L39 Sepsis and bacteraemia Flashcards
List 4 red flags of sepsis.
Any 4
- Responds only to voice/pain/ Unresponsive
- Acute confusional state
- Systolic BP <90 mmHg (or drop from >40 from normal)
- Heart rate >130/min
- Respiratory rate >25/min
- Needs oxygen to keep SpO2 >92%
- Non-blanching rash, mottled/ashen/cyanotic
- Not passed urine in last 18h/ UO <0.5ml/kg/hr
- Lactate >2 mmol/L
- Recent chemotherapy
What is the definition of sepsis?
- SIRS (Systemic inflammatory response syndrome) +
2. documented evidence of infection = Positive culture
What is SIRS (Systemic inflammatory response syndrome)?
- Temperature <36/ >38
- Heart rate >90/min
- Respiratory rate >20/min or PaCO2 <32 mmHg
- WBCs <4x10^9, >12 x 10^9
What is bacteraemia and septicaemia?
Presence of bacteria in blood, as confirmed by culture
Can be transient/ continuous
Septicaemia is an old term = more severe bacteraemia.
What are the possible sources of infection that we should try to locate in bacteraemia?
- Endogenous
- CNS/H&N
- Lungs
- Abdomen/intestine
- Skin/soft tissue
- Bone and joints - Exogenous
- instrumentation sites
- inhalation equipment
- IV fluids
List 2 G+ and G- bacteria that are common causes of bacteraemia.
Viruses, parasites, fungi infection are mostly in immunocompromised patients
G+
- Staph. aureus
- Strep. pyogenes
- Strep. pneumoniae
G-
- Escherichia coli
- Klebsiella pneumoniae
- Enterobacter spp.
- Pseudomonas aeruginosa
What are the MC causative agents that causes lung infections?
i) Community
ii) Nosocomial
i)
- Hemophilus influenzae
- Strep. pneumoniae
ii)
- Gram-ve bacteria
- MRSA
What are the MC causative agents that causes abdominal infections?
i) Community
ii) Nosocomial
i)
- Escherichia coli
- Anaerobes
ii)
- G-ve bacteria, anaerobes
- Candida spp.
What are the MC causative agents that causes skin and soft tissue infections?
i) Community
ii) Nosocomial
i)
- S.aureus
- S.pyogenes
- Clostridium spp.
ii)
- S.aureus (MRSA)
- G- bacteria
What are the MC causative agents that causes UTI?
i) Community
ii) Nosocomial
i)
- E.coli
- Enterococcus spp.
ii)
- G-ve bacteria
- Candida app.
What are the MC causative agents that causes CNS infection?
i) Community
ii) Nosocomial
i)
- S.pneumoniae
- N.meningitidis
ii)
- Staph spp.
- GNB
The SIRS criteria are rarely used clinical, instead _____________ is used.
An increase of ______ points indicates sepsis.
- PaO2/FiO2 ratio
- GCS
- MAP
- Administrations of vasopressors
- SCr/ UOP
- Bilirubin
- Platelet count
SOFA score
- Sequential organ failure assessment
=>2 points
What is septic shock?
- Sepsis with refractory hypotension (after adequate volume resuscitation, requiring use of inotropes)
+ - Hypoperfusion abnormalities
List 3 risk factors for sepsis.
- Age
- Underlying diseases: e.g. Malignancy - leukaemia, solid tumors; DM, cirrhosis
- Drugs: immunosuppressant, broad-spectrum Abx
- Surgery/instrumentation: catheters, ventilators, prostheses
- Burns/trauma
Pathogenesis of sepsis? (5)
- Endotoxin: Lipopolysaccharide (LPS) of GN bacterial cell wall > binds to TLR-4 (toll-like receptors)
- Activation of macrophages
- Release of cytokines: TNF-alpha, IL-1, IL-6
- Coagulation cascade (> acute respiratory distress syndrome ARDS + DIC)
+ Complement cascade
+ increase Prostaglandins and Leukotrienes
> endothelial cell damage
cytokines/PG/inflammatory and vasodilator mediators
hypotension in severe sepsis
MODS (multiple organ dysfunction syndrome)
What are the non-specific clinical features of sepsis?
- Fever
- Chills
- Malaise
- Fatigue
- Can be absent in elderly patients
Neurological: anxiety, confusion
Suggest clinical complications of sepsis (organ-based). (7)
- Lungs
- ARDS (adult respiratory distress syndrome) [Tachypnea Hypoxia] - Kidney
- AKI [oliguria/ anuria, proteinuria] - Heart
- Heart failure - GI
- N/V, diarrhoea, ileus - Liver
- liver failure - Skin
- Petechiae, purpura - Vascular
- DIC (disseminated intravascular coagulation)
What specimens should be sent to laboratory upon sepsis?
- Blood, sputum, CSF, urine, pus, tissue from obvious infected sites
Note for blood specimen for sepsis? (3)
- 2 separate sets of blood culture is required
[(aerobic + anerobic) x2] - collected 1h apart/ emergency situation at the same time at different sites before Abx therapy
- blood cultures should be taken with aseptic technique to avoid contamination by skin flora
Laboratory diagnosis of sepsis: Specimens Microscopy Culture Serology Molecular
List examples for the last 4.
- Microscopy: Gram stain, special stain
- Culture: 5-day protocol (-ve if no growth after 5 days, prolonged culture in IE/ PUO - pyrexia of unknown origin)
- Serology: ELISA, IF, Latex agglutination
- Molecular: PCR etc.
General management for sepsis? (5)
- Nutrition (Diet)
- Organ support: Cardiovascular (fluids, inotropes - force heart contractions); Ventilation
- Antibiotics
- Adjunctive therapy: (=other tx tgt with primary tx)
- activated protein C, steroids, antibodies to endotoxins - Surgical intervention: drainage, debridement
A specific toxic syndrome is the Waterhouse-Friderichsen syndrome that causes overwhelming sepsis.
What is it caused by (2)
What is the main clinical manifestation?
- Neiserria meningitidis (MC)
- Pseudomonas aeruginosa
Clinical:
- Acute bilateral adrenal haemorrhage: adrenal insufficiency
Toxic shock syndrome is an infection by _____________ with the release of _____________(2)?
What is another possible causative agent?
Staphylococcus aureus
- TSST-1 (TSS toxin-1)
- Enterotoxin B/C
Also can be Strep pyogenes with release of streptococcal pyogenic toxins A,B,C
What are the 4 criteria of Toxic shock syndrome? (4)
- Fever >38.9
- Hypotension systolic BP <90 mmHg
- Rash with subsequent desquamation (sunburn-like rash)
- Multisystem dysfunction =>3 organ systems
What is the MC cause of TSS?
use of tampons, vaginal colonisation of toxin-producing S.aureus
Which of the following are risk factors for IE?
A. Mitral valve prolapse or Aortic Stenosis
B. IV drug addict > right sided IE
C. Prosthetic heart valve
D. Poor dental hygiene
E. DM patients
F. HIV patients
All of the above
List causative pathogens of
- Acute IE
- Subacute IE
- IE associated with prosthetic heart valve
- Endocarditis in IVDA
- Acute IE
- S.aureus (MC), Group A strep - Subacute IE
- Strep. viridans (MC overall) - IE associated with prosthetic heart valve
- S. epidermidis (early <60 days), S.aureus (late >60 days) - Endocarditis in IVDA
- S.aureus (MC), HACEK organisms
What antibiotics can be given for prophylaxis?
Single dose amoxicillin PO
In what individuals antibiotic prophylaxis should be given during dental procedures? (3)
- Prosthetic heart valve
- Previous IE
- Congenital heart disease (unrepaired, repaired with residual defects, completely repaired within the 1st 6 months)
Case study
- 32/M 3-month history of tiredness and weightless. Had been previously well although a heart murmur had been noted in childhood.
- Diastolic and systolic murmurs, slight splenomegaly and sphincter haemorrhages. 37.8 degrees. Anemic, raised WBC.
- Broth culture yielded G+ cocci in chains.
Most likely diagnosis? (1)
Most likely pathogen? (1)
Subacute bacterial endocarditis/infective endocarditis
(- 4-6 weeks of penicillin + gentamicin should be given)
Streptococci viridans
What is the expected colonial morphology of Strep. viridans in subacute IE, when grown on blood agar?
How to differentiate it form other similar looking bacterial colonies?
Alpha haemolytic cocci
- differentiate from Strep. pneumoniae by
optochin test - Viridans is optochin resistant, pneumoniae is optochin sensitive
The patient has visited the dentist and was diagnosed with subacute IE.
What is the significance of the dental visit? (2)
Can this infection be prevented? How?
- Manipulation of gingival tissue/ tooth extraction > entry of bacteria into bloodstream
- Platelet fibrin deposits - turbulent blood flow allows easier inoculation of bacteria in heart valves
Yes, by antibiotic prophylaxis - Amoxicillin
> if not: erythromycin
> if not: vancomycin
25/M 1-week history of fever and SOB. No murmur was audible. but echocardiogram revealed a large vegetation on tricuspid valve.
Large abscess was noted on the groin.
G+ cocci in clusters can be seen.
Trilobe nucleus of WBC at the background of cocci can be seen in Gram stain of pus swab.
Likely identity of bacteria? (1)
2 biochemical tests to identify this bacteria? (2)
Staphylococcus aureus
- Catalase +ve
- Coagulase +ve
(common source: nostril, hardline, throat swab, perineum , skin)
25/M 1-week history of fever and SOB. No murmur was audible. but echocardiogram revealed a large vegetation on tricuspid valve.
Large abscess was noted on the groin.
G+ cocci in clusters can be seen.
Trilobe nucleus of WBC at the background of cocci can be seen in Gram stain of pus swab.
What is the significance of the groin abscess?
Which group of patients are more at risk of right-sided endocarditis caused by this organism?
- IVDA (injection site) [forearm/groin]
- right-sided endocarditis = 1st wale enchanted from venous system
= IV drug addicts
68/F with fever, SOB, cough, right sided chest pain.
40 degrees, BP 90/60, 89% O2 saturation.
CXR: right middle lobe consolidation
Microscopy of blood: G+ cocci in pairs.
Most likely diagnosis?
Most likely pathogen?
Community acquired pneumonia Streptoccocus pneumoniae (MC cause of pneumonia)
What are the preventive measures advocated by the HKSAR government for community acquired pneumonia?
- PPSV23 (T-cell independent) for asplenic patients, elderly > 65 years old, immunocompromised patients
- PCV13 (more immunogenic, recruiting CRM197-specific type 2 helper T cells, allow immunoglobulin type switching) for children <2 years old
15/M right lower abdominal pain. Febrile, BP 110/65, pulse 85/min RLQ tenderness and guarding Surgery for appendicitis Blood microscopy: G+ cocci in clusters Coagulase -ve isolated
Usual habitat of coagulase negative staphylococci? (1)
What is the significance of the result?
Usual habitat of coagulase negative stphylococci: skin
- Staphylococcus epidermidis
– Contamination: coagulase -ve staph in skin flora, will not appear and appendix
If the patient is bacteraemic during appendicitis, what pathogens would you expect?
Polymicrobial
- With Enterobacteriaceae and Anaerobes
e. g. E.coli, Bacteroides, Clostridium - peritonitis with perforated bowel
48/F acute myeloid leukaemia.
Chemotherapy give, but drug can result in severe tissue damage id leak into nearby tissue.
CVC was inserted for venous access.
1 month later: chills shortly after the injection of drugs.
febrile. Skin overlying the catheter not inflamed.
Blood culture x2 (2 sets are taken)
Both: G+ cocci in clusters, coagulase -ve
Interpretation of blood results?
Raised a concern that they are not contaminants.
Patient also has risk factor of coagulase negative staphylococci *with CVC.
Coagulase -ve staph
> should take again
48/F acute myeloid leukaemia.
Chemotherapy give, but drug can result in severe tissue damage id leak into nearby tissue.
CVC was inserted for venous access.
1 month later: chills shortly after the injection of drugs.
febrile. Skin overlying the catheter not inflamed.
Blood culture x2 (2 sets are taken)
Both: G+ cocci in clusters, coagulase -ve
Gave empirical Abx > no response
Taken 3d blood culture from CVC lumen > G+ cocci in clusters, coagulase -ve.
Interpretation? Management?
CVC itself is infected
- Remove CVC
- Catheter lock solution for low virulence bacteria but not for high virulence bacteria (pseudomonas)
After CVC is removed in infected case, how do you confirm catheter associated infection? (1)
Adv? (1)
Disadv? (1)
Maki’s roll method: 5cm up cultured by rolling onto agar plate >15 colony forming units will be counted as significant catheter related infection.
Adv: technically easy to perform
Disadv: Miss out colonising bacteria inside the lumen
