Module D Sepsis, Septic Shock, and DIC NUR 203. Page 1 of 24

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1 Module D Sepsis, Septic Shock, and DIC NUR 203 Page 1 of 24

2 Shock Patho: a response to poor tissue oxygenation Etiology: Any problem that impairs oxygen delivery to tissues and organs can start the syndrome of shock; if shock progresses the hypoxia can lead to multiple organ dysfunction syndrome (MODS) and death Key Features: Respiratory Neuro Integumentary Kidney respiratory rate Shallow depth of respirations Paco2; PaO2 Cyanosis, especially around lips & nail beds Anxiety Restlessness Thirst Cool to cold Pale to mottled to cyanotic Moist, Clammy Mouth dry; pastelike coating present urine output specific gravity Sugar & acetone present in urine Page 2 of 24

3 Shock Key Features Continued Cardio GI Late Motility Diminished or absent bowel sounds N & V Constipation CO Pulse Rate Thready pulse BP Narrowed Pulse Pressure Postural Hypotension Low CVP (central venous pressure) Flat neck & hand veins in dependent positions Slow Capillary Refill in nail beds Diminished peripheral pulses central nervous system activity (lethargy to coma) Generalized muscle weakness Diminished or absent deep tendon reflexes Sluggish pupillary response to light Page 3 of 24

4 Tissue and organ perfusion is related to mean arterial pressure (MAP) Factors that influence MAP Total blood volume Cardiac Output Size of vascular bed Sympathetic tone Types of Shock Hypovolemic shock when too little circulating blood vol. causes a MAP O2 Cardiogenic shock when the actual heart muscle is unhealthy & pumping is impaired Distributive shock blood vol. not lost; distribut to interstitial tissues/cannot deliver O2 o Neural induced o Chemical induced Anaphylaxis Sepsis Capillary leak syndrome Obstructive shock caused by problems that impair ability heart muscle to pump effectively Page 4 of 24

5 Hypovolemic Shock Pathophysiology: Loss of blood volume from the vascular space; Decreased MAP; Loss of O2 carrying capacity from loss of circulating RBC s; Decrease in MAP of 5-10 mmhg below baseline is detected by baroreceptors; Compensatory mechanisms can halt the progression; If MAP continues to fall, cell damage can be so severe that the client cannot survive Page 5 of 24

6 Stages of Shock Initial (Early) Early shock; baseline MAP is decreased by less than 10 mm Hg; Compensatory mechanisms are effective at returning MAP to normal perfusion to vital organs; Lactic acid will cause compensation of sympathetic system; vasoconstriction and increased heart rate; Symptoms are so mild it is hard to detect shock Nonprogressive (Compensatory) When MAP 10 to 15 mm Hg from baseline Kidney and baroreceptors sense an ongoing decrease in MAP and trigger the release of renin, ADH, aldosterone, epinephrine and norepinephrine Tissue hypoxia occurs in nonvital organs and in the kidney, it is not enough to cause permanent damage Mild acidosis and hyperkalemia; HR/R Progressive (Intermediate) Sustained decrease in MAP of more than 20 mm Hg from baseline Compensatory mechanisms are functioning but no longer deliver sufficient oxygen, even to vital organs Overall metabolism is anaerobic: moderate acidosis and hyperkalemia; tissue ischemia Life threatening emergency; Cold Refractory (Irreversible) Severe tissue hypoxia with ischemia and necrosis Release of myocardial depressant factor from the pancreas Buildup of toxic metabolites MODS Death MODS Sequence of cell damage caused by the massive release of toxic metabolites and enzymes Metabolites trigger small clots to form Occurs first in the liver, heart, brain, and kidney Damage to the heart muscle is severe (one cause is the release of MDF from ischemic pancreas) Page 6 of 24

7 Shock Assessment Assessment History PE/Clinical manifestations Cardiovascular changes Respiratory changes Kidney/Urinary changes Skin changes CNS changes Skeletal muscle changes Page 7 of 24

8 Shock Psychosocial Assessment Is it necessary to repeat questions to obtain response? Does the response answer the question asked? Does the client have difficulty making word choices? Is the client irritated or upset by the questions? Can the client concentrate on a question long enough to answer appropriately, or is the attention span limited? Laboratory Assessment ph decreased PaO 2 decreased PaCO 2 increased Lactic acid increased Hct increased with fluid shift and dehydration; decreased with hemorrhage Hgb as above K + --increased Page 8 of 24

9 Best Nursing Practice for Shock Ensure airway IV access Administer supplemental oxygen Elevate client s feet Examine client for overt bleeding Apply direct pressure to overt bleeding Administer medications as prescribed Increase the rate of IV fluids DO NOT LEAVE CLIENT Page 9 of 24

10 Nursing Interventions for Shock Nonsurgical management o Oxygen o IV therapy (Crystalloids and Colloids) o Drug therapy: Vasoconstrictors (Dopamine, Norepinephrine, Phenylephrine); Inotropic Agents (Dobutamine, Milirinone Primacor); Agents Enhancing Myocardial Perfusin (Sodium Nitroprusside Nitropress, Nipride) o Monitoring Surgical management Community-based care Page 10 of 24

11 Sepsis and Septic Shock Patho: Infection Sepsis/SIRS sepsis is a condition in which infectious microorganisms have entered the bloodstream. As the numbers of organisms increase, an inflammatory response, known as systemic inflammatory response syndrome (SIRS), is triggered as a result of infection escaping local control. Severe sepsis the progression of sepsis w/an amplified inflammatory response. Septic shock the stage of sepsis and SIRS when multiple organ failure is evident and uncontrolled bleeding occurs. Even w/appropriate intervention, the death rate among patients in this stage of sepsis exceeds 50%. Page 11 of 24

12 Risk Factors for Shock (Nursing Focus on the Older Adult) Hypovolemic Cardiogenic Distributive Obstructive Diuretic therapy; Diminished thirst reflex; Immobility; Use of ASAcontaining products; Use of complimentary therapies such as Ginkgo biloba; Anticoagulant therapy Diabetes mellitus; Presence of cardiomyopathies Diminished immune response; Reduced skin integrity; Presence of cancer; Peripheral neuropathy; Strokes; Institutionalization (hospital or extended care facility); Malnutrition; Anemia Pulmonary HTN; Presence of cancer Page 12 of 24

13 Changes in Selected Parameters during Sepsis and Septic Shock Parameter Normal Early Sepsis Late Sepsis Cardiac Output Normal 3-5 L/min Decreased Increased Normal ml Decreased Increased Septic Shock Greatly Decreased Greatly Decreased Stroke Volume Serum Lactate Normal to (Arterial) < 2 mmol/l slightly increased 2-4 mmol/l > 4 mmol/l Blood Glucose <110 mg/dl mg/dl mg/dl >150 mg/dl Oxygen Saturation % <95% < 85% <80% Serum Creatinine Segmented Neutrophils Band Neutrophils mg/dl (men) mg/dl (women) Normal to slightly increased > 2 mg/dl (men) > 1.4 mg/dl (women) > 3.0 mg/dl (either gender) 55% - 70% of WBC count Increased Decreased < 10% 2%-5% of total Normal to WBC count slightly increased > 10% > 20% Page 13 of 24

14 Left Shift Page 14 of 24

15 Oxygen Therapy Drug Therapy Antibiotics Steroids Insulin Anticoagulants Activated Protein C Blood replacement therapy Interventions Table 39-6 Page 15 of 24

16 DIC (Disseiminated Intravascular Coagulation) The body s blood clotting mechanisms are activated throughout the body instead of being localized to an area of injury Small blood clots form throughout the body, and eventually the blood clotting factors are used up and unavailable to form clots at sites of real tissue injury Bleeding cannot be stopped Also called consumption coagulopathy Page 16 of 24

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19 Clients at Risk for DIC Recent sepsis Injury or trauma Recent surgery or anesthesia Complications of delivery (retained placenta) Leukemia or disseminated cancer Recent transfusion reaction Severe liver disease Page 19 of 24

20 Signs and symptoms of DIC Bleeding from multiple body sites Clot formation Hypotension Bruising and petechiae Tests for DIC Fibrin degradation products increased PT/PTT increased Platelet count decreased Serum fibrinogen decreased D-dimer positive Page 20 of 24

21 DIC Treatments Treat the underlying cause Improve oxygenation, replace fluids, correct electrolyte imbalances, administer vasopressor medications Cryoprecipitate FFP Heparin Activated protein C Nursing Care for DIC Be aware of at risk clients Assess clients thoroughly and frequently for signs and symptoms of DIC Page 21 of 24

22 DIC Things to avoid Procedures/activities that increase ICP Medications that interfere with platelet function Rectal probes/rectal medications IM injections High-pressure suctioning Lemon-glycerin swabs and commercial mouthwash for oral care Dislodging any clots, including those around IV sites Page 22 of 24

23 DIC Things to DO Monitor VS closely, including neuro checks, hemodynamics, abdominal girth, and urine output Monitor amount of external bleeding carefully number of dressings saturated, time to saturate a dressing, pad count in women with vaginal bleeding Low-pressure suctioning Administer oral hygiene carefully use sponge-tipped swabs with baking soda rinses Assess skin q.2h and reposition carefully Use lamb s wool between digits Page 23 of 24

24 DIC Things to DO Continued Auscultate breath sounds q.2h Monitor edema Monitor volume of IVF s, blood products Administer diuretics as prescribed Monitor fibrinogen levels Identify previous coping mechanisms Explain all procedures in terms the client and family can understand Page 24 of 24