8. Rupture
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Objectives: The mechanisms by which microbial invasion of the amniotic cavity leads to membrane weakening and rupture are poorly understood. Recently, endogenous host enzymes have been implicated in this process. Matrix metalloproteinases are a family of potent enzymes that degrade components of the extracellular matrix. Collagen type I provides the main tensile strength of the fetal membranes. Matrix metalloproteinase 8 (MMP-8), or neutrophil collagenase, degrades interstitial collagens, acting preferentially on collagen type I. This study was undertaken (1) to determine whether MMP-8 is present in amniotic fluid and whether its concentrations are changed in preterm and term labor and membrane rupture with and without intra-amniotic infection and (2) to determine whether the amniotic fluid concentrations of MMP-8 in labor at term are different in the lower and upper uterine compartments.
Study design: A cross-sectional study was conducted and transabdominal amniocentesis was performed in women in the following categories: (1) midtrimester (n = 25), (2) preterm labor in the presence and absence of microbial invasion of the amniotic cavity (n = 86), (3) preterm premature rupture of the membranes in the presence and absence of microbial invasion of the amniotic cavity (n = 51), (4) term patients in labor and not in labor (n = 51), and (5) term premature rupture of membranes (n = 20). Additional paired samples of amniotic fluid were retrieved by transabdominal amniocentesis (upper compartment) and transvaginal amniocentesis (lower or forebag compartment) from 14 term patients (28 samples) in spontaneous labor with intact membranes. Amniotic fluid MMP-8 concentrations were determined with a sensitive and specific immunoassay.
In caesarean section patients, the spontaneous rupture of the posterior wall of the uterus is extremely rare, with nonspecific signs and symptoms being present. Perinatal and maternal morbidity and mortality are high.
Silent uterine rupture is very rare and easy to ignore due to nonspecific clinical symptoms, unexplained haemoglobin reduction and haemoperitoneum, but these features caution us to more closely consider uterine rupture in patients.
Spontaneous rupture of the posterior wall of the uterus in pregnancy is rare and potentially a catastrophic event for both the mother and the foetus [3, 4]. Nonspecific signs and symptoms lead to misdiagnosis and delayed treatment. In this case, no predisposing factors, classic signs and symptoms, including decreased foetal heart rate, uterine contraction, abdominal pain, changes in the station of the presenting part, bleeding or shock were found. The patient felt only uterine contraction aggravations and abdominal swelling. We performed an urgent laparotomy based on the previous caesarean delivery history in breech presentation. Both the patient and the newborn were fortunate to have a good outcome.
In 2011, Stefano Uccella [5] wrote a review of spontaneous pre-labour uterine rupture in a primigravida. Some risks in those cases included a history of uterine surgeries, such as caesarean section or myomectomy, uterine damage due to trocar insertion, uterine perforation and other risk factors, such as uterine anomaly, uterine curettage, uterine diverticula, and Ehlers-Danlos syndrome. The patient had only a history of caesarean section, with no other uterine operations, but the rupture site was not found in the uterine scar. She had no other risk factors.
Le-Ming Wang [6] reported a spontaneous uterine rupture on the posterior wall due to placenta percreta. In this case, the placenta was located on the right lateral and anterior wall of the uterus so that its occurrence should not be related to placenta factors. Unscarred uterus multiparity is one of the most important factors in uterine rupture. The stretching, tearing or bruising of repeated childbirth makes the uterine wall very weak, so the chances of rupture increase with every subsequent pregnancy. The patient had a medical termination of a missed miscarriage at seven weeks and a caesarean section. It was not clear if this rare event of spontaneous rupture may be attributed to the weakening of the uterine wall.
Traditionally, spontaneous rupture of the posterior wall of the uterus is rare, and the rupture is often easily covered by the intestinal loop and omentum so that some minor symptoms are ignored. Ultrasonography plays a critical role in diagnosing uterine rupture based on the demonstration of a myometrial defect associated with intraperitoneal and extraperitoneal haemorrhage [7]. In this case, we failed to find extraperitoneal haemorrhage. However, it is important to maintain a high index of suspicion for uterine rupture in women presenting with some or all of these features, regardless of any known risk factor [8]. Prompt recognition of uterine rupture, early diagnosis and expeditious recourse to laparotomy are critical to influencing perinatal and maternal morbidity.
Silent uterine rupture, especially that occurring in the posterior wall, is very rare and easy to ignore due to nonspecific clinical symptoms. Haemoglobin reduction and haemoperitoneum in patients caution us to closely consider uterine rupture.
The Department of Transportation's Pipeline and Hazardous Materials Safety Administration (PHMSA) has been an integral partner in investigations into this tragic pipeline incident. PHMSA staff were on scene in San Bruno the day after the pipeline rupture to assist the National Transportation Safety Board (NTSB) as it began its investigation to determine the cause of the rupture. PHMSA also participated in NTSB public meetings and provided factual information required for the NTSB report.
On September 9, 2010 at 6:11 pm, a 30 inch diameter natural gas transmission pipeline in San Bruno, CA ruptured and released vast quantities of natural gas. The escaping gas ignited and initiated structure fires in the community surrounding the pipeline. Local emergency responders utilized air drops of fire retardant and water to limit the spread of the fire. At 7:40 pm, PG&E completed the isolation of the ruptured pipeline from sources of gas supply by closing valves upstream and downstream of the rupture site. Approximately 5 hours after the rupture, PG&E reported the pipeline rupture to the National Response Center (NRC). The consequences of the rupture and fire were devastating. Eight people lost their lives, 51 people required in-patient hospitalization, and 38 homes were destroyed. PG&E has estimated the property damage from the rupture to be over $220 million.
Spontaneous atraumatic splenic rupture is a rare but dramatic occurrence that is most commonly attributed to infection or neoplasia. Deciphering the etiology can be challenging with many cases remaining unclear despite full investigation.
We report the case of a previously healthy and immunocompetent 52-year-old Caucasian woman with a remote history of clinically diagnosed infectious mononucleosis who experienced sudden atraumatic splenic rupture after an untreated stray cat bite.
Regardless of etiology, the immediate management of ASR can be varied, depending on the degree of splenic injury[4]. If the degree of splenic injury is mild, then conservative therapy consisting of fluids, with or without blood transfusion(s) and intensive care unit (ICU) admission for close monitoring may be sufficient[4]. If severe, then splenic artery embolization, splenic salvage, or splenectomy may be indicated when conservative management fails to achieve hemodynamic stabilization[4]. Approximately 20 to 40% of patients require surgical intervention[5]. Finally, patients should be advised to avoid high impact sports post-injury between 1 and 6 months post-rupture, depending on the degree of splenic injury[6]. Evidence for serial CT imaging to document splenic healing prior to resumption of activities is poor and is only recommended in select individuals and activities[7]. In patients post-splenectomy, there is strong evidence to encourage patients to receive pneumococcal vaccination due to reduced immunity towards encapsulated organisms[8]. Vaccination for patients undergoing nonoperative conservative management remains controversial[9].
A case for EBV infection is also possible given the EBV serological findings. Hepatic involvement is observed in approximately half of adults with infectious mononucleosis, resulting in up to 5-fold elevation in liver enzymes[16]. Here, liver involvement was noted clinically, radiologically and biochemically. While the patient convalesced on anti-Bartonella antibiotics, EBV is a self-limiting infection with a typical clinical course that resolves over 1 to 3 months. Thus, it may be possible that the improvement in clinical status had no relationship with antimicrobial therapy. A negative Monospot test is not inconsistent with an EBV infection as this test is specific, but lacks sensitivity, and has a negative likelihood ratio of 0.14[17]. However, there are several factors in this case that argue against EBV. Infectious mononucleosis is diagnosed most commonly using the Hoagland criteria: 1) greater than 50% lymphocytes and more than 10% atypical lymphocytes; 2) clinically as a triad of fever, pharyngitis and lymphadenopathy; 3) positive serology for EBV. In this case, there were no atypical lymphocytes and her clinical presentation was not entirely consistent with the classical triad. Splenomegaly is seen in 50 to 60% of patients with infectious mononucleosis, yet splenic rupture is rare, occurring in an estimated 0.1 to 0.5% of cases and occurring almost exclusively in males[18]. Thus, this patient does not fit the profile of a high-risk patient for ASR secondary to EBV infection. Furthermore, although the patient reported two previous episodes of infectious mononucleosis in her teenage years, the EBV serological profile does not fit the categorization of either past infection or reinfection of EBV and thus is inc
