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Immunology & ID > Sepsis > Flashcards

Sepsis Flashcards

1
Q

sepsis

A

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)

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2
Q

Sepsis is a syndrome

A

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

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3
Q

Sepsis Criteria (pwpt slide 8)

A

(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)

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4
Q

Normal response to infection:

A

Local infectoin

non-specific inflamm response

3 phases: vasodilation, vessel permeability, tissue repair

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5
Q

Pathophysiology of Sepsis:

A

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

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6
Q

Revisit notes on slide 11

A

Revisit notes on slide 11

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7
Q

What can cause SIRS aside from infections?

A

trauma, burns, pancreatitis, etc. (body ticked off from irritation)

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8
Q

SIRS

A

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

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9
Q

Risk Factors for Sepsis

A

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

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10
Q

Increased Risk for Sepsis

A

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)

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11
Q

Increased Risk for Sepsis

A

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)

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12
Q

Signs/Symptoms

A

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

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13
Q

Revisit notes slide 18

A

Revisit notes slide 18

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14
Q

Causes of Sepsis

A

Pneumonia
UTI
Infection after abdominal surgery
skin infection (MRSA abscess)

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15
Q

United Effort to Improve Survival from Sepsis

A

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

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16
Q

EMS role in Sepsis

A

Decreased time to intravenous fluids
Decreased time to antibiotics
Decreased mortality
Shorter hospital stay

EMS can have a significant impact on patients

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17
Q

Identifying Sepsis Patient

A

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!!

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18
Q

Identifying Sepsis Patient

A

Look for SIRS criteria in the vital signs
Look for shock/dehydration
Check end-tidal CO2

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19
Q

Treating Sepsis

A

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

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20
Q

Sepsis Alert

A

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

21
Q

What about Dopamine?

A

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

22
Q

Respiratory Component of Sepsis

A

increased O2 demand

Keep sats ≥ 92 % (NRB, CPAP, intubation)

Respiratory failure can happen quickly

Acute Respiratory Distress Syndrome

23
Q

Sepsis Pitfalls

A

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

24
Q

note:

A

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

25
Q

EtCO2 and Lactate (??)

A

Low EtCO2 associated with high lactic acid

Low EtCO2 predicts mortality

26
Q

Emergent Conditions: Necrotizing Fasciitis

A

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”)

27
Q

Necrotizing Fasciitis

A

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

28
Q

Necrotizing Fasciitis: Lab Findings

A

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

29
Q

What is kinase?

A

creatine kinase?

30
Q

NF: Imaging

A

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

31
Q

NF: Meds

A

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

32
Q

NF: Initial therapy

A

Carbap(enem) + agent against MRSA + clindamycin for its antitoxin effects against strains of streptococci + staphylococci

33
Q

NF: Therapy cont.

A

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

34
Q

NF: Surgery

A

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

35
Q

NF: Follow up

A

Antibiotic therapy should be continued until all infected tissue has been removed and the patient has stabilized

36
Q

Toxic Shock Syndrome

A

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 ^)

37
Q

Staph aureus:

A

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

38
Q

Streptococcal infection

A

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

39
Q

Clostridium sordellii

A

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

40
Q

S aureous

A

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

41
Q

S aureous

A

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

42
Q

Streptococcal TSS

A

Invasion of skin or soft tissues

Acute respiratory distress syndrome

Kidney failure

Skin rash and desquamation may not be present

43
Q

C sordellii

A

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

44
Q

easy test question:

A

If we see desquamation, what’s the bacteria? Strept TSS

45
Q

S aureus vs C sordellii

A

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

46
Q

S aureus Treatment

A

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

47
Q

Strept TSS Treatment

A

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

48
Q

C sordellii Treatment

A

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

49
Q

Small differences in treatment

A

Brush summarized this shit in five seconds, figure out a way to do the same for studying

Immunology & ID (15 decks)

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