Acute Sepsis Flashcards

1
Q

Define sepsis

A

Sepsis is life threatening organ dysfunction due to a dysregulated host response to infection

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2
Q

What is sepsis shock

A

Sepsis shock is persisting hypotension requiring treatment to maintain blood pressure despite fluid resuscitation

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3
Q

What is septicaemia

A

Sepsis in the blood

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4
Q

What is the early warning score and when should a patient be checked for sepsis

A

Early warning score = basic observations (blood pressure, temp, heart rate, respiratory rate etc)
EWS > 3 means patient should be checked of sepsis

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5
Q

What are sepsis red flags

A

Check for red flags (high respiratory rate, low blood pressure, unresponsive)
Immediate action required (within an hour) - send urgent investigations
Complete sepsis six bundle

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6
Q

What are common signs of sepsis

A
Slurred speech or confusion
Extreme shivering or muscle pain
Passing no urine (in a day)
Severe breathlessness
"I feel like I might die"
Skin mottled or discoloured
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7
Q

What are common features of a history for a septic patient

A

Sudden sickness, temperature and chills

Fever, severe headache, nausea, weakness, general muscles aches, abdominal pain, eye pain on exposure to light

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8
Q

What common examination findings would you see on a septic patient

A

Pale, looks sick , high temperature, high pulse, high respiratory rate,
Purpuric rash - red legions when pressed do not change color
Neck stiffness, mentally alert

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9
Q

Understand the mechanism by which micro-organisms trigger the inflammatory cascade

A

○ Endotoxins binds to macrophages
○ Local control include cytokines (tissue necrosis factors, TNF-a, IL-1) stimulate inflammatory response to promote wound repair and recruit RE system
○ Systemic control where cytokines released into circulation and stimulates growth factor, macrophages and platelets to control infection
○ Sepsis is when infection is not controlled, cytokines lead to activation of humoral cascades and RE system

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10
Q

How does the inflammatory cascade cause sepsis

A

○ Cytokines initiate production of thrombin and thus promote coagulation
○ Cytokines also inhibit fibrinolysis
○ Coagulation cascade leads to microvascular thrombosis and hence organ ischaemia, dysfunciton and failure
○ Microvascular injury is the major cause of shock and multiorgan failure

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11
Q

What are supportive and specific treatment of sepsis

A

•Supportive treatment- consider early referral to ITU (intensive care unit)
○ Sepsis six
○ Regular monitoring and reassessment
• Specific treatment - Antibiotic treatment - an agent likely to be active against the pathogens that cause meningitis in this age group (mode of transmission)
○ An agent that penetrates into the site of infection
○ Empiric choice is ceftriaxone

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12
Q

What are some life threatening complications of sepsis

A

○ Irreversible hypotension (not enough blood circulation)
○ Respiratory failure (give oxygen and monitor look gas)
○ Acute kidney injury (renal failure)
○ Raised intracranial pressure
○ Ischaemic necrosis of digits/hands/feet

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13
Q

What investigations would you do for a suspected septic patient

A

• Confirming the diagnosis
○ Blood culture
○ PCR of blood - look for fragments of organism
○ Lumbar puncture (if safe)
§ Microscopy and culture of cerebrospinal fluid (CSF), PCR of CSF
• Examination of CSF
○ Urgent transport of CSF to laboratory
§ Glucose and protein estimation in biochemistry, microscopy and culture in microbiology
○ Appearance - turbidity and colour
○ Microscopy WBCs, RBCs
○ Gram stain

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14
Q

List the sepsis six bundle

A
  • Give oxygen to 94%
  • Take blood cultures
  • Give IV antibiotics
  • Fluid challenge - check if patient can be able to increase stroke volume with increased fluids
  • Measure lactate
  • Measure urine output
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15
Q

Describe features of Neisseria meningitidis and of meningococcal disease

A

• Meningococcal meningitis - meningococcus
○ Gram negative bacteria
○ Spread by direct contact with respiratory secretions
○ Most people are harmlessly colonised (cleared or act as carrier)
○ In some, rapid progressive and potentially fatal disease if not recognised and treated properly
• Polysaccharide capsular antigen - evades immune response by preventing phagocytosis
• Outer membrane acts as an endotoxin

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