Pathophysiology of sepsis | Case Study

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11th Feb 2020 Nursing Case Study Reference this

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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.

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 Thomas’s case, the stress response is initiated by infection.

Under the influence of stress, the body steady 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 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 production 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 cortisol and aldosterone through the adrenal cortex. Those corticosteroids can result in increased metabolism, sodium and water retention (Seaward 2015).

Therefore, it is obvious that Thomas was under the effect of stress. He was tachycardic, tachypnoeic and slightly hyperglycaemic due to the effect of sympathetic nervous response. He was oliguric because of the 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 compromise 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 amount of cytokines go into the circulation. This promotes the production of growth factor and adhesion 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 made 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 indirect contribution 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, general 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 clotting 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 Thomas’s fever is highly likely 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 Thomas’s 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 failure 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 mandatory ventilation volume control will be explained as Thomas’s 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 ventilator 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 patient’s 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 patient’s 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 constant 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 patient’s 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 Thomas’s case, the volume controlled synchronised intermittent mandatory ventilation would be the better option of managing his severe pneumonia and respiratory distress.

Reference

Better Health Channel 2012, Stress, viewed 12th March 2015, http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/stress

Bone, RC, Balk, RA, Cerra, FB, Dellinger, RP, Fein, AM, Knaus, WA, Schein, RM & Sibbald, WJ 1992, ‘Definitions for sepsis and organ failure 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. KGaA, Germany

Esmon, CT 2005, ‘The interactions between inflammation and coaulation’, British Journal of Haematology, vol. 131, no. 4, pp. 417-430.

Goldsworthy, S & Graham, L 2014, Compact Clinical Guide To Mechanical Ventilation : Foundations Of Practice For Critical Care Nurses, New York, NY

Jaffer, U, Wade, RG & Gourlay, T 2010, ‘Cytokine in the systemic inflammatory response syndrome: a review’, HSR Proceedings in Intensive Care & Cardiovascular Anaesthesia, vol. 2, no.3, pp. 161-175.

Kaplan, LJ 2014, Systemic inflammatory response syndrome, viewed 19th March 2015, http://emedicine.medscape.com/article/168943-overview#a0101

Kyrou, I, Chrousos, Kassi, E & Tsigos, C 2012, Stress, Endocrine physiology and pathophysiology, viewed 12th March 2015, http://www.endotext.org/chapter/stress-endocrine-physiology-and-pathophysiology/#h23

Neviere, R 2015, Sepsis and the systemic inflammatory response syndrome: Definition, epidemiology and prognosis, viewed 19th March 2015, http://www.uptodate.com/contents/sepsis-and-the-systemic-inflammatory-response-syndrome-definitions-epidemiology-and-prognosis

O’brien, JM, Ali, NA, Aberegg, SK & Abraham, E 2007, ‘Sepsis’, The American Journal of Medicine, vol.120, no.12, 1012-1022.

Pierce, LNB 2007, Management of Mechanically Ventilated Patient, 2nd edn, Saunders Elsevier, London

Plevkova, J 2011, Systemic inflammatory response syndrome, viewed 24th March 2015, http://eng.jfmed.uniba.sk/fileadmin/user_upload/editors/PatFyz_Files/Handouty/angl/Systemic_inflammatory_response_syndrome_2011.pdf

Sagy, M, Al-Qaqaa, Y & Kim, P 2013, ‘Definitions and pathophysiology of sepsis, Current Problems in Paediatric and Adolescent Health Care, vol. 43, no. 10, pp. 260-263.

Seaward, BL 2015, ‘Physiology of stress’, Managing Stress, Jones & Bartlett Learning, Burlington, MA.

Singh, S, Singh, P & Singh, G 2009, ‘Systemic inflammatory response syndrome outcome in surgical patients’, Indian Journal of Surgery, vol.71, no.4, pp. 206-209.

Sprague, AH & Khalil RA 2009, ‘Inflammatory cytokines in vascular dysfunction and vascular disease’, Biochemical Pharmacology, vol. 78, no. 6, pp. 539-552.

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