Bacteraemia and Septicaemia Flashcards
Define bacteriaemia
The presence of viable bacteria in the blood, which may be transient and inconsequential.
Define septicaemia/sepsis
Presence of microorganisms and/or their products in the blood that induces a Systemic Inflammatory Response Syndrome (SIRS)
SEPSIS = SIRS + Infection (documeted/or presumed presence of infection)
SIRS diagnosis
SIRS can be diagnosed by the presence of at least two or more of the following four signs:
- Fever or hypothermia (core body temperature >38.5; or <36 degrees celcius)
- Leukocytosis or leukopaenia (WBC count >12x10^9 L or <4x10^9/L, or immature (bands) form >10%)
- Tachycardia (rapid heart rate, >90bpm)
- Tachypnoea (rapid breating >20 bpm) or partial pressure of CO2 in arterial blood (PaCO2) <32 mmHg
Note: other signs and symptoms including fatigue, malaise, anxiety or altered mental status (confusion) may be apparent at time of presentation.
Examples of non-infectious causes of SIRS
Examples including tissue injury caused by:
- Trauma
- Burns
- Venous thrombosis (clots/thrombus)
- Myocardial or pulmonary infarcts
- Pancreatitis (inhereted abnormalities; or formation of gallstones block normal flow of enzymes through drainage ducts, for example).
- Hyperthyroidism (excessie thyrpod hormones increasing basal level metabolism)
- Drug product reaction (hypersensitivity)
- Malignant hyperthermia (in response to certain drugs used in general anaesthesia)
Epidemiology of Sepsis
Often rapid onset.
Increasing incidence in elderly and chronically ill and mortality rates vary with age (much higher in <1 year)
Each one hour delay in institution of appropriae treatment leads to a 7-9% increase in mortality.
Sepsis risk factors
- Underlying disease (ie. HIV/AIDS) with associated immunosuppression.
- Use of foreign devices (urinary/central venous catheters)
- Surger/trauma/burns patients
- Chronic renal/liver (cirrhosis) failure
- Intestinal ulceration
- IVDU
- Extremes of age
- Alcohol-dependence
- Diabetes
- Malnutrition
Origins of infection
Infections can originate from multiple sources, including:
- Primary blood stream infection (meningococcaemia, meningitis)
- Wounds (also postoperative infections) and abscesses
- Lungs (pneumonia)
- Gastrointestinal tract (organisms cross the interstinal epithelium)
- Urinary tract
- Infected heart valves (bacterial endocarditis)
- Colonised IV lines, drains or shunts.
Pathophysiology and progression of sepsis
Bacterial component
LPS = lipopolysaccharide
Immune response
LPS complex binds to receptors (i.e. CD14) on macrophages, leading to cytokine production.
- Cytokines: TNF, IL’s, IFN
DIC
Disseminated intravascular coagulation.
May be triggered by infectious (microorganisms and/or their products) or non-infectious sources (various malignancies [lung, pancrease, stomach]. trauma, burns for example).
Imbalance in coagulation produces small red blood clots within the blood vessels (systemic microvascular clots); clotting, increasingly consumes more platelets and other clotting protein factors, resulting in abnormal bleeding (haemorrhages) and possible organ dysfunction (and even death).
Always consult a haematologist and an infectious disease physician.
Severe sepsis
SEPSIS + one or more sepsis-related organ dysfunction or hypoperufsion *or *hypotension
Organ dysfunction
Defined as evidence of:
- Acute lung injury
- Renal, liver or cardiac failure
- Coagulation abnormalities
- Thrombocytopenia
- Altered mental status
- Hypoperfusion with lactic acidosis
- Digestive tract abnormalities (nausea, vomiting, diarrhoea, ileus)
- Skin/cutaneous manifestations (petechial rash; ecthyma gangrenosum; generalised erythoderma).
Fulminant meningococcal sepsis
- Ecchymoses
- Intraocular hamorrhage
- Thrombosis and gangrene of the fingers
Ecthyma gangrenosum (necrotic blister)
Lesions begin as papules surrounded by erythema, and then evolve into haemorrhagic necrotic ulcers. Often associated with P. aeruginosa but cultures can show the presence of *Klebsiella *species, Serratia species, Aeromonas hydrophila or E. coli.
Septic shock
Severe sepsis + hypotension.
Hypotension: systolic BP of <90mmHg, or MAP <65mmHg, or a 40mmHg drop in SBP compared to baseline.
Unresponsive to fluid challenge and requires the adminisration of vasopressors.
Diagnosis of sepsis, severe sepsis and septic shock.
No one bedside test or laboratory test provides a definitive diagnosis. It is based on:
Clinical history: travel, animal/occupational exposure, medications being used, alcohol use, any underlying disease that predisposes to infection; and
Physical examination: pelvic (signs of pelvic inflammaotry disease), rectal (signs of perineal/perirectal abscesses)
Laboratory tests: take cultures.
Complete blood cell count (CBC) with the differential (looking for signs of leukocytosis, bandemia [immature blood cells])
Where would you take cultures from to diagnose sepsis?
Blood
- At least two culture sets over a 24 hour period, divide for aerobic/anaerobic incubation) ; take before administration of abx therapy.
Urine
- Urinary tract infection
- Renal dysfunction?
_Wound/abscess _
Cerebral spinal fluid (possible CNS infection)`
Other signs of organ dysfunction
- Acute lung injury
- Renal dysfunction
- Hepatic dysfunction
- Haematologic dysfunction
- Coagulation abnormalities
- Increase presence of biomarkers in the blood
- Capillary refilling time 3 seconds or greater
- Hyperlactatemia
- Electrolyte imbalances
- Hyperglycemia
Acute lung injury
Arterial hypoxemia (PaO2/FiO2 <300) which may lead to acute respirtaory distress syndrome (ARDS)
Renal dysfunction
- Acute oliguria (urine output <0.5mL/kg/h for at least 2 hours)
- Azotemia (waste products like creatine increas {>5 mg/L] in the serum)
Hepatic dysfunction
Plasma total bilirubin >17-19umol/L; elevated amounts of various liver enzymes in the blood including, alkaline phosphatase; alanine transaminase (ALT) and asparate transaminase (AST).
Hetatologic dysfunction
Thrombocytopenia (platelet counts <100 x 10^9/L (signs of disseminated intravascualar coagulation)).
Coagultion abnormalities
International normalised ratio (INR) >1.5 [reference range 0.8-1.2] or activated partial thromboplastin time [aPTT] > 60s [reference range, 10-14 s]
Increase presence of biomarkers in the blood
Procalcitonin [easured in nanograms/L
C-reactive protein [CRP] produced in the liver in response to cytokines/inflammation to active complement to help contain infection.
Hyperlactatemia
Lactate >2mmol/L; hence, glucose is being converted to pyruvate, and the pyruvate is then converted to lactate.
