Sepsis Flashcards
sepsis
When the body’s immune system becomes overactive in response to an infection, causing inflammation which can affect how well other tissues and organs work
(sepsis=bacterial infection)
(anaphylaxis=allergic reaction)
Sepsis is a syndrome
A group of body dysfunctions found together
Dysfunctions that progress together in a predictable way
High mortality rate, variable clinical presentations
Severe Sepsis is very deadly
Sepsis Criteria (pwpt slide 8)
(Systemic inflammatory response syndrome) SIRS: High HR, high RR, high Temp, abnormal WBC count, low pCO2(low cell metabolism)
Sepsis: 2 SIRS + infection
Severe Sepsis: Sepsis + hypotension, end organ damage, elevated lactate
Septic Shock: Severe sepsis + hypotension + persistent signs of end organ dysfunction (50% mortality)
Normal response to infection:
Local infectoin
non-specific inflamm response
3 phases: vasodilation, vessel permeability, tissue repair
Pathophysiology of Sepsis:
Uncontrolled, exaggerated immune response
Endothelium damage, cell mediator activation, disruption of coagulation system homeostasis
Vasodilation and capillary permeability
Systemic inflammatory response
End-organ damage, death
Revisit notes on slide 11
Revisit notes on slide 11
What can cause SIRS aside from infections?
trauma, burns, pancreatitis, etc. (body ticked off from irritation)
SIRS
Systemic Inflammatory Response Syndrome
A constellation of abnormal signs
Many triggers, infection is most common
EMS uses a version of SIRS that doesn’t rely on blood test results (WBC count, ABG)
Temp, HR, RR, glucose, mental status
Risk Factors for Sepsis
Extremes of age (old and young):
-Can’t communicate, need careful assessment
-Patients with developmental delay
-Cerebral Palsy
Recent surgery, invasive procedure, illness, childbirth/pregnancy termination/miscarriage
Reduced immunity
Increased Risk for Sepsis
DIABETES, DIABETES, DIABETES (TEST)
Liver cirrhosis
Autoimmune diseases (lupus, rheumatoid arthritis, body already attacks itself)
HIV/AIDS
Para/quadriplegics
Sickle cell disease
Splenectomy patients
Compromised skin (chronic wounds, burns, ulcers)
Increased Risk for Sepsis
Chemotherapy
Post-organ transplant (bone marrow, solid organ)
Chronic steroid use
Recent antibiotic use
Indwelling catheters of any kind (dialysis, Foley, IV, PICC, PEG tubes, etc)
Signs/Symptoms
Symptoms of sepsis are often nonspecific and include the following:
Fever = most common (elderly patients often do NOT mount a febrile response)
Flu-like symptoms
Chills/shaking (mistaken for seizure)
Nausea/vomiting
Mental status changes/fatigue/lethargy
Revisit notes slide 18
Revisit notes slide 18
Causes of Sepsis
Pneumonia
UTI
Infection after abdominal surgery
skin infection (MRSA abscess)
United Effort to Improve Survival from Sepsis
Research from past 20 years is saving lives
Rapid identification, fluids, antibiotics
Education to all physicians, nurses, technicians
“Care bundles” monitored by Feds
Sepsis alert teams in hospitals
Chart review
Administrative support at all levels
EMS role in Sepsis
Decreased time to intravenous fluids
Decreased time to antibiotics
Decreased mortality
Shorter hospital stay
EMS can have a significant impact on patients
Identifying Sepsis Patient
Look for and ask about infection
Did you look at all the skin???
Look for and ask about risk factors for infection
Check a temperature accurately
> 38°C (100.4°F)
< 36°C (96°F) more dangerous!!
Identifying Sepsis Patient
Look for SIRS criteria in the vital signs
Look for shock/dehydration
Check end-tidal CO2
Treating Sepsis
Airway/breathing
-Get sats > 92%
-NRB, CPAP, invasive
airway
Circulation
-2 large bore IV,
consider IO
-20 cc/kg NS bolus
-May repeat if lungs
remain clear
Sepsis Alert
Communicate your suspicion early!
It doesn’t matter if accepting facility has a formal sepsis alert response process
Explicitly communicate abnormal vitals (especially temp) just as you would in trauma
What about Dopamine?
Dopamine traditionally used for shock in EMS
Studies show that survival is WORSE when dopamine is used to treat septic shock
Probably better to stick with fluids and rapid transport
Hospitals and other EMS use norepinephrine for best survival in septic shock
Respiratory Component of Sepsis
increased O2 demand
Keep sats ≥ 92 % (NRB, CPAP, intubation)
Respiratory failure can happen quickly
Acute Respiratory Distress Syndrome
Sepsis Pitfalls
Beta blockers block tachycardia response (tachy was notable but actually a good thing at that moment in a way)
Altered mentation not recognized as “end-organ failure”
Temperatures not checked
EtCO2 not checked or recognized
Discouragement due to hospital response
note:
As sepsis progresses, circulatory abnormalities lead to an imbalance of systemic oxygen delivery and demand, resulting in global tissue hypoxia.
Global tissue hypoxia is a key development preceding multi-organ failure and death
EtCO2 and Lactate (??)
Low EtCO2 associated with high lactic acid
Low EtCO2 predicts mortality
Emergent Conditions: Necrotizing Fasciitis
Distinguishing necrotizing fasciitis from necrotizing myositis may be difficult as skeletal muscle and fascia are involved in both syndromes
Necrotizing fasciitis:
-Most often monomicrobial
-Usual causative agent is Streptococcus pyogenes (Group A beta-hemolytic streptococci)
-Can also be caused by other streptococcal species, and occasionally by Staphylococcus aureus
-Infections can be polymicrobial (mixed aerobic and anaerobic bacteria)
-A history of exposure to brackish water or MARINE LIFE should raise suspicion for Vibrio vulnificans or Aeromonas species
-Patients with burn injuries are susceptible to Pseudomonas species
Necrotizing myositis
-Often caused by Clostridia species (clostridial myonecrosis or “gas gangrene”)
Necrotizing Fasciitis
Presentation is similar to cellulitis but way worse
rapid progression
systemic toxicity
severe pain (pain often subsides as nerve are destroyed)
multi-organ failure is common as infection progresses
Necrotizing Fasciitis: Lab Findings
Elevated white blood cell count, erythrocyte sedimentation rate and C-reactive protein
Elevated creatine kinase may indicate muscle involvement
Blood, wound, and tissue cultures should be obtained
Histologic specimens may demonstrate
Extensive tissue destruction
Thrombosis of blood vessels
Bacteria spreading along fascial planes
What is kinase?
creatine kinase?
NF: Imaging
CT or MRI of the affected area may show gas in tissues or fascial plane infection
Imaging may also appear normal, so rely on clinical suspicion and surgical evaluation
NF: Meds
Antibiotic therapy should then be tailored to culture results
Broad-spectrum antibiotic therapy
Should be initiated whenever the diagnosis is suspected
Should cover aerobic and anaerobic organisms
NF: Initial therapy
Carbap(enem) + agent against MRSA + clindamycin for its antitoxin effects against strains of streptococci + staphylococci
NF: Therapy cont.
Patients with exposure histories that suggest less common etiologies should have additional therapy targeted to those organisms (sea world worker)
Intravenous immunoglobulin for streptococcal necrotizing soft tissue infections
-Has been shown to reduce mortality when added to surgical and antibiotic therapy
NF: Surgery
Early and extensive debridement is essential for survival
Surgical evaluation should not be delayed while awaiting imaging or other diagnostic tests, especially in the setting of rapid progression of clinical manifestations
NF: Follow up
Antibiotic therapy should be continued until all infected tissue has been removed and the patient has stabilized
Toxic Shock Syndrome
Multiple organisms that can cause toxic shock syndrome (TSS) include:
Staphylococcus aureus
Streptococcus
Certain Clostridium species (C perfringens, C sordellii)
(TSS defined as a systemic shock response to ^)
Staph aureus:
Strains of staphylococci may produce toxins that can cause three important entities
-Scalded skin syndrome, typically in children, or bullous impetigo in adults
-TSS
-Enterotoxin food poisoning
Streptococcal infection
Any streptococcal infection—and necrotizing fasciitis in particular, can cause TSS
TSS is due to pyrogenic erythrotoxin superantigen that stimulates massive release of inflammatory cytokines believed to mediate the shock
Invasive disease
-Risk factors are age (very young or older persons) and underlying medical conditions
-Bacteremia occurs in most cases
Clostridium sordellii
C sordellii is a rare cause of endometritis and toxic shock syndrome following childbirth
Fatal cases of uterine infection following medically induced abortion with mifepristone have been reported
S aureous
Toxic shock is characterized by abrupt onset of high fever, vomiting, and watery diarrhea
Sore throat, myalgias, and headache are common
A diffuse macular erythematous rash and nonpurulent conjunctivitis (like allergic eyes) are common, and desquamation (skin pealing off), especially of the palms and soles, is typical during recovery
S aureous
Toxic shock is characterized by abrupt onset of high fever, vomiting, and watery diarrhea
Sore throat, myalgias, and headache are common
A diffuse macular erythematous rash and nonpurulent conjunctivitis (like allergic eyes) are common, and desquamation (skin pealing off), especially of the palms and soles, is typical during recovery
Streptococcal TSS
Invasion of skin or soft tissues
Acute respiratory distress syndrome
Kidney failure
Skin rash and desquamation may not be present
C sordellii
Abdominal pain
Absence of fever
Onset of illness was within 4–5 days of ingestion of mifepristone
Clinical course is fulminant
Infection appeared to be limited to the uterus, which shows
Necrosis
Edema
Hemorrhage
Acute inflammatory changes
easy test question:
If we see desquamation, what’s the bacteria? Strept TSS
S aureus vs C sordellii
S aureus
Blood cultures classically are negative because symptoms are due to the effects of the toxin and not to the invasive properties of the organism
C sordellii
Tachycardia, severe hypotension, capillary leak syndrome with edema
Profound leukocytosis, hemoconcentration
S aureus Treatment
Rapid rehydration, antistaphylococcal antibiotics (eg, parenteral nafcillin or oxacillin or, in the penicillin allergic patient, clindamycin), management of kidney or heart failure, and most importantly removal of sources of toxin (eg, removal of tampon, drainage of abscess)
Intravenous immune globulin may be considered, although there are limited data compared to streptococcus TSS
Strept TSS Treatment
β-Lactam, such as penicillin, plus clindamycin, (potent inhibitor of toxin production) 600 mg every 8 hours intravenously
Consider giving immune globulin as source of specific antibody to streptococcal exotoxins
C sordellii Treatment
Early recognition
Aggressive resuscitation from shock
Immediate surgical debridement with hysterectomy
Administration of an antimicrobial active against C sordellii, including:
Penicillin
Ampicillin
Macrolide
Clindamycin
Tetracycline
Metronidazole
Small differences in treatment
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