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Co-existing Test 1 > Infection and Immunity > Flashcards

Infection and Immunity Flashcards

1
Q

What percentage of nosocromial infections are surgical site infections?

A

14-16%

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2
Q

What is the surgery with the highest rate of cases of SSI?

A

Intra-abdominal

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3
Q

What are patient related factors for risk factors for SSI?

A
  1. Extremes of age
  2. poor nutritional status
  3. ASA status >2
  4. DM
  5. Smoking
  6. Obesity
  7. co-existing infections
  8. colonization
  9. immunocompromise
  10. longer reop hospital stay
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4
Q

What are some microbial factors for risk of developing SSI?

A
  • Enzyme production
  • polysaccharuide capsule
  • ability to bind to fibronectin
  • biofilm and slime formation (implants)
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5
Q

What are some wound related factors for development of SSI?

A
  1. Devitilized tissue
  2. dead space
  3. hematoma
  4. contaminated surgery
  5. presence of foreign material
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6
Q

What is the most common cause of SSI?

A

S. aureus, including MRSA is most common

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7
Q

What is the normal presentation of an SSI? Timeframe? Gold standard dx?

A
  • Presentation w/in 30 days post op
    • local inflammation
    • poor wound healing
    • sx of systemic infection
  • gold standard dx: aseptically obtained wound culture
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8
Q

What are some coniderations in anesthetic managmeent to prevent SSI?

A
  • Manage pain
    • acute pain can suppresses NK cell activity
  • prevent hypothermia
    • exacerbates stress response
  • minimize catecholamine surges
    • this can increase blood glucose, which increases risk of infection
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9
Q

SSI prevention in general?

A
  • appropriate admin of prophylactic antibiotics
    • usually within 1 hour prior to incision (2 hours for vancomycin and fluoroquinolones)
    • redose in prolonged surgery >4hr
    • most commom is first generation cephalosporin
      • broad specturm, low side effects, high tolerability
    • small bowel also need gram-negative coverage
    • large bowel and femail need anaerobic coverage
  • NO SMOKING FOR 4-8 WEEKS
  • No alcohol 1 month
  • optimize daibetics
  • optimize nutritional status in cachexia or obesity
  • postpone sx until active infection gone (if possible)
  • optimize oxygenation with titration Fio2
  • prevent hypothermia
  • adequate analgesia
  • hypocapnia should be avoided due to vasoconstrction
  • optimize glucose control
    • hyperglycemia inhibits leukocyte function
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10
Q

What are common antibiotics used for general srugery?

what surgery needs gram-negative coverage?

what needs anaerobic coverage?

A
  • Most common abx is first-generation cephalosporin
    • broad spectrum, low side effects, high tolerability
  • small bowel needs gram-negative
  • large bowel and female genital tract needs anearobic
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11
Q

What is recommendation for smoking prior to surgery?

A

stop 4-8 weeks beforehand

smoking increases respriatory and wound infection

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12
Q

What is recommendation for ETOH abstinence?

A

one month

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13
Q

What are CDC’s “Top 5 Recommendation” to prevent central line infections?

A
  1. handwashing prior to insertion or maintenance
  2. using full barrier precautions (hat, mask, sterile gown, sterile area covering) during insertion
  3. cleaning skin iwth chlorhexidine
  4. avoiding the femoral and peripheral arms whne possible
    1. IJ and SCL with lower risk; consider pneumo risk in SCL
  5. RoutinE daily inspection of catheters with removal ASAP
  • Routine practice of hand sanitizer and scrubbing ports with alchol before every use of CVL
  • Best “treatment” is prevention
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14
Q

What is risk of bacterial contamination in platelets? PRBC?

A

1: 5000 for platelet (think stored at room temp)
1: 50,000 for PRBC

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15
Q

What is the risk for viral transmission from blood transfusion?

A

Very low, HIV and hep C transmission 1:2 million

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16
Q

Why is there immunosuppression when receiving blood transfusion?

A

NK cell inhibition (even in autologous blood. it’s the storage process that kill NK cells)

irradiation decreases this risk

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17
Q

What decreases risk of bacterial contamination of blood product?

A

irradiation of blood

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18
Q

What is septic shock?

A

defined by hypotension not reversed with IV fluids

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19
Q

What is SIRS?What can a sirs response lead to?

A

Systemic Inflammatory Response Syndrome

  • reaciton of body’s inflmmatory response in the absences of infection. Can be stimulated by
    • trauma
    • burns
    • pancreatitis
    • other
  • SIRS can lead to
    • systemic vasodilation
    • altered capillary permeability
    • MSOF
  • Need volume resuscitation and pressors on board prior to sx!
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20
Q

What is distributive shock?

A
  • high output cardiac failure with hypotension
  • bounding pulses
  • wide pulse pressure

can treat c norepi

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21
Q

Which gram bacteria is notorious for patients getting very sick, very fast?

A

gram negative

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22
Q

If pt has narrow PP, tachycardic, hypotensive with gram negative sepsis, what can be a first drug of choice?

A

Epinephrine

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23
Q

What is source control in OR for sepsis?

A

4 D’s

  • Drainage
    • intra abdominal abcess
    • thoracic empyema
    • septic arthritis
    • pyelonephritis, cholangitis
  • debridement
    • necrotizing soft tissue
    • pancreatic necrosectomy
    • mediastinitis
  • Device removal
    • infected intravascular device
    • urinary catheter
    • infected IUCD
  • Definitive contorl
    • bowerl reseciton
    • chole

finding underlying cause of infection requires urgent sx

ex- abscesses, infective endocarditis, power perforation or infarction, infected prosthetic device, endometritis, necrotizing fasciitis

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24
Q

Diagnosis of sepsis?

A

Dx via culture- all source

blood, urine, sputum minimum

narrow abx coverage ASAP

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25
Q

Treatment for sepsis?

What are some goal directed therapies?

A
  • Time sensitive
  • empiric antibiotics, then tailor to organism ASAP
  • goal directed therapy with end organ perfusion a a goal
    • MAP >65,
    • CVP 8-12,
    • UOP Adequate,
    • correction metabolic acidosis,
    • mixed venous O2 sat >70
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26
Q

What are some anesthetic consideration in someone with sepsis?

A
  • Note limited reserve
  • prone to hypoxemia and hypotension
  • willl need invasive monitoring
  • adequate vascular access for resuscitation
  • prioritize abx admin
  • anticipate ICU admission
  • careful dosing with anesthetic, sedatives
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27
Q

What is the concern with the use of etomiade in patient with sepsis?

A

adrenal insufficiency may already be present and may be worsened even with a single dose

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28
Q

What might happen with surgical manipulation of infection?

A

cytokine release cauing rapid decompensation–> cardiovascular collapse

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29
Q

What is some direction for early goal-directed therapy (first few hours) in a patient with sepsis?

A
  • Fluid ressuscitation
    • crystalloid 500-1000mL or colloid 300-500mL over 30 minutes
    • repeat according to response
  • invasive monitoring
    • a line
    • Central line
  • vasopressors
    • NE 0.05-0.5 mcg/kg/min
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30
Q

What can be done in cases with refractory shock after early goal-directed therapy?

A
  • Measurement of cardiac output
    • esophageal doppler, PA cath, echo
    • consider epi or dobutamine
  • steroid administration
    • hydrocortsone 50-100 mg IV q 6 hours
  • Vasopressin 0.01-0.04 unit/min
    • can test dose. Dilute vial to 40 mL and give 2-4 mL at time
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31
Q

Target BG in sepsis?

A

80-150 mg/dL

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32
Q

WHat are some considerations for use of blood product in patient with sepsis?

A
  • Keep hgb between 7-9 g/dL
  • FFP only to cover invasive procedures and surgery
  • PLT transfusion to keep counts >5000 or 50,000/mm3 for invasive sx
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33
Q

Considerations for mechnical ventilation in septic patient?

Use of hymodilysis?

Other consideration?

A
  • Mechnical ventilation
    • 6-8 mL/kg TV
    • Plateau pressure <30
  • Hemodialysis
    • support ARF
      • continuous VV hemofiltration
      • intermittent HD
  • OTher
    • DVT prophylaxis
    • Stress ulcer prophylaxis
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34
Q

What are some guidlines for administration of ABX in septic patient?

A
  • Broad spectrum IV
    • collection of microbio speciments
      • blood ctx
      • urine cx
      • CSF
    • Source control
      • pus drainage, sx
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35
Q

What are the 4 pillars of sepsis management?

A
  • Immediate resuscitation
  • empiric therapy
  • source control
  • prevention of further complication
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36
Q

What are some CVP, SVO2 and SV values that show adequately resuscitated patient

A
  • CVP 12
  • SVO2 70%
  • SV 79 mL
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37
Q

What CVP, SVO2 SV show an udnerfilled patient?

A

CVP 8

SVO2 55%

SV 45 mL

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38
Q

What CVP, SVO2, SV show on an overfilled patient?

A

CVP 18

SVO2 80%

SV 110mL

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39
Q

AHA 2017 infective endocarditis guidelines?

A

Antibioitic prophylaxis with dental procedures i reasonable for patients with cardiac conditions associated with the highest risk of adverse outcomes from endocarditis, including:

  • prosthetic cardiac valves
  • prosthetic material for cardiac valve repair
  • previous endocarditis
  • CHD only in following categories
    • unrepaired cyanotic CHD (palliative shunts and conduits)
    • completele repaird CHD with prosthetic material/device during the first 6 months after procedure
    • repaired CHD with residual shunt/valvular regurge at site or adjacent to site of prosthetic patch/device
  • cardiac transplantation recipients with valve regurg d/t structurally abnomal valve

no evidence for use of ABX with GI GU tract procedures with devleopment of IE

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40
Q

What is c. diff?

A
  • anaerobic, gram positive, spore forming bacteria
  • most common cause in hospital diarrhea
    • due to increased abx admin
  • alchol based sanitizer does not kill spores
  • Tx: oral metronidazole (flagyl)
    • vancomycin
    • fecal transplant
  • Spores resistant to heat, acid, abx
  • risk doubles 3 days after abx
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41
Q

What are some considerations for patient with C diff going to OR?

A
  • will be very ill
  • anticipate dehydration
  • a/b abnormalities
  • electrolyte imbalance
    • plan for invasive monitoring to guide fluid resuscitationa nd vasopressor admin
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42
Q

What is necrotizing soft tissue infection?

A
  • Variety: fourniers, gas gangrene, flesh eating bacteria
  • Presentation may not reveal severity
    • pain is often out of proportion to symptoms
  • SIRS likely
  • often in genital area (fournier’s) . Crepitus at site may be present
  • Surgical emergencies with high mortality (75%)
43
Q

Treatment for necrotizing fasciitis? Anesthetic consideration?

A
  • Definitive treamtnet is surgical debridement along with ABX
  • Anesthetic considerationg:
    • tx like severe sepsis
    • aggressive fluid resus.
    • goal directed therapy
    • avoid etomidate
    • anticipate cytokine release intraoperativley
      • have vasopressin on standby
    • ensure vascular access for resus.
44
Q

What is Ludwig Angina?

A

SL/Submandibular infection in mouth.

Potential airway issue 40-60% need trach

plan for awake intubation

45
Q

What is tetanus?

A
  • Gram negative - occurs with spore contamination of wound
  • symptoms from neurotoxic “tetanospasmin” CNS effects
    • trismus is presenting sx
    • SNS responses are labile and exaggerated
      • expect tachycardia and HTN
      • Prone to skeletal muscle spasms that can lead to increased O2 consumption
    • hyperthermia
    • death
  • laryngeal, pharyngeal, intercostal and diaphragmatic spasms can affect adequate ventilation
    • need early airway protection
46
Q

Treatment of tetanus?

A
  • Controlling muscle spasms
    • diazepam/lorazepam
    • NVNMB and vent support may be needed
  • prevent SNS hyperactivity
    • beta blockers
  • support ventilation
  • neutralizing toxin
    • exotoxin neutralized by intrathecal or IM admin of human antitetanus immunoglobulin
  • surgical debridmenet
    • delayed until a few hours after antitoxin
47
Q

Anesthesia considerations for tetanus?

A
  • anticipate SNS hyperacitivty
    • give BB
  • Titration VA
  • Lidocaine
  • esmolol
  • metoprolol
  • Mg
  • nicardipine and SNP for refractory HTN
48
Q

What is pneumonia?

A
  • Variety of causes:
    • community acquired
    • atypical (more common in younger adults)
    • aspiration
    • postperative
    • VAP
    • legionnaires (hotels and whirlpools)
    • fungal (immunocompromised)
    • chlamydia psittaci (exposure to birds)
  • CXR
    • diffuse infiltarates suggestiv eof atypical PNA
    • Lobar opacification suggestive of typical PNA
49
Q

What are some risks associated with aspiration PNA?

A
  • Risk in patients with depressed consciouness and abnormal swallowing or esophageal motility. induction of anesthesia increases risk
  • Increased risk: NG tube, esophageal Ca, bowel obstruction, repeated vomiting
  • Poor oral hygiene and periodontal disease increases pneumonia risk following aspiration
50
Q

Anesthetic considerations with pneumonia?

A
  • defer sx if possible in acute PNA
  • expect hypoxemia despirate oxygenation in severe cases
    • because no SA for gas exchange
  • Carefully titrate fluids, may present dehydrate but overhydration may lead to worsening
  • use lung protective strategies of 6-8 mL/kg ideal body mass
  • mean airway pressre <30
    • meticuluous pulmonary hygeien with suctioning
  • use peep valve for transprot to minimize de recruitment in PEEP dependent patient
    • clamp and unclamp ETT
51
Q

What is tuberculosis? Symptom? dx? tx?

A
  • primarily spread through aerosolized droplets
  • now have MDR and XDR (extremely drug resistant) strains
  • Sx:
    • persisnt non productive cough
    • anorexia
    • weight loss
    • CP
    • hymoptysis
    • night sweats
  • Increased incidence: minority racial and thnic gourps, people form areas where TB is endemic (asia, africa), IVDA, HIV/AIDS
  • Dx:
    • mantoux, interferon release assay, CSR, sputum culture for acid-fast bacilli
  • Treatment
    • isoniazid, rifampicin, pyrazinamide, streptomycin, ethambutol
    • Isoniazid toxicity- peripheral nervous sytem in slow acetylators
      • hepatotoxicity worsened in rapid acetylators
    • Rifampicin: thrombocypopenia, leukopenia, anemia, renal failure, heptitis in 10%

TB treatment must continue to 6 months to be curative

90% with - sputum after 3 months but still need txmt

52
Q

Anesthetic considerations with TB?

A
  • Increased risk of provider exposure especially during bronch
    • postpone elective procedures until 3 negative sputum cultures
  • Perform high risk procedures in negative pressure room
    • need N95 for patient on transport
  • high efficiency particulate air filtre should be placed in anesthesai delivery circuit b/w Y connector and mask, LMA or ETT
    • adds dead space and resistance
  • Bacterial filter should b eplaced on exhalation limb of anesthesia delivery circuit to decrease d/c of tubercle bacilli into ambient air
  • Sterilize anesthesia equipment with standrard methods
    • using disinfectant that destoys tubercle bacilli
  • PACU negativ epressure room
53
Q

Infection s/p transplant?

A
  • Infection w/in 1 month- likely source is allograft (transplant)
  • 2-6 monhts- opportunistic infection, reactivation diesease syndromes (TB)
    • semptra- prophylaxis for pneumocystis PNA for at least 6 months
  • inflammatory response blunted: sometimes difficult ot ID source of infection
    • may not have typical s/s of infection d/t immunosuppression
  • >6 MOnths: many do well, infection risk decreases
    • some deal with chronic or progressive viral infection
      • hep B, hep c, CMB, EBV, herpes
54
Q

Anesthesai considerations post transplants?

A
  • Preop- focus on determining degree of immunosuppression and transplanted organ function
    • evaluate for co-existing infection
    • review comorbidities
  • Minimium: cbc cmp, lft, viral panel/viral loads, CXR, EKG
  • Strict aseptic technique with all invasive procedures
  • Active rejection requiring explantation= emergent case!
    • elective/non urgent cases should be postponed in active rejection or in patient with evidence of active infection
  • continue antimicrobial and antirejection drugs through perioperativ eperiod
  • regional anesthesia controversial
  • avoid nasal intubation
  • GA thought to have increased immunosuppressant effects over regional
  • Cyclosporine: delayed metabolism of NMB!! (esp pancuronium/vec)
55
Q

What is HIV & AIDS?

A
  • Retrovirus leading to severe immune dysfunciton
    • lymphotrophic; affinity for CD4 cells
  • Acute, latent and end stage phases
    • seroconversion 2-3 eweks following inoculation
      • flu-like symptoms
      • positive ELISA 4-8 weeks after incoulation
  • Nucleic acid testing HIV RNA is most specific and sensitive test for HIV
  • Generalized lymphadenopathy is hallmark sx until HAART started
  • halmark of pregression from chornic latent phaes HIV to AIDS is weight loss and FTT
56
Q

What is the hallmark of HIV infection?

A

subclinical and clinical multiple organ system involvement

57
Q

How many people in US have HIV/AIDS? How many unaware?

A
  1. 2 million in US
    1: 8 unaware
58
Q

What is treatment for HIV?

A
  • Highly active antiretroviral therapy (HAART)
  • Tailored to individual patients based on viral genotype/phenotype sensitivity and resistance ot drug regimens
59
Q

What are some cardiac involvements of HIV/AIDS?

A
  • High affinicty for myocardium and torphic effects on vascular structures
  • manifestations: LV dilation
    • cardiac dysfunciton
    • pulmonary HTN in 1%
    • pericardial effusion 25%
    • myocarditis in advanced dx
    • increased risk aneurysma nd aortic dissections
  • HAART therapy : premature artheroscleosis and diastolic dysfunction
60
Q

CNS invovlement in HIV/AIDS?

A
  • CNS reservoir for infeciton
  • variety of infectious nad neoplstic dx
  • AIDS dementia
  • peripheral neuropathy is most frequent neuro complication in HIV
61
Q

PUlmonary implications in HIV/AIDS?

A
  • Prone to opportunistic infections
  • PCP PNA- less common now with HAART
    • risk increase with CD4 < 200
    • CXR shows B ground glass opacities
62
Q

Endocrine implications in HIV/AIDS?

A
  • Prone to adrenal insufficiency
    • coritsol levels should be monitored
  • protease inhibitors: glucose intolerance
    • altered lipid metabolism
    • fat redistribution
      • can cause difficult airway
63
Q

Hematological implications in HIV aids?

A
  • anemia is most common early finding of HIV
  • Bone marrow suppression with zidovudine
  • thrombocytopenia worsens with CD 4<250
  • Coagulopathies (hypercoagulable vs bleeding)
64
Q

Renal implications in HIV/AIDS?

A
  • Protease inhibitors cna cause ATN, kidney stones
  • HIV associated nephropathy can lead to renal failure
65
Q

What is HAART?

A
  • Highly active antiretroviral therapy
  • Combo of at least 3 drugs
  • life long commitmenet
  • Longterm metabolic effects
    • lgucose intolerance
    • lipid abnormalities
    • increased risk CAD and CVD
    • fat redistribution to neck and abdomen
  • does not offer protective effects for anesthesi
  • variable effects on liver enzyme induction/inhibiton depending on combination
66
Q

Anesthesia specific drug interactions with Nucleoside reverse transcriptase inhibitors (NRTIs)?

A
  • HAART potentially changes drug clearance and effects of methadone
67
Q

Nonnucleoside reverse transcriptase inhibitors NNRTIs have what anesthetic interactions?

A

prolongs half life and or effects of:

  • Sedatives: diazepam, midazolam, triazolam
  • Opiates: fentanyl, meperidine, methadone
68
Q

Anesthesia drug interactions with protease inhibitors?

A

Prolongs half -life or effects of:

  • Antidysrhythmics: amiodarone, digoxin, quinidine
  • Sedatives: diazepam, midazolam, triazolam
  • Opiates: fentanyl, meperidine, methadone
  • local anesthetic: lidocaine
69
Q

Anesthetic interactions with integrase strand transfer inhibitors? (INSTIs)

A

No interactions!

70
Q

Anesthetic reactions with entry inhibitors?

A

changes drug clearance and effects of midazolam

71
Q

In general, how do you dose opiates/sedatives in patient on HAART?

A

decrease fentanyl and midazolam doses

72
Q

Periop considerations for patient with HIV/AIDS?

A
  • Periop risk correlates with CD4 cell count <200 puts pt at sig risk for opportunistic infectiosn and increased infectious risk associated with sx
  • presence of pulmonary, cardiac or renal dx may lead to periop complications
  • thorough multi-system work up preop (CBC, CMP, LFT, Coag, CXR, EKG, echo, cardiac clearance
  • Consider difficult airway d/t fat redistribution
    • no speicfic anesthetic recommended
  • be sure to document pre-existing neuropathy/vision loss
  • neurological involvement can affect choice of anesthetic- keep short acting
    • spinal cord involvement- avoid succ d/t proliferation of fAChR
73
Q

Anesthetic consideration for HIV/Aids?

A
  • Baseline tachycardia under anesthesia
  • potential for hemodynamic instability d/t autonomic dysfunction
  • may have chronic diarrhea w/ hypovolemia and electolyte imbalances
  • may need steroid supplementation (adrenal insuff)
  • protease inhibitors- prolonges DOA of hepatically metabolized drugs (fentayl, midz, morphine)
  • Perinatal- c-section decreases vertical transmission
  • exposure transmission 0;.3% risk percutaneously 0.09% mucus membrane
74
Q

When do you need to start antiretroviral treatment if you’re exposed?

A

within 1 hour

75
Q

What are prions?

A
  • Proteinaceous infective particles- are infectious proteins, many preferentially infect neuro tissue
    • ex CJD (mad cow)
  • Universally lethal; highly infectious
  • may come to OR for tonsillar or brain bx (diagnostic)
  • prions are not destroyed by standard mechanisms of decontamination
    • limit OR personnel
    • remove unnecessary equipment
    • use disposable instruments
    • wear full barrier
    • use TIVA nad ICU/portable vent
    • no pipeline scavenging
  • essentially everything gets thrown away/incinerated after case
76
Q

WHat are the 2 pathways of immunity?

A

Innate and adaptive

  • Innate- rapid and nonspecific
  • Adaptibe: delayed onset of activation. capable of memory
    • humoral (B lymphocytes)
    • cellular component (t lymphocytes)
77
Q

What is neutropenia?

A
  • Neutrophil granulocyte count <1500
    • increased risk for infection if <500
  • May be drug induced, autoimmune related
  • G-CSF: reduces duration of neutropenia after chmemo or bone marrow transplant
  • Liver is primary organ of somplement protein synthesis: advanced liver dx increases risk of infection
  • hyposplenism: most common cause of autoinfarction from vasoocclusive crises in sickle cell anemia
78
Q

What is hereditary angioedema?

A
  • Hereditary or acquired
  • Episodic subcutaneous and submucosal edema formation, can compromise airway
  • most common hereditary form: autosomal dominant deficiency or dysfunciton of C1 esterase inhibitor
    • leads to release of vasoactive mediators that increase vascular permeability and produce edema via bradykinin
    • repeated bouts of facial and/or laryngeal edema lasting 24-72 hours
    • episodes may b etriggered by menses, trauma, infeciton, stress, estorgen containing OC
    • Dental sx can be an important trigger of laryngeal attacks
79
Q

What is acquird angioedema?

A
  • Acquired: Lymphoproliferative dx, ACE inhibitors (0.5% of pt taking ACE inhibitors)
    • due to increased bradykinin, may develop unexpectedly after prolonged drug use with ace inhibitor
  • Androgens: mainstay of prophylactic therapy. antifibrinolytic therapy is another option- prophylactics NOT helpful in acut eepisodes not are drug susually used to treat allergic reaction (catecholamines, antihistamines)
80
Q

What is treatment for acquired angioedema during an acute attack?

A
  • C1 inhibitor concentrate (plasma derived or recombinant)
  • icatibant- synthetic bradykinin receptor antagonist
  • ecallantide- recombinant plasma kallikrein inhibitor that blocks conversion of kininogen to bradykinin
  • FFP (2-4 units) to replace deficient enzyme
81
Q

Anesthesia considerations for angioedema?

A
  • Life threatening airway obstruciton- requires intubation, personnel and equipment for trach should be available
  • prior to anesthesia- require prophylaxis before dental procedure or any procedure requiring intubation
  • C1 inhibitor concnetrates should be available
  • minimize trauma to oropharynx (ex sucitoning)
  • regional anesthesia is well tolerated
82
Q

Types of allergic reactions?

A
  • Type 1- IgE mediated and involve mast cells and basophils
  • Type II- mediate cyctoxicity with IgG, IgM and complenet
  • Type III- Tissue damage via immune complex formation or deposition
  • Type IV- T lymphocyte-mediated delayed hypersensitivity

Anaphylactoid reaction- mediator release from mast cells and basophils through non-immune mechanism. txmt same as anaphylaxis

83
Q

Type 1 allergic reaction?

A
  • Mediator- IgE
  • Timing- immediate
  • ex- anaphylaxis, urticaria
84
Q

Type II reaction

A
  • Mediators- IgG, IgM, complement
  • Timing- may be delayed
  • ex- autoimmune hemolytic anemia
    • immunes thrombocytopenia
    • incompatible blood reaction
85
Q

Type III reaction?

A
  • Mediators- immune complex formation and deposition
  • Timing- delayed
  • Ex- glomerulonephritis
    • serum sickness
    • vasculitis
      *
86
Q

Type IV reaction?

A
  • Mediator- T lymphocytes
  • timing- delayed
  • examples- dermatitis, chornic transplant rejection, TB test
87
Q

Anaphylaxis in anesthesia?

A
  • Incidence 1:3500 to 1:20,000 anesthetics
  • CV collapse, interstitial edema and bronchospasm
  • Risk: not reliably predictable; note patients with hx of asthma and/or fruit and drug allergies
  • degranulation of mast cells and basophils
    • epi stabilizes mast cells (only one!)
  • sx usually within 5-10 min of exposure to antigen
    • tachycardia, bronchospasm, laryngeal edema, cutaneous manifestation
    • intial sx difficult to appreciate under anesthesia. 1st sign may be CV collapse
  • confirm with histoamine in tryptase levles; time sensitive
  • skin testing post event must take place >6 weeks after
    • d/t depletion of mast cells an basophils may cause false negative
88
Q

What are most common triggers for anaphylaxis around anesthesia?

A
  • Muscle relaxants
    • roc and succ most common<– this is in european patients. in US, this is lower
  • antibiotics (b-lactam drugs, sulfonamides, vancomycin, quinolones)
    • PCN and cephalosporin cross reactiity 2%
  • latex
    • distinguishing feature is delayed onset >30 min after exposure
      • spina bifida, multple previous sx, fruit allergy and healthcare workers have higher wisk
        *
89
Q

Other common considerations for allergies around anesthesia?

A
  • esters metabolized to PABA
    • no cross-sensitivity b/w esters and amides
    • use preservative free LA in hx of LA allergic rxn
  • propofol and food allergy concerns unsubstantiated
  • halothane hepatitis
  • promatine: histamine release r/t rate of injeciton, not allergic
    • allergic reaction potential in diabetics givne NPH insulin
90
Q

Transfusion reaction?

A
  • Hemolytic reactions occur in 1:10,000-50,000 blood transfusions
  • IgM and IgG
    • acute hemolytic reactions ABO incompatibility; renal failure and DIC
      • Treatment- aggressive hydration, heparin for DIC +/-
    • delayed reaction are often due to Kidd or Rh antibodies: usually require no txmt
  • Anaphylactic reactions to blood are rare
    • tx: stop transfusion. fluids, epi, pressors
91
Q

What is TRALI?

A
  • Transfusion related acute lung injury
    • leading cause of transfusion-related morbiity and mortality
      • FFP and PLT most common culprit
  • sx: hypoxia, b pulmonary edema within 6 hours of transfusion
  • pathophys: activation of neutrophils on pulmonary vascular endothelium from donor leukocyte antibodies
  • tx- supportive
92
Q

What is TRIM?

A
  • Transfusion-related immunomodulatory
  • increased susceptibilty to infection; promotion of tumor growth
  • decreased NK cell and phagocytic function
    • impaired antigen presentation
    • suppression of lymphocyte production
  • seen in Ca
93
Q

What is the physiologic effect of histamines?

A
  • Increased capillary permeability
  • peripheral vasodilation
  • bronchoconstriction
94
Q

What ar ephysiologic effects of leukotrienes?

A
  • Increased capillary permeability
  • bronchoconstriciton
  • negative inotropy
  • coronary artery vasoconstriction
95
Q

What are physio effects of prostaglandins?

A

Bronchoconstriction

96
Q

What is primary treatment of anaphylaxis durign anesthesia?

A
  • General measures
    • inform surgeon
    • request immediate assistanc
    • estop admin of drugs, colloid and blood products
    • maintain airway with 100% o2
    • elevate legs if practical
  • Epinephrine administration
    • titrate dose accoring to symptom severity and clincal response
    • Adults: 10-100 ug by IV bolus every 1-2 min
    • IV infusion starting at 0.05-1 ug/kg/min
    • Chilren- 1-10 ug/kg by IV bolus repeat every 102 min
  • Fluid therapy:
    • Cystalloid NS 10-25mL/kg over 20 min more as needed
    • colloid 10mL/kg over 20 min
  • Anaphylaxis resistant to epi
    • glucagon- 1-5 mg IV bolue
    • NE 0.05-0.1 ug/kg/min IV infusion
    • vasopressin 2-10 unit IV bolus followed by 0.01-0.1 unit/min IV
97
Q

What is the secondary treatment of anaphylaxis after anesthesia?

A
  • Bronchodilator
    • b2 agnoist for symptomatic txmt of bronchospasm
  • Antihistamines
    • histamine 1 antagonist- diphenhydramine 0.5-1 mg/kg IV
    • Histamine 2 antagonist- ranitidine 50 mg IV
  • Corticosteroids
    • adults- hydrocortison 250 mg IV or methylprednisolone 80 mg IV
    • children- hydrocortisone 50-100 mg or methylprednisolone 2mg/kg IV
98
Q

Aftercare for anaphylaxis?

A
  • Patient may experience relapse; admit for observation
  • obtain blood samples
  • arrange allergy testing at 6-8 weeks postop
99
Q

Anesthesia immune implications for anesthesia?

A
  • Cervical instability with RA
  • Renal injury with SLE
  • Liver failure with chornic autoimmune hepatitis
  • addisonian crisis in pt treated long term with corticosteroids
  • newer therapies for autoimmune disorders inhibit immune response: increased risk of periop infection
  • Risk of accelerated atherosclerosis, heart disease, and storke
    • autoimmune disease may increase CV morbidity/mortality 50 fold
    • long term steroid therapy is associated with HTN and DM
100
Q

Regional anesthesia ____ the neuroendocrine surgical stress resposne

A

attenuates

101
Q

Selective IgA deficiency?

A
  • 1:600-800 adults
    • recurrent pulmonary/sinus infections
    • must get blood transfusion from IgA deficient donor or will have anaphylaxis
102
Q

Cryoglobulinemia and cold hemagglutinin disease?

A

microvascular thrombosis with end organ damage from hypothermia (<33). must maintain normothermia

103
Q

Amyloidosis?

A
  • accumulation of insoluble fibrillar proteins in various tissue can be primary or secondary
  • note macroglossia in 20%, englarged, stiff tongue. enlargmenet of salivary glands. overall difficult airways
  • cardiac involvement with conduction defects
  • also severe reanl, GI and hepatic effects
104
Q

Di Geroge syndrome?

A

gene deletion; absent or diminished thymus development

other congenital abnormal (cardiac; facial deformities)

immunocompromised

Co-existing Test 1 (4 decks)

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