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Surgery > Burns, Shock, and Sepsis Surgery Module > Flashcards

Burns, Shock, and Sepsis Surgery Module Flashcards

1
Q
  1. Highest risk is ______ years old and 2:1 (gender?) in both injury and death
  2. In children the highest incidence is what?
A
  1. 18-35, male to female

2. scalding injuries from hot drinks or bath

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2
Q 
Burn Management
Pathophysiology 
1. Skin is how many layers?
-what are they?
2. Thickness varies with what?
3. Skin is semipermeable barrier for what?
4. Skin also responsible for what?
A
  1. Skin is 2 layers: Dermis and epidermis
  2. Thickness varies with age
  3. Skin is semi-permeable barrier for evaporative loss
  4. Skin also responsible for control of body temp
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3
Q

Burn Management
Pathophysiology
1. Cellular changes seen in burns? 4

  1. Burn shock with depression of what?
    - what accompanies this?
A
    • Intracellular influx of Na/H2O
    • Extracellular migration of K
    • Disruption of cell membrane function
    • Failure of “sodium pump”
  2. Burn Shock with depression of myocardium
    - metabolic acidosis
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4
Q

Burn Management
Pathophysiology
-Hematologic changes? 3

A
  1. Increase in hematocrit
  2. Increase in blood viscosity
  3. Anemia due to RBC destruction
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5
Q

Burn Management
Pathophysiology
-Local Progressive injury? 3

A
  1. Liberation of vasoactive substances
  2. Disruption of cellular function
  3. Edema formation
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6
Q 
Burn Management
Pathophysiology 
1. Cell damage occurs at temp > what?
2. Due to?
3. What are the three zones that contribute to burn injury? 3
A
  1. 113F
  2. due to denaturation of protein
    • Zone of coagulation
    • Zone of stasis
    • Zone of hyperemia
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7
Q

Describe what happens in the following zones:

  • Zone of coagulation? 1
  • Zone of stasis? 2
  • Zone of hyperemia? 1
A
  1. Zone of coagulation
    Irreversibly destroyed
  2. Zone of stasis
    - Stagnation of microcirculation
    - Can/will extend if not treated appropriately
  3. Zone of hyperemia
    Increase blood flow
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8
Q 
Burn Management
Clinical Features – Burn Size
1. Quantified as what?
2. Rapid method is based on what ?
3. Whats the Rule of 9s?
4. What is the best diagram for burns?
A
  1. Quantified as percentage of body surface area (BSA) burned
  2. Rapid method is based on the area of the back of patient’s hand is approximately 1% of BSA
  3. Rule of 9’s breaks portions of body into multiples of 9 with the perineum being 1%
  4. Lund and Browder burn diagram is best
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9
Q

Burn Management
Clinical Features – Burn Depth
First Degree characteristics? 3

A
  1. Erythema of skin
  2. Possibly minimal surrounding edema
  3. Minimal pain
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10
Q

Burn Management
Clinical Features – Burn Depth
Second degree characteristics? 3

A
  1. Deeper than first degree
  2. Involve partial thickness
  3. Usually much more painful than third degree
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11
Q

Examples of 2nd degree burn? 3

A
  1. deep sunburn,
  2. contact with hot liquids,
  3. flash burns from gasoline flames
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12
Q

How does the skin appear in a 2nd degree burn? 6

A
  1. Red or mottled;
  2. blisters with broken epidermis;
  3. considerable swelling;
  4. wet/weeping surfaces;
  5. painful;
  6. sensitive to the air
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13
Q

Burn Management
Clinical Features – Burn Depth
Third Degree Burns:
1. Damage what? 3

  1. How does the skin appear? 6
A
  1. Damage to all
    - skin layers,
    - subcutaneous tissues, and
    - nerve endings
  2. Skin appears:
    - Pale white or charred appearance,
    - leathery;
    - broken skin with fat exposed;
    - dry surface;
    - painless to pinprick;
    - edema.
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14
Q

Burn Management
Specific Issues

Inhalation injury signs? 4

Be thinking what? 2

Treat? 1

A
  1. Carbon around nose
  2. Burns involving mouth
  3. Significant Resp problems
  4. Fires in enclosed areas
  5. Remember CO exposure
  6. Toxic gases from combustion
  7. Intubate early
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15
Q 
Burn Management
Specific Issues
-Chemical burns 
1. What can cause burns? 2
2. Do not try to do what?
3. Tx?
4. Which burns are more serious and why?
A
  1. Alkali or acids can cause burns
  2. DO NOT TRY TO NEUTRALIZE
  3. “The solution to pollution is dilution” - - IRRIGATE, IRRIGATE, IRRIGATE
  4. Alkali burns are more serious than acid burns because the alkalis penetrate deeper
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16
Q

Burn Management
-Specific Issues
Electrical burns
1. What do we need to remember about this?

  1. Where are we going to find the most damage?
  2. Occult destruction of muscle can cause ___________ which causes the release of myoglobin and can lead to ________________?
A
  1. Always more serious than they appear
  2. Skin has more resistance than bone, muscle, blood vessels or nerves; therefore deeper structures have more damage
  3. rhabdomyolysis, acute renal failure
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17
Q

Electrical Burns

  1. If urine is dark think what?
  2. If urine doesnt clear?
  3. Control metabolic acidosis by what?
A
  1. If urine is dark, assume myoglobin and increase fluids to achieve a urine output of 100ml/hr
  2. If urine doesn’t clear…….mannitol to ensure continued diuresis
  3. Control metabolic acidosis by perfusion and add sodium bicarbonate as needed to alkalinize urine to solubilize myoglobin
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18
Q

Burn Management
Emergency Department Management
1. By definition, major burn patients are multiple injury trauma patients: So remember your what?

  1. Check for evidence of what?
  2. and if present; consider what?
  3. Start what as soon as possible?
  4. Place these where?
  5. Do secondary survey and look closely at what?
  6. Estimate what and record this?
A
  1. ABCDE
  2. airway involvement
  3. endotracheal intubation EARLY!
  4. 2 large bore IVs
  5. in non-burned areas if practical
  6. eyes for evidence of corneal burns
  7. depth and extent of burn
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19
Q

Burn Management
Emergency Department Management
1. Any patient with >____% BSA partial-thickness burn needs what?

  1. Labs? 5
  2. Labs for inhalation injury? 4
  3. Urine for what? 2
  4. Check med records for what?
A
  1. 20, NG tube placed as ileus is likely
    • CBC,
    • electrolytes,
    • BUN,
    • Creatinine,
    • Glucose (Chem 7) should be obtained
    • ABGs,
    • carboxyhemaglobin level,
    • CXR and
    • EKG on any suspected inhalation injury
    • Urine for myoglobin and
    • CPK
  5. Check Tetanus status and when in doubt, give
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20
Q 
Burn Management
Emergency Department Management
1. Remove what?
2. Monitor what with circumferential burns?
3. What procedure may need to be done?
  1. Every patient with significant burns gets a what?
  2. WHY? 2
  3. Pain control: Especially in patients with what?
A
  1. Remove any jewelry…
  2. closely monitor distal pulses in extremities with circumferential burns….
  3. escharotomy PRN
  4. Foley catheter
    • Critical in monitoring resuscitation
    • Until a Swan-Ganz or CVP line is placed, it is the only way to ensure adequate renal perfusion
  6. widespread second-degree burns
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21
Q

Burn Management
Emergency Department Management
Fluid Resuscitation Requirements
1. Adults?

  1. Children?
A

NS or RL 4ml x weight (kg) x % BSA for 1st 24hr

  • Half of above over the first 8h from time of burn
  • Other half over subsequent 16 hours
  • Example: 70kg with 40% 2nd and 3rd degree burns
  • Do not memorize this stuff…know that there is a formula
  1. Children:
    NS or RL 3ml x weight (kg) x %BSA (admin schedule same as adult)
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22
Q

Burn Management
Emergency Department Management
Dressings: Minimal burns or burns that are being treated as an outpatient
1. What agent?
2. Re-evaluate when?
3. Dressing changes when?
4. Commercial preparations containing ______ shown to be of benefit?

A
  1. 1% silver sulfadiazine (silvadene)
  2. Re-evaluate every 24 hours until full extent is known
  3. Dressing changes BID until burn stops weeping
  4. honey shown to be of benefit
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23
Q

Burn Management
Emergency Department Management
Transfer Guidelines?
6

A
  1. Partial thickness burns of > 10% BSA
  2. Burns involving face, hands, feet, genitalia, perineum, or major joints
  3. Third-degree burns in any age group
  4. Electrical burns, especially lightening injuries
  5. Burns with preexisting complicating medical disorders
  6. Children with significant burns that are not in a children’s hospital

WHEN IN DOUBT CALL THE REFERRAL BURN CENTER

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24
Q

Regional Burn Centers

6

A
  1. University of Colorado Burn Center, Aurora, CO
  2. Western States Burn Center, North Colorado Medical Center, Greely, CO
  3. Hennepin County Medical Center, Minneapolis, MN
  4. Regions Hospital Burn Center, St. Paul, MN
  5. University of Utah Hospital Burn Center, SLC, UT
  6. University of Washington Burn Center, Seattle, WA
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25
Q

Peri and Post-operative Surgical Complications

2

A
  1. Shock

2. Sepsis

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26
Q

Shock defined as?

Caused by? 3

A

Defined as inadequate tissue/organ perfusion

  1. Pump failure
  2. Decreased peripheral resistance
  3. Hemorrhage
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27
Q

Shock Cardiac Response? 3

A
  1. Tachycardia
  2. Increased myocardial contractility/oxygen demand
  3. Constriction of peripheral blood vessels
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28
Q

Shock Renal Response? 3

A

1 stimulating an increase in renin secretion.

  1. vasoconstriction of arteriolar smooth muscle
  2. stimulation of aldosterone secretion by the adrenal cortex.
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29
Q

Shock Nueroendocrine response? 1

A

increase in circulating antidiuretic hormone.

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30
Q

What are the types of shock?

A
  1. Hypovolemic
  2. Septic
  3. Cardiogenic
  4. Neurogenic
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31
Q

Describe the following types of shock:

  1. Hypovolemic? 2
  2. Septic?
  3. Cardiogenic?
  4. Neurogenic?
A
  1. Hypovolemic
    - Decreased vascular volume
    - Hemorrhagic
  2. Septic
    - Systemic infections leads to hypotension, decreased vascular volume
  3. Cardiogenic
    - Shock resulting from some abnormal cardiac function
  4. Neurogenic
    - Due to failure of vasomotor regulation and pooling of blood in dilated capacitance vessels – suddenly the tank is too big
32
Q

Signs of shock: 4

whats the earliest manifestations of shock?

A
  1. Tachycardia (The EARLIEST manifestation)
  2. Hypotension
  3. Decreased urine output
  4. Altered mental status
33
Q
  1. Shock: Fluids with?
  2. Clinical signs, including? 4
  3. The development of peripheral edema is often due to what?
    - Should it be used as a marker for fluid resuscitation and why?
A
  1. Fluid repletion with isotonic saline.
    • blood pressure,
    • urine output,
    • mental status, and
    • peripheral perfusion, are often adequate to guide resuscitation.
  3. acute dilutional hypoalbuminemia and should not be used as a marker for adequate fluid resuscitation or fluid overload.
34
Q

What colliods might you use for shock?

A
  1. Albumin
  2. Hespan
    In summary, saline solutions are generally preferred
35
Q

HEMORRHAGIC SHOCK

Physiological Responses To Blood Loss? 4

A
  1. Heart Rate Increases
  2. Cardiac Contractility Increases
  3. Blood Shunted To Vital Organs
  4. Conservation of Water and Sodium
36
Q
  1. What causes pale extremeties in hemorrhagic shock?

2. Why do we have decreased urine output?

A
  1. Blood Shunted To Vital Organs

2. Conservation of Water and Sodium

37
Q

Physiological Effects @ Site of Loss in hemorrhagic shock?

5

A
  1. Local activation of coagulation system
  2. Affected blood vessels contract
  3. Activated platelets adhere to damaged vessels
  4. Activated platelets release Thromboxane A2
  5. Thromboxane A2 causes increased vessel contraction ….wound healing
38
Q

HEMORRHAGIC SHOCK….don’t miss:
Classic Clinical Presentation?
9

A
  1. Tachycardia
  2. Tachypnea
  3. Narrow Pulse Pressure
  4. Decreased Output
  5. Cool Clammy Skin
  6. Poor Capillary Refill
  7. Decreased CVP- Flat neck veins
  8. Hypotension (late)
  9. Altered Mental Status
39
Q 
HEMORRHAGIC SHOCK
TREATMENT 
IV Lines
1. How many?
2. Whats preferred?
3. Min of what size?
A
  1. Minimum of two lines
  2. Peripheral preferred
  3. Minimum 16 guage
40
Q

HEMORRHAGIC SHOCK
1. Initial Fluid Bolus
Give as rapidly as possible
How much? (adults and children)

  1. Requires how much crystalloid for how much blood loss?
  2. Monitor what for adequate fluid?
    - What levels for adults and children?
A
    • 1-2 Liters in adult
    • 20ml/kg in peds
  2. Requires 3 ml crystalloid for every 1 ml blood loss
  3. Monitor urine for adequate fluid
    - 30-50ml/hr for adults
    - 1ml/kg/hr for peds (2ml/kg/hr for peds less than 1 year)
41
Q

HEMORRHAGIC SHOCK
Blood Requirements based upon response to initial fluid bolus
1. VS return to normal after bolus treat how? 2

  1. VS return to normal then again drop treat how? 2
A
  1. VS return to normal after bolus
    - Type/Cross/Hold
    - Monitor Urine output and vitals
  2. VS return to normal then again drop
    - Give type specific if available…..O neg in a pinch
    - Plan to go back to OR
42
Q

HEMORRHAGIC SHOCK
TREATMENT: If hemorrhagic and severe how do we need to manage?
4

A
  1. Replace blood (PRBC’s)
  2. May have to replace platelets and give fresh frozen plasma.
  3. Reversal of the clinical manifestations of severe hypovolemia is often adequate to guide resuscitation
  4. Identify source of bleeding!
43
Q

HEMORRHAGIC SHOCK

Monitor what? 3

A
  1. Monitor ABGs- Persistent acidosis should be treated with fluids
  2. Monitor Calcium
  3. Monitor for Coagulopathy
44
Q

Persistent acidosis should be treated with what?

A

fluids

45
Q

HEMORRHAGIC SHOCK

Hypothermia is a big concern: treat how? 3

A
  1. Use warm fluids
  2. Use warm blankets
  3. Keep recovery rooms warm
46
Q
  1. The goal of therapy in hemorrhagic shock is what?

2. Signified by? 4

A
  1. Restoration of organ perfusion and adequate tissue oxygenation
  2. signified by:
    - appropriate urinary output
    - central nervous system function
    - skin color
    - return of pulse and blood pressure towards normal.
47
Q

Cardiogenic Shock

  1. Shock resulting from what?
  2. 10-20% due to what?
  3. Hallmark is what?
  4. Inadequate organ perfusion manifested by what? 2
  5. Identify abnormality and address….may need what?
A
  1. Shock resulting from some abnormal cardiac function
  2. 10-20% due to AMI with > 50% fatality
  3. Hallmark is hypotension with signs of increased PVR
  4. Inadequate organ perfusion:
    - Altered mental status and
    - decreased UO
  5. Identify abnormality and address….may need pressors
48
Q

What are signs of increased PVR? 2

A
  1. Weak, thready pulse

2. Cool, clammy skin

49
Q
  1. Septic Shock is what?
  2. along with the presence of perfusion abnormalities which may include, but are not limited to what?
    3
A
  1. Sepsis induced with hypotension despite adequate resuscitation
  2. along with the presence of perfusion abnormalities which may include, but are not limited to:
    - lactic acidosis
    - oliguria
    - or an acute alteration in mental status.
50
Q
  1. Septic Shock: Usually due to a what? Causing what?
  2. Toxic Shock Syndrome is the exception and is caused by what?
  3. Predisposing co-morbid states are common like? 3
  4. Relative hypovolemia occurs due to what? 2
  5. Direct depression of ___________ also possible
A
  1. Gram Negative bacteria causing “endotoxic shock”
  2. staphylocccal toxin
    • Diabetes,
    • leukemia,
    • immunosupression
    • pooling of blood in microcirculation and
    • loss of fluid into interstital spaces due to increased capillary permeability
  5. myocardium
51
Q

Septic Shock

  1. Wide what?
  2. Signs of TSS? 3
A
  1. Shock………wide pulse pressure
  2. TSS:
    - Diffuse red rash,
    - thrombocytopenia, and
    - usually within 5 days of menses
52
Q 
Septic Shock
Common sites and bugs:
1. GU: 4
2. Resp: 2
3. Below diaphragm: 2
A
    • E. coli,
    • Klebsiella,
    • Proteus,
    • Pseudomonas
    • Strep pneumoniae,
    • Staph aureus
    • Aerobic Gm negative bacilli,
    • Clostridium
53
Q

Neurogenic Shock
1. Most often caused by what?

  1. Due to?
  2. NOT CAUSED BY?
A
  1. Most often caused by spinal cord injury
  2. Due to failure of vasomotor regulation and pooling of blood in dilated capacitance vessels – suddenly the tank is too big
  3. Isolated head injuries do not cause shock
    - In a trauma patient with isolated head injury and shock, look for another cause
54
Q

Shock Therapy and Special Considerations
1. Do not use colloids in septic shock: why?

  1. Do not use inotropic agents (vasopressors) in any shock state except what? 2
    - unless central venous monitoring shows what? 2
  2. There is no ultimate substitute for blood when that is what the patient has lost
    - What temporize, but do not treat?
A
  1. Increased capillary permeability will cause pulmonary edema
  2. septic or cardiogenic shock
    - patient to be normovolemic and they remain hypotensive
  3. Crystalloids
55
Q
  1. What is sepsis?

2. Clinical manifesation? 4

A
  1. Presence of bacteria or other infectious organisms or their toxins in the blood (septicemia) or in other tissue of the body.
    • Fever, chills,
    • malaise ,
    • low blood pressure, and
    • mental status changes.
56
Q 
Sepsis: Etiology
Common portals of entry into the bloodstream
1. GI tract: 3
2. Skin:  2 
3. GU tract:  2
4. Respiratory tract: 2
5. Oral:  2
A
    • Enterobactericeae,
    • Pseudomonas,
    • anaerobes
    • Staphylococcus,
    • beta-hemolytic streptococci
    • Enterobactericeae,
    • Neisseria gonorrhea
    • Pneumococcus,
    • Hemophilus, viruses
    • Alpha-hemolytic streptococci,
    • anaerobes
57
Q

Sepsis: Risk Factors
1. Gram negative bacillary bacteremia? 6

  1. Gram positive bacteremia? 4
  2. Fungemia? 2
A
    • Diabetes mellitus
    • Cancer
    • Cirrhosis
    • Burns
    • Invasive procedures/devices
    • Neutropenia
    • Vascular devices
    • Indwelling mechanical devices
    • IV drug administration/use
    • Burns
    • Immunosuppressed with neutropenia
    • Broad-spectrum antimicrobial therapy
58
Q

Risk Factors for Severe Sepsis

4

A
  1. Age > 50
  2. Primary pulmonary disease
  3. Abdominal infection site
  4. CNS infection
59
Q

Clinical Signs of Sepsis

6

A
  1. Fever.
  2. Leukocytosis.
  3. Tachypnea.
  4. Tachycardia.
  5. Reduced Vascular Tone.
  6. Organ Dysfunction.
60
Q

Systemic Inflammatory Response Syndrome (SIRS),which may have an infectious or noninfectious etiology, is defined by the presence of 2 or more of the following:
4

A
  1. Fever (oral temp > 38C….100.4F) or hypothermia (less than 36C…96.8F)
    - Hypothermia is especially common in elderly, neonates, uremic patients and alcoholics
  2. Tachypnea (>24 breaths/minute) - early sign of systemic illness
  3. Tachycardia (HR > 90 beats/minute)
  4. Leukocytosis (WBC >12,000/microliter), Leukopenia (WBC less than 4000/microliter), or neutrophilic bands >10% (left shift)
61
Q

SIRS….differential diagnosis
Non-septic causes of Systemic Inflammatory Response Syndrome (SIRS)
12

A
  1. Pancreatitis
  2. Burns
  3. Trauma
  4. Adrenal insufficiency
  5. Pulmonary embolism
  6. Dissecting or ruptured aortic aneurysm
  7. Myocardial infarct
  8. Occult hemorrhage
  9. Cardiac tamponade
  10. Post-cardiopulmonary bypass surgery
  11. Drug overdose
  12. Anaphylaxis
62
Q

Sepsis….Clinical Manifestations

-Hypotension and DIC predispose patient to development of what? 2

A
  1. acrocyanosis

2. peripheral ischemic necrosis (digits)

63
Q

What is acrocyanosis?

4

A
    • cyanosis of the extremities with
    • mottled discoloration of skin of the digits, wrists, ankles and
    • profuse sweating and
    • coldness of the digits
64
Q

Sepsis: Dermatologic lesions
Secondary seeding of skin and soft tissue, produces cellulitis, pustules, bullae, hemorrhagic lesions

Skin lesions may be suggestive of specific pathogen?
3

A
  1. Petechiae/purpura…. N. meningitis (and H. influenzae)
  2. Tick bites in endemic areas….petechiae….think RMSF
  3. Erythema gangrenosum lesions
65
Q

Sepsis: Dermatologic lesions
How will the following present:
1. N. meningitis (and H. influenzae) caused lesions?

  1. Tick bites in endemic areas
  2. Erythema gangrenosum lesions
  3. Lab value? Usually what bug?
  4. Generalized erythoderma in septic patient. What do we have to rule out? 2
A
  1. Petechiae/purpura
  2. Tick bites in endemic areas….petechiae….think RMSF
    • bullous lesion surrounded
    • by edema that
    • undergoes central hemorrhagic necrosis)….
  4. neutropenia & usually Ps. aeruginoa
  5. R/O
    - toxic shock syndrome (TSS) secondary to S. aureus or
    - Streptococcus pyogenes (Group A streptococci)
66
Q

GI manifestations of Sepsis?

3

A
  1. Nausea, vomiting,
  2. diarrhea & ileus suggest acute gastroenteritis
  3. Cholestatic jaundice may precede sepsis
67
Q

Major Complications of Sepsis

Cardiopulmonary? 4

A
  1. Hypotension secondary to abnormal distribution of blood fluids/volume with resulting hypovolemia and dehydration
  2. Hypoxemia
  3. Hypercapnia
  4. Acute Respiratory Distress Syndrome (ARDS)
68
Q

Major Complications of Sepsis: Renal? 2

Renal failure secondary to what?
-Caused by what? 2

A
  1. Oliguria,
  2. azotemia,
  3. proteinuria,
  4. nonspecific urinary casts, and
  5. polyuria may occur
  6. Renal failure secondary to acute tubular necrosis (ATN)
  7. induced by
    - hypotension and
    - capillary injury
69
Q

Major Complications of Sepsis
1. Coagulopathies? 2

  1. Neurocomplications occur when?
A
  1. Coagulopathies
    - Thrombocytopenia (in 10-30% of patients)
    - DIC (platelets less than 50,000/microliter)
  2. Neurologic complications
    - Usually only occur after prolonged periods of sepsis (weeks to months)
70
Q

Systemic response to infection usually intensifies over time from mild sepsis to extremely severe septic shock
Severe Sepsis: Defined by (1)-there are 5 or (2) below?

A

(1) Sepsis with one or more signs of organ dysfunction, such as:
- Metabolic acidosis
- Acute encephalopathy
- Oliguria
- Hypoxemia
- Disseminated intravascular coagulation (DIC)

or (2) Hypotension

71
Q

Septic Shock: Severe Sepsis (organ dysfunction) with hypotension (defined by arterial SBP less than 1.___ mmHg or 2.____ mmHg less than patient’s normal BP) that is unresponsive to 3._____________?

A
  1. 90
  2. 40
  3. fluid resuscitation
72
Q
  1. What is Refractory Septic Shock?

2. Multiple-Organ-Dysfunction Syndrome (MODS)?

A
  1. Septic shock that lasts for > 1 hour and does not respond to fluid or pressor administration
  2. Dysfunction of more than one organ, requiring intervention to maintain homeostasis
73
Q

Sepsis-Induced Organ Injury

  1. Multiple Organ Dysfunction (MODS) and Multiple Organ Failure (MOF) result from what?
  2. Mechanisms of cell injury / death? 4
A
  1. diffuse cell injury/ death resulting in compromised organ function.
    • Cellular Necrosis (ischemic injury)
    • Apoptosis
    • Leukocyte-mediated tissue injury
    • Cytopathic Hypoxia
74
Q

Pathophysiology of Sepsis-Induced Ischemic Organ Injury
1. Cytokine production leads to what?

  1. Structural changes in the endothelium result in what? 2
  2. Plugging of select microvascular beds with neutrophils, fibrin aggregates, and microthrombi impair what?
  3. Organ-specific what?
A
  1. massive production of endogenous vasodilators.
    • extravasation of intravascular fluid into interstitium and
    • subsequent tissue edema.
  3. microvascular perfusion.
  4. vasoconstriction.
75
Q

What four things lead to Maldistribution of Microvascular Blood Flow
which subsequaently leads to ischemia, cell death and organ dysfunction?

A
  1. Hypotension
  2. Microvascular Plugging
  3. Vasoconstriction
  4. Edema
76
Q

Therapeutic Strategies in Sepsis

12

A
  1. Renal replacement therapies….dialysis
  2. Surgical intervention
  3. Drainage
  4. Cardiovascular support (vasopressors, inotropes).
  5. Culture directed Antimicrobial therapy
  6. Mechanical ventilation.
  7. Transfusion for hematologic dysfunction.
  8. Enteral/parenteral nutritional support
  9. Minimize exposure to hepatotoxic and nephrotoxic therapies.
  10. Optimize organ profusion
  11. Expand effective blood volume
  12. Hemodynamic monitoring.

Surgery (20 decks)

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