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SURGERY EXAM II > BURNS SHOCK SEPSIS > Flashcards

BURNS SHOCK SEPSIS Flashcards

1
Q

EPIDEMIOLOGY OF BURNS

  • burn mortality = highest in patients ________ (age)
  • highest risk for burns = ________ (age range)
  • ratio of male : female for both injury & death = __:__
  • In children, the highest incidence for burns = scalding injuries from _______ & __________
A

> 65

18-35 years old

2:1

hot drinks or baths

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2
Q

2 layers of skin = _______ & ________

  • People have skin of various thickness
  • skin thickness varies with _____
A

Dermis + Epidermis

age

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3
Q

Skin is a __________ barrier for evaporative loss

Skin is also responsible for the control of ___________

A

SEMI-PERMEABLE

body temperature

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4
Q

1st degree burn =
2nd degree burn =
3rd degree burn =

A

superficial - epidermis
partial thickness - either superficial partial (epidermis + superficial part of dermis - papillary) or deep partial (epidermis + extends into deep portion of dermis - reticular layer)
full thickness - extends through entire skin (epidermis + dermis)

4th degree = entire skin into underlying fat / muscle / bone

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5
Q

CELLULAR CHANGES WITH BURNS

A

o Intracellular influx of sodium & H2O (sodium mostly outside cell, potassium inside)

o Extracellular migration of potassium

o Disruption of cell membrane function

o Failure of “sodium pump”

  • Burns can lead to shock with depression of the myocardium & metabolic acidosis
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6
Q

local progressive injury with burns

A

o Liberation of vasoactive substances
o Disruption of cellular function
o Edema formation

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7
Q

cell damage with burns - occurs at temps > ______ due to ___________

A

113F

denaturation of protein

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8
Q

3 zones

A

zone of coagulation
zone of stasis
zone of hyperemia

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9
Q

describe

zone of coagulation
zone of stasis
zone of hyperemia

A

⦁ Zone of Coagulation - irreversibly destroyed

⦁ Zone of Stasis - stagnation of microcirculation; decreased tissue perfusion –> ischemia; can and will extend to necrosis if not treated appropriately

⦁ Zone of Hyperemia - increased blood flow; tissue perfusion is increased

innermost = coagulation, middle = stasis, outer = hyperemia

Zone of coagulation is the area that sustained maximum damage from the heat source. Proteins become denatured, and cell death is imminent due to destruction of blood vessels, resulting in ischemia to the area. Injury at this area is irreversible (coagulative necrosis & gangrene)

Zone of stasis surrounds the coagulation area, where tissue is potentially salvageable. This is the main area of focus when treating burn injuries

Zone of hyperemia is the area surrounding the zone of stasis. Perfusion is adequate due to patent blood vessels, and erythema occurs due to diapedesis

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10
Q

which zone is the main area of focus when treating burn injuries

A

zone of stasis

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11
Q

TRIAD OF DEATH FOR BURNS

A
  1. Acidosis
  2. Coagulopathy
  3. Hypothermia
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12
Q

Burns are quantified as percentage of

A

BSA

Rule of 9’s - breaks down body portions into multiples of 9, and perineum = 1%

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13
Q

back of hand is approximately ______ BSA

perineum is ______ BSA

A

1%

1%

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14
Q

which burn diagram is best

A

Lund & Browder

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15
Q

which degree burn is a sunburn

A

first

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16
Q

clinical presentation of 1st degree superficial burn

A

erythema (NO BLISTERS), red
pain
possibly minimal surrounding edema
DRY

painful & tender to touch
Refill intact* - blanches with pressure

Heals within 7 days
no scarring

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17
Q

2nd degree superficial partial thickness burn

A

⦁ deeper than 1st degree burn

⦁ involves partial thickness - epidermis & top part of dermis (papillary)

⦁ ex: deep sunburn, contact with hot liquids, flash burns from gasoline flames
⦁ usually MORE PAINFUL than 3rd degree burns
⦁ Skin appearance: red or mottled, blisters with broken epidermis, considerable swelling; wet/weeping surfaces; VERY PAINFUL, sensitive to the air

**Most painful of all burns; very tender to touch

Refill intact* - blanches with pressure

Heals within 14-21 days
no scarring, but may leave pigment changes

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18
Q

examples of 2nd degree superficial partial thickness burn

A

deep sunburn
contact with hot liquids
flash burns from gasoline flames

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19
Q

skin appearance with 2nd degree superficial partial thickness burn

A 
red or mottled skin
blisters with broken epidermis
WET / WEEPING SURFACES
considerable swelling
VERY PAINFUL
sensitive to the air
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20
Q

most painful of all burns

A

superficial partial thickness burns

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21
Q

2nd degree deep partial thickness burn

A

⦁ Extends into deep dermis (epidermis + deep dermis - reticular)
⦁ Yellow or white, less blanching (absent capillary refill)
⦁ DRY
⦁ BLISTERING
⦁ Pressure and discomfort
⦁ Can cause scarring and contractures
⦁ May require skin grafting
⦁ Not usually painful, but may have pain with pressure
⦁ May have decreased 2 point discrimination

Absent capillary refill
NOT USUALLY PAINFUL; may have pain/discomfort with pressure

Takes 3 weeks - 2 months to heal
Scarring is common; may need skin graft or excision to prevent contractures (a permanent shortening of muscle, tendon, or scar tissue, producing deformity or distortion)

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22
Q

dry, no blisters, pain

A

1st degree

no scarring
painful
blanching
red/erythematous

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23
Q

wet, blisters, pain

A 
2nd degree superficial
no scarring - may have pigment changes
PAIN
blanching
erythematous / pink
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24
Q

dry, blisters, usually no pain

A

2nd degree deep

yellow or white
absent capillary refill - no blanching
usually not painful - discomfort with pressure
scarring - may need skin graft/excision to prevent contractures

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25
Q

3rd degree = full thickness burn

A

Damage to all skin layers, subcutaneous tissues, and nerve endings

Extends through entire dermis

Skin appears: Pale white or charred appearance, leathery; broken skin with fat exposed; dry surface; painless to pinprick; edema

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26
Q

skin appearance with full thickness 3rd degree burn

A 
pale white or charred (waxy, white)
leathery
broken skin with fat exposed
DRY
PAINLESS
edema

capillary refill absent (just like with 2nd deep)

takes months to heal
- does NOT spontaneously heal well

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27
Q
  • extends through entire skin & into underlying fat, muscle and bone
A

FOURTH DEGREE BURN - FULL THICKNESS

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28
Q

INHALATION BURNS

A 
⦁	carbon around nose
⦁	burns involving mouth
⦁	significant respiratory problems
⦁	from fires in enclosed areas
⦁	remember CO exposure
⦁	Toxic gases from combustion
⦁	INTUBATE EARLY
  • burns to the airway can cause swelling that blocks the flow of air into the lungs
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29
Q

CHEMICAL BURNS

A

⦁ alkali or acids can cause burns
⦁ DO NOT TRY TO NEUTRALIZE** (can end up making much worse)
⦁ “The solution to pollution is dilution” - IRRIGATE IRRIGATE IRRIGATE
⦁ ***Alkali burns are more serious than acid burns, because alkali penetrates deeper

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30
Q

how to treat chemical burns

A

dilution - IRRIGATE IRRIGATE IRRIGATE

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31
Q

with chemical burns: __________ are more serious than ________ burns

A

***Alkali burns are more serious than acid burns, because alkali penetrates deeper

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32
Q

why are alkali burns more serious that acid burns

A

alkali burns penetrates deeper

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33
Q

ELECTRICAL BURNS

A

⦁ ***Always more serious than they appear

⦁ Skin has more resistance than bone, muscle, blood vessels or nerves, therefore deeper structures have more damage

⦁ Occult destruction of muscle can cause RHABDOMYOLYSIS (breakdown of skeletal muscle - do UA to check for myoglobinuria), which causes the release of myoglobin and can lead to ACUTE RENAL FAILURE

Myoglobin = a red protein containing heme (iron containing compound) that carries and stores oxygen (and iron) in muscle cells. It is structurally similar to a subunit of hemoglobin. Myoglobin = iron & oxygen binding protein found in muscle tissue

too much myoglobin in blood - is quickly filtered through by glomeruli, can accumulate in tubules and lead to kidney damage…or myoglobin breaks down into substances that can damage kidney cells

  • if urine is DARK = assume myoglobin, and increase fluids to achieve a urine output of 100ml/hr
  • if urine doesn’t clear = give Mannitol to ensure continued diuresis (mannitol = diuretic used to prevent cerebral edema & treat/prevent kidney failure)
    ⦁ The aim is to ‘wash’ the myoglobin out of the tubules and prevent it precipitating there with obstruction and development of acute renal failure.
  • Control metabolic acidosis by perfusion, and add sodium bicarb as needed to alkalinize the urine to solublize the myoglobin (hypoxia to muscles –> muscle breakdown –> lactic acid release –> metabolic acidosis)
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34
Q

with electrical burns = causes ________ = now worried about __________

A

rhabdomyolysis

acute kidney failure

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35
Q

treatment for myoglobinuria

A

if urine is DARK = assume myoglobin, and increase fluids to achieve a urine output of 100ml/hr

  • if urine doesn’t clear = give Mannitol to ensure continued diuresis

(mannitol = diuretic used to prevent cerebral edema & treat/prevent kidney failure)

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36
Q

ABCDEs of major burn patients

A 
⦁	Airway
⦁	Breathing
⦁	Circulation
⦁	Disability
⦁	Exposure or Environment - (want to keep pt warm, but also need to expose the pt to look everywhere on body for trauma)
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37
Q

burn management in ER

A
  • check for evidence of airway involvement; if present, consider endotracheal intubation EARLY!
  • start 2 large bore IVs asap - place in non-burned areas if possible
  • do secondary survey: look closely at eyes for evidence of corneal burns
  • estimate depth & extent of burn and record
  • should obtain CBC, electrolytes / BUN / Creatinine / Glucose (CMP)
  • ABGs, carboxyhemoglobin level, CXR and EKG on any suspected inhalation injury
  • Urine for myoglobin & CPK
    (creatinine phosphokinase - enzymes present in brain, heart and skeletal muscles - elevates with MI, skeletal muscle injury, strenuous exercise, drinking too much alcohol, certain meds/supplements) (CKMB - specific to cardiac muscle)
  • check tetanus status - when in doubt, give tetanus shot
  • Remove any jewelry…closely monitor distal pulses in extremities with circumferential burns….escharotomy PRN
  • Every patient with significant burns gets a Foley catheter*****
  • Pain control: Especially in patients with widespread second-degree burns
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38
Q

burn management in ER

look closely at eyes for evidence of

A

corneal burns

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39
Q

Any patient with > 20% BSA partial thickness burn needs NG tube placed, as an _____ is likely

A

ileus

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40
Q

Any patient with > 20% BSA partial thickness burn needs __________ placed, as an ileus is likely

A

NG tube

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41
Q

emergency department burn victims: what should be obtained on any suspected inhalation injury

A

ABGs
carboxyhemoglobin level
CXR
EKG

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42
Q

emergency department burns: check urine for

A

myoglobin & CPK

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43
Q

every patient with significant burns needs a

A

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

44
Q

what is an escharotomy

A

surgical incision of the eschar and superficial fascia in order to permit the cut edges to separate and restore blood flow to unburned tissue. Edema may form beneath the inelastic eschar of a full-thickness burn and compress arteries, thus impairing blood flow and necessitating an escharotomy.

45
Q

fluid resuscitation requirements for burn patients = called the Parkland formula

A

⦁ Adults: NS or RL 4ml x weight (kg) x % BSA for 1st 24hr; Give half of that amount during first 8 hours, and the other half over the next 16 hours

⦁ Children: NS or RL 3ml x weight (kg) x %BSA (admin schedule same as adult = half in first 8 hours, other half in next 16 hours)

  • called the Parkland Formula
    ex: For example, an adult person weighing 75 kg with burns to 20% of his or her body surface area would require 4 x 75 x 20 = 6,000 mL of fluid replacement within 24 hours. 3,000 mL given in first 8 hrs after incident, remaining 3,000 given over following 16 hrs
46
Q

DRESSINGS

-For minimal burns or burns that are being treated as an outpatient:

A

⦁ 1% silver sulfadiazine (silvadene)
⦁ Re-evaluate every 24 hours until full extent of burn is known
⦁ Dressing changes BID until burn stops weeping
⦁ Commercial preparations containing honey shown to be of benefit

  • silvadene
  • honey
  • BID
  • re-eval q24hrs until extent of burn is known
47
Q

TRANSFER GUIDELINES FOR BURNS

A

Partial thickness burns of > 10% BSA

Burns involving face, hands, feet, genitalia, perineum, or major joints

Third-degree burns in any age group

Electrical burns, especially lightning injuries

Burns with preexisting complicating medical disorders

Children with significant burns that are not in a children’s hospital

WHEN IN DOUBT CALL THE REFERRAL BURN CENTER

48
Q

what is shock

A

defined as inadequate tissue/organ perfusion

⦁ pump failure
⦁ decreased peripheral resistance
⦁ hemorrhage

49
Q

cardiac response to shock

A
  • tachycardia
  • increased myocardial contractility / oxygen demand
  • constriction of peripheral blood vessels (to perfuse tissues rapidly?)
50
Q

renal response to shock

A
  • stimulates an increase in renin secretion
  • vasoconstriction of arteriolar smooth muscle
  • stimulation of aldosterone secretion by adrenal cortex
51
Q

neuroendocrine response to shock

A
  • increase in circulating ADH (water retention)
52
Q

metabolic acidosis causes vaso____________

A

vasoconstriction

53
Q

shock cascade

A
  • inadequate perfusion –> cell hypoxia –> energy deficit –> lactic acid accumulation & decrease in pH –> metabolic acidosis (–> vasoconstriction –> failure of pre-capillary sphincters –> peripheral pooling of blood) –> cell membrane dysfunction & failure of sodium pump –> intracellular lysozymes release digestive enzymes (-> efflux of potassium and influx of sodium & water) –> toxic substances enter circulation –> capillary endothelium damaged –> further destruction / dysfunction / cell death
54
Q

TYPES OF SHOCK

A

o HYPOVOLEMIC
o SEPTIC
o CARDIOGENIC
o NEUROGENIC

o HYPOVOLEMIC
⦁ decreased vascular volume
⦁ hemorrhagic

o SEPTIC
⦁ systemic infections lead to hypotension & decreased vascular volume

o CARDIOGENIC
⦁ shock resulting from some abnormal cardiac function

o NEUROGENIC
⦁ due to failure of vasomotor regulation & pooling of blood in dilated vessels –> suddenly the tank is too big

55
Q

the earliest manifestation of shock

A

TACHYCARDIA

56
Q

SIGNS OF SHOCK

A

⦁ TACHYCARDIA = **earliest manifestation
⦁ Hypotension
⦁ Decreased urine output
⦁ Altered mental status

57
Q

Fluid repletion for shock

A
  • fluid repletion with LR or NS
  • clinical signs (BP, urine output, mental status, peripheral perfusion) are often adequate to guide resuscitation
  • the development of peripheral edema is often due to acute dilutional hypoalbuminemia (which is normal after surgery) - so peripheral edema should not be used as a marker for adequate fluid resuscitation or fluid overload

COLLOIDS FOR SHOCK

  • Albumin
  • Hespan
  • however, isotonic crystalloid solutions are preferred for shock fluid repletion
58
Q

what clinical sign should NOT be used as a marker for adequate fluid resuscitation or fluid overload?

A

PERIPHERAL EDEMA (due to acute hypoalbuminemia)

59
Q

physiologic responses to hemorrhagic shock (blood loss is cause of inadequate perfusion)

A

⦁ Tachycardia (HR increases)
⦁ Cardiac contractility increases
⦁ Blood is shunted to vital organs (peripheral vasoconstriction) - causes pale extremities
⦁ Decreased urine output (to conserve water & sodium)

60
Q

physiologic effects at site of blood loss during hemorrhagic shock

A

⦁ Local activation of coagulation system
⦁ Affected blood vessels contract
⦁ Activated platelets adhere to damaged vessels
⦁ Activated platelets release Thromboxane A2 - which has prothrombotic properties: stimulates activation of new platelets as well as increases platelet aggregation

61
Q

TXA2 is released from

action of TXA2

A

Activated platelets release Thromboxane A2

stimulates activation of new platelets as well as increases platelet aggregation

62
Q

clinical presentation of hemorrhagic shock

A 
⦁	Tachycardia
⦁	Tachypnea
⦁	Narrow Pulse Pressure
⦁	Decreased Output
⦁	Cool Clammy Skin
⦁	Poor Capillary Refill
⦁	Decreased CVP --> Flat neck veins
⦁	Hypotension (late)
⦁	Altered Mental Status (late)
63
Q

hemorrhagic shock treatment

A 
- IV Lines
⦁	Minimum of 2 lines
⦁	Peripheral preferred***
⦁	minimum = 16 gauge
⦁	2 tries max, if unsuccessful = use IO (intraosseus)
  • Initial Fluid bolus
    ⦁ give as rapidly as possible
    ⦁ 1-2 L for adults
    ⦁ 20 mL/kg for kids
  • then - continued fluids = 3 mL crystalloid for every 1mL blood loss
  • monitor urine for adequate fluid
    ⦁ 30-50 mL/hr for adults
    ⦁ 1 mL/kg/hr for kids (2 mL/kg/hr for peds < 1 year)
64
Q

hemorrhagic shock treatment: IV LINES

minimum of ________ lines

________ lines preferred

minimum ____ gauge

2 tries max, if unsuccessful =

adults initial bolus

peds initial bolus

after initial bolus = infusion of

monitor urine for adequate fluid: adult vs peds

A

2

peripheral

16

IO (intra-osseous)

1-2 L

20 mL/kg

3 mL crystalloid for every 1 mL blood lost

urine output adults = 30-50 mL/hr
urine output peds = 1 mL/kg/hr
urine output peds < 1 = 2 mL/kg/hr

65
Q

kids fluid dose/weight

A

20 mL/kg

66
Q

treatment for SEVERE hemorrhagic shock

A

⦁ replace blood (Packed RBCs)
⦁ May have to replace platelets and give FFP
⦁ The reversal of clinical manifestations of severe hypovolemia is often adequate to guide resuscitation
⦁ Identify the source of bleeding!**
⦁ Monitor ABGs: persistent acidosis should be treated with fluids
⦁ Monitor calcium
⦁ Monitor for coagulopathy (DIC - clotting to prevent bleeding, but then still bleeding out due to having used up all clotting factors)
⦁ Hypothermia is a big concern! - use warm fluids & warm blankets, and keep recovery rooms warm

67
Q

goal of therapy with hemorrhagic shock

A

Restoration of organ perfusion and adequate tissue oxygenation

- this is signified by
⦁	appropriate urinary output
⦁	 central nervous system function
⦁	 skin color
⦁	 return of pulse and blood pressure towards normal.

**urine output & level of mentation = more important than BP

68
Q

Restoration of organ perfusion and adequate tissue oxygenation is signified by

A

⦁ appropriate urinary output
⦁ central nervous system function
⦁ skin color
⦁ return of pulse and blood pressure towards normal.

**urine output & level of mentation = more important than BP

69
Q

Shock resulting from some abnormal cardiac function

A

cardiogenic shock

⦁ 10-20% due to AMI with > 50% fatality

70
Q

***HALLMARK OF CARDIOGENIC SHOCK =

A

HYPOTENSION WITH SIGNS OF INCREASED PVR***

71
Q

clinical manifestations of cardiogenic shock

A

HYPOTENSION WITH SIGNS OF INCREASED PVR*** = hallmark

also have weak, thready pulse
have cool, clammy skin
altered mental status
decreased urine output

72
Q

hemorrhagic shock signs/symptoms summary

A

tachycardia, decreased cardiac output, hypotension, vasoconstriction / increased PVR (to prevent bleeding out), decreased pulmonary capillary pressure

73
Q

cardiogenic shock signs/symptoms summary

A

HYPOTENSION & INCREASED PVR (from vasoconstriction) - want to maintain perfusion to heart. Have increased pulmonary capillary resistance

74
Q

what is septic shock

A

SIRS = 2/4 (fever, pulse > 90, RR > 20 or PaCO2 < 32, WBC count > 12,000 or < 4000)

Sepsis = SIRS + Infection (often associated with increased lactate)

Severe Sepsis = SIRS + MSOF (multi-system organ failure)

Septic shock = Sepsis + refractory hypotension despite fluid administration (SBP < 90)

SEPTIC SHOCK = - Sepsis + hypotension (despite adequate resuscitation) along with the presence of perfusion abnormalities; may include but aren’t limited to
⦁ lactic acidosis
⦁ oliguria
⦁ or an acute alteration in mental status

75
Q

septic shock usually caused by gram

A

NEGATIVE bacteria

exception = TSS = usually caused by staph

76
Q

Predisposing co-morbid states are common with septic shock

A

Diabetes
leukemia
immunosuppression

77
Q
  • Relative hypovolemia occurs with septic shock due to
A

pooling of blood in microcirculation and loss of fluid into interstitial spaces due to increased capillary permeability

78
Q

what shock has wide pulse pressure

A

septic shock (but still hypotensive…)

79
Q

septic shock from TSS

A

exception of gram positive (staph)

Diffuse red rash
thrombocytopenia
usually within 5 days of menses

80
Q

common sites & bugs for sepsis

A

⦁ GU: E. coli, Klebsiella, Proteus, Pseudomonas

⦁ Resp: Strep pneumoniae, Staph aureus

⦁ Below diaphragm: Aerobic Gram negative bacilli, Clostridium

81
Q

neurogenic shock is most often caused by

A

spinal cord injury

82
Q
  • do NOT use colloids in _____ shock; as increased capillary permeability will cause _______________
A

septic

pulmonary edema

83
Q

do NOT use inotropic agents (vasopressors) in ANY shock state except

A

septic or cardiogenic shock

unless central venous monitoring shows patient to be normo-volemic and they remain hypotensive

84
Q

CLINICAL SYMPTOMS OF POST-OP SEPSIS

A 
⦁	 fever
⦁	 chills
⦁	 malaise
⦁	 hypotension
⦁	 mental status changes
85
Q

explaining post-op sepsis

A
  • “blood poisoning” = presence of bacteria or other infectious organisms or other toxins in the blood (septicemia) or in other tissues of the body
86
Q

ETIOLOGY OF SEPSIS

A

Any microorganism: bacteria, virus, parasite, or fungus
Common portals of entry into the bloodstream
⦁ GI tract: Enterobactericeae, Pseudomonas, anaerobes
⦁ Skin: Staphylococcus, beta-hemolytic streptococci
⦁ GU tract: Enterobactericeae, Neisseria gonorrhea
⦁ Respiratory tract: Pneumococcus (strep pneumo), Hemophilus, viruses
⦁ Oral: Group A beta-hemolytic streptococci, anaerobes

87
Q

o Risk Factors for Gram Negative Bacillary Sepsis

A 
⦁	Diabetes mellitus
⦁	Cancer
⦁	Cirrhosis
⦁	Burns
⦁	Invasive procedures/devices
⦁	Neutropenia
88
Q

o Risk Factors for Gram Positive Sepsis

A

⦁ Vascular devices
⦁ Indwelling mechanical devices
⦁ IV drug administration/use
⦁ Burns

89
Q

o Risk Factors for Fungemia

A

⦁ Immunosuppressed with neutropenia

⦁ Broad-spectrum antimicrobial therapy

90
Q

RISK FACTORS FOR SEVERE SEPSIS

A

⦁ Age > 50
⦁ Primary pulmonary disease
⦁ Abdominal infection site
⦁ CNS infection

91
Q

CLINICAL SIGNS OF POST-OP SEPSIS

A 
⦁	Fever
⦁	Leukocytosis
⦁	Tachypnea
⦁	Tachycardia
⦁	Reduced Vascular Tone
⦁	Organ Dysfunction
92
Q

SIRS

A
  • Presentation and progression varies greatly
  • 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:
    ⦁ Fever (oral temp > 38C….100.4F) or hypothermia (<36C…96.8F); Hypothermia is especially common in elderly, neonates, uremic patients and alcoholics
    ⦁ Tachypnea (>24 breaths/minute) - early sign of systemic illness
    ⦁ Tachycardia (HR > 90 beats/minute)
    ⦁ Leukocytosis (WBC >12,000/microliter), Leukopenia (WBC <4000/microliter), or neutrophilic bands >10% (left shift)
  • SIRS = just inflammation - can be infectious or non-infectious…don’t know yet
93
Q

non-septic causes of SIRS

A

Pancreatitis, Burns, Trauma, Adrenal insufficiency
Pulmonary embolism, Dissecting or ruptured aortic aneurysm, Myocardial infarct
Occult hemorrhage, Cardiac tamponade, Post-cardiopulmonary bypass surgery
Drug overdose, Anaphylaxis

94
Q

CLINICAL MANIFESTATIONS OF SEPSIS

A

Hypotension and DIC predispose patient to development of:

acrocyanosis (cyanosis of the extremities with mottled discoloration of skin of the digits, wrists, ankles and profuse sweating and coldness of the digits) and

peripheral ischemic necrosis (digits)

SO…

1) Acrocyanosis
2) Peripheral ischemic necrosis

  • Dermatological Lesions
    ⦁ secondary seeding of skin & soft tissue produces cellulitis, pustules, bullae, and hemorrhagic lesions
    ⦁ petechiae/purpura = think N. meningitis and H. flu
    ⦁ Tick bites in endemic areas & petechiae = think RMSF
    ⦁ Erythema gangrenosum lesions (bullous lesion surrounded by edema that undergoes central hemorraghic necrosis) & neutropenia = think Pseudomonas
    ⦁ Generalized erythroderma in septic patient . . . R/O toxic shock syndrome (TSS) secondary to S. aureus or Streptococcus pyogenes (Group A streptococci)
95
Q
  • Dermatological Lesions
    ⦁ secondary seeding of skin & soft tissue produces cellulitis, pustules, bullae, and hemorrhagic lesions
    ⦁ petechiae/purpura = think _________
    ⦁ Tick bites in endemic areas & petechiae = think __
    ⦁ Erythema gangrenosum lesions (bullous lesion surrounded by edema that undergoes central hemorraghic necrosis) & neutropenia = think ______
A

N. meningitis and H. flu

RMSF

Pseudomonas

96
Q

SEPSIS & GI MANIFESTATIONS

⦁ Nausea, vomiting, diarrhea & ileus suggest

_____________may precede sepsis

A

acute gastroenteritis

cholestatic jaundice**

97
Q

________________ (GI) may precede sepsis

A

cholestatic jaundice

98
Q

MAJOR COMPLICATIONS OF SEPSIS

A

o Cardiopulmonary
⦁ Hypotension secondary to abnormal distribution of blood fluids/volume with resulting hypovolemia and dehydration
⦁ Hypoxemia
⦁ Hypercapnia
⦁ Acute Respiratory Distress Syndrome (ARDS)

o Renal
⦁ Oliguria, azotemia, proteinuria, nonspecific urinary casts, and polyuria may occur
⦁ Renal failure secondary to acute tubular necrosis (ATN) induced by hypotension and capillary injury

o Coagulopathies
⦁ Thrombocytopenia (in 10-30% of patients)
⦁ DIC (platelets < 50,000/microliter)

o Neurologic complications
⦁ Usually only occur after prolonged periods of sepsis (weeks to months)

99
Q

severe sepsis

A

Defined by (1) or (2) below

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

o or (2) Hypotension

100
Q

septic shock =

A

Severe Sepsis (organ dysfunction) with hypotension (defined by arterial SBP < 90 mmHg or 40 mmHg less than patient’s normal BP) that is unresponsive to fluid resuscitation

101
Q

refractory septic shock

A

Septic shock that lasts for > 1 hour and does not respond to fluid or pressor administration

102
Q

multiple organ dysfunction syndrome

A

Dysfunction of more than one organ, requiring intervention to maintain homeostasis

103
Q

mechanisms of cell injury / death

A

Cellular Necrosis (ischemic injury)
Apoptosis
Leukocyte-mediated tissue injury
Cytopathic Hypoxia

104
Q

PATHOPHYS OF SEPSIS INDUCED ORGAN-FAILURE

A

1) CYTOKINE PRODUCTION leads to massive production of endogenous vasodilators
2) Structural changes in the endothelium –> fluid leaks out into interstitium –> edema
3) Plugging of microvascular beds with neutrophils / fibrin / microthrombi to repair endothelium –> impaired perfusion
4) organ-specific vasoconstriction

105
Q

THERAPEUTIC STRATEGIES FOR POST-OP SEPSIS

A 
Renal replacement therapies….dialysis
Surgical intervention
Drainage
Cardiovascular support (vasopressors, inotropes)
Culture directed Antimicrobial therapy
Mechanical ventilation.
Transfusion for hematologic dysfunction
Enteral/parenteral nutritional support
Minimize exposure to hepatotoxic and nephrotoxic therapies.
Optimize organ perfusion 
Expand effective blood volume 
Hemodynamic monitoring

SURGERY EXAM II (7 decks)

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