Ectopic pregnancy outcomes in patients discharged from the emergency department.

OBJECTIVE: The objective of this study was to determine the proportion of women who had a ruptured ectopic pregnancy after being discharged from the emergency department (ED) where ectopic pregnancy had not yet been excluded. METHODS: This was a retrospective chart review of pregnant (<12-week gestational age) women discharged home from an academic tertiary care ED with a diagnosis of ectopic pregnancy, rule-out ectopic pregnancy, or pregnancy of unknown location over a 7-year period. RESULTS: Of the 550 included patients, 83 (15.1%) had a viable pregnancy, 94 (17.1%) had a spontaneous or missed abortion, 230 (41.8%) had an ectopic pregnancy, 72 (13.1%) had unknown outcomes, and 71 (12.9%) had other outcomes that included therapeutic abortion, molar pregnancy, or resolution of ßHCG with no location documented. Of the 230 ectopic pregnancies, 42 (7.6%) underwent expectant management, 131 (23.8%) were managed medically with methotrexate, 29 (5.3%) were managed with surgical intervention, and 28 (5.1%) patients had a ruptured ectopic pregnancy after their index ED visit. Of the 550 included patients, 221 (40.2%) did not have a transvaginal ultrasound during their index ED visit, and 73 (33.0%) were subsequently diagnosed with an ectopic pregnancy. CONCLUSION: These results may be useful for ED physicians counselling women with symptomatic early pregnancies about the risk of ectopic pregnancy after they are discharged from the ED.

Effects of glycol-split low molecular weight heparin on placental, endothelial, and anti-inflammatory pathways relevant to preeclampsia.

Low molecular weight heparin (LMWH) is being investigated as a potential preventative therapy against preeclampsia. There is evidence suggesting that LMWH may prevent preeclampsia through anticoagulation-independent mechanisms. In this study, we compared the in vitro placental, endothelial, and anti-inflammatory effects of an LMWH (dalteparin) with a nonanticoagulant, glycol-split heparin derivative (gsHep). In contrast with dalteparin, gsHep did not interact with antithrombin III, possess significant anti-Factor Xa activity, or significantly prolong in vitro plasma clotting time. However, dalteparin and gsHep were otherwise mechanistically similar, both interacting with soluble fms-like tyrosine kinase-1 (sFlt1) and promoting release of the pro-angiogenic protein placental growth factor, but not the antiangiogenic sFlt1, from healthy placental villous explants. Placental explant media pretreated with dalteparin or gsHep significantly stimulated endothelial cell tube formation compared to untreated explants. Lastly, dalteparin and gsHep both significantly suppressed inflammation by inhibiting complement activation and leukocyte adhesion to endothelial cells that were activated using serum from preeclamptic women. Our data suggest that nonanticoagulant heparin derivatives may be utilized as a tool to distinguish the anticoagulation-independent mechanisms of LMWH, and provide insight into the role of anticoagulation in the prevention of preeclampsia.

Enhanced cell-volume regulation in cyclosporin A cardioprotection.

AIMS: Cyclosporin A (CsA) has been shown to protect against ischaemia/reperfusion injury presumably by its inhibition of mitochondrial permeability transition pore opening through cyclophilin D inhibition. We examine if CsA cardioprotection involves a cell-volume regulatory mechanism. METHODS AND RESULTS: To address this issue, cultured rabbit cardiomyocytes were subjected to the following protocols: (i) cardiomyocytes were treated with 200 nM CsA either given for 10 min followed by 10 min of washout prior to 30 min hypo-osmotic stress (200 mOsm) or administered throughout 75 min simulated ischaemia/60 min simulated reperfusion. Cell necrosis and cell swelling were determined by trypan blue staining and cell-volume measurements, respectively; (ii) SPQ(6-methoxy-N-(3-sulfopropyl)quinolinium) dye loaded cardiomyocytes were treated with 200 nM CsA for 10 min followed by 10 min washout and intracellular Cl(-) concentration measured (Cl(-) efflux); (iii) 5,5',6,6'-tetrachloro-1,1',3,3'- tetraethylbenzimi-dazolylcarbocyanine iodide(JC-1) loaded cardiomyocytes were treated with 200 nM CsA to inhibit mitochondrial membrane potential (ΔΨm) dissipation (an index of mitochondria permeability transition pore opening) by either valinomycin (2 µM) or ischaemia/reperfusion injury. Cl(-) channels were blocked by indanyloxyacetic acid 94 (IAA-94, 50 µM). CsA not only significantly (P < 0.001) reduced the % of dead cells following simulated ischaemia/reperfusion but it also triggered an efflux of Cl(-), hence enhancing cardiomyocyte cell-volume regulatory response. CsA protection against cell necrosis and its effect on Cl(-) transport/volume regulation were all blocked by IAA-94. IAA-94 had no effect on ΔΨm. CONCLUSION: These data indicate that CsA protects against cell necrosis at least in part by enhancing cardiomyocyte volume regulation, and not simply by inhibiting MPTP opening.

Cardiac failure following inadvertent administration of high-dose epinephrine subcutaneously.

Our aim is to report the consequences of epinephrine toxicity leading to cardiac failure in a child and the successful management with dopamine and milrinone. A previously healthy 13-year-old girl undergoing a left tympanomastoidectomy was inadvertently administered 10 mL of 1:1000 epinephrine subcutaneously (0.175 mg/kg) on the left post auricular region in lieu of lidocaine. She developed sudden supraventricular tachycardia, hypertension and flash pulmonary edema. She was initially treated with propofol, nitrogycerin and increased peak end-expiratory pressure. Within 4 h, she remained tachycardic, but was hypotensive with an increased central venous pressure. Electrocardiogram and echocardiogram investigations showed ST changes indicative of myocardial ischemia and globally reduced function, respectively. Dopamine infusion was administered, together with milrinone, resulting in a gradual improvement of cardiac function within 3 days. She was transitioned to enalapril and discharged home. This case highlights the clinical features of high dose epinephrine toxicity secondary to iatrogenic subcutaneous overdose followed by hypotension and pulmonary edema as a possible late effect of epinephrine and the successful management of secondary cardiac failure with administration of dopamine, milrinone and enalapril.