In addition to cell-derived mediators, several acellular biochemical cascade systems—consisting of preformed plasma proteins—act in parallel to initiate and propagate the inflammatory response. These include the complement system activated by bacteria and the coagulation and fibrinolysis systems activated by necrosis (e.g., burn, trauma).Acute inflammation may be regarded as the first line of defense against injury. Acute inflammatory response requires constant stimulation to be sustained. Inflammatory mediators are short-lived and are quickly degraded in the tissue. Hence, acute inflammation begins to cease once the stimulus has been removed. Chronic
Chronic inflammation is inflammation that lasts for months or years. Macrophages, lymphocytes, and plasma cells predominate in chronic inflammation, in contrast to the neutrophils that predominate in acute inflammation. Diabetes, cardiovascular disease, allergies, and chronic obstructive pulmonary disease (COPD) are examples of diseases mediated by chronic inflammation. Obesity, smoking, stress and insufficient diet are some of the factors that promote chronic inflammation. A 2014 study reported that 60% of Americans had at least one chronic inflammatory condition, and 42% had more than one. Cardinal signs
Common signs and symptoms that develop during chronic inflammation are:
Body pain, arthralgia, myalgia
Chronic fatigue and insomnia
Depression, anxiety and mood disorders
Gastrointestinal complications such as constipation, diarrhea, and acid reflux
Weight gain or  loss
Frequent infections

Vascular component
Vasodilation and increased permeability
As defined, acute inflammation is an immunovascular response to inflammatory stimuli. This means acute inflammation can be broadly divided into a vascular phase that occurs first, followed by a cellular phase involving immune cells (more specifically myeloid granulocytes in the acute setting).
Pneumopericardium is a medical condition where air enters the pericardial cavity. This condition has been recognized in preterm neonates, in which it is associated with severe lung pathology, after vigorous resuscitation, or in the presence of assisted ventilation. This is a serious complication, which if untreated may lead to cardiac tamponade and death. Pneumomediastinum, which is the presence of air in the mediastinum, may mimic and also coexist with pneumopericardium. It can be congenital, or introduced by a wound. Presentation
The symptomatic patient may present with dyspnea, cyanosis, chest pain, pulsus paradoxus, bradycardia or tachycardia. Pathophysiology
The mechanism responsible for pneumopericardium is the ‘Macklin effect’ – There is initially an increased pressure gradient between the alveoli and the interstitial space. Increased pressure leads to alveolar rupture, resulting in air getting through to the pericapillary interstitial pulmonary space. This space is continuous with the peribronchial and pulmonary perivascular sheaths. From here, the air tracks to the hilum of the lung and then to the mediastinum. In case of a pericardial tear, this air enters the pericardial cavity and pneumopericardium develops. The condition may remain asymptomatic or may progress to life-threatening conditions like tension pneumopericardium or cardiac tamponade. Diagnosis
On physical examination, the patient may have the classic “Beck’s triad” – hypotension, raised JVP and distant heart sounds, when complicated by cardiac tamponade. Extension of the mediastinal air to the subcutaneous tissues via the fascial planes may lead to subcutaneous emphysema.