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Surgery > Burns, Shock, & Sepsis > Flashcards

Burns, Shock, & Sepsis Flashcards

1
Q

Epidemiology of Burns

A

65+ is highest in mortality

18-35 years old 2:1 (M:F)

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2
Q

Cellular Changes in Burns

A

Intracellular influx of Na/H2O
Extracellular migration of K
Disruption of cell membrane function
Failure of “sodium pump”

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3
Q

Hematologic Changes in Burns

A

Increased hematocrit
Increase in blood viscosity
Anemia due to RBC destruction

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4
Q

At what temperature does cell damage occur?

A

113+ F

Denatures protein

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5
Q

What happens to the zone of coagulation with a burn?

A

Irreversibly destroyed

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6
Q

What happens in the zone of stasis with a burn?

A

Stagnation of microcirculation

Can/will extend if not treated appropriately

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7
Q

What occurs in the zone of hyperemia with a burn?

A

Increase blood flow

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8
Q

How to Determine What Percentage of Patient is Burned

A 
9%: each arm
9%: front of each leg
9%: back of each leg
9%: chest
9%: abdomen
18%: back
9%: head
1%: genitals
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9
Q

1st Degree Burn

A

Erythema of skin
Minimal surrounding edema
Minimal pain

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10
Q

2nd Degree Burn

A 
Partial thickness
Painful
Red or mottled skin
Blisters with broken epidermis
Edema
Wet/weeping surfaces
Sensitive to air
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11
Q

3rd Degree Burn

A 
Full thickness
Damage to all skin layers, subQ tissues, & nerve endings
Pale white or charred appearance
Leathery
Broken skin with fat exposed
Dry surface
Painless to pinprick
Edema
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12
Q

Specific Issues with Burn Management

A 
Carbon around nose
Burns involving the mouth
Significant respiratory problems
Fires in enclosed places
CO exposure
Toxic gases from combustion (cyanide)
Intubate early
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13
Q

Chemical Burns

A

Irrigate

Alkali burns more serious

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14
Q

Why are alkali burns more serious than acid burns?

A

Alkali’s penetrate deeper

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15
Q

Electrical Burns

A

Always more serious than they appear
Deeper structures have more damage
Rhabdomyolysis -> acute renal failure
Dark urine: assume rhabdomyolysis

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16
Q

What can you do to help clear up the urine from rhabdomyolysis?

A

Increase fluids to achieve a UO of 100 mL/hr

Mannitol if necessary

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17
Q

ABCDE of Burn Patients

A 
A: airway
B: breathing
C: circulation or control of hemorrhage
D: disability (neurologic)
E: environmental control/exposure
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18
Q

What needs to be observed in a burn patient?

A

Eyes: corneal ulcers
Need 2 large bore IVs
Estimate depth & extent of burn

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19
Q

Management of the Burn Victim

A 
20%+ BSA partial thickness burn: NG tube placement
CBC, CMP
ABGs, carboxyhemaglobin level
CXR & EKG on suspected inhalation injury
Urine: myoglobin & CPK
Tetanus status
Remove jewelry
Foley placement
Pain control
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20
Q

Dressings for Burn Victims

A

1% silver sulfadiazine (sivadene)
Re-evaluate every 24 hours until full extent is known
Dressing changes BID until weeping stops
Honey shown to be effective

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21
Q

Guidelines for Transferring Burn Patients

A

Partial thickness >10% BSA
Burns involving the face, hands, feet, genitalia, perineum, or major joints
Third-degree burns in any age group
Electrical burns
Burns with complicated co-morbidities
Children with significant burn that are not in a children’s hospital

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22
Q

Define Shock

A

Inadequate tissue/organ perfusion

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23
Q

Reasons for Shock

A

Pump failure
Decreased peripheral resistance
Hemorrhage

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24
Q

Cardiac Response to Shock

A

Tachycardia
Increased myocardial contractility/oxygen demand
Constriction of peripheral blood vessels

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25
Q

Renal Response to Shock

A

Stimulating an increase in renin secretion
Vasoconstriction of arteriolar smooth muscle
Stimulation of aldosterone secretion by the adrenal cortex

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26
Q

Neuroendocrine Response to Shock

A

Increase in circulating antidiuretic hormone

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27
Q

Types of Shock

A

Hypovolemic
Septic
Cardiogenic
Neurogenic

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28
Q

Reasons for Hypovolemic Shock

A

Decreased vascular volume

Hemorrhagic

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29
Q

Reasons for Septic Shock

A

Systemic infections lead to hypotension & decreased vascular volume

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30
Q

Reasons for Cariogenic Shock

A

Some abnormal cardiac function

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31
Q

Reasons for Neurogenic Shock

A

Disruption of the autonomic pathways within the spinal cord

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32
Q

Signs of Shock

A

Tachycardia
Hypotension
Decreased urine output
Altered mental status

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33
Q

Reversal of Hypovolemic Shock

A

Fluids: isotonic saline
Colloids: albumin, hespan

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34
Q

Systemic Physiologic Responses to Hemorrhagic Shock

A

Increased HR
Cardiac contractility issues
Blood shunted to vital organs
Conservation of water & sodium

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35
Q

Local Physiologic Responses to Hemorrhagic Shock

A

Local activation of coagulation system
Affected vessels contract
Activated platelets adhere to damaged vessels
Activated platelets release Thromboxane A2
Thromboxane A2 increases vessel contraction

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36
Q

Clinical Presentation of Hemorrhagic Shock

A 
Tachycardia
Tachypnea
Narrow pulse pressure
Decreased output
Cool clammy skin
Poor capillary refill
Decreased CVP
Hypotension
Altered mental status
37
Q

Treatment for Hemorrhagic Shock

A

2 large bore IVs
Give 1-2 L as rapidly as possible (3 mL/ 1 mL blood loss)
Monitor urine for adequate fluid (30-50 cc/hr)
Blood transfusion based on response to fluid bolus
Monitor ABGs
Monitor calcium
Monitor for coagulopathy (DIC)
Prevent hypothermia

38
Q

Vital Signs Return to Normal After Fluid Bolus in Hemorrhagic Shock

A

Type, cross, hold

Monitor urine output & vitals

39
Q

Vital Signs Return to Normal then Drop Again After Fluid Bolus in Hemorrhagic Shock

A

Give type specific blood

Plan to go to OR

40
Q

Treatment for Severe Hemorrhagic Shock

A

Replace blood (PRBCs)
Possible replacement of platelets & FFP
Reversal of clinical manifestations often adequate to guide resuscitation
Identify source of bleeding

41
Q

Goal of Therapy in Hemorrhagic Shock

A

Restoration of organ perfusion & adequate tissue oxygenation

42
Q

How is organ perfusion & adequate tissue oxygenation assessed?

A

Appropriate urine output
CNS function
Skin color
Return of pulse & BP towards normal

43
Q

Define Cardiogenic Shock

A

Shock resulting from some abnormal cardiac function (MI)

44
Q

Hallmark Sign of Cardiogenic Shock

A

Hypotension

Signs of increased peripheral vascular resistance

45
Q

How to Determine Inadequate Organ Perfusion

A

Altered mental status

Decreased urine output

46
Q

Treatment of Cariogenic Shock

A

Identify abnormality

Address abnormality

47
Q

Define Septic Shock

A

Sepsis induced with hypotension despite adequate resuscitation along with the perfusion abnormalities

48
Q

Perfusion Abnormalities in Septic Shock

A

Lactic acidosis
Oliguria
Acute alteration in mental status

49
Q

What is septic shock usually due to?

A

Gram negative bacteria

50
Q

Predisposing Co-Morbid States with Septic Shock

A

DM
Immunosuppression
Leukemia

51
Q

Why does relative hypovolemia occur?

A

Pooling of blood in microcirculation & loss of fluid into the interstitial spaces (leaky capillaries)

52
Q

Toxic Shock Syndrome

A

Diffuse red rash
Thrombocytopenia
Usually within 5 days of menses

53
Q

Common Bugs of Sepsis from GU Origin

A

E. coli
Klebsiella
Proteus
Pseudomonas

54
Q

Common Bugs of Sepsis from Respiratory Origin

A

Strep pneumoniae

Staph aureus

55
Q

Common Bugs of Sepsis from Below the Diaphragm

A

Aerobic gram negative bacilli

Clostridium

56
Q

What is neurogenic shock most often caused by?

A

Spinal cord injury

57
Q

Special Considerations for Shock

A

Do not use colloids in septic shock
Cardiogenic & Septic: can use inotropic medications
All other shock: can use inotropic medications IF CVP monitoring shows patient to be normovolemic & they remain hypotensive
No substitute for blood in hemorrhagic shock

58
Q

Define Sepsis

A

Presence of bacteria or other infectious organisms or their toxins in the blood or other tissues of the body

59
Q

Clinical Manifestations of Sepsis

A

Fever/chills
Malaise
Hypotension
Mental status changes

60
Q

Etiology of Sepsis from the GI Tract

A

Enterobactericeae
Pseudomonas
Anaerobes

61
Q

Etiology of Sepsis from the Skin

A

Staphylococcus

Beta hemolytic streptococci

62
Q

Etiology of Sepsis from the GU Tract

A

Enterobactericeae

N. gonorrhea

63
Q

Etiology of Sepsis from the Respiratory Tract

A

Pneumococcus
Hemophilus
Viruses

64
Q

Etiology of Sepsis from the Oral Cavity

A

Alpha-hemolytic streptococci

Anaerobes

65
Q

Risk Factors for Gram Negative Bacillary Bacteremia

A 
DM
CA
Cirrhosis
Burns
Invasive procedures/devices
Neutropenia
66
Q

Risk Factors for Gram Positive Bacteremia

A

Vascular devices
Indwelling mechanical devices
IV drug administration/use
Burns

67
Q

Risk Factors for Fungemia

A

Immunosuppressed with neutropenia

Broad-spectrum antibiotic therapy

68
Q

Risk Factors for Severe Sepsis

A

Age 50+
Primary pulmonary disease
Abdominal infection site
CNS infection

69
Q

Clinical Signs of Sepsis

A 
Fever
Leukocytosis
Tachycardia
Tachypnea
Reduced vascular tone
Organ dysfunction
70
Q

Define Systemic Inflammatory Response Syndrome (SIRS)

A

Infectious or non-infectious etiology with the presence of 2+ of the following
Fever or hypothermia
Tachypnea
Tachycardia
Leukocytosis, leukopenia, or neutrophilic bands

71
Q

Non-Septic Causes of SIRS

A 
Pancreatitis
Burns
Trauma
Adrenal insufficiency
Pulmonary embolism
Dissecting or ruptured aortic aneurysm
MI
Occult hemorrhage
Cardiac tamponade
Post-cardiopulmonary bypass surgery
Drug overdose
Anaphylaxis
72
Q

Skin Manifestations of Sepsis

A

Acrocyanosis
Peripheral ischemic necrosis
Dermatologic lesions

73
Q

Define Acrocyanosis

A

Cyanosis of the extremities with mottled discoloration of skin of the digits, wrists, ankles, and profuse sweating & coldness of the digits

74
Q

Dermatologic Lesions of Sepsis

A

Cellulitis
Pustules
Bullae
Hemorrhagic lesions

75
Q

Pathogens with Petechiae/Purpura in the Presence of Sepsis

A

N. meningitis

H. influenza

76
Q

Pathogen of Petechiae in Tick Bite Endemic Areas in the Presence of Sepsis

A

Rocky mountain spotted fever

77
Q

Pathogen with Erythema Gangrenosum Lesions in the Presence of Sepsis

A

Pseudamonas aeruginosa

78
Q

GI Clinical Manifestations of Sepsis

A

N/V
Diarrhea
Ileus
Cholestatic jaundice

79
Q

Major Cardiopulmonary Complications of Sepsis

A

Hypotension secondary to abnormal distribution of blood fluids/volume
Hypoxemia
Hypercapnia
Acute respiratory distress syndrome (ARDS)

80
Q

Major Renal Complications of Sepsis

A 
Oliguria
Azotemia
Proteinuria
Non-specific urinary casts
Polyuria
Renal failure secondary to acute tubular necrosis induced by hypotension & capillary injury
81
Q

Other Major Complications of Sepsis

A

Thrombocytopenia
DIC
Neurologic complications

82
Q

Define Severe Sepsis

A

Sepsis with 1+ signs of organ dysfunction
OR
Hypotension

83
Q

Signs of Organ Dysfunction

A 
Metabolic acidosis
Acute encephalopathy
Oliguria
Hypoxemia
Disseminated intravascular coagulation (DIC)
84
Q

Define Septic Shock

A

Severe sepsis with hypotension that is unresponsive to fluid resuscitation

85
Q

Define Refractory Septic Shock

A

Septic shock that lasts for 1+ hour & does not respond to fluid or pressor administration

86
Q

Define Multiple Organ Dysfunction Syndrome (MODS)

A

Dysfunction of more than one organ requiring intervention to maintain homeostasis

87
Q

Mechanisms of Cell Injury/Death

A

Cellular necrosis
Apoptosis
Leukocyte mediated tissue injury
Cytopathic hypoxia

88
Q

Pathophysiology of Sepsis-Induced Ischemic Organ Injury

A

Cytokine production leads to massive production of endogenous vasodilators
Structural changes in endothelium result in extravasation of intravascular fluid into interstitium
Plugging of microvascular beds with neutrophils, fibrin aggregates, & micro thrombi impair microvascular perfusion
Organ-specific vasoconstriction

89
Q

Therapeutic Strategies in Sepsis

A 
Renal placement therapies: dialysis
Surgical intervention
Drainage
Cardiovascular support
Culture directed antimicrobial therapy
Mechanical ventilation
Transfusion for hematologic dysfunction
Enteral/parenteral nutritional support
Minimize exposure to hepatotoxic & nephrotoxic therapies
Optimize organ perfusion
Expand effective blood volume
Hemodynamic monitoring

Surgery (20 decks)

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