, respectively [ n = 6–10, P < 0.001, (−/−) vs. others]. Volume influx for AQP4 knockout mice was 100 ± 8 μl/min. In the absence of an osmotic gradient,3H2O uptake [half time = 2.3 and 2.2 min in (+/+) and (−/−) mice, respectively], [14C]urea uptake [half time = 7.9 and 7.7 min in (+/+) and (−/−) mice, respectively], and spontaneous isosmolar fluid absorption from the peritoneal cavity [0.47 ± 0.05 and 0.46 ± 0.04 ml/h in (+/+) and (−/−) mice, respectively] were not affected by AQP1 deletion. Therefore, AQP1 provides a major route for osmotically driven water transport across the peritoneal barrier in peritoneal dialysis.

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