Acture Sepsis In The Emergency Department Flashcards

(23 cards)

1
Q

What are the features of acute sepsis?

A

F

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2
Q

List 10 important facts about Neisseria meningitidis.

A

•  Spread by direct contact with respiratory
secretions

  •   Most people are harmlessly colonised
  •   In the unlucky few - rapidly progressive (and potentially fatal) disease if not recognised and treated promptly
  • Often in association with polymorphonuclear leukocytes when viewed under a microscope
  • It is a nonmotile, gram-negative diplococcus, shaped like a kidney bean, which always appears in pairs. It is also piliated and the pili allow attachment of the organism to the nasopharyngeal mucosa where it is harbored both in carriers and in those with meningococcal disease. When meningococcus is isolated from blood or spinal fluid, it is invariably encapsulated. The meningococcal polysaccharide capsule is antiphagocytic and, therefore, the most important virulence factor. [Note: Antibodies to the capsule carbohydrate are bactericidal.]
  • Transmission occurs through inhalation of respiratory droplets from a carrier or a patient in the early stages of the disease. In addition to contact with a carrier, risk factors for disease include recent viral or mycoplasma upper respiratory tract infection, active or passive smoking, and complement deficiency. In susceptible persons, pathogenic strains may invade the bloodstream and cause systemic illness after an incubation period of 2 to 10 days.
  • Humans are the only natural host.
  • Antiphagocytic properties of the meningococcal capsule aid in the maintenance of infection.
  • N. meningitidis initially colonizes the nasopharynx, the epithelial lining of the nasopharynx normally serves as a barrier to bacteria. Therefore, most persons colonized by N. meningitidis remain well. As a rare event, meningococci penetrate this barrier and enter the bloodstream where they rapidly multiply (meningococcemia).
  • The organism can seed from the blood to other sites, for example, by crossing the blood-brain barrier and infecting the meninges. There they multiply and induce an acute inflammatory response
  • Within several hours the initial fever and malaise can evolve into severe headache, a rigid neck, vomiting, and sensitivity to bright lights—symptoms characteristic of meningitis. Coma can occur within a few hours.
  • Meningococci can cause a life-threatening septicemia in an apparently healthy individual in less than 12 hours. Up to 30 percent of patients with meningitis progress to fulminant septicemia. In this condition, the clinical presentation is one of severe septicemia and shock, for which the bacterial endotoxin (LOS) is largely responsible. Acute, fulminant meningococcal septicemia is seen mainly in very young children
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3
Q

What investigations would you request to assess a patient with sepsis?

A

Full Blood Count – looking for features of sepsis with raised white cell count and raised neutrophils. Neutrophils are part of the inflammatory response to infection

CRP (C Reactive Protein) – an Acute Phase Protein that is raised in acute infections.
C Reactive Protein is produced by the liver as part of the response to infection. Since this is a protein that has to be made by the liver, it takes a few hours to be produced and then measured in the blood. It is nevertheless a useful (although non-specific) indicator of inflammation and infection.

U&E (Urea and Electrolytes) – Since patients with acute sepsis may develop renal and other metabolic problems.

Blood cultures – to confirm and identify the bacteria causing the infection.

Imaging – such as abdominal X-ray or abdominal CT scan to look for pathology related to the tumour

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4
Q

What does it mean if a rash in “non-blanching”? Give an example of such a rash

A

The group called ‘non-blanching’ doesn’t disappear when you press it with a glass/tumbler.

An example of this is a purpuric rash.

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5
Q

What is sepsis?

A

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

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

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6
Q

Define bacteraemia

A

It is the presence of bacteria in the blood

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7
Q

What is septicaemia?

A

Septicaemia is an outdated clinical term meaning generalised sepsis

Or sepsis in the blood

The term is not interchangeable with Sepsis

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8
Q

How do we recognise sepsis?

A

Clinical assessment of patients who look sick
or have raised Early Warning Score (EWS).

Clinical features suggesting source (e.g. pneumonia, UTI, meningitis, etc)

Check for Red Flags (e.g. high RR, low BP, unresponsive)

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9
Q

What is measured for EWS?

A

EWS = Early warning score

They are basic observations e.g. RR, HR, temp and BP

Score of 3 or more should be reviewed for sepsis - to make sure we don’t miss it even though there are a range of reasons why people can get that score

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10
Q

What should you do if a patient has red flag sepsis?

A
  •   Immediate action required
  •   Inform senior doctor for review
  •   Send urgent investigations
  •   Complete Sepsis Six Bundle
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11
Q

What is within the sepsis six bundle?

A
–  Oxygen 
–  Blood cultures 
–  IV antibiotics 
–  Fluid challenge 
–  Lactate 
–  Measure urine output
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12
Q

What should be urgently investigated if sepsis is suspected?

A
  •   Full blood count, Urea and Electrolytes
  •   EDTA bottle for PCR
  •   Blood sugar
  •   Liver Function Tests
  •   C-Reactive protein (CRP)
  •   Coagulation (clotting) studies
  •   Blood gases
  •   Other microbiology samples (CSF, urine, etc)
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13
Q

How is Meningitis treated?

A

Prevented by vaccines

High fever, headache, and a rash typical of meningococcal infection are treated immediately in an effort to prevent progression to fulminant septicemia which has a high mortality rate.

Blood cultures should be drawn and antibiotic therapy should not be delayed while waiting for lumbar puncture to be performed.

Pretreatment with antibiotics can substantially diminish the probability of a positive CSF culture but the diagnosis can often still be established from the pretreatment blood cultures; and organisms may continue to be visible on Gram stain of the CSF.

Meningitis can be effectively treated with penicillin G or ampicillin (both of which can pass the inflamed blood-brain barrier) in large intravenous doses.

When the etiology of the infection is unclear, cefotaxime or ceftriaxone is recommended. Prompt treatment reduces mortality to about 10 percent.

Because of the intense inflammatory reaction that accompanies bacterial meningitis, many authorities recommend a dose of the corticosteroid dexamethasone shortly prior to, or together with, the first dose of antibiotic.

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14
Q

Which antibiotics would you use for meningitis treatment?

A

•   An agent likely to be active against the
pathogens that cause meningitis in this
age group (different in neonates and the
elderly)

  •   An agent that penetrates into the CSF (cerebrospinal fluid)
  •   Empiric choice is CEFTRIAXONE
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15
Q

WHat are some life threatening complications of meningitis?

A
  •   Irreversible hypotension
  •   Respiratory failure
  •   Acute kidney injury (renal failure)
  •   Raised intracranial pressure
  •   Ischaemic necrosis of digits/hands/feet
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16
Q

How would you confirm a meningitis diagnosis?

A
•   Blood culture 
•  PCR of blood 
•  Lumbar puncture (if safe)
    –  Microscopy & Culture of cerebrospinal fluid
(CSF) 
    –  PCR of CSF
17
Q

How would you examine the Cerebrospinal fluid of a patient with meningitis?

A
•   Lumbar puncture only performed after
checking contraindications 
•  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 
•  Referral for PCR
18
Q

Briefly outline the meningococcus bacterium

A

•   Neisseria meningitidis
•  Gram-negative diplococcus
•  Numerous serogroups (e.g. A, B, C, W-135 based on the
•  Polysaccharide capsular antigen
–  evades immune response by preventing phagocytosis
•  Outer membrane acts as an endotoxin
•   Up to 25% young adults may be carriers
•  Spread by aerosols and nasopharyngeal secretions
•  Fatality rate ~10%

19
Q

How can meningitis be prevented?

A

Prevention 1. vaccination

  •   Meningococcal C conjugate vaccine
  •   ACWY vaccines

•  Serogroup B vaccine has been introduced in the UK (Sep 2015)
- Given to babies at 2, 4 & 12 months and adults at increased risk

Prevention 2. antibiotic prophylaxis

  •   Meningitis is a Notifiable disease
  •   Cases reported to the local Health Protection Unit of Public Health England
  •   Close contacts can be given antibiotic prophylaxis & considered for vaccination
20
Q

What must be carried out in the supportive care part of treatment?

A
  •   Consider early referral to ITU
  •   Sepsis Six
  •   Regular monitoring and reassessment
21
Q

Outline the three main structures of the meningitis organism that makes it so successful at targeting host cells.

A

1) Endotoxic lipopolysaccaride cell wall - This triggers inflammation
2) Pilus - enhances attachment of the bacteria to host cell. This allows for colonisation. Conjugative pill also allow the transfer of DNA between bacteria
3) Polysaccaride Capsule - Promotes adherence and prevents phagocytosis by the host cell

22
Q

Compare the local, systemic and septic inflammatory cascade

A

In all three, the endotoxin binds to macrophages.

Local - Cytokines stimulate inflammatory response to promote wound repair and recruit reticuloendothelial system

Systemic - Cytokines released into circulation and sti mate growth factor, macrophages and platelets to control infection and clot for wound formation

Sepsis - Sepsis represents an imbalance, cascade gets out of control, things that were supposed to help, start to compromise the body.

  • The principle problem is a circulatory insult; body is not managing circulation and so bloody supply to viral organs, kidneys heart etc is compromised.
  • Cytokines released by immune system as a result of this microorganism promote thrombin clotting
23
Q

What happens to coagulation in a patient with 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, dysfunction and failure
  •   Microvascular injury is the major cause of shock and multiorgan failure