Occurrence Of Pulmonary Hemorrhage Research Articles

The prognostic value of the level of lactate in umbilical cord blood in predicting complications of neonates with meconium aspiration syndrome

Background In spite of significant advances in therapeutic, diagnostic and even medical modalities, meconium management continues to be a concern for management. It has been recently assumed that trace of lactate in both serum and urine can be a sign of the asphyxia in neonates. However, no study has been done on the prognostic value of increasing lactate concentration in umbilical cord blood for predicting the outcomes of meconium aspiration syndrome (MAS), which was our aim in this study. Methods Thin cross-sectional study was performed on 150 neonates suffering meconium aspiration syndrome who were admitted to Akbar Abadi hospital in Tehran between 2016 and 2018. Samples of umbilical cord blood were extracted from neonates and sent to the reference laboratory to measure lactate level as well as arterial blood gas analysis. The neonatal characteristics as well as postdelivery complications were also collected by reviewing the hospital recorded files. Results Thick meconium stained amniotic fluid (TKMSF) was found in 40.0% and thin meconium stained amniotic fluid (TNMSF) in 60.0%. The mean level of lactate was significantly higher in those neonates with morbidities including pulmonary hemorrhage, persistent pulmonary hypertension of the neonate (PPHN), intraventricular hemorrhage (IVH), and respiratory failure requiring ventilation support. According to the ROC curve analysis, increasing lactate in umbilical cord blood could predict occurrence of pulmonary hemorrhage (AUC = 0.885), PPHN (AUC = 0.832), IVH (AUC = 0.898), and requiring ventilation (AUC = 0.833). Comparing the two groups with TKMSF and TNMSF showed higher gestational age, lower Apgar score, lower BE, higher PCO2, lower PO2, lower PH as well as higher serum lactate. In this regard and using the ROC curve analysis (Table 4), increased lactate could effectively discriminate TKMSF from TNMSF (AUC = 0.998) with the best cut-off value of 4.10. Conclusion The increase in lactate in the umbilical cord blood (>4.1 mmol/L with high sensitivity and specificity) can distinguish between thick meconium and thin meconium forms in amniotic acid and thus can determine the severity of MAS. Also, increasing serum lactate levels is an accurate indicator for predicting complications such as pulmonary hemorrhage, PPHN, IVH, and need for ventilation in newborns with this syndrome. This diagnostic accuracy is even beyond the usual markers for arterial gas analysis, such as PH, PCO2, PO2 and BE.

Pulmonary arteriovenous malformation with spontaneous haemothorax

Pulmonary arteriovenous malformation (PAVM) is a very rare congenital vascular abnormality of the lung. PAVM are usually asymptomatic in presentation. The occurrence of Pulmonary haemorrhage in patients with Pulmonary arterio -venous malformation is very rare. Pulmonary haemorrhage is a very lethal complication of Pulmonary arteriovenous malformation and it should be treated aggressively. Depending upon the location, either massive haemoptysis or haemothorax will occur. We report a case of 36 year old female who was evaluated for spontaneous massive haemothorax on the right side and detected to have large PAVM. She was successfully treated with right lower lobectomy.

Patient selection in non-small cell lung cancer: Histologic versus molecular subtypes?

Until recently, the selection of systemic therapy has not varied according to histologic subtypes of non-small cell lung cancer (NSCLC) and is largely empirical. Thus, the diagnosis of “non-smallcell lung cancer not otherwise specified” (NSCLC-NOS) has been a frequently-used, acceptable term for clinical decision-making, despite the fact that it is not recognized by the World Health Organization Classification of Lung Tumors (1). This paradigm has been challenged by new generation of rational cancer therapeutics. The first emphasis on histology in treatment decision in NSCLC came from safety concerns about the first-in-class angiogenesis inhibitor bevacizumab. A randomized Phase II trial of carboplatin and paclitaxel alone or with lowor high-dose bevacizumab revealed a severe (and even fatal) occurrence of pulmonary hemorrhage in NSCLC patients with squamous histology receiving bevacizumab (2). Thus, patients with squamous histology were subsequently excluded from Phase III trials of bevacizumab and most of anti-angiogenesis inhibitors in advanced NSCLC (3-6). The identification of molecularly-defined cohorts of NSCLC patients who demonstrate dramatic clinical response to targeted agents has changed the landscape of lung cancer therapy. An epidermal growth factor receptor tyrosine kinase inhibitor (EGFR TKI), gefinitb or gefitinib, was the first targeted therapy used for the treatment of NSCLC patients (7,8). Initial clinical experiences suggested that high tumor responses were observed among patients with adenocarcinoma and a light or never smoking history (9-11). These clinical observations led to the development of a Phase III trial of gefinitb compared with first-line chemotherapy doublets in this clinically selected patient population (12). Surprisingly, correlative molecular analyses in this Phase III study reveals that the key driver of response to EGFR TKIs is the presence of TK-activating EGFR mutations rather than histology, Asian ethnicity or clinical characteristics (13). The higher clinical responses observed in never or light smokers and NSCLC patients with adenocarcinoma rather than squamous histology are due to the higher prevalence of TK-activating EGFR mutations present in these patients. These results led to world-wide clinical testing for EGFR mutations for selecting those NSCLC patients for first-line therapy of an EGFR TKI in 2009 (14). Of note, papillary and micropapillary adenocarcinoma subtypes have been correlated with lung adenocarcinomas with EGFR mutations (15). However, the clinical value of subtyping histologic-genetic correlations in NSCLC remains to be determined as the genetic features for the majority of NSCLC have yet to be characterized and the histologic diagnosis of lung adenocarcinoma or squamous carcinoma could vary significantly between pathologists. Nevertheless, the cancer armentarium that might be selected by molecular biomarker status is quickly increasing. The echinoderm microtubule-

Pulmonary haemorrhage

The occurrence of pulmonary haemorrhage in an already sick neonate is a serious complication, representing haemorrhagic pulmonary oedema. Known risk factors include prematurity, intrauterine growth restriction and significant respiratory distress syndrome treated with surfactant. The mortality remains high especially with severe pulmonary haemorrhage. There have been concerns about the causative role of surfactant therapy in pulmonary haemorrhage, but the evidence suggests only a marginal increase with surfactant, certainly not enough to outweigh the proven beneficial effects of surfactant. There is some supportive evidence for the use of surfactant in the treatment of pulmonary haemorrhage, despite concerns about its role in the causation. The mainstay of treatment, however, remains vigorous resuscitation of a shocked and critically ill infant.

Influence du surfactant sur l'hémodynamique du syndrome de détress respiratoire néonatal

The neonatal respiratory distress syndrome tends to delay the circulatory adamation to extra-uterine life and leads to systematic hypotension. Haemodynamic changes following the instillation of surfactant are not stereotyped. They depend on the type of surfactant, the time of the instillation, the degree of prematurity, the severity of the respiratory disease and the mode of instillation. They are characterized by a transient haemodynamic instability with variable consequences on arterial pressure and systemic blood flow. The use of surfactant tends to decrease pulmonary arterial resistances and pulmonary arterial pressures but this effect is variable and is not obviously accompanied by long-term deleterious effect on the arterial duct. Haemodynamics and blood gases changes due to surfactant instillation have a variable effect on cerebral blood flow. The potential role of blood gas and haemodynamics changes on the occurrence of pulmonary haemorrhage or cerebral damage following instillations of surfactant remains poorly established but has to be taken into account.

Clinical Trials of Synthetic Surfactant in the Respiratory Distress Syndrome of Premature Infants

This article outlines the controlled clinical trials that have been performed with synthetic surfactant preparations in the management of premature newborn infants. The results have shown impressive reductions of mortality and in the incidence of air-leak complications. Complications appear to be few and mild, although the occurrence of pulmonary hemorrhage is increased in very small infants. The 1- and 2-year follow-up data suggest that there is not an increase in the number of impaired surviving children.

Association of IgM with IgG ANCA in patients presenting with pulmonary hemorrhage.

ANCA are markers for systemic vasculitis such as Wegener's granulomatosis (WG) and microscopic polyarteritis (MPA) and are usually of the IgG isotype. However, IgM ANCA may rarely occur in isolation, and in these circumstances, we have found that they are associated clinically with a syndrome of pulmonary hemorrhage and systemic vasculitis. How frequently IgM ANCA may occur in conjunction with IgG has not previously been investigated. We report here a study of 24 consecutive patients with IgG ANCA-positive systemic vasculitis (14 WG, 10 MPA) in whom we determined whether IgM ANCA occurred in association with IgG ANCA, and if so, whether this had clinical importance. Eight patients were found to have IgM ANCA as well as IgG ANCA, and of these, seven presented with severe pulmonary hemorrhage. None of the IgM ANCA-negative patients presented with pulmonary hemorrhage. Although the occurrence of pulmonary hemorrhage in ANCA positive vasculitis was closely correlated with the presence of IgM ANCA, the antigen specificity of these IgM autoantibodies was variable, since both myeloperoxidase (4 patients), PR3 (3 patients), and an unknown ANCA antigen (1 patient) were found to be targets. We conclude that knowledge of ANCA isotype may have important clinical and therapeutic implications for the management of patients with systemic vasculitis.

Marked hyperbilirubinemia with Gilbert syndrome and immunohemolytic anemia

The etiology of pulmonary hemorrhage in lupus is unclear. Fayemi 7 identified fibrinoid necrosis and vasculitis in pulmonary vessels of autopsied patients. Reports of electron-dense deposits in alveolar basement membranes observed by electron microscopy, low levels of C3, and the occurrence of pulmonary hemorrhage during the acute phases of SLE suggest that pulmonary hemorrhage may result from vascular injury mediated by immune complexes. Hemoptysis in a patient with SLE is more commonly associated with pulmonary infection, pulmonary emboli, and congestive heart failure. To ensure appropriate therapy, each of these possibilities must be investigated in the patient who has SLE with hemoptysis. However, pulmonary hemorrhage per se is a known, but often fatal, complication of SLE and prompt recognition is essential; early diagnosis and prompt treatment with steroids and positive end expiratory pressure, and concomitant therapy of thrombocytopenia with platelet transfusions, permitted the survival of our patient.