Essay about Sepsis: Inflammation and White Cell Count

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This is the case study of Mr. Jones, a 65 year old male, who was admitted to the emergency department with persistent cough and episodes of chest pain over the last five days. He appeared to be experiencing worsening dyspnoea, fever and feeling unwell. It was also noted that he had a poor urine output over the last 24 hours. An indwelling catheter was inserted which only obtained 20 mLs of amber urine.

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
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Leukocytes and macrophages secrete pyrogens which increases body temperature, decreases haemoglobin affinity for oxygen, worsening hypoxia (Marieb, 2004). Sepsis producing endotoxins TNFa and IL-1 or PAF may cause tissue damage by directly activating nitric oxide (NO), a free radical and potent vasodilator. NO can accumulate in high numbers and react with other free radicals leading to endothelial damage, further stimulating the inflammatory response (Edwards, 2003:636).

In addition, sepsis causes enhanced coagulation with stimulation of the coagulation cascade. This produces a reduction a reduction in the level of protein C and antithrombin III which results in the formation of micro emboli, further impairing blood flow and organ perfusion (Porth, 2005). Inflammatory mediators cause activation of intrinsic and extrinsic clotting pathways. Thrombosis, intravascular fibrin deposits and bleeding develop. Inhibitory pathways of protein C and Protein S are impaired and depleted and clotting increases in plasminogen activator inhibitor levels. Coagulation factors are depleted, and bleeding worsens. Disseminated intravascular coagulation (DIC) may result (Munford, 2001).

The three major effects of septic shock within the vascular system are vasodilation, maldistribution of blood volume and

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