NURSING 203 NOTE TAKING GUIDE Sepsis and Multiple Organ Dysfunction Syndrome 1.

Sepsis and septic shock a. Sepsis is widespread infection. Septic shock the stage of sepsis and SIRS when multiple organ failure is evident and uncontrolled bleeding occurs. Severe hypovolemic shock is present along with hypodynamic cardiac fx. (Both result in hypoperfusion to the tissues). Mortality= >60%. b. Type of distributive shockresults in under-perfusion to the tissues. c. Pts at risk: immunocompromised, very young, very old, people w/o spleen or thymus, invasive procedures (nosocomial infections), pt. In a weakened state (pt. Mouth can be colonized within 6 hours of admission- mouth care is important!) d. Causes: bacterial : gram + or =. Most common = are sudamonis, or e. coli. Most common + are staff A or clostridium. Fungus and virus are less common but can cause sepsis. e. Usual progression-which can >> SIRS Local infection can >>>>>systemic infection

i. STAGE I Sepsis--- SIRS kicked in from burns, MI, or trauma. When SIRS kills the organisms and the bacterial cells dies, endotoxins from within those cells are released into the blood. This can lead to a continueation of SIRS. Sepsis is present when two or more of the following CRITERIA are present: 1. Temp > 100.4 OR lower that 96.8 2. HR > 90 3. RR> 20 or a PCO2 <32 mmHg 4. WBC count of >12,000 or lower than 4,000 or with more than 10% band cells 5. Pts. could be TX on a med-surg floor, but with close monitoring for S & S of worsening. ii. Stage 2 sepsiswhen 2 or more SIRS criteria are present along with a known infection. 1. Pt may get 2nd hit- causes SIRS to go into overdrive w/ release of these mediators (not tested on individual mediators) a. Capillaries become leaky and vessels dilate = increased intersitial fluid= decreased vascular volume and pulmanary edema.

b. Increased plt aggregation (clumping) = decreased perfusion c. This >>> decreased cell nutrients, cell hypoxia and acidosis (lactic acid buildup which kills even more cells) this depressess myocardio contracions 2. Four factors associated with transition from SIRS to MODS a. Failure to control the source of infection or insultit's not the bacteria as much as it is the bodies response to the bacteria that kills the patient. b. Persistent hypoperfusion to the tissues- i.e. prolonged shock, clotting, or leaky vessels. c. Presence of necrotic tissue or absess- wound care! Putting off wound care can increase risk of sepsis. Cleaning will also decrease circulating mediators. d. altered cellular O2 consumption (hypermetabolism)- cells are so sick, that they don't take in o2 normally. Lung injury does occur. Protein calorie malnutrition begins. iii. Stage 3= severe sepsis/ MODS BEGINSPt meets the sepsis criteria and shows one of the S & S of organ failure. Hypermetabolism state continues and auto catabolism begins results in decrease in lean body mass. This affects a lot of muscles including diaphragmatic muscle, cardiac muscle, and intestinal viscera cachexia- emaciated state (end stage=cachexic) S & S OF ORGAN FAILURE: 1. CV a. SBP < 90, HR < 54 or drop from baseline pressure of >40 mm Hg b. MAP <65 (needs to be >40 to perfuse the corinary arteries) c. Poor response to inotropic support (= poor contractility) d. V. tach or V. fib (from hypoxia to the cardiac muscle) 2. Hematologicin association with MODS its DIC a. Platelets < 100,000 (nl = 130,000-400,000) b. Platelets decreased by 50% over 3 days c. Acutely abnormal prothrombin time (nl: 10-13 sec)or partial thromboplastin time (PTT) (nl: 21-35 sec) without anticoagulation therapy (INR > 1.5: PTT >60 seconds. d. Blood cell death3. Hepatic a. Bilirubin level > 2 mg/dl (nl = 0.1-1.0 mg/dL). Hemolysis

b. Alkaline phosphatase level > 250 units per liter (nl = 42-136 units/L. Think Liver or bone if elevated. c. Aspartate aminotransferase ( SGOT) level > 100 Units/ L. ( nl = 8-38 ). liver and heart muscle. Can be elevated 10x's or more. d. Alanine animotransferase level = > 100 u/L. (nl = 10-35) Enzyme in liver helpful in Dxing hepatocellular destruction. e. The underperfused liver: functions poorly in removing toxins & mediators from the body= continuation of SIRS. Can't kill or rid organisms from body so they enter systemic circulation. Endotoxins inhibit protein synthesis in liver= depressed immune system, decreased albumin (3rd spacing), and ascites f. To meet increasing demands of the body ,the liver increases its rate of gluconeogenesis and protein catabolism >> elevated NH 3 (ammonia).

4. Metabolic a. Serum lactate levels > 2 mmol/L . (nl = 0.5-2.0 mmll/L. Mucles.... into pyruvic acid which = cellular energy. 5. Neurologic a. Mental state acutely altered from baseline b. Glasgow Coma Scale score of < 15 6. Pulmonary a. RR> 24 b. SaO2 < 92% with pt on O2 at 6L /min using face mask (avoid using 100% o2 for long periods). Inability to saturate lungs despite O2 is called ARDS. c. Elevated SvO2- represents the amount of o2 in venous blood when it returns to the right atrium. Nl: 60-80. (higher because cells are too sick to take up o2) 7. Renal a. UOP < 0.5 mL/kg/hr despite volume resuscitation b. Increase in CR level over 1.5 mg/dL (normal is 0.51.5) iv. Stage 4septic shock 1. severe sepsis + HoTN 2. doesn't respond to fluid resucitation. 3.high mortality rate

Pathophysiology Microorganism invades the body >>>>>an immune response which provokes activation of mediators. Mediators are released to regulate cellular function when you have minor or major insult. Problem is that one activator stimulates others and their effects are enhanced in this hypermetabolic phase. Initially a hyperdynamic response occurs. High CO, Normal BP, will respond to fluid resuscitation, tachycardia, hyperthermia, warm flush skin, bounding pulse, and increased RR. GI may be compromised, N/V/D, Decreased Bowel sounds, other signs: elevated BS, slight neuoro changes from cerebral hypoxia, Progression: tissues become more underprofused and acidotic. Mechanisms begin to fail and don't respond to Tx. Assess end organ perfusion (UO, Neuro status, stool character, CV status, etc.) Sepsis then can progress to septic shock

2. Management / Nursing Caregoal is to control the initiating event and aggressive care to prevent nosocomials a. blood cultures before antibx. If lactate > 4 mmol/L., give crystalloids. If BP DOESNT RESPONDgive vasopressors (raise BP). See PAGE 1786, Table 67-8 b. Start 2 IVs with large bore needles (14-16ga) c. low dose corticosteroids: 200-300 mg hydrocortisone IV daily in divided doses. d. insulin to keep BS < 150. e. Xigris IV med to decrease thrombotic effects in sepsis & antiinflammatory. s/e.bleed (if pt. Becomes confused, then may be sign of bleeding in brain) f. Other drug therapy like that given for hypovolemic shockPg. 1787, Table 67-9. Goal is to increase CO and restore vascular volume. g. Increase assessment frequency- look for trends! i. Once sepsis is suspected, its crucial to watch closely for S & S of its rapid progression such as: fever or hypothermia Tachycardia Tachypnea Hypotension Decreasing urine output Change in mental status from time of admission Abnormal lab values ii. Initiate nursing interventions while awaiting patient transfer to the ICU. 1. Alert the MD ask for orders for labwork (stat) to start Tx. (ex. ABG's, Blood clx, fibrin split products (DIC), D-dimer

2. Begin O2 administration. (about twice normal) a. Ways to decrease O2 demand i. Promote comfort decreases circulating catecholamine (which vasoconstrict), this includes emotional ii. Decrease anxiety decr. catecholamine iii. Prevent infection decr. Mediators iv. enteral feedings- check placement and residual q 4hr. Turn tube feeding off to reposition. R/F aspiration v. Promote wound healing- decr. mediators vi. Planned rest periods- vital in healing. vii. Treat fever, anxiety, shivering and pain- to decr. Metabolic demands b. Ways to increase O2 supplygoal is PaO2 >80. Avoid 100%. i. Promote ventilation (improve O2 saturation) elevate the HOB. Ask about putting pt. On PEEP (positive end expiratory pressure) ii. Maintain adequate circulating blood volume and transport, administer blood products as ordered. Hemodynamic monitoring to eval and adjust blood o2 content, o2, and other drugs. iii. Maintain airway (improves O2 sat) iv. Promote UOP to prevent FVE(fluid volume excess)- diuretics or fluid restrictions v. Maintain nutritional status decr. Hyperglycemia and liver workload. Prevents skeletal muscle loss. vi. Treat increased WOB (work of breathing)- morphine, o2, hyperoxygenate prior suction -hypervent after suction vii. Maintain tissue perfusion decreases clotting viii. Maintain patent IV lines, admin inotropes as ordered ix. Continuous lateral rotation or?? prone positioning ( studies show that pt. With ARDS do better in prone) c. Fluid resuscitation- of the microcurculation is the 1 st step in maintaining tissue perfusion. Disadvantage is that mediators and bacteria get flushed back into circulation- this is called re-perfusion injury. Adjust preload, afterload and contractility by medications (1786- table 67-8). goal is to have ventral venous pressure at about 15.

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3. Suggest establishing a CVL and begin fluids for circulatory support to restore circulatory volume to increase tissue perfusion. 4. Place a urinary catheter and track output closely. Diuretics amy increase r/t decrease glomerular filtration. Dopamine increases renal perfusion. Document complete and measurable assessments 1. Be specific in describing to oncoming nurse. Trends, amounts, etc. 2. Watch for any changes obvious and non-obvious signs of bleeding (i.e. Abdomen getting bigger, hemocult stools), monitor F&E, look and lab levels, o2 saturatio, ascites can decrease pulmonary excursion (elevate HOB). DIC have both clotting and hemorrhage phase. LOC 3. Remember that some of these immunocompromised pts may not develop Usual S & S of sepsis. Confusion may be 1st sign. 4. Temp. may not be treated until 101+ until then, the pt. Immune system is taking care of things. After 101, the immune system is overwhelmed. Cooling blanket- put sheet between it and pt., turn off when temp= 99 5. Monitor lab values: meds may not be excreted normally so they stay in the body longer, pt. May develop s/e of drugs. Nutritional Supportwithin 48-72 hours from insult 1. If the gut works, use it. Feeding = deification which gets rid of toxins, maintains integrity of the gut. secretes GI hormones = less stress ulcers. 2. Energy expenditure in hypermetabolic phase is 1.5 -2 times normal. 3. Hepatamineenteral feeding, achieves nitrogen retention (will be negative nitrogen balance). Metabolized in muscle, not liver. -Lactulose/ Neomycin (lower ammonia levels) 4. Omega 3 fatty acids + fish oils- enter cell membrane and alter release of inflammatory mediators. Oxepa is an example 5. Daily wt., I & 0 6. DIC- avoid sticks and increased ICP (via cough, sneeze, strain), do neuro checks. Use low pressure when suctioning. 7. Albumin levels and daily wts help determine pts protein needs REVIEW QUESTIONS pg. 1797.