pituitrin and Airway-Obstruction

Bleeding from esophageal varices remains a difficult clinical problem, carrying a high likelihood both of rebleeding and of mortality. The initial approach requires adequate but not overly vigorous volume replacement with blood and other fluids. Once the patient is resuscitated, upper gastrointestinal endoscopy should be performed to establish the source of bleeding. Both endoscopic variceal sclerotherapy and balloon tamponade appear to be effective in achieving temporary control of acute ongoing hemorrhage from esophageal varices. The value of intravenous vasopressin remains controversial. Rebleeding can be prevented in most patients by shunt surgery. However, surgery carries both considerable early morbidity and mortality (related mainly to the severity of the underlying liver disease) and substantial longer-term morbidity and mortality from hepatic encephalopathy and liver failure. The role of pharmacologic agents (eg, propranolol) intended to prevent variceal hemorrhage by reducing portal pressure remains to be established. At present, we recommend use of endoscopic variceal sclerotherapy for the control of active variceal bleeding, with employment of balloon tamponade and intravenous vasopressin if sclerotherapy is successful. Emergency shunt surgery should be reserved only for those patients whose bleeding cannot be controlled by these other means. For prevention of rebleeding in Child class C patients, we attempt to obliterate the varices by repeated endoscopic sclerotherapy. Patients who have two to three episodes of rebleeding despite this approach are considered for shunt surgery. For better-risk patients who do not have ascites, which is difficult to control, we are currently recommending a distal splenorenal shunt. Alternatively, repeated endoscopic variceal sclerotherapy is used for these better-risk patients (Child class A or B) in some centers, with shunt surgery reserved for patients who continue to rebleed. Which approach to preventing rebleeding in the better-risk patient is more effective, as well as the role of pharmacologic therapy with propranolol or other agents, remains to be settled by well-controlled randomized clinical trials.

Topics: Airway Obstruction; Catheterization; Esophageal and Gastric Varices; Fluid Therapy; Gastrointestinal Hemorrhage; Hemostatic Techniques; Humans; Hypertension, Portal; Liver Diseases, Alcoholic; Propranolol; Sclerosing Solutions; Vasopressins

The two life-threatening signs of anaphylactic shock (AS) are severe arterial hypotension and bronchospasm. Guidelines recommend epinephrine as first-line treatment. Arginine vasopressin (AVP) has been proposed as an alternative if epinephrine does not correct arterial hypotension. These two drugs may have beneficial, neutral or deleterious effects on airflow either directly or by modifying factors that regulate vasodilatation and/or edema in the bronchial wall.. To compare the effects of epinephrine and AVP on airflow and airway leakage in a rat model of AS.. Thirty-two ovalbumin-sensitized rats were randomized into four groups: control (CON), AS without treatment (OVA), AS treated with epinephrine (EPI), and AS treated with AVP (AVP). Mean arterial pressure (MAP), respiratory resistance and elastance and microvascular leakage in the airways were measured.. All OVA rats died within 20 minutes following ovalbumin injection. Ovalbumin induced severe arterial hypotension and airway obstruction (221 ± 36 hPa.s.L. Epinephrine was superior to AVP for alleviating the airway response in a rat model of AS. When bronchospasm and severe arterial hypotension are present during AS, epinephrine should be the drug of choice.

Topics: Airway Obstruction; Anaphylaxis; Animals; Arterial Pressure; Bronchial Spasm; Capillary Leak Syndrome; Epinephrine; Hypotension; Neurophysins; Ovalbumin; Protein Precursors; Rats; Respiratory System; Vasopressins

We describe two children who after cardiopulmonary arrest developed hypernatremia at the terminal stage. Urinary antidiuretic hormone concentration was very low, indicating central diabetes insipidus. These cases illustrate the necessity of alertness to the development of central diabetes insipidus in patients with severe hypoxic brain damage.

Topics: Adolescent; Airway Obstruction; Brain Damage, Chronic; Cerebral Palsy; Diabetes Insipidus; Humans; Hypoxia, Brain; Infant; Male; Pituitary Gland, Posterior; Resuscitation; Vasopressins; Water-Electrolyte Balance