Burns, Shock, & Sepsis Flashcards
1
Q
Epidemiology of Burns
A
65+ is highest in mortality
18-35 years old 2:1 (M:F)
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”
3
Q
Hematologic Changes in Burns
A
Increased hematocrit
Increase in blood viscosity
Anemia due to RBC destruction
4
Q
At what temperature does cell damage occur?
A
113+ F
Denatures protein
5
Q
What happens to the zone of coagulation with a burn?
A
Irreversibly destroyed
6
Q
What happens in the zone of stasis with a burn?
A
Stagnation of microcirculation
Can/will extend if not treated appropriately
7
Q
What occurs in the zone of hyperemia with a burn?
A
Increase blood flow
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
9
Q
1st Degree Burn
A
Erythema of skin
Minimal surrounding edema
Minimal pain
10
Q
2nd Degree Burn
A
Partial thickness Painful Red or mottled skin Blisters with broken epidermis Edema Wet/weeping surfaces Sensitive to air
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
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
13
Q
Chemical Burns
A
Irrigate
Alkali burns more serious
14
Q
Why are alkali burns more serious than acid burns?
A
Alkali’s penetrate deeper
15
Q
Electrical Burns
A
Always more serious than they appear
Deeper structures have more damage
Rhabdomyolysis -> acute renal failure
Dark urine: assume rhabdomyolysis
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
17
Q
ABCDE of Burn Patients
A
A: airway B: breathing C: circulation or control of hemorrhage D: disability (neurologic) E: environmental control/exposure
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
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
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
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
22
Q
Define Shock
A
Inadequate tissue/organ perfusion
23
Q
Reasons for Shock
A
Pump failure
Decreased peripheral resistance
Hemorrhage
24
Q
Cardiac Response to Shock
A
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
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