dinoprost and Respiratory-Insufficiency

A case of severe reaction to extraamniotically administered prostaglandin F2 alpha, with cardiorespiratory collapse and pulmonary oedema necessitating transfer to an intensive care unit, is presented. Attention is drawn to the profound haemodynamic effects of systemically administered prostaglandin, and the need for caution and ready availability of facilities for resuscitation when this potent substance is administered. Treatment for the effects of intravascular absorption of prostaglandin F2 alpha is discussed.. A case of severe vasoconstriction treated as cardiorespiratory collapse in a woman given extraamniotic PGF2alpha for midtrimester abortion is described, with comments on management of this rare reaction. The patient was having elective termination because of confirmed spina bifida with hydrocephalus by ultrasound and elevated AFP at 18 weeks gestation. She was given a 4 mg test dose of PGF2alpha (Dinoprost, Upjohn Pty, Ltd) in viscous gel (Tylose MH300, Hoechst Australia Ltd) via extraamniotic Foley catheter. She immediately developed dyspnea, abdominal and breast pain, hypotension of 50 mm Hg systolic, peripheral vasoconstriction, cyanosis and confusion. She was treated with iv Hartmann's solution 600 ml, oxygen 8 1/min, and sc adrenaline 1/1000 0.5 ml. She seemed to improve after receiving 500 ml 3.5% polygeline colloid (Haemaccel, Behringwerke AG), and 5 ml 1/10,000 adrenaline iv, as her systolic blood pressure rose to 70 mm Hg measured indirectly. 500 ml more iv colloid was given, and blood pressure rose to 90 mm Hg. Then she suddenly deteriorated with florid pulmonary edema. Oxygen saturation fell and positive pressure ventilation was begun. She was given furosemide 160 mg iv and hydrocortisone 500 mg iv. Anaphylactic reaction was ruled out on the basis of blood count; amniotic fluid embolism was ruled out because of minor changes in clotting parameters. The events seen here most likely occurred as a result of inadvertent injection of PGF2alpha into the arterial circulation, causing increased pulmonary arterial pressure and vascular resistance, systemic vasoconstriction interpreted as hypotension, all exacerbated by adrenaline and exogenous fluid load. Severe hypertension after extraamniotic PGF2alpha has been reported before in a similar case of apparent hypotension treated with agents to increase blood pressure. PGF2a should not be used without facilities to treat such adverse reactions.

Topics: Abortion, Therapeutic; Adult; Cardiac Output, Low; Dinoprost; Female; Humans; Pregnancy; Pregnancy Complications, Cardiovascular; Pregnancy Trimester, Second; Pulmonary Edema; Respiratory Insufficiency

Arterial plasma concentrations of thromboxane B2 (TxB2), prostaglandin F2 alpha (PGF2 alpha) and 6-keto-prostaglandin F1 alpha (PGF1 alpha) were measured during endotoxin-induced acute respiratory failure (ARF) in anesthetized 10-12 wk old pigs. A 4.5 hour (hr) infusion of endotoxin resulted in a biphasic pattern of ARF. Phase 1 (0-2 hr) was characterized by increased pulmonary artery pressure, pulmonary vascular resistance (PVR), and alveolar-arterial O2 gradient (delta A-aO2), and decreased cardiac index (CI) and lung dynamic compliance (LDC). Following a return of PVR and CI values towards baseline, a second phase (2-4.5 hr) of deteriorating function occurred and was characterized by additional increases in PVR and delta A-aO2 and decreases in CI and LDC. Baseline (i.e., 0 hr) plasma TxB2 concentrations were 241 +/- 24 pg/ml; these values peaked at 0.5 hr (3228 +/- 712 pg/ml) and declined to 1635 +/- 453 pg/ml at 4.5 hr. Plasma concentrations of PGF2 alpha slowly increased from a baseline value of 154 +/- 32 pg/ml to 2355 +/- 738 pg/ml at 4.5 hr, while PGF1 alpha values increased from 54 +/- 2 pg/ml at 0 hr to 503 +/- 172 pg/ml at 4.5 hr. Time-matched control pigs showed no changes in pulmonary hemodynamics or in plasma TxB2, PGF2 alpha or PGF1 alpha levels. These results indicate that cyclooxygenase products are increased during both phases of endotoxin-induced ARF in pigs.

Topics: 6-Ketoprostaglandin F1 alpha; Acute Disease; Animals; Arteries; Dinoprost; Endotoxins; Escherichia coli; Hemodynamics; Lung; Prostaglandins F; Respiratory Insufficiency; Swine; Thromboxane B2

Topics: Adult; Aspirin; Dinoprost; Female; Humans; Middle Aged; Prostaglandins F; Pulmonary Alveoli; Respiration, Artificial; Respiratory Insufficiency; Thromboxane A2

The porcine pulmonary vascular and airway responses to exogenous 5-hydroxytryptamine (5-HT), norepinephrine, prostaglandin F2 alpha (PGF2 alpha), and angiotensin II were evaluated before and after ketanserin, a 5-HT2 receptor antagonist. Ketanserin blocked the 5-HT-induced increases in airway and pulmonary artery pressures, whereas the increases in airway and pulmonary artery pressures caused by norepinephrine, PGF2 alpha, or angiotensin II were not significantly modified by ketanserin, indicating a relatively high degree of specificity for 5-HT2 receptors. The role of endogenous 5-HT in mediating endotoxin-induced respiratory failure was evaluated by treating pigs with ketanserin. Escherichia coli endotoxin (055-B5) was infused intravenously into anesthetized 10- to 14-wk-old pigs at 5 micrograms/kg the first h, followed by 2 micrograms/kg/h for 3.5 h. Ketanserin was infused at 300 micrograms/kg before endotoxin plus 67 micrograms/kg/h during endotoxemia. During Phase 1 (i.e., 0 to 2 h), the endotoxin-induced increases in pulmonary vascular resistance and room air alveolar-arterial oxygen difference and the decreased cardiac index and lung dynamic compliance were not significantly modified by ketanserin. However, during Phase 2 (i.e., 2 to 4.5 h) endotoxemia, ketanserin attenuated the endotoxin-induced pulmonary hypertension and the increases in pulmonary vascular resistance, alveolar dead space ventilation, and alveolar-arterial oxygen difference. Ketanserin also attenuated the Phase 2 bronchoconstriction and the decreased cardiac index, but did not modify the endotoxin-induced increase in alveolar-capillary permeability. These results indicate that 5-HT plays little or no role in mediating the early (i.e., less than 2 h) response to endotoxin.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Disease; Angiotensin II; Animals; Bronchi; Constriction, Pathologic; Dinoprost; Disease Models, Animal; Dose-Response Relationship, Drug; Endotoxins; Escherichia coli; Ketanserin; Norepinephrine; Prostaglandins F; Pulmonary Artery; Pulmonary Veins; Respiratory Insufficiency; Serotonin; Swine; Swine Diseases; Vascular Resistance

An evaluation was made of 106 surgical patients with Gram-negative septic shock, both for clinical criteria as well as the biochemical mediators endotoxin, prostaglandin F2 alpha, prostaglandin I2 (prostacyclin), and thromboxane. These data were correlated to various defined shock phases, functional data of vital organs, and clinical outcome. Patients underwent invasive organ function monitoring and the usual laboratory tests of intensive care. Prostaglandins and thromboxane were measured radioimmunologically, endotoxin by the limulus amebocyte lysate test. Endotoxin proved to be a more accurate predictor of severe sepsis than did positive blood cultures. Endotoxin as well as prostaglandins and thromboxane are predominantly released in early shock phases, appearing in plasma concentrations, which correlate with the severity of organ failure. Sepsis-induced respiratory failure coincides with a deterioration of pulmonary prostaglandin inactivation, which contributes to the release mechanism. High systemic prostacyclin activity benefits the patients' organ functions and clinical outcomes, while a predominance of thromboxane seems to effect the opposite. Transpulmonary-thromboxane gradients correlate significantly with pulmonary hypertension in the early phases of septic shock.

Topics: 6-Ketoprostaglandin F1 alpha; Acute Kidney Injury; Adolescent; Adult; Aged; Dinoprost; Endotoxins; Epoprostenol; Humans; Middle Aged; Peritonitis; Prostaglandins; Prostaglandins F; Respiratory Insufficiency; Shock, Septic; Surgical Wound Infection; Thromboxanes