Role of antidiuretic hormone in hyponatremia in patients with isolated adrenocorticotropic hormone deficiency.

We found symptomatic hyponatremia in four elderly patients in which serum sodium (Na) levels ranged from 101 to 122 mEq/l. All 4 patients had low levels of plasma adrenocorticotropic hormone (ACTH), serum cortisol, and urinary excretion of 17-OHCS, and poor responses of ACTH to exogenous insulin and antidiuretic hormone (ADH). Other pituitary hormones were all normal. They were therefore diagnosed as having isolated ACTH deficiency. Plasma ADH was relatively high despite hypoosmolality which was associated with the hyponatremia. Water loading test revealed impaired water excretion and poor suppression of plasma ADH. Replacement with 20-30 mg hydrocortisone completely restored the serum Na level and restored the plasma ADH level to the normal range in all 4 patients. Other factors such as decreased glomerular filtration, enhanced urinary Na loss and decreased Na intake were also included. These results indicate that there is marked hyponatremia and that in the presence of hypoosmolality the sustained secretion of ADH is the key factor in causing the impaired water excretion and hyponatremia in isolated ACTH deficiency.     

Maternal dehydration: impact on ovine amniotic fluid volume and composition

Maternal dehydration consistent with mild water deprivation or moderate exercise results in maternal and fetal plasma hyperosmolality and increased plasma arginine vasopressin (AVP). Previous studies have demonstrated a reduction in fetal urine and lung fluid production in response to maternal dehydration or exogenous fetal AVP. As fetal urine and perhaps lung liquid combine to produce amniotic fluid, maternal dehydration may affect the amniotic fluid volume and/or composition. In the present study, six chronically-prepared pregnant ewes with singleton fetuses (128 +/- 1 day) were water deprived for 54 h to determine the effect on amniotic fluid. Maternal plasma osmolality (306.5 +/- 0.9 to 315.6 +/- 1.9 mOsm/kg) and AVP (1.9 +/- 0.2 to 22.2 +/- 3.2 pg/ml) significantly increased during dehydration. Similarly, fetal plasma osmolality (300.0 +/- 0.9 to 312.7 +/- 1.7 mOsm/kg) and AVP (1.4 +/- 0.1 to 10.4 +/- 2.4 pg/ml) increased in parallel to maternal values. Amniotic fluid osmolality (276.8 +/- 5.7 to 311.6 +/- 6.5 mOsm/kg) and sodium (139.8 +/- 4.8 to 154.0 +/- 5.4 mEq/l) and potassium (9.1 +/- 1.3 to 13.9 +/- 2.4 mEq/l) concentrations increased while a significant (35%) reduction in amniotic fluid volume occurred (871 +/- 106 to 520 +/- 107 ml). These results indicate that maternal dehydration may have marked effects on maternal-fetal-amniotic fluid dynamics, possibly contributing to the development of oligohydramnios.     

Vascular responses to plasma hypoosmolality in man.

To study limb vascular responses to plasma hypoosmolality in man, we infused test solutions of hypoosmolar NaCl (145 mOsm/kg) and control solutions of isosmolar NaCl (290 mOsm/kg) into the brachial arteries of 14 mornotensive and 13 essential hypertensive patients. Limb blood pressures were monitored, limb blood flow was measured by indicator-dilution, and limb vascular resistance was calculated as mmHg/ml flow/min/100 cm3 limb volume. The infusions did not significantly change systemic plasma osmolality, sodium concentration, or blood pressure. Compared to control infusions, the hypoosmolar infusions decreased limb venous plasma osmolality and serum sodium concentrations by an average of 12 mOsm/kg and 7 mEq/1, respectively. Compared to control infusions, limb venous serum concentrations of potassium, calcium, magnesium, or blood hematocrit were not altered by the hypoosmolar infusions. In response to the hypoosmolar infusions, limb resistance increased by 28% in normotensives and by 26% in hypertensives. We conclude that the acute local vascular response to a small reduction in plasma osmolality in the limb of man is a large increase in vascular resistance. We found no evidence for abnormal responses to plasma hypoosmolality in essential hypertensives.     

Role of vasopressin in rats with bilateral ureteral obstruction

After unilateral release of bilateral ureteral obstruction (BUO), there is a significant increase in renal vasoconstriction that accounts for the marked decrease in glomerular filtration rate and effective renal plasma flow seen in this setting. We examined the potential role of antidiuretic hormone (ADH), a vasoconstrictor of the renal circulation, on renal hemodynamics in female Sprague-Dawley rats with BUO of 24-hr duration. Rats with BUO had significantly higher plasma values of ADH 65.1 +/- 12.2 vs. 12.1 +/- 4.1 pg/ml), sodium (145.4 +/- 0.91 vs 138.6 +/- 1.06 mEq/liter), and osmolality (375.6 +/- 2.0 vs 310.1 +/- 3.6 mOsm/kg) than sham-operated rats. Rats with BUO pretreated with enalapril, an angiotensin-converting enzyme inhibitor, before obstruction had somewhat higher, but not significantly different, plasma values for ADH (84.6 +/- 20.8 pg/ml) than rats with BUO not given enalapril. Rats with unilateral ureteral obstruction of 24-hr duration had plasma levels of ADH (8.2 +/- 1.3) not different from those in sham-operated rats. Rats with BUO pretreated with a specific antagonist of the V1-type receptor for ADH had significantly greater values for the glomerular filtration rate (2.31 +/- 0.24 vs 1.44 +/- 0.08 ml/min/kg body wt) and the effective renal plasma flow (8.95 +/- 0.71 vs 3.81 +/- 0.44 ml/min/kg body wt) and significantly lower values for mean arterial pressure (140.3 +/- 2.0 vs 159.1 +/- 5.5 mm Hg) than did BUO rats not given the antagonist. The results indicate that high levels of ADH play an important role in the decrease in the glomerular filtration rate and effective renal plasma flow observed in rats with BUO of 24 hr. The significant increase in ADH levels after BUO of 24-hr duration may be due to an increase in osmotic stimulation as a consequence of hypernatremia. Activation of the renin-angiotensin axis, known to occur after BUO or unilateral ureteral obstruction of 24-hr duration, does not appear to have a role in the increased circulating levels of ADH.     

Plasma arginine vasotocin and angiotensin II in the water deprived Kelp gull (Larus dominicanus), Cape gannet (Sula capensis) and Jackass penguin (Spheniscus demersus)

1. The basal levels of the osmoregulatory hormones, arginine vasotocin (AVT) and angiotensin II (AII) were measured (by radioimmunoassay) in the plasma of conscious Kelp gulls, Cape gannets and Jackass penguins. 2. The responses of the hormones to similar degrees of hypertonicity and hypovolemia caused by water deprivation have also been determined. 3. Dehydration elevated plasma AVT and plasma AII in all three species. 4. The AVT concentration was increased by 2-4 fold and although in each case the correlation between plasma osmolality and plasma AVT was highly significant (2P less than 0.01), the sensitivity of release was greater in the gull (1.13 pg/ml per mOsm/kg) than in the gannet (0.36 pg/ml per mOsm/kg) or penguin (0.44 pg/ml per mOsm/kg). 5. Dehydration increased plasma AII 3-fold in the three bird types.     

Empty sella following spontaneous resolution of a pituitary macroadenoma

BACKGROUND/AIM: Empty sella is a radiological finding characterized by the presence of arachnoid herniation into the sella, resulting in compression of the pituitary against the sella wall. The objective of this case presentation is to discuss secondary empty sella in a patient with spontaneous resolution of a pituitary macroadenoma. METHODS: A case of empty sella syndrome is presented. Static and dynamic testing was performed. Etiology, pituitary function, and imaging are discussed. RESULTS: A 69-year-old African-American woman was referred by her primary care physician for evaluation and treatment of 'hypothyroidisim'. Thyroid tests were performed because of muscle and joint tenderness and revealed low free thyroxine and normal thyroid-stimulating hormone levels. The diagnosis of secondary hypothyroidism was made, and magnetic resonance imaging (MRI) of the pituitary revealed an empty sella turcica. In retrospect, the patient had presented 11 years earlier with tinnitus, and an MRI of her auditory canals demonstrated an 'incidental' 1.5-cm pituitary tumor. No endocrine evaluation was done at that time, and neurosurgical follow-up of the pituitary tumor by serial MRIs demonstrated the genesis into empty sella. CONCLUSIONS: In our patient the natural history of her pituitary tumor was that it involuted and resulted in an empty sella. Although oftentimes speculated as a cause of empty sella, tumor involution has rarely been shown to be causative. In this instance, empty sella was associated with hypopituitarism. This case illustrates the importance of endocrine evaluation of patients with this radiological finding.     

Plasma levels of arginine vasotocin,prolactin, aldosterone and corticosterone during prolonged dehydration in the domestic flowl: effect of dietary NaCl

Three groups of White Plymouth Rock laying hens were adapted to three levels of dietary NaCl: low-NaCl food with tap water (LOW), high-NaCl food (1% NaCl w/w added) with tap water (HT), and high-NaCl food with 0.5% NaCl for drinking (HS). The birds were subjected to water deprivation (dehydration) for 18 days. Blood sampling was done at 2-4 day intervals. Plasma concentrations of arginine vasotocin (AVT), prolactin (PRL), aldosterone (ALDO) and corticosterone (CS) were determined by radioimmunoassay. Plasma osmolality, sodium, chloride, and potassium were also determined. In the normally hydrated hens fully adapted to the diets, there was a stepwise increase from LOW to HS in plasma osmolality (305, 315, 332 mOsm, for LOW, HT and HS, respectively), [Na+] (144, 153, 161 mM) and [Cl-] (109, 119, 127 mM) as well as in [AVT] (6, 14, 18 pg/ml) and [PRL] (16, 24, 34 ng/ml). Regressing [AVT] on osmolality gave a slope of 0.30 pg . ml-1/mOsm and a threshold of 273 mOsm. The slope of [PRL] on osmolality was 0.73 ng . ml-1/mOsm. The correlation coefficient of [AVT] and [PRL] was 0.67. LOW had high [ALDO] (165 pg/ml) which was suppressed to low levels in HT and HS (5-8 pg/ml), while [CS] was the same in all groups (0.9-1.1 ng/ml). Plasma [K+] was decreased in the high-NaCl groups (5.8 mM in LOW, 4.4 and 4.7 mM in HT and HS). Dehydration resulted within 2 days generally in a sharp (5-15%) increase in osmolality, [Na+] and [Cl-], which thereafter increased more slowly during the remaining 16 days in all groups, with the slowest increase in LOW. The levels of osmolality [Na+] and [Cl-] were 5% lower in LOW than in HT and HS, which showed the same levels during the dehydration period. Plasma [AVT] and [PRL] increased 2-4 fold within 2 days of dehydration; [AVT] reached a plateau at 29 pg/ml in all groups, but [PRL] continued to rise in all groups, fastest in LOW, reaching similar levels in all groups after 14-18 days of dehydration, about 85 ng/ml. The correlation coefficient of [AVT] and [PRL] was decreased by half (to 0.32) during dehydration. Plasma [ALDO] increased in all groups with dehydration, 1.7 fold in LOW and 3-6 fold in HT and HS, but the levels reached in HT and HS were only 15-30% of that seen in LOW.(ABSTRACT TRUNCATED AT 400 WORDS)     

May primary empty sella turcica be a cause of isolated ACTH deficiency? A case report and the review of related literature

Isolated ACTH deficiency is an uncommon cause of secondary adrenocortical insufficiency and accompaniment with primary empty sella has been reported in several cases. We present a case of isolated ACTH deficiency associated with empty sella. A sixty-two year old woman was admitted to our endocrine clinic with complaints of weakness, fatigue, weight loss, nausea, vomiting, and lack of appetite for about one month. Physical examination indicated orthostatic hypotension and epigastric tenderness. Laboratory investigations revealed hypoglycemia, hyponatremia and anemia, in addition low plasma cortisole and ACTH levels. Serum cortisole responses to short and prolonged ACTH stimulation were tested and partial and accurate responses were obtained, respectively. Plasma ACTH and serum cortisole levels failed to respond after intravenous injection of human corticotropin releasing hormone. Other hypophysial hormone levels were within the normal reference ranges. Although cranial and abdominal computerized tomography images were evaluated as normal, cranial magnetic resonance imaging of the pituitary gland revealed 'primary empty sella turcica'. Replacement therapy with methylprednisolon resulted in the improvement of hypoglycemia, hyponatremia and clinical symptoms. Based on these results, the patient was diagnosed as isolated ACTH deficiency and was scheduled for follow up by our outpatient clinic. Our report is consistent with other reports pointing out that primary empty sella may be responsible for pathogenesis of isolated ACTH deficiency.     

Osmotic stimuli and NaCl-intake in the fowl; release of arginine vasotocin and prolactin

White Plymouth Rock hens were fed a high- and a low-NaCl content of the diet. The two groups were exposed to moderate dehydration, to intra-arterial hyperosmotic NaCl-loading, or to injection of physiological doses of arginine vasotocin (AVT). The plasma levels of AVT and prolactin were measured by accurate and sensitive radioimmunoassay and the osmolality and Na, K (and Cl) concentrations also measured for 48 h after dehydration, and for 60-90 min after NaCl-loading or AVT-injection. The plasma concentration of AVT after a given increase of plasma osmolality was in all experiments found higher in the low- as compared to the high-NaCl diet group. The average difference was 0.2 pg/ml X mOsm. The intra-arterial injection of AVT resulted in a strictly mono-exponential fall over the next hour with an average half-life of 6.3 min without any difference between the high- and the low-NaCl diet groups. It is concluded (a) that the release of prolactin after osmotic stimulation is most likely caused by a direct effect of osmolality (or Na concentration) and not by AVT, (b) that the release of AVT is influenced by the NaCl-intake in a direction which tends to maintain extracellular volume.     

Central and systemic antidiuretic hormone and angiotensin II in salt and fluid balance of birds as compared to mammals

1. Tonicity dominates the release of ADH with similar sensitivities (0.2-1 pg/ml per mOsm/kg) for both birds and mammals. 2. There is an inverse relationship between the volume of the extracellular fluid compartments and the plasma level of ADH. 3. Angiotensin II formation is governed by volume factors. 4. In birds the factors reducing the delivery of Na+ to the nephron distal tubules stimulate ANGII formation. 5. Mammals have a high vascular constrictor sensitivity to ADH and ANGII; there is little or no vascular sensitivity to these in birds. 6. In birds and mammals the subfornical organ and other circumventricular organs have receptors that specifically bind ANGII. 7. Dog and duck CSF levels of ADH and AII indicate their function as specific mediators of intrinsic neuronal systems controlling salt and fluid balance.     

Syndrome of Inappropriate Antidiuretic Hormone Secretion Associated with Coproporphyria: Case Report and Review of Literature

ObjectiveTo remind physicians to consider the hepatic porphyrias in the differential diagnosis of the syndrome of inappropriate antidiuretic hormone secretion.MethodsWe present a case report of a patient seen in the hospital for severe hyponatremia, who was discovered to have the syndrome of inappropriate antidiuretic hormone secretion attributable to coproporphyria. Results of laboratory tests of the patient and her family are presented.ResultsA 54-year-old woman was seen in the hospital because of severe hyponatremia accompanied by generalized seizures. Her serum sodium concentration was 112 mEq/L, with concomitant serum and urine osmolalities of 235 and 639 mOsm/kg, respectively. Renal, thyroid, and adrenal functions were normal. Brain, chest, abdominal, and pelvic imaging studies were negative for occult malignant disease. Urinary excretions of porphobilinogen and aminolevulinic acid were substantially elevated. Results of follow-up urine, plasma, and fecal porphyrin studies were consistent with coproporphyria. Results of porphyrin metabolic studies of the patient’s family showed normal findings in her parents and a minimally increased fecal coproporphyrin concentration and urinary uroporphyrin excretion in her sister.ConclusionAn endocrinology consultation is often requested for patients with hyponatremia. It is important to consider the acute hepatic porphyrias in the differential diagnosis, even though these are rare disorders and the family history may not always be helpful because of the high frequency of asymptomatic carriers. (Endocr Pract. 2007;13:164-168)     

Plasma concentration of antidiuretic hormone in patients with chronic renal insufficiency on maintenance dialysis.

Radioimmunoassay of plasma arginine-vasopressin (AVP) in regularly dialyzed patients with chronic renal insufficiency revealed a parallel increase of AVP and plasma osmolality (POsm) before dialysis (4.16 +/- 0.36 pg/ml and 312.6 +/- 1.80 mOsm/1) and their parallel declin to the normal range (1.93 +/- 0.27 pg/ml and 292.0 +/- 1.27 mOsm/1) during dialysis. Plasma AVP correlated with POsm before and after dialysis (r = 0.611 and 0.453, p less than 0.01 and less than 0.05 respectively). The increase of AVP before dialysis was lower than would correspond to the rise of POsm and lower than that recorded in healthy subjects during dehydration. Statistical correlation between plasma AVP and indicators of body fluid volume changes between or during dialysis were not proved. We found statistical correlation between the mean blood pressure and AVP before dialysis (r = 0.468, p less than 0.05). These findings suggest that in chronic renal insufficiency changes of POsm remain primary regulating factor of AVP secretion. The expansion of extracellular fluid volume has probably only a modifying effect. It remains to be elucidated whether the revealed statistical relationship between the mean blood pressure and AVP before dialysis plays also a pathogenetic role in the development of hypertension in chronic renal insufficiency.     

Hyponatremia-induced brain edema in guinea pigs is reduced by treatment with the novel anion transport inhibitor L-644,711

Cerebral edema in various disease states may result from astroglial swelling due to increased NaCl uptake mediated by enhanced Cl-HC03 exchange. We evaluated this mechanism in the pathogenesis of cerebral edema in acute hyponatremia by administering L-644,711, a fluorenyloxyacetate derivative that functions as an anion exchange inhibitor, to guinea pigs with severe reductions in serum Na+ concentration. Acute hyponatremia was induced for 54 hr by daily injections of arginine vasopressin (10 U/day) and 5% dextrose in water (7.5% body wt/day). Experimental animals received L-644,711, 20 mg/kg/day, while controls were given an equal volume of the diluent. This regimen lowered the serum Na from normal levels to 108 +/- 3 and 109 +/- 4 mM in experimental and control animals, respectively. Drug treatment resulted in less cerebral edema characterized by a reduction in brain total tissue water 432 +/- 4 vs 466 +/- 8 ml/100 g dry wt experimental vs control, P less than 0.005. This difference was composed mainly of less expansion of the intracellular water space, 287 +/- 11 vs 323 +/- 9 ml/100 g dry wt experimental vs control, p less than 0.005. The cerebral cortical Na+ +Cl content was reduced from 55.5 +/- 1.3 (control) to 39.5 +/- 1.1 mEq/100 g dry wt (experimental), p less than 0.01. These results indicate that treatment of guinea pigs with L-644,711 decreases brain NaCl content and attenuates cerebral edema during severe acute hyponatremia without normalizing the serum Na+ concentration.     

A case of partial hypopituitarism with empty sella following normal course of pregnancy and delivery

A 28 year-old woman was admitted to Jichi Medical School Hospital because of amenorrhea, cold intolerance, easy fatigability and body weight loss. She was pregnant at the age of 26 years. She delivered a 3230 g healthy girl at full term without any complications. However, she did not have any lactation or recurrence of menstruation after the delivery. Serum cortisol was 0.7 micrograms/dl, and plasma adrenocorticotropic hormone (ACTH) was less than 10 pg/ml. Both hormones failed to increase in response to insulin-induced hypoglycemia or exogenous arginine vasopressin. However, serum cortisol and urinary excretion of 17-hydroxycorticosteroids (17-OHCS) were significantly increased by the repeated administration of ACTH. Serum prolactin was 2.2 ng/ml and the level did not rise after the administration of thyrotropin releasing hormone (TRH). Responses of release of adenohypophysial hormones including gonadotropins, growth hormone and thyroid stimulating hormone (TSH) were normal. Serological studies showed an antibody to the pituitary gland which was demonstrated by an indirect immunofluorescence technique. Plain skull X-ray film and brain computerized tomography revealed an empty sella of the normal size. These results indicate the presence of partial deficiency of ACTH and prolactin, and that autoimmune disorders may be involved in the pathogenesis of her hypopituitarism.     

Plasma antidiuretic hormone (ADH) concentrations in cattle, during various water and feed regimes

Twelve steers of three different breeds were exposed to five feed and water regimes in order to characterize changes in plasma antidiuretic hormone (ADH) concentrations. No breed differences were found in plasma ADH concentration. Plasma ADH concentration rose (4.2 to 22.0 pg/ml) during dehydration. By 3 hr hydration, plasma ADH concentrations dropped dramatically (over 50%) to 9.2 pg/ml. No changes in plasma ADH concentrations occurred during feed restriction and refeeding. Hematocrit percentages were also determined and differences are hypothesized to relate to probable differences in environmental adaptability and genetic selection for meat or milk production among the three breeds.     

Responses of the rat kidney to the water load test and vasopressin administered during normal feeding and fasting

Parameters of water-salt balance in Wistar rats were compared on empty stomach and at standard alimentary regimen (satiated animals). On empty stomach, the blood serum osmolatity amounted to 284 +/- 2, while in satiated rats--to 290 +/- 5 mOsm/kg H2O (p < 0.05); sodium ion concentration on empty stomach lower, whereas no difference in potassium concentration was found. After an intragastric administration of water (5 ml/100 g body mass) to unanaesthetised rats, the blood serum osmolality decreased, while diuresis increased to an equal extent in both groups of rats. For 120 min after the water administration the rats on an empty stomach excreted 92.9% of the administrated fluid, whereas the satiated animals--80.7%. The urine composition differed qualitatively: in fasting rats the increment of diuresis was due to a rise of osmotic free water excretion, whereas in satiated rats--to an increase of excretion of osmotic active substances (including Na and K ions) with water and a simultaneous increase of the osmotic free water reabsorption in the kidney. After the water load and injection of 0.005 nmole/100 g body mass of arginine-vasopressin for 2 hr of the study, diuresis in both groups of animals decreased to an equal extent, but in fasting animals this was due mostly to an increase of the osmotic free water. The data obtained indicate that, under conditions of usual alimentary regimen, the response of kidney to the water load had a character of a volume-regulating response, whereas in fasting rats--of the specific osmorequlating one. A problem is discussed of the concept of norm under usual conditions and at certain clinically accepted restrictions, for instance, on empty stomach.     

Profound Hypokalemia in Diabetic Ketoacidosis: A Therapeutic Challenge

ObjectiveTo describe profound hypokalemia in a comatose patient with diabetic ketoacidosis.MethodsWe present a case report, review the mechanisms for the occurrence of hypokalemia in diabetic ketoacidosis, and discuss its management in the setting of hyperglycemia and hyperosmolality.ResultsA 22-year-old woman with a history of type 1 diabetes mellitus was admitted in a comatose state. Laboratory tests revealed a blood glucose level of 747 mg/dL, serum potassium of 1.9 mEq/L, pH of 6.8, and calculated effective serum osmolality of 320 mOsm/kg. She was intubated and resuscitated with intravenously administered fluids. Intravenous administration of vasopressors was necessary for stabilization of the blood pressure. Intravenous infusion of insulin was initiated to control the hyperglycemia, and repletion of total body potassium stores was undertaken. A total of 660 mEq of potassium was administered intravenously during the first 12.5 hours. Despite such aggressive initial repletion of potassium, the patient required 40 to 80 mEq of potassium daily for the next 8 days to increase the serum potassium concentration to normal.ConclusionProfound hypokalemia, an uncommon initial manifestation in patients with diabetic ketoacidosis, is indicative of severe total body potassium deficiency. Under such circumstances, aggressive potassium repletion in a comatose patient must be undertaken during correction of other metabolic abnormalities, including hyperglycemia and hyperosmolality. Intravenously administered insulin should be withheld until the serum potassium concentration is ≥ 3.3 mEq/L. (Endocr Pract. 2005;11:331-334)     

Plasma concentrations of arginine vasotocin, prolactin, aldosterone and corticosterone in relation to oviposition and dietary NaCl in the domestic fowl

The osmolality and concentrations of Na, K, Cl and the hormones arginine vasotocin (AVT), prolactin, aldosterone and corticosterone were measured in plasma as functions of time in relation to oviposition, changing NaCl content of the diet, and feeding-inanition. AVT was significantly increased immediately after oviposition (but not during the hour before) with a calculated average value of 38.0 +/- 4.1 pg/ml at oviposition. A moderate increase in concentrations of prolactin and corticosterone were observed immediately after oviposition. Oviposition was not associated with detectable changes in plasma osmolality (and electrolyte concentrations) nor with the concentration of aldosterone. After a sudden change from a high NaCl diet to a low NaCl diet the plasma osmolality and concentrations of NaCl, AVT and prolactin reached new stable levels in 24 hr, whereas the plasma aldosterone concentration required more than 4 days to reach a steady level. After resalination plasma aldosterone was suppressed in less than 8 hr. Both osmolality and concentrations of AVT and prolactin showed transient overshoots during the first 24 hr. NaCl depletion resulted in a transient increase of corticosterone.     

Hypodypsia and selective dysfunction of osmoreceptors in the hypernatremia syndrome

We studied a patient with the rare syndrome of chronic hypernatremia associated with a frontal expansive process. The pituitary function was evaluated during dynamic tests bearing on radioimmunoassay of serum neurophysins levels. A test of water restrictionloading was performed during which urine appeared diluted (190-200 mOsm/kg) while the degree of serum osmolality was high (310-317 mOsm/kg). An hemodynamic stimulation resulted in a significant increase in serum neurophysins (from 3.5 +/- 0.3 to 5.5 +/- 0.2 ng/ml). After one intravenous injection of 2 mg nicotine, vomiting was observed, followed by a sharp rising of serum neurophysins levels (from 3.2 +/- 0.5 to 10.6 +/- 0.2 ng/ml). During hypertonic saline infusion, serum osmolality increased from 270 to 310 mOsm/kg, while neurophysins showed no significant change. Such results evidence a selective impairment of the hypothalamic-neurohypophyseal response to osmotic stimuli, with intact mechanisms of non-osmotic stimulation. In this patient, natremia was brought back to normal values by adequate water supply.     

Hyponatremia in the postoperative craniofacial pediatric patient population: a connection to cerebral salt wasting syndrome and management of the disorder.

Hyponatremia after cranial vault remodeling has been noted in a pediatric patient population. If left untreated, the patients may develop a clinical hypoosmotic condition that can lead to cerebral edema, increased intracranial pressure, and eventually, to central nervous system and circulatory compromise. The hyponatremia has traditionally been attributed to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH); however, in our patients the treatment has been resuscitation with normal saline as opposed to fluid restriction (the accepted treatment of SIADH), thus placing the diagnosis of SIADH in question. Patients who developed hyponatremia after intracranial injury or surgery were, until recently, grouped together as having SIADH. However, there are diagnosis and treatment differences between SIADH and another distinct but poorly understood disorder that is designated cerebral salt wasting syndrome (CSW). CSW is associated with increased urine output and increased urine sodium concentration and volume contraction, and it is frequently seen after a central nervous system trauma. We therefore developed a prospective study to evaluate the cause of the sodium imbalance.Ten consecutive pediatric patients who underwent intracranial surgery for various craniosynostotic disorders were postoperatively monitored in the pediatric intensive care unit for hemodynamic, respiratory, and fluid management. The first four patients were evaluated for electrolyte changes and overall fluid balance to determine the consistency with which these changes occurred. The remaining six patients had daily (including preoperative) measurement of serum electrolytes, urine electrolytes, urine osmolarity, serum antidiuretic hormone (ADH), aldosterone, and atrial natriuretic hormone (ANH). All patients received normal saline intravenous replacement fluid in the postoperative period.All of the patients developed a transient hyponatremia postoperatively, despite normal saline resuscitation. Serum sodium levels as low as 128 to 133 mEq per liter (normal, 137 to 145 mEq per liter) were documented in the patients. All patients had increased urine outputs through the fourth postoperative day (>1 cc/kg/h). The six patients who were measured had an increased ANH level, with a peak value as high as 277 pg/ml (normal, 25 to 77 pg/ml). ADH levels were low or normal in all but one patient, who had a marked increase in ADH and ANH. Aldosterone levels were variable. On the basis of these results, all but one patient showed evidence of CSW characterized by increased urine output, normal or increased urine sodium, low serum sodium, and increased ANH levels. The other patient had similar clinical findings consistent with CSW but also had an increase in ADH, thus giving a mixed laboratory picture of SIADH and CSW.The association of CSW to cranial vault remodeling has previously been ignored. This study should prompt reevaluation of the broad grouping of SIADH as the cause of all hyponatremic episodes in our postoperative patient population. An etiologic role has been given to ANH and to other, as yet undiscovered, central nervous system natriuretic factors. All of the patients studied required normal saline resuscitation, a treatment approach that is contrary to the usual management of SIADH. These findings should dictate a change in the postoperative care for these patients. After cranial vault remodeling, patients should prophylactically receive normal saline, rather than a more hypotonic solution, to avoid sodium balance problems.