Week 15: Impaired Immunity Flashcards
1
Q
Systemic inflammatory response syndrome (SIRS), triggers, criteria needed, what does it advance to?
A
*Generalized inflammation in organs remote from initial insult
*Consider fairly reversible. Problem is that it advances to MONS
Criteria (2 or more needed):
- Fever greater than 38.0 or less than 36
- hr greater than 90
- RR greater than 20
- WBC above 12,000, less than 4,000
- Bands greater than 10%
Triggers
- Mechanical tissue trauma: burns, crush injuries, surgical procedures
- Abscess formation: intra-abdominal, extremities
- Ischemic or necrotic tissue: pancreatitis, vascular disease, MI
- Microbial invasion: Bacteria, viruses, fungi
- Endotoxin release: Gram-negative bacteria
- Global perfusion deficits: Post–cardiac resuscitation, shock states
- Regional perfusion deficits: Distal perfusion deficits
2
Q
Multiple organ dysfunction syndrome (MODS)
A
- failure of two or more organ systems
- Homeostasis cannot be maintained without intervention-Results from SIRS
- SIRS and MODS represent ends of a continuum
- Transition from SIRS to MODS DOES NOT occur in a clear-cut manner
3
Q
Consequences of inflammatory response
A
- Low BF
- Release of mediators
- Direct damage to endothelium
- Hypermetabolism
- Vasodilation leading to dec SVR
- Inc in vascular permeability
- Activation of coagulation cascade
- Inflammation can travel to other organs and cause the same response in other organs
4
Q
SIRS and MODS patho and stages
A
- Organ and metabolic dysfunction
- Hypotension
- Decreased perfusion
- Formation of microemboli
- Redistribution or shunting of blood
Stage 1:
local cytokine relase
Stage 2:
release of cytokines into systemic system
stage 3:
Humoral cascade (clotting cascade being released systemically in multiple organs)
5
Q
SIRS/MODS in respiratory system
A
- Alveolar edema
- Decrease in surfactant
- Increase in shunt
- V/Q mismatch
- End result: ARDS
- 70% will go into MODS, so the VAP protocols are essential
6
Q
Cardiovascular system SIRS/MODS patho
A
- Myocardial depression and massive vasodilation
- decreased CO, decreased preload, increased afterload leading to ischemia to the heart
- Depressed cardiac muscle function
7
Q
Renal system SIRS/MODS patho
A
Acute renal failure
- Hypoperfusion leading to ischemia
- Release of mediators
- Activation of renin–angiotensin– aldosterone system to compensate (which causes vasoconstriction, furthering ischemia)
- Nephrotoxic drugs, especially antibiotics further the insult. Quinolines, Sulfas, Vancomycins
8
Q
GI system SIRS/MODS patho
A
- Motility decreased: Abdominal distention and paralytic ileus
- Decreased perfusion: Risk for ulceration and GI bleeding
- Potential for bacterial translocation
Hypermetabolic state
- Hyperglycemia–hypoglycemia
- Insulin resistance
- Catabolic state
- Liver dysfunction
- Lactic acidosis
9
Q
Hematologic system SIRS/MODS patho
A
- DIC
- Electrolyte imbalances
- Metabolic acidosis
10
Q
SIRS/MODS collaborative care prevention
A
- Prognosis for MODS poor
- Goal: Prevent progression of SIRS to MODS
- Vigilant assessment-ongoing monitoring to detect early signs of deterioration or organ dysfunction-critical
- Prevention and treatment of infection
- Aggressive infection control strategies to dec risk for nosocomial infections
- Once an infection suspected, institute interventions to control source !~
11
Q
SIRS/MODS collaborative care oxygenation
A
Maintain tissue oxygenation
- Dec O2 demand
- Sedation
- Mechanical ventilation (on volume control)
- Paralysis
- Analgesia
- Optimize O2 delivery
- Maintain normal hemoglobin level
- Maintain normal PaO2
- Individualize tidal volumes with PEEP ( don’t want too much volume, can cause barotrauma)
12
Q
Maintenance of tissue oxygenation with SIRS/MODS
A
Maintenance of tissue oxygenation
Enhance CO
- Increase preload or myocardial contractility: dopamine and dobutamine
- Reduce afterload: Nipride or nitro drip,
- Give levofed to cause vasoconstriction: cuts circulation into the periphery increasing SVR and preload
13
Q
SIRS/MODS collaborative care with nutrition
A
- Nutritional and metabolic needs
- Goal of nutritional support: Preserve organ function-total energy expenditure-often inc 1.5 to 2.0 times: need HIGH PROTEIN feed.
- Nutritional and metabolic needs
- Use of enteral route preferred to parenteral nutrition
- Monitor plasma transferrin & prealbumin levels to assess hepatic protein synthesis
14
Q
SIRS/MODS failiing organs
A
Support of failing organs
- ARDS: Aggressive O2 therapy and mechanical ventilation
- DIC: Appropriate blood products
- Renal failure: Continuous renal replacement therapy or dialysis
15
Q
Shock, classifications
A
- Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism
- Imbalance in supply/demand for O2 and nutrients
-
Classification of shock
Cardiogenic:
Hypovolemic:
Distributive:
Obstructive:
16
Q
cardiogenic shock
A
Definition
- Systolic or diastolic dysfunction
- Compromised cardiac output (CO)
Precipitating causes
- Myocardial infarction
- Cardiomyopathy
- Blunt cardiac injury
- Severe systemic or pulmonary hypertension
- Cardiac tamponade
- Myocardial depression from metabolic problems
17
Q
patho of cardiiogenic shock
A
decrease in filling that leads to a decrease in stroke volume. Up to 85% die
CO lesss than 4 or cardiac input of less than 2.5
18
Q
Manifestations of Cardiogenic shock
A
Early manifestations
- Tachycardia; Hypotension
- Narrowed pulse pressure
- ↑ myocardial O2 consumption
Physical examination
- Tachypnea, pulmonary congestion
- Pallor; cool, clammy skin
- Dec capillary refill time
- Anxiety, confusion, agitation
- ↑ in pulmonary artery wedge pressure
- Dec renal perfusion and UO
19
Q
Absolute hypovolemia
A
loss of intravascular fluid volume
- Hemorrhage; GI loss (e.g., vomiting, diarrhea)
- Fistula drainage; Diabetes insipidus
- Hyperglycemia; Diuresis
20
Q
relative hypovolemia
A
- Results when fluid volume moves out of vascular space into extravascular space (e.g., interstitial or intracavitary space)
- Termed third spacing
21
Q
patho of hypocolemic shcok
A
- greater than 40% volume loss is irreversible and there will be permanent damage. Body tries to autoregulate, but can’t past this 40%, causing ischemia and damage to all organs
- Look at H&H, (see an increase with diabetes insipidous or third spacing, otherwise it will go down), look at electrolytes (increase in K+), ABGS, CV o2 sat, watching UO hourly (have to be cathed)
22
Q
clinical manifestations of hypovolemic shock
A
- Anxiety
- Tachypnea
- Inc in CO, heart rate
- Dec in stroke volume, PAWP, urinary output
- If loss is >30%, blood volume is replaced.
23
Q
Distributive shock/neurogenic shock and clinical manifestations
A
- Hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and last up to 6 weeks
- Can occur in response to spinal anesthesia
- Results in massive vasodilation > lead to pooling of blood in vessels
Clinical manifestations
- Hypotension
- Bradycardia
- Temperature dysregulation (resulting in heat loss) (warm skin from vasodilation, then it cools and get hypothermia)
- Dry skin
- Poikilothermia (taking on the temperature of the environment)
24
Q
distributive shock/anaphylactic shock, manifestations, treatment
A
Acute, life-threatening hypersensitivity reaction
- Massive vasodilation; Release of mediators
- ↑ capillary permeability
Clinical manifestations
- Anxiety, confusion, dizziness
- Sense of impending doom; Chest pain
- Incontinence
- Swelling of the lips and tongue, angioedema
- Wheezing, stridor; Flushing, pruritus, urticaria
- Respiratory distress and circulatory failure
Treatment
- A (establish this quick) BCDE
- If you don’t have an epi pen, have them in a position to help with vasodilation, so you want their feet elevated
- Epi (adrenaline) lasts only 20 minutes, then it needs to be repeated (give every 3-5 minutes in hospital until you get a response)
- High flow oxygen is appropriate for these patients (veni mask, face mask)
- IV fluids: Adults 500-1,000, children crisiloid 20ml/kg
- Give steroids and medications to help with allergic reactions (hydrocortisone, chloriphenamine
25
Q
Distributive/Septic shock, clinical manifestations
A
- Sepsis: systemic inflammatory response to documented or suspected infection
- Severe sepsis = Sepsis + Organ dysfunction
- Presence of sepsis with hypotension despite fluid resuscitation
- Presence of tissue perfusion abnormalities
Clinical manifestations
- ↑ coagulation and inflammation
- ↓ fibrinolysis
- Formation of microthrombi
- Obstruction of microvasculature
- Hyperdynamic state: increased CO and decreased SVR
- Tachypnea/hyperventilation
- Temperature dysregulation
- ↓ urine output
- Altered neurologic status
- GI dysfunction
- Respiratory failure common.
26
Q
obstructive shock
A
(pulmonary embolis) Develops when physical obstruction to blood flow occurs with decreased CO
- From restriction to diastolic filling of right ventricle due to compression
- Abdominal compartment syndrome
Patient experience
- Dec CO
- Increased afterload
- Variable left ventricular filling pressures
Rapid assessment and immediate treatment important
27
Q
initial stage of shock
A
- Usually not clinically apparent
- Usually considered reversible
- Metabolism changes from aerobic to anaerobic.
- Lactic acid accumulates -must be removed by blood and broken down by liver.
- Process requires unavailable O2.
- Clinically apparent –Neural, Hormonal &Biochemical compensatory mechanisms
- Attempts aimed to overcome consequences of anaerobic metabolism and maintaining homeostasis.
28
Q
compensatory (or initial?) stage of shock
A
- Baroreceptors in carotid and aortic bodies activate SNS in response to ↓ BP.
- Vasoconstriction while blood to vital organs maintained-
- ↓ blood to kidneys > activates renin– angiotensin system ↑ venous return to heart, CO, BP
- Impaired GI motility- Risk for paralytic ileus
- Cool, clammy skin from blood
- Except septic patient who is warm and flushed
29
Q
complensatory stage
A
- Shunting blood from lungs increases physiologic dead space.
- ↓ arterial O2 levels
- Increase in rate/depth of respirations
- V/Q mismatch
- SNS stimulation increases myocardial O2 demands.
- If perfusion deficit corrected, patient recovers with no residual sequelae
- If deficit not corrected, patient enters progressive stage
30
Q
progressive stage of shock
A
- Begins when compensatory mechanisms fail
- Aggressive interventions to prevent multiple organ dysfunction syndrome (MODS)
- Hallmarks -↓ cellular perfusion & altered capillary permeability
- Leakage of protein into interstitial space
- ↑ systemic interstitial edema
Anasarca
- Fluid leakage affects solid organs and peripheral tissues.
- ↓ blood flow to pulmonary capillaries
Movement of fluid from pulmonary vasculature to interstitium
- Pulmonary edema
- Bronchoconstriction
- ↓ residual capacity
Fluid moves into alveoli
- Edema-Dec surfactant
- Worsening V/Q mismatch
- Tachypnea, Crackles
- Inc work of breathing
CO begins to fall
- Dec peripheral perfusion
- Hypotension
- Weak peripheral pulses
- Ischemia of distal extremities
Myocardial dysfunction results in
- Dysrhythmias
- Ischemia; Myocardial infarction
- End result: complete deterioration of cardiovascular system
Liver fails to metabolize drugs and waste.
- Jaundice; Elevated enzymes
- Loss of immune function
- Risk for DIC and significant bleeding
Mucosal barrier of GI system becomes ischemic
- Ulcers
- Bleeding
- Risk of translocation of bacteria
- Dec ability to absorb nutrients
54
Q
cutaneous anthrax
A
- Accounts for 80% of naturally occurring Anthrax cases
- Enters through openings in skin from abrasions, lacerations
- 20% progress to systemic form if untreated
- Most cases recover
55
Q
anthrax inhalation
A
- Inhalation of spores
- Incubation, 2-3 days (range up to 60 days)
- Spores engulfed by macrophages and transported to mediastinal and peribronchial lymph nodes
- Insidious onset: malaise, low grade fever, nonproductive cough
- Abrupt development of respiratory distress
- Hemorrhagic mediastinitis
- Hematogenous spread
- Meningitis in 50%, usually fatal
59
Q
smallpox characteristics
A
- Febrile Syndrome – occurring 1-4 days prior to rash.
-
Classic Smallpox lesion – deep-seated, firm/hard, round, well-circumscribed; lesion may become umbilicated or confluent.
- Can be mistaken chicken-pox
- Febrile Syndrome – occurring 1-4 days prior to rash.
- Lesion in Same Stage of Development – Evolve from macules → papules → pustules at the same time.
- Centrifugal distribution – First lesion on oral mucosa, face, or forearms.
- lesions on palms and soles
60
Q
smallpox vs. Chickenpox distribution
A
Spares the trunk: Smallpox
Primarily the trunk: chickenpox
