SEARCH RESULTS FOR: Endometritis

Endometritis

Endometritis: Pathogenesis and clinical findings Prolonged rupture of membranes > 24 hours between amnion rupture and delivery ↑Time for vaginal flora to ascend into the uterus Assisted vaginal delivery Use of forceps or vacuum Multiple digital vaginal exams Manual examination of the vagina to assess cervical dilation Internal monitoring Intrauterine device to monitor the fetus or contractions Group B Streptococcus colonization Opportunistic bacteria present in the normal vaginal flora of up to 30% of women Bacterial Vaginosis Overgrowth of anaerobic bacteria with associated decrease in protective Lactobacillus species Foreign bacterial ascension into the uterus Sepsis Cesarean delivery ↑ Exposure of vaginal flora to the uterus Introduction of bacteria directly into the uterus Spread of infection to myometrial and parametrial layers of uterus Authors: Gabrielle Wagner Reviewers: Danielle Chang Crystal Liu Aysah Amath* * MD at time of publication ↑ Susceptibility to bacterial invasion of the uterine lining Endometritis Postpartum infection of the uterine endometrial lining Activation of innate Fever, immune response Inflammation of uterus Leukocytosis Accumulation of WBCs within vaginal discharge Purulent or foul-smelling lochia (vaginal discharge) Uterine tenderness Pelvic and/or abdominal pain Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published November 26, 2019 on www.thecalgaryguide.com

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Maternal complications of labour and vaginal delivery Author: Yan Yu Reviewers: Kayla Nelson, Radhmila Parmar, Jemimah Raffe-Devine, Alina Constantin* * MD at time of publication Labour and vaginal delivery Detachment of placenta disrupts uterine blood vessels Intense pressure on vaginal walls during fetal passage and/or use of forceps or vacuumà physical damage vagina and perineum Urinary tract catheterization during labour Foreign tube inserted into bladder allows easier colonization of bladder & urinary tract by bacteria Urinary Tract Infections Passage of fetus distends pubo-vesicular and pubo- rectalis sling muscles Urethra /rectum no longer kinked enough to prevent high intra-abdominal pressures from forcing out urine or feces Stress incontinence (of bladder & bowel; usually temporary) Scar tissue forms at site of placental detachment After complete hemostasis (cessation of bleeding) and vessel healing, scar tissue is shed from uterus Lochia (vaginal discharge/ bleeding) & eschar (scar tissue) shedding Placental tissue may be retained in the uterus Uterus fails to contract fully to seal off uterine blood vessels Post-partum hemorrhage (See relevant slide) Foreign substances trigger systemic inflammatory response in mother Disseminated Intravascular Coagulation, DIC (see relevant slide) Rarely, torn blood vessels let amniotic fluid (with fetal cells & meconium) enter maternal circulation Amniotic fluid embolism (clumps of foreign fetal cells and meconium in maternal circulation) Viscous amniotic fluid can block maternal blood vessels Obstructing blood flow out of lungs Blood backs up before lungsàless preload for heart Damaged tissue & blood in the uterus Ample nutrients for bacteria to infect uterus Endometritis Uterine pain, radiating throughout the abdomen Pulmonary edema Hypotension Perineal tears (1st-4th degree); Hemorrhoids Perineal Pain Unilateral leg pain & swelling Dyspnea, Cough If profound Cardiac arrest Tissue damage activates blood coagulation factors ­ Coagulation in areas of hemostasis (e.g. veins) Deep Vein Thrombosis Post-partum fever (see relevant slide) Cardiovascular collapse Lack of perfusion to heart Note: Post-partum depression is commonly seen in at least 10% of newly-delivered mothers. Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Initially published September 5, 2013 on www.thecalgaryguide.com Updated and re-published January 23, 2021

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Postpartum (Puerperal) Fever: Pathogenesis and complications Author: Lindey Felske Reviewers: Brianna Ghali Ran (Marissa) Zhang Ingrid Kristensen* * MD at time of publication Breast Feeding Delayed gastric emptying in pregnancy ↑ Risk of aspiration during delivery Inhalation of gastric contents Chemical burn of the airways from gastric acid Tissue injury Chemokines released by alveolar cells recruit neutrophils Accumulation of neutrophils and plasma exudate in alveoli Aspiration Pneumonia Delivery (Vaginal or Cesarean Section) Tissue damage: Urinary tract catheterization Foreign body can: Introduce bacteria into bladder Provide a biofilm surface for bacterial adhesion Cause mucosal irritation Invasion of bacteria into urinary tract mucosa • • • • Perineal tear/episiotomy (perineal incision) Abdominal incision site Uterine damage Retained products of conception (RPOC) Bacteria enter open tissue Production of antimicrobial peptides and proinflammatory mediators in epidermis Cellulitis Necrosis of RPOC (good medium for bacterial growth) Post-operative pain Hypoventilation from shallow breathing Low volume in alveoli Alveolar collapse Endogenous cervicovaginal flora migrate into the uterine cavity Infiltration of bacteria into endometrium Endometrial TLR4 receptors recognize the endotoxin of Gram-negative bacteria Secretion of proinflammatory cytokines (IL-6, IL-8) and prostaglandin E(2) Activation of coagulation cascade Coagulation in areas of hemostasis (e.g., deep veins) Deep vein thrombosis Dislodged DVT travels to pulmonary arteries Pulmonary embolism • • • Skin openings in breasts (milk ducts +/- cracks) Bacteria from skin and/or saliva enter body Milk backup from blocked duct or poor breastfeeding technique Milk stasis provides environment for bacterial growth Upregulation of IFN- γ, and IL-12A cytokines in milk ducts Mastitis Collection of inflammatory exudate Breast abscess Cytokine expression and inflammatory cell infiltration Sloughing of urinary tract lining to reduce bacterial load Atelectasis Maternal fever (> 38.0°C) within 6 weeks of delivery Urinary tract infection Endometritis Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published July 4, 2022 on www.thecalgaryguide.com The image part with relationship ID rId4 was not found in the file.

Spontaneous Rupture of Membranes

Pre-Labour Rupture of Membranes: Pathogenesis and clinical findings Gestational age approaching term (>37 weeks) Authors: Wendy Xu Reviewers: Riya Prajapati Michelle J. Chen Dr. Jadine Paw* * MD at time of publication Intrauterine inflammation Fetal maturation Fetal growth Uterine contractions ↑ Pro-inflammatory cytokine & chemokine release in fetal membranes & amniotic fluid ↑ Stretch forces on fetal membranes ↑ Pro-apoptotic factors induces cellular apoptosis of fetal membranes Changes in collagen and protein composition drive extracellular matrix remodeling in fetal membranes ↓ Tensile strength Structural weakening of fetal membranes Occurs primarily in the focal area of fetal membranes overlying the cervix ↑ Matrix metalloproteinases triggers extracellular matrix degradation in fetal membranes Amnion and choriodecidua separation Amniotic fluid flows from vagina Amniotic fluid pools in posterior fornix on speculum exam Pre-labour rupture of membranes Membranes rupture before onset of uterine contractions Chorioamnionitis (infection of the fetal membranes and amniotic fluid) Neonatal infection Endometritis (infection of the endometrium) Amniotic fluid leaks through the cervix Prolonged rupture of membranes (>18hrs) before delivery Microbes ascend through vaginal canal Low amniotic fluid volume on ultrasound Amniotic fluid (pH 7.0-7.5) mixes with normal vaginal fluid (pH 4.5-6.0) which increases vaginal fluid pH to > 6.5 Positive nitrazine (pH indicator) test Ion- and estrogen-containing amniotic fluid enters vaginal canal Ferning (branching pattern) of vaginal fluid under microscope Accompanies uterine contractions, cervical effacement & cervical dilation Delivery/birth Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Oct 4, 2024 on www.thecalgaryguide.com