Septic Shock - Dissertation Example

Septic Shock Introduction Septic shock is a life-threatening, debilitating medical emergency wherein the toxins released by microorganisms produces complex systemic reactions leading to massive vasodilatation, systemic blood misdistribution and decreased cardiac output, which eventually deprives oxygen to cells and tissues around the system, resulting to death (Black & Hawks, 2005). My patient to be presented in this case is a 55 year old post-operative male admitted to surgical ICU where I am working. He was hooked on cardiac monitor and Two hours after admission, my patient had a low BP (blood pressure) of 75/40 mmHg, HR (heart rate) of 130 per minute, RR (respiration rate) of 30 breaths per minute, spiking high fever, oxygen saturation of 88%, and positive abdominal pain. The patient’s skin appears warm, dry and flushed. I called the resident-on-call to report these deviations in the vital signs, and he ordered 2 intravenous boluses of NSS (normal saline solution) 500cc and oxygen administration of 2 liters per minute via nasal prongs (NP). There is no order for serum lactate measurement or arterial blood gas analysis. There are also no orders for blood culture, blood chemistry, or even antibiotics. Four hours after surgical ICU admission, my patient was still in high fever, having a systolic BP of 75 mmHg, HR of 145 per minute, RR of more than 40 breaths per minute, low oxygen saturation, decreased LOC (level of consciousness) and decreased urine output (see table 1 for summary of the trend). I called the resident-on-call again, but there was no response. I called the RRT (rapid response team) instead. See the following Table for the trend: Vital Signs 2 hours later 4 hours later BP 75/40 mmHg 75 mmHg systolic HR 130 per minute 145 per minute RR 30 per minute 40 per minute Oxygen Saturation 88% It would appear that this was not recognized appropriately as management of the patient did not improve the cardiovascular status. Within the four-hour span of surgical ICU admission, most assessment, diagnostic procedures, medical and evaluation necessary for septic shock management were absent, and there was only two hours remaining for the 6-hour crucial period of the Sepsis Resuscitation Bundle. Case Outline In a normal physiology, the three components of blood circulation compensate each other to maintain the normal circulation, which are the heart, the vascular tone and the blood volume in maintaining adequate systemic perfusion. For example, if there is inadequate circulating blood volume, the baroreceptors of the aortic arch will signal the heart to increase the heart rate to raise blood pressure. Other organs in the circulation, like the kidneys, will compensate as well, like the activation of rennin-angiotensin-aldosterone system, which will also increase the vascular tone and stimulate fluid retention. When these compensatory mechanisms fail to maintain an effective systemic perfusion, shock occurs as a result (Black & Hawks, 2005). The inadequacy of systemic perfusion in septic shock is only an aftermath of the systemic effects of microorganisms present in the body, whether it is in the bloodstream (septicemia) or localized infection. A number of risk factors are associated with septic shock: age, co-existing infection, co-existing hepatic, renal and heart failure, decreased white blood cells, unknown source of infection, corticosteroid use, and retention of foreign body in the system (Leibovici et al, 1997; Labelle et al, 2008; Annane et al, 2003; Brun-Buisson et al, 1995). It is uncertain whether infection occurred from the patient’s previous abdominal surgery or otherwise. Black and Hawks (2005) gives an excellent pathophysiology of septic shock. The invading pathogen releases endotoxins which generates a myriad of reactions in the body. One is the activation of kinins, specifically bradykinin, which is the main responsible for the hypovolemic state in septic shock since it causes vasodilation, decreasing blood pressure and venous return. When the offending microorganism is destroyed, tumor necrosis factor and interleukin is released, which increases nitric oxide, further promoting vasodilation. Endotoxins also activate the myocardial depressant factor which decreases the end diastolic volume, ejection fraction and cardiac output, along with cardiac arrhythmias. Endotoxins will also activate clotting and complement cascades which predispose the body to thrombus formation and then to disseminated intravascular coagulation. Another effect of endotoxins is the release of thromboxane which constricts pulmonary blood vessels, causing impairment in gas exchange, leading to acute respiratory distress syndrome. Septic shock impairs all organs of the body, leading to myriad of complex manifestations presented by my patient in this case. Impaired cerebral tissue perfusion decreased his LOC. Impaired circulatory tissue perfusion is responsible for the hypotensive state, low systolic BP and mean arterial pressure (MAP) of 52 mmHg, while the heart compensates for the decreased cardiac output by inducing tachycardia (130 then 145 per minute). Ineffective renal tissue perfusion was manifested by decreased urine output. Impaired peripheral tissue perfusion was evidenced by below normal oxygen saturation (88%). Impaired gas exchange was manifested by increased respiration rate (30 then 40+ breaths per minute). The only manifestation of infection available is the high fever and abdominal pain. These manifestations reveal that the patient is still in “warm shock” as the body is still able to compensate for the decreased circulating blood volume (Black and Hawks, 2005). Assessment Based from my patient’s manifestations, he presents evidences of ineffective circulatory, cerebral and peripheral tissue perfusion, as well as the signs of infection. Circulation There is still evidence of circulation, though ineffective, on the fourth hour prior to admission at surgical ICU: a hypotensive blood pressure and elevated heart rate. However, the patient should also be hooked on cardiac monitoring and 12-lead ECG (electrocardiogram) to assess deadly cardiac rhythms such as complete AV block, ventricular tachycardia, torsades des pointes and ventricular fibrillation, the latter being the most life-threatening (Black and Hawks, 2005). Part of assessment of circulation, particularly on the brain, is the LOC, utilizing the Glasgow Coma Scale (GCS) for accurate determination of consciousness, but was missing from the given case. Airway and Breathing Since ARDS complicates septic shock, assessment of the airway is important in maintaining oxygenation. Microbial toxins activate thromboxane which constricts pulmonary blood vessels, impairing gas exchange. The only data I obtained about the patient’s airway status is the increased respiration rate (more than 40 breaths per minute). Many vital airway and breathing assessment interventions that should be ordered by the resident-on-call were missing, which contributes to the ineffectiveness of oxygen administration of 2 liters per minute via NP to improve oxygen saturation and level of consciousness. Moreover, no arterial blood gas (ABG) analysis was performed to evaluate the effectiveness of gas exchange. The increased respiratory rate may be a compensatory mechanism to the elevated carbon dioxide levels in the blood (PaCO2 more than 45 mmHg) and acidic blood pH (below 7.35), or a compensatory mechanism to the constricted pulmonary blood vessels (Black and Hawks, 2005). It is also missing an important value in determination of oxygen levels in the blood (PaO2) to support the oxygen saturation reading. Sepsis Resuscitation Bundle (Society of Critical Care Medicine, 2007). After the assessment and establishment of the circulation, airway and breathing, the use of the Sepsis Resuscitation Bundle is known to increase the rate of survival by half (Gao et al, 2005). See the Appendix for the elements of the Sepsis resuscitation Bundle. The steps 1, 2 and 5 of the Bundle are assessment procedures that should be implemented within 6 hours of admission. These are the (1) measurement of serum lactate, (2) obtaining blood cultures and (3) CVP (central venous pressure) and ScvO2 (central venous oxygen saturation). These important assessments were missing from the physician’s orders as they were important (significance of these is explained in the succeeding paragraphs). It is believed that serum lactate is a more reliable determinant in predicting the patient outcomes incases of septic shock than oxygen-related values (Bakker et al, 1991). Deprivation of oxygen in some organ systems will trigger an anaerobic respiration, when the metabolism of pyruvate was reduced. The end product of this alteration is lactic acid, and will trigger a metabolic acidosis leading to death (Black and Hawks, 2005). Moreover, since the liver metabolizes lactate, hepatic failure will further aggravate the elevation of serum lactate. The high mortality rate of lactic acidosis, which is above 50% (Gutierrez & Wulf, 1996), contributes to the high mortality rate in septic shock secondary to lactic acidosis. As the value of serum lactate reflects the degree of cellular damage by oxygen deprivation of cells, it remains to be the good indicator in determining the extent of multiple organ failures (Bakker et al, 1996). For the given case, obtaining the results of serum lactate concentrations within the remaining 2 hours of the Sepsis Resuscitation Bundle is a must, as well as ABG to confirm the acidity of blood due to lactic acidosis. Possibly, the increased rate of respirations of the patient is a compensatory mechanism to increased serum lactate, but it is to be confirmed. Obtaining blood cultures will determine the causative factor/s of septic shock to determine the appropriate antimicrobial medication (except when caused by viruses which will not be present in blood cultures) suitable for the offending organism. It is also one of the strongest recommendations by the international experts in managing septic shock (Dellinger et al, 2008). However, even without the results of the blood culture, a broad spectrum antibiotic should be administered within one hour of the surgical ICU admission (in this case, it is already delayed by 3 hours). Nevertheless, the blood culture is necessary to prevent the inappropriate use of antimicrobial therapy (Kumar et al, 2009). Measurement of the central venous pressure assesses the blood volume being pumped by the left ventricle while the central venous oxygen saturation determines the oxygen concentrations. This will assess the level of the decrease in the circulating blood volume secondary to systemic vasodilatation, and the level of compensation by the heart. Low central venous oxygen saturation is also responsible to the mortality in septic shock (Bracht et al, 2007). Decision Making In the nursing field, decision-making is fundamental in the role of the nurse which portrays her knowledge and practice (Buckingham & Adams, 2000a; Bakalis, 2006). As there was abundance of available theories in decision-making, problems arise when applied in practice (Buckingham & Adams, 2000b) as many factors like personal characteristics, hierarchy, power, responsibility, interpersonal relationships, etc. that influence the nurse’s decision-making capability (Hancock & Easen, 2005; Bucknall, 2003). Like for example in this case, I experienced a difficulty in communicating the elements of the Sepsis Resuscitation Bundle to the resident-on-call that was missed, and other interventions that are dependent on physician’s order. It seems that there was a personal barrier within me that hinders me from giving suggestions to the resident-on-call, assuming that I am at the lower hierarchy to remind him of ordering serum lactate laboratory and antibiotics. There’s some kind of border between the nurse and the physician. Perhaps it is the reason why I called, by intuition, the rapid response team after the resident-on-call made no reply to my report of changes in patient’s status at the 4th hour of admission. I should have tried to reach the resident-on-call wherever he may have been after I called the rapid response team. I might have as well a mishap of having strategy due to my limitations. Instead of enforcing the Sepsis Resuscitation Bundle, even to the resident-on-call, I employed a simple strategy of simply obeying the physician’s orders while not questioning the absence of those that I think appropriate for my patient. I have the thinking of “What if he tells me that the patient is not yet being diagnosed of septic shock for me to suggest those?” Perhaps this is my cognitive limitation, as described by Elstein & Schwartz (2002) as a problem in clinical problem solving. My intuition, backed up by the manifestations of the patient, tells me that the patient should already be diagnosed with septic shock, but I might be crossing the boundaries of physician’s power and responsibility. There must be a way for me to communicate this matter in a way that I won’t sound as someone better than the physician, but I’m hindered by my personal fear. This is where I should improve, to enhance my decision-making capabilities. There are other things I can do aside from discussing the patient’s probable diagnosis of septic shock. It is my independent nursing power to thoroughly assess the patient and report all the significant findings that would convince the resident-on-call to diagnose the patient with septic shock and make orders to address it. According to Dellacroce (2009), the nurse indeed has a role in improving the prognosis of a patient undergoing septic shock, and one of which is to document and report my assessment, as suggested by Nelson et al (2009). It is in my power in determining whether the patient is manifesting signs and symptoms of SIRS and MODS and report them immediately (King, 2007). I might not have the power and responsibility to diagnose the patient with septic shock, but by using the right strategy, I can influence the physician in his diagnosis and treatment. Conclusion Assessment and decision-making, especially in a heightened perceived difficulty of a case, is an integral part of nursing management of a case of septic shock. Even if a nurse thinks that it is problematic to assess her decisions and whether she can make improvement (Buckingham & Adams, 2000a), she should equip herself with strategies that might improve her ability to assess and decide what might be the best for the patient, even those interventions that require her to coordinate with others who are at a different level of power and hierarchy. There is certainly a need for a nurse to consider how good her decisions are and to consider other approaches (Harbison, 2001). References Bakalis, N. (2006). Clinical decision-making in cardiac nursing:a review of the literture, Art and science cardiology, vol. 21, no. 29, pp. 39-46. Bakker, J. et al (1991). 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Initiation of Inappropriate Antimicrobial Therapy Results in a Fivefold Reduction of Survival in Human Septic Shock, CHEST, vol. 136, no. 5, pp. 1237-1248. Labelle, A. et al (2008). Treatment-related risk factors for hospital mortality in Candida bloodstream infections, Critical Care Medicine, vol. 36, issue 11, pp. 2967-972. Leibovici, L. et al (1997). Septic Shock in Bacteremic Patients: Risk Factors, Features and Prognosis, Scandinavian Journal of Infectious Diseases, vol. 29, no.. 1, pp. 71-75. Nelson, D. P. (2009). Recognizing sepsis in the adult patient, The American Journal of Nursing, vol. 109, no. 3, pp. 40-45. Riley (2003). Removing chest drains a critical reflection of a complex clinical decision. Nursing in Critical Care, vol. 8, no. 5, pp. 212-221. Society of Critical Care Medicine (2007). Implement the 6-hour Bundle: Sepsis Resuscitation Bundle. [Online], Available: http://www.survivingsepsis.com/6hr_bundles [17 Mar 2011] Read More