BURNS SHOCK SEPSIS Flashcards
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 _______ & __________
> 65
18-35 years old
2:1
hot drinks or baths
2 layers of skin = _______ & ________
- People have skin of various thickness
- skin thickness varies with _____
Dermis + Epidermis
age
Skin is a __________ barrier for evaporative loss
Skin is also responsible for the control of ___________
SEMI-PERMEABLE
body temperature
1st degree burn =
2nd degree burn =
3rd degree burn =
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
CELLULAR CHANGES WITH BURNS
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
local progressive injury with burns
o Liberation of vasoactive substances
o Disruption of cellular function
o Edema formation
cell damage with burns - occurs at temps > ______ due to ___________
113F
denaturation of protein
3 zones
zone of coagulation
zone of stasis
zone of hyperemia
describe
zone of coagulation
zone of stasis
zone of hyperemia
⦁ 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
which zone is the main area of focus when treating burn injuries
zone of stasis
TRIAD OF DEATH FOR BURNS
- Acidosis
- Coagulopathy
- Hypothermia
Burns are quantified as percentage of
BSA
Rule of 9’s - breaks down body portions into multiples of 9, and perineum = 1%
back of hand is approximately ______ BSA
perineum is ______ BSA
1%
1%
which burn diagram is best
Lund & Browder
which degree burn is a sunburn
first
clinical presentation of 1st degree superficial burn
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
2nd degree superficial partial thickness burn
⦁ 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
examples of 2nd degree superficial partial thickness burn
deep sunburn
contact with hot liquids
flash burns from gasoline flames
skin appearance with 2nd degree superficial partial thickness burn
red or mottled skin blisters with broken epidermis WET / WEEPING SURFACES considerable swelling VERY PAINFUL sensitive to the air
most painful of all burns
superficial partial thickness burns
2nd degree deep partial thickness burn
⦁ 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)
dry, no blisters, pain
1st degree
no scarring
painful
blanching
red/erythematous
wet, blisters, pain
2nd degree superficial no scarring - may have pigment changes PAIN blanching erythematous / pink
dry, blisters, usually no pain
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
3rd degree = full thickness burn
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
skin appearance with full thickness 3rd degree burn
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
- extends through entire skin & into underlying fat, muscle and bone
FOURTH DEGREE BURN - FULL THICKNESS
INHALATION BURNS
⦁ 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
CHEMICAL BURNS
⦁ 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
how to treat chemical burns
dilution - IRRIGATE IRRIGATE IRRIGATE
with chemical burns: __________ are more serious than ________ burns
***Alkali burns are more serious than acid burns, because alkali penetrates deeper
why are alkali burns more serious that acid burns
alkali burns penetrates deeper
ELECTRICAL BURNS
⦁ ***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)
with electrical burns = causes ________ = now worried about __________
rhabdomyolysis
acute kidney failure
treatment for myoglobinuria
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)
ABCDEs of major burn patients
⦁ 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)
burn management in ER
- 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
burn management in ER
look closely at eyes for evidence of
corneal burns
Any patient with > 20% BSA partial thickness burn needs NG tube placed, as an _____ is likely
ileus
Any patient with > 20% BSA partial thickness burn needs __________ placed, as an ileus is likely
NG tube
emergency department burn victims: what should be obtained on any suspected inhalation injury
ABGs
carboxyhemoglobin level
CXR
EKG
emergency department burns: check urine for
myoglobin & CPK
every patient with significant burns needs 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
what is an escharotomy
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.
fluid resuscitation requirements for burn patients = called the Parkland formula
⦁ 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
DRESSINGS
-For minimal burns or burns that are being treated as an outpatient:
⦁ 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
TRANSFER GUIDELINES FOR BURNS
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
what is shock
defined as inadequate tissue/organ perfusion
⦁ pump failure
⦁ decreased peripheral resistance
⦁ hemorrhage
cardiac response to shock
- tachycardia
- increased myocardial contractility / oxygen demand
- constriction of peripheral blood vessels (to perfuse tissues rapidly?)
renal response to shock
- stimulates an increase in renin secretion
- vasoconstriction of arteriolar smooth muscle
- stimulation of aldosterone secretion by adrenal cortex
neuroendocrine response to shock
- increase in circulating ADH (water retention)
metabolic acidosis causes vaso____________
vasoconstriction
shock cascade
- 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
TYPES OF SHOCK
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
the earliest manifestation of shock
TACHYCARDIA
SIGNS OF SHOCK
⦁ TACHYCARDIA = **earliest manifestation
⦁ Hypotension
⦁ Decreased urine output
⦁ Altered mental status
Fluid repletion for shock
- 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
what clinical sign should NOT be used as a marker for adequate fluid resuscitation or fluid overload?
PERIPHERAL EDEMA (due to acute hypoalbuminemia)
physiologic responses to hemorrhagic shock (blood loss is cause of inadequate perfusion)
⦁ Tachycardia (HR increases)
⦁ Cardiac contractility increases
⦁ Blood is shunted to vital organs (peripheral vasoconstriction) - causes pale extremities
⦁ Decreased urine output (to conserve water & sodium)
physiologic effects at site of blood loss during hemorrhagic shock
⦁ 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
TXA2 is released from
action of TXA2
Activated platelets release Thromboxane A2
stimulates activation of new platelets as well as increases platelet aggregation
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 (late)
hemorrhagic shock treatment
- 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)
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
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
kids fluid dose/weight
20 mL/kg
treatment for SEVERE hemorrhagic shock
⦁ 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
goal of therapy with hemorrhagic shock
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
Restoration of organ perfusion and adequate tissue oxygenation 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
Shock resulting from some abnormal cardiac function
cardiogenic shock
⦁ 10-20% due to AMI with > 50% fatality
***HALLMARK OF CARDIOGENIC SHOCK =
HYPOTENSION WITH SIGNS OF INCREASED PVR***
clinical manifestations of cardiogenic shock
HYPOTENSION WITH SIGNS OF INCREASED PVR*** = hallmark
also have weak, thready pulse
have cool, clammy skin
altered mental status
decreased urine output
hemorrhagic shock signs/symptoms summary
tachycardia, decreased cardiac output, hypotension, vasoconstriction / increased PVR (to prevent bleeding out), decreased pulmonary capillary pressure
cardiogenic shock signs/symptoms summary
HYPOTENSION & INCREASED PVR (from vasoconstriction) - want to maintain perfusion to heart. Have increased pulmonary capillary resistance
what is septic shock
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
septic shock usually caused by gram
NEGATIVE bacteria
exception = TSS = usually caused by staph
Predisposing co-morbid states are common with septic shock
Diabetes
leukemia
immunosuppression
- Relative hypovolemia occurs with septic shock due to
pooling of blood in microcirculation and loss of fluid into interstitial spaces due to increased capillary permeability
what shock has wide pulse pressure
septic shock (but still hypotensive…)
septic shock from TSS
exception of gram positive (staph)
Diffuse red rash
thrombocytopenia
usually within 5 days of menses
common sites & bugs for sepsis
⦁ GU: E. coli, Klebsiella, Proteus, Pseudomonas
⦁ Resp: Strep pneumoniae, Staph aureus
⦁ Below diaphragm: Aerobic Gram negative bacilli, Clostridium
neurogenic shock is most often caused by
spinal cord injury
- do NOT use colloids in _____ shock; as increased capillary permeability will cause _______________
septic
pulmonary edema
do NOT use inotropic agents (vasopressors) in ANY shock state except
septic or cardiogenic shock
unless central venous monitoring shows patient to be normo-volemic and they remain hypotensive
CLINICAL SYMPTOMS OF POST-OP SEPSIS
⦁ fever ⦁ chills ⦁ malaise ⦁ hypotension ⦁ mental status changes
explaining post-op sepsis
- “blood poisoning” = presence of bacteria or other infectious organisms or other toxins in the blood (septicemia) or in other tissues of the body
ETIOLOGY OF SEPSIS
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
o Risk Factors for Gram Negative Bacillary Sepsis
⦁ Diabetes mellitus ⦁ Cancer ⦁ Cirrhosis ⦁ Burns ⦁ Invasive procedures/devices ⦁ Neutropenia
o Risk Factors for Gram Positive Sepsis
⦁ Vascular devices
⦁ Indwelling mechanical devices
⦁ IV drug administration/use
⦁ Burns
o Risk Factors for Fungemia
⦁ Immunosuppressed with neutropenia
⦁ Broad-spectrum antimicrobial therapy
RISK FACTORS FOR SEVERE SEPSIS
⦁ Age > 50
⦁ Primary pulmonary disease
⦁ Abdominal infection site
⦁ CNS infection
CLINICAL SIGNS OF POST-OP SEPSIS
⦁ Fever ⦁ Leukocytosis ⦁ Tachypnea ⦁ Tachycardia ⦁ Reduced Vascular Tone ⦁ Organ Dysfunction
SIRS
- 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
non-septic causes of SIRS
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
CLINICAL MANIFESTATIONS OF SEPSIS
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)
- 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 ______
N. meningitis and H. flu
RMSF
Pseudomonas
SEPSIS & GI MANIFESTATIONS
⦁ Nausea, vomiting, diarrhea & ileus suggest
_____________may precede sepsis
acute gastroenteritis
cholestatic jaundice**
________________ (GI) may precede sepsis
cholestatic jaundice
MAJOR COMPLICATIONS OF SEPSIS
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)
severe sepsis
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
septic shock =
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
refractory septic shock
Septic shock that lasts for > 1 hour and does not respond to fluid or pressor administration
multiple organ dysfunction syndrome
Dysfunction of more than one organ, requiring intervention to maintain homeostasis
mechanisms of cell injury / death
Cellular Necrosis (ischemic injury)
Apoptosis
Leukocyte-mediated tissue injury
Cytopathic Hypoxia
PATHOPHYS OF SEPSIS INDUCED ORGAN-FAILURE
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
THERAPEUTIC STRATEGIES FOR POST-OP SEPSIS
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
