misoprostol and Multiple-Organ-Failure

This study compared prophylactic administration of either intragastric misoprostol (200 micrograms four times a day), a prostaglandin E1 analog, or bolus intravenous cimetidine (300 mg every 6 hours) in preventing stress lesions and stress bleeding in 127 adult postoperative patients who required mechanical ventilation and also had developed hypotension or sepsis. Both drug treatments were equally effective in preventing the development of diffuse gastritis (greater than 10 gastric hemorrhagic lesions) and in preventing upper gastrointestinal hemorrhage (UGIH). The combined data from both groups showed that for the 44 (35%) patients who died, death was significantly associated with the presence at study entry of renal failure (64% of 25 patients with renal failure died), hepatic failure (57% of 23 patients) or coagulopathy (62% of 29 patients) (p less than 0.02 for each), and with the number of organ system failures at study entry (48% of 69 patients with multiple organ system failures died, p less than 0.001). Death was also significantly associated with the presence of adult respiratory distress syndrome (ARDS) at study entry or the development of ARDS (63% of 24 patients with ARDS died, p less than 0.001), and the development of UGIH (5% of 93 patients with known bleeding outcome died, p less than 0.05). The number of stress lesions that developed was significantly associated with subsequent UGIH (p less than 0.001). Additional organ system failure developed during the study in 31% of the 127 patients, as did diffuse gastritis in 20% of 111 patients who had a follow-up endoscopy. These results demonstrate that postoperative patients who require mechanical ventilation and have hypotension or sepsis are at significant risk for the development of stress gastric lesions and multiple organ system failure even when prophylaxis for stress ulcers is provided. Furthermore, the presence of ARDS, renal failure, hepatic failure, coagulopathy, and UGIH are significantly associated with death.

Topics: Cause of Death; Cimetidine; Critical Care; Double-Blind Method; Female; Follow-Up Studies; Gastroscopy; Humans; Male; Middle Aged; Misoprostol; Multiple Organ Failure; Peptic Ulcer; Peptic Ulcer Hemorrhage; Placebos; Pneumonia; Postoperative Complications; Prospective Studies; Respiratory Distress Syndrome; Stress, Physiological; Surgical Procedures, Operative; Survival Rate; Treatment Outcome; Wound Healing

Heat stroke is a life-threatening disorder triggered by thermoregulatory failure. Hyperthermia-induced splanchnic hypoperfusion has been reported to induce intestinal barrier dysfunction and systemic immune response that ultimately cause multiple-organ failure and death. Intestinal goblet cells contribute greatly to the formation of mucus barrier, which hinders translocation of gut microorganisms. Studies have reported that misoprostol can not only alleviate ischemic injury but also protect GI mucosal layer. Therefore, we evaluated the effects of misoprostol on intestinal goblet cells after heat stress and on multiple-organ dysfunction in heat stroke rats.. Heat stress was established in the heating chamber and followed by misoprostol treatment. Changes in hemodynamics, organ function indices, inflammation, oxidative stress, and survival rate were analyzed. Furthermore, ilea and LS174T cells were used to examine intestinal functions.. Heat stress caused dysfunction of intestinal goblet cells and damage to ilea by increasing oxidative stress and apoptosis. Increased nitrosative stress and inflammation accompanied by hypotension, hypoperfusion, tachycardia, multiple-organ dysfunction, and death were observed in the heat stroke rat model. Treatment of LS174T cells with misoprostol not only decreased oxidative stress and apoptosis but also reduced cytotoxicity caused by heat stress. Moreover, misoprostol prevented disruption of the enteric barrier, multiple-organ injury, and death in rats with heat stroke.. This study indicates that misoprostol could alleviate intestinal damage and organ injury caused by heat stress and be a potential therapy for heat-related illnesses.

Topics: Alprostadil; Animals; Goblet Cells; Heat Stroke; Heat-Shock Response; Inflammation; Intestinal Mucosa; Misoprostol; Multiple Organ Failure; Rats

A 31-year-old G3P2002 with history of two prior caesarean sections presented with influenza-like illness, requiring intubation secondary to acute respiratory distress syndrome. Investigations revealed intrauterine fetal demise at 30-week gestation.She soon deteriorated with sepsis and multiple organs impacted. Risks of the gravid uterus impairing cardiopulmonary function appeared greater than risks of delivery, including that of uterine rupture. Vaginal birth after caesarean was achieved with misoprostol and critical care status rapidly improved.Current guidelines for management of fetal demise in patients with prior hysterotomies are mixed: although the American College of Obstetricians and Gynecologists recommends standard obstetric protocols rather than misoprostol administration for labour augmentation, there is limited published data citing severe maternal morbidity associated with misoprostol use. This case report argues misoprostol-augmented induction of labour can be a reasonable option in a medically complex patient with fetal demise and prior hysterotomies.

Topics: Administration, Intravaginal; Adult; Delivery, Obstetric; Female; Fetal Death; Humans; Hysterotomy; Intubation, Intratracheal; Labor, Induced; Labor, Obstetric; Misoprostol; Multiple Organ Failure; Oxytocics; Pregnancy; Pregnancy Complications, Infectious; Pregnancy Trimester, Third; Respiratory Distress Syndrome; Treatment Outcome; Uterine Rupture

Misoprostol is an important drug in obstetrics and gynecology because of its uterotonic and cervical-ripening activities. The side effects are dose-related, usually transitory, and well tolerated. The toxic dosage in humans is unknown, and there is no specific antidote.. An adolescent developed upper gastrointestinal bleeding after self-medication with misoprostol orally (12 mg) to cause abortion. She presented with multiorgan failure, acute abdominal signs, and hemodynamic instability. Emergency laparotomy showed gastric and esophageal necrosis. After several episodes of cardiac arrest, and despite resuscitation efforts, the patient died.. Temporal relationship (48 hours after the beginning of medication) strongly suggests that misoprostol was the agent directly involved in the maternal death. The mechanism implicating misoprostol in gastrointestinal ischemia and necrosis is unknown.

Topics: Abortifacient Agents, Nonsteroidal; Abortion, Induced; Adolescent; Diagnosis, Differential; Esophagus; Fatal Outcome; Female; Gastrointestinal Hemorrhage; Humans; Misoprostol; Multiple Organ Failure; Necrosis; Pregnancy; Stomach

Live E. coli were infused i.v. in cats to induce gastrointestinal mucosal injury and the gastric mucosa was exposed to bile and a luminal pH of 1. A gastric lesion index was calculated and intestinal injury was graded. The effects of i.v. methylprednisolone before and after induction of bacteremia were compared with those of intragastric misoprostol combined with i.v. superoxide dismutase (SOD) and catalase and with a control group. Methylprednisolone, but not misoprostol/SOD/catalase, significantly reduced the gastric lesion index (p less than 0.05). The duodenum/small intestine was significantly injured in 4/6, 2/6 and 4/6 cats in the misoprostol/SOD/catalase, methylprednisolone and control groups, respectively (NS). End gastric luminal pH was 3.9, 2.7 and 4.5 in the respective groups (p less than 0.05), with systemic arterial pH 7.15, 7.15 and 7.32 (NS). Mean arterial pressure and cardiac output were improved with methylprednisolone. Misoprostol/SOD/catalase reduced late hypotension. Pulmonary arterial pressure rose to c. 200% of basal in all groups. Methylprednisolone, but not misoprostol/SOD/catalase, thus protected the gastric mucosa from sepsis-induced gastric injury concomitant with reduced disappearance of protons from the gastric lumen, but did not significantly affect small-bowel damage. Hemodynamic responses were significantly improved in methylprednisolone-pretreated cats.

Topics: Acid-Base Equilibrium; Alprostadil; Animals; Anti-Ulcer Agents; Catalase; Cats; Drug Therapy, Combination; Escherichia coli Infections; Gastric Acidity Determination; Gastric Mucosa; Hemodynamics; Hydrogen-Ion Concentration; Intestinal Mucosa; Methylprednisolone; Misoprostol; Multiple Organ Failure; Shock, Septic; Stomach Ulcer; Superoxide Dismutase