1.02 - Core Surgical Concepts Flashcards
Name the 4 main types of injury that can occur during surgery.
- Bisection from sharp dissection
- Blunt injury from instrumentation or retraction
- Diathermy injury from the instrument directly or burns from the pads
- Entrapment pressure or incarceration due to suturing or closure of structures
What structures are most frequently damaged during surgical procedures?
- Vascular structures: arteries and veins
- Neurological structures: nerves and nerve plexuses
- Musculoskeletal structures: tendons, ligaments and muscles
- Abdominal viscera: small bowel, large bowel, bladder, ureter, spleen and liver.
NB: patients should be consented before any operation about the risks of damage to local structures.
Injury to local structures in surgery can be reduced by:
- excellent anatomical knowledge
- suitable planning of the surgical approach
- careful and meticulous dissection
- retracting vulnerable structures carefully
Post-operatively, the patient should be examined for signs of damage to the local structures.
Define inflammation.
The initial physiological response to tissue damage, such as that caused by mechanical, thermal, electrical, irradiation, chemical or infection.
Give the 4 characteristic features of acute inflammation.
Acute inflammation begins within seconds to minutes following injury to tissues. It is characterised by four key features:
- Rubor (redness) secondary to vasodilation and increased blood flow.
- Calor (heat) due to a localised increase in temperature, and increased blood flow.
- Tumour (swelling) resulting from increased vascular permeability, allowing fluid loss into the interstitial space.
- Dolor (pain) caused by stimulation of local nerve endings, from mechanical and chemical mediators.
What are the two stages of acute inflammation?
- vascular phase
- cellular phase
Outline the changes that occur during the vascular phase of acute inflammation.
a) small blood vessels adjacent to the injury vasodilate and blood flow to the area increases.
b) endothelial cells initially swell, then contract to increase the space between them, thus increasing the permeability of the vascular barrier.
c) exudation of fluids leads to a net loss of fluid from the vascular space into the interstitial space, resulting in oedema.
d) increased production of tissue fluid acts as a medium for which inflammatory proteins can migrate through; it may also help to remove pathogens and cell debris via lymphatic drainage.
Outline the changes that occur during the cellular phase of acute inflammation.
Neutrophils are attracted to the site of injury by the presence of chemotaxins - for example IL-8 and histamine - that are released into the blood immediately after the insult.
a) margination - neutrophils line up against the endothelium
b) rolling - neutrophils are in close contact with and roll along the endothelium
c) adhesion - neutrophils connect to the endothelial wall
d) emigration - neutrophils move through the vessel wall to the affected area
Once in the region, neutrophils recognise the foreign body and begin phagocytosis.
What is the predominant cell of acute inflammation?
The neutrophil
Following the process of acute inflammation, what are the possible outcomes?
a) complete resolution - total repair and destruction of the insult
b) fibrosis and scar formation - occurs in stages of significant inflammation
c) chronic inflammation - from persisting insult
d) formation of an abscess - result of pyogenic infection
What is an abscess?
A localised collection of pus surrounded by granulation tissue, forming when the primary insult is a pyogenic bacterium and extensive tissue necrosis occurs.
Outline how an abscess forms.
The initial inflammatory exudate forces the tissue apart, leaving a centre of necrotic tissue with the neutrophils and pathogens. The abscess acts as a harbour for the infection, and can result in pain and destruction of local structures as it expands.
Over time, the acute inflammation will cease and - if not surgically drained - the abscess will be replaced by scar tissue.
Name 3 mediators responsible for vasodilatation in acute inflammation.
- histamine
- bradykinin
- prostaglandins (PGE2)
Name the mediator responsible for mast cell degranulation in acute inflammation.
Complement proteins (C3a, C5a)
Name 3 mediators responsible for chemotaxis in acute inflammation.
- IL-8
- complement proteins (C5a)
- histamine
Name 3 mediators responsible for lysosomal granule release in acute inflammation.
- complement proteins (C5a)
- IL-8
- PAF
Name the mediator responsible for phagocytosis in acute inflammation.
Complement proteins (C3b)
Name 3 mediators responsible for pain in acute inflammation.
- prostaglandins (PGE2)
- bradykinin
- histamine
Name 3 mediators responsible for fever in acute inflammation.
- IL-1, IL-6
- TNF-a
- prostaglandins (PGE2)
What is the aetiology of chronic inflammation?
Chronic inflammation is the ongoing inflammatory response from an unresolved insult, resulting as a continuation of acute inflammation or arising de-novo.
What is the predominant cell of chronic inflammation?
Macrophages - acting to engulf and destroy foreign material and/or pathogens.
Lymphocytes - act to coordinate the response between the innate and adaptive immune cells.
What is the function of macrophages in chronic inflammation?
- phagocytosis of foreign material and/or pathogens
- antigen presentation (APC) to the adaptive immune cells
- fusion to form giant cells
- secrete growth factors to aid cell repeair
- secrete complement proteins and cytokines to help coordinate the immune response
Which type of giant cell would be present in response to a foreign body?
Foreign-body giant cell
Which type of giant cell would be present in response to mycobacterium tuberculosis?
Langhans giant cell
Which type of giant cell would be present in response to fat necrosis?
Touton giant cell
Outline the role of T lymphocytes in chronic inflammation.
T-helper lymphocytes (CD4+) act to coordinate further targeted inflammatory response, from both innate and adaptive immune cells.
T-killer lymphocytes (CD8+) act to coordinate the targeted destruction of infected cells.
What is a granuloma?
In chronic inflammation, macrophages and lymphocytes can combine to form a granuloma, allowing the immune system to ‘wall off’ an agent particularly resistant to destruction.
A granuloma contains a collection of epithelioid cells (elongated macrophages), surrounding a core of lymphocytes and giant cells attempting to break down the particles.
NB as granulomatous inflammation progresses, fibroblasts lay down scar tissue.
Describe the four stages of wound healing by primary intention.
- Haemostasis - activation of platelets and cytokines forms a haematoma and causes vasoconstriction, to limit blood loss at the affected area.
- Inflammation - a cellular inflammatory response acts to remove any cell debris and pathogens.
- Proliferation - inflammatory cells release cytokines that drive the proliferation of fibroblasts and the formation of granulation tissue. Growth mediations (e.g. VEGF) promote angiogenesis, and 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.
The end result of healing by primary intention is a complete return to function, with minimal scarring and loss of skin appendages.
Describe the four stages of wound healing by secondary intention.
- Haemostasis - activation of platelets and cytokines forms a large fibrin mesh, which fills the wound to limit blood loss.
- Inflammation - a cellular inflammatory response acts to remove any cell debris and pathogens (response stronger than in primary intention)
- Proliferation - granulation tissue forms at the bottom of the wound and fills it 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 myofibroblasts facilitate contraction of the wound.
Outline the physiology in the formation of keloid scars.
Keloid scars form when there is excessive collagen production by fibroblasts, typically affecting people with darker skin.
What is wound dehiscence?
Where a wound fails to heal, often re-opening a few days after surgery - most common in abdominal surgery.
Define
a) superficial wound dehiscence
b) full thickness wound dehiscence
a) the skin wound alone fails, with the rectus sheath remaining intact (occurs secondary to SSI, poorly controlled diabetes mellitus, or poor nutritional status).
b) the rectus sheath fails to heal and bursts, with protrusion of abdominal contents (occurs secondary to raised intra-abdominal pressure, poor surgical technique and if the patient is critically unwell).
