The Incidence of Severe Sepsis and Septic Shock - Essay Example

Septic Shock Introduction: Severe sepsis and septic shock are quite often seen in the hospital environments. The issue for concern is that the incidence of severe sepsis and septic shock are on the rise in spite of the ever increasing range of powerful antibiotics available and the increased knowledge of the patho-physiological processed involved in septic shock. Septic shock presents itself in hospital environments in different forms with particular emphasis in patients of advanced ages and in patients with immuno-compromise problems (Balk, 2000). Definition: Attempts at providing clarity of sepsis through a better definition led to a new set of definitions in 1991. The objective of these definitions was to give a more differentiated understanding of sepsis to enable precise management. As a result the concept of systemic inflammatory response syndrome (SIRS) evolved with its diagnostic criteria put in place. Then sepsis was defined on the basis of SIRS, whereby sepsis was defined as “suspected or microbiologically proven infection together with SIRS”. Severe sepsis was then defined as “sepsis together with sepsis-induced organ dysfunction”. Finally septic shock was defined as “sepsis-induced hypotension persisting despite adequate fluid resuscitation” (Marik & Lipman, 2007). A very valid question arises as to the need for such differentiated definitions. There is justification for these differentiated definitions, which is provided from the study of recent data on the mortality rates associated with each of these differentiated definitions. Mortality from sepsis ranges ten to fifteen percent; severe sepsis ranges from seventeen to twenty percent and septic shock ranges from forty-three to fifty-four percent. Thus the hierarchical definitions get justified by this. (Marik & Lipman, 2007). Deeper examination of this data suggests that there is a wide difference in the mortality figures for severe sepsis and septic shock. This finding clearly indicates that it is most important to distinguish between severe sepsis and septic shock, so that they can be grouped into low and high mortality risk groups. It is in this aspect that the hierarchical definitions as created in 1991 are found to be deficient. The diagnostic criteria for septic shock still remain unclear and vague. To remove this deficiency Marik and Lipman, 2007, suggest that septic shock be defined as “ a systolic blood pressure less than 90mmHg (or a fall in systolic blood pressure of > 40mmHg), or a mean arterial pressure less than 65mmHg after a crystalloid fluid challenge of 30mL per kg body weight in a patient with severe sepsis. Prevalence of Septic Shock: The prevalence of sepsis and septic shock is quite common and in the United States of America alone about 750,000 people are afflicted by either sepsis or septic. The annual death rate as a result of sepsis and septic shock, with the major contribution from septic shock is around 215,000 just in the United States of America. Thus mortality as a result of septic shock and sepsis contributes to 9.3 % of all deaths in the United States of America and is almost equal to the mortality rate as a result of acute myocardial infection. The mortality rate of septic shock and sepsis far exceed the more dreaded diseases like AIDS and breast cancer (Sharma & Kumar, 2003). Besides the concern on mortality rates as a result septic shock and sepsis is the economic burden. The average length of stay at a hospital for such patients is 19.6 days and the cost per patient $22,100, which amounts to a total economic burden of $16.7 billion in the United States of America alone (Sharma & Kumar, 2003). The alarming part of these figures is that such a high prevalence and mortality rate is despite the significant advances that have been made in the understanding of the patho-physiologic processes associated with septic shock, the enhanced ability to monitor, support and manage critically ill patients and the developments in science and technology that have provided an ever increasing range of antibiotics (Sharma & Kumar, 2003). Patho-physiology of Septic Shock: Septic shock results from the progress of the sepsis syndrome to severe hypotension and tissue anoxia, as a result of which organs like the heart, lungs, liver and kidneys start failing. In spite of supportive and anti-biotic therapy prognosis in septic shock is poor. Gram-negative bacteria are most often associated with septic shock, with occasional occurrence due to Gram-positive bacteria. Current research is centred on the role of endotoxin found in the cell membrane of Gram-negative bacteria. This role of endotoxin has led to septic shock also being called endotoxic shock. Endotoxin activates the complement system, leading to the release of vaso-active substances and pro-inflammatory cytokines (Sleigh & Timbury, 1998). The excessive inflammatory response as a result of severe sepsis is caused by the pro-inflammatory cytokines with special emphasis on the tumour necrosis factor-alpha (TNA-alpha) and interleukin-1 (IL-1), which are produced by monocytes as a reaction to infection or endotoxin. These pro-inflammatory cytokines are capable of causing diffuse pan-endothelial and microvascular injury. Traditionally septic shock has been linked to excessive inflammatory response. Understanding has now developed that both pro-inflammatory and anti-inflammatory response play a role in the pathogenesis of septic shock. The compensatory anti-inflammatory response (CARS) that ensues as a consequence of the initial pro-inflammatory response is an important contributor to mortality in septic shock. During CARS the cytokine receptor antagonists and soluble cytokine receptors reduce the pro-inflammatory response. The onset of CARS sees a shift from pro-inflammatory cytokines to anti-inflammatory cytokines like IL-10, IL-4, prostaglandin E2 and soluble inhibitors of IL-1 and TNA. Apoptosis of lymphocytes is also witnessed in CARS. The net effect of CARS is that a state of immuno-suppression is produced. This improved understanding of sceptic shock has led to the realization that in the management of septic shock mere suppression of the excessive pro-inflammatory response does not lead to successful outcomes. Genetic factors are an added influence in the exacerbation of the condition in septic shock. Genetic factors can increase susceptibility to infection and increased risk of mortality. Changed gene expression is involved in inflammation and cellular dysfunction. This is because the cytokine cascade, expression of endothelial adhesion molecules and iNOS are reflective of the effects of up-regulation of gene expression. Heat shock proteins have a likely significant role in apoptosis seen in septic shock. Increased apoptosis may be an important pathogenic event leading to acute organ dysfunction. In addition single nucleotide polymorphisms in those genes that are responsible for the host response in infection could result in severe impairment in the immune response. Finally the TNF2 allele enhances polymorphism in the production of TNF-alpha. Patients with such polymorphism face a higher risk of mortality (Lemaout, Gonzales, Aboab & Annane, 2006). Clinical Presentation of Septic Shock: Patients with septic shock are likely to present with general symptoms of sweats, chills or rigours, breathlessness and headache. Confusion, disorientation and coma are also seen in thirty percent of the patients, particularly if the patient is elderly. Nausea, vomiting and diarrhoea are also likely to be present (Ramrakha & Moore, 2005). Examination of the patient is likely to show hyperpyrexia, though hypothermia is also seen in some patients. Therefore the temperature of a patient in sceptic shock could be either more than 38 degrees Centigrade or less than 37 degrees Centigrade. Other abnormalities likely to be presented include tachycardia, wild pulse pressures, tachypnea and hypotension. Examination of the eyes is likely to show retinal haemorrhages, cotton wool spots and conjunctival petechiae (Gough, 2000). Multiple organ failure is associated with septic shock. As a result of this cardiovascular manifestations are likely to be seen. Vaso-dilation could result causing warm extremities. The tachycardia observed is the result of compensation to cardiovascular stress in septic shock, Myocardial depression leads to hypotension presented in septic shock, with the patient likely to show diminished response to volume replacement. (Gough, 2000). Respiratory stress in septic shock is the reason for tachypnea and hypoxemia demonstrated by patients with septic shock. Azotemia, oliguria and active urinary sedimentation are associated with renal failure in septic shock. Liver dysfunction is commonly seen in septic shock and presents as cholestatic jaundice. Cutaneous lesions are seen in septic shock as a result of cellulitis or fasciitis; consequence of hypotension or disseminated intravascular coagulation; and microemboli or complex vasculitis. Haematological changes associated with septic shock include neutropenia, neutrophilia, thrombo-cytopenia and disseminated intravascular coagulation. There is increased release of catecholamines, cortisol and glucagen in septic shock, which result in hyperglycemia and is demonstrated by enhanced blood sugar levels. The hyperglycaemic condition is also contributed to by increased insulin resistance, decreased insulin production and impaired use of insulin. Determination of blood-gas may show hypoxemia and respiratory alkalosis (Gough, 2000). This example of a clinical presentation of a patient in septic shock with a groin mass provided by Cynthia, R., 2000, gives clarity to the clinical presentation, with particular emphasis on laboratory findings, of a patient with septic shock. The patient presented with low-grade pyrexia, hypotension and tachycardia. White blood cell count was 19.1 x 1000 cells/cubic mm with five percent bands. Haemoglobin was 9.4g/dl, hematocrit was 29.1% and platelet count 461 x 1000 cells/cubic mm. Laboratory results suggested acute renal failure with creatinine of 1.6 mg/dl, urea nitrogen of 89 mg/dl and serum lactate of 3.0 mmol/L. Serum sodium was 129 mmol/L; potassium 5 mmol/L; chloride 90 mmol/L; and serum carbon dioxide 20 mmol/L. Total bilirubin and alkaline phosphatase demonstrated a slight increase, while lactate dehydrogenase, serum aspartate aminotransferase, serum alanine aminotransferase, amylase and lipase levels remained within normal range. Prothrombin time was 14.8 sec; partial thromboplastin time was 35.3 sec and ammonia at 69.5 mcmol/L (Cynthia, 2006) Patient Profile: There are three major components to the patient profile in septic shock, namely, hypovolemic profile, distributive profile and cardiogenic profile. The hypovolemic profile is veno-dilation and capillary leak; and poor cardiac filling in patients with septic shock. Distributive profile is arterial hypotension; shunting of blood supply to vital organs; and splanchnic hypoperfusion from a macro-vascular perspective and vaso-dilation or low systemic vascular resistance; pre-capillary shunting; impaired micro-circulatory flow; and micro-vascular thrombosis from a micro-vascular perspective and mitochondrial dysfunction resulting in impaired oxygen utilization from a cell level perspective. The cardiogenic profile is myocardial depression demonstrated through decreased ejection fraction and modulated through ventricular dilation in an attempt to maintain stroke volume. The advantage of such a profiling is that it is exhaustive in providing the various possible dysfunctions that are likely to occur as a result of septic shock. (Craft, Nolan & Parr, 1999). Treatment of Septic Shock: Treatment strategies in septic shock are two pronged consisting of combating the infection that has caused the septic shock and reducing the impact of septic shock on the body by maintaining adequate blood pressure and improving oxygen delivery and tissue perfusion. Paul Wade 1999, points out that no single antimicrobial agent is likely to prove sufficient in combating the infection, and so a combination antimicrobial therapy will be required. In normal circumstances a combination of third-generation cephalosporins, aminoglycoside and metronidazole provides sufficient cover against gram-positive, as well as gram-negative bacteria. In case pseudomonal infection is suspected, then it is better to use ceftazidime, quinolones and carbapenems in place of cephalosporins. When there is a strong suspicion of gram positive infection it is essential that vancomycin or teicoplanin are considered in the combination antimicrobial therapy. Use of pristinamycin comes into play, when vancomycin-resistant enterococci are suspected to be the cause of the infection (Wade, 1999). To maintain adequate blood pressure and improve oxygen delivery and tissue perfusion multiple therapeutic therapies are required. Colloids are given to restore intravascular volume. In the event that even after resuscitation cardiac output remains inadequate inotrope therapy is started by employing an agent with strong inotropic action like adrenaline. Noradrenaline is gradually provided to increase systemic vascular resistance (SVR) and maintain blood pressure. In septic shock, where cardiac output is low, the rationale for using adrenaline is that it increases cardiac output and tissue oxygen delivery, thus preserving organ function. The use of a vassopressor like noradrenaline is to induce vasoconstriction and increase SVT and blood pressure in combination with the increased cardiac output and right ventricular ejection that results from the use of adrenaline (Badcott, 1999). Fluid replacement strategies are required in conjunction with ionotropic support. The large vasodilation due to septic shock along with capillary permeability calls for of large volumes of fluid to restore and maintain the circulatory system. Colloids meet this requirement, as they restore volume quickly. Usually a combination of colloids and crystalloids is given. Colloids prevent oedema and sodium overload, as a result of crystalloid use, and crystalloid prevents fluid overload resulting from the use of colloids (Elliott, 1999). The benefit of corticosteroids in septic shock is still in doubt, but some clinicians recommend the use of corticosteroids after an evaluation test. If the corticotrophin test reveals adequate reserves of adrenal, then corticosteroids are discontinued. In septic shock cases with inadequate adrenal reserve use of hydrocortisone and fludrocortisone over a period of seven days may be beneficial (Annane, Fan & Herridge, 2006). An evolving therapeutic strategy in septic is the use of recombinant human activated protein C, which has been found to inhibit thrombosis and inflammation, while promoting fibrinolysis. Further studies would determine the role that activated protein C would play in the pathogenesis of septic shock (Kanji, Devlin, Piekos & Racine, 2001). Stress induced hyperglycaemia and insulin resistance is observed in septic shock and indicates the severity of the condition and the possibility of complications. Tight glycaemic control reduces the possibility of complications and morbidity and mortality (Liolios, 2007). Nursing Strategies in Septic Shock: In any critical illness resuscitation means assessment and support to airway, breathing and circulation. Hence the nursing professional must be prepared to intubate the patient, provide oxygen therapy and target rapid restoration of organ perfusion and perfusion pressure. Once the patient is stabilized nursing strategies removal of necrotic tissue, debriding burn eschar, stabilising fractures and maintaining adequate antibiotic regime. Other intervention strategies of the nursing professionals are to address the possibility of failure of vital organs. Monitoring of comprehensive haemo-dynamic activity is essential for an understanding of the extent of cardio-vascular derangement. For this purpose a pulmonary artery thermodilution catheter needs to be in place and cardiac output, PAWP and systemic resistance monitored. Further supportive action by the nursing professionals is in the form optimizing intravascular fluid volume, with the objective of continuing volume loading until the cardiac output and stroke volume show no improvement. The mean arterial needs to be maintained at more than 60-70mmHg. There is difficulty in ascertaining cerebral perfusion. Yet, conscious level and alertness of the patient are important indications to this. Use of inotropes and vassopressors to aid in maintaining required perfusion will have to be considered by the nursing professionals, with the choice depending on the practice in that particular ICU. Supranormal delivery of oxygen is known to reduce the risk of mortality and nursing professionals need to use this strategy in septic shock (Adam & Osborne, 1997). Conclusion: Septic shock is a critical condition that results from the response of the body to infection that has not been controlled. Rapid deterioration of the condition is demonstrated by hypovolemia, disruption of the distribution process of the circulatory system and cardiogenic shock. All this could lead to failure of multiple organs and the risk of mortality is high. Treatment in septic shock targets the causative infection through appropriate antimicrobials and reducing the manifestations of the condition in the functioning of the systems and organs of the body. Thus the approach in treating septic shock is multi-faceted. This makes the role of the nursing vital in septic shock, as it involves monitoring the condition of the patient, initiating action, evaluating the result of the action and initiating changes based on the evaluation with the objective of preventing the possibility of further complications in septic shock and the mortality that may result. Literary References Adam, K. S. & Osborne, S. 1997. ‘Critical Care Nursing: Science and Practice’. Oxford University Press. Oxford. Annane, D., Fan, E. & Herridge, M. S. 2000. ‘Pro-con debate: steroid use in ACTH non-responsive septic shock patients with high baseline cortisol levels’. Critical care, vol. 10, no.2, pp. 210. Badcott, S. 1999. ‘Inotropic and vasoactive support in acute cardiac failure and shock states’. In Ed Rachel Elliot, Critical Care Therapeutics, Pharmaceutical Press. London. pp 109-119. Balk, R. A. 2000. ‘Severe sepsis and septic shock. Definitions, epidemiology, and clinical manifestations’. Critical care clinics, vol. 16, no. 2, pp. 179-192. Craft, T.M., Nolan, J.P. & Parr, M. J. A. 1999. KEY TOPICS IN CRITICAL CARE. BIOS Scientific Publishers. Oxford. Cynthia, R. 2006. ‘A 58-Year-Old Man With a Groin Mass and Septic Shock’. Medscape Gastroenterology, vol. 6, no.1 [Online] Available at: http://www.medscape.com/viewarticle/474658 (accessed on March 15, 2007). Elliott, R. 1999. ‘Fluid Replacement Strategies’. . In Ed Rachel Elliot, Critical Care Therapeutics, Pharmaceutical Press. London. pp 97-108. Gough, E. J. 2000. Therapeutic Approach to the Hypotensive Patient. In Eds. David M. Cline, O. John Ma, Judith E. Tintinalli, Gabor, D. Kelen & J. Stephan Stapczynski, EMERGENCY MEDICINE. Fifth Edition. McGraw Hill. New York, pp. 57-69. Kanji, S., Devlin, W. J., Piekos, A. K. & Racine, E. 2001. ‘Recombinant Human Activated Protein C, Drotrecogin Alfa (Activated): A Novel Therapy for Severe Sepsis’. Pharmacotherapy, vol.21, no. 11, pp. 1389-1402. Liolios, A. 2007. ‘Highlights of the 19th European Society of Intensive Care Medicine (ESICM 2006). Medscape Critical Care, [Online] Available at: http://www.medscape.com/viewarticle/550223 (accessed on March 15, 2007). Marik, P. E. & Lipman, J. 2007. ‘The definition of septic shock: implications for treatment’. Critical care and resuscitation, vol. 9, no. 1, pp. 103. Ramrakha, P. & Moore, K. 2005. OXFORD HANDBOOK OF ACUTE MEDICINE. Second Edition. OXFORD UNIVERSITY PRESS. Oxford. Sharma, S. & Kumar, A. 2003. ‘Septic Shock, Multiple Organ Failure, and Acute Respiratory Distress Syndrome’. Current Opinion in Pulmonary Medicine, vol. 9, no.3, pp. 199-209. Sleigh, D. & Timbury, C. M. 1998. Notes on Medical Bacteriology. Fifth Edition. CHURCHILL LIVINGSTONE. Edinburgh. Wade, P. 1999. ‘Prevention and treatment of infection’. In Ed Rachel Elliot, Critical Care Therapeutics, Pharmaceutical Press. London. pp 140-152. Read More