Mr. Jones clinical assessment revealed that his Glasgow Coma Score was 11/15. He was opening his eyes to speech, only making inappropriate words and localizes to pain. He was also pyrexial with a temperature of 39.0 ˚C, diaphoretic with hot peripheries, hypotensive BP 90/45 mmHg (MAP 60 mmHg), and tachyopneic at 30breaths/min and tachycardic at 120beats/min.
This paper will not only define SIRS/sepsis but will also discuss the clinical manifestations in relation to the pathophysiology of systemic inflammatory response syndrome (SIRS)/sepsis in relation to Mr. Jones.
Mr. Jones appeared to be in distressed. He is now using his accessory muscles to breathe, crackles are heard on auscultation and there is decreased air entry in the left and right bases. Chest X ray revealed consolidation on the left lower lobe and atelectasis in the right lower lobe.
After a series of investigation in the emergency department, Mr. Jones was commenced on Normal Saline at 125 mls/hr and he was given oxygen via non rebreather mask at 10L/min. He was then transferred to the intensive care unit for respiratory and circulatory support and a provisional diagnosis of sepsis due to a respiratory source.
Sepsis is a condition characterized by a systemic inflammation response syndrome (SIRS) and the presence of infection (Steen 2009:48). This is the cascade of inflammatory events that are part of the body’s response to an insult in an attempt to maintain homeostasis (Lever and Mackenzie, 2007:879). Systemic inflammatory response syndrome (SIRS) is a systemic reaction to infection as evidenced by two or more of the following symptoms: Temperature > 38˚C or < 36˚C; Heart rate > 90 beats per minute; Respiratory rate > 20 breaths per minute; White blood count > 12,000 or < 4000 per ml (Levy et al, 2003:1250).
In December 2001, the American College of Chest Physician (ACCP), the Society of Critical Care Medicine (SCCM), American Thoracic Society and European Society of Intensive Care Medicine met and expanded this list of signs and symptoms to include chills, decreased urine output, decreased skin perfusion, poor capillary refill, skin mottling, decreased platelet count, petechiae, hypoglycaemia, and unexplained change in mental state (Urden, et al. 2006:1023).
When a confirmed systemic response to infection is associated with SIRS, sepsis has developed (Wagenlehner et al. 2007:30). Sepsis can be caused by pathogens other than bacteria, such as fungi, viruses, and protozoa (Munford, 2001:63). Regardless of the causative organism, sepsis can result in systemic complications that occur as circulating chemical mediators released by the inflammatory response compromised the patients cardiovascular system (Cunha, 2003:24). Severe sepsis occurs when hypoperfusion, hypotension and organ dysfunction develop. If hypotension and perfusion abnormalities, lactic acidosis, oligoria and acute onset of mental deterioration occur despite aggressive fluid resuscitation and inotropic therapy, septic shock is present (Munford, 2001:65).
Mr. Jones CX-ray confirmed to have consolidation on the left lower lobe and atelectasis in the right lower lobe. Respiratory infection is the likelihood of the source of sepsis in Mr. Jones’s case. Once a microbial infection develops, a general but complex inflammatory response develops, resulting in increased capillary permeability and blood flow (Urden et al. 2006:1032). These responses allow immunologic cells to migrate toward the site of infection; phagocytic actions begin and activate the complement system. Munford...