Massive obstetric hemorrhage: Current approach to management

Guasch, E.; Gilsanz, F.

doi:10.1016/j.medine.2016.02.003

Cited by 26 publications

(35 citation statements)

References 60 publications

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“…Hypertension can damage the endothelium of blood vessels in heart, increase shear and tear forces on vessel walls that change cell osmotic stability (Jiao et al, 2017) and fasten lipid deposition in arteries (Lawes et al, 2008). Cigarette smoking can damage the endothelium of arteries, stimulate inflammation (Hussien and Mousa, 2016), increase blood pressure (BP) and cause cardiac hypertrophy (Guasch and Gilsanz, 2016). People with diabetes have a much higher incidence of CAD because of dyslipidemia and metabolic disorders, particularly the formation of glycated proteins that cause inflammation, stiffening arteries, trapping other macromolecules, and disrupting enzyme activities, hormone regulation, immune function and activities of dendritic cells (Price and Knight, 2007).…”

Section: Atherosclerosis and Cardioprotective Effect Of Otmentioning

confidence: 99%

Therapeutic Potential of Oxytocin in Atherosclerotic Cardiovascular Disease: Mechanisms and Signaling Pathways

Wang

Yang

et al. 2019

Front. Neurosci.

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Coronary artery disease (CAD) is a major cardiovascular disease responsible for high morbidity and mortality worldwide. The major pathophysiological basis of CAD is atherosclerosis in association with varieties of immunometabolic disorders that can suppress oxytocin (OT) receptor (OTR) signaling in the cardiovascular system (CVS). By contrast, OT not only maintains cardiovascular integrity but also has the potential to suppress and even reverse atherosclerotic alterations and CAD. These protective effects of OT are associated with its protection of the heart and blood vessels from immunometabolic injuries and the resultant inflammation and apoptosis through both peripheral and central approaches. As a result, OT can decelerate the progression of atherosclerosis and facilitate the recovery of CVS from these injuries. At the cellular level, the protective effect of OT on CVS involves a broad array of OTR signaling events. These signals mainly belong to the reperfusion injury salvage kinase pathway that is composed of phosphatidylinositol 3-kinase-Akt-endothelial nitric oxide synthase cascades and extracellular signal-regulated protein kinase 1/2. Additionally, AMP-activated protein kinase, Ca 2+ /calmodulin-dependent protein kinase signaling and many others are also implicated in OTR signaling in the CVS protection. These signaling events interact coordinately at many levels to suppress the production of inflammatory cytokines and the activation of apoptotic pathways. A particular target of these signaling events is endoplasmic reticulum (ER) stress and mitochondrial oxidative stress that interact through mitochondria-associated ER membrane. In contrast to these protective effects and machineries, rare but serious cardiovascular disturbances were also reported in labor induction and animal studies including hypotension, reflexive tachycardia, coronary spasm or thrombosis and allergy. Here, we review our current understanding of the protective effect of OT against varieties of atherosclerotic etiologies as well as the approaches and underlying mechanisms of these effects. Moreover, potential cardiovascular disturbances following OT application are also discussed to avoid unwanted effects in clinical trials of OT usages.

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Section: Atherosclerosis and Cardioprotective Effect Of Otmentioning

confidence: 99%

Therapeutic Potential of Oxytocin in Atherosclerotic Cardiovascular Disease: Mechanisms and Signaling Pathways

Wang

Yang

et al. 2019

Front. Neurosci.

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“…It is defined (among others) as the loss of >2,500ml of blood, and is associated to a need for admission to critical care and/or hysterectomy. 6 It is not only life threatening situation but also an obstetrician's nightmares. 7 Anticipation of risk factors and active management of the third stage of labor, including the prophylactic application of uterotonics, are Many national and international studies show that uterine atony is the commonest cause of PPH followed by trauma to genital tract, adherent placenta, uterine angle extension and retained placenta.…”

Section: Introductionmentioning

confidence: 99%

Clinical study of post partum haemorrhage from a teaching hospital in Maharashtra, India

Tasneem

Sirsam

Shanbhag

2017

Int J Reprod Contracept Obstet Gynecol

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Background: To study the cases of postpartum haemorrhage, their causes and management in a tertiary care centre.Methods: A retrospective study of cases of postpartum haemorrhage for a period of 3yrs was conducted in Dept. of OBGY at a rural tertiary care center and teaching hospital in Maharashtra. The major causes, management modalities, morbidity and mortality associated with it were discussed.Results: Out of 37515 deliveries over the period of 3 years (2014-2016), there were 1333 cases of PPH out of which accounted for a prevalence of 3.55%. Study showed that 86% of cases were due to atonic PPH, 9.9% due to traumatic PPH, and 0.97% were due to both atonic and traumatic PPH. 2.7% of cases were due to retained placenta, 0.07% were due to bleeding diathesis.Conclusions: In an era with availability of excellent uterotonics and active management of 3rd stage of labour even today postpartum haemorrhage stands first as the cause of maternal morbidity and mortality. Even though with excellent medical and surgical interventions, maternal mortality due to PPH has been significantly reduced, the field still needs extensive research and new modalities to prevent and manage post-partum haemorrhage.

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“…However, the uterus did not contract at all, and hemorrhage increased. We speculated that the replacement was easy because massive hemorrhage and concomitant coagulopathy might have caused remarkable atony of the uterus [6,7]. However, hemorrhage increased on replacement of the uterus because the blood flow was reperfused into the ischemic uterus.…”

Section: Discussionmentioning

confidence: 99%

Uncontrollable uterine atony after replacement of uterine inversion managed by hysterectomy: a case report

et al. 2020

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Background Uterine inversion may cause massive hemorrhage, resulting in maternal deterioration and death. Replacement of the inverted uterus must be performed as soon as possible. As time passes, the inverted uterus becomes atonic and necrotic, and a surgical approach may be required. Case presentation A 27-year-old Japanese woman was admitted to our hospital 4 hours postpartum with increased hemorrhage after the replacement of an inverted uterus. Recurrent inversion was diagnosed, and though the atonic uterus was replaced again by the Johnson maneuver, hemorrhage persisted. Balloon tamponade was not successful in stopping the hemorrhage, and uterine artery embolization was performed. Bleeding resumed the next day on removal of the balloon, and hysterectomy was performed. Massive hemorrhage, coagulopathy, and uterine necrosis caused uterine atony, and the reperfused blood flow on replacement of the ischemic uterus increased hemorrhage. Conclusions Cases of uterine inversion with coagulopathy lasting for more than 4 hours may require a surgical intervention, and uterine replacement may have to be delayed until the maternal hemodynamic condition is stabilized. Uterine replacement under laparotomy may be also be considered due to the risk of increased hemorrhage.

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Massive obstetric hemorrhage: Current approach to management

Cited by 26 publications

References 60 publications

Therapeutic Potential of Oxytocin in Atherosclerotic Cardiovascular Disease: Mechanisms and Signaling Pathways

Therapeutic Potential of Oxytocin in Atherosclerotic Cardiovascular Disease: Mechanisms and Signaling Pathways

Clinical study of post partum haemorrhage from a teaching hospital in Maharashtra, India

Uncontrollable uterine atony after replacement of uterine inversion managed by hysterectomy: a case report

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