Ultimate Occlusion Nottingham
Jarrell Campbell
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Objective: To determine the effectiveness of resuscitative endovascular balloon occlusion of the aorta (REBOA) when used in the emergency department along with standard care vs standard care alone on mortality in trauma patients with exsanguinating hemorrhage.
Design, setting, and participants: Pragmatic, bayesian, randomized clinical trial conducted at 16 major trauma centers in the UK. Patients aged 16 years or older with exsanguinating hemorrhage were enrolled between October 2017 and March 2022 and followed up for 90 days.
Main outcomes and measures: The primary outcome was all-cause mortality at 90 days. Ten secondary outcomes included mortality at 6 months, while in the hospital, and within 24 hours, 6 hours, or 3 hours; the need for definitive hemorrhage control procedures; time to commencement of definitive hemorrhage control procedures; complications; length of stay; blood product use; and cause of death.
Results: Of the 90 patients (median age, 41 years [IQR, 31-59 years]; 62 [69%] were male; and the median Injury Severity Score was 41 [IQR, 29-50]) randomized, 89 were included in the primary outcome analysis because 1 patient in the standard care alone group declined to provide consent for continued participation and data collection 4 days after enrollment. At 90 days, 25 of 46 patients (54%) had experienced all-cause mortality in the REBOA and standard care group vs 18 of 43 patients (42%) in the standard care alone group (odds ratio [OR], 1.58 [95% credible interval, 0.72-3.52]; posterior probability of an OR >1 [indicating increased odds of death with REBOA], 86.9%). Among the 10 secondary outcomes, the ORs for mortality and the posterior probabilities of an OR greater than 1 for 6-month, in-hospital, and 24-, 6-, or 3-hour mortality were all increased in the REBOA and standard care group, and the ORs were increased with earlier mortality end points. There were more deaths due to bleeding in the REBOA and standard care group (8 of 25 patients [32%]) than in standard care alone group (3 of 18 patients [17%]), and most occurred within 24 hours.
Conclusions and relevance: In trauma patients with exsanguinating hemorrhage, a strategy of REBOA and standard care in the emergency department does not reduce, and may increase, mortality compared with standard care alone.
Fetal endoscopic tracheal occlusion (FETO) is a promising treatment for severe congenital diaphragmatic hernia, a condition that carries significant morbidity and mortality. It is hypothesised that balloon occlusion of the fetal trachea leads to an improvement in lung growth and development. The major documented complications of FETO to date are related to preterm delivery.
Congenital diaphragmatic hernia (CDH) is a relatively common disorder, with an incidence between 1 in 2,000 and 1 in 5,000. Its aetiology is unknown [1, 2]. There is significant associated morbidity and mortality secondary to pulmonary hypoplasia and pulmonary hypertension [3]. Other complications include recurrent herniation, repeated hospitalisations, growth failure and gastro-oesophageal reflux disease [3, 4].
In addition to primary surgical repair, several other treatments have been used in the past, including prenatal corticosteroids, high-frequency oscillatory ventilation, liquid ventilation, surfactant therapy, extracorporeal membrane oxygenation and delayed surgical repair. Despite these efforts, the morbidity and mortality remain high. In fact, each apparent improvement in survival over the last decade was associated with an increase in antenatal death rate [5]. Fetal surgery has been reported to be of no benefit [6].
It is hypothesised that antenatal obstruction of the trachea improves lung growth and development. Effective and sustained obstruction can be achieved by endoscopic deployment of a detachable balloon between the carina and vocal cords, a procedure known as fetal endoscopic tracheal occlusion (FETO). Intrauterine reversal of obstruction improves surfactant production [7, 8].
Occlusion of the fetal trachea has been shown to stimulate fetal lung growth in animal models [9]. Although FETO carries the risk of amniorrhexis and consequent preterm delivery, no serious maternal complications or direct adverse effects on the fetus have been reported to date. In particular, no tracheal damage has been demonstrated in experimental studies [10, 11]. Data on long-term morbidity continue to be collected. There is a single report of a baby with severe developmental delay following FETO [12]. We now report five infants who developed tracheomegaly subsequent to FETO.
Case 2. a Tracheal dilatation is seen on an upper GI study with b tracheal collapse in expiration denoting tracheomalacia. c Volume-rendered CT coronal reformatted images of the trachea in inspiration and d expiration again show tracheomegaly with inspiration and tracheomalacia, respectively. The arrow points to an air-filled oesophagus, not seen on the previous inspiratory image
Case 4. Chest radiograph on day 3 of life shows ET and NG tubes, a right chest drain and an umbilical venous catheter. Marked tracheal dilatation is evident on this film and was also seen on all other chest radiographs (white arrows). The small radiodense opacity on the left side, which was present on all films, was assumed to be due to a collapsed tracheal occlusion catheter in the left main bronchus (black arrow). This child died aged 8 days and did not have an autopsy
Tracheomegaly, which generally manifests as diffuse dilatation of the trachea, typically occurs as a result of weakness of the airway wall or abnormal collapsibility. Causes of tracheomegaly include connective tissue disorders, lung fibrosis and prior intubation, but true tracheomegaly is rarely seen in childhood [13]. Tracheomegaly is characterised by atrophy or absence of elastic fibres and thinning of smooth muscle layers in the trachea but, unfortunately, our two babies who died did not have autopsies [14]. Tracheomalacia refers to a weakness of the tracheal wall, resulting in expiratory collapse, typically with >50% decrease in tracheal diameter. Tracheomalacia is usually due to focal or diffuse cartilage deficiency. It may be congenital, manifesting in neonates, when it is commonly seen in association with oesophageal atresia or cardiovascular anomalies. Alternatively, tracheomalacia may be acquired later in life as a result of diffuse tracheal disease, prolonged intubation or extrinsic compression.
There are no reports to date of tracheomegaly as a complication of FETO. However, we have now described five such cases. Two infants also had tracheomalacia proven radiologically. Our five infants with tracheomegaly suggest that the tracheal cartilage can be damaged by the prolonged intratracheal balloon deployment method of FETO. An alternative explanation for the tracheal abnormality would be damage to the trachea from balloon removal, but we believe this is unlikely as two of our children had tracheomegaly documented prior to removal of the balloon.
Mounier-Kuhn syndrome is a rare but noteworthy congenital abnormality that manifests with marked widening of the trachea and major bronchi [14]. Although it has been reported in children as young as 18 months of age, the condition is usually seen in adults [14]. Our cohort does not, strictly speaking, fit the criteria for this syndrome as only one (case 5) had involvement of a bronchus in addition to tracheal dilatation.
Although tracheal damage is not known to be a complication, the sites of the tracheal abnormalities in these cases correspond to the previous sites of the in utero tracheal balloons. The proximal airways are known to be very compliant early in gestation. A balloon can stretch the tracheal circumference by 15% [10]. Studies in animal models have revealed changes to the tracheal architecture at a microscopic level, with loss of the typical epithelial folding pattern, squamous metaplasia and elongation of the pars membranacea, but without obvious flattening or structural damage to the cartilage [11]. Changes also occur distal to the balloon, probably due to higher airway pressures [11]. One fetal lamb sacrificed early had tracheal dilatation, but this study concluded that these changes disappear almost completely for the remainder of gestation following in utero unplugging [11]. No cartilaginous effects were reported [11]. Harrison et al. [16] reported a small cohort who had stridor and vocal cord paralysis secondary to in utero intervention. Two of their children also had tracheomalacia, but that group had undergone tracheal dissection, transtracheal occluding clips (and tracheal lacerations) rather than simpler balloon placement [16].
We are particularly grateful to Professor Kypros Nicolaides for furnishing much of the antenatal detail of the children and for the information regarding FETO. We are also grateful to innumerable paediatricians in Nottingham and Leeds for allowing us to report two of their patients. We are also grateful to the other members of the tracheal team at Great Ormond Street Hospital for Children, London, for their assistance with these difficult cases. These other team members include Ben Hartley, Colin Wallis, Mike Broadhead, Quen Mok, Alex Barnacle, Clare McLaren, Catherine Dunne, Clair Noctor and Caroline Doyle.
When a plaque inside a coronary artery ruptures, the process of platelet aggregation, linked to the creation of "fibrin", can cause a partial or complete occlusion of the artery. (see flow chart to come on Thrombosis).
Platelets, in their normal state, float around in the blood like smarties: nice and smooth and oval shaped. It is only when platelets receive biochemical signals that they start to react and, when an arterial plaque is ruptured, it releases these biochemical signals.
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