Care of surgical patients III Flashcards
VTE
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
RF for VTE
- 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)
pathophysiology of VTE
THINK Virchow’s triad
-
Stasis of blood
- immobility
-
Endothelial injury
- direct trauma
- atheroma
-
Hypercoagulability
- cancer
- pregnancy
- inflammation
Prevention of VTE
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.
-
Mechanical thromboprophylaxis
- Antiembolic stockings
- Intermittent pneumatic compression
-
Pharmacological thromboprophylaxis (after surgery)
- LMWH
- Unless eGFR <30 (then consider Unfractionated heparin)
- DOAC after hip or knee replacement
- LMWH
-
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
DVT
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
D-dimer
-
is sensitive but not specific
- may also be raised due to infection, trauma, surgery, inflammation, liver disease, pregnancy and prolonged hospital stay
measuring circumference of leg
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
thrombophlebitis
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).
pulmonary embolism
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
three layers of the skin
epidermis
dermis
hypodermis
epidermis
- 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
dermis
- 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
hypodermis
- Subcutaneous tissue
- Major body store of adipose tissue
4 stages of wound healing
- Haemostasis
- Inflammation
- Proliferation
- Remodelling
complications of wound healing
- 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
wounds can either heal by
primary or secondary intention
primary intention
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.
Secondary intention
Occurs when sides of the wound are not opposed, therefore healing must happen from the bottom up
cells vital to secondary intention
- 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.
outline healing by primary intention
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
outline healing by secondary intention
- 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
local factors which affect wound healing
type, size, location
local blood supply
infection
contamination
systemic factors which affect wound healing
increasing age
co-morbidities e.g. DM or CB
obesity
nutritional deficiencies e.g. Vit C
smoking
contamination classification
- Clean
- Clean-contaminated
- Contaminated
- Dirty
wound management
The basic principles for the management of a wound or laceration are:
- Haemostasis
- Cleaning the wound
- Analgesia
- Skin closure
- Dressing and follow-up advice
cleaning the wound
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
which propylaxis to infection should be fiven
Abx
tetanus porphylaxis if pt not upr to date
skin closure
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
