Burns, Shock, Sepsis Flashcards
1
Q
Epidemiology of Burns?
A
- mortality in pts over 65
- highest risk is 18-35 yo and 2:1 male to female in both injury and death
- in kids highest incidence is scalding injuries from hot drinks to bath
2
Q
Fxn of the skin?
PP of burns - cell changes?
A
- skin: dermis and epidermis
- various thickness
- thickness varies w/ age
- skin is semi-permeable barrier for evaporative loss
- skin also responsible for control of body temp
cellular changes seen in burns:
- intracellular influx of Na/H2O
- extracellular migration of K
- disruption of cell membrane fxn
- failure of Na pump
- Burn shock w/ depression of myocardium and metabolic acidosis
3
Q
Heme changes in burns? Local progressive injury?
A
heme changes:
- increase in hematocrit
- increase in blood viscosity
- anemia due to RBC destruction
local progressive injury:
- liberation of vasoactive substances
- disruption of cellular fxn
- edema formation
4
Q
At what temp does cell damage occur? Diff zones?
A
- occurs when above 113F due to denaturation of protein
- zone of coag: irreversibly destroyed
- zone of stasis: stagnation of microcirculation, can/will extend if not tx appropriately
- zone of hyperemia: increase blood flow
5
Q
How is burn size quantified?
A
- as % of BSA burned
- rapid method based on area of back of pt’s hand 1% of BSA
- Rule of 9’s
6
Q
Characteristics of 1st degree burn?
A
- erythema of skin
- possibly minimal surrounding edema
- minimal pain
7
Q
Characteristics of 2nd degree burn?
A
- deeper than 1st degree
- involve partial thickness
- ex: deep sunburn, contact w/ hot liquids, flash burns from gas flames
- usually much more painful than 3rd degree
- skin appears: red or mottled, blisters w/ broken epidermis, considerable swelling, wet/weeping surfaces, painful, sensitive to air
8
Q
Characteristics of 3rd degree?
A
- damage to all skin layers, subq tissues, and nerve endings
- skin appears: pale white or charred appearance, leathery, broken skin w/ fat exposes, dry surface, painless to pinprick, edema
9
Q
Signs of airway damage in burn pt? Tx?
A
- carbon around nose
- burns involving mouth
- sig resp problems
- fire in enclosed areas
- remember CO exposure
- toxic gases from combustion (house fires)
- intubate early
10
Q
What are chemical burns? Tx?
A
- alkali or acids can cause burns
- alkali burns more serious than acid burns b/c alkalis penetrate deeper
- Don’t try to neutralize, soln to poln is dilution - Irrigate!!
11
Q
What can occur w/ electrical burns? Tx?
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 rhabdomylosis which causes the release of myoglobin and can lead to acute renal failure
tx: - if urine dark - assume myoglobin and increase fluids to achieve a urine output of 100ml/hr
- if urine doesn’t clear: mannitol to ensure cont diuresis
- control metabolic acidosis by perfusion and add Na bicarb as needed to alkalinize urine to solubilize myoglobin
12
Q
ED management of burns?
A
- major burn pts are mult injury trauma pts: ABCDE
- check for evidence of airway involvement and if present - consider endotracheal intubation
early - start 2 large bore IVs ASAP: place in non-burned areas if practical (if no access - IO)
- do secondrary survey and look closey at eyes for evidence of corneal burns
- est depth and extent of burn and record
- any pt w/ greater than 20% BSA partial thickness burn needs NG tube placed as ileus is likely
- remove any jewelry: closely monitor distal pulses in extremities w/ circumferential burns - escharotomy PRN
- pain control: esp in pts w/ widespread 2nd degree burns
13
Q
What tests, labs are needed in burn pt? What does q pt w/ sig burns need?
A
- CBC, lytes, BUN, Cr, glucose (chem 7) should be obtained
- ABGs, carboxyhemaglobin level, CXR and EKG on any suspected inhalation injury
- urine for myoglobin and CPK
- check tetanus status and when in doubt, give
- q pt w/ sig burns gets a Foley catheter:
criticla in monitoring resuscitation, until Swan-Ganz or CVP line placed- only way to ensure adequate renal perfusion
14
Q
Fluid resuscitation in burn pts?
A
- adults: NS or RL
- half of above over the first 8h from time of burn
- other half over next 16 hrs
15
Q
Dressings for burn pts w/ minimal burns or burns that are being tx as an oupt?
A
- 1% silver sulfadiazine (silvadene)
- re-evaluate q 24 hrs until full extent is known
- dressing changes BID until burn stops weeping
- commercial preps containing honey shown to be of benefit
16
Q
Transfer guidelines for Burn pts?
A
- partial thickness burns of more than 10% BSA
- burns involving face, hands, feet, genitalia, perineum or major jts
- 3rd degree burns in any age group
- electrical burns, especially lightening injuries
- burns w/ preexisting complicating medical disorders
- kids w/ significant burns that aren’t in a children’s hosp
- when in doubt call referral burn center
17
Q
Definition of shock?
A
inadequate tissue/organ perfusion:
- pump failure
- decreased peripheral resistance
- hemorrhage
18
Q
Cardiac, renal, and neuroendocrine response?
A
cardiac response:
- tachycardia
- increased myocardial contractility/O2 demand
- constriction of peripheral blood vessels
renal response:
- stimulating an increase in renin secretion
- vasoconstriction of arteriolar smooth muscle
- stimulation of aldosterone secretion by adrenal cortex
neuroendocrine response:
- increase in circulating ADH
19
Q
Progression of shock?
A
- inadequate perfusion
- cell hypoxia
- energy deficit
- lactic acid accum and fall in ph - leads to anaerobic metabolism
- metabolic acidosis - leads to vasoconstriction and failure of pre-capillary sphincters - and then to peripheral pooling of blood
- cell membrane dysfxn and failure of Na pump
- intracellular lysosomes release digestive enzymes lead to efflux of K and influx of Na and H2O
- toxic substances enter circulation
- capillary endothelium damaged
- further destruction, dysfxn, and cell death
20
Q
Diff types of shock?
A
- hypovolemic: decreased vascular volume, hemorrhagic
- septic: systemic infections lead to hypotension, decreased vascular volume
- cardiogenic: shock resulting from some abnormal cardiac fxn
- neurogenic: due to failure of vasomotor regulation and pooling of blood in dilated capacitance vessels - suddenly tank is too big
21
Q
What are the signs of shock?
A
- tachycardia (earliest manifestation)
- hypotension
- decreased urine output
- altered mental status
22
Q
Tx of shock?
A
- fluids: fluid repletion w/ isotonic saline
- clinical signs, including BP, urine output, mental status, and peripheral perfusion are often adequate to guide resuscitation
- development of peripheral edema is often due to acute dilutional hypoalbuminemia and shouldn’t be used as marker for adequate fluid resuscitation or fluid overload
- colloids: albumin, hespan for bleeding (but saline solns are still generally preferred)
23
Q
Physiological responses to blood loss?
A
physiological responses to blood loss:
- HR increases
- cardiac contractility increases
- blood shunted to vital organs: causes pale extremities
- conservation of H2O and Na: decreased urine output
24
Q
Physiological effects at site loss in hemorrhagic shock?
A
- local activation of coagulation system
- affected blood vessels contract
- activated platelets adhere to damaged vessels
- activated platelets release thromboxane A2
- thromboxane A2 causes increased vessel contraction – stimulates wound healing
25
Classic clinical presentation of hemorrhagic shock?
- tachycardia
- tachypnea
- narrow pulse pressure
- decreased output
- cool clammy skin
- poor capillary refill
- decreased CVP: flat neck veins
- hypotension (late)
- altered mental status
26
tx of hemorrhagic shock?
- minimum of 2 lines
- peripheral preferred
- minimum 16 gauge
- initial fluid bolus:
give as rapidly as possible, 1-2 L in adults, 20ml/kg in preds
- reqrs 3 ml crystalloid for q 1 ml blood loss
- monitor urine for adequate fluid (get foley in):
30-50ml/hr for adults
1 ml/kg/hr for peds (2ml/kg/hr for peds if younger than yr
- blood requirements based upon response to initial fluid bolus:
VS return to normal after bolus: type/cross/hold, and monitor urine output and vitals
if
VS return to normal and then drop - give type specific if available, O- if in pinch, plan to go back to OR
27
Tx of severe hemorrhagic shock?
- replace blood (PRBCS)
- may have to replace platelets and give FFP
- reversal of clinical manifestations of severe hypovolemia is often adequate to guid resuscitation
- ID source of bleeding
28
What needs to be monitored in hemorrhagic shock?
- monitor ABGs: persistent acidosis should be tx w/ fluids
- monitor Ca
- monitor for coagulopathy (DIC)
29
What else is a big concern for hemorrhagic shock? how can this be tx?
- hypothermia
- use warm fluids
- use warm blankets
- keep recovery rooms warm
30
Goal of therapy in hemorrhagic shock? How is this signified?
- restoration of organ perfusion and adequate tissue O2
- signified by:
approp urinary output
CNS fxn
skin color
return of pulse and BP towards normal
31
What is cardiogenic shock? Hallmark?
- shock resulting from some abnormal cardiac fxn: 10-20% due to AMI w/ over 50% fatality
- hallmark is hypotension w/ signs of increased PVR: weak thready pulse, and cool clammy skin
- inadequate organ perfusion: altered mental status and decreased UO
- ID abnormality and address - may need pressors
32
What is septic shock?
- sepsis induced w/ hypotension despite adequate resuscitation along w/ presence of perfusion abnormalities which may include but aren't limited to:
lactic acidosis
oliguria
or an acute alteration in mental status
33
Usual cause of septic shock? Why does relative hypovolemia occur?
- usually due to gram (-) bacteria causing endotoxic shock (TSS is an exception and is caused by staphyloccal toxin - present w/ diffuse red rash, thrombocytopenia, and usually w/in 5 days of menses)
- predisposing co-morbid states are common: diabetes, leukemia, immunosupression
- relative hypovolemia occurs due to pooling of blood in microcirculation and loss of fluid into interstitial spaces due to increased capillary permeability
- direct depression of myocardium also possible
34
classic hallmark sign of septic shock?
wide pulse pressure
35
Common sites and bugs of septic shock?
- GU: E. Coli, Klebseilla, proteus, pseudomonas
- Resp: strep pneumoniae, staph aureus
- below diaphragm: aerobic gram (-) bacilli, clostridium
36
What is neurogenic shock?
- Most often caused by spinal cord injury
- isolated head injuries don't cause shock
- in a trauma pt w/ isolated head injury and shock - look for another cause
- Due to failure of vasomotor regulation and pooling of blood in dilated capacitance vessels - suddenly tank is too big
- skin will be warm n neurogenic shock (compared to hemorrhagic - cold and clammy)
37
Tx don'ts in diff types of shock?
- don't use colloids in septic shock: increased capillary permeability will cause pulmonary edema
- don't use inotropic agents (vasopressors) in any shock state except septic or cardiogenic shock unless central venous monitoring shows pt to be normovolemic and they remain hypotensive
- there is no ultimate sub for blood when that is what the pt has lost: crystalloid temporize but don't tx
38
What is sepsis? Common presentation?
- "blood poisoning"
- presence of bacteria or other infectious organisms or their toxins in the blood (septicemia) or in other tissue of the body
- fever, chills, malaise, low BP, and mental status changes
39
Etiology of sepsis? Common portals?
- any microorganism: bacteria, virus, parasite, or fungus
common portals of entry into bloodstream:
- GI: enterobactericeae, pseudomonas, anaerobes
- skin: staph, beta-hemolytic strep
- GU: enterobactericeae, neisseria gonorrhea
- resp: pneumococcus, hemophilus, viruses
- oral: alpha-hemolytic strep, anaerobes
40
RFs for gram (-) bacillary bacteremia?
- DM
- Cancer
- cirrhosis
- burns
- invasive procedures/devices
- neutropenia
41
RFs for gram (+) bacteremia?
- vascular devices
- indwelling mechanical devices
- IV drug admin/use
- burns
42
RFs for fungemia?
- immunosuppressed w/ neutropenia
| - broad spectrum antimicrobial therapy
43
RFs for severe sepsis?
- over 50
- primary pulmonary disease
- abdominal infection site
- CNS infection
44
Clinical signs of sepsis?
- fever
- leukocytosis
- tachypnea
- tachycardia
- reduced vascular tone
- organ dysfxn
45
Clinical signs of sepsis?
- fever
- leukocytosis
- tachypnea
- tachycardia
- reduced vascular tone
- organ dysfxn
46
What is SIRS? Presentation?
- may have infectious or noninfectious etiology, is defined by presence of 2 or more of the following:
- fever (oral temp over 100.4F) or hypothermia (under 96.8F)
- tachypnea (over 24) - early sign of systemic illness
- tachycardia (HR over 90bpm)
- leukocytosis: WBC over 12000 or leukopenia under 4000, or neutrophilic bands: greater than 10% L shift
47
Diff b/t sepsis and SIRS?
- sepsis is SIRS that is proven or suspected microbial etiology
48
DDx for SIRS?
non-septic causes of SIRS:
- pancreatitis
- burns
- trauma
- adrenal insufficiency
- PE
- dissecting or ruptured aortic aneurysm
- MI
- occult hemorrhage
- cardiac tamponade
- post-cardiopulmonary bypass surgery
- drug overdose
- anaphylaxis
49
Clinical manifestations of sepsis?
- hypotension and DIC predispose pt to development of acrocyanosis (cyanosis of extremities w/ mottlied discoloration of skin of the digits, wrists, ankles, and profuse sweating and coldness of digits) and peripheral ischemic necrosis (digits)
- derm lesions:
secondary seeding of skin and soft tissue, produces cellulitis, pustules bullae, hemorrhagic lesions
skin lesions may be suggestive of specific pathogen:
-petechiae/purpura: N. meningitis (and H influenzae)
-tick bites in endemic areas - petechiae - RMSF
- erythema gangrenosum lesions (bullous lesion surrounded by edema that undergoes central hemorrhagic necrosis) - neutropenia and usually P. aeruginoa
- generalized erythoderma in septic pt: R/o TSS secondray to Staph aureus or strep pyogenes (Grou A)
-GI: N/V/D, and ileus suggest acute gastroenteritis
Cholestatic jaundice may precede sepsis
50
What are cardiopulm complications of sepsis?
- hypotension secondary to abnormal distribution of blood fluids/volume w/ resulting hypovolemia and dehydration
- hypoxemia
- hypercapnia
- ARDS
51
What are renal complications of sepsis?
- oliguria, azotemia, proteinuria, nonspecific urinary casts, and polyuria
- renal failure secondary to acute tubular necrosis (ATN) induced by hypotension and capillary injury
52
Coagulopathies complications of sepsis?
- thrombocytopenia (in 10-30% of pts)
| - DIC (platelets less than 50,000/microliter)
53
Neuro complications of sepsis?
- usually only occur after prolonged periods of sepsis (weeks - months)
54
What is the clincial course of sepsis? How is severe sepsis defined?
- systemic response to infection usually intensifies over time from mild sepsis to extremely severe septic shock
- severe sepsis defined by 1 or 2 below:
1 - sepsis w/ one or more signs of organ dysfxn, such as:
metabolic acidosis
acute encephalopathy
oliguria
hypoxemia
DIC
2- hypotension
55
What is septic shock?
- severe sepsis (organ dysfxn) w/ hypotension (defined by arterial SBP less than 90 mmHg or 40 mmHg less than pt's normal BP) that is unresponsive to fluid resuscitation
56
Pathogenesis of severe sepsis - excessive response?
- infection leads to microbrial products (endotoxin/exotoxin) - leads to cellular responses:
platelet activation, coag activation, oxidases, kinins complement and cytokines: TNF, IL-1, and IL-6 - lead to coagulopathy/DIC/ vasular and organ system injury and ultimately leads to multi-organ failure and death
57
What is refractory septic shock? Multiple organ dysfxn syndrome (MODS)?
- refractory septic shock: septic shock that lasts for over an 1 hr and doesn't respond to fluid or pressor admin
- MODS: dysfxn of more than one organ, requiring intervention to maintain homeostasis
58
MODs and MOF result from what? Mechanisms of cell injury/death?
- MODS and MOF result from diffuse cell injury/death resulting in compromised organ fxn
- mechanisms of cell injury/death:
- cellular necrosis (ischemic injury)
- apoptosis
- leukocyte-mediated tissue injury
- cytopathic hypoxia
59
PP 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 and subsequent tissue edema
- plugging of select microvascular beds w/ neutrophils, fibrin aggregrates, and microthrombi impair microvascular perfusion
- organ specific vasoconstriction
60
Pathway of organ dysfxn in sepsis?
infection leads to stim of inflammatory mediators which lead to:
- vasodilation leads to hypotension
- microvascular plugging
- vasoconstriction
- endothelial dysfxn leads to edema
- these all lead to maldistribution of microvasacular blood flow then to ischemia and cell death and ultimately organ dysfxn
61
What are the therapeutic strategies in sepsis?
- renal replacement therapies: dialysis
- surgical intervention
- drainage
- CV support (vasopressors, inotropes)
- culture directed antimicrobrial therapy
- mechanical ventilation
- transfusion for hematologic dysfxn
- enteral/parenteral nutritional support
- minimize exposure to hepatotoxic and nephrotoxic therapies
- optimize organ profusion
- expand effective blood volume
- hemodynamic monitoring
