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Flashcards in Burns, Shock, & Sepsis Deck (89):
1

Epidemiology of Burns

65+ is highest in mortality
18-35 years old 2:1 (M:F)

2

Cellular Changes in Burns

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

3

Hematologic Changes in Burns

Increased hematocrit
Increase in blood viscosity
Anemia due to RBC destruction

4

At what temperature does cell damage occur?

113+ F
Denatures protein

5

What happens to the zone of coagulation with a burn?

Irreversibly destroyed

6

What happens in the zone of stasis with a burn?

Stagnation of microcirculation
Can/will extend if not treated appropriately

7

What occurs in the zone of hyperemia with a burn?

Increase blood flow

8

How to Determine What Percentage of Patient is Burned

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

9

1st Degree Burn

Erythema of skin
Minimal surrounding edema
Minimal pain

10

2nd Degree Burn

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

11

3rd Degree Burn

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

12

Specific Issues with Burn Management

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

13

Chemical Burns

Irrigate
Alkali burns more serious

14

Why are alkali burns more serious than acid burns?

Alkali's penetrate deeper

15

Electrical Burns

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

16

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

Increase fluids to achieve a UO of 100 mL/hr
Mannitol if necessary

17

ABCDE of Burn Patients

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

18

What needs to be observed in a burn patient?

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

19

Management of the Burn Victim

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

20

Dressings for Burn Victims

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

21

Guidelines for Transferring Burn Patients

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

22

Define Shock

Inadequate tissue/organ perfusion

23

Reasons for Shock

Pump failure
Decreased peripheral resistance
Hemorrhage

24

Cardiac Response to Shock

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

25

Renal Response to Shock

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

26

Neuroendocrine Response to Shock

Increase in circulating antidiuretic hormone

27

Types of Shock

Hypovolemic
Septic
Cardiogenic
Neurogenic

28

Reasons for Hypovolemic Shock

Decreased vascular volume
Hemorrhagic

29

Reasons for Septic Shock

Systemic infections lead to hypotension & decreased vascular volume

30

Reasons for Cariogenic Shock

Some abnormal cardiac function

31

Reasons for Neurogenic Shock

Disruption of the autonomic pathways within the spinal cord

32

Signs of Shock

Tachycardia
Hypotension
Decreased urine output
Altered mental status

33

Reversal of Hypovolemic Shock

Fluids: isotonic saline
Colloids: albumin, hespan

34

Systemic Physiologic Responses to Hemorrhagic Shock

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

35

Local Physiologic Responses to Hemorrhagic Shock

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

36

Clinical Presentation of Hemorrhagic Shock

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

37

Treatment for Hemorrhagic Shock

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

Vital Signs Return to Normal After Fluid Bolus in Hemorrhagic Shock

Type, cross, hold
Monitor urine output & vitals

39

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

Give type specific blood
Plan to go to OR

40

Treatment for Severe Hemorrhagic Shock

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

41

Goal of Therapy in Hemorrhagic Shock

Restoration of organ perfusion & adequate tissue oxygenation

42

How is organ perfusion & adequate tissue oxygenation assessed?

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

43

Define Cardiogenic Shock

Shock resulting from some abnormal cardiac function (MI)

44

Hallmark Sign of Cardiogenic Shock

Hypotension
Signs of increased peripheral vascular resistance

45

How to Determine Inadequate Organ Perfusion

Altered mental status
Decreased urine output

46

Treatment of Cariogenic Shock

Identify abnormality
Address abnormality

47

Define Septic Shock

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

48

Perfusion Abnormalities in Septic Shock

Lactic acidosis
Oliguria
Acute alteration in mental status

49

What is septic shock usually due to?

Gram negative bacteria

50

Predisposing Co-Morbid States with Septic Shock

DM
Immunosuppression
Leukemia

51

Why does relative hypovolemia occur?

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

52

Toxic Shock Syndrome

Diffuse red rash
Thrombocytopenia
Usually within 5 days of menses

53

Common Bugs of Sepsis from GU Origin

E. coli
Klebsiella
Proteus
Pseudomonas

54

Common Bugs of Sepsis from Respiratory Origin

Strep pneumoniae
Staph aureus

55

Common Bugs of Sepsis from Below the Diaphragm

Aerobic gram negative bacilli
Clostridium

56

What is neurogenic shock most often caused by?

Spinal cord injury

57

Special Considerations for Shock

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

Define Sepsis

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

59

Clinical Manifestations of Sepsis

Fever/chills
Malaise
Hypotension
Mental status changes

60

Etiology of Sepsis from the GI Tract

Enterobactericeae
Pseudomonas
Anaerobes

61

Etiology of Sepsis from the Skin

Staphylococcus
Beta hemolytic streptococci

62

Etiology of Sepsis from the GU Tract

Enterobactericeae
N. gonorrhea

63

Etiology of Sepsis from the Respiratory Tract

Pneumococcus
Hemophilus
Viruses

64

Etiology of Sepsis from the Oral Cavity

Alpha-hemolytic streptococci
Anaerobes

65

Risk Factors for Gram Negative Bacillary Bacteremia

DM
CA
Cirrhosis
Burns
Invasive procedures/devices
Neutropenia

66

Risk Factors for Gram Positive Bacteremia

Vascular devices
Indwelling mechanical devices
IV drug administration/use
Burns

67

Risk Factors for Fungemia

Immunosuppressed with neutropenia
Broad-spectrum antibiotic therapy

68

Risk Factors for Severe Sepsis

Age 50+
Primary pulmonary disease
Abdominal infection site
CNS infection

69

Clinical Signs of Sepsis

Fever
Leukocytosis
Tachycardia
Tachypnea
Reduced vascular tone
Organ dysfunction

70

Define Systemic Inflammatory Response Syndrome (SIRS)

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

71

Non-Septic Causes of SIRS

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

Skin Manifestations of Sepsis

Acrocyanosis
Peripheral ischemic necrosis
Dermatologic lesions

73

Define Acrocyanosis

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

74

Dermatologic Lesions of Sepsis

Cellulitis
Pustules
Bullae
Hemorrhagic lesions

75

Pathogens with Petechiae/Purpura in the Presence of Sepsis

N. meningitis
H. influenza

76

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

Rocky mountain spotted fever

77

Pathogen with Erythema Gangrenosum Lesions in the Presence of Sepsis

Pseudamonas aeruginosa

78

GI Clinical Manifestations of Sepsis

N/V
Diarrhea
Ileus
Cholestatic jaundice

79

Major Cardiopulmonary Complications of Sepsis

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

80

Major Renal Complications of Sepsis

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

81

Other Major Complications of Sepsis

Thrombocytopenia
DIC
Neurologic complications

82

Define Severe Sepsis

Sepsis with 1+ signs of organ dysfunction
OR
Hypotension

83

Signs of Organ Dysfunction

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

84

Define Septic Shock

Severe sepsis with hypotension that is unresponsive to fluid resuscitation

85

Define Refractory Septic Shock

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

86

Define Multiple Organ Dysfunction Syndrome (MODS)

Dysfunction of more than one organ requiring intervention to maintain homeostasis

87

Mechanisms of Cell Injury/Death

Cellular necrosis
Apoptosis
Leukocyte mediated tissue injury
Cytopathic hypoxia

88

Pathophysiology of Sepsis-Induced Ischemic Organ Injury

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

Therapeutic Strategies in Sepsis

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