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Y5 Infection > List I - Act Core Conditions > Flashcards

List I - Act Core Conditions Flashcards

1
Q

How can the risk of infection be reduced in the pre-operative phase for patients?

A
  • Pre-operative showering
  • Nasal decolonisation
  • Antibiotic prophylaxis
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2
Q

What can be used for nasal decolonisation prior to surgery?

A
  • Nasal mupirocin in combination with a chlorhexidine body wash before procedures with Staphylococcus aureus is a likely cause of a surgical site infection
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3
Q

What is the advise to patients if hair needs removal prior to surgery?

A
  • Use electrical clippers with single use head (razors increase the infeciton risk)
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4
Q

In which situations prior to surgery are antibiotics required as prophylaxis?

A
  • Clean surgery involving the placement of prosthesis or valve
  • Clean-contaminated surgery
  • Contaminated surgery
  • Use local formulary
  • Aim to give single dose of IV antibiotic on anaesthesia
  • If a tourniquet is to be used, give prophylactic antibiotics earlier
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5
Q

How is the risk of surgical site infection managed intra-operatively?

A
  • Prepare the skin with alcoholic chlorhexidine

* Cover surgical site with dressing

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6
Q

What is the advice from NICE regarding the use of diathermy for skin incisions?

A
  • NICE do not advocate the use of diathermy for skin incisions
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7
Q

What is healing by primary intention?

A
  • Occurs when a wound has been sutured after an operation and heals to leave a minimal cosmetically acceptable scar
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8
Q

What is healing by secondary intention?

A
  • Occurs when a wound is deliberately left open at the end of an operation because of excessive bacterial contamination, particularly anaerobes or when there is a risk of devitalised tissue which leads to infection and delayed healing
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9
Q

How is a wound healing by secondary intention managed?

A
  • May be sutured within a few days (delayed by primary closure) or much later when the wound is clean and granulating (secondary closure) or left to complete healing naturally without suturing
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10
Q

How are surgical wounds classified?

A
  • Clean
  • Clean-contaminated
  • Contaminated
  • Dirty or infected
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11
Q

What is a clean wound?

A
  • Clean - incision in which no inflammation is encountered in a surgical procedure without a break in sterile technique and during which the respiratory, alimentary or genitourinary tracts are not entered
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12
Q

What is a clean-contaminated wound?

A
  • Clean-contaminated - incision through which the respiratory, alimentary or genitourinary tract is entered under controlled conditions but with no contamination encountered
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13
Q

What is a contaminated wound?

A
  • Contaminated - incision undertaken during an operation in which there is a major break in sterile technique or gross spillage from the GI tract or an incision in which acute, non purulent inflammation is encountered
  • Open traumatic wounds that are more than 12 to 24 hours old also fall into this category
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14
Q

What are dirty or infected wounds?

A
  • Dirty or infected - incision undertaken during an operation in which the viscera are perforated or when acute inflammation with pus is encountered (for example, emergency surgery for faecal peritonitis) and for traumatic wounds if treatment is delayed, there is faecal contamination, or devitalised tissue is present
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15
Q

What is infectious mononucleosis?

A
  • Glandular fever
  • Eptein Barr virus (EBV)
  • Human herpes virus 4 (HHV-4)
  • As above in 90% of cases
  • Less frequently caused by CMV and human herpes virus 6 (HHV-6)
  • It is most common in adolescents and young adults
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16
Q

Who more commonly gets infectious mononucleosis?

A
  • Most common in people aged 15-24 years
  • Lower socio-economic groups
  • Have frequently acquired EBV in early childhood when the primary infection is often sub clinical
  • Higher socioeconomic groups also show a higher incidence of infectious mononucleosis - acquiring EBV in adolescence or early childhood results in symptomatic disease
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17
Q

What is the classic triad of infectious mononucleosis?

A
  • Seen in around 98% of patients:
  • Sore throat
  • Lymphadenopathy - anterior and posterior triangles of the neck, in contrast to tonsillitis which typically only results in the upper anterior cervical chain being enlarged
  • Pyrexia
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18
Q

What are the other features that might present with infectious mononucleosis?

A
  • Malaise, anorexia, headaches
  • Palatal petechiae
  • Splenomegaly - in 50% and may rarely predispose to splenic rupture
  • Hepatitis, transient rise in ALT
  • Lymphocytosis - in 50% with at least 10% atypical lymphocytes
  • Haemolytic anaemia secondary to cold agglutins (IgM)
  • Maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis
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19
Q

How long should patients be advised that the symptoms take to resolve?

A
  • Incubation period is about 4-7 weeks (contagious during this time)
  • 2-4 weeks for symptoms to resolve
  • Risk of malignancy - long term (Burkitt lymphoma, nasopharnygeal carcinoma)
  • Due to being herpes virus type (DNA virus)
  • DNA viruses stay latent in body therefore can reactivate
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20
Q

How is infectious mononucleosis diagnosed?

A
  • Heterophil antibody test (Monospot test)

* NICE guidance suggests FBC and Monospot in the 2nd week of the illness to confirm a diagnosis of glandular fever

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21
Q

What is the management for a patient with infectious mononucleosis?

A

Management is supportive, it includes the following:

  • Rest during the early stages, drink plenty of fluid, avoid alcohol
  • Simple analgesia for any aches or pains - paracetamol and ibuprofen
  • Avoid playing contact sports for 8 weeks after having glandular fever to avoid the risk of splenic rupture
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22
Q

What is sepsis?

A
  • Defined as an infection that triggers a particular systemic inflammatory response syndrome (SIRS)
  • Characterised by a body temperature outside 36c - 38c, HR, >90 BPM, RR >20/min, WBC count >12000/mm3 or <4000/mm3
  • Patients with infections and two or more elements of SIRS meet the diagnostic criteria for sepsis
  • Patients with organ failure have severe sepsis and those with refractory hypotension - septic shock
23
Q

What is the pathophysiology of sepsis?

A
  • During the septic process there is marked activation of the immune system with extensive cytokine release
  • May be coupled with or triggered by systemic circulation of bacterial toxins
  • All cause endothelial cell damage and neutrophil adhesion
  • Hallmarks are therefore excessive inflammation, coagulation and fibrinolytic suppression
24
Q

What is septic shock?

A
  • Subset of sepsis which describes circulatory cellular and metabolic abnormalities which are associated with a greater risk of mortality than sepsis alone
  • In the hospital setting septic shock is defined as sepsis with persisting hypotension despite fluid correction and ionotropes (requiring vasopressors to maintain a mean arterial pressure (MAP) of 65 mmHg or more) and hyperlactataemia with a serum lactate level of >2 mmol/L where MAP is the driving pressure of tissue perfusion
25
Q

What are the risk factors for developing sepsis?

A
  • Infants (under one year) and older people (over 75 years)
  • People who are very frail
  • Immunocompromised (DBM, HIV, cirrhosis, SCD or asplenia)
  • Immunosuppressed due to drug treatments such as anticancer treatment, oral corticosteroids or other immunosuppressive drugs
  • People who have had trauma, surgery or other invasive procedures in the past 6 weeks
  • People with any breach of skin integrity
  • People who misuse intravenous drugs or alcohol
  • People with indwelling lines or catheters
  • Women who are pregnant or miscarriage in the past 6 weeks including those who have had:
  • C section, forceps delivery or removal of retained products of conception
  • Prolonged rupture of membranes
  • Close contact with people with group A streptococcal infection for example scarlet fever
  • Ongoing vaginal bleeding or an offensive vaginal discharge
26
Q

What are the complications of sepsis?

A
  • Between 1/5 and 1/2 of sepsis survivors following hospital admission experience long term sequelae (post sepsis syndrome)
  • Sepsis is the leading cause of avoidable death from infection
  • Organ failure - may be multi system and includes AKI, cholestasis, heart failure, acute respiratory distress syndrome or acute lung injury and bone marrow suppression
  • Recurrent and secondary infections - people who survive sepsis may develop hospital acquired infections with atypical organisms and may have reactivation of latent viruses due to an impaired ability to mount an appropriate response to superadded infections
  • Malnutrition - partly due to impaired intestinal barrier function
  • Coagulopathy - may cause thromboembolism or DIC (microthrombosis and haemorrhage)
  • Physical impairments
  • Encephalopathy and delirium
  • Psychological sequelae - may include anxiety about recurrent infection and sepsis, post traumatic stress disorder, loss of confidence and self esteem
27
Q

How is a diagnosis of sepsis made?

A
  • Suspect sepsis in any person presenting with:
  • Symptoms or signs indicating possible infection causing significant illness or deterioration, includes people who are deteriorating unexpectedly or failing to improve as expected
  • One or more risk factor for sepsis and who looks unwell
  • Concern from a relative or carer that there is a change in appearance or behaviour
  • Be aware:
  • People with sepsis may present with non-specific, non-localised clinical features for example general malaise, agitation or behavioural change
  • People with sepsis may not present with a high temperature and may present with hypothermia
  • Sepsis may result from infection with almost any pathogen therefore may be a wide range of possible clinical features depending on the site of infection and host response
  • Suspect neutropenic sepsis in any person who becomes unwell who is receiving anticancer treatment
28
Q

If you suspect a patient has sepsis what should you ask them about to assess them?

A
  • Any recent fever or rigors.
  • Any symptoms suggesting specific infection, such as dysuria or productive cough.
  • Clinical features suggesting dehydration, such as reduced urine output in the past 18 hours.
  • Any altered behaviour, mental state, or cognition, such as not responding normally to social cues or waking only with prolonged stimulation, or new irritability (in children); new-onset confusion (in adults). See the CKS topic on Delirium for more information.
  • Any sudden change or deterioration in functional ability.
  • Possible risk factors for sepsis, including co-morbidities and drug treatments.
  • Possible risk factors for antibiotic resistance, such as recent or previous antibiotic therapy, previous hospital admissions, and residency in a care home, for example.
  • Immunization status (particularly in infants and young children)
29
Q

If you suspect a patient has sepsis how should you examine them?

A
  • General appearance
  • Temperature
  • Heart rate, respiratory rate and signs of respiratory distress and blood pressure
  • Capillary refill time and O2 sats
  • Mottled or ashen skin; pallor or cyanosis of skin, lips or tongue; cold peripheries
  • Non-blanching rash which may suggest meningococcal disease
  • Weak high pitched or continuous cry in children under 5 years
  • Any breach of skin integrity (cuts, burns or infections)
  • Dry mucous membranes
  • Possible underlying source of infection
  • Use a sepsis risk stratification tool to assess the risk fo clinical deterioration including severe illness or death from sepsis depending on the persons age, risk factors and clinical features of concern
30
Q

What is the sepsis six specialist assessment and treatment all patients with suspected sepsis should receive in the first hour in the acute hospital setting?

A
  1. Oxygen therapy 15L NRBM
  2. Blood cultures, blood gas, FBC, CRP, U and E’s, LFT’s Clotting screen, urine analysis and culture, CXR
  3. Give IV broad spectrum antibiotics at the maximum recommended dose
  4. Give IV fluid bolus to restore tissue perfusion
  5. Check serial lactate measurement
  6. Check urine output, monitor fluid balance hourly and monitor the persons clinical condition - track and trigger system to identify people at risk of deterioration
31
Q

According to the surviving sepsis campaign care bundle, how should hypotension that does not respond to initial fluid resuscitation be managed?

A
  • Apply vasopressors to maintain a mean arterial pressure (MAP) >65 mm Hg
  • If there is persistent arterial hypotension despite volume resuscitation (septic shock) or initial lactate > or = 4 mmol/L (36mg/dL):
  • Measure central venous pressure (CVP)
  • Measure central venous oxygen saturation (ScvO2)
  • Remeasure the lactate if initial lactate was elevated
  • Targets for quantative resuscitation included in the guidelines are CVP of >8 mm Hg, ScvO2 of > 70% and normalisation of lactate
32
Q

What are the main vasopressors?

A
  • Phenylephrine
  • Norepinephrine
  • Epinephrine
  • Vassopressin
33
Q

What type of shock is caused by severe sepsis (and neutrogenic and anaphylaxis)?

A
  • Distributive shock
34
Q

How is organ dysfunction identified in the context of sepsis?

A
  • Acute change in total Sequential Organ Failure Assessment (SOFA) score >2 points consequence to the infection
35
Q

How is the SOFA score calculated?

A
  • Can be used on all patients admitted to an intensive care unit
  • Includes the following:
  • PaO2
  • FiO2
  • On mechanical ventilation including CPAP
  • Platelets
  • GCS
  • Bilirubin level
  • MAP or administration of vasoactive agents required
  • Creatinine
36
Q

What is Clostridium difficile?

A
  • Gram positive rod often encountered in hospital practice

* Produces an exotoxin which causes intestinal damage leading to a syndrome called pseudomembranous colitis

37
Q

How is infection with Clostridium difficile caused?

A
  • C. diff develops when the normal gut flora is suppressed by broad spectrum antibiotics
  • Clindamycin is historically associated with causing c. diff, now 2nd and 3rd generation cephalosporins are the leading cause of c. diff
38
Q

What are the other risk factors for developing c.diff infection?

A
  • Proton pump inhibitors
39
Q

What are the clinical features of clostridium difficile infection?

A
  • Diarrhoea
  • Abdominal pain
  • Raised WBC count is characteristic
  • If severe, toxic megacolon may develop
40
Q

How is a diagnosis of c. diff made?

A
  • Detecting c. diff toxin in the stool

* C. diff antigen positivity only shows exposure to the bacteria rather than the current infection

41
Q

How is Clostridium difficile infection managed?

A
  • Oral metronidazole for 10-14 days is first line therapy
  • If severe or not responding to metronidazole then oral vancomycin may be used
  • Recurrent infection can happen in 20% and this increases to 50% after the second episode
  • Fidaxomicin may also be used for patients who are not responding, particularly those with multiple co-morbidities
  • Life threatening infections - use a combination of oral vancomycin and intravenous metronidazole
  • Other therapies include - bezlotoxumab a monoclonal antibody which targets c. difficile toxin B - not widely used
42
Q

How might a patients’ abdominal film appear with a c. difficile infection?

A
  • Loss of bowel wall architecture
  • ‘Thumb printing’ consistent with colitis
  • Moderate free fluid in the pelvis and peritoneum
  • Colon oedematous throughout with enhancing walls, but normal calibre
43
Q

What type of c. diff produces more toxins than most other types?

A
  • Type 027 - causes a greater proportion of severe disease and appears to have a higher mortality
44
Q

What dose of metronidazole is recommended for c. diff infections?

A
  • Metronidazole 400mg or 500mg 3 times daily for 10-14 days for mild to moderate infections
45
Q

What dose of vancomycin is recommended for c.diff infections?

A
  • Vancomycin 125mg 4 times per day for 10-14 days is an option for second episodes or in the infection is severe or caused by type 027
46
Q

What dose of vancomycin or fidaxomicin is recommended for recurrent c. diff infection?

A
  • Vancomycin or fidaxomicin 200mg x 2 per day for 10 days may be used
47
Q

How is pyrexia of unknown origin defined?

A
  • Prolonged fever on several occasions (>38.3c or higher) of >3 weeks which no cause has been found despite 7 days of basic investigations in hospital
48
Q

What are the common causes of pyrexia of unknown origin?

A
  • Most are unusual presentations of common diseases:
  • Tuberculosis
  • Endocarditis
  • Gall bladder disease
  • HIV infection
  • In adults, infections and cancer account for most PUO’s
  • Autoimmune disorders account for 10-20% of cases
  • In children, infectious disease is the main cause of PUO and malignancy, miscellaneous disease and collagen vascular disease
49
Q

What other causes of PUO are there?

A
  • Bacterial
  • Viral
  • Fungi
  • Parasites
  • Rickettsial organisms
  • Psittacosis
  • Lymphogranuloma venereum
  • Neoplasms
  • Drug fever
  • Collagen vascular and autoimmune diseases
  • Granulomatous diseases
  • Vasculitides
  • Peripheral pulmonary emboli
  • Inherited diseases
  • Hyperthyroid and subacute thyroiditis
  • Kikuchi’s disease
  • Undiagnosed
50
Q

What are the important features of history to ask about in a patient with PUO?

A
  • Inquire about symptoms from all major systems. Include general complaints - eg, fever, weight loss, night sweats, headaches and rashes.
  • Record all complaints, even if not currently present. Previous illnesses, including surgery and psychiatric problems, are important.
  • Discuss nutrition, including consumption of dairy products and the source of these products.
  • Drug history should be recorded, to include over-the-counter medications, prescription medications and any illicit substances.
  • Immunisation status should be documented.
  • Enquire about family history of illness.
  • Occupational history should include exposure to chemicals/animals.
  • Take a history of travel and recreational habits - including possible exposure to ticks and other vectors.
  • Sexual history should be recorded.
51
Q

How should a patient with PUO be examined?

A
  • Diseases such as brucellosis, borreliosis and Hodgkin’s disease tend to cause recurrent episodes of fever.
  • Physical examination should be repeated daily while the patient is in hospital. Particularly, watch for:
  • Rashes.
  • Lymph node enlargement.
  • Signs of arthritis.
  • New/changing cardiac murmurs.
  • Abdominal tenderness or rigidity.
  • Fundoscopic changes and neurological deficits
52
Q

Which investigations can be done for PUO?

A
  • FBC, ESR, CRP, LFT’s, ANA, Rh factor, TFT’s
  • Labelled white cell scan
  • Blood cultures
  • Urine culture, sputum, stool, CSF and morning gastric aspirates (if TB suspected)
  • CXR, abdominal CT scan and ECG
  • CT, IV pyelogram, MRI and PET scan
  • Hybrid F18-FDG PET/CT
  • Invasive procedures for abnormal findings include:
  • Lumbar puncture for headache
  • Skin biopsy for rash
  • Lymph aspiration or biopsy for lymphadenopathy
  • In an HIV positive patient - bone marrow aspiration or biopsy
  • Abnormal LFTs should prompt a liver biopsy
53
Q

What is the management of PUO?

A
  • Dependent on diagnosis, although empirical treatment has never been advocated in cases of PUO, there are 3 important exceptions to this:
  • Meeting criteria for culture negative endocarditis
  • Cryptic disseminated tuberculosis (or other granulomatous infections)
  • Suspected temporal arteritis (with vision loss) is suspected

Y5 Infection (2 decks)

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