Chronic dehydration stone disease

A study was made of 819 patients attending a metabolic stone clinic. A firm diagnosis was made in 708 (86%) and in 132 of these (19%) the diagnosis was thought to be chronic dehydration. The records were available for study for 87 males and 11 females in the chronic dehydration group. The mean age at presentation was 43 years. The causes of chronic dehydration were hot climate (62%), with hot occupation and low water intake almost equal in second place. In patients with a single cause of chronic dehydration, 57% also had a dietary risk factor for urolithiasis and this was most commonly high oxalate intake. Following dietary advice, the mean urinary volume increased from 1720 to 2475 ml/24 h. This was accompanied by a rise in mean urinary calcium from 6.02 to 6.96 mmol/24 h, presumably due to the calcium in the additional water drunk. Urinary oxalate did not change significantly. The mean follow-up time was 4.85 years and the stone recurrence rate was low. It was concluded that chronic dehydration is a common cause of urolithiasis; this can be treated satisfactorily by increasing water intake plus dietary advice in certain cases.     

Salt depletion and dehydration in hypertensive preterm infants

Three preterm infants presented with both severe or moderate arterial hypertension and dehydration due to increased water and sodium urinary excretion. In patient 1, water and sodium wasting were extremely severe and peaked at 575 ml/kg per day and 73 mEq/kg per day, respectively. In all infants, urinary water and sodium excretion dramatically decreased when hypertension resolved. The overall clinical data suggest a pressure natriuresis phenomenon. Received May 15, 1996; received in revised form and accepted September 12, 1996     

The problem of dehydration and healing of burn wounds

In an experiment on rats, a partial thickness burn wound 20 mm in diameter was produced on the dorsum. Half the wound area was left untreated, the other half painted with elastic collodion. Examination on the l0th day following the intervention confirmed that prevention of dehydration can save a good proportion of thermally damaged tissue. It was also shown that prevention of dehydration results in a marked delay in wound healing.     

Six cases of rhabdomyolysis induced by dehydration

Rhabdomyolysis results from a variety of causes. We experienced 6 cases of rhabdomyolysis induced by dehydration in psychoneurosis patients or seniors. We should know dehydration as a risk factor for rhabdomyolysis especially in psychoneurosis patients or seniors.     

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.     

Hyponatremic dehydration: An analysis of 78 cases

Our purpose was to determine the frequency of convulsion in children with hyponatremic dehydration (HD). We also investigated whether or not there was a relationship between the severity of hyponatremia and the degrees of malnutrition in our region (Eastern Anatolia of Turkey) in where malnutrition is frequently observed. In this study, the clinical and laboratory findings of 78 patients with diarrhoea (acute, persistent or chronic diarrhoea) and HD were studied. When diarrhoea lasts longer than 2 and 4 weeks they were accepted as persistent and chronic diarrhoea, respectively. Patients were said to have HD if they had the clinical findings of dehydration associated with hyponatremia [Serum sodium (SNa) <130 mmol/L)]. Nutritional status of the children was assessed by the Gomez classification using weight for age; it was accepted as normal those were between 90%-110%, mild malnutrition 75%-89%, moderate malnutrition 60%-74% and severe malnutrition <60%. Of 78 patients, 40 were boys, 38 were girls. The age and weight of the patients ranged from 40 days to 36 months (8.94 +/- 5.49 months) and from 2000 to 10,300 g (5535.25 +/- 1702.10 g) respectively. All patients except four had malnutrition; 15 (20.3%) had mild malnutrition, 30 (40.5%) had moderate malnutrition and 29 (39.2%) had severe malnutrition. Forty-seven patients had acute, 16 patients had persistent, and 15 patients had chronic diarrhoea. SNa levels were between 104 and 129 mmol/L (121.21 +/- 6.12 mmol/L). There was not statistically a significant difference between SNa level and the degree of malnutrition, and SNa level and the types (acute, persistent or chronic) of diarrhoea (p > 0.05). Of 78 patients, 12 (15.3%) patients had convulsion, of whom eight had convulsion associated with fever. Convulsion was noted in nine (19.1%) and three (18.7%) patients with acute and persistent diarrhoea, respectively (p > 0.05). Also, we observed that when hyponatremia was severer, convulsions tended to be more occuring (p < 0.05). Five (6.4%) children died and all of them had severe malnutrition and septicemia. We determined that the frequency of convulsion in HD was 15.3% (12/78), and there was not a difference between the cases of acute, persistent and chronic diarrhoea for the frequency of convulsion. We also found a significant difference was not present between SNa level and the degree of malnutrition, and between SNa level and the types (acute, persistent or chronic) diarrhoea. However, we observed that when hyponatremia was severer, convulsions tended to be more occuring.     

Reversible renal medullary hyperechogenicity in neonatal hypernatremic dehydration

Three exclusively breastfed term neonates were admitted with lethargy, poor feeding, and oligoanuria. All three babies were severely dehydrated and had a weight loss ranging from 18% to 40%. Serum sodium of more than 180 mEq/l and renal failure were observed in all three. Two had very high creatinine levels of 9.5 mg/dl and 6.7 mg/dl. Both these babies also had multiple seizures. One baby required mechanical ventilation. All three babies showed markedly hyperechoic renal medullary pyramids with speckled foci suggestive of crystal deposition that reversed completely on therapy. Urine showed abundant urate crystals in two and an elevated calcium/creatinine ratio of 1.6 in one. There was no evidence of distal renal tubular acidosis, Bartter syndrome, or high serum calcium. Supersaturation of the ions in a markedly hypertonic renal medulla may have led to crystallization, with resolubilization with hydration and restoration of good urine output. The hypernatremic dehydration was primarily due to lactation failure leading to inadequate fluid intake in the face of ongoing insensible losses. High breast milk sodium may have been a contributory factor in one patient.     

Extracellular fluid and its proteins: dehydration, shock, and recovery

This review highlights characteristics of extracellular fluid (ECF) that are often overlooked. ECF has, in addition to plasma and interstitial fluid (ISF) surrounding cells, a third large compartment, the ISF of skin and connective tissue. This acts as a reservoir that gives up ECF to plasma volume (PV) in order to sustain circulation in the event of either shock or dehydration. While Starling forces drive filtration, ECF is returned to PV more by lymph and less by Starling forces than previously appreciated. Lymph return to PV is dependent on physical activity and muscle contraction to overcome gravity. Regional change in metabolic rate alters the need for oxygen and nutrients that is met by a regional increase in capillary blood flow. Blood flow is controlled by vasoactive compounds released in response to a drop in PO₂; these relax capillary smooth muscle to increase blood flow and delivery of oxygen and nutrients. Plasma proteins, including albumin, are filtered into the interstitium through larger pores than those filtering ECF. The rate of protein filtration is set by size and charge of these larger endothelial pores and by size and charge of proteins. Charge of these pores, hence albumin permeability, is regulated by many of the same vasoactive compounds that control capillary flow. As a consequence, in response to gravitational stress and other forms of shock that reduce effective circulation, albumin as well as ECF is rapidly shifted from plasma and sequestered in ISF. When this has occurred, as in burn shock, restoration is better effected by generous expansion of ECF with Ringer’s solution alone, rather than with Ringer’s solution supplemented with human serum albumin or other colloid. Restoring both PV and ISF volume restores lymph circulation and returns sequestered albumin to PV. Received: 12 November 1998 / Revised: 30 March 1999 / Accepted: 2 April 1999