Sepsis & Meningococcal Flashcards
Meningococcal disease - definition
A life threatening infection caused by meningocous bacteria where the bacteria enters the blood stream.
Can causes meningitis and/or sepsis
Meningococcal disease - signs & symptoms
- Fever
- Joint pain
- Headache
- Cold hands/feet
- Skin mottling and leg pain
- Altered conscious state
- Hypotension
- Tachycardia
- Purpuric rate (non-blanching)
Groups most at risk of meningoccocal
Babies up to 5 years old are at most risk due to under developed immune system.
Meningococcal disease - signs and symptoms specific for paedicatrics
- Fever, irritable, poor feeding, nausea/vomiting, drowsiness, petechiae
Criteria for Abx administration in Meningococcal Disease
Any one of the following:
- Altered conscious state
- stiff neck, photosphobia
- petechial (non blanching) rash
Meningococcal disease management
- ICP back up
- IV access
- Ceftriaxone (600mg/kg) or 2g max
- Sepsis management
How to draw up and administer ceftriaxone
- IV: Dilute each 1g of Ceftriaxone with 9.5 mLs of normal saline and administer over 2 min (e.g. 2g over 4 mins).
- If unable to obtain IV/IO access or not accredited in IO access, dilute each 1 g of ceftriaxone with 3.5mLs 1% Lignocaine HCl and administer into the upper lateral thigh or large muscle mass.
What is the ETAT criteria?
Emergency Triage Assessment and treatment for paediatric shock criteria
- Cold extremities
- Cap refill <3 secs
- Fast, rapid pulse (SV is unable to increase, therefore, usually first sign of distributive shock)
Sepsis management for paediatrics
Treatment is administered if ETAT criteria is met.
1. O2 if SpO2 <94%.
2. Fluid: 10mg/kg bolus repeated once after 15 mins.
3. Ceftriaxone 50mg/kg if transport time >60 mins.
4. Manage hypoglycaemia
How to prepare ceftriaxone for administration
IV administration: dilute 1g ceftriaxone with 9.5ml NaCl and administer over 2 mins.
IM Administration: dilute each 1 g of ceftriaxone with 3.5mLs 1% Lignocaine HCl and administer into the upper lateral thigh or large muscle mass.
Sepsis definition
Life-threatening organ dysfunction caused by dysregulated host response to infection
Septic shock definition
Sepsis + hypotension; subset of sepsis with profound circulatory, cellular and metabolic disregulation.
Generally required vasopressors to maintain MAP >65mmHg
Sepsis Pathophysiology
- Cytokines (immune cells) mitigate to antigen and elicit an immune response (complement system).
- Histamine and mast cell degranulation occurs to lyse foreign cells.
- Activated coagulation factors result coagulation cascade and sticky mesh preventing microbe spread. Bradykinin is released, facilitating vasodilation and increased capillary leakage = increased tissue swelling oedema.
- Systemic release of cortisone, adrenaline and prostaglandins which inhibit immune response systemically.
- In sepsis, there is low levels of activated protein C, an anticoagulation system that results in fibrin deposited widely and small clots forming throughout vasculature. This contributes to DIC which is widespread clot formation, impaired tissue perfusion and thrombosis.
qSOFA definition and uses
Quick Sequential Organ Failure Assessment. A risk stratification tool that is used to identify the adult who is at risk of deterioration from sepsis. DOES NOT DIAGNOSE.
qSOFA criteria
Hypotension <90mmHg
Altered conscious state
Tachypnoea >22
Sepsis management for adult
a. Adults:
i. qSOFA 2-3:
i. ICP pack up
ii. 500mL boluses titrated to maintain SBP >100mmHg (max. 3L)
iii. Ceftriaxone if tansport time >60mins
iv. Adrenaline infusion is SBP still remains <100mmHg
qSOFA <2:
i. 500ml Nomral Saline bolus
If SBP <100mmHg, continue 500mL fluid bolus (Max. 3L)
Sepsis signs and symptoms
Hypotension <90mmHg
HR >90bpm
RR>22
Altered conscious state
Temp <36 or >38
SpO2 <94%
BGL >7mmol/L
Raised lactate
Decreased urination
Metabolic acidosis
Non-blanching rash
How is meningococcal infection colonised and transmitted
Transmitted via respiratory droplets: coughing, sneezing and breathing.
Colonises within the nasopharyngeal area > incubation period of 1-10 days. If penetrates the submucosal tissue, enters the bloodstream
Pathophysiology of meningococcal disease
- Bacterium may penetrate submucosal in URT in 10-20% of infections which N. Meningitidis enters the blood stream.
- Bacteria produces cytotoxins, causing damage to inner surface of blood vessel, resulting in leakage of plasma/blood into surrounding tissues/organs.
- This causes a decrease in plasma volume, leading to decreased O2 carrying-ability. Increased RR and WOB as a result to increase O2 availability for end-organ perfusion.
- Decreased blood flow to extremities to allow adequate perfusion to vital organs.
- As blood enters surrounding tissues, a non-blanching rash occurs.
How does meningococcal causes meningitis
Bacteria may cross the BBB, into the meninges. Colonises in freely moveable CSF, leading to inflammation and swelling
