Sepsis Flashcards
1
Q
Chest Tubes - purpose of seal chamber**
A
with chest tube (20ml) water seal is what keep air from going back into the lungs (pleural cavity) – so most important part of chest tube
2
Q
chest tube and pneumothorax
A
- if pneumnothorax will see bubbling in the water seal chamber, will also see a little floatation
- don’t clamp chest tube while pt has pneumothorax
- if come in and don’t see bubbling then listen to lung sounds and should hear bilateral breath sounds
- can clamp it if lung is expanded for small amount of time to see how they do but watch carefully
3
Q
chest tube components:
A
- Water seal 2. Drainage 3. Suction
4
Q
chest tube dressing
A
baseline gauze – foam top
5
Q
Thoracotomy: *
A
surgical opening into thoracic cavity
6
Q
Thoracostomy: *
A
incision made into chest wall to provide opening for purpose of drainage in order to put in a chest tube
7
Q
Laparotomy: *
A
surgical incision into peritoneal cavity
• Exploratory – trauma, bleed, infection
8
Q
Lacerated:*
A
torn, jagged
9
Q
Ligated: *
A
to tie off a blood vessel or duct with suture or wire
10
Q
Peritoneum: *
A
extensive serous membrane that lines abdominal wall of body; coverscontained viscera
• Semipermiable
• GI tract surrounded by blood vessels
11
Q
Thoracentesis –
A
placing needle into the thoracic cavity
12
Q
MAST
A
Medical antishock trousers, pressurized, trying to get output back to brain
13
Q
Pulmonary artery (swan guanz) put in bc
A
it will help to see volume in left end diastolic volume in ventricle
• Filling pressure – care bc that amount of pressure to be ejected when ventricle contracts
14
Q
when give vasopressor make sure
A
pt has volume first
15
Q
Oxyhemoglobin shift in sepsis
A
to the right – loose bond
16
Q
Warm, dry flushed skin in sepsis **
A
early sepsis vasodilation, bacteria in the blood produce toxins that cause vasodilation or lose of tone of vessels
17
Q
Consider infection if:
A
- Sputum specimen has 25 or greater WBCs
- Urinalysis shows greater than 10-15 WBCs = infection
- Positive wound or line culture
- Positive blood cultures
18
Q
Infection vs Bacteremia
A
- Infection: invasion of body with organisms
* Bacteremia: bacteria in the blood
19
Q
SIRS
A
body’s response to an insult that results in activation of the immune response
• Systemic inflammatory response syndrome
20
Q
SIRS as 2 or more: **
A
- Temp >100.4 or < 96.8 some pts won’t be able to have fever bc so immocompromised
- HR > 90 beats/min
- RR > 20 breaths/min
- PaCO2 < 32 mmHg respiratory alkalosis
- WBC > 12,000 or 10% bands
- Hyperglycemia
21
Q
Causes of SIRS: **
A
Infection is certainly a trigger BUT ALSO NON-infection causes: • Trauma • Burns • Myocardial infarction • Pancreatitis • Note: it is possible for a patient to have SIRS without having sepsis *
22
Q
Sepsis**
A
infection + 2 ≥ SIRS criteria
• Sometimes the source of infection cannot be identified: called “sterile sepsis” – cannot identify pathogen
• Its hard to detect fungal/viral infections
23
Q
Severe Sepsis**
A
- infection 2 + ≥ SIRS criteria + 1 ≥ organ dysfunction
• Common organs: kidney or lungs, hepatic dysfunction
• Mr. S is in septic shock
24
Q
Septic Shock **
A
severe sepsis + hypotension despite IVF and vasopressors; presence of lactic acidosis, oliguria, mental status changes
25
MODS*
Multi Organ Dysfunction Syndrome (2 or more failing organs)
26
Septic Shock info
* Global hypotension: peripheral vascular failure/vasodilation, decreased SVR, increased HR (possible high CO, early)
* Leads to hypoperfusion and low oxygenation of vital organs and tissues; changes in microcirculation: leaky capillary membranes, maldistribution of blood and fluids, cellular dysfunction
* Blood going to pool in vessels so tissues not getting good O2 and nutrients leads to organ hypoperfusion, so blood sitting in tissue but not being delivered to tissues
* By the time we see clinical s/s that the patient has severe sepsis, usually several body organs are already affected
27
Intrinsic Factors (who is at risk)*
• Age: most vulnerable – elderly, newborns
#1 cause of sepsis in elderly is urosepsis (UTI leads to this)
• Coexisting disease: diabetes, COPD, cancer, HIV, immunocompromised
• Malnutrition
28
Extrensic factors (who is at risk)*
* Invasive devices: central lines, foley catheters, ETT’s
* Drug therapy
* Surgical wounds
* Invasive diagnostic procedures
* Immunosuppressive Rx
* Infected “hidden” organs: kidneys, bowel, liver, gallbladder, pancreas
29
Gram-negative bacteria:*
Escherichia coli, Klebsiella, Enterobacter, Serratia, Pseudomonas aeruginosa, Bacteriodides, Proteus
• Produce exdotoxins that stimulate production of inflammatory mediators (cytokines) interleukins
• These bacteria are known as pyrogenic because they stimulate fever, inflammatory process
30
Gram-positive bacteria:*
staphylococcus aureus, Staphlyococcus epidermidits, Streptococcus pyrogenes, Listeria, pneumococcal pathogens
• See text: p. 991 – (“gm + are responsible for more than ½ of septic cases”)
• Produce exotonxins – more vicious than endotoxins
• Viruses
• Fungus
31
THE BIG THREE PROBLEMS OF SEPSIS:*
1. Exaggerated inflammatory response
2. Endothelial dysfunction – leaky capillaries
3. Coagulation dysfunction
32
Bacteria entering body are seen as a foreign substances or
ANTIGENS. Body responds by making ANTIBODIES that link with antigen, forming antigen/antibody complex.
33
Bacteria also release Endotoxins, triggering:
Leukocyte migration to site of infection
Neutrophils – 1st responders that release oxygen cadicals to destroy the antigen (bacteria)
Monocytes/macrophages-2nd responders that release inflammatory mediators:
• Interleukin – 1 (1L-1), Cytokines
• Tumor necrosis factor (TNF)
• Platelet activating factor (PAF)
• Tissue Necrosis Factor
• Myocardial depressant factor
34
Septic Shock early signs*
* Massive vasodilation
* ↑ temp
* ↑ RR
* respiratory alkalosis
* normal - ↓ BP (due to >CO and vasodailation)
* bounding to pull pulses
* widened pulse pressure
* ↓ CVP
* ↓ PAP
* ↓ PWP
* ↓ SVR (8)
* clear or congested lung sound depending on dx
* ↓ UO
* warm flushed skin
* ↓ or ↑ WBC
* + BC
* ↑ lactate
35
Septic Shock late signs*
* ↑ HR
* ↑ RR and hypoxemia
* ↓ BP (MAP) (SBP < 90)
* ↓ LOC obtunded
* weak pulses
* narrow pulse pressure
* ↑ CVP
* ↑ PAP
* ↑ PWP
* ↑ SVR (<600)
* ↓ CO/CI
* clear or congested lung sound depending on dx
* needs mechanical ventilation
* ↓ UO
* cold, mottled skin
* respiratory alkalosis/ metabolic acidosis
36
The release of these inflammatory mediators contribute to septic shock.
```
Interleukin (1L-1)
• Fever
• Vasodilation
• Hypotension
• Edema
• > WBC
Tumor necrosis factor (TNF)
Cytokines
```
37
Result of Mediators of Inflammatory Response
• Massive Vasodilation: ↓ SVR, ↓ preload, ↓ afterload
Vessels lose ability to respond to SNS
• Sluggish Blood Flow: increased blood viscosity, microemboli develop
• Leaky capillary membrane: 3rd spacing, edema in lungs (acute lung injury), around heart, in skin
• Myocardial Depression
38
Vascular endothelium regulates:
* Blood vessel tone
* Vascular permeability
* Coagulation
* WBC and platelet activity
* Phagocytosis of bacteria
39
Tissue Factor
* With vessel damage, Tissue Factor that normally is contained in the vessel is now released
* Tissue Factor activates abnormal clotting – massive clot production through activation of Hageman Factor (factor XII)
40
clotting overproduction
* Hageman factor stimulates “clotting cascade” resulting in Thrombin formation
* Thrombin stimulates fribrin production
* Fibrin: a sticky weblike material that traps platelets, RBC’s WBC’s, forming a Fibrin Clot
* Clots become trapped in capillaries, blocking oxygen and blood flow leading to death of tissue
* 1st see petechiae then eventually see loss of digits (black toes)
41
COAGULOPATHY
* Inflammatory mediators also activate the clotting cascade
* All clotting factors are eventually used up
* “Micro-clots” dispersed everywhere
* Leads to ischemic organs/necrosis
* Increased thrombin production attracts platelets, resulting in thrombocytiopenia
* Activation of fibrinogen, Fibrin split products to break down clots
* Inhibition of activated Protein C (a substance that blocks microvascular coagulation)
* Now see bleeding all over the place
* Now will see ↑ in D-dimers
42
Signs related to microthrombi
```
Neuro
• Stroke
Pulmonary
• RF
• PE
Heart
• MI, angina
• Dysrhythmias
GI
• Liver ischemia
• Bowel infarct
GU
• Renal failure
```
43
From clotting to bleeding
* Under normal circumstances, Fibrin Spilt Products are “cleared” by Reticuloenothelial System. In sepsis, the system is overwhelmed
* Fibrin Split Products remain in circulation
* Fibrin Split Products have an ANTICOAGULANT effect
* INCREASED BLEEDING EVERYWHERE
* DISSEMINATED INTRAVASCULAR COAGULATION (DIC) petechiae
44
Clinical Symptoms related to hemorrhage
* Bleeding from gums, venipunctures, surgical sites
* Hemoptysis
* Heamturia
* Abdominal hemorrhage
* Subarachoid hemorrhage
45
expected lab results
* ↑ Prothrombin Time
* ↑ Partial Thromboplastin Time
* ↑ Fibrin Degradation Products
* ↑ D-dimers
46
Treatment of DIC**
DISSEMINATED INTRAVASCULAR COAGULATION *
need to stop the clotting – having over clotting problems, use heprin
• elimination of underlying pathology
• Restoring hemostasis
• Maintaining organ function
• Heprin
• Replacement therapy (fluids, platelets, FFP)
47
Compensation*
High cardiac output shock
• Early s/s:
* Fever
* Warm, flushed skin
* Bounding pulses
* Widened pulse pressure
* Tachycardia, tachypnea
* Altered LOC
48
Decompensation *
Low cardiac output shock
• Late s/s:
* Hypotension
* Weak pulses
* < cap refilling
* skin mottling
* < UO
* edema/ + fluid balance
* > BS (>120mg/dl is DM)
* Altered LOC
49
Role of nurse
key to prevention
• HOB at > 30 degrees elevation
• Oral care
• Aggressive mobility plan
• Early enteral feeding – so gut doesn’t sit and become susceptible to a paralytic illeus
• Reduction on ventilator circuit changes
50
Primary goal
```
Remove the cause
Maintain tissue/organ perfusion (blood flow)/ cellular oxygenation by:
• Optimizing volume status
• Optimizing BP
• Optimizing CO
```
51
Treatment
* IVF, Levophed
* Blood cultures
* Sputum culture
* Intubated, high FIO2
* CVL and arterial line
52
Xigris: Drotrecogin Alfa (x)
```
(Activated Protein C)
• First approved cogin
• Inhibits coagulation
• Promotes fibrinolysis
• Decreases inflammatory response
• Now off market (2012)
• Contraind: bleeding
• Side effect: bleeding
• 24 mg/kg/hr for 96 hrs
• effects gone within 2 hrs after D/C
• cone bottle lasts about 15 hours
• costs $12,000/bottle
• Xigris has anti-coagulant, anti-inflammatory, and fibrinolytic properties
• It reduces IL-1 and IL-6, TNF, and other proinflammatory cytokines
• (sepsis depletes levels of protein C)
• Xigiris inhibits factors Va and Viiia, inhibiting trombotic effect
• Inhibits TNF production by monocytes, blocking leukocyte adhesion
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