Acute Bacterial Skin and Skin Structure Infections

Acute bacterial skin and skin-structure infection (ABSSSI) is a frequent cause of morbidity in both the community and hospital settings.1 According to the US Food and Drug Administration (FDA) definition, ABSSSI includes cellulitis, erysipelas, major skin abscesses and wound infections with a minimum lesion surface area of 75 cm2. Common bacterial pathogens causing ABSSSI are Streptococcus pyogenes and Staphylococcus aureus including methicillin-resistant S. aureus (MRSA). Less common causes include other Streptococcus species, Enterococcus faecalis, or Gram-negative bacteria.2

Recent epidemiological data of the European Antimicrobial Resistance Surveillance (EARS) Network from 28 participating countries suggested that, overall, MRSA accounted for 16.7% of all S. aureus isolates, with national differences from <1% to ≥50%.1 There were more than 4.8 million hospital admissions of adults with ABSSSI from 2005 through 2011, which included patients with cellulitis, erysipelas, wound infection and major cutaneous abscess. In fact, hospital admissions for ABSSSI significantly increased by 17.3 percent during this timeframe.3 The estimated mean cost of an ABSSSI hospitalization in the United States is $8,023 with a 4.9-day length of stay and associated risks.4

The majority of all skin and soft tissue infections in hospitalized patients are caused by streptococci and Staphylococcus aureus, and approximately 59 percent of these S. aureus infections in the U.S. are estimated to be caused by MRSA.5 Early and effective treatment of ABSSSI is critical to optimize patient recovery and for certain patients may also help to avoid potentially lengthy and costly hospital stays.

Please consult your local healthcare professional for more information.

References:

  • Russo A, Concia E, Cristini F, et al. Current and future trends in antibiotic therapy of acute bacterial skin and skin-structure infections. Clin Microbiol Infect. 2016 Apr;22 Suppl 2:S27-36.
  • US Food and Drug Administration, Center for Drug Evaluation and Research. Guidance for Industry. Acute Bacterial Skin and Skin Structure Infections: Developing Drugs for Treatment. Draft Guidance [monograph]. 2010. Clinical/antimicrobial revision 1.
  • Khachatryan A, Patel D, Stephens J, et al. Rising Us Hospital Admissions for Gram+ Acute Bacterial Skin and Skin Structure Infections (ABSSSI) [abstract]. Journal of Hospital Medicine. 2014; 9 (suppl 2). http://www.shmabstracts.com/abstract/rising-us-hospital-admissions-for-gram-acute-bacterial-skin-and-skin-structure-infections-absssi/. Accessed July 7, 2016.
  • Pollack CV Jr, Amin A, Ford WT Jr, et al. Acute bacterial skin and skin structure infections (ABSSSI): practice guidelines for management and care transitions in the emergency department and hospital. J Emerg Med. 2015 Apr;48(4):508-19.
  • Moran GJ, Krishnadasan A, Gorwitz RJ, et al. Methicillin-Resistant S. aureus Infections among Patients in the Emergency Department. N Engl J Med. 2006;355:666-74.

Acute Coronary Syndromes

Acute Coronary Syndromes (ACS) is a term that refers to a variety of conditions consistent with acute myocardial ischemia and/or infarction that are usually due to an abrupt reduction in coronary blood flow.1 Thrombus (i.e. blood clot that forms inside a blood vessel or chamber of the heart) formation and possible coronary vasospasm reduce blood flow in the affected coronary artery and cause ischemic chest pain. Patients presenting with ACS generally fall under the categories of:

  • ACS-STEMI (ST-elevated MI): patients with acute chest pain and persistent ST-segment elevation (>20 mins) on the electrocardiogram (ECG), cardiac biomarkers are generally elevated2
  • ACS-NSTEMI (Non-ST-elevated MI): patients with acute chest pain but no persistent ST-segment elevation, cardiac biomarkers are generally elevated2
  • Unstable angina: myocardial ischemia at rest or minimal exertion in the absence of cardiomyocyte necrosis, cardiac biomarkers are generally not elevated2

Research from Datamonitor estimates that in 2013, >880,000 persons in the US experienced an ACS event, while in the major 5 EU markets, this figure was >650,000.3 Furthermore, The number of ACS incidences is expected to grow nearly 40% by 2033.3

The presence of STEMI is usually indicative of a totally occluded artery resulting in no blood flow into the affected area, whereas NSTEMI is indicative of a partially occluded artery resulting in reduced blood flow into the affected area. The mortality rate for patients with STEMI has declined over the last two decades, but remains substantial with approximately 4% in-hospital and 7% within the first year.5,6 Mortality and morbidity in NSTE-ACS remain high and equivalent to those of patients with STEMI during long-term follow-up.4

The goals of treatment in ACS are the relief of ischemia and the prevention of MI and death.1 Timely initiation of reperfusion therapy is key in the management of STEMI, since the greatest benefit gained from reperfusion therapy occurs within the first 2–3 hours of symptom onset. Similarly, current guidelines both form the ESC and the American Heart Association /American College of Cardiology now advise high risk NSTE-ACS patients to undergo early reperfusion within 24 hours and unstable very high risk patients reperfusion within 2 hours of diagnosis.1,2,4 Depending on the severity of the occlusion, reperfusion is achieved through the use of antithrombotic agents in combination with myocardial revascularization procedures, such as percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG). PCI involves the insertion of a metal stent to the lesion, thereby mechanically maintaining an open artery to improve blood flow and reduces the risk of (re)infarction. Antithrombotic agents (such as aspirin, platelet P2Y12 receptor blockers, glycoprotein (GP) IIb/IIIa inhibitors, and parenteral anticoagulants) are used peri- and post-procedurally to decrease the risk of new thrombus formation and microembolization. GP IIb/IIIa antagonists inhibit the final stage of platelet aggregation and therefore represent the most powerful antiplatelet therapy.7

Please consult your local healthcare professional for more information.

References:

  • Amsterdam EA et al. 2014 AHA/ACC guideline for the management of patients with non–ST-elevation acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;64:e139–228.
  • Roffi M et al. 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J. 2016 Jan 14;37(3):267-315.
  • Datamonitor. Acute Coronary Syndrome: Epidemiology. October 2014.
  • Windecker S et al. 2014 ESC/EACTS Guidelines on myocardial revascularization. Eur Heart J. 2014;35:2541-2619.
  • Van de Werf F, Bax J, Betriu A, et al. Management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2008;29:2909-2945.
  • Lenzen MJ, Boersma E, Bertrand ME, Management and outcome of patients with established coronary artery disease: the Euro Heart Survey on coronary revascularization. Eur Heart J. 2005;26:1169-79.
  • De Luca G. Glycoprotein IIb-IIIa inhibitors. Cardiovasc Ther. 2012;30:e242-254.

Atrial Fibrillation

Atrial Fibrillation (also known as AFib or AF) is a supraventricular tachyarrhythmia with uncoordinated atrial activation resulting in ineffective atrial contraction and if left untreated, structural and/or electrophysiological atrial tissue abnormalities.1 AF is a common cardiac rhythm disturbance that increases in prevalence with advancing age.1 According to the American Heart Association, estimates of the prevalence of AF in the US ranged from 2.7M to 6.1M in 2010 and is expected to rise to between 5.6M to 12M in 2030.2 In the EU, the prevalence of AF in adults >55 years of age was estimated to be 8.8M in 2010, and is projected to more than double to 17.9M by 2060.3

AF is associated with a 5-fold increased risk of stroke, 3-fold risk of heart failure, and 2-fold risk of dementia and mortality.1 One in five of all strokes is attributed to atrial fibrillation; these are often severe and result in long-term disability or death. Short duration AF episodes carry the same stroke risk as permanent AF, furthermore, undiagnosed ‘silent AF’ is a likely cause of some ‘cryptogenic’ strokes.5 Hospitalizations account for the majority of the cost burden associated with the treatment of AF, which was estimated to cost ~$8,500 per patient in the US or ~$3.5B nationwide.4

There are two strategies to manage AF, namely, rhythm- or rate-control. A rhythm-control strategy may be used in patients who are severely compromised, remain symptomatic despite adequate rate control, when adequate rate control is difficult to achieve, when long term rhythm control therapy is preferred, younger patient age, presence of tachycardia-mediated cardiomyopathy, and first episode of AF.1, 5 Early intervention with a rhythm-control strategy to prevent progression of AF may be beneficial to the AF patient.1

There are two common approaches to convert a patient with AF back to normal sinus rhythm: 1) use of an antiarrhythmic drug (also referred to as chemical or pharmacological cardioversion); or 2) use of electrical shock(s) (also known as direct current (DC) or electrical cardioversion).

Choosing between pharmacological or electrical cardioversion depends on several considerations, with the duration of AF episode being the key element.6 Pharmacological cardioversion is usually most effective (range 50% – 70%) if initiated within a week after the onset of the arrhythmia.6 The conversion rate with antiarrhythmic drugs is lower than DC cardioversion, but unlike DC cardioversion, drug cardioversion does not require general anaesthesia or conscious sedation and fasting, and may have lower psychological impact on some patients.5,6 Furthermore, with electrical cardioversion, delays in the cardioversion of patients are common due to the required scheduling of facilities, staff and other resources.

Early cardioversion not only reduces AF symptoms and inconvenience for the patients, but also increases success rates, reduces the risk of stroke and other thromboembolic complications, and may prevent AF progression.7 The recent FinCV study found that a delay to cardioversion of 12 hours or longer from symptom onset was associated with a greater risk of thromboembolic complications (1.1%) compared to a cardioversion delay of less than 12 hours (0.3%).8

AF is also the most common complication after cardiac surgery with peak incidence occurring between post-operative days 2 and 4.5 Number of studies have reported that post-operative AF is associated with increased early and late mortality after cardiac surgery, stroke, and prolonged length of stay.9 The risk of death is increased by 9.7% (range 3 – 33.3%).9 Similar to non-surgical patients, pharmacological or electrical cardioversion are treatment options to manage the highly symptomatic post-operative AF patient or when rate control is difficult to achieve.5 Short-acting beta-blockers may be used when haemodynamic instability is a concern.5

Please consult your local healthcare professional for more information.

References:

  • January CT et al. 2014 AHA/ACC /HRS guideline for the management of patients with atrial fibrillation. J Am Coll Cardiol. 2014;34:e1 – e76.
  • Mozaffarian D et al. Heart Disease and Stroke Statistics-2016 Update: A Report From the American Heart Association. Circulation. 2016 Jan 26;133(4):e38-60.
  • Krijthe BP et al. Projections on the number of individuals with atrial fibrillation in the European Union, from 2000 to 2060. Eur Heart J. 2013;34:2746-2751.
  • Patel NJ et al. Contemporary trends of hospitalizations for Atrial Fibrillation in the United States, 2000 through 2010. Circulation. 2014;129:2371-2379.
  • Camm AJ et al. Guidelines for the management of atrial fibrillation, The Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology (ESC). Eur Heart J. 2010;31:2369-2429.
  • Savelieva I et al. Pharmacological cardioversion of atrial fibrillation with vernakalant: evidence in support of the ESC Guidelines. Europace. 2014;16:162-173.
  • Tse HF and Lau CP. Does sinus rhythm beget sinus rhythm? Effects of prompt cardioversion on the frequency and persistence of recurrent atrial fibrillation. Card Electrophysiol Rev. 2003;7:359–365.
  • Tse HF and Lau CP. Does sinus rhythm beget sinus rhythm? Effects of prompt cardioversion on the frequency and persistence of recurrent atrial fibrillation. Card Electrophysiol Rev. 2003;7:359–365.
  • Kaireviciute, D et al. Atrial fibrillation following cardiac surgery: clinical features and preventative strategies. Eur Heart J. 2009;30:410-425.

Hospital Acquired Pneumonia & Community Acquired Pneumonia

Hospital acquired pneumonia (HAP) is a very common hospital acquired infection that presents a major cause of morbidity and mortality1. HAP is defined as an acute infection of the lung parenchyma caused by an infectious agent that is not present prior to hospital admission; an infection that occurs 48 hours or more after hospital admission1,2. Community acquired pneumonia (CAP) is defined as an acute infection of the lung parenchyma in individuals who have not been hospitalized recently and have not had regular exposure to healthcare settings2. Increasing incidence of bacterial strains resistant to many commonly used antibiotics is a major concern in HAP and CAP.

Methicillin-resistant Staphylococcus aureus (MRSA), which was initially almost exclusive to infections acquired in hospital settings (e.g. HAP), has become more common in communit acquired infections, such as CAP4. Since the frequency of MRSA is increasing in CAP and HAP, MRSA is an important public health problem4.

HAP is the second most common hospital acquired infection after urinary tract infections (UTI)5. The incidence of HAP ranges from 5 to 15 cases per 1000 hospital admissions5. The incidence of HAP can range from 1.6-3.7 cases per 1000 admissions in the general ward, to as high as 25% of all intensive care unit (ICU) patients5. Since community acquired pneumonia (CAP) is not well reported and only 20%-50% require hospitalization, its true incidence is difficult to quantify5. The overall annual incidence of CAP in European adults ranges between 1.07-1.2 cases per 1000 population5.

References:

  • Rotstein, C. et al. Clinical practice guidelines for hospital-acquired pneumonia and ventilator-associated pneumonia in adults. Canadian Journal of Infectious Diseases & Medical Microbiology. 2008. 19(1):19-53
  • National Institute for Health and Clinical Excellence (NICE). Pneumonia: diagnosis and management of community- and hospital-acquired pneumonia in adults. NICE clinical guideline: Pneumonia scope. 2012.
  • Musher, D.M. et al. Community-Acquired Pneumonia. Review Article. The New England Journal of Medicine. 2014. 371:1619-28
  • Defres, S. et al. MRSA as a cause of lung infection including airway infection, community acquired pneumonia and hospital-acquired pneumonia. European Respiratory Journal. 2009. 34: 1190–1196
  • Torres A., Cillóniz C. (2015) Epidemiology, etiology, and risk factors of bacterial pneumonia. In: Clinical Management of Bacterial Pneumonia. Adis, Cham

Pulmonary Arterial Hypertension

Pulmonary Arterial Hypertension (PAH) is a life threatening, progressive disease caused by narrowing or tightening (constriction) of the pulmonary arteries, which connect the right side of the heart to the lungs.1

PAH is an rare disease with no known cure, and it worsens over time. The most common symptoms associated with the disease include breathlessness, fatigue, weakness, angina, syncope, and abdominal distension.1 In addition to these physical symptoms, PAH has a profound social, practical and emotional impact on the lives of patients and their families and caregivers. Diagnosis is difficult, but as awareness of PAH grows and diagnosis improves, the number of patients requiring PAH therapy will continue to increase.

PAH disease severity is classified in WHO functional classes, graded I to IV, from most mild to most severe limitations.1 PAH disease progression dictates pharmacologic intervention. While treatment patterns vary, and therapies are tailored to meet an individual patient’s needs, the typical progression of drug therapy will incorporate parenteral compounds in more advanced stages of the disease.1 For patients with moderate to severe limitation (WHO functional class III or IV disease), prostacyclin analogs are often a key part of the treatment regimen.2 Prostacyclin based therapy is currently the only continuously infused parenteral option approved for use for the management of PAH.

Please consult your local healthcare professional for more information.

References:

  • Galiè N, Humbert M, Vachiery JL, et al. 2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension: The Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS): Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Heart and Lung Transplantation (ISHLT). Eur Heart J. 2016;37(1):67-119.
  • LeVarge BL Prostanoid therapies in the management of pulmonary arterial hypertension. Ther Clin Risk Manag. 2015 Mar 31;11:535-47. doi: 10.2147/TCRM.S75122. eCollection 2015.

For information about Correvio’s products, please click here

By following this link you will be leaving the correvio.com website. Please note that Correvio does not take responsibility for the content displayed on other websites:

ContinueClose