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Treatment of a Patient with Septic Shock - Essay Example

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The paper "Treatment of a Patient with Septic Shock" outlines septic shock is of great importance in intensive care medicine. To decrease the mortality early recognition of septic shock, resolution of the inflammatory response, elimination of the causative organism, and supportive care is needed…
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Treatment of a Patient with Septic Shock
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Role of Registered Nurse in the Initial Assessment, Investigation, and Nursing Management/ Treatment of a Patient with Septic Shock INTRODUCTION: Septic shock, according to Bridges; Dukes (2005: p.14), is one of the most feared medical conditions. Mortality due to severe sepsis is approximately 29%, with 215,000 deaths each year, which is comparable to the number of deaths due to acute myocardial infarction. The keys to decreasing the mortality include early recognition of septic shock, resolution of the inflammatory response, elimination of the causative organism, and provision of supportive care. Septic shock is of great importance in intensive care medicine. The condition has a high risk potential and extensive therapy is required to be carried out in intensive care settings. The mortality of septic shock patients is about 50% (Fazi, et al, 2002: p.42). The nurse is presented with a wide range of problems and challenges which test knowledge, abilities and skills, by patients with medical emergencies. The nurse must respond quickly and effectively to prevent further harm, by means of skillful assessment of the patient’s condition. Emergency may be defined as: Any trauma or sudden illness that requires immediate intervention to prevent immediate severe damage or death (Ford, 1986, as quoted in Sheppard; Wright 2000: p.213). Sepsis is defined as infection with evidence of systemic inflammation, consisting of two or more of the following: increased or decreased temperature or leucocyte count, tachycardia and rapid breathing. Septic shock is sepsis with hypotension that persists after resuscitation with intravenous fluid (Annane, et al, 2005: p.63). Normally the immune and neuroendocrine systems tightly control the local inflammatory process to eradicate invading pathogens. When this control mechanism fails, systemic inflammation occurs, converting the infection from sepsis to severe sepsis, and then to septic shock. Impending onset of septic shock immediately calls upon several types of health care professionals to attend to the emergency situation. Among them, the role of the registered nurse is crucial, in the initial assessment of the condition, the investigations and tests that are required to be conducted, the treatment, and nursing interventions and management to be carried out to ensure the patient’s return to a normal condition from a critically ill stage (Fazi, et al, 2002:p.42). DISCUSSION: Annane, et al (2005: p.63) reiterate that the time available for intervention is short, and treatment must promptly control the source of infection and restore hemodynamic homoeostasis. Clinical Signs and Symptoms of Septic Shock: A person in septic shock will display all the signs and symptoms of septicemia, plus most crucially: Hypotension (systolic pressure < 90 mm Hg, and diastolic < 60 mm Hg). Consequent impaired blood flow to all parts of the body may result in: 1) Low urine output indicating renal failure. 2) Cyanosis indicating respiratory failure. 3) Jaundice indicating liver failure. Disseminated intravascular coagulation results in: reduced platelets and clotting proteins, increased tendency to bleed (Higgins, 2000: pp.318-319). RECOGNIZED FRAMEWORK FOR ASSESSING PATIENTS: Emergency conditions such as septic shock and traumatic injuries are currently assessed and treated according to a rapid systematic process known as Advanced Trauma Life Support (ATLS), as stated by Alexander and Procter (1993), quoted in Sheppard; Wright (2000: p.214). According to the ATLS, a rapid search for and correction of life-threatening problems is carried out in the correct sequence by health professionals. Stead; Thomas (2000: p.441, p.501) state that each of the criteria are quickly assessed for particular symptoms. The full form of the letters A B C D E which denote the Advanced Trauma Life Support sequence of rapid assessment, are as follows: A - Airway (with C-spine control), B - Breathing, C - Circulation, D - Disability, and E - Exposure with temperature control. In the case of septic shock, the following assessments will be made rapidly, state Sheppard; Wright (2000: p.214) and Stead; Thomas (2000: p.441, p.501): A. Airway: Suction and modified jaw thrust are used as needed to visualize the field. Signs of impending loss of airway (dyspnea, stridor, expanding hematoma, bleeding into airway, dysphagia, hoarseness) are monitored. Loss of the gag reflex, or vomitus in the oropharynx are also looked for. Early intubation may be needed to maintain control of the airway. B. Breathing: The frequency and depth of breathing are noted. Slow, deep breathing may indicate the need for ventilatory support, rapid shallow breathing may indicate an underlying metabolic acidosis or hypoxemia. Respiratory effort, rate and chest-wall excursion are assessed. Breath sounds are assessed to ensure that they are present and equal. The chest is percussed to listen for hyperresonance or dullness. Supplemental oxygen is given as needed. C. Circulation: Blood pressure and pulse are obtained to assess baseline circulatory status. Bradycardia may indicate cardiotoxicity or parasympathetic overload, whereas tachycardia may be due to cholenergic blockade or central nervous system stimulation. Intravenous access should be obtained, using at least two large-bore IV catheters. If damage to the subclavian vessels is suspected, at least one line should be established in the lower extremities. D. Disability: A quick, neurological examination is performed including size and reactivity of pupils, ability to move all four extremities, and the presence of reflexes. Mental status is assessed using the AVPU (Alert, responds to Verbal stimuli, responds to Painful stimuli, or Unresponsive). A rectal examination is performed to assess rectal tone, presence of blood or bony defect and position of the prostate. E. Exposure: The patient must be undressed completely, to allow a complete physical examination and eliminate the possibility that any injuries could be overlooked. In the case of septic shock, this criterion is optional, depending on the case (Stead; Thomas 2000: pp.441,501). THE PATHOPHYSIOLOGY OF SEPTIC SHOCK: According to Bayley; Turcke (1992: p.106), the main contributing factors are: 1) Hemodynamic instability, metabolic derangement, and coagulation disturbances resulting from overwhelming systemic infection. This is most commonly due to Gram-negative bacteremia. Also caused by Gram-positive bacteria, viruses, fungi and rickettsiae 2) Endotoxins found in cell walls of Gram-negative organisms, are released into the systemic circulation, resulting in activation of various hormonal and chemical mediators. The mediators have numerous effects, ultimately decrease tissue perfusion. Massive arterial and venous vasodilation causes decreased total peripheral resistance, decreased venous return to the heart, and reduced CO. Activation of clotting factors and platelet aggregation causes results in micro-circulatory coagulation, and impedes capillary blood flow. Pre-disposing factors associated with Septic Shock: (Bayley; Turcke,1992: p.106) state that pre-existing chronic disease, age, debilitation, immunosuppression, intravascular lines, indwelling urinary catheter, ventriculostomy catheter, endotracheal intubation, tracheostomy, peritonitis, open wounds, soft tissue trauma, burns, retained foreign bodies, inadequate debridement, surgical procedures, hypovolemic shock, and diagnostic indicators like positive blood cultures are precipitating factors. In the patient with a hyper coagulablity, treatment of the underlying malignancy is vital, because the tumour is the ultimate stimulus. All other therapy, although effective on a short term basis, provides only an inteval of symptomatic relief (Yarbro, et al, Oncology Nursing Review, p.180) Bridges; Dukes (2005: p.14), focus on the cardiovascular aspects of septic shock, including cardiovascular pathophysiology, cardiovascular monitoring and treatment options. Septic shock is associated with three major pathophysiological effects, within the cardiovascular system: Vasodilation, Maldistribution of blood flow, and Myocardial depression. According to the authors Bridges; Dukes (2005: p.14) shock is an imbalance between oxygen supply and demand, which results in a systemic clinical syndrome, characterized by hypotension and hypoperfusion, leading to cellular dysfunction. Sepsis is systemic response to infection, and septic shock is sepsis with hypotension and abnormalities in perfusion. There are four general types of shock: hypovolemic, cardiogenic, obstructive and distributive. Recognizing the early signs and symptoms of septic shock is pivotal in improving patients’ outcomes (p.19). Appropriate monitoring of patients with septic shock is imperative, with specific consideration given to detecting changes in perfusion and tissue oxygenation. Basic monitoring should include pulse oxymetry, electrocardiography, and invasive blood pressure monitoring. Central venous pressure monitoring or pulmonary artery catheterization, along with measurements of venous oxygen saturation are useful in evaluating cardiovascular status. Higgins (2000: p.318) states that whilst antibiotic therapy is effective in combating the underlying infection and preventing septic shock from arising, it has little or no effect in combating septic shock. This is because shock is caused not by the bacteria themselves, but by the body’s response to bacterial infection. A destructive cascade of chemical release by the body’s own cells, monocytes, macrophages, etc, recruited to fight the infection accompanies release of toxins from invading bacteria. Tumor necrosis factor (TNF) and interleukin 1 (IL-1) are among the many chemicals released from the body’s own cells. These two proteins and endotoxin (released from the walls of dying gram-negative bacteria) are particularly significant in the pathogenesis of septic shock. Damage mediated by these chemicals to the cells of the vascular endothelium results in disruption of the microvascular circulation, because of the tiny vessels of the microvasculature becoming dilated and leaky. The combination of hypovolaemia (low blood volume due to leaky vessels) and vessel dilatation cause a reduction in blood pressure (hypotension) which is the most significant clinical sign of septic shock. The resulting reduced blood supply to all tissue cells leads to hypoxia and tissue death. All organs may be affected, and without successful treatment, multiple organ dysfunction progresses to multiple organ failure and death. Besides hypotension, the triggering of the clotting cascade leads to the inappropriate coagulation of blood within blood vessels. Due to exhaustion of clotting factors, an increased tendency to bleed and a high risk of fatal hemorrhage results. The immediate cause of death for many patients with septic shock is intracerebral hemorrhage (Higgins,2000: p.319). LABORATORY INVESTIGATIONS IN SEPSIS: A variety of laboratory tests should be performed emergently when sepsis is suspected. Other diagnostic tests may be required and obtained later if the diagnosis remains unclear (Cunha, 1998: p.51). Rationale for the Microbial Examination of Blood: The primary objective of the laboratory is to determine whether a patient’s blood contains bacteria. If is not possible to confirm or exclude the presence of bacteria in blood by simply examining a sample under the microscope. There simply are not sufficient bacteria present. Instead, bacteria must first be grown in a liquid called the culture medium which contains the nutrients necessary for bacteria to grow and multiply. In practice, if there is no evidence of bacterial growth afte three days of incubation, it is highly unlikely that the culture and therefore the blood sample added to the culture is infected with bacteria (Higgins, 2000: p.319). Other Laboratory Investigations: The following tests have to be performed frequently: complete blood count including platelet count, serum electrolytes, blood urea nitrogen and creatinine, lactate levels, calcium, phosphate, magnesium, coagulation parameters, liver function, arterial blood gases and mixed venous oxygenation (if a pulmonary artery catheter has been placed), Cunha (1998: p.51). These tests help identify correctable electrolyte and metabolic disturbances, including anemia, hypokalemia, hyponatremia, bleeding abnormalities, thrombocytopenia, lactic acidosis and impending renal, hepatic or respiratory failure. During the acute stages of sepsis, patients may need to have some tests repeated frequently. Serial measurements of arterial blood gases, lactic acid levels, platelet counts, and renal, hepatic and coagulation profiles, help estimate the severity of the sepsis, associated organ dysfunction, and the response to therapy. The intervals between blood testing can be gradually increased as the patient improves and stabilizes. Other laboratory tests include cardiac enzymes and fibrinogen. Some more important physical and physiological tests: 1) Vital signs: fever, hypothermia, tachycardia, tachypnea and hypotension 2) Central nervous sytem: confusion, obtundation and coma. 3) Cardiovascular: Tachycardia, hypotension, normal or increased cardiac output, low systemic vascular resistance. 4) Respiratory: Tachypnea, hypocapnea, hypoxemia, ARDS. 5) Renal: Oliguria, acute renal failure. 6) Gastrointestinal: Impaired gastrointestinal motility, SRMD, hyperbilirubinemia, elevation of liver enzymes. 7) Hematologic: Leucocytosis, leukopenia, thrombocytosis, thrombocytopenia, disseminated intravascular coagulation. 8) Metabolic, electrolyte: Hypoalbuminemia, hyperglycemia, hypoglycemia, lactic acidosis, hypokalemia, hyponatremia, hypocalcemia, hypomagnesemia, hypophosphatemia. Other tests that need to be done are: degradation products, D-dimer assays, serum protein and albumin concentrations, urinalysis and antibiotic peak and trough levels. Diagnostic services that need to be available on a 24-hour emergent basis include: portable chest and abdominal roentgenography, head, chest and abdominal computed tomography, ultrasonography of the abdomen and chest, pulmonary angiography, and appropriate consultation services (Cunha, 1998: p.52). Some Proposed Laboratory Markers of Sepsis: Markers of inflammation are useful in the diagnosis of sepsis. Some of the markers are: White blood cell count, C-reactive protein (CRP), Cytokine levels: TNF, IL-6, IL-8, IL-10, TNF receptors, Procalcitonin, Serum amyloid protein, Neopterin, Elastase, Phospholipase A2, Endothelin 1, Nitrates/ nitrites, P-selectin/ E-selectin, Prolactin, Lactoferrin, Lipopolysaccharide binding protein. C-reactive protein has been shown to be a useful indicator of the presence of sepsis, and more indicative of infection than the white blood count or fever. CRP levels > 17 mg/dl have been suggested as a means of separating patients with sepsis from those with a non-inflammatory response due to trauma. Precalcitonin has also been proposed as a marker of infection. Neopterin is also a marker of sepsis (Eichacker, 2001: p.20). MANAGEMENT AND TREATMENT OF SEPTIC SHOCK: Picard, et al (2006: p.44) give the background of the protocol for management and treatment of septic shock. Treatment is focused on supporting failing organ systems. Interventions include fluid replacement, airway management, antibiotic therapy, use of vasoactive medications, and hemodialysis. Various treatments used to improve patients’ outcome, can paradoxically contribute to organ dysfunction. Examples of these treatments include the use of high-tidal-volume ventilation to improve oxygenation which may cause barotrauma or damage of the lung parenchyma; use of antimicrobial agents that cause nephrotoxic effects; and hemodialysis in renal dysfunction, which may worsen a pre-existing coagulopathy. Current management includes early goal-directed therapy, activated protein C for severe sepsis, intensive insulin therapy, steroids for patients with adrenal suppression, and protective lung ventilation. The authors Picard et al (2006: pp.44-45) state that significant improvement in mortality could be achieved by therapy which included: manipulating preload by using fluids and blood transfusions, manipulating oxygen delivery by using vasopressors, inotropic agents and blood transfusions. Hemodynamic support for patients with septic shock can be classified into three main categories: fluid resuscitation, vasopressor therapy, and inotropic therapy (Bridges; Dukes 2005: p.30). The treatment of septic shock can be viewed as having three main goals: maintain an adequate mean arterial pressure (MAP), identify and eliminate the cause of infection, and interrupt the pathogenic process leading to septic shock. While these goals are being addressed, adequate organ system perfusion and function should be maintained, on the basis of cardiovascular monitoring. Fluid resuscitation is the initial therapy of choice for the treatment of hypotension in septic shock, because most patients with sepsis have inadequate preload due to peripheral vasodilation. Although exact end points of resuscitation have not been specified, a general goal is a central venous pressure of 8 to 12 mm.Hg, a pulmonary arterial pressure of 12 to 15 mm. of Hg, or fluid resuscitation to a point at which additional infusions of fluid are not accompanied by an increase in cardiac output. Additionally, other indicators of adequate tissue perfusion, for example: increased urine output, decrease in serum level of lactate, and improved mental status should be assessed. NURSING INTERVENTION IN SEPTIC SHOCK: The nursing intervention that is most important in preventing septic shock is administering intravenous fluid replacement therapy as ordered (Billings, 2004: p.284). The main focus is on correcting and maintaining adequate tissue perfusion (p.294). Inadequate tissue perfusion may be caused by massive vasodilatation of the vascular bed as seen in the condition of septic shock. Fluid deficit, not fluid overload occurs in shock. Urine output provides the most sensitive indication of the client’s response to therapy for hypovolemic shock. Urine output should be consistently greater than 30 to 35 ml/ hour. Blood pressure is a more adequate reflection of vasoconstriction than of tissue perfusion. The client who is receiving Dopamine hydrochloride requires continuous blood pressure monitoring with an invasive or a non-invasive device. The nurse may titrate the intravenous infusion to maintain a systolic blood pressure of 90 mm. Hg. Administration of a pain medication is not an essential nursing action for a client who is in shock, with already low hemodynamic values. Arterial blood gas concentrations should be monitored according to the patient’s respiratory status and acid-base balance status, and are not directly related to the dopamine hydrochloride dosage (p.295). Warm, flushed skin from a high cardiac output with vasodilatation occurs in the hyperdynamic or first phase of septic shock. Other signs and symptoms of early septic shock include fever with restlessness and confusion, decreased blood pressure with tachypnea and tachycardia, increased or normal urinary output, and nausea and vomiting or diarrhoea. Cool, clammy skin occurs in the hypodynamic cold phase or later phase. The nurse monitors for the blood levels of antibiotics, white blood cells, serum creatinine, and blood urea nitrogen because of the decreased perfusion to the kidneys. Nursing diagnoses, expected outcomes and interventions. Two examples are as follows: According to Bayley; Turcke (1992: p.112). 1. Diagnosis: Impaired gas exchange related to decreased blood flow, obstructed airway or pulmonary edema. Expected outcome: 1) Normal respiratory rate and rhythm. 2) Clear and equal breath sounds. 3) Adequate ABGs: pH 7.35 to 7.45, PaO2 more than 80mm. Hg. Oxygen saturation more than 95%. 4) Normal chest x-ray. Nursing Interventions: 1) Maintain patent airway. 2) Administer high flow humidified Oxygen. 3) Assist with intubation and mechanical ventilation. Monitor peak inspiratory Pressure. 4) Suction pro re nata (prn). Preoxygenate and limit actual suction time (prevents Vasovagal reflex and subsequent bradycardia). 5) Monitor respiratory rate, rhythm, chest Excursion and use of accessory muscle. 6) Assess breath sounds for rales, rhonchi, and Wheezes. 7) Obtain ABGs and monitor for signs of hypoxemia and/ or hypercapnia. 8) Monitor arterial oxygenation via pulse oximeter. 9) Assist with thoracostomy tube placement, and monitor functioning of system and drainage. 10) Position patient for optimal perfusion of lungs and lung function. 11) Administer chest physiotherapy and encourage use of incentive spirometry. 12) Prevent aspiration by inserting nasoorogastric tube and connecting to straight drainage or suction. 2. Diagnosis: Fluid volume deficit related to loss of fluid from the intravascular compartment. Expected outcome: Hemodynamic stability as evidenced by: 1) Heart rate 60 to 100 beats per minute. 2) Normal sinus rhythm. 3) Systolic blood pressure more than 90 mm Hg. 4) Peripheral pulses normal (+2). 5) CO four to six litres per minute. 6) Cardiac index 2.8 to 4.2 litres / minute/ m2. 7) Pulmonary artery diastolic pressure 8 to 15 mm. Hg. 8) Systemic vascular resistance 900 to 1400 dynes/ second/ cm2. 9) Central venous pressure 5 to 8 mm. H2O. 10) Mixed venous oxygen saturation 60 to 80%. 11) Normal serum electrolytes. Other important nursing interventions: 1) Control bleeding with direct pressure, or PASG. 2) Observe for early signs of shock. 3) Insert large-bore peripheral intravenous catheters. 4) Assist with insertion of arterial and central venous catheters. 5) Administer warmed crystalloids, colloids and blood components for Phase I/ II shock via large-bore administration set. 6) Administer warmed crystalloids, colloids and blood components for Phase III/ IV shock via large-bore administration set; provide calcium supplements as prescribed. 7) Prepare for autotransfusion, monitor blood loss, and re-infuse autologous blood as needed. 8) Obtain and monitor initial and serial blood studies, including hemoglobin and hematocrit, platelets, coagulation factors, and serum calcium. 9) Monitor vital signs and hemodynamic parameters, including Pulmonary Artery Pressure (PAP), pulmonary capillary wedge pressure (PCWP), CO, Cardiac Index, and mixed venous oxygen saturation. 10) Insert urinary catheter, measure intake and output. 11) Anticipate need and assist with emergency thoracotomy and diagnostic peritoneal lavage. The nurse also needs to check whether the client’s orientation to person, place and time are adequate, and check whether pupils are equal and reactive to light ( Bayley; Turcke,1992 p.113). Current Best Practice, Evidence-Based: There are usually four components to the clinical evidence-based practice question, according to Reynolds (2000) as quoted in (Smallwood, 2005: 231): Nursing is central to effective health care, thus for nurses to be equal partners in clinical and health care decision making, accessing and applying evidence in their work is essential. In a study by Claude et al (2000: p.2758), special attention was paid to hemodynamic management and to the choice of vasopressor used, to determine whether the use of norepinephrine was associated with increased mortality. The research was conducted on 97 adult patients with septic shock. The 57 patients who were treated with norepinephrine had significantly lower hospital mortality, than the 40 patients treated with vasopressors other than norepinephrine. The results were thus in favour of norepinephrine in the treatment of septic shock. According to Kleinpell (2003: p.16), the efficacy of drotrecogin alfa (activated) was recently studied in a large international multi-centred placebo-controlled trial. Treatment with the drug produced a 6.1% absolute reduction in mortality and 19.4% reduction in the relative risk of mortality due to all causes in patients with severe sepsis. The number of lives saved among patients at high risk of death, was increased. Drotrecogin alfa (activated), a recombinant human protein with anti-inflammatory, anti-thrombotic and profibrinolytic properties, resulted in the first successful outcome in reducing mortality rates in patients with severe sepsis. The Actions of Medications Prescribed: In septic shock, dopamine is probably the most widely used agent, producing improvement in cardiac output and stroke volume, and a variable increase in arterial blood pressure, according to Skinner (Ed.) (1997: p136). Even at low dosage, vasoconstriction may occur, and result in reduced microcirculatory oxygen availability. Dobutamine does not demonstrate a vasoconstrictive effect, and also has the ability to reduce pulmonary capillary wedge pressure, thereby allowing increased fluid volume infusion. For these reasons, Dobutamine in conjunction with noradrenaline to counteract hypotension, is becoming increasingly popular (Edwards, 1993b) as quoted in Skinner (1997:136). To be of value, the dose of catecholamines should be adjusted to meet the needs of the individual septic shock patient, therefore the patient needs to be transferred to the intensive care unit and should be intensively monitored, often with pulmonary artery flotation catheter. Vasodilators may be indicated when cardiac failure is present, but low mean arterial blood pressure limits their use in septic shock. Treatment which attains high levels of oxygen delivery and consumption is under investigation. Until recently high-dose corticosteroids were recommended in the early management of septic shock. In spite of beneficial effects, there was no improvement in mortality, and there was an increase in infection attributable to the corticosteroids, hence the drug has been discontinued. CONCLUSION: Septic shock has remained a serious medical condition with high mortality (Evans, 2000: p.v). Though several novel therapies had been developed for septic shock, having excellent theoretical grounds for their efficacy, they failed in altering mortality attributable to sepsis. Recent developments in pharmacology, producing drugs like Dobutamine in combination with noradrenaline, are bringing a positive turn to the treatment of septic shock. Further research is required in the future, drawing upon a number of disciplines like Physiology, Molecular and Cell Biology, and related areas. The nurse practitioner’s role is increasing to include crucial decision-making responsibilities, in conditions of emergency and intensive care. The area of septic shock is a very challenging one for health care professionals, due to the high level of trauma and the short period available for intervention, before the patient succumbs to the onset of the disease. The nurse’s skills, knowledge and critical thinking abilities are required for prevention and treatment of septic shock. ---------------------------------------------------------- REFERENCES Annane, Djillali; Bellisant, Eric; Cavaillon, Jean Marc. “Septic Shock”. The Lancet, Vol.365, pp.63-78. Bayley, Elizabeth W; Turcke, Susan Allyn. (1992). A Comprehensive Curriculum for Trauma Nursing. London: Jones and Bartlett Publishers. Billings, Diane McGovern. (2004). Lippincott’s Review for NCLEX-RN. Lippincott Williams and Wilkins. Bridges, Elizabeth J; Dukes, Major Susan. (2005). “Cardiovascular Aspects of Septic Shock: Pathophysiology, Monitoring, and Treatment”. Critical Care Nurse, Vol.25, No.2, April 2005. Claude, Martin; Xavier, Viviand; Marc, Leone; Xavier, Thirion. (2000). “Effect of Norepinephrine on the Outcome of Septic Shock”. Critical Care Medicine, Vol 28, No.8, pp.2758-2765. Cunha, Burke A. (1998). Infectious Diseases in Critical Care Medicine. U.S.A.: Marcel Dekker. Eichacker, Peter Q; Pugin, Jerome. (2001). Evolving Concepts in Sepsis and Septic Shock. Massachusett: Springer. Evans, Thomas J. (2000). Septic Shock Methods and Protocols. New Jersey, Humana Press. Fazi, Paola; Luzi, Daniela; Ricci, Fabrizio L; Vignetti, Marco. (2002). The Conceptual Basis: Medical Data Analysis, Third International Symposium, ISMDA 2002, Proceedings. Springer. Higgins, Chris. (2000). Understanding Laboratory Investigations: A Text for Nurses and Other Health Care Professionals. United Kingdom: Blackwell Publishing. Kleinpell, Ruth. (2003). “Advances in Treating Patients With Severe Sepsis: Role of Drotrecogin alfa (activated)”. Critical Care Nurse, Vol.23, No.3. pp.16-31. Picard, Kathy M; O’Donoghue, Sharon C; Young-Kershaw, Duane A; Russell, Kristin J. (2006). “Development and Implementation of a Multidisciplinary Sepsis Protocol”. Critical Care Nurse, Vol.26, No.3, June 2006. Sheppard, Amanda; Wright, Mike. (2000). Principles and Practice of High-Dependency Nursing. U.K.: Elsevier Health Sciences. Skinner, David (Ed). (1997). Cambridge Textbook of Accident and Emergency Medicine. United Kingdom: Cambridge University Press. Smallwood, Andrew. (2005). “Nurse-led Elective Cardioversion: An Evidence-Based Practice Review”. Nursing in Critical Care. 2005, Vol.10, No.5. pp.231-242. Stead, Latha G; Thomas, Stephen H. (2000). Emergency Medicine. Lippincott Williams and Wilkins. Yarbro, Connie Henke; Frogge, Margaret Hansen; Goodman, Michelle. (2004). Oncology Nursing Review. United Kingdom: Jones and Bartlett Publishers. Read More
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