UNIT 3: Care Of A Septic Patient Flashcards
What should we know about CBC lab values across the SIRS & Sepsis specturm?
- Hgb/Hct
- Females 12-16 g/dl, 37-47%
- Males: 14-18g/dl, 42%-52%
- WBC: 5,000-10,000/Ul
- **bands- if this number is more than 10% it shows that the blood has a lot of immature WBCs circulating =shift to the left
- Platelet: 150,000-400,000/ul if under 100,000 =thrombocytopenia
What should we know about CMP lab values across SIRS & Sepsis spectrum?
- Albumin: 3.4-5.4 g/dl
- Total protien 6.0 to 8.3 g/dl
- BUN & CR
- BUN normal level 6 to 20mg/dL
- Cr normal level is 0.6 to 1.3 mg/dl
- Measures kidney function - Electrolytes
- Soidum 135-145
- K+: 3.5-5.5
- Glucose 70-110g/dL
- Liver
- ALT 5-40 u/L
- AST 7-56 u/L
- Total bilirubin 0.1 to 1.2 mg/dl
What should we know about ABG lab values across the SIRS & Sepsis specturm?
- PH: 7.34-7.45
- Pa02: 80-100
- Paco2: 35-45
- Hco3: 22-26
- O2 sats 95%
What should we know about procalcitonin levels across the SIRS & Sepsis spectrum?
Procalcitonin: less than 0.1mg/dl
1. Increases when there is an infection present
2. Rises within 2-4 hours of inflammation
3. If present, can help identify tx methods
What do we need to know about lactate levels in the SIRS and sepsis spectrum
Lactate (lactic acid) less than 1.0 mmol/l
1. excess production from tissue hypoperfusion (anaerobic metabolism)
2. Elevated levels (hyperlactemia) have a strong association with high mortality rates
3. Lactate serves as metabolic feul for the heart and brain when the body is stressed which correlates with illness severity
What should we know about PT lab values across the SIRS and Sepsis spectrum?
PT (prothrombin time) 11-12.5 seconds
1. Thrombin time reflects the time to clot
2. aPTT is more senstive to monitor heparin therapy
What should we know about CRP (c reactive protein) in the SIRS & Sepsis specturm?
CRP (c reactive protien) less than 10mg/l
1. Measures inflammation
What do we need to know about the CPK (creatine phosphokinase) in the SIRS & sepsis specturm?
Creatine phosphokinase (CPK) or creatine kinase (CK): 26-192 u/l for females and 39-308 U/L males
1. Elevation are related to injury (inflammation) or stress on muscle tissue, the heart or the brain
2. When muscles are damaged, CPK is rereleased into the bloodstream. Typically seen in MI
What happens when inflammation occurs in the body?
There is an activation of macrophages, neutrophils, platelets to the area which causes the endothelium (lining of the vessels) to release cytokins which activate the inflammatory pathways.
If the bands are elevated in a serum blood draw what is this called?
Shift to left. This means that there are young/immature white blood cells present commonly showing that there is either an infection or inflammation present and that the bone marrow is producing more WBCs and releasing them into the blood before they are full mature
Whats happening in SIRS?
- Chemical messengers release widespread histamine
- Widespread seperation of endothelial cells = vasodilation
- Increased blood flow = need for greater CO= TACHYCARDIA
- TACHYCARDY = increased need for o2= TACHYPNEA =HYPOCAPNIA
- Body reads widespread WAR= LEUKOCYTOSIS initally and then as the WBC are decreased = leukopenia = increased production = increased immature wbcs in blood (bands)= shift to the left
- Body reads WAR= immune response stimulated = “thermostat” of hypothalmus altered= hyperthermia (proper response) or hypothermai (improper response)
What causes systemic inflammatory response syndrome (SIRS)?
- Caused by stressors that are either infectious or noninfectious that cause acute inflammation
SIRS defined by the presence of 2 or more of the following?
MUST KNOW
- Temp greater than or equal to 100.5 (38c) or 96.8(36c)
- Heart reate: greater than or equal to 90
- Resp. Rate greater than or equal to 20bpm or paCo2 less than or equal to 32
- WBC count greater than 12,000 or less than or equal to 4,000 or more than 10& immature bands
What is the nursing managment of SIRS?
- Maintain tissue oxygenation (BIGGEST THING)
- Monitor labs: hemoglobin greater than 7
- Maintain room to encourage sleep (cluster car, low stem)d
- Administer sedation as ordered
- Prevent & treat infection
- Advocate for removal of removal of times
- Urinary caths
- CVL
- Mobility (increases circulation and fluid moving to different places but only in the beginning)
- Encourage mobility by active ROM (walking)
- Passive ROM
- Nutritional and metabolic support
- Start within 24 hours of admission
- Enteral feeding best (tube feeding NGT, OGT)
- Parenteral (IV) may be needed if enteral contraindicated
What is our treatment for SIRS?
Identify and tx the primary cause
1. Infectious:
- Bacterial, fungal, viral
2. Non-infectious
- control symptoms
- dehydration: give fluids
- Autoimmune disorder: RA (give RA meds), DM (control glucose)
Infection control
1. Broad spectrum antibiotics (levofloxacin, piperacillin/tazobactam, ceftriaxone, meropenem, cefepime)
2. Narrow spectrum antibiotics (vancomycin)
3. antivirals (oseltamvir: tamiflu, interferon, acyclovir)
4. antifungals (amphotericin, nystatin)
Inflammatory control
1. Glucocorticoids (hydrocortisone, dexamathasone, methylprednisolone, prenidosne)
2. Antipyretics
Glucose control
1. Maintain less than 180mg/dl
2. Scheduled insulin or insulin drip
What is sepsis?
- It is the body’s response to an infection that has moved from the original starting point (pneumonia in the lungs or cut on the leg) and spread through the bloodstream to all parts of the body
- Remember sepsis begins with a systemic inflammatory response which can lead to widespread inflammation and clotting
- Inflammation and coagulation are closely linked
What are risk factors that contribute to sepsis?
- Invasive devices/lines
- Extremes of age (elderly/very young)
- Malignancies
- Burns
- AIDS
- DM
- Substance abuse
- Wounds
- Immunosuppresive therapy
How is inflammation and coagulation closely linked?
inflammation> coagulation pathways forms thrombin (clots)> tiny clots (microthrombi)> blocks blood flow to organs> hypoxia or hypoperfusion to organs> eventually fibrinolysis occurs (breakdown of clots) but can use up all fibrin available, so they have clots all over
when the patient runs out of clotting facors, they lose the ability to clot, and they can bleed out
What is “SOFA”
- Scoring system for sepsis to identify severity, higher the score, the hyper the risk for septic shock and dealth
- Changes in 2 or more of the ares along with an infection = septicemia
- Systems include cardiac, resp, neuro, kidney, liver, hematologic
What signs are clinically significant in sepsis?
- Pa02/FiO2
- 300-500=normal
- 200-300: acute lung injury
- <200 significant lung injury
- Hypotension or use of vasopressors
- Systolic <90, dialstolic <60
- Map <70mmgh
- 1,2 or 3 vasopressors
- (decreased platelets) Thrombocytopenia <150,000ul
- Decreased GCS <14
- Bilirubin >1.2
- Creatinine > 1.2mg/dl or urine output (oliguria)<500ml/day
What is our treatment for sepsis?
- Administer crystalloid bolus for hypotension and/or lactate >2
- 30mL/kg
- Administer as quickly as the patient can tolerate
- Max of 3 hours for sepsis
- Max of 1 hour for septic shock
- Blood cultures
- 2 different sites
- takes time for cultures to grow, usually several days
- Antibiotics quickly but within 3 hours
- Recommend antibiotics within 1 hour for septic shock
- Continue antibiotic therapy until WBC <10,000
- Measure lactate level
- Repeate if lactate is greater than or equal to 2
- Vasopressors if not responsive to fluid resuscitation
- 1st line- Norepinephrine then vasopressin and then dopamine
What is our nursing managment of sepsis?
- assess perfusion & oxygenation
- Early identification of SIRS
- Monitor vital signs for trends
- Assess need for fluid resuscitation
- Passive leg raises
- Provides internal bolus to patient 450mL
- If BP increases, patient is responsive and needs fluids
- Monitor effectiveness of fluid resuscitation
- Monitor i/o & daily weight
- Monitor labs
How can we know if our fluid resuscitation in our sepsis managment has been effective?
fluid responsiveness is determined by clinical assessment
1. Vital signs- increase bp
2. cap refil 2-3 seconds
3. skin temp warm
4. urine output >0.5 ml/kg/hr
5. Central venous pressure (CVP) 8-12mmHG
6. MAP greater than 65
What is the criteria for Septic shock?
- SIRS plus a confirmed infection
- Map less than 65MMHG
- Serum lactate greater than or equal to 2 mmol/l
- vassopressors
- Organ dysfunction
Septic shock Summary
Dont have to know all the detail just bolded
**1. Confirmed infection systemically
**
- WBC recruitment
**2. Massive vasodilation
**
- Increased vessel diameter & permeability
- Decreases systemic vascular resistence (SVR)—>decrease in blood pressure
- Initally increased CO to compensate for decreased SVR
- Continual feedback causes decreased CO
- WARM skin initally but as progresses will become cool
3. Damage to vessels systemically causing coagulation factors to clot
- Eventually clotting factors used up
- Causing disseminated intravascular coagulopathy (DIC)
4. Hypoperfusion = organs not recieving oxygen and anaerobic metabolism occurs
- lactic acid produced and levels begin to rise rapidly
5. Respiratory blood vessels damaged
- Acute resp. distress syndrome (ARDS)
- Severe hypoxemia
- Need to be mechanically ventilated
How do we manage septic shock?
- Assessments- vital signs
- Cardiac- SBP less than 90 or MAP less than 65
- Resp. Failure and need for mechanical ventilation
- Monitor diagnostics
- Blood cultures
** - Lactate (Lactic ACID)- drawn put on ice and sent immediately to lab. Redone if equal to or more than 2 mmo/l** - ABG (Pao2<60)
- Blood cultures
- Organ specific labs
- Kidneys: Cr more than 2.0, or urine output less than 0.5ml/kg/hr
- Liver: Bilirubin more than 2mg/dL
- Hematology: Platelets less than 100k, INR more than 1.5 or PTT more than 60 seconds, Inflammatory markers: C-reactive protien (CRP) & Erythrocyte Sedimentation rate
How do we treat septic shock?
Maintain perfersion
1. Fluid resuscitation
- 30mL/kg is goal
- Add vasopressors if fluid resuscitation is not effective
Maintain Oxygenation
1. Maintain Pao2 of more than 75, prefer 80
2. Monitor lactate levels to determine hypoperfusion
Control infection
1. Broad spectrum antibiotics
- Can narrow down once culture comes back.
What is DIC?
It occurs when there is tissue damage or endothelial injury which triggers clotting in the body (microvascular thrombi) everywhere in the body. The body tries to break down these clots by releasing fibrinolytic mediators. Chaos occurs
Clots are forming- the body is trying to break down clots resulting in consumption of clotting factors and therefore the bodies begins to lose its ability to clot and bleeding occurs.
What should we know about vasopressors and there role in the tx of shock? Which vassopressors will we see?
Used if fluid resuscitation is not effective in managing septic shock
1. Norepinephrine, vasopressin, phenlyephrine, dopamine
2. Vasocontrictors may decrease coronary artery perfusion so montior for chest pain or pressure
3. Used to increase blood pressure due to decreased systemic vascular resistance (SVR)
What are the inital signs of DIC?
Initally excessive clotting that can lasts hours to weeks
1. Ischemic toes, fingers & or tip of the nose
This may lead to
1. THrombosis
2. Gangrene
3. Altered LOC, CVA
4. SOB,PE
5. Bowel obstruction/infarction
6. Acute renal failure
What are later signs of DIC?
After inital symptoms progress it leads to excessive bleeding
1. Bleeding from various sites
2. Petechiae
3. Hematuria
4. Oozing from IV sites
5. GI bleeds
6. Oozing gums
More hypovolemic symptoms
What lab values are important too look at if you suspect your patient is in DIC and will they be increased or decreased?
MUST KNOW
- Decreased Fibrinogen
- Decreased platelet
- Increased PTT & PT
- Increased D-dimer
It takes fibrinogen and platelets to clot so as your patient progresses in DIC this is why you have decreased values.
D-Dimer is increased when your body is trying break down clots. Also indicates that there is clotting happening.
What is our volume and/or DIC treatment
- Blood or blood product transfusion
- Requires physican order and patient written consent for the prodect
What are the different types of blood products?
- Plasma- filtered portion that provides volume, coagulation factors, and other protiens
- Platelets- small fragments (thrombocytes) that control bleeding
- Cryoprecipitate- concentrated levels of fibrinogen and clotting factors from multiple donors
- RBCs
- Contain hemaglobin but NOOOO clotting factors
- Replaces volume and o2 carrying components
- must use blood tubing with filter and prime with NS
- must be crossmatched
- Albumin- large protien to pull fluid back into vessels and increases intravascular volume
What must you get prior to admin blood products besides concent?
Baseline vitals
What do you do if you believe your patient is having an adverse reaction to blood products?
- Stop the infusion
- Notify the MD
- disconnect the tubing.
- DO NOT FLUSH LINE
What is MODS?
Progressive compensation that leads to severe organ dysfunciton and eventually failure and dealth
What are signs of pulmonary dysfunction?
- Tachypenea-1st organ to initiating MODS cascade
- Dyspnea
- Shallow breathing
- Hypoxemia
- Crackels
- ABG <70 paO2 or >50 Paco2
- Pao2/fiO2 <200
- Resp failure with high fio2
- Mechanical vent
What are signs of cardiovascular dysfunction?
- Tachycardia
- Hypotension
- Cap refil greater than 4
- Skin mottling
- Cool skin
- Weak pulse
- Map lower than 65
- Low SVR
- Dysrhythmias r/t electroltes like Hyperkalemia (peaked twaves)
- BP <90/60 or a decrease more than 40 points from baseline
What are signs of neurological dysfunciton?
- Confusion/delirum
- headache
- agitiation
- lethargic
- seizures
- no cough/gag reflex
- slow or no pupil response
- pupils mid-position and dilated (4-9mm)
- GCS <8
What are signs of renal dysfunction?
- Oliguria leading to possible anuria
- Fluid retention
- Urine output less than 0.5ml/kg/hr
- Hyperkalemia more than 5.5
- Protienuria
- Creatinine greater than 1.2
- Hematuria
What are s/s of hepatic dysfunciton?
- Jaundice
- confusion
- edema
- fatigue
- nausea
- upper abdominal pain
- coagulation disorders
- hyperbilrubinemia greater than 2mg/dL
- Hyper ammoonemia
- Hyperalbuminemia less than 2g/dl
- Elevated AST ALT
- Hepatic Encephalopathy
What are signs of gi dysfunciton?
- Abomdinal pain
- distention
- hypoactive bowel sounds
- no bowel sounds
- tarry stool (upper bleed)
- Bright right stool (lower bleed)
- Peristalsis leading to ileus
- Permeability of GI tract
- Bacterial translocation
What are signs of endocrine dysfunciton?
- Hyperglycemia
- Hot & dry “Sugar high”
- Thirsty w/poluria, irritable, stomache pain, dry mouth
- Hypoglycemia
- Cold and clammy “need some candY”
- Lethargic, pallor, hungry
- Dcreased wound healing
What are some signs of hematologic and metabolic dysfunciton in MODS
- Thrombocytopenia
- Platelet count less than 100k
- Coagulopathy
- Decreased fibrinogen
- INR more than 1.5 or PTT more than 60 seconds
- Increased d-dimer
- Lactate
- more than 2 mmol/L
- Metabolic acidosis
How is MODS managed?
- Provide hemodynamic monitoring
- maintain strict I&O/daily weights
- monitor labs closely
- Assess central lines daily and change dressing PRN
- Assist with agressive pulmonary managment
- Ambulation or passive ROM
- TCDB
- Oral care
How do we treat MODS
- Prevention/treatment of infection
- Remove sources of infection; foley, central lines
- cultures
- antibiotics
- Maintenance of tissue oxygenation
- Increase supply: Fi02, hgb
- Decrease demand: sedation, rest cluster care, maintain normal temp
- Nutritional and metabolic needs
- Enteral nutrition within 24 hours
- glycemic control 140-180mg/dl
What are some pharm. considerations in the treatment of MODS?
- Perfusion- vasopressors, fluids
- CNS: Benzos, opioids, diuretics, steriods
- Blood transfusions (albumin, PRBC)
- Proton pump inhibitors,
- Insulin therpay.
