Pathophysiology of sepsis | Case Study

Pathophysiology of sepsis Case Studydoubting Thomas, a 70-year-old man, admitted to hospital with a five-day history of coughing with yellow green sputum, pyrexia, rigors, vile appetite, mild chest pain and increasing difficulty of breathing.The initial observations areNeurological Altered neurological status, GCS 11/15. Agitated and confused.Cardiovascular venous sinus tachycardia, HR 135bpm. Hypotension, 90/45 mmHg.Respiratory Tachypnoeic, RR 35bpm. Decreased saturation while receiving 6L O2 through Hudson mask.Metabolic Febrile, 39 degreeRenal Oliguric with 20ml/hr urine output. intrinsic catheter (IDC) was inserted.The blood test revealed that the unhurried was suffering from hypernatremia, hyperkalaemia, hyperglycaemia, elevated urea, poor creatinine, increased WCC and low thrombocyte expect. The ABG indicated that Thomas was experiencing combined respiratory and metabolic acidosis. Thomas was at long last diagnosed as sepsis complicated by the right middle lobe streptoc occus pneumonia. He required intubation and invasive respiration support.In this case study, the pathophysiology of sepsis depart be discussed and the mechanism of synchronised intermittent mandate ventilation (SIMV) volume cut back ventilation mode will be explained.Sepsis is defined as the dysregulated inflammatory rejoinder caused by onerous transmitting (Neviere 2015). It has the interchangeable definition as systemic inflammatory receipt syndrome (SIRS) while the SIRS is military issueed by a suspected or substantiate infectious source (Neviere 2015). The concept of SIRS was first introduced by the American College of Chest Physicians (ACCP) and Society of captious Care Medicine (SCCM) in 1992 (Kaplan 2014). It is characterised by two or more following symptoms. They are fever of gamy than 38 degree or hypothermia tachycardia tachypnoea or partial pressure of arterial carbon dioxide (PaCO2) less than 32 mmHg deranged discolor cell count of more than 12,000/L or les s than 4,000/L (Obrien et al. 2007). Associated with Thomass symptoms, it is clear to see that he was decidedly 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 spark off by the body immune system. Due to the severe infection, a large number of proinflammatory mediators are released which in countermand result in the serial inflammatory answer 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. thither are a few elements that need to be emphasised. They are acute focussing resolution, inflammatory process and cytokine storm.Firstly, stress response is the acute phrase reaction when the body tries to defence against the threatening triggers. Those triggers are also known as stress. Stress can be caused by daily life events, environmental factors or physical illness (Better Health Channel 2012). In Thomass case, the stress response is initiated by infection.Under the influence of stress, the body settle down state is disrupted. To maintain the homeostasis, the stress response is activated to reverse the body balance and redistribute the oxygen and energy to maintain the function of vital organs (Kyrou et al. 2012). Hypothalamus plays a vital role in processing the distress signals (Seaward 2015). Once it senses the stress, it triggers the activation of sympathetic nervous system. The sympathetic nervous system then stimulates the adrenal gland gland to produce epinephrine. It is also known as adrenaline. The adrenaline can lead to increased heart rate and myocardial contractility dilated pupils and bronchi peripheral vasoconstriction accelerated respiratory rate decreased digestive activity and increased performance of glucose from liver (Seaward 2015).In addition, stress can also activate another pathway of stress response. That is the hypothalamic-pituitary-adrenal (HPA) axis (Seaward 2015). It means the stress triggers the release of corticotrophin-releasing factor (CRF) from anterior hypothalamus. The CRF then promotes the pituitary gland to produce adrenocorticoid trophic hormone (ACTH). The ACTH stimulates the production of hydrocortisone and aldosterone through the adrenal cortex. Those corticosteroids can result in increased metabolism, sodium and water retention (Seaward 2015). on that pointfore, it is obvious that Thomas was under the effect of stress. He was tachycardic, tachypnoeic and pretty hyperglycaemic due to the effect of sympathetic nervous response. He was oliguric because of th e acute kidney injury secondary to the vasoconstriction. His hypernatremia status can be contributed by the impact of aldosterone. He had poor oral intake can be cause by the suppressed digestion function.Secondly, the inflammatory cascade plays an essential role in the pathophysiology of systemic inflammatory response syndrome. Sagy et al. (2013) summarised the inflammation mediator related mechanisms in the systemic inflammatory response. It is indicated that the excessive release of pro-inflammatory mediators result in the inflammation, inhibit the function of compensatory anti-inflammatory response, and agree the immune system eventually (Sagy et al. 2013).Cytokines are the essential components of immune system. Bone et al. (1992) explained that the local cytokines are activated immediately after an insult in order to repair the wound and initiate the innate immune system. Because of the release of local cytokines, a small measurement of cytokines go into the circulation. Thi s promotes the production of growth factor and affixation of macrophages and platelets to help with the recovery of the local damage. However, when the infection is severe and the homeostasis is unable to be restored, cytokine storm occurs.More specifically, cytokine storm is formed from a complex progression. Cytokines are do up by macrophages, monocytes, mast cells, platelets and endothelial cells, which are the initial immune defensive components (Plevkova 2011). The multitude of cytokines can soon induce the cytokine tissue necrosis factor-alpha (TNF-a) and interleukin-1 (IL-1). Those two elements result in the removal of nuclear factor-KB (NF-KB) inhibitor. This in turn prompts the production of more proinflammatory mediators, such as IL-6, IL8 and interferon gamma (Plevkova 2011). In other words, cytokines stimulate the production of immune cells, which in turn induce more cytokines in the circulation.The cytokines have a great impact on the body, including direct or indirec t constituent of mortality in SIRS. TNFa is discovered causing fever, abnormal haemodynamic values, low white cell count, increased liver enzymes and clotting problems (Jaffer et al. 2010). IL-1 is reported having connection with fever, haemodynamic abnormality, loss of appetite, usual weakness, headache and neutrophilia (Jaffer et al. 2010). IL-6 is found having strong relationship with fever and impaired lung function as well as acting a determinant of severity of SIRS and mortality rate (Jaffer et al. 2010). The massive accumulation of cytokines can cause widespreading vasodilatory effect. It is because the cytokines stimulate the release of vasodilators such as nitric oxide (Sprague and Khalil 2009). Additionally, cytokines promotes adhesion of the immune cells and the endothelial cells, which in turn leads to leaky endothelium and loss of fluid from intercellular space to extracellular space (Sprague and Khalil 2009). Moreover, the cytokines cascade can also lead to the clott ing disorder. It is because of the high concentration of fibrinogen in the inflammation process (Esmon 2005). The fibrinogen is converted from thrombin, which is generated by tissue factor. Tissue factor is a substance that is expressed by the surface of white cell. It can also be induced by TNFa and endotoxin from the infection (Esmon 2005). The fibrinogen can be transferred into fibrin which in turn forms clots. As the excessive amount of fibrin in the inflammation status, it can result in extensive clotting disorder.To sum it up, it can be concluded that Thomass fever is highly promising related to the release of TNFa, IL-1 and IL-6. IL-1 could be one of the contributors of his poor appetite and elevated white cell count. IL-6 could worsen Thomass existing affected lung function. Thomas had increased white cell count can be contributed by the immune response and IL-1. The hypotension is related to the vasodilation effect. Due to the hypotensive, the kidney perfusion dropped and then led to the acute kidney trial and poor urine output. The acute kidney injury may affect the elimination of potassium so that Thomas was found having high potassium level. The low platelet count could be related to the massive production of cytokines and damaged endothelium.In the next section, the synchronised intermittent mandate ventilation volume control will be explained as Thomass mechanical ventilation management.The synchronised intermittent mandatory ventilation (SIMV) is commonly used in ICU. With the volume control mode, the patient is given the ventilation support with a set tidal volume during the mandatory breaths (Deden 2010). To provide the effective ventilation support, there are a few specific values that need to be set up for the SIMV volume controlled mode. They are tidal volume and respiratory rate. The tidal volume refers to the amount of oxygen delivered by the breathing machine or the amount of oxygen the patient breathes voluntarily. The respiratory rate is set up for mandatory breaths. In the SIMV volume controlled mode, the ventilation is trigger by the ventilator or patient self. It means the actual respiratory rate can be upon the preset rate (Goldsworthy and Graham 2014). There is a window of time for the ventilator to sense the patients inspiratory effort. This trigger window helps avoid the ventilator deliver the oxygen when the patient exhales (Deden 2010). If the patient is able to trigger the ventilation within the time frame, the patient-triggered mandatory breath is induced. After reaching the demand tidal volume, the inspiratory phrase ends and expiratory starts. Between each mandatory breaths, the patient is able to initial own spontaneous breath, the breathing volume and length depend on the patients respiratory effort (Pierce 2007). If the patient is heavily sedated and unable to initiate the spontaneous breath within the trigger window, the machine-triggered mandatory breath will be activated to provide constan t ventilation support according to the set respiratory rate and tidal volume (Deden 2010). Once the ventilator delivers the demand tidal volume, the inspiratory cycle ends and expiratory phrase starts until the next scheduled inspiratory cycle. If the patients attempt of breathing is not strong enough to trigger the patient-triggered mandatory breath, the assisted synchronised breath will be provided to achieve the desired the tidal volume. Like the other mode, the inspiratory cycle ends once the set tidal volume is delivered (Deden 2010).It is believed that Thomas would be beneficial from the SIMV volume controlled mode. It is because that SIMV mode could help him reduce the work of breathing, especially when he was in the high energy-consuming septic status. In addition, due to the SIMV mode, the ventilator allows him to have extra breath to blow off the accumulative carbon dioxide. This can improve his acidosis. Moreover, because of the systemic inflammatory response syndrome and severe pneumonia, his lungs could be stiff and fragile secondary to the inflammation effect and accumulation of cytokines. The volume controlled ventilation acts as a protective strategy to avoid the ventilator related complications, such as volutrauma. It is recommended not to set the tidal volume more than 8-10ml/kg (Deden 2010).In conclusion, sepsis is a systemic inflammatory response syndrome resulted by the infection. The stress response, inflammation reaction and cytokines play essential roles in the progression of SIRS. As SIRS can cause high mortality rate, it is vital to control the infection and manage the widespreading inflammation as well as providing appropriate support to treat the symptoms. In Thomass case, the volume controlled synchronised intermittent mandatory ventilation would be the better option of managing his severe pneumonia and respiratory distress.ReferenceBetter Health Channel 2012, Stress, viewed 12th March 2015, http//www.betterhealth.vic.gov.au/bhcv2/ bhcarticles.nsf/pages/stressBone, RC, Balk, RA, Cerra, FB, Dellinger, RP, Fein, AM, Knaus, WA, Schein, RM Sibbald, WJ 1992, Definitions for sepsis and organ misery and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine, Chest, vol. 101, no. 6, pp. 1644-1655.Deden, K, 2010, Ventilation modes in intensive care, Dragerwerk AG C0. 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