Thomas, a 70-year-old man, admitted to hospital with a five-day history of coughing with yellow-green sputum, pyrexia, rigors, poor appetite, mild chest pain and increasing difficulty of breathing.
The initial observations are:
Neurological: Altered neurological status, GCS 11/15. Agitated and confused.
Cardiovascular: Sinus tachycardia, HR 135bpm. Hypotension, 90/45 mmHg.
Respiratory: Tachypnoeic, RR 35bpm. Decreased saturation while receiving 6L O2 through Hudson mask.
Metabolic: Febrile, 39 degree
Renal: Oliguric with 20ml/hr urine output. Indwelling catheter (IDC) was inserted.
The blood test revealed that the patient was suffering from hypernatremia, hyperkalaemia, hyperglycaemia, elevated urea, poor creatinine, increased WCC and low platelet count. The ABG indicated that Thomas was experiencing combined respiratory and metabolic acidosis. Thomas was finally diagnosed as sepsis complicated by the right middle lobe streptococcus pneumonia. He required intubation and invasive ventilation support.
In this case study, the pathophysiology of sepsis will be discussed and the mechanism of synchronised intermittent mandatory ventilation (SIMV) volume control ventilation mode will be explained.
Sepsis is defined as the dysregulated inflammatory response caused by severe infection (Neviere 2015). It has the interchangeable definition as Systemic inflammatory response syndrome (SIRS) while the SIRS is resulted by a suspected or confirmed infectious source (Neviere 2015). The concept of SIRS was first introduced by the American College of Chest Physicians (ACCP) and Society of Critical Care Medicine (SCCM) in 1992 (Kaplan 2014). It is characterised by two or more following symptoms. They are fever of high than 38 degree or hypothermia; tachycardia; tachypnoea or partial pressure of arterial carbon dioxide (PaCO2) less than 32 mmHg; deranged white cell count of more than 12,000/µL or less than 4,000/µL (O’brien et al. 2007). Associated with Thomas’s symptoms, it is clear to see that he was definitely experiencing sepsis. It is because that he was febrile up to 39 degree, tachycardic with heart rate of 135 bpm, and had increased respiratory rate of 35bpm as well as the elevated leucocytes count of 14,000 per microliter. The clinical signs are related to the inflammation process which is activated by the body immune system. Due to the severe infection, a large number of proinflammatory mediators are released which in turn result in the serial inflammatory reaction and extensive tissue damage (Neivere 2015). It is reported that SIRS can lead to high mortality rate because of high occurrence of SIRS induced multiple organ dysfunction syndrome (MODS) (Singh et al. 2009). In the following paragraphs, the pathophysiology of sepsis/SIRS will be more comprehensively examined.
The pathophysiology of SIRS is complex. There are a few elements that need to be emphasised. They are acute stress response, inflammatory process and cytokine storm.