Catheterization ; Endoscopy ; Esophageal and Gastric Varices ; complications ; drug therapy ; surgery ; therapy ; Gastrointestinal Hemorrhage ; drug therapy ; etiology ; surgery ; therapy ; Humans ; Octreotide ; therapeutic use ; Somatostatin ; therapeutic use ; Vasopressins ; therapeutic use

Two patients with post-traumatic diabetes insipidus (DI) are reported. One had suffered a fatal injury and the other a mild contusion without amnesia before DI developed. These two instances exemplify the wide spectrum of post-traumatic DI and, hence, the importance of ruling out DI even afer a mild closed-head injury.
Adult ; Case Report ; Central Nervous System/*injuries ; Desmopressin/therapeutic use ; Diabetes Insipidus/drug therapy/*etiology/physiopathology ; Diuresis/drug effects ; Female ; Human ; Male ; Middle Age ; Vasopressins/therapeutic use ; Wounds and Injuries/*complications/mortality

OBJECTIVETo explore the effect and mechanism of dexamethasone (DEX) in the prevention of central pontine myelinolysis (CPM) in rats.

METHODSHyponatremia was induced in rat by subcutaneous injection of Vasopressin Tannate and intraperitoneal injection of 2.5% dextrose in water for 3 d, the rats of Group A received a bolus of 1 mol/L NaCl (2 ml/kg) and DEX (5 mg/kg) simultaneously at the 4th day; the rats of Group B were treated with DEX after 24 h of the injection of 1 mol/L NaCl; the rats in Group C received a bolus of 1 mol/L NaCl and saline simultaneously; Group D was the control group. The demyelinative lesions were evaluated by myelin staining. The Evans blue (EB) contents of brain were detected to evaluate the blood-brain-barrier permeability after rapid correction of hyponatremia. The expression of inducible nitric oxide synthase (iNOS) in brains was evaluated by Western blotting.

RESULTCPM was induced successfully in rats. The EB contents of Group A, B and C had no significant difference at 0 h after injection of hypertonic saline compared with Group D. The EB contents of Group C began to increase significantly at 6 h after injection of hypertonic saline, peaked at 24 h; the expression of iNOS in brains began to increase after 3 h after the rapid correction of hyponatremia. The rate of morbidity in Group C was 66.7%. The demyelinative lesions were rarely seen in Group A, the EB contents of brain decreased significantly compared with Group C at the same time point (P<0.05), the iNOS expression was also inhibited. DEX could not prevent the attack of CPM at Group B, the rate of morbidity (75%) had no significant difference compared with Group C (P>0.05).

CONCLUSIONEarly treatment with DEX can protect blood-brain-barrier and inhibit the expression of iNOS to prevent the attack of CPM.

Animals ; Arginine Vasopressin ; Blood-Brain Barrier ; drug effects ; physiopathology ; Dexamethasone ; therapeutic use ; Glucocorticoids ; therapeutic use ; Glucose ; Male ; Myelinolysis, Central Pontine ; chemically induced ; physiopathology ; prevention & control ; Nitric Oxide Synthase Type II ; metabolism ; Rats ; Rats, Sprague-Dawley ; Time Factors ; Vasopressins

This is a report on a case of severe skin necrosis in a vasodilatory septic shock patient after the infusion of low-dose vasopressin through a central venous catheter. An 84-year-old male was hospitalized for edema on both legs at Asan Medical Center, Seoul, Korea. On hospital day 8, the patient began to complain of dyspnea and he subsequently developed severe septic shock caused by E. coli. After being transferred to the medical intensive care unit, his hypotension, which was refractory to norepinephrine, was controlled by an infusion of low-dose vasopressin (0.02 unit/min) through a central venous catheter into the right subclavian vein. After the infusion of low-dose vasopressin, severe skin necrosis with bullous changes developed, necessitating discontinuation of the low-dose vasopressin infusion. The patient expired from refractory septic shock. Although low-dose vasopressin can control hypotension in septic shock patients, low-dose vasopressin must be used with caution because ischemic complications such as skin necrosis can develop even with administration through a central venous catheter.
Vasopressins/administration & dosage/*adverse effects/therapeutic use ; Vasoconstrictor Agents/administration & dosage/*adverse effects/therapeutic use ; Skin/*drug effects/*pathology ; Shock, Septic/*drug therapy ; Necrosis/chemically induced/pathology ; Male ; Infusions, Intravenous ; Humans ; Fatal Outcome ; Dose-Response Relationship, Drug ; Catheterization, Central Venous ; Aged, 80 and over