ABSTRACT
Hypertensive heart disease refers to changes in the myocardium that result from hypertension. The relationship between hypertensive heart disease and sudden cardiac death is well established, but there are few pathological studies. We examined the clinical and pathological features of hypertensive heart disease in sudden cardiac death victims from a national cardiovascular pathology registry. We investigated 5239 cases of sudden cardiac death between 1994 and 2018. Hearts were examined by two expert cardiac pathologists. Diagnostic criteria included history of hypertension, increased heart weight and left ventricular wall thickness in the absence of other causes. Collagen was quantified using picrosirius red staining and imaging software. Of 75 sudden cardiac death cases due to hypertensive heart disease (age at death: 54 ± 16 years; 56% males), 56 (75%) reported no prior cardiac symptoms. Thirty-four (45%) recorded a BMI ≥ 30. Only two (2.7%) had hypertensive heart disease diagnosed antemortem. Four (5%) were diagnosed clinically with hypertrophic cardiomyopathy, but lacked myocyte disarray at autopsy. All hearts showed concentric left ventricular hypertrophy and myocyte hypertrophy. Fibrosis was identified microscopically in 59 cases (81%). The posterior left ventricular wall showed the greatest increase in the percentage of collagen in hypertensive diseased hearts compared to controls (25.2% vs 17.9%, p = 0.034). Most sudden deaths due to hypertensive heart disease occur without prior cardiac symptoms; thus, clinical risk stratification is challenging. Hypertensive heart disease can be misdiagnosed in life as hypertrophic cardiomyopathy which has major implications for relatives. Pathologists require a history of hypertension and histology for a definitive diagnosis of hypertensive heart disease.
Subject(s)
Cardiomyopathy, Hypertrophic , Heart Diseases , Hypertension , Adult , Aged , Cardiomyopathy, Hypertrophic/complications , Cardiomyopathy, Hypertrophic/pathology , Collagen , Death, Sudden, Cardiac/epidemiology , Death, Sudden, Cardiac/etiology , Female , Heart Diseases/complications , Heart Diseases/pathology , Humans , Hypertension/complications , Hypertension/pathology , Male , Middle Aged , MyocardiumABSTRACT
BACKGROUND: Emergency abdominal surgery is associated with a high risk of postoperative pulmonary complications (PPCs). The primary aim of this study was to determine whether patients undergoing emergency laparotomy are ventilated using a lung-protective ventilation strategy employing tidal volume ≤8 ml kg-1 ideal body weight-1, PEEP >5 cm H2O, and recruitment manoeuvres. The secondary aim was to investigate the association between ventilation factors (lung-protective ventilation strategy, intraoperative FiO2, and peak inspiratory pressure) and the occurrence of PPCs. METHODS: Data were collected prospectively in 28 hospitals across London as part of routine National Emergency Laparotomy Audit (NELA). Patients were followed for 7 days. Complications were defined according to the European Perioperative Clinical Outcome definition. RESULTS: Data were collected from 568 patients. The median [inter-quartile range (IQR)] tidal volume observed was 500 ml (450-540 ml), corresponding to a median tidal volume of 8 ml kg-1 ideal body weight-1 (IQR: 7.2-9.1 ml). A lung-protective ventilation strategy was employed in 4.9% (28/568) of patients, and was not protective against the occurrence of PPCs in the multivariable analysis (hazard ratio=1.06; P=0.69). Peak inspiratory pressure of <30 cm H2O was protective against development of PPCs (hazard ratio=0.46; confidence interval: 0.30-0.72; P=0.001). Median FiO2 was 0.5 (IQR: 0.44-0.53), and an increase in FiO2 by 5% increased the risk of developing a PPC by 8% (2.6-14.1%; P=0.008). CONCLUSIONS: Both intraoperative peak inspiratory pressure and FiO2 are independent factors significantly associated with development of a postoperative pulmonary complication in emergency laparotomy patients. Further studies are required to identify causality and to demonstrate if their manipulation could lead to better clinical outcomes.
Subject(s)
Laparotomy/adverse effects , Postoperative Complications/prevention & control , Respiration, Artificial/methods , Ventilator-Induced Lung Injury/prevention & control , Adult , Aged , Emergency Medical Services , Female , Humans , Inspiratory Capacity , London , Male , Middle Aged , Oxygen/blood , Positive-Pressure Respiration , Postoperative Complications/epidemiology , Prospective Studies , Tidal Volume , Ventilator-Induced Lung Injury/epidemiologyABSTRACT
This randomised controlled trial investigated the efficacy of Epi-Fix(™) , LockIt Plus(®) and Tegaderm(™) as fixation devices for intrapartum epidural catheters. One hundred and sixty-five women requesting intrapartum epidural analgesia were randomised to receive different fixation devices to secure their epidural catheter. The amount of epidural catheter migration (measured to the nearest 0.5 cm) was analysed for three devices: Epi-Fix (n = 55); LockIt Plus (n = 54); and Tegaderm dressing (n = 51). Median (IQR [range]) catheter migration for Epi-Fix was 1.0 cm (0.0-2.0 [-2.0 to 9.5]), vs 0.0 cm (0.0-0.5 [-1.0 to 5.5]) for LockIt Plus and 0.5 cm (0.0-1.8 [-1.5 to 8.0]) for Tegaderm (p = 0.003). Thirty-eight (69.1%) epidural catheters secured with Epi-Fix migrated < 2.0 cm, compared with 49 (90.7%) with LockIt Plus and 40 (78.4%) with Tegaderm. Sixteen epidural catheters required resiting due to failure of analgesia of which 12 (75.0%) occurred in patients with epidural catheters that had migrated ≥ 2.0 cm. This study shows that intrapartum epidural catheters secured with the LockIt Plus device exhibit less catheter migration compared with fixation with Epi-Fix and Tegaderm.
