1/47. Transient pseudo-hypoaldosteronism following resection of the ileum: normal level of lymphocytic aldosterone receptors outside the acute phase.Pseudo-hypoaldosteronism (PHA) is due to mineralocorticoid resistance and manifests as hyponatremia and hyperkalemia with increased plasma aldosterone levels. It may be familial or secondary to abnormal renal sodium handling. We report the case of a 54-year-old woman with multifocal cancer of the colon, who developed PHA after subtotal colectomy, ileal resection and jejunostomy. She was treated with 6 g of salt daily to prevent dehydration, which she stopped herself because of reduced fecal losses. One month later she was admitted with signs of acute adrenal failure, i.e. fatigue, severe nausea, blood pressure of 80/60 mmHg, extracellular dehydration, hyponatremia (118 mmol/l); hyperkalemia (7.6 mmol/l), increased blood urea nitrogen (BUN) (200 mg/dl) and creatininemia (2.5 mg/dl), and decreased plasma bicarbonates level (HCO3-: 16 mmol/l; N: 27-30). However, the plasma cortisol was high (66 microg/100 ml at 10:00 h; N: 8-15) and the ACTH was normal (13 pg/ml, N: 10-60); there was a marked increase in plasma renin activity (>37 ng/ml/h; N supine <3), active renin (869 pg/ml; N supine: 1.120), aldosterone (>2000 pg/ml; N supine <150) and plasma AVP (20 pmol/l; N: 0.5-2.5). The plasma ANH level was 38 pmol/l (N supine: 5-25). A urinary steroidogram resulted in highly elevated tetrahydrocortisol (THF: 13.3 mg/24h; N: 1.4 /-0.8) with no increase in tetrahydrocortisone (THE: 3.16 mg/24h; N: 2.7 /-2.0) excretion, and with low THE/THF (0.24; N: 1.87 /-0.36) and alpha THF/THF (0.35; N: 0.92 /-0.42) ratios. The number of mineralocorticoid receptors in mononuclear leukocytes was in the lower normal range for age, while the number of glucocorticoid receptors was reduced. Small-bowel resection in ileostomized patients causes excessive fecal sodium losses and results in chronic sodium depletion with contraction of the plasma volume and severe secondary hyperaldosteronism. Nevertheless, this hyperaldosteronism may be associated with hyponatremia and hyperkalemia suggesting PHA related to the major importance of the colon for the absorption of sodium. In conclusion, this case report emphasizes 1) the possibility of a syndrome of acquired PHA with severe hyperkalemia after resection of the ileum and colon responding to oral salt supplementation; 2) the major increase in AVP and the small increase in ANH; 3) the strong increase in urinary THF with low THE/THF and alpha THF/THF ratios; 4) the normal number of lymphocytic mineralocorticoid receptors outside the acute episode.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
2/47. Dual facets of hyponatraemia and arginine vasopressin in patients with ACTH deficiency.OBJECTIVE: Hyponatraemia is often observed in patients with ACTH deficiency who are thought not to suffer from volume depletion. Their high plasma AVP levels relative to plasma osmolality are presumed to be maintained by non-osmotic mechanisms. We attempted to assess volume status from changes in selected clinical measurements related to body fluid balance in the course of i.v. fluid supplementation and following glucocorticoid (GC) replacement in ACTH-deficient patients, and to interpret plasma AVP levels in the context of the estimated volume status. patients AND DESIGN: This report consists of three parts. First, an ACTH-deficient patient with hyponatraemia and volume depletion who was followed through volume replacement to recovery after GC replacement is described (case report). Secondly, medical records of five ACTH-deficient patients with hypovolaemia and hyponatraemia were surveyed retrospectively to observe changes in serum levels of sodium, uric acid (UA) and haematocrit (Hct) following i.v. fluid supplementation of low sodium content (retrospective study). Thirdly, five ACTH-deficient patients with or without overt dehydration were studied with regard to body weight, blood pressure, serum sodium, total proteins, Hct and blood urea nitrogen before and after GC replacement (prospective study). Plasma AVP levels were measured after i.v. fluid supplementation without GC replacement in the patients of the retrospective study, and before and after GC replacement in the patients of the prospective study. RESULTS: The first patient became more hyponatraemic after i.v. fluid supplementation and recovered ultimately from hyponatraemia after GC replacement. In five patients studied retrospectively, the serum sodium levels fell progressively following i.v. fluid supplementation, concurrent with reduction in UA levels and Hct, which indicated the dilutional nature of the hyponatraemia. In the patients observed prospectively, the accumulation of fluid and sodium was indicated by a rise in body weight, blood pressure and serum sodium levels and a decline in Hct and total proteins after GC replacement. Plasma AVP levels rose similarly in patients with dilutional hyponatraemia and in patients with borderline hyponatraemia before GC replacement. CONCLUSION: patients with untreated ACTH deficiency may have either of two kinds of hyponatraemia--i.e. borderline hyponatraemia associated with subclinical hypovolaemia, or dilutional hyponatraemia. Similarity of plasma AVP levels in two hyponatraemic states suggests their AVP secretion is regulated by non-osmotic, non-volume mechanisms, possibly released from GC suppression at low plasma osmolality.- - - - - - - - - - ranking = 2keywords = pressure (Clic here for more details about this article) |
3/47. syndrome of inappropriate secretion of antidiuretic hormone associated with idiopathic normal pressure hydrocephalus.A 79-year-old woman suffering from urinary incontinence and unsteady gait was diagnosed as having idiopathic normal pressure hydrocephalus (NPH) with hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The concentration of antidiuretic hormone was high while the plasma osmolality was low in the presence of concentrated urine during the episodes of hyponatremia. magnetic resonance imaging (MRI) of the head showed enlargement of the third and lateral ventricles. After ventriculoperitoneal shunt surgery, the symptoms of NPH and hyponatremia improved. It may be possibly explained that mechanical pressure on the hypothalamus from the third ventricle is responsible for hyponatremia.- - - - - - - - - - ranking = 6keywords = pressure (Clic here for more details about this article) |
4/47. hyponatremia-induced metabolic encephalopathy caused by Rathke's cleft cyst: a case report.Rathke's cleft cysts are sometimes associated with aseptic meningitis or metabolic encephalopathy due to hyponatremia. We treated such a case manifest by lethargy, fever and electroencephalographic abnormalities. A 68-year-old man was admitted to our ward after experiencing general malaise, nausea and vomiting and then high fever and lethargy. On admission, he was drowsy and had nuchal rigidity and Kernig's sign. Physically, he was pale with dry, thickened skin. He had lost 5.0 kg of body weight in the last month. His serum sodium was 115 mEq/l. He had a low serum osmotic pressure (235 mOsmol/l) and a high urine osmotic pressure (520 mOsmol/l). His urine volume was 1200-1900 ml/24 h with a specific gravity of 1008-1015. The urine sodium was 210 mEq/l. He did not have an elevated level of antidiuretic hormone. Electroencephalograms showed periodic delta waves over a background of theta waves. With sodium replacement, the patient become alert and symptom free, and his electroencephalographic findings normalized. However, the serum sodium level did not stabilize, sometimes falling with a recurrence of symptoms. magnetic resonance imaging clearly delineated a dumbbell-shaped intrasellar and suprasellar cyst. The suprasellar component subsequently shrunk spontaneously and finally disappeared. An endocrinologic evaluation showed panhypopituitarism. The patient was given glucocorticoid and thyroxine replacement therapy, which stabilized his serum sodium level and permanently relieved his symptoms. A transsphenoidal approach was performed. A greenish cyst was punctured, and a yellow fluid was aspirated. The cyst proved to be simple or cubic stratified epithelium, and a diagnosis of Rathke's cleft cyst was made. The patient was discharged in good condition with a continuation of hormonal therapy. Rathke's cleft cyst can cause aseptic meningitis if the cyst ruptures and its contents spill into the subarachnoid space. Metabolic encephalopathy induced by hyponatremia due to salt wasting also can occur if the lesion injures the hypothalamus and pituitary gland.- - - - - - - - - - ranking = 2keywords = pressure (Clic here for more details about this article) |
5/47. syndrome of inappropriate antidiuretic hormone secretion associated with lisinopril.OBJECTIVE: To describe a case of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) associated with lisinopril therapy. CASE SUMMARY: A 76-year-old white woman who was being treated with lisinopril and metoprolol for hypertension presented with headaches accompanied by nausea and a tingling sensation in her arms. Her serum sodium was 109 mEq/L, with a serum osmolality of 225 mOsm/kg, urine osmolality of 414 mOsm/kg, and spot urine sodium of 122 mEq/L. diclofenac 75 mg qd for osteoarthritic pain and lisinopril 10 mg qd for hypertension was begun in 1990. lisinopril was increased to 20 mg qd in August 1994 and to 20 mg bid pm in August 1996 for increasing blood pressure; metoprolol 50 mg qd was added in July 1996. A diagnosis of SIADH was postulated and further evaluation was undertaken to exclude thyroid and adrenal causes. After lisinopril was discontinued and the patient restricted to 1000 mL/d of fluid, serum sodium gradually corrected to 143 mEq/L. The patient was discharged taking metoprolol alone for her hypertension; serum sodium has remained > or =138 mEq/L through April 1999, 32 months after discharge, despite daily use of diclofenac. DISCUSSION: Angiotensin-converting enzyme (ACE) inhibitors in antihypertensive doses may block conversion of angiotensin I to angiotensin ii in the peripheral circulation, but not in the brain. Increased circulating angiotensin I enters the brain and is converted to angiotensin ii, which may stimulate thirst and release of antidiuretic hormone from the hypothalamus, eventually leading to hyponatremia. CONCLUSIONS: SIADH should be considered a rare, but possible, complication of therapy with lisinopril and other ACE inhibitors.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
6/47. hypertension-hyponatremia syndrome in neonates: case report and review of literature.hypertension hyponatremia syndrome occurred in a 32-week male neonate following septicemic shock on Day 9. The systolic blood pressure rose from 60 to 85 mmHg as the serum sodium dropped from 136 to 121 mmol/L associated with natriuresis, polyuria, and dehydration. Convulsions occurred at a systolic blood pressure of 102 mmHg. Investigations for hypertension revealed hyper-reninemia without cardio/renovascular or neuroendocrine abnormalities. Salt supplementation and antihypertensive therapy with captopril led to resolution of natriuresis and hyponatremia. review of literature revealed associated renovascular pathology in all neonatal cases of the syndrome reported so far. Renal ischemia from possible renal microthrombi may have been the triggering event in our case. Decline in renin levels during follow-up favors this hypothesis.- - - - - - - - - - ranking = 2keywords = pressure (Clic here for more details about this article) |
7/47. The hyponatraemic hypertensive syndrome in a 2-year-old child with behavioural symptoms.In this case report we present a 2-year-old girl with the classical signs of the hyponatraemic hypertensive syndrome. She initially presented with a history of behavioural abnormalities and hyponatraemia (126 mmol/l) and her blood pressure was as high as 220/160 mmHg. After admission, somnolence developed. Intravenous anti-hypertensive therapy was started immediately. The hyponatraemia was treated with i.v. sodium supplementation. The cause of this syndrome proved to be fibromuscular dysplasia of the left renal artery. Finally, a left nephrectomy was performed. With this therapy, blood pressure and serum sodium normalised and the girl promptly regained normal consciousness and behaviour. CONCLUSION: Behavioural abnormalities in the history of a child without any other neurological symptoms might be one of the first signs of hypertensive encephalopathy. In combination with hyponatraemia, these symptoms should alert the physician to consider the hyponatraemic hypertensive syndrome.- - - - - - - - - - ranking = 2keywords = pressure (Clic here for more details about this article) |
8/47. One-step hysteroscopic removal of sinking submucous myoma in two infertile patients.OBJECTIVE: To report one-step resectoscopic removal of submucous myomas that were pushed back into the muscular layer by increased intrauterine pressure during hysteroscopic procedures. DESIGN: Case report. SETTING: Kawasaki Municipal Hospital, Kawasaki, japan. PATIENT(S): Two infertile women presenting with menorrhagia in whom submucous myoma with a broad base was diagnosed. INTERVENTION(S): One patient was pretreated with GnRH agonist for 4 months; the other patient did not receive this treatment. Resectoscopic myomectomies were performed under close sonographic monitoring. MAIN OUTCOME MEASURE(S): Clinical symptoms and conception status. RESULT(S): Tumor sinking occurred during the hysteroscopic procedures, but complete resectoscopic removal of the submucous myomas was achieved under sonographic and hysteroscopic visualization. One patient experienced hyponatremia but recovered after conservative treatment. Both patients conceived after myoma removal. CONCLUSION(S): Sinking myomas, which may cause infertility, can be removed with a one-step hysteroscopic procedure. Sinking of submucous myomas during hysteroscopy might be caused by pretreatment with GnRH agonist and by increased intrauterine pressure during hysteroscopy. We recommend that intrauterine pressure be <45 mmHg, equivalent to hanging a bag of fluid under gravity control 70 cm above the patient's uterus, at the beginning of operations for sinking myomas.- - - - - - - - - - ranking = 3keywords = pressure (Clic here for more details about this article) |
9/47. Hyponatremic hypertensive syndrome.We report on a 4-year-old girl with hyponatremic-hypertensive syndrome (HHS), a rare entity in childhood. The girl was referred to us from a local hospital with a history of recurrent fever, vomiting, and seizures. On admission she was markedly dehydrated. Initial investigations revealed severe hyponatremia (serum Na 120 mmol/l), hypochloremia (serum Cl 68 mmol/l), and mild hypokalemia (serum K 3.3 mmol/l), while serum calcium and magnesium were normal. serum urea was 5 mmol/l and serum creatinine was 62 mumol/l. Despite hyponatremic dehydration, her urine output was high (2050 ml/24 h), as was her urinary sodium (168 mmol/24 h). She had massive transient proteinuria (maximal 1642 mg/24 h) while being severely hypertensive (blood pressure 210/160 mmHg). Further investigations revealed right kidney scarring, hyper-reflexive bladder dysfunction, massive brain infarcts, and myocardial left ventricular hypertrophy. Renal arteries were normal on arteriography. blood pressure control resulted in normalization of serum and urinary electrolytes and decrease of proteinuria. hyponatremia and transient massive proteinuria in this patient seem to be caused by high-pressure-forced diuresis due to malignant renoparenchymal hypertension.- - - - - - - - - - ranking = 3keywords = pressure (Clic here for more details about this article) |
10/47. glycine toxicity and unexpected intra-operative death.A rare complication of the use of glycine irrigation fluid during prostatic surgery in a 69-year-old man is described. Following cystolithopexy and transurethral resection of the prostate for benign prostatomegaly, abdominal distension developed with increasing ventilatory pressures. Despite retroperitoneal fluid evacuation at subsequent urgent laparotomy, cardiac arrest occurred that was not amenable to resuscitation. At autopsy a traumatic defect in the posterior bladder wall filled with calculus debris was confirmed that did not communicate with the peritoneal cavity. hyponatremia with markedly elevated levels of blood, urine, and body fluid glycine were demonstrated. death was, therefore, attributed to glycine toxicity following tracking of glycine through a surgical defect in the posterior bladder wall. Careful dissection of surgical sites is required in such cases to demonstrate any additional trauma that may be associated with the fatal episode. Analysis of body fluids for glycine and electrolytes is also necessary to assist in the determination of possible mechanisms of death.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
| | Next -> |