Care of surgical patients III Flashcards

1
Q

VTE

A

venousthromboembolism

  • DVT
  • PE

All patients being admitted to hospital or undergoing surgery should be assessed for VTE risk on admission and re-assesed if a change occurs in clinical situation

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2
Q

RF for VTE

A
  • Increasing age
  • Previous VTE
  • Smoking
  • Pregnancy or recently post-partum
  • Recent surgery (especially abdominal surgery, pelvic surgery, or hip or knee replacements)
  • Prolonged immobility (> 3 days)
  • Hormone replacement therapy or the combined oral contraceptive pill
  • Current active malignancy
  • Obesity
  • Known thrombophilia disorder (e.g. antiphospholipid syndrome or Factor V Leidin)
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3
Q

pathophysiology of VTE

A

THINK Virchow’s triad

  • Stasis of blood
    • immobility
  • Endothelial injury
    • direct trauma
    • atheroma
  • Hypercoagulability
    • cancer
    • pregnancy
    • inflammation
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4
Q

Prevention of VTE

A

All patients undergoing surgery should be offered mechanical prophylaxis (except those with PAD). Some patients at risk of VTE/ depending on the surgery will have medication after.

  1. Mechanical thromboprophylaxis
    • Antiembolic stockings
    • Intermittent pneumatic compression
  2. Pharmacological thromboprophylaxis (after surgery)
    • LMWH
      • Unless eGFR <30 (then consider Unfractionated heparin)
    • DOAC after hip or knee replacement
  3. Other measures:
    • postoperative mobilisation, adequate hydration, avoiding pressure on calves
    • stop oestrogen containing tablets 6 weeks before surgery (HRT, COCP)

Warfarin- impractical for many surgeons- risk of operative haemorrhage

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5
Q

DVT

A

formation of blood clot int he deep veins of limbs

Presentation

  • unilateral leg pain or swelling
  • pyrexia
  • pitting oedema
  • tenderness
  • prominent superficial veins

Investigations

  • WELLS score
    • <1 - DVT is unlikely → reuqire D-dimer to exclude
    • >1- likely and DVT should be confirmed by US
  • Measuring circumference of leg
  • D-dimer

Management

  • First line: DOAC/ or LWMH depending on guidelines
  • Direct factor Xa inhibitors
    • Apixaban
    • Rivaroxaban
    • Edoxaban
    • Direct thrombin inhibitor: dabigatran
    • Dabigatran and edoxaban – initial treatment with LMWH
    • Contraindicated in those with chronic renal impairment
  • Second line: Warfarin (if DOAC contraindicated)
    • Requires therapeutic LMWH to cover until INR levels are therapeutic
  • Cancer associated VTE: LMWH alone
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6
Q

D-dimer

A
  • is sensitive but not specific
    • may also be raised due to infection, trauma, surgery, inflammation, liver disease, pregnancy and prolonged hospital stay
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7
Q

measuring circumference of leg

A

10 cm below the tibial tuberosity and compare with the asymptomatic leg. A difference of more than 3 cm between the extremities increases the probability of DVT

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8
Q

thrombophlebitis

A

is an inflammatory process that causes a blood clot to form and block one or more veins, usually in the legs. The affected vein might be near the surface of the skin (superficial thrombophlebitis) or deep within a muscle (deep vein thrombosis, or DVT).

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9
Q

pulmonary embolism

A

Blockage of pulmonary artery by a substance that has travelled there in the bloodstream e.g. thrombosis that has broke. Off and migrated e.g. DVT

Cause

  • DVT
  • Right sided mural thrombosis (post-MI)
  • AF
  • Neoplastic cells
  • Fat cells after tibial fracture

Presentation

  • Sudden onset dyspnoea
  • Pleuritic chest pain
  • Cough
  • Haemoptysis (rate)
  • Tachycardia
  • Pyrexia
  • Raised JVP (rare)

Pleural rub or pleural effusion (rare

Investigations

  • Wells score
    • <4- PE unlikely- requires further D-dimer
    • >4 PE likely- requires CTPA
  • ECG incase of MI
    • PE can show RBBB, inverted T waves V1-4

Management

  • Haemodynamically stable
    • DOAC +- LMWH
  • Hemodynamic compromise (massive or high risk PE)
    • thrombolysis
  • Recurrent PE
    • IVC filter
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10
Q

three layers of the skin

A

epidermis

dermis

hypodermis

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11
Q

epidermis

A
  • Layers:
    • Stratum basale
    • Stratum spinosum
    • Stratum granulosum
    • Stratum lucidum
    • Stratum corneum
    • Features
      • Layers of keratinocytes undergoing terminal maturationà cornification
      • Melanocytes
      • Langerhans cells- APC dendritics
      • Merkel cells- sensory mechanoreceptors
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12
Q

dermis

A
  • Two layers
    • Superficial papillary layer
    • Deeper reticular layer
      • Thicker- thick bundles of collagen that provide durability
  • Features
    • Fibroblasts- collogen and elastin
    • Mast cells0 histamine granule containing cells
    • Blood vessels and cutaneous sensory nerves
    • Skin appendages
      • Hair follicles
      • Sebaceous glands
      • Sweat glands
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13
Q

hypodermis

A
  • Subcutaneous tissue
  • Major body store of adipose tissue
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14
Q

4 stages of wound healing

A
  • Haemostasis
  • Inflammation
  • Proliferation
  • Remodelling
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15
Q

complications of wound healing

A
  • Keloid scars
    • Excessive collagen production- extensive scaring
    • Extra connective tissue that forms extends beyond the original wound area
  • Hypertrophic scar
    • Thick raised scar that an abnormal response to wound healing
    • Extra connective tissue that forms within original wound stays within that area
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16
Q

wounds can either heal by

A

primary or secondary intention

17
Q

primary intention

A

Occurs when wound with dermal edges are close together e.g. a scalpel incision

  • Faster than secondary intention
  • End result of healing by primary intention is (in most cases) a complete return to function, with minimal scarring and loss of skin appendages.
18
Q

Secondary intention

A

Occurs when sides of the wound are not opposed, therefore healing must happen from the bottom up

19
Q

cells vital to secondary intention

A
  • Myofibroblasts are vital cells in secondary intention. They are modified smooth muscle cells that contain actin and myosin, and act to contract the wound; decreasing the space between the dermal edges. They also can deposit collagen for scar healing.
20
Q

outline healing by primary intention

A

Stages

  • Haemostasis
    • Haematoma formation (platelet and cytokines)
    • Vasoconstriction- limiting blood loss at the affected area
    • The close proximity of the wound edges allows for ease of clot formation and prevents infection by forming a scab
  • Inflammation – a cellular inflammatory response acts to remove any cell debris and pathogens present
  • Proliferation – cytokines drive proliferation of the fibroblasts and the formation of granulation tissue
    • Angiogenesis is promoted by the presence of growth mediators (e.g VEGF), allowing for further maturation of the granulation tissue; the production of collagen by fibroblasts allows for closure of the wound after around a week
  • Remodelling – collagen fibres are deposited within the wound to provide strength in the region, with the fibroblasts subsequently undergoing apoptosis
21
Q

outline healing by secondary intention

A
  • Haemostasis – a large fibrin mesh forms, which fills the wound
  • Inflammation – an inflammatory response e.g. neutrophils acts to remove any cell debris and pathogens present
    • There is a larger amount of cell debris present, and the inflammatory reaction tends to be more intense than in primary intention
  • Proliferation – granulation tissue forms at the bottom of the wound
    • This is an important step, as the epithelia can only proliferate and regenerate once granulation tissue fills the wound to the level of the original epithelium; once the granulation tissue reaches this level, the epithelia can completely cover the wound
  • Remodelling – the inflammatory response begins to resolve, and wound contraction can occur- fibromyoblasts
22
Q

local factors which affect wound healing

A

type, size, location

local blood supply

infection

contamination

23
Q

systemic factors which affect wound healing

A

increasing age

co-morbidities e.g. DM or CB

obesity

nutritional deficiencies e.g. Vit C

smoking

24
Q

contamination classification

A
  • Clean
  • Clean-contaminated
  • Contaminated
  • Dirty
25
Q

wound management

A

The basic principles for the management of a wound or laceration are:

  • Haemostasis
  • Cleaning the wound
  • Analgesia
  • Skin closure
  • Dressing and follow-up advice
26
Q

cleaning the wound

A

To reduce infection and promote healing. Five aspects:

  • Disinfect the skin around the wound with antiseptic
    • Avoid getting alcohol or detergents inside the wound
  • Decontaminate the wound by manually removing any foreign bodies
  • Debride any devitalised tissue where possible
  • Irrigate the wound with saline
    • If there is no obvious contamination present, low pressure irrigation is sufficient* (pouring normal saline from a sterile container carefully into the wound)
  • Antibiotics for high-risk wounds or signs of infection (follow local antibiotic guidelines)
    • Risk factors for wound infection include foreign body present or heavily soiled wounds, bites (including human), puncture wounds, and open fractures
27
Q

which propylaxis to infection should be fiven

A

Abx

tetanus porphylaxis if pt not upr to date

28
Q

skin closure

A

The aid wound healing, the edges of the wound can be manually opposed. There are four main methods of doing so:

  • Skin adhesive strips (e.g. Steri-StripsTM) are suitable if no risk factors for infection are present
  • Tissue adhesive glue (e.g. Indermil®) can be used for small lacerations with easily opposable edges (a popular choice in paediatrics)
  • Sutures are typically used for any laceration greater than 5cm, deep dermal wounds, or in locations that are prone to flexion, tension, or wetting
  • Staples can be used for some scalp wounds