Hemodynamic effects of acute tension pneumothorax in a term newborn. A case report.

1. Katherine Cashen, DO* 2. Tara L. Petersen, MD† 1. *Department of Pediatrics, Children's Hospital of Michigan/Wayne State University School of Medicine, Detroit, MI 2. †Division of Critical Care, Department of Pediatrics, The Children’s Hospital of Wisconsin/The Medical College of Wisconsin, Milwaukee, WI * Abbreviations: BTS: : British Thoracic Society CHF: : congestive heart failure CT: : computed tomography VATS: : video-assisted thoracoscopic surgery 1. Clinicians should be aware of the causes and clinical presentation of pleural effusions and pneumothoraces. 2. Clinicians should understand the current role of diagnostic tests, imaging modalities, and timing of minimally invasive treatments. After completing this article, readers should be able to: 1. Describe the pathogenesis of pleural fluid accumulation. 2. Identify the most likely causes of pleural effusion and pneumothorax. 3. Understand the basic clinical presentation, diagnostic tests, and management of pleural effusions and pneumothoraces. 4. Differentiate between transudative and exudative pleural effusions. 5. Understand the natural history of spontaneous pneumothorax. The pleural space is created by the parietal and visceral pleura that line the chest wall and the lung surface, respectively. Normally, only a small amount (0.3 mL/kg) of hypotonic fluid is present within the pleural space due to homeostatic balances in physiologic fluid production and absorption. Various infectious and noninfectious processes can lead to pathologic filling of the pleural space with fluid (effusion) or air (pneumothorax). Such pathologic changes create a true space that can interfere with normal lung mechanics and, in severe cases, cardiac function. Although much less common in pediatric than adult populations, pleural effusions and pneumothoraces in both groups can lead to substantial complications, resulting in significant morbidity and mortality if unrecognized or untreated. Overall, the cause of pleural effusions and pneumothoraces differs in children compared to adults. In adults, congestive heart failure (CHF) and malignancy account for a substantial number of pleural effusions, but these are uncommon causes in children. Infectious pleural effusions in the setting of pneumonia (parapneumonic effusions) remain the most common cause of effusions in both children and adults. Unlike the adult population, children experience spontaneous …

Tuberculosis remains as one of the top 10 infectious diseases causing mortality worldwide. In year 2022, Tuberculosis has caused an estimated 1.30 million deaths with 1.13 million of death caused by tuberculosis alone, while 167000 cases in TB-HIV coinfection. Secondary Spontaneous Pneumothorax has been well known as a complication of Tuberculosis, although the incidence is quite rare, it could be life threatening especially if the pneumothorax progress to tension pneumothorax. Patient, male 19 years old came to the emergency room with a sudden shortness of breath for 3 hours prior to hospital admission. X-ray thorax examination showed collapse of the right lung with hyperlucent avascular findings on the right lung, which suggest secondary spontaneous tension pneumothorax. He was treated with chest tube insertion and WSD placement, 2 hours after WSD placement, he became pulseless. ACLS protocols were given and unfortunately, we were unable to achieve ROSC on him. Tuberculosis remains one of the deadliest infection diseases, but can still be treated with the DOTS regimen. Some condition can make tuberculosis difficult to treat, such as immunodeficiency patient like HIV/AIDS. Spontaneous Pneumothorax has been well known as a complication of tuberculosis, although the incidence rate of pneumothorax in tuberculosis are quite low, however it could be life-threatening if it develops into a tension pneumothorax, especially in the settings of advanced stage HIV patients. Spontaneous pneumothorax can be fatal especially when it develops to tension pneumothorax. Further research is needed to know what population who are at risk of developing pneumothorax.

The myocardial performance index (MPI) is a noninvasive method to measure global systolic and diastolic myocardial function. In both term and premature neonates, changes in the systolic and diastolic function of the left ventricle (LV) and right ventricle (RV) reflect the degree of neonatal myocardial immaturity and the co-existence of foetal circulation. To assess MPI (or Tei indices) of both ventricles in term and preterm newborns, and to observe MPI trends throughout the neonatal period. Heart ultrasound imaging was performed on the first day of life (DOL), after patent ductus arteriosus (PDA) closure, and on the 28th DOL, in 29 term and 29 preterm newborns. RVMPI and LVMPI were measured within the preterm group at 40 weeks of post-conception age (PCA). A statistically significant reduction in RVMPI was observed in both term and preterm newborns. In term newborns, the RVMPI value on the first DOL was 0.42 ± 14, dropping to 0.29 ± 0.09 after PDA closure, and finally reaching 0.22 ± 0.09 on the 28th DOL. The respective RVMPI values for the preterm newborns were 0.44 ± 0.15, 0.30 ± 0.12, and 0.21 ± 0.08. Little variability in the mean values of LVMPI was observed in both groups throughout the neonatal period. The LVMPI for term neonates in successive measurements was 0.37 ± 0.10, 0.39 ± 0.07, and 0.37 ± 0.11, respectively, and for the preterm neonates it was 0.37 ± 0.10, 0.35 ± 0.09, and 0.36 ± 0.10, respectively. The MPI values from preterm newborns taken at 40 weeks PCA (RVMPI = 0.28 ± 0.09; LVMPI = 0.37 ± 0.05) were comparable to those measured in term newborns after PDA closure. Observed postnatal changes in RVMPI correspond to changes in ventricular function, reflecting the haemodynamic changes of the transitional circulation. The relatively small postnatal changes in LVMPI in term and preterm newborns may reflect an immature myocardium. The RVMPI and LVMPI values at 40 weeks PCA in preterm newborns correlate best with MPI values in term newborns just after PDA closure.

FROM A SIMPLE COLD SORE TO SEVERE CYSTIC LUNG DISEASE

Performing lung ultrasound at rest and/or after an exercise stress test to better identify high-risk ambulatory patients with heart failure.

This article refers to ‘Lung ultrasound-guided treatmentin ambulatory patients with heart failure: a random-ized controlled clinical trial (LUS-HF study)’ by M.Rivas-Lasarteet al., published in this issue on pages1605–1613.

Subclinical pulmonary congestion is prevalent in nephrotic syndrome.

Spontaneous pneumothorax resulting in tension physiology

IntroductionTo compare the clinical characteristics and outcomes of patients with acute heart failure (AHF) according to the 2016 European Society of Cardiology (ESC) guidelines taking into account isolated right HF (RHF) with left HF (LHF) phenotypes. Volume status was assessed by the clinical manifestations and lung ultrasound (LUS). The secondary aim was to study the role of echocardiography in congestion based on LUS and their relations with outcomes.MethodsThis study included AHF patients, who referred to the emergency department (ED) at AL-Mouwasat and AL-Assad University Hospitals in Syria between May and August 2024. The same cardiologist reviewed medical reports, signs/ symptoms of decompensation, echocardiographic assessment, diagnosis, and treatment therapies.ResultsOf 100 patients, 10 patients (10%) had isolated RHF and 90 patients (90%) had LHF, including warm-wet (n = 65, 65%), followed by cold-wet (n = 13, 13%), warm-dry (n = 10, 10%), and cold-dry (n = 2, 2%). Most discharged patients without admission were Warm-dry, meanwhile most of patients with cold-wet (76.9%) were admitted to intensive care unit (ICU). The longest in-hospital stays were in cold-wet (11.9 days) followed by isolated RHF (7.5 days). While in-hospital mortality was mainly in cold-wet (38.5%) followed by isolated RHF (20%). Diuretics dose was highest in cold-wet followed by isolated RHF, while hydration was predominantly in cold-wet. Using vasopressors and inotropes were predominantly in cold-wet. Systolic blood pressure (SBP), hemoglobin (Hb), sodium (Na), proximal right ventricular outflow tract (RVOT1), left ventricular end-diastolic internal diameter (LVIDd), Tricuspid annular systolic plane excursion (TAPSE), and systolic pulmonary atrial pressure (SPAP) correlated with hospital stays, while only SBP and Cr correlated with in-hospital mortality. The cut-off values of E/e’ ratio, isovolumic relaxation time (IVRT), and deceleration time (DT) were (12.5, 55ms, and 131.5 ms; respectively) and could predict congestion (guided by LUS) with sensitivities of (96%, 74%, and 62%; respectively) and specificities of (53%, 92%, and 84%; respectively).ConclusionClassifying AHF patients into these five groups, based on clinical examination supporting by echocardiography and LUS evaluation can give better assessment of the AHF phenotypes and gives more details for management. The bedside diagnostic assessment by LUS and echocardiography is an easy tool and seems to be of great benefit in detecting congestion that enhances the treatment protocols.

Tension pneumothorax is a cause of potentially preventable death in prehospital and battlefield settings and 14-gauge angiocatheter (14G AC) decompression remains the current treatment standard, despite its high incidence of failure. Traumatic pneumothorax is often associated with hemothorax, but 14G AC has no proven efficacy for associated hemothorax. We sought to compare the 14G AC to three alternative devices for treatment of tension hemopneumothorax (t-H/PTX) in a positive-pressure ventilation swine model. Our tension model was modified to incorporate a persistent air leak and pleural blood. Tension physiology was achieved with escalating carbon dioxide insufflation via transdiaphragmatic trocar, and 10% estimated blood volume was instilled into each chest. Intervention was randomized between 14G AC, 10-gauge angiocatheter (10G AC), modified Veress-type needle (mVN), and 3-mm laparoscopic trocar (LT). After recovery, serial tension-induced pulseless electrical activity (PEA) events were induced and decompressed. Success of rescue, time to rescue, and physiologic data were recorded. One hundred ninety-five t-H/PTX and 88 PEA events were conducted in 25 swine. Laparoscopic trocar and 10G AC were more successful and had faster median time to rescue for t-H/PTX compared with 14G AC, whereas mVN performed comparably. Following PEA, 14G AC and mVN succeeded at rescue only 50% and 57% of the time, whereas 10G AC and LT had 100% success at return of spontaneous circulation. Time to successful return of circulation following PEA did not differ between devices; however, there was a noticeable difference in the rate of meaningful hemodynamic recovery following PEA favoring LT and 10G AC. There were no significant injuries noted. While mVN performed comparably to 14G AC, both have unacceptable failure rates. Ten-gauge AC and LT performed superiorly in both t-H/PTX and PEA. We believe there is now ample evidence supporting replacement of the 14G AC with 10G AC in current treatment recommendations.

Tension pneumothorax is a life threatening condition which requires prompt diagnosis and treatment. We report a case of delayed tension pneumothorax caused by blunt chest trauma, which was diagnosed intraoperatively and successfully treated by chest tube insertion. In this case, the tension pneumothorax was thought to be due to blunt chest trauma and precipitated by positive pressure ventilation during anesthesia. The diagnosis and treatment of intraopetative pneumothorax is discussed together with a review of the literature.

Background Acute heart failure (AHF) presents as either new-onset heart failure (de novo AHF) or acute decompensation of chronic heart failure (ADCHF). Studies comparing the detailed cardiac characteristics of these groups remain limited. Purpose We sought to identify clinical characteristics and compare mortality and AHF readmission outcomes in patients with de novo AHF and ADCHF. Methods In a prospective, two-centre observational cohort study, adults hospitalised with clinical signs of AHF were enrolled from 2022 to 2024. Echocardiography, 8-zone lung ultrasound (LUS), and laboratory tests were performed shortly after admission. Medical chart reviews provided a detailed medical history at the time of admission. We analysed the composite outcome of AHF readmission or all-cause mortality at 90 and 180 days after discharge. Results A total of 567 patients admitted with AHF were prospectively included (mean age 78.2 ± 11.6; 43.7% female). Among these, 299 (52.7%) had de novo AHF and 268 (47.3%) had ADCHF. Compared to ADCHF, patients with de novo AHF were younger (77.1 ± 12.1 vs. 79.4 ± 10.8 years, p=0.020), had fewer comorbidities (Figure 1), including a lower prevalence of atrial fibrillation (57.5% vs. 72.8%, p<0.001), and were more likely to present with acute coronary syndrome as AHF aetiology (19.4% vs. 6.0%, p<0.001). On echocardiography, patients with ADCHF had higher filling pressures (E/e’: 18.0 ± 8.69 vs. 15.5 ± 8.17, p=0.002), larger left atrial volume index (41.6 ± 18.4 vs. 36.2 ± 15.2 mL/m2, p=0.005), and lower tricuspid annular plane systolic excursion (1.81 ± 0.39 vs. 1.89 ± 0.35 cm, p=0.023). There was no significant difference in left ventricular ejection fraction between groups (ADCHF: 37.8% vs. de novo AHF: 37.4%, p=0.749). On LUS, patients with ADCHF presented with a higher B-line count compared to patients with de novo AHF (10 ± 9 vs. 7 ± 8, p<0.001). At 90- and 180-days post-discharge, 140 (24.7%) and 185 (32.6%) patients were either readmitted with AHF or died. Although 90-day outcome rates were comparable (de novo AHF: 21.7% vs. ADCHF: 28.0%, p=0.10), patients with ADCHF had worse 180-day outcomes (38.4% vs. 27.4%, p=0.039). In univariable Cox regression, ADCHF was associated with a higher 180-day composite outcome risk (HR 1.51, 95% CI 1.13–2.02, p=0.005) (Figure 2). This association remained after adjusting for age and comorbidities (HR 1.45, 95% CI 1.05–1.99, p=0.022). Conclusions In this real-life prospective cohort of patients admitted with clinical signs of AHF, cases of de novo AHF and ADCHF were evenly distributed. Patients with de novo AHF tended to be younger, had fewer comorbidities, better diastolic and right ventricular function, and less pulmonary congestion on LUS. While short-term outcomes were similar, ADCHF patients had significantly higher 180-day readmission or mortality rates. ADCHF was independently associated with a higher risk of the 180-day composite outcome.Figure 1 Figure 2

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Unileaflet Mitral Valve in Patient With Marfanoid Habitus

This article refers to 'Lung ultrasound-guided treatment in ambulatory patients with heart failure: a randomized controlled clinical trial (LUS-HF study)' by M. Rivas-Lasarte et al., published in this issue on pages 1605–1613. In the last few years, lung ultrasound (LUS) has moved from a niche research tool to the clinical arena, and from intensive care units and emergency departments to cardiology and internal medicine.1 LUS is part of point-of-care ultrasound, which is the quintessence of clinical ultrasound. Its primary purpose is less about the examination of an organ (the lungs), but as a tool to answer a specific clinical question. While LUS is indeed an imaging study, it is fundamentally clinical in nature; some describe its clinical application as a kind of 'extended' physical examination. Indeed, insonation has recently been described as the 'fifth pillar' of bedside physical examination.2 Applying insonation to the lungs allows a rough semi-quantification of the degree of pulmonary deaeration. Thus, the utility of LUS spans multiple clinical settings, as documented by hundreds of studies worldwide.3 Ironically, visualization of B-lines is the most counterintuitive LUS sign: they are artefacts, appearing as comet tails across the screen. They do not directly depict the lung parenchyma; rather, B-lines indirectly inform us of the level of deaeration, which in a patient with heart failure (HF) represents, with very high probability, interstitial pulmonary oedema. A substantial body of work confirms the value of LUS in the HF setting (Table 1). The presence of B-lines narrows the differential diagnosis of acute dyspnoea.4 A recent randomized trial demonstrated B-lines together with clinical assessment improved diagnostic accuracy when compared to the current diagnostic approach of clinical assessment plus chest X-ray and N-terminal pro-B-type natriuretic peptide (NT-proBNP), and significantly reduced the time needed for a correct diagnosis.5 B-lines also predict outcomes; subclinical persistent congestion – defined by persistent B-lines at discharge – predicts rehospitalization.6, 7 Similarly, the presence of a higher number of B-lines in HF patients in the outpatient setting, predicts rehospitalization with acute pulmonary oedema and death.8-10 Despite the diagnostic and prognostic value of B-lines, what is unknown is whether B-lines are a target for therapy. Does LUS-guided therapy, even in the absence of clear signs and symptoms, improve HF patients' outcomes? Diagnosis Inpatients Outpatients ++++ +++ ++++ ++ Multiple, diffuse, bilateral B-lines rule in AHF. Absence of multiple, diffuse, bilateral B-lines rules out AHF ≥14 total B-lines Monitoring Inpatients ++ Variation of B-lines, with first significant reduction already less than 1 h after diuretic therapy A significant reduction of B-lines during hospitalization predicts rehospitalization for HF and death at 6 months Prognosis Inpatients Outpatients +++ +++ Persistent significant B-lines at discharge (>20/30 total B-lines) predicts rehospitalization for HF and death at 3 months A higher number of B-lines during out-office visit predicts hospitalisation for HF and death at 6 months The paper by Rivas-Lasarte et al.11 begins to fill this knowledge gap. In this single-blind trial, 123 patients hospitalized for HF were randomized to either standard follow-up or LUS-guided (plus usual care) follow-up. Both study arms required scheduled visits at 2 weeks, 1, 3, and 6 months after discharge. In the LUS-guided arm, treating physicians were encouraged to modify diuretic therapy according to the number of B-lines present on LUS. Ultimately, LUS-guided patients had better outcomes (hazard ratio 0.518, 95% confidence interval 0.268–0.998; P = 0.049) as defined by the primary composite endpoint (number of urgent visits, hospitalizations for worsening HF, and death from any cause). Compared to standard follow-up, the absolute risk reduction was 17%, resulting in a number needed to treat of 5. At first glance, this is a stunning accomplishment. Yet such a strong effect, coupled with wide confidence intervals and a marginally significant P-value warrants caution. Outcome differences were driven solely by a lower number of urgent visits for HF. No differences in rehospitalization or mortality were observed. Nor were there any differences in quality of life or NT-proBNP values. On the other hand, the LUS-guided arm had significantly greater improvements in the 6-min walk test, nearly doubling the distance (37 m vs. 60 m) compared with those in the standard follow-up group. They also received higher doses of loop diuretics, suggesting insonation may add to the traditional physical exam in detecting congestion.10 Nevertheless, these discordant secondary signals combined with no reduction in rehospitalization or mortality highlight the need for continued investigation. Other limitations of this study are worth noting as they highlight current limitations in the field. There are no clear cut-off values for B-lines to establish when a patient can be considered decompensated. In truth, different cut-offs likely apply to different patient populations, since the same number of B-lines in a patient with acute symptoms of HF have a different meaning than a patient with chronic HF or in patients without a history of HF. LUS studies in patients with HF continue to vary in protocol technique, both in terms of number of thoracic sites scanned12 and in the quantification/semi-quantification of B-lines.13 At present, the number of B-lines (quantity) is the dominant concern. Yet quality of B-lines, such as location in the chest (apical B-lines may highlight greater severity) and distribution may also matter. Importantly, B-lines, similar to any other biomarker, should not be viewed in isolation. Context matters: sonographic information must be integrated with our knowledge, experience and clinical judgment. Finally, as a single-centre study, it should be viewed more as a pilot experience; one that is promising and will hopefully lead to a multicentre study. Other studies are ongoing: the BLUSHED-HF study, which is a multicentre randomized pilot trial designed to test whether a LUS-guided treatment protocol outperforms usual care for reducing pulmonary congestion during emergency department stay14; and the LUST study, which shifts the idea of LUS-guided treatment to dialysis patients and has already provided some preliminary results.15 If confirmed by larger multicentre studies, the implications would be remarkable. LUS is easy to learn and patient friendly. Integrating LUS in the management of HF patients might tailor the approach to titrating therapies. The detection of B-lines, even in asymptomatic patients, would lead to further optimization of treatment, which in turn might reduce hospitalization. Ultimately, Rivas-Lasarte and colleagues are to be congratulated for their significant contribution towards HF management. Patients want to feel well and stay well; the LUS-HF study suggests adding ultrasound assessment will reduce urgent HF visits. Given the safety of LUS and its well established diagnostic and prognostic benefits, we strongly encourage its use. The next few years will yield greater insights into the value of LUS in HF; perhaps ultrasound lung comets will indeed guide us. Conflict of interest: none declared.