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Diseases > Sepsis and Septic Shock, Diseases- Yr 3, Wk 1 > Flashcards

Sepsis and Septic Shock, Diseases- Yr 3, Wk 1 Flashcards

1
Q

Give the definition of sepsis:

A

-Sepsis derives from the Greek work “sepo” meaning decay or decomposition
-systemic illness caused by microbial invasion of normally sterile parts of the body
(you will get sepsis if a microorganism enters a part of the body that is normally sterile eg the brain or the meninges)

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2
Q

Describe the 4 different stages that comprise the traditional model of sepsis:

A

1) SIRS (Systemic Inflammatory Response Syndrome): temp >38 or <36, HR >90, RR >20 or PaCo2 <32
WBCs >12,000 or <4,000 (High or Low WCC) or >10% bands (2 or more of the above criteria)
2) Sepsis: SIRS + infection
3) SevereSepsis: Sepsis + End Organ Damage
4) Septic Shock: Severe Sepsis + Hypotension

(-you can get SIRS with pancreatitis, following burns, post-surgery, trauma)
(-there are things that can cause SIRS without infection e.g the point above)

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3
Q

Definition of sepsis:

a) Sepsis
b) Septic shock

A

a) Sepsis: is defined as life-threatening organ dysfunction caused by dysregulated host response to infection
- organ dysfunction can be identified as an acute change in total SOFA score >2 points consequent to the infection
- SOFA score >2 reflects an overall mortality risk of approx 10% in a general hospital population with suspected infection

b) Septic Shock: can be identified with a clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain MAP
>65mmHg and having serum lactate of >2mmol/l despite adequate volume resuscitation
-patients with septic shock have a hospital mortality of 40%

(septic shock means that the person has sepsis and they have hypotension or else they have a very high lactate despite giving them fluids)

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4
Q

What does the SOFA score stand for?

A

Sequential Organ Failure Assessment Score

(-intensive care uses this scoring system to tell whether a patient is going to do well or not
-patients with a low score will do better than patients with a high score)

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5
Q

What is the name for the new definition of sepsis?

A

qSOFA

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6
Q

What is the basis of qSOFA?

A

patients with suspected infection who are likely to have a prolonged ICU stay or die in the hospital can be promptly identified with a qSOFA

(it doesn’t tell you if the patient has sepsis or not but it tells us if the patient will do well or badly)

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7
Q

Give the criteria of qSOFA:

A
  • Hypotension Systolic BP <100 mmHg
  • Altered mental status
  • Tachypnea RR >22/ min

Score of > or equal to 2 criteria suggests a greater risk of a poor outcome

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8
Q

Why is sepsis important?

A
  • common condition
  • becoming more common
  • increased morbidity
  • increased mortality

(more common as patients living longer or on medication that alter their immune system eg chemotherapy

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9
Q

Describe survival in septic shock based on antimicrobial delay:

A

Very important graph: (look it up in the lecture)

  • If you delay giving antibiotics even by minutes (x axis) - the longer it takes to give antibiotics - the survival goes down dramatically
  • giving antibiotics at the onset of septic shock is v important
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10
Q

For each hour’s delay in administering antibiotics in septic shock…….(finish this sentence)

A

…..mortality increases by 7.6%

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11
Q

Name the guideline used to help in the treatment options in sepsis:

A

SEPSIS 6

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12
Q

SEPSIS

A

time is life

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13
Q

List some of the body’s defence against sepsis:

A
  • Physical barrier: skin, mucosa, epithelial lining
  • Innate immune system: IgA in GI tract, dendritic cells/ macrophages
  • Adaptive Immune system: lymphocytes, immunoglobulins

(IgA in GI tract keeps organisms away)

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14
Q

Describe the origin of sepsis:

A
  • originates from a breach of integrity of host barrier, whether physical or immunological
  • organism enters the bloodstream creating a septic state
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15
Q

Describe the pathophysiology of sepsis:

A

-Uncontrolled inflammatory response
-Patients with sepsis have features consistent with immunosuppression;
: loss of delayed hypersensitivity
: inability to clear infection
: predisposition to nosocomial infection
-Probable change of the sepsis syndrome over time
: initially there is an increase in inflammatory mediators
: Later, there is a shift toward an anti-inflammatory immunosuppressive phase
:depends on the health of the individual patient

(-patient loses ability to fight infection and patient is predisposed to other infections
-initially, an increase in inflammatory markers)

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16
Q

List the 3 phases in the pathogenesis of sepsis:

A

1) Release of bacterial toxins
2) Release of mediators
3) Effects of specific excessive mediators

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17
Q

Describe phase 1: Release of bacterial toxins:

A
  • Bacterial invasion into body tissues is a source of dangerous toxins
  • May or may not be neutralised and cleared by existing immune system
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18
Q

Name some commonly released toxins:

a) Gram positive
b) Gram negative

A

a) Gram positive: Lipopolysaccharide (LPS)

b) Gram negative:
-Microbial-associated molecular pattern (MAMP);
: lipoteichoic acid (important gram -ve to remember)
: muramyl dipeptides
-Superantigens
:staphylococcal toxic shock syndrome toxin (TSST)
: streptococcal exotoxins

(2 types of toxins- endotoxins and exotoxins)

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19
Q

Describe phase 2: Release of mediators in response to infection:

A
  • effects of infections due to endotoxin release
  • effects of infections due to exotoxin release
  • mediator role on sepsis
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20
Q

Describe endotoxin release in sepsis:

A

-LPS needs an LPS-binding protein to bind to macrophages
-LTA do not need such proteins
-pro-inflammatory response
-small amounts of superantigens will cause a large amount of mediators to be secreted: cascade effect
(exotoxin release you get these super antigens which bind immediately to T-lymphocytes which releases cascade of other mediators and patient then becomes extremely unwell)

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21
Q

MEDIATOR ROLE IN SEPSIS: Name the 2 types of mediators that can be released:

A

Th1 and Th2 (T-helper)

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22
Q

What happens as the result of pro-inflammatory mediators?

A

pro-inflammatory mediators- causes inflammatory response that characterises sepsis
(Th1- provides pro-inflammatory mediators
Th2- is a compensatory anti-inflammatory reaction)

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23
Q

What can happen as a result of the compensatory anti-inflammatory reaction?

A

can cause immunoparalysis

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24
Q

Name some

a) pro-inflammatory mediators and
b) anti-inflammatory mediators

A

a) IL-2, IL-8, IL-15

b) IL-4, IL-10, IL-13

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25
Q

describe the first step in the pathophysiology of sepsis:

A

bacteria come in and breach the first line of defence (skin, epithelial lining)

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26
Q

PHASE 3: Effects of specific excessive mediators
Describe the action of
a) pro-inflammatory mediators
b) Anti-inflammatory mediators

A

a) pro-inflammatory mediators:
- promote endothelial cell-leukocyte adhesion
- release of arachidonic acid metabolites
- complement activation
- vasodilatation of blood vessels by NO
- Increase coagulation by release of tissue factors and membrane coagulants
- cause hyperthermia

b) Anti-inflammatory mediators:
-Inhibit TNF alpha
-Augment acute phase reaction
-Inhibit activation of coagulation system
Provide negative feedback mechanisms to pro-inflammatory mediators

(-brings in leukocytes and those T-cells will stay in the area where the infection is
-vasodilation- more circulation around the infected area (hence why you get erythema in cellulitis)

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27
Q

Normally, there is a balance between the various immue responses, name these 2 “normally” balanced immune responses

A

Pro-inflammatory and compensatory anti-inflammatory

28
Q

What would be the mismatch in terms of balance of the 2 various immune responses when septic shock with multiorgan failure and death occurs?

A

Greater: Pro-inflammatory
Less: Compensatory anti-inflammatory

29
Q

What would be the mismatch in terms of balance of the 2 various immune responses when immunoparalysis with uncontrolled infection and multiorgan failure occurs?

A

Greater: compensatory anti-inflammatory
Less: Pro-inflammatory

30
Q

Describe the balance of immune responses in

a) the hyperimmune state
b) the hypoimmune state

A

a) too much pro-inflammatory

b) too much compensatory anti-inflammatory

31
Q

There are various clinical features of sepsis…..what are the 3 main categories which this depends on?

A
  • host
  • organism
  • environment
32
Q

Organ dysfunction can occur in sepsis: name some different effects sepsis has on

a) the CNS
b) the Respiratory system
c) the liver
d) the renal system
e) the CVS
f) blood tests

A

a) altered consciousness, confusion, psychosis
b) tachypnoea, PaO2: <70mmHg, sats <90%
c) Jaundice, inc liver enzymes, decreased albumin, inc PT
d) oliguria, anuria, increased creatinine
e) Tachycardia, hypotension
f) dec platelets, protein C
inc PT/ APTT, D-Dimer
(increased D-DIMER indicates a problem with the coagulation system of the body)

33
Q

List some of the general features of sepsis:

A

-Fever >38- presents as chills, rigors, flushes, cold sweats, night sweats etc
-Hypothermia <36- esp in elderly, very young, immunosuppressed
-tachycardia (>90 BPM)
-tachypnoea (>20 BPM)
-altered mental status- esp in elderly
-hyperglycaemia (>8mmol/L in the absence of diabetes)
(Fever is most common, impaired glucose tolerance: in sepsis their sugars tend to rise)

34
Q

List some of the inflammatory variables in sepsis:

A

-leucocytosis
-leucopenia
-normal WCC with greater than 10% immature forms
-High CRP
-High procalcitonin
(Low WCC is a poor prognostic indicator usually- cant produce white cells, High crp IS V COMMON AND MARKER to tell how severe the infection is although quite non-specific
Procalcitonin is only elevated in bacterial infection)

35
Q

List some haemodynamic variables in sepsis:

A

-Arterial hypotension (systolic <90mmHg or MAP <70mmHg)
-SvO2 >70%
(Systolic BP less than 90- indication the patient might be going down the route of septic shock)

36
Q

List some organ dysfunction variables in sepsis:

A
  • arterial hypoxaemia (Pao2/FiO2 <50mmHg)
  • oliguria (<0.5ml/Kg/h)
  • creatinine increase compared to baseline
  • coagulation abnormalities (PT>1.5 or APTT >60s)
  • Ileus (not able to produce stools and get abdominal distension)
  • thrombocytopenia (<150,000/ml)
  • Hyperbilirubinaemia
37
Q

List some Tissue perfusion variables in sepsis

A

-High lactate
-Skin mottling and reduced capillary perfusion
(The blood investigation most important for someone presenting with sepsis is LACTATE!
Lactate tells us whether the patient has tissue hypoperfusion
If you can’t correct lactate in the first 30 mins-1 hour then high chance of death)

38
Q

Give some risk factors which may effect someone who presents with sepsis (effect of host on sepsis presentation):

A
  • Age
  • Co-morbidities (COPD, DM, CRF, disseminated malignancy)
  • Immunosuppression
  • Previous surgery- (splenectomy)
39
Q

Give some of the effects of organism on presentation of sepsis:

A

-Gram positive vs gram negative
-Virulence factors (ex: MRSA, toxin secretion, ESBL, KPC, NDM-1)
-Bioburden
(ESBL, KPC, NMD1, bioburden- drug resistant)

40
Q

True or false: the same organism can give you different presentations?

A

TRUE

41
Q

List some of the effects of the environment on presentation of sepsis:

A
  • Occupation
  • Farmers (aspergillosis)
  • Travel
  • Abroad (malaria for ex, hotel (legionella))
  • Hospitalisation
  • Previous hospitalisation (possibility of getting multi drug resistant organisms)
42
Q

Case 1: 55 year old man, history of dm, smoker and IHD, admitted through A and E with FEVER, NAUSEA, VOMITING AND ABDOMINAL PAIN X 4 HOURS:

a) examination
b) Investigations
c) Treatment in A and E
d) Why didn’t he improve?
e) On post-take round another blood test was carried out- serum amylase- with a result of 1450, what is your diagnosis?
f) What is his management now?

A

a) Temp: 38.3, resp rate 24/min, pulse: 120 bpm, BP: 160/85, HS: normal, chest: clear, abdomen: tenderness in epigastrium, no rebound, BS present
(QSofa: doesn’t trigger QSofa SO NOT OVERLY CONCERNED WITH HIM AT THIS POINT)

b) WCC: 15,600/ml
Platelets: 240,000/ml
INR: 1.2
U&amp;E: Normal
LFT: Bil 80; AAT 20; ALP 35; GGT 40
Lactate 2.2mmol/l
Glucose: 8.8mmol/l
CXR and AXR: normal

(lactate of 2.2 which is slightly increased, Glucose; 8.8; diabetic)

c) Sepsis 6
Started on Amoxicillin, Gentamicin and Metronidazole for intra-abdominal sepsis
6 hours later patient failed to improve

d) Admitted with SIRS
e) Acute pancreatitis
f) Antibiotics stopped and patient transferred to surgery for further management

43
Q

What is the main method of treatment followed in a patient with sepsis?

A

the sepsis 6

44
Q

The earlier you start with the sepsis 6….(finish this sentence)…

A

…..the higher the likelihood the patient will have a good outlook

45
Q

Give the 2 acronyms// phrase used when using the sepsis 6 for treatment:

A

Take 3: Give 3

OR

2 As, 2 Bs, 2 Cs

46
Q

Describe Take 3: Give 3

A 
Take 3: Give 3;
Take: 
1) Blood cultures 
2) Blood lactate 
3) Measure urine output 
TAKE ALL OF THE ABOVE 
Give: 
1) Oxygen aim sats 94-98% 
2) IV Antibiotics 
3) IV fluid challenge 
GIVE ALL OF THE ABOVE
47
Q

Describe 2 As, 2 Bs, 2 Cs:

A

2 As: -Air enriched with o2
-Antibiotics after blood culture

2 Bs: -Blood culture
-Blood gas with lactate

2 Cs: -crystaloid Bolus
-Catheter (urinary) if severe sepsis or septic shock

48
Q

Describe the Diagnostic criteria for sepsis:

A

Infection, documented or suspected, and some of the following:
General variables
Fever (> 38.3°C)
Hypothermia (core temperature < 36°C)
Heart rate > 90/min–1 or more than two sd above the normal value for age
Tachypnea
Altered mental status
Significant edema or positive fluid balance (> 20 mL/kg over 24 hr)
Hyperglycemia (plasma glucose > 140 mg/dL or 7.7 mmol/L) in the absence of diabetes
Inflammatory variables
Leukocytosis (WBC count > 12,000 μL–1)
Leukopenia (WBC count < 4000 μL–1)
Normal WBC count with greater than 10% immature forms
Plasma C-reactive protein more than two sd above the normal value
Plasma procalcitonin more than two sd above the normal value
Hemodynamic variables
Arterial hypotension (SBP < 90 mm Hg, MAP < 70 mm Hg, or an SBP decrease > 40 mm Hg in adults or less than two sd
below normal for age)
Organ dysfunction variables
Arterial hypoxemia (Pao2/Fio2 < 300)
Acute oliguria (urine output < 0.5 mL/kg/hr for at least 2 hrs despite adequate fluid resuscitation)
Creatinine increase > 0.5 mg/dL or 44.2 μmol/L
Coagulation abnormalities (INR > 1.5 or aPTT > 60 s)
Ileus (absent bowel sounds)
Thrombocytopenia (platelet count < 100,000 μL–1)
Hyperbilirubinemia (plasma total bilirubin > 4 mg/dL or 70 μmol/L)
Tissue perfusion variables
Hyperlactatemia (> 1 mmol/L)
Decreased capillary refill or mottling
(Take 3 and give 3)

49
Q

The 3 that you “TAKE”….why do you “take” these?

A

1) Blood cultures: -make microbiological diagnosis (30-50% positive)
- if spike in temperature, take 2 sets

2) Lactate: Marker of generalised hypoperfusion/ severe sepsis/ poorer prognosis
3) Low Urine output: marker of renal dysfunction

(Fever, chills, hypothermia, leukocytosis, left shift of neutrophils, neutropenia, and the
development of otherwise unexplained organ dysfunction (e.g., renal failure or signs of
hemodynamic compromise) are specific indications for obtaining blood for culture. Blood
cultures should be taken as soon as possible after the onset of fever or chills

Take 3 sets in the possibility of infective endocarditis)

50
Q

What antibiotics do you GIVE in sepsis?

A
  • Based on working diagnosis from History and examination
  • Local antibiotic guidelines
  • BUT consider allergy
  • BUT consider previous MRSA, ESBL, CPE
  • BUT consider Abx toxicity/ interactions
51
Q

Give some information on the administration of antibiotics in sepsis:

A

Administer effective intravenous antimicrobials within the first hour of recognition of septic
shock (Grade 1B) and severe sepsis without septic shock (Grade 1C) as the goal of therapy.
■ Initial empiric anti-infective therapy of one or more drugs that have activity against all likely
pathogens (bacterial and/or fungal or viral) and that penetrate in adequate concentrations
into tissues presumed to be the source of sepsis (Grade 1B) should be employed.
■ Antimicrobial regimen should be reassessed daily for potential deescalation (Grade 1B).

Its very important to come up with diagnosis as will be different antibiotic requirements for chest infection and for meninigitis

52
Q

What is the tool that is used when giving antibiotic treatment ?

A

INFECTION MANAGEMENT GUIDELINES: Empirical Antibiotic Therapy

53
Q

Name a biomarker that can identify the possibility of adverse outcomes:

A

LACTATE

54
Q

what are the 2 types of lactate?

A

Type A and Type B

55
Q

Describe lactate type A:

A

Hypoperfusion

Type A is the type we are interested in when referring to sepsis

56
Q

Describe lactate type B

A

mitochondrial toxins, alcohol, malignancy, metabolism errors

57
Q

Give some extra information on lactate and IV fluids:

A

Patients with severe sepsis and septic shock may experience ineffective arterial circulation
due to the vasodilatation associated with infection or impaired cardiac output. Poorly perfused
tissue beds result in global tissue hypoxia, which is often found in association with an elevated
serum lactate level. A serum lactate value greater than 4 mmol/L (36 mg/dL) is correlated
with increased severity of illness and poorer outcomes even if hypotension is not yet present.
As such, patients who are hypotensive or have a lactate greater than 4 mmol/L (36 mg/dL)
require intravenous fluids to expand their circulating volume and effectively restore
perfusion pressure.

Fluid challenges require the definition of four components: 1) the type of fluid to be
administered; 2) the rate of fluid infusion (e.g., 500 mL to 1,000 mL over 30 minutes); 3) the
end points (e.g., mean arterial pressure of >65 mm Hg, heart rate of <110 beats per minute);
and 4) the safety limits (e.g., development of pulmonary edema).
Stop any antihypertneisve therapy that they are on

58
Q

IV fluids, what is the guideline recommendation?

A
  • 30ml/ kg fluid challenge (expert opinion)

- 2.1L 70kg patient

59
Q

When should you consider referral to High Dependency Unit (HDU)?

A
  • Low BP responsive to fluids
  • Lactate >2 despite fluid resuscitation
  • Elevated creatinine
  • Oliguria
  • Liver dysfunction, Bil, PT, Pit
  • Bilateral infiltrates, hypoxaemia
60
Q

Give the definition of severe sepsis:

A

sepsis-induced tissue hypoperfusion or organ dysfunction (any of the following thought to be due to the infection):

  • Sepsis-induced hypotension
  • Lactate above upper limits laboratory normal
  • Urine output < 0.5 mL/kg/hr for more than 2 hrs despite adequate fluid resuscitation
  • Acute lung injury with Pao2/Fio2 < 250 in the absence of pneumonia as infection source
  • Acute lung injury with Pao2/Fio2 < 200 in the presence of pneumonia as infection source
  • Creatinine > 2.0 mg/dL (176.8 μmol/L)
  • Bilirubin > 2 mg/dL (34.2 μmol/L)
  • Platelet count < 100,000 μL
  • Coagulopathy (international normalized ratio > 1.5)

(HDU is different to intensive care as it can do everything apart from intubating the patient)

61
Q

When should you consider ITU?

A
  • Septic shock
  • Multi organ failure
  • Requires sedation, intubation and ventilation
62
Q

There is a good diagram in the lecture slide 75- have a look)

A

have a look at picture in the lecture

63
Q

Case:

  • 68 y/old woman admitted with worsening shortness of breath
  • History of IHD, CVA and bed bound
  • On examination: Alert, temp 38, resp rate 26/min, pulse 120/min irreg, BP 85/60, chest dullness right base

What has the patient got?

A

…..qSOFA= ?? BE ABLE TO CALCULATE qSOFA score

Right sided pneumonia,

Is it community acquired- or is it aspirated (Previous stroke) ?

64
Q

What scoring system will you use in this patient with pneumonia?

A

CURB65 score

slide 80 has all the requirements in giving someone a CURB65 score

65
Q

What should be done in the next 60 mins for this patient?

A 
oxygen 
IV fluid challenge 
Blood cultures
Blood lactate 
IV antibiotics 
Monitor urine output

(SEPSIS 6!!)

Diseases (9 decks)

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