Burn, Shock, Sepsis Flashcards

1
Q

Burn Pathophysiology:

-describe the cellular changes seen

A

Cellular Changes:

  • intracellular influx of Na/H2O (edema)
  • extracellular migration of K
  • Disruption of cell membrane function
  • failure of Na pump

Burn shock with depression of myocardium and metabolic acidosis

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2
Q

Burn Pathophysiology:

  • hematologic changes
  • cell damage occurs at what temperatures?
A

Heme:

  • increase in HCT
  • increase blood viscosity
  • anemia d/t RBC destruction

Cell damage at temperatures greater than 113F

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3
Q

Burn Size:

-how is this quantified? also, describe two methods.

A

Quantified as a % of body surface area (BSA) burned.

Rapid method: based on the area of the back of the pts hand is approximately 1% of BSA

Rule of 9’s breaks portion of body into multiples of 9 with the perineum being 1% (Lund and Browder burn diagram)

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4
Q

First degree burn:

  • signs/sx
  • ex

2nd degree burn:

  • sx/signs
  • ex

3rd degree:

  • signs/sx
  • ex
A

Signs/Sx:

  • erythema
  • possibly edema
  • minimal pain
    (e. g. sunburn)

2nd degree:

Signs/sx:

  • partial thickness
  • much more painful than 3rd degree burn
  • skin appears:
  • -red/mottled
  • -blisters with broken epidermis
  • -considerable swelling
  • wet/weeping surfaces
  • -sensitive to air

e.g. deep sunburn, contact with hot liquids, flash burns from gasoline flames

3rd degree:

Signs/sx:

  • damage to all skin layers, subQ tissues, and nerve damage
  • pale white or charred
  • leathery
  • broken skin with fat exposed
  • dry surface
  • painless to pin prick
  • edema
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5
Q

Inhalation Burns:

  • signs
  • causes
  • management
A

signs:
- carbon around nose
- burns involving the mouth
- peri oral edema
- talking in raspy voice
- significant resp problems

Cause:

  • fire in enclosed area
  • remember CO exposure
  • Toxic gases from combustion*

Management: intubate early

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6
Q

Chemical Burns:

  • types
  • -which type is worse?
  • tx
A

Types:

  • alkali
  • acids

Alkali burns are more serious than acid burns b/c the alkalis penetrate deeper

Tx:
-the solution to pollution is dilution (IRRIGATE!!!)

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7
Q

Electrical Burns:
-more damage is done to the skin or deeper structures such as bone, muscle, blood vessels, and nerves?

  • what are the consequences of muscle destruction?
  • How would we tell muscle destruction has occurred and how do we manage that?
  • how do we control metabolic acidosis?
A

More damage is done to the deeper structures.

Consequences:
-occult destruction of muscle can cause rhabdomyolysis which causes the release of myoglobin and can lead to acute renal failure

Rhabdo

  • if urine is dark, assume myoglobin and increase fluids to achieve a urine output of 100 ml/hr
  • if urine doesn’t clear, use mannitol to ensure continued diuresis

Metabolic acidosis controlled by perfusion and sodium bicarbonate to alkalinize urine to soluble myoglobin.

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8
Q

Burn Management

A
  • check for evidence of airway involvement and if present consider endotracheal intubation early!
  • start 2 large bore IVs ASAP
  • inspect for corneal burns
  • estimate depth and extent of burn and record.
  • greater than 20% BSA partial thickness burn needs NG tube placed as ileus is likely
  • CBC, CMP
  • ABGs, carboxyhemaglobin level
  • CXR and EKG

Urine for myoglobin and CPK

Tetanus Status

Foley catheter placement (every pt with significant burns gets one)**

Pain control

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9
Q

Burn Management:

-adult/child fluid resuscitation, what type of fluids are used?

A

Adult fluid resuscitation: NS or RL

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10
Q

Minimal burns/outpatient burns Tx

Which burns require admission to burn center?

A

Minimal:

  • sulfadiazine/silvadene
  • re-evaluate every 24hrs
  • change dressings BID until burn stops weeping

Admission to burn center:

  • partial thickness burns of greater than 10% BSA
  • burns involving face, hands, feet, genitalia, perineum, or major joints
  • 3rd degree burns in any age group
  • electrical burns
  • burns with preexisting complications (medical disorders)
  • children with significant burns taht are not in a childrens hospital
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11
Q

Shock:

  • definition
  • cardiac response
  • renal response
  • neuroendocrine response
A

Definition:

  • inadequate tissue/organ perfusion
  • -pump failure, decreased peripheral resistance, hemorrhage

Cardiac response:

  • tachycardia
  • increased myocardial contractility/oxygen demand
  • constriction of peripheral blood vessels.

Renal Response:

  • stimulating an increase in renin secretion
  • vasoconstriction of arteriolar smooth muscle
  • stimulation of aldosterone secretion by the adrenal cortex

Neuroendocrine Response:
-increase in circulating ADH

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12
Q

What are the types of shock?

A

Types:

  • hypovolemic:
  • -decreased vascular volume
  • -hemorrhagic

-Septic: systemic infections leads to hypotension, decreased vascular volume

  • Cardiogenic:
  • -shock resulting from some abnormal cardiac function (pump failure)
  • Neurogenic:
  • -failure of vasomotor regulation and pooling of blood in dilated capacitance vessels
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13
Q

Signs of shock

A

Tachycardia
Hypotension
Decreased urine output
Altered Mental Status

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14
Q

What clinical signs can be relied on to guide fluid resuscitation?

Which fluids do we use for resuscitation in shock?

A

Clinical signs:

  • BP
  • Urine output
  • Mentals Status
  • Peripheral perfusion (warm, cold)

Fluids used in resuscitation:

  • **Isotonic saline
  • colloids
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15
Q

What are the physiological responses to blood loss?

A

Heart Rate Increases

Cardiac contractility increases

Blood shunted to vital organs (pale extremities)

Conservation of water and sodium (decreased urine output)

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16
Q

Hemorrhagic Shock:

-physiologic effects @ site of loss

A

Local activation of coagulation system

affected blood vessels contract

activated platelets adhere to damaged vessels

Activated platelets release thromboxane A2 causing platelet aggregation and increased vessel contraction.

17
Q

Hemorrhagic Shock clinical presentation

A

tachycardia

tachypnea

narrow pulse pressure

decreased output

cool clammy skin

poor capillary refill

Decreased CVP (flat neck veins)

hypotension (late)

AMS

18
Q

Hemorrhagic Shock:

  • Tx
  • -how many IV lines?
  • -what size needle/catheter
  • -administer how much fluid for initial bolus in adults/children?
  • -normal urine output/hr in adults and peds
  • -if VS return to normal after initial bolus then what? if they responed and then drop?
A

Tx:

  • 2 large bore IVs
  • 16 gauge
  • 1-2L in adults as rapidly as possible
  • 20ml/kg

Normal urine output/hr:

  • adults 30-50ml/hr
  • peds: 1ml/kg/hr

If VS return to normal after initial bolus then
type/cross/hold blood and monitor urine output and vs.

If vs return to normal and then drop you give them blood and plan to go back to OR.

19
Q

Hemorrhagic Shock:

  • Tx:
  • -other than blood replacement what are some other blood products may need to be infused?
  • Labs to monitor
  • management of hypothermia
A

Other blood products:

  • FFP
  • Platelets

Labs:

  • ABG
  • Calcium
  • Coagulopathy

Hypothermia:

  • use warm fluids
  • use warm blankets
  • keep recovery rooms warm
20
Q

What is the goal of therapy in hemorrhagic shock?

A

Restoration of organ perfusion and adequate tissue oxygenation

21
Q

Signs of restoration of organ perfusion and adequate tissue oxygenation?

A

Appropriate urine output

central nervous system function

skin color (pink up)

return of pulse and blood pressure towards normal.

22
Q

Cardiogenic Shock:

  • hallmark sign
  • other signs
  • tx
A

Hallmark signs:
-hypotension with signs of increased peripheral vascular resistance (weak, thready pulse, cool, clammy skin)

  • Other:
  • -inadequate organ perfusion: AMS and decreased urine output

Tx:
-pressors

23
Q

Septic Shock:

  • define
  • gram -/+ bug
  • explain why there is relative hypovolemia in septic shock.
A

Define:

  • sepsis induced with hypotension despite adequate resuscitation along with the presence of perfusion abnormalities with may include but are not limited to:
  • lactic acidosis
  • oliguria
  • acute alteration in mental status

Gram - bacteria causing endotoxic shock, except for TSS this is usually caused by Staph

Relative Hypovolemia occurs d/t loss of fluid into the interstitial spaces d/t increased capillary permeability. (decreased volume in vessels)

24
Q

Septic Shock:

  • wide or narrow pulse pressure?
  • what are the common bugs causing Septic shock in each of the following:
  • -GU
  • -Resp
  • -Below diaphragm
A

Wide pulse pressure

GU:
-e. Coli, Klebsiella, proteus, pseudomonas

Resp: strep pneumo, staph aureus

Diaphragm:
-aerobic gram - bacilli like clostridium

25
Q

Neurogenic Shock:

  • MC cause
  • pathophys
A

MC cause: spinal cord injury

Pathophys:
-failure of vasomotor regulation and pooling of blood in dilated capacitance vessels- suddenly the tank is too big.

26
Q

Shock Therapy and Special considerations:
-do you use colloids in septic shock? why/why not?

-Can you use inotropic agents (vasopressors) in shock states?

A

Septic shock DO NOT use colloids, increased capillary edema will cause pulmonary edema.

Do NOT use inotropic agents in any shock state EXCEPT for septic and cardiogenic shock UNLESS central venous monitoring shows pt to be normovolemic and remain hypotensive.

27
Q

Skin is warm/cold and dry/clammy in each of the following:

  • hemorrhagic shock
  • cardiogenic shock
  • septic shock
  • neurogenic shock
A

Hemorrhagic, cardiogenic, and septic shock are cool and clammy.

Neurogenic shock is warm.

28
Q

Sepsis:

  • define
  • sx & signs
  • risk factors
A

Define: presence of bacteria or other infectious organisms or their toxins in the blood (septicemia) or in other tissues of the body.

Sx:

  • fever
  • chills
  • malaise
  • hypotension
  • AMS
  • leukocytosis
  • tachypnea
  • tachycardia
  • pale, cold, sweat
  • organ dysfunction
  • acrocyanosis
  • peripheral ischemic necrosis

Risk factors:

  • greater than 50YO
  • primary pulmonary dz
  • abd infection site
  • CNS infection
29
Q

SIRS:

-definition

A

infectious or noninfectious etiology defined by 2 or more of the following:

  • fever (38C), hypothermia (less than 36C)
  • Tachypnea (greater than 24)
  • Tachycardia (greater than 90)
  • Leukocytosis (greater than 12K)
  • Leukopenia (less than 4K)
  • Neutrophilic bands greater than 10% (left shift)

*Sepsis is SIRS that has a proven or suspected microbial etiology

30
Q

Sepsis:

  • dermatologic lesions
  • GI manifestations
A

Dematologic:

  • cellulitis
  • pusutles, bullae
  • hemorrhagic lesions
  • purpura/petechiae (N. meningitis and H. flu)
  • Erythema gangrenosum lesions (pseudomonas aeruginosa)
  • generalized erythroderma
  • GI: N/V, diarrhea
  • cholestatic jaundice may precede sepsis
31
Q

Major complications of Sepsis:

  • cardiopulmonary
  • renal
  • coagulopathies
  • neurologic:
A

Cardiopulmonary:

  • hypotension (resulting in hypovolemia and dehydration)
  • hypoxemia
  • hypercapnia
  • ARDS

Renal:

  • oliguria, azotemia, proteinuria, urinary casts, polyuria
  • renal failure secondary to acute tubular necrosis (induced by hypotension and capillary injury)

Coagulopathies:

  • thrombocytopenia
  • DIC

Neurologic:
-only occur prolonged periods of sepsis

32
Q

Clinical course of sepsis?

A

Mild sepsis, severe sepsis, severe septic shock, multiple organ dysfunction (MODS), Multiple organ failure (MOF)

33
Q

Define:

  • severe sepsis

- septic shock

A

Severe sepsis:

  • (1) or (2) below:
  • -(1) sepsis with one or more signs of organ dysfunction such as:
  • metabolic acidosis
  • acute encephalopathy
  • oliguria
  • hypoxemia
  • DIC

– or (2) hypotension.

Severe Septic Shock:
-severe sepsis WITH hypotension (defined by SBP less than 90 or 40mmHg less than pts normal BP) that is unresponsive to fluid resuscitation.