Dressings, Pharmacology, Hematoma/Seroma/DVT Flashcards

Question 1

Q

WHY DO WE USE DRESSINGS THAT HAVE INORANIC SILVER?

Answer

A

inoragnic sliver is strongly bacteriocidal and broad spectrum antimicrobial, including vs. pseudomonas
tri-prong MOA:
- increases permeability
- decreases cell respiration
- denatures nucleic acid

Question 2

Q

why do we use sulfa-containing dressings

Answer

A

broad spectrum, bacteriostatic, including vs. pseudomonas
inhibits folic acid metabolism - cells can’t make nucleic acids or purines

Question 3

Q

what are the advantages, disadvantages and side effects of SSD?

Answer

A

advantages:
- broad spectrum, bacteriostatic, anti pseudomonal
- moderate eschar penetration
- soothing, painless application
- cleaner vs. silver
Disadvantages
- pseudoeschar
- inhibits fibroblast (bad for superficial PT wounds)
side effects
- neutropenia (controversial)
- sulfa allergy
- hemolytic reaction in newborns (contraindicated in late pregnancy)

Question 4

Q

what are the advantages, disadvantages and side effects of sulfamylon (sodium mafenide?)

Answer

A

advantages
- bacteriostatic
- strongly penetrates eschar
- useable with exposed cartilage
Disadvantages
- poor against MRSA, s aureus, candida (“least broad spec”)
- painful
- carbonic anhydrase inhibitor: risk of hyperchloremic metabolic acidosis
- allergy/rash

Question 5

Q

advantages, disadvantages and side effects of sodium hypochlorite (dakins, hygoel)

Answer

A

advantages
- bacteriocidal, fungicidal, viricidal (MOA produces hypochlorous acid that denatures protein)
- breaks up clot
- inexpensive
disadvantages
- hemorrhage
- inhibits wound healing (harms healthy tissue)
- inactivated by light (brown class bottle, in bag)
- short duration only
ideal for infected necrotic wounds

Question 6

Q

what are advantages, disadvantages and side effects of acetic acid

Answer

A

advantage: antipseudomonal
disadvantage: ltd against other bugs, corrosive to eyes

Question 7

Q

what are the advantages disadvantages and side effects of silver nitrate?

Answer

A

advantages
- broad spec bacteriocidal
- painless
- no skin hypersensitivity
disadvantages
- stains everything
- poor penetration
Side effects
- hypotonic solution, causing low Na, K, Cl
- rare risk methemoglobinemia

Question 8

Q

discuss the antibacterial activity of the common ointments

Answer

A

bacitracin - GPC, GPB
polymyxin - GN
neomycin - GN, some GP
mupirocin - for MRSA
fucidin - GP and anaerobes
polysporin - bacitracin and polymyxin (broad spec)
neosporin - bacitracin, polymyxin, neomycin (broad spec)

Question 9

Q

list characteristics of ideal dressing

Answer

A

Would be identical to Skin
Barrier to bacteria
Prevents fluid loss
Prevents Heat Loss
Allow gas exchange
Comfortable and conformable
Non-allergenic and non-toxic
Infrequent changes
Inexpensive, long shelf life

Question 10

Q

what is the MOA of NPWT

Answer

A

Macrodeformation

Draws edges of the wound closer together
Removal of Exudate & Inflammatory mediators

Microdeformation

Promotes Granulation tissue formation
Angiogenesis
Cellular Mitosis
Enhances perfusion and local oxygen delivery.

Question 11

Q

What is the mechanism of action of local anaesthetics?

Answer

A

Ester and amine anaesthetic block nerve conduction
They diffuse in the non-charged state through the neuron cell membrane.
Here they become charged, and block voltage-gated Na+ channels
This blocks Na conductance, and therefore neurons cannot reach their threshold potential to generate an action potential
This blocks sensory fibres (no sensation/pain) prior to motor fibures

Question 12

Q

Differentiate between bactericidal and bacteriostatic

Answer

A

Bactericidal Agent – Antimicrobial able to kill susceptible microorganisms without the intercession of host humoral or cellular immune defenses
Bacteriostatic Agent – Antimicrobial which reversibly inhibits essential bacterial metabolic processes, which can recommence when levels become subinhibitory; ultimate destruction of infecting organism depends on host defenses

Question 13

Q

List guideline to antimicrobial useage

Answer

A

Specimens – prior to initiating treatment
Drug Choice – as narrow as possible, consider allergies, toxicity, side effects, resistance patterns
Dose – adequate dose, appropriate interval
Duration – complete course or until clinical cure (e.g. OM & TB), resist changing abx unless good reason
Remove Barriers – e.g. drain abscesses, remove foreign bodies

Question 14

Q

list examples of bacteriocidal and bacteriostatic antibiotics

Answer

A

Bactericidal (Very Finely Proficient At Cell Murder)
Glycopeptides (Vancomycin)
Fluoroquinolones
Penicillins
Aminoglycosides
Cephalosporins
Metronidazole
Bacteriostatic
Macrolides (Erythromycin)
Lincosamines (Clindamycin)
Folate antagonists (Sulphonamides)
Tetracyclines

Question 15

Q

List bacteria endogenous to skin

Answer

A

AP-LEAD

s. Aureus
c. Perforingens
Lactobacillus
s. Epidermidis
p. Acnes
Diphtheroids spp

Question 16

Q

What are bacteria endogenous to the mouth?

Answer

A

aerobic and anaerobic strep
Actinomyces
Bacterioides
Fusobacterium

Question 17

Q

what is red man syndrome?

Answer

A

associated w/ vancomycin administration; specifically rapid administration
from 4-10 mins after infusion starts (to 1 hr later) have pruritus, an erythematous rash of the face, neck, and upper torso +/- hypotension, angioedema; Treat (pre-treat) w/ anti-histamine; other support as needed

Question 18

Q

List organisms associated w/ Dog/Cat; Human; Reptile bite

Answer

A

Source

Organisms

Dog / cat

Pasteurella multocida
Staph aureus
Streptococci
Anerobes

Human

Eikenella corrodens
Streptococci
Staph aureus
Anaerobes (Bacteroides, Peptostreptococcus)

Reptile

Enteric Gram negative bacteria
Anerobes

Question 19

Q

What are features of a tetanus prone wound?

Answer

A

Age > 6 hrs without treatment
Mechanism: crush, trauma, burn, frostbite, missile etc
Configuration - stellate, avulsion, abrasion
Depth > 1cm
Signs of infection
Devitalized tissue
Contaminants
Denervated or ischemic

Question 20

Q

discuss when you would give tetanus booster and IG

Answer

A

History of Adsorbed Tetanus Toxoid (doses)

Nontetanus-Prone Wounds

Tetanus-Prone Wounds

Td

TIG

Td

TIG

Unknown or ≤ three

Yes

No

Yes

≥ Three

No (Yes if > 10 yrs since last dose)

No

No (Yes if > 5 yrs since last dose)

No

Td (0.5mL) – Tetanus and diptheria toxoids adsorbed – for adult use (given IM)
TIG (250mL IM) – Tetanus Immune Globulin
Simultaneous administration of Td and TIG – Given at different sites via different syringes

Question 21

Q

What are risk factors for CA-MRSA? What populations are at risk?

Answer

A

· 5 C’s implicated in transmission of CA-MRSA

o Crowding

o frequent skin Contact

o Compromised skin

o sharing Contaminated personal care items

o lack of Cleanliness

· Populations at increased risk of CA-MRSA

o <2 years, minority populations (Native or Aboriginal, African-American), athletes (mainly contact-sport participants), injection drug users, men who have sex with men, military personnel, inmates, veterinarians, pet owners and pig farmers

Question 22

Q

what antibiotics are potentially available to treat CA-MRSA?

Answer

A

PO: Clinda, septra, doxycycline, minocycline, linezolid, IV: vancomycin, daptomycin (for invasive infections)

Question 23

Q

describe the MOA of local anaesthetic

Answer

A

Neural conduction is interrupted by inhibiting influx of sodium ions through voltage-gated sodium channels (receptor site) within the neuronal membrane
Penetration of nerve membrane requires un-ionized (base) form
pKa determines the ratio of ionized to un-ionized local anesthetic
The closer the pKa is to the body pH, the faster the onset
Stability is enhanced by adjusting pH of solutions to mildly acidic

Question 24

Q

Why does local anaesthetic not work as well in infection/inflammatory states?

Answer

A

tissue pH is acidic & much lower than the pKA of LA –> greater % of agent is in cationic form and only neutral form will diffuse

Question 25

Q

what is the benefit of adding bicarb to LA

Answer

A

decrease pain on injection, ↑pH, closer to pKA, more in neutral form à faster onset

Question 26

Q

Contrast amide to ester local anaesthetic

Answer

A

Esters

·Cocaine, Procaine, Tetracaine, Benzocaine

·Disadvantage – greater risk of allergy (due to PABA metabolite); metabolized in plasma (pseudocholinesterase)

·*Cocaine met in liver and blood

·Renally excreted

Amides (two ‘i’s in generic name, ‘i’ in liver)

·Lidocaine, bupivicaine, prilocaine, mepivicaine

·Metabolized in liver

·Low risk of allergy to preservative

·Liver failure: can lead to amide toxicity

·Renally excreted

Question 27

Q

List toxicity to local anaesthetic

Answer

A

Local toxicty

Local Toxicity of LA

·Skin necrosis (epi)
·Muscle necrosis
·Intraneural injection – fibrosis
·Prolonged motor/sensory deficit
·Vasodilatation

Systemic toxicity: EXAM

·CNS

oLow level (depression, tinnitus, perioral numbness, dizziness metallic taste)
oHigh level (anxiety, fine tremor, sz)
oVery high (depression, coma, resp depression, cardiac arrest)

·CVS

oLow levels = ↓conduction velocity, bradyarrhythmia
oHigh level: negative inotropic effect, vasodilation –> CV collapse
oBupivicaine –> longer duration –> more cardiotoxic

·Hematologic

oMethemoglbinemia (prilocaine); Risk Factors: G6PD, meds (sulfonamides, antimalarials)

· Allergic rxn (ester >>> amide)

Question 28

Q

What are steps in treatment of local anaesthesia (lidocaine, bupivicaine) toxicity?

Answer

A

Call 911; alert facility with cardiopulmonary bypass
A – Maintain AW
B – 100% O₂ face mask or ventilator (prevent respiratory acidosis)
C – Support BP: IV fluids, pressors, CPR
D - Diazepam for seizures
E – Lipid emulsion for refractory amide cardiac toxicity
Lidocaine toxicity Rx – infusion of 20% lipid emulsion
Bolus 1.5 ml/kg (lean body mass) intravenously over 1 minute (~100 ml)
Provide continuous infusion at 0.25 ml/kg/minute (~18 ml/minute; adjust by roller clamp)
Repeat bolus once or twice for persistent cardiovascular collapse
Double the infusion rate to 0.5 ml/kg/minute if blood pressure remains low
Continue infusion for at least 10 minutes after circulatory stability is achieved
Max dose 12ml/kg over first 30 minutes
Consider also direct evacuation if possible: open abdominoplasty, evacuate from rectus sheath

Question 29

Q

what is the “antidote” to lidocaine toxicity?

Answer

A

20% lipid emulsion

Question 30

Q

what is the maximum dose of epinephrine delivered for purposes of prevention of hemostasis / w/ local anaesthetic

Answer

A

Maximum dose – 10 μg/kg
1:100 000 = 10 μg/ml, 1:200 000 = 5 μg/ml
so, if 1:100 000, can give same mls as patient weight

Question 31

Q

How do you treat epinephrine toxicity?

Answer

A

Toxicity Treatment **ACLS**
Drugs: α-blocker – phentolamine,
β-blocker - propranolol
Phentolamine (1.5-3 mg) Reversible, nonselective alpha-adrenergic antagonist causing vasodilation
Accidental EpiPen digit inj à phentolamine
- dilute 1.5mg (0.15ml) in 1ml 2% lido and inject subcutaneous into site of epipen until finger pink
- Topical/systemic nitro
- Warm water immersion

Question 32

Q

What is the antidote / reversal agent to local over-administration of epinephrine (epipen, during local procedure)

Answer

A

Phentolamine

Question 33

Q

what are the advantages and disadvantages of regional anesthesia

Answer

A

Advantages

·Less post-op pain

·Less systemic complications associated with GA

·Less narcotic use

·Less N&V

Disadvantages

·↑ preparation time

·Technically demanding

·Risk a/w, numb/flaccid extremity

·Urinary retention

Question 34

Q

Define BIER block, and list advantages and limitations

Answer

A

Definition: Intravenous regional anaesthesia (IVRA): relies on diffusion of local anesthesia from the venous system to nearby nerves
Should be used for duration of < 1 hr
Advantages of IVRA
safety (esp vs. GA), similicity, reliability, fast onset (and offset) of analgesia
Limitations of IVRA
short procedures, no post-op analgesia, tourniquet pain, no muscle relaxation, risk of systemic toxicity

Question 35

Q

what is the sequence for execution of a BIER block?

Answer

A

apply 2-cuff tourniquet
PIV on OR site
elevate and exsanguinate
inflate distal cuff
inflate proximal cuff
deflate distal cuff - so LA will infiltrate this area
inject local - 3mg/kg max; no epi (50cc of 0.5% lidocaine is common)
remove PIV; ensure contralateral arm has PIV access
rapid onset of analgesia
for tourniquet pain (often around 30mins):
- inflate distal cuff
- double check distal cuff is inflated
- release proximal cuff
release tourniquet - not before 30 mins have elapsed to avoid toxicity
- TIME <40 min: release tourniquet for 15s, then re-inflate x 30s before final deflation
- >40min can deflate safely
rapid resolution of anesthesia

Question 36

Q

How do you execute a wrist block?

Answer

A

Wrist block: median, ulnar, superficial radial n block (see below)
D1-3 – block median & superficial radial nerves
- Median – b/w FCR & PL, just proximal to carpal tunnel
- Superficial radial – 3 fingerbreadths proximal to radial styloid
D5 – block ulnar & dorsal sensory branch
- Ulnar – Transverse injection under FCU just proximal to wrist crease (nerve ulnar to artery)
- Dorsal sensory branch – dorsal to 5^th MC base
D4 – median, superficial radial, ulnar, dorsal ulnar sensory branch

Question 37

Q

how do you do a foot/ankle block?

Answer

A

Tibial

Heel/sole
Post to artery, 1cm above malleolus

Deep peroneal

1st web
Between TA&EHL @ level of malleolus

Sup peroneal

Dorsum
Subcut from EHL to the lateral malleolus

Sural

Lat foot
Between the lateral malleolus and Achilles 1cm above malleolus

Saphenous

Medial foot
Between tib-ant and medial malleolus

Question 38

Q

what is malignant hyperthermia

Answer

A

Autosomal dominant disorder of skeletal muscle characterized by intracellular skeletal muscle hypercalcemia and ATP consumption

Question 39

Q

What is the pathophysiology of maligant hypertermia? What triggers malignant hyperthermia?

Answer

A

Pathophysiology
- Ryanodine receptor problem –> uncontrolled influx of Ca into cytoplasm of skeletal myocyte à sustained uncontrolled contractile hyperactivity –> consumption of ATP
Triggers: halothane & flurothane gases, succinylcholine (currently agreed that amides are not triggers)

Question 40

Q

What are signs of malignant hyperthermia?

Answer

A

Vitals: first sign is hypercapnia, also hyperthermia, tachycardia, hypertension, tachypnea,
Clinical: rigidity, myoglobinuria/hemoglobinuria
Labs: electrolyte abn (hyper K, hyper Ca), increased CK, metabolic acidosis

Question 41

Q

What are ways to diagnose malignant hyperthermia?

Answer

A

definitive is muscle biopsy: caffiene halothane test
in pt w/ positive family history, many have baseline elevated CK

Question 42

Q

How do you treat malignant hyperthermia?

Answer

A

Prevention – at risk pt can be pretreated: Dantrolene PO 5mg/kg/day (div in 4 doses) over 1-3 days
Stop offending agent
Immediate dantrolene: IV Dantrolene: 1-2 mg/kg IV q 5-10 mins until patient stable
Ventilate with 100% O2
Cooling measures
Correct electrolyte/acid-base abn
Diuresis to prevent renal injury
ICU
Inform patient/family refer for testing/need card

Question 43

Q

What are side effects of NSAID?

Answer

A

o Allergy, also implicated in SJS & TENS

o Teratogenic in 1st trimester

o CVS – HTN, stroke, MI

o Renal - ARF

o GI – upset, GERD, ulcer, bleed

o Only mild antiplatelet effects (except ASA) – easy bruising in high doses or combo with ASA

Question 44

Q

describe hematolgoic MOA for ASA

Answer

A

· inhibits platelet aggregation through inhibition of cyclooxygenase in thromboxane pathway

· low dose inhibits thromboxane not prostacyclin

· stop 10d prior to surgery

Question 45

Q

what is the MOA for glucocorticoids?

Answer

A

Mechanism of Action
Anti-inflammatory : inhibit WBC & macrophage function
↓ interleukins; ↓ Production of prostaglandins & leukotrienes

Question 46

Q

Describe how local complicaitons of glucocorticoid w/ wound healing

Answer

A

Complications
Wound healing: (by phases)
- Inflammatory: less PMN activation; less chemotaxis, phagocytosis, angiogenesis
- Proliferative phase: ↓ fibroblast proliferation/collagen synthesis
- Remodeling: less contraction d/t less collagen remodeling
Skin: Think layers
- Local: Atrophy, striae, fragile, Epidermis (thin, less basal mitosis) dermis (thin, less ground sub and collagen), capillary vasoconstriction, hypopigmentation, telangiectasia

Question 47

Q

what is one therapy that can counteract local wound healing effects of steroid administration?

Answer

A

Vitamin A orally

Question 48

Q

Describe when and how you would use stress dose steroid admin?

Answer

A

Indications for peri-op steroid coverage (within past 1 year)
- Previous high dose >60mg daily x 7 days
- Moderate dose >20mg qd x 12w (for RA say if taking chronic > 5mg/d)
- Prev peri-op std coverage
Dosage
- Minor procedure: double daily dose day of OR, then normal
- Major:
Solucortef 100 mg IV pre-op
Solucortef 100 mg IV q 8 h x 24 hrs post op day 0 then
Solucortef 50 mg IV q 8h x 24 hrs – post op day 1
Restart usual daily dose PO/IV post op day 2

Question 49

Q

what is addisonian crisis?

Answer

A

Addisonian crisis: acute adrenal insufficiency
hypotension, hypercalcemia, pain legs/back abdo, vomiting/diarrhea, syncope, hypoglycemia, confusion/psychosis, fever

Question 50

Q

describe drugs that influence hemostasis

Answer

A

HEPARIN

·binds antithrombane AIII; inhibiting thrombin and Xa

HERUDIN

·naturally occurring in salivary glands of medicinal leaches

·hirudin inhibits thrombin

DEXTRAN

·LMW polysaccharide:

ovolume expansion

oinactivates vWF

onegative charge on platelets

ofibrinolytic

·anaphylaxis 1:70,000; pulmonary edema, nephrotoxic

ASA

· inhibits platelet aggregation through inhibition of cyclooxygenase in thromboxane pathway

· low dose inhibits thromboxane not prostacyclin

Question 51

Q

describe complications of a GA

Answer

A

Medications:
Pain, nausea, vomiting, headache, memory changes/dementia
Allergy, unrecognized malignant hyperthermia, other
Intubation
Tube displacement, airway obstruction
Aspiration, aspiration or chemical pneumonitis, delayed extubation/prolonged intubation
Atelectasis, tooth injury
2’ to insult/injury/process aand/or PMHx
cardiac problem: troponitis, ischemia
cardiorespiratory failure
death

Question 52

Q

WHAT are the four phases of coagulation?

Answer

A

primary hemostasis - initiation & formation of platelet plug
secondary hemostasis - propogation by coagulation cascade & formation of fibrin clot
termination by antithrombotic control mechanisms
removal of clot

Question 53

Q

list intrinsic, extrinsic and common pathway clotting factors

Answer

A

intrinsic: XII, XI, IX, necessary cofactors: Ca, PL, VIII
extrinsic: TF, VII
common: X, II, I, necessary cofactor V

Question 54

Q

what are vitamin K dependent cofactors (and thus those inhibitied by coumadin)

Answer

A

X
IX
VII
II
also protein C, protein S
“1972” Canada vs. soviety

Question 55

Q

compare characteristics of bleeding disorders - primary vs. secondary hemostasis

Answer

A

1° Hemostatic Disorders (Platelet defects)

2° Hemostatic Disorders (Coagulation Defects)

Onset after injury

Immediate
Delayed- hours to days

Sites of Bleeding

Superficial- mucosal membranes (nasal, gingival, GIT, GUT), skin
Deep-joints, muscles, retroperitonium

Physical findings

Petechiae, ecchymosis
Hematomas, hemathroses

Family History

Autosomal dominant (AD)
Autosomal or X-linked recessive

Response to therapy

Immediate; local measures effective
Requires sustained systemic therapy

Question 56

Q

describe tests used to measure hemostasis

Answer

A

Type of Hemostasis

Test

Purpose

Examples of Associated Diseases

Primary

Platelet count

platelet number (quantitative)
↓: DIC, ITP, HUS/TTP

Bleeding time

Plt function and vessel wall function (qualitative)
↑: vWD, plt. dysfunction, severe thrombocytopenia

Secondary

aPTT

measures intrinsic pathway (factors VIII,IX,XI,XII) and common pathway
used to monitor heparin therapy
↑: haemophilia A & B

PT

extrinsic + common pathway
↑: factor VII deficiency

INR

extrinsic pathway
used to monitor warfarin therapy

Mixing studies

differentiate inhibitors of clotting factor(s) from a deficiency in clotting factor(s)
mix pt.’s plasma with normal plasma in 1:1 ratio & repeat abnormal test
Normal - clotting factor (s) deficiency
Abnormal - presence of inhibitors of clotting factor(s) - HIT

Question 57

Q

what is the MOA of heparin?

Answer

A

binds and potentiates ATIII, inactivating thrombin (II) and factor X

Question 58

Q

what blood test measures heparin effectiveness on clotting?

Question 59

Q

what is the antidote to heparin

Answer

A

protamine sulfate

Question 60

Q

what is the antagonist to coumadin?

Answer

A

vitamin K, FFP

Question 61

Q

what is MOA of fragmin

Answer

A

also potentiates ATIII but more selectively inhibits factor X

Question 62

Q

what are the advantages of LMWH over UFH

Answer

A

less risk HIT
OD dosing
less blood tests
less bleeding
more reliable weight-based dosing

Question 63

Q

what is a lab test for efficacy of ASA

Answer

A

bleeding time

tests platelet function

Question 64

Q

what is the MOA of ASA

Answer

A

for thrombogenic prophylaxis, low doses irreversibly inhibit platelet aggregation through the TAX2 pathway & COX inhibition
at higher doses, also inhibits PGI2 for antiinflammatory

Answer 64

A

platelets
DDAVP

Answer 65

A

technical: inadequate coagulation, large dead space, use of epinephrine
patient: clotting disorder, baseline htn
systemic: post-op HTN, hypothermia (induces vasodilation), depletion of clotting factors

Answer 66

A

blood as space occupying lesion: compression of pedicle or NAC, overlying tenuous skin flap (ischemia/necrosis), compression of vital structures (globe/optic nerve, airway, cartilage etc)
blood as potential source of infection
blood as an irritant - free radical formation generated during break down by anaerobes (OH-, H2O2, superoxide O2-) can cause inflammation, direct necrosis, scar formation, contraction/contracture
other: ossification, wound dehiscene, pigmentation, fibrosis

Answer 67

A

BEFORE THE OR

identification of clotting disorder
stopping anticoagulant medicines
stopping natural supplements
optimization of blood pressure through FMD or GIM consult
take anti-htn in am of OR & continue afterwards

DURING THE OR

prophylactic hemostasis
tying or clipping vessels
maintaining normal BP (avoiding permissive hypotension or without bringing back to normal before you leave the room - may unmask other bleeders)
wide exposure & knowledge of anatomy
use of drains

POST OP

avoid HTN
compression dressings

Answer 68

A

blood plasma without clotting factors

Answer 69

A

electrocautery
large dead space
extensive dissection
lymphatic disruption
fat necrosis
US assisted liposuction

Answer 70

A

identification of seroma, history, physical, +/- imaging as necessary

management can then be grouped in 3 ways

prevention
1. minimize undermining
2. use tumescent to cool tissues with adjacent electrocautery
3. in abdominoplasty, leave some sub-scarpal fat on abdo wall fascia
4. minimize deadspace: closed-suction drains, quilting sutures, pressure garments, fibrin sealant
non-operative management
1. close observation and expectant management for resorption
2. pressure dressing
operative intervention
1. percutaneous drainage using large bore or angiocath, +/- under image-guidance, +/- serial percutaneous drainages, with pressure dressing afterwards
2. re-insertion of closed suction drain
3. open drainage and excision of seroma cavity
4. injection of sclerosant under radiological guidance: EtOH, Bleomycin, docycycline, erythromycin

Answer 71

A

nothing - may be seen as a complication or expected in many people after certain types of surgery with no sequellae after absorption
chronic seroma
chronic seroma cavity
infection
delayed wound healing/dehiscence
organization of seroma, overlying distortion of tissues, fibrosis

Answer 72

A

~ 50% develop at induction of GA

Answer 73

A

patient-based risk factor stratification
- ex: Caprini Risk Assessment Model develops an aggregate risk score based on presence/absence of individual patient risk factors
procedure-based risk factor stratification
- ex: Total hip arthroplasty (all pts get chemoproph unless c/i)
- risk w/ MWL, abdoplasty combined procedures etc.

Answer 74

A

Hypercoagulable states - congenital
- AT deficiency
- Factor V Leiden
- Protein C/S deficiency
- Hyperhomocysteinuria
Hypercoagulable states - acquired
- APLA syndrome,
- Endo: OCP, HRT, tamoxifen
- Malignancy (excluding skin), myeloproliferative do
Venous stasis RFs
- Immobilization: recent long GA, travel/flight, cast immobilization, bed-bound or hospitalized on bedrest
- Obesity
- Pelvic mass
- Pregnancy or 4-6wks post-partum
Other RFs
- Major: prev VTE, FHx VTE, recent stroke, polytrauma / major bone #
- Minor: varicose veins, smoking, certain comorb: AMI, COPD, IBD, kidney disease
Procedure RFs
- Total hip/knee arthroplasty
- Abdominoplasty
- MWL body contouring
- combined procedures

Answer 75

A

venous stasis 2’ plication of rectus diastasis
disruption to superficial venous drainage
post-operative decrease mobilization or immobilization

Answer 76

A

elective procedures under GA > 1 hr
breast reconstruction
H&N cancer surgery/recon
Body contouring
Abdominoplasty
Lower extremity surgery

Answer 77

A

appropriate risk stratification
discontinuation of prothombotic meds: OCP, HRT, TAMOXIFEN, SMOKING 2-3 wks prior and 2-3 wks post
consider conscious sedation vs GA
early ambulation
proper patient positioning
mechanical prophylaxsis: TEDS (thromboembolic deterrernt stockings), SCD (sequential compression device)

Answer 78

A

recent IC bleed or stroke
epidural < 24 hrs
active bleeding
plts < 100
HIT
coagulopathy

Answer 79

A

FFP all clotting factors, fibrinogen
Cryo: VIII, XIII, vWF, fibrinogen, fibronectin

Answer 80

A

prothormbin complex concentrate
contains vit k dependent coagulation factors: 10, 9, 7, 2
for use in rapid reversal of elevated INR 2’ warfarin

Answer 81

A

anticoagulant
- arnika
- garlic
- ginger
- ginko
- vit e
coagulant
- ginsing
- golden seal
- mistle toe

Answer 82

A

expect 50% reduction in size by 4 wks (MM)

Brainscape's Knowledge GenomeTM

Dressings, Pharmacology, Hematoma/Seroma/DVT Flashcards

Brainscape's Knowledge Genome^TM