Use of oxycodone in polytrauma patients: the "Gemelli" experience.

INTRODUCTION: This is the first study investigating the effect of oxycodone in polytrauma patients. The management of pain in polytrauma patients has become a very relevant issue. Nonsteroidal anti-inflammatory drugs (NSAIDs) represent the most used drugs in polytrauma patients, even though their use is associated with an increased hemorrhagic risk. Previous studies have demonstrated the efficacy of oxycodone for the treatment of acute pain. The aim of this study was to assess the efficacy of oxycodone administration in polytrauma patients, with minor injuries. PATIENTS AND METHODS: 15 polytrauma patients (10 males, mean age 40 +/- 13 years; 5 females, mean age 49 +/- 26 years) were admitted to the Emergency Department of the Catholic University, A. Gemelli Hospital in Rome, Italy. All patients underwent physical examination, FAST ultrasound, total body CT scanning and blood tests. Three patients had multiple costal fractures, three had pelvic fracture, two had tibial fracture, five had vertebral fractures, one patient had clavicle fracture and ulnar fracture, one patient a severe trauma of the left leg, which required amputation. Five patients also reported minor head trauma, with a Glasgow Coma Score (GCS) 15. All patients reported abdominal trauma, while none of them had severe thoracic or kidney damage. Patients with head trauma also underwent a second CT head scanning 12 hours after admission, which excluded the occurrence of cerebral damage. All patients were then treated with oral administration of oxycodone 10 mg two times per day (bid) for 3 days. Pain intensity, before and after the administration of oxycodone, was evaluated using a scale ranging from 0 to 10. RESULTS: The mean pain score at admission was 8 +/- 0.7. All patients reported significant pain improvement after the administration of oxycodone (8 +/- 0.7 vs 1.8 +/- 0.9; p < 0.0001). A dosage increase of oxycodone from 20 to 40 mg bid was required in only one patient with a clavicle fracture. The main side effects were light-headache (5 patients), constipation (4 patients) and nausea (3 patients). CONCLUSIONS: These data indicate that oxycodone is a safe and effective drug for pain relief in polytrauma patients without severe thoracic, kidney or brain damage.

The use of non-invasive ventilation in the treatment of acute cardiogenic pulmonary edema.

The patient with acute heart failure may present with acute cardiogenic pulmonary edema (ACPE), a condition accompanied by severe respiratory distress, with crackles over the lung and orthopnea, and an O2 saturation usually < 90% on room air, prior to treatment. Non-invasive ventilation is the delivery of assisted ventilation without the need for endotracheal intubation and an invasive artificial airway. Two techniques are used for ventilatory support: continuous positive airway pressure (CPAP) and non-invasive positive-pressure ventilation (NPPV). There is a strong consensus that one of these two techniques should be used before endotracheal intubation and mechanical ventilation because non-invasive techniques dramatically reduce the need for mechanical ventilation via endotracheal intubation and its complications. The aim of this review is to evaluate and resume the evidence for the use of non-invasive positive pressure ventilation in the treatment of acute cardiogenic pulmonary edema according recent literature in order to guide physicians in using CPAP and NPPV in patients affected by ACPE in clinical practice. Recent literature showed that CPAP and NPPV both significantly decrease the need for endotracheal intubation, and CPAP significantly decreases mortality when compared to standard medical treatment. These techniques resulted safe and there is no evidence of increased risk of acute myocardial infarction (AMI) with either of them. Although both CPAP and NPPV present similar efficacy, CPAP has been shown to be cheaper and easier to implement in clinical practice and it could be considered the preferred intervention in patients with ACPE especially in the Emergency Department setting.

Amiodarone-induced thyroid dysfunction in clinical practice.

Amiodarone is a potent class III anti-arrhythmic drug used in clinical practice for the prophylaxis and treatment of many cardiac rhythm disturbances, ranging from paroxismal atrial fibrillation to life threatening ventricular tachyarrhythmias. Amiodarone often causes changes in thyroid function tests mainly related to the inhibition of 5'-deiodinase activity resulting in a decrease in the generation of T3 from T4 with a consequent increase in rT3 production and a decrease in its clearance. In a group of amiodarone-treated patients there is overt thyroid dysfunction, either amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH). AIT is primarily related to excess iodine-induced thyroid hormone synthesis in an abnormal thyroid gland (type I AIT) or to amiodarone-related destructive thyroiditis (type II AIT). The pathogenesis of AIH is related to a failure to escape from the acute Wolff-Chaikoff effect due to defects in thyroid hormonogenesis, or, in patients with positive thyroid autoantibody test, to concomitant Hashimoto's thyroiditis. Both AIT and AIH may develop either in apparently normal thyroid glands or in glands with preexisting, clinically silent abnormalities. AIT is more common in iodine-deficient regions of the world, whereas AIH is usually seen in iodine-sufficient areas. In contrast to AIH, AIT is a difficult condition to diagnose and treat, and discontinuation of amiodarone is usually recommended. In this review we analyse, according to data from current literature, the alterations in thyroid laboratory tests seen in euthyroid patients under treatment with amiodarone and the epidemiology and treatment options available of amiodarone-induced thyroid dysfunctions (AIT and AIH).

Heart failure and therapy.

The clinical syndrome of heart failure is the final outcome of a number of diseases affecting the heart. Several studies undertaken over the past decade, have led to a significant change in the therapies available and a growing understanding of the physiopathological mechanisms. Increasingly, the current treatment of heart failure, is not just symptomatic but also etiologic and physiopathologic. In this paper we will try to furnish guidelines, as practical as possible, for the treatment of this syndrome, addressing the physiopathologic and experimental principles which underlie it. The present suggestions are based on the updated literature review, they conform to the latest guidelines of the European Society of Cardiology and are in agreement with the classification in grades, proposed by the American Heart Association and the American College of Cardiology.

Brain natriuretic peptide and acute coronary syndrome.

The natriuretic peptide system (atrial natriuretic peptide, brain natriuretic peptide, BNP, and C natriuretic peptide) is an important marker of cardiac failure. These peptides are synthesized in atrial or ventricular myocytes in response to wall tension. In several studies the correlation between high BNP levels and mortality, in patients with acute coronary syndrome and heart failure, has been demonstrated. On the other hand, plasma levels of BNP could be considered as independent predictors of mortality in patients with heart failure. BNP could be used, for instance, as an early diagnostic marker for the differential diagnosis between cardiogenic and non cardiogenic dyspnea. In the Emergency Department its use will be important in the diagnosis of thoracic pain origin since it may help in the diagnostic and therapeutic course of this patient and to define the modality of hospitalization. Moreover, it can be used as a marker of heart failure severity and as an important negative prognostic factor. Some studies have confirmed that plasma BNP reflects the degree of left ventricular dysfunction and the prognostic significance after acute myocardial infarction and chronic heart failure.

How to use the C-reactive protein in cardiac disease?

Inflammation is an important contributor to atherothrombosis. The C-reactive protein (CRP) is not only an excellent biomarker of inflammation, but it is also a direct participant in atherogenesis. CRP consistently predicts new coronary events, including myocardial infarction and death, in patients with ischemic heart disease. The predictive value of CRP is, in the majority of the studies, independent of and additive to that of the troponins and its levels can be modulated by statins. Prospective observational studies show that moderately elevated levels of CRP are associated with an adverse cardiovascular prognosis among healthy individuals. The availability of high sensibility assays for CRP should provide a valuable tool for identifying patients at risk of cardiovascular events in primary prevention in conjunction with lowering LDL cholesterol and may also have utility in the treatment of acute coronary syndromes with percutaneous coronary intervention (PCI) therapy. High CRP levels, associated with a higher risk, should suggest a more aggressive medical therapy in the long term and also an aggressive and invasive therapy in the short term, including the use of GP IIb/IIIa inhibitors, high doses of statins, and when a PCI is necessary, provisional stenting. Finally, CRP will provide a readily accessible marker for further testing of the inflammatory hypothesis in atherosclerosis.

Review of dilated cardiomyopathies. Dilated cardiomyopathies and altered prothrombotic state: a point of view of the literature.

Heart failure is an enormously important clinical problem that, if not faced, may overwhelm health care resources. Primary and secondary cardiomyopathies cause the majority of cases of clinical heart failure, which is thus better approached from the utility point of view of myocardial failure. Furthermore, the risk of thromboembolic complications presenting in such disease may be higher than in ischemic cardiomyopathy. Intracardiac thrombi and mural endocardial plaques (from the organization of thrombi) are present at necropsy in more than 50% of patients with dilated cardiomyopathy (DCM). Several studies have shown that systemic and pulmonary emboli are more frequent in patients with ventricular thrombi or plaques. Dilated cardiomyopathy has been associated with left ventricular thrombosis which leads to substantial morbidity and mortality as a site for peripheral emboli. There are some studies on patients with dilated cardiomyopathy showing altered hemostasis and platelet behavior despite sinus rhythm. Platelet activation, thrombin activation and fibrinolytic activity are increased in patients with DCM compared to normal subjects. However, these markers reflecting coagulation activation in patients with left ventricle thrombus are comparable to those in patients without thrombus in the left ventricle. The pathophysiology and clinical issues concerning the susceptibility to develop left ventricular (LV) thrombosis and its complications like cerebrovascular disease in patients with DCM are summarized and the most recent articles present in the medical literature are reviewed.

[Usefulness of magnetic resonance imaging for the diagnosis of acute myocarditis. A case of acute myocarditis as myocardial infarction-like]. / Ruolo della risonanza magnetica nucleare nella diagnosi di miocardite acute. Un caso di miocardite acuta ad esordio simil-infartuale.

According to the Dallas criteria, myocarditis is defined histologically as an inflammatory process involving the myocardium with an inflammatory infiltrate and myocyte necrosis or damage. Clinically, myocarditis is an insidious disease that is usually asymptomatic and commonly underdiagnosed. Infact, the symptoms are often non-specific and the majority of cases recover fully with no sequelae. At present, endomyocardial biopsy remains the gold standard for the diagnosis of myocarditis, despite its limited sensitivity and specificity. However, the lack of an association between biopsy evidence of myocarditis and the presence of autoantibodies in patients with clinical signs of myocarditis, the paucity of the positive biopsy findings in large cohorts of patients with suspected myocarditis, the potential discordance between clinical and histologic features and the inherent limitation of histologic diagnosis, suggest that the diagnosis shouldn't be based on histologic examination alone. The magnetic resonance imaging (MRI) with gadolinium can be useful to visualize the localization, activity and extent of inflammation and may be a powerful noninvasive diagnostic tool in acute myocarditis. Infact, MRI achieves a 100% sensitivity and a 90% specificity. We report the case of a 31-year-old male patient with an acute myocarditis with electrocardiographic manifestations like to acute myocardial infarction, whose diagnosis was based on the clinical signs and on the characteristic pattern of the MRI with paramagnetic contrast. The MRI with gadolinium is suggested as noninvasive study to support the diagnosis of acute myocarditis in the correct clinical setting.