Case Scenario 3: Shock and Sepsis

Transcription

1 Name: Molly Boyle 1. Define the term shock (Lewis textbook): Shock is a syndrome characterized by decreased perfusion and impaired metabolism. Shock can have a number of causes that result in damage to multiple organs and can be fatal. 2. Fill in the table: Hypovolemic Shock Definition: Hypovolemic shock occurs when there is a decrease in the amount of blood circulating in the body, thus causing hypoperfusion Examples of causes: hemorrhage, pooling of blood (bowel obstruction), internal bleeding, extreme vomiting/diarrhea/diuresis (dehydration) Clinical signs and symptoms: tachycardia, hypotension, tachypnea bradypnea(late), oliguria, confusion, mental status change, decreased Hct, Hg Obstructive Shock Definition: develop when there is a physical obstruction to diastolic filling, causing decreased CO Examples of causes: cardiac tamponade, tension pneumothorax, uperior vena cava syndrome, abdominal compartment syndrome, pulmonary embolism Clinical signs and symptoms: JVD, tachycardia, tachypnea, hypotension Cardiogenic Shock Definition: cardiogenic shock occurs when cardiac output is reduced due to a dysfunction of the hearts ability to pump blood Examples of causes: MI, pulm HTN, dysrhythmias, ventricular hypertrophy Clinical signs and symptoms: tachycardia, hypotension, tachypnea, oliguria, confusion, mental status change Distributive Shock Definition: distributive shock is caused by extreme vasodilation resulting in hypoperfusion Types: neurogenic, anaphylactic, septic Examples of causes: neurogenic (spinal cord injury, spinal anesthesia), anaphylactic (allergies), septic (infection) Clinical signs and symptoms: decreased oxygen saturation, hypotension, increased/decreased temperature, oliguria, increased/decreased temperature, positive blood cultures 3. Describe the three stages of shock (include what occurs and a brief description of what your patient would demonstrate): Compensatory: reversible stage during which compensatory mechanisms are effective and homeostasis is maintained - tachycardia, tachypnea, hypotension, slight confusion Progressive: compensatory mechanisms are becoming ineffective and fail to maintain perfusion to vital organs - decreased responsiveness to stimuli, disoriented, hypotension, tachycardia, GI bleeding, erosive ulcers, oliguria, jaundice, DIC, hypothermia, cold and clammy

2 2 Irreversible: compensatory mechanisms are not functioning or are totally ineffective, leading to multiple organ dysfunction syndrome - unresponsive, loss of reflexes, pupils nonreactive and dilated, profound hypotension, bradycardia, respiratory failure, anuria, hypothermia, mottled and cyanotic skin, metabolic acidosis, hypoglycemia, increase in serum lactate levels Read the following case scenario and answer the questions using Surviving Sepsis Guidelines ( and your textbook. Do not print out the Guideline- far too many pages. This link will take you to the full guidelines as well as the tables to direct care. The whole guideline essentially describes the evidence based care and the rationale, where the tables are strictly the care recommended. Judd is a previously healthy 26yo, 100kg male admitted after being stabbed in his abdomen in a home robbery. He required emergent surgery to his duodenum in addition to being fluid resuscitated for blood loss. He was extubated on post op day (POD) 1. On POD 2 his JP drain is draining a moderate amount of sero- sanginous drainage, NG tube is to low intermittent suction and draining green bilious fluid. He has absent bowel sounds and his abdomen is distended. Incision is intact with a small amount serous drainage. On POD 3, he is found to be difficult to arouse but responds to commands. His JP drainage is appearing thicker in consistency and his incision is weeping purulent drainage. His respiratory rate is 28, shallow and labored. His urine output is down to 20mL/hr for the last two hours. His skin is warm, dry and flushed. BP 80/50, HR 132, T 35.8, CVP 2, Glucose is 270 and a WBC of 22,000. A culture and sensitivity was sent on his JP drainage and incision and indicated gram- negative bacilli. 4. What is the definition of sepsis? Sepsis is a systemic inflammatory response to a documented or suspected infection 5. What is the definition of severe sepsis? Severe sepsis is sepsis complicated by organ dysfunction and hypoperfusion. 6. Which does he qualify for and why? Based on Judd s presenting signs and symptoms and the diagnostic criteria determined by the Surviving Sepsis Campaign, Judd has sepsis because he is positive for arterial hypotension with a systolic blood pressure less than 90, HR >90, hypothermia with a temperature less than 36, hyperglycemia with a serum glucose >140, leukocytosis with a WBC count >12,000, and acute oliguria having a urine output less than 50mL/hour.

3 7. What are the goals of initial resuscitation during the first 6 hours for Judd? CVP 8-12 mmhg MAP >65 mmhg Urine output >/= 0.5mL/kg/hr Central venous or mixed venous O2- saturation 70% or 65% respectively In pt s w/ elevated lactate levels, normalized lactate levels 8. What is the significance of lactate or lactic acid (what can it tell us)? What is a normal value? Hypoperfusion causes cells to go into anaerobic metabolism, releasing lactic acid and because liver function is impaired, it is unable to properly filter it out. A normal value is: mmol/l 9. By attempting to meet these early goal- directed therapy goals how much reduction in 28- day mortality as we possibly giving to this patient? (you will need to review the guidelines for this) A 17.7% absolute reduction in 28- day mortality rate if early goal- directed therapy is initiated 10. What is the possible mortality if both hypotension and a lactate > 4mmol are present? Approximately 46% 11. What are the recommendations about drawing blood cultures when sepsis is suspected? Obtain 2 sets of blood cultures before antimocrobial therapy, 1 of them being drawn percutaneously and 1 drawn through each vascular access device, unless it was accessed in the last 24 hours The Surviving Sepsis Campaign has created bundles - groups of interventions with evidence to support improved outcomes when completed together. 12. Within the first 3 hours of Judd s care, what should be our priorities based on these bundles? (page 591) Measure lactate level Obtain blood cultures prior to administration of antibiotics Administer broad spectrum antibiotics Administer 30 ml/kg crystalloid for hypotension or lactate >/= 4 mmol/l

4 4 Four hours later Judd s condition deteriorates dramatically. Antibiotics had been started after drawing blood cultures and he had received 3 liters of NS. He was re- intubated for potential symptoms of ARDS and sedated. His VS are: HR 140, RR 14, BP 70/52, Temp 35.8, CVP 8. ABG: ph 7.14, CO2 49, PO2 46, HCO3 12. Saturations 85%. Lactate 3. SVO2 55%. 13. What should be completed next according to the bundle? Administer vasopressors to maintain a MAP >/= 65 mmhg 14. Identify three reasons Norepinephrine is recommended over Dopamine to increase the BP in severe sepsis (will need to refer to guideline rationale). NE increases MAP with little changes in heart rate NE is more potent than dopamine and may be more effect at reversing hypotension in patients with septic shock Dopamine causes more tachycardia and may be more arrhythmogenic than NE, it also influences the endocrine response and has immunosuppressive effects 15. Why would his SVO 2 be low? (Refer to Lewis text for this answer) Because he is in a state of metabolic acidosis, his oxygen consumption goes up, thus decreasing his SVO2 16. When should IV hydrocortisone be used to treat adult septic shock patients? IV hydrocortisone should only be used if fluid resuscitation and vasopressor are unable to restore hemodynamic stability 17. Because ARDS is likely with Judd, what standards should be maintained for the following? a. Tidal Volume: 6 ml/kg b. PEEP: >5 cmh20 c. HOB: prone 18. Briefly describe other supportive treatment of severe sepsis (do not copy all the interventions, use bullet points to identify key points). Administer blood products blood glucose control, administer insulin per protocol CRRT DVT prophylaxis: compression devices, pharmacological interventions (heparin, lovanox, etc) stress ulcer prophylaxis (H2- blocker, PPI s)

5 oral or enteral feedings as tolerated, supplement as needed 19. Under stress ulcer prophylaxis what is defined as bleeding risk factors? (p. 611) Does Judd qualify? Coagulopathy, on mechanical ventilation for at least 48 hours, or possibly hypotension I am uncertain of Judd s coagulation labs, though he does have hypotension which could put him at risk for bleeding