Sepsis Flashcards
Chest Tubes - purpose of seal chamber**
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
chest tube and pneumothorax
- 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
chest tube components:
- Water seal 2. Drainage 3. Suction
chest tube dressing
baseline gauze – foam top
Thoracotomy: *
surgical opening into thoracic cavity
Thoracostomy: *
incision made into chest wall to provide opening for purpose of drainage in order to put in a chest tube
Laparotomy: *
surgical incision into peritoneal cavity
• Exploratory – trauma, bleed, infection
Lacerated:*
torn, jagged
Ligated: *
to tie off a blood vessel or duct with suture or wire
Peritoneum: *
extensive serous membrane that lines abdominal wall of body; coverscontained viscera
• Semipermiable
• GI tract surrounded by blood vessels
Thoracentesis –
placing needle into the thoracic cavity
MAST
Medical antishock trousers, pressurized, trying to get output back to brain
Pulmonary artery (swan guanz) put in bc
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
when give vasopressor make sure
pt has volume first
Oxyhemoglobin shift in sepsis
to the right – loose bond
Warm, dry flushed skin in sepsis **
early sepsis vasodilation, bacteria in the blood produce toxins that cause vasodilation or lose of tone of vessels
Consider infection if:
- Sputum specimen has 25 or greater WBCs
- Urinalysis shows greater than 10-15 WBCs = infection
- Positive wound or line culture
- Positive blood cultures
Infection vs Bacteremia
- Infection: invasion of body with organisms
* Bacteremia: bacteria in the blood
SIRS
body’s response to an insult that results in activation of the immune response
• Systemic inflammatory response syndrome
SIRS as 2 or more: **
- 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
Causes of SIRS: **
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 *
Sepsis**
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
Severe Sepsis**
- infection 2 + ≥ SIRS criteria + 1 ≥ organ dysfunction
• Common organs: kidney or lungs, hepatic dysfunction
• Mr. S is in septic shock
Septic Shock **
severe sepsis + hypotension despite IVF and vasopressors; presence of lactic acidosis, oliguria, mental status changes
MODS*
Multi Organ Dysfunction Syndrome (2 or more failing organs)
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
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
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
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
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
THE BIG THREE PROBLEMS OF SEPSIS:*
- Exaggerated inflammatory response
- Endothelial dysfunction – leaky capillaries
- Coagulation dysfunction
Bacteria entering body are seen as a foreign substances or
ANTIGENS. Body responds by making ANTIBODIES that link with antigen, forming antigen/antibody complex.
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
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
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
The release of these inflammatory mediators contribute to septic shock.
Interleukin (1L-1) • Fever • Vasodilation • Hypotension • Edema • > WBC Tumor necrosis factor (TNF) Cytokines
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
Vascular endothelium regulates:
- Blood vessel tone
- Vascular permeability
- Coagulation
- WBC and platelet activity
- Phagocytosis of bacteria
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)
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)
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
Signs related to microthrombi
Neuro • Stroke Pulmonary • RF • PE Heart • MI, angina • Dysrhythmias GI • Liver ischemia • Bowel infarct GU • Renal failure
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
Clinical Symptoms related to hemorrhage
- Bleeding from gums, venipunctures, surgical sites
- Hemoptysis
- Heamturia
- Abdominal hemorrhage
- Subarachoid hemorrhage
expected lab results
- ↑ Prothrombin Time
- ↑ Partial Thromboplastin Time
- ↑ Fibrin Degradation Products
- ↑ D-dimers
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)
Compensation*
High cardiac output shock
• Early s/s:
- Fever
- Warm, flushed skin
- Bounding pulses
- Widened pulse pressure
- Tachycardia, tachypnea
- Altered LOC
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
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
Primary goal
Remove the cause Maintain tissue/organ perfusion (blood flow)/ cellular oxygenation by: • Optimizing volume status • Optimizing BP • Optimizing CO
Treatment
- IVF, Levophed
- Blood cultures
- Sputum culture
- Intubated, high FIO2
- CVL and arterial line
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
