Septic Shock: Causes and Treatments

1285 words (5 pages) Essay

21st Sep 2017 Health Reference this

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  • Jessica Jensen
  • North Mohave Community College
  • Nursing 222
  • Monika V. Wise, RN, BSN, MS

Septic Shock

It knows no boundaries. It is not biased or racist, and it is a killer. It will affect any age or gender. It is cunning, quick to manifest itself, and life-threatening, it is septic shock. Sepsis is a crafty syndrome that most people may not even realize they have until a family member realizes they are acting different and takes them to the emergency department. First it starts with an infection, then early sepsis, which if not treated it turns into septic shock.

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Sepsis is defined by the Surviving Sepsis Campaign as a “life-threatening organ dysfunction caused by a dysregulated host response to infection (Society of Critical Care Medicine, 2017, p. 489).” Septic shock is defined as a “subset of sepsis with circulatory and cellular/metabolic dysfunction associated with a higher risk of mortality (Society of Critical Care Medicine, 2017, p. 489).”Sepsis and septic shock are major health problems around the world, killing millions of people each year. It is estimated that one in four people die from sepsis each year (Society of Critical Care Medicine, 2017, p. 489).

Septic shock starts from an infection, the invading bacteria go untreated and invade the body’s tissues. This invasion provokes an inflammatory response that activates inflammatory mediators, such as tumor necrosis factor and interleukins, and biochemical mediators like cytokines. These inflammatory mediators impair the microvasculature, which results in increased capillary permeability and vasodilation (Hinkle & Cheever, 2014, p. 302; Wagner & Hardin-Pierce, 2014, p. 866). The increased capillary permeability and vasodilation interrupt the body’s ability to provide adequate oxygenation and perfusion to the tissues and cells (Hinkle & Cheever, 2014, p. 302). When the proinflammatory and anti-inflammatory mediators (cytokines, interleukins, etc.) are released it activates the coagulation system, and clots begin to form regardless of bleeding being present (Hinkle & Cheever, 2014, p. 302). These cascades of clotting and inflammation are critical elements of the progression of sepsis.

The clinical manifestations of sepsis are the patient has a temperature of more than 38 degree Celsius or less than 36 degree Celsius, heart rate greater than 90 beats per minute, respiratory rate greater than 20 breaths per minute, and a white blood cell count greater than 12,000 mL or less than 4,000 mL, or an immature (band) forms greater than 10%, and an infection is confirmed (Wagner & Hardin-Pierce, 2014, table 36-8). Severe sepsis is associated with organ dysfunction, hypotension, and hypoperfusion. Along with the previous symptoms lactic acidosis, oliguria, or acute alteration in mental status are evident (Wagner & Hardin-Pierce, 2014, table 36-8). Septic shock is associated with hypotension despite fluid resuscitation, and the other manifestations already mentioned (Wagner & Hardin-Pierce, 2014, table 36-8). As sepsis worsens the patient’s extremities will be cold and mottling may be present, lactate levels rise, and ScvO2 decreases (Wagner & Hardin-Pierce, 2014, p. 867).

It is important for hospitals to have a protocol in place to recognize and treat sepsis. The Surviving Sepsis Campaign has suggested that all hospitals have a sepsis screening for critically ill and high risk patients. It is recommended that blood cultures be obtained immediately before antibiotic therapy is started, and antibiotics should be administer one hour after the diagnosis of sepsis is made (Society of Critical Care Medicine, 2017, p. 494). An empiric broad spectrum antibiotic with one or more antimicrobial is usually chosen, to cover all likely pathogens, until the invading pathogen is identified. When the pathogen is identified the patient is switched to an antibiotic that is more effective for the pathogen found (Society of Critical Care Medicine, 2017, p. 494-495). A lactate level should also be drawn because it is an indicator of tissue oxygenation and a high level is closely associated with shock (Wagner & Hardin-Pierce, 2014, p. 268). Fluid resuscitation should begin within the first three hours and 30 mL/kg IV crystalloid fluids should be given (Society of Critical Care Medicine, 2017, p. 491).

If the patient is in severe sepsis heading toward septic shock vasoactive drugs are recommended to increase the patient’s hemodynamic status. Norepinephrine is the recommended first-line drug for sepsis, and low-dose dopamine should be used to for renal protection. If the patient is not responding to vasopressors and fluids, IV corticosteroids can be used at a dose of 200 mg per day (Society of Critical Care Medicine, 2017, p. 504-506). Tight glucose control should be maintained. It is recommended that glucose levels should be under 180 mg/dL (Society of Critical Care Medicine, 2017, p. 514). If the patient is ventilated they should be sedated and given analgesic medication (Society of Critical Care Medicine, 2017, p. 513.) Venous thromboembolism prophylaxis should be initiated to prevent blood clots. It is recommended that a low molecular weight heparin be used along with sequential compression devices (mechanical prophylaxis). A proton pump inhibitor or histamine-2 receptor antagonist should be used to prevent stress ulcers if there is a high risk for gastrointestinal bleeding (Society of Critical Care Medicine, 2017, p. 516-518). Nutritional therapy should be initiated twenty-four to forty-eight hours after admission to address the hypermetabolic state (Hinkle & Cheever, 2014, p.304). Enteral nutrition is recommended route of administration (Society of Critical Care Medicine, 2017, p. 518).

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It is also very important to communicate with the patient and family. Septic shock can be fatal. If the patient is in multiple organ dysfunction syndrome, and the patient is refractory to treatment, end-of-life care should be discussed with the family. Treatment is aggressive and it could take time for the patient to get better. Keeping the family updated and educated in the process assist with the patient’s outcome.

Sepsis is no laughing matter. It takes lives. That is why it is essential to know what the signs of sepsis are, and once the patient is diagnosed, strict measures of treatment need to be enforced. It is also important to know the hospitals sepsis policy. Immediate action will assist in a more positive outcome for the patient.

References

Hinkle, J. L., & Cheever, K. H. (2014). Shock and multiple organ dysfunction syndrome. In Brunner & Studdarth’s Textbook of Medical-Surgical Nursing (13th ed.) (pp. 285-309). Philadelphia, PA: Wolters Kluwer Health Lippincott Williams & Wilkins.

Society of Critical Care Medicine. (2017). Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Critical Care Medicine, 45(3), pp. 486-552. http://dx.doi.org/10.1097/CCM.0000000000002255

Wagner, K.D., & Hardin-Pierce, M.G. (2014). Shock states. In High-Acuity Nursing (6 ed.) (pp. 850-874). Boston, MA: Pearson.

  • Jessica Jensen
  • North Mohave Community College
  • Nursing 222
  • Monika V. Wise, RN, BSN, MS

Septic Shock

It knows no boundaries. It is not biased or racist, and it is a killer. It will affect any age or gender. It is cunning, quick to manifest itself, and life-threatening, it is septic shock. Sepsis is a crafty syndrome that most people may not even realize they have until a family member realizes they are acting different and takes them to the emergency department. First it starts with an infection, then early sepsis, which if not treated it turns into septic shock.

Sepsis is defined by the Surviving Sepsis Campaign as a “life-threatening organ dysfunction caused by a dysregulated host response to infection (Society of Critical Care Medicine, 2017, p. 489).” Septic shock is defined as a “subset of sepsis with circulatory and cellular/metabolic dysfunction associated with a higher risk of mortality (Society of Critical Care Medicine, 2017, p. 489).”Sepsis and septic shock are major health problems around the world, killing millions of people each year. It is estimated that one in four people die from sepsis each year (Society of Critical Care Medicine, 2017, p. 489).

Septic shock starts from an infection, the invading bacteria go untreated and invade the body’s tissues. This invasion provokes an inflammatory response that activates inflammatory mediators, such as tumor necrosis factor and interleukins, and biochemical mediators like cytokines. These inflammatory mediators impair the microvasculature, which results in increased capillary permeability and vasodilation (Hinkle & Cheever, 2014, p. 302; Wagner & Hardin-Pierce, 2014, p. 866). The increased capillary permeability and vasodilation interrupt the body’s ability to provide adequate oxygenation and perfusion to the tissues and cells (Hinkle & Cheever, 2014, p. 302). When the proinflammatory and anti-inflammatory mediators (cytokines, interleukins, etc.) are released it activates the coagulation system, and clots begin to form regardless of bleeding being present (Hinkle & Cheever, 2014, p. 302). These cascades of clotting and inflammation are critical elements of the progression of sepsis.

The clinical manifestations of sepsis are the patient has a temperature of more than 38 degree Celsius or less than 36 degree Celsius, heart rate greater than 90 beats per minute, respiratory rate greater than 20 breaths per minute, and a white blood cell count greater than 12,000 mL or less than 4,000 mL, or an immature (band) forms greater than 10%, and an infection is confirmed (Wagner & Hardin-Pierce, 2014, table 36-8). Severe sepsis is associated with organ dysfunction, hypotension, and hypoperfusion. Along with the previous symptoms lactic acidosis, oliguria, or acute alteration in mental status are evident (Wagner & Hardin-Pierce, 2014, table 36-8). Septic shock is associated with hypotension despite fluid resuscitation, and the other manifestations already mentioned (Wagner & Hardin-Pierce, 2014, table 36-8). As sepsis worsens the patient’s extremities will be cold and mottling may be present, lactate levels rise, and ScvO2 decreases (Wagner & Hardin-Pierce, 2014, p. 867).

It is important for hospitals to have a protocol in place to recognize and treat sepsis. The Surviving Sepsis Campaign has suggested that all hospitals have a sepsis screening for critically ill and high risk patients. It is recommended that blood cultures be obtained immediately before antibiotic therapy is started, and antibiotics should be administer one hour after the diagnosis of sepsis is made (Society of Critical Care Medicine, 2017, p. 494). An empiric broad spectrum antibiotic with one or more antimicrobial is usually chosen, to cover all likely pathogens, until the invading pathogen is identified. When the pathogen is identified the patient is switched to an antibiotic that is more effective for the pathogen found (Society of Critical Care Medicine, 2017, p. 494-495). A lactate level should also be drawn because it is an indicator of tissue oxygenation and a high level is closely associated with shock (Wagner & Hardin-Pierce, 2014, p. 268). Fluid resuscitation should begin within the first three hours and 30 mL/kg IV crystalloid fluids should be given (Society of Critical Care Medicine, 2017, p. 491).

If the patient is in severe sepsis heading toward septic shock vasoactive drugs are recommended to increase the patient’s hemodynamic status. Norepinephrine is the recommended first-line drug for sepsis, and low-dose dopamine should be used to for renal protection. If the patient is not responding to vasopressors and fluids, IV corticosteroids can be used at a dose of 200 mg per day (Society of Critical Care Medicine, 2017, p. 504-506). Tight glucose control should be maintained. It is recommended that glucose levels should be under 180 mg/dL (Society of Critical Care Medicine, 2017, p. 514). If the patient is ventilated they should be sedated and given analgesic medication (Society of Critical Care Medicine, 2017, p. 513.) Venous thromboembolism prophylaxis should be initiated to prevent blood clots. It is recommended that a low molecular weight heparin be used along with sequential compression devices (mechanical prophylaxis). A proton pump inhibitor or histamine-2 receptor antagonist should be used to prevent stress ulcers if there is a high risk for gastrointestinal bleeding (Society of Critical Care Medicine, 2017, p. 516-518). Nutritional therapy should be initiated twenty-four to forty-eight hours after admission to address the hypermetabolic state (Hinkle & Cheever, 2014, p.304). Enteral nutrition is recommended route of administration (Society of Critical Care Medicine, 2017, p. 518).

It is also very important to communicate with the patient and family. Septic shock can be fatal. If the patient is in multiple organ dysfunction syndrome, and the patient is refractory to treatment, end-of-life care should be discussed with the family. Treatment is aggressive and it could take time for the patient to get better. Keeping the family updated and educated in the process assist with the patient’s outcome.

Sepsis is no laughing matter. It takes lives. That is why it is essential to know what the signs of sepsis are, and once the patient is diagnosed, strict measures of treatment need to be enforced. It is also important to know the hospitals sepsis policy. Immediate action will assist in a more positive outcome for the patient.

References

Hinkle, J. L., & Cheever, K. H. (2014). Shock and multiple organ dysfunction syndrome. In Brunner & Studdarth’s Textbook of Medical-Surgical Nursing (13th ed.) (pp. 285-309). Philadelphia, PA: Wolters Kluwer Health Lippincott Williams & Wilkins.

Society of Critical Care Medicine. (2017). Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Critical Care Medicine, 45(3), pp. 486-552. http://dx.doi.org/10.1097/CCM.0000000000002255

Wagner, K.D., & Hardin-Pierce, M.G. (2014). Shock states. In High-Acuity Nursing (6 ed.) (pp. 850-874). Boston, MA: Pearson.

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