A 56 year old lady with idiopathic thrombocytopenic purpura has a platelet count of
50. She is due to undergo a splenectomy. What is the optimal timing of a platelet
transfusion in this case?
A. 24 hours pre-operatively
B. 2 hours pre-operatively
C. Whilst making the skin incision
D. After ligation of the splenic artery
E. On removal of the spleen
ITP causes splenic sequestration of platelets. Therefore a platelet transfusion should
be carefully timed. Too soon and it will be ineffective. Too late and unnecessary
bleeding will occur. The optimal time is after the splenic artery has been ligated.
Splenectomy
Indications
Trauma: 1/4 are iatrogenic
Spontaneous rupture: EBV
Hypersplenism: hereditary spherocytosis or elliptocytosis etc
Malignancy: lymphoma or leukaemia
Splenic cysts, hydatid cysts, splenic abscesses
Post splenectomy changes
Platelets will rise first (therefore in ITP should be given after splenic artery
clamped)
Blood film will change over following weeks, Howell Jolly bodies will appear
Other blood film changes include target cells and Pappenheimer bodies
Increased risk of post splenectomy sepsis, therefore prophylactic antibiotics
and pneumococcal vaccine should be given.
Post splenectomy sepsis
Typically occurs with encapsulated organisms
Opsonisation occurs but then not recognised
A 19 year old man has a skin lesion excised from his back. He is reviewed clinically
at 4 months post procedure and the surgeon notes that the scar has begun to contract.
Which of the following facilitates this process?
, A. Myofibroblasts
B. Neutrophils
C. Granuloma formation
D. Macrophages
E. Fibroblasts
As wounds mature the fibroblast population differentiates into myofibroblasts, these
have a contractile phenotype and therefore help in contracting the wound. Immature
fibroblasts, though able to adhere to the ECM, do not have this ability.
Wound healing
Surgical wounds are either incisional or excisional and either clean, clean
contaminated or dirty. Although the stages of wound healing are broadly similar their
contributions will vary according to the wound type.
The main stages of wound healing include:
Haemostasis
Vasospasm in adjacent vessels, platelet plug formation and generation of
fibrin rich clot.
Inflammation
Neutrophils migrate into wound (function impaired in diabetes).
Growth factors released, including basic fibroblast growth factor and vascular
endothelial growth factor.
Fibroblasts replicate within the adjacent matrix and migrate into wound.
Macrophages and fibroblasts couple matrix regeneration and clot substitution.
Regeneration
Platelet derived growth factor and transformation growth factors stimulate
fibroblasts and epithelial cells.
Fibroblasts produce a collagen network.
Angiogenesis occurs and wound resembles granulation tissue.
Remodeling
Longest phase of the healing process and may last up to one year (or longer).
, During this phase fibroblasts become differentiated (myofibroblasts) and these
facilitate wound contraction.
Collagen fibres are remodeled.
Microvessels regress leaving a pale scar.
The above description represents an idealised scenario. A number of diseases may
distort this process. It is obvious that one of the key events is the establishing well
vascularised tissue. At a local level angiogenesis occurs, but if arterial inflow and
venous return are compromised then healing may be impaired, or simply nor occur at
all. The results of vascular compromise are all too evidence in those with peripheral
vascular disease or those poorly constructed bowel anastomoses.
Conditions such as jaundice will impair fibroblast synthetic function and overall
immunity with a detrimental effect in most parts of healing.
Problems with scars:
Hypertrophic scars
Excessive amounts of collagen within a scar. Nodules may be present histologically
containing randomly arranged fibrils within and parallel fibres on the surface. The
tissue itself is confined to the extent of the wound itself and is usually the result of a
full thickness dermal injury. They may go on to develop contractures.
Image of hypertrophic scarring. Note that it remains confined to the boundaries of the
original wound:
Image sourced from Wikipedia
Keloid scars
Excessive amounts of collagen within a scar. Typically a keloid scar will pass beyond
the boundaries of the original injury. They do not contain nodules and may occur
following even trivial injury. They do not regress over time and may recur following
removal.
, Image of a keloid scar. Note the extension beyond the boundaries of the original
incision:
Image sourced from Wikipedia
Drugs which impair wound healing:
Non steroidal anti inflammatory drugs
Steroids
Immunosupressive agents
Anti neoplastic drugs
Closure
Delayed primary closure is the anatomically precise closure that is delayed for a few
days but before granulation tissue becomes macroscopically evident.
Secondary closure refers to either spontaneous closure or to surgical closure after
granulation tissue has formed.
hich of the following blood products can be administered to a non ABO matched
recipient?
A. Whole blood
B. Platelets
C. Packed red cells
D. Fresh frozen plasma
E. Cryoprecipitate
50. She is due to undergo a splenectomy. What is the optimal timing of a platelet
transfusion in this case?
A. 24 hours pre-operatively
B. 2 hours pre-operatively
C. Whilst making the skin incision
D. After ligation of the splenic artery
E. On removal of the spleen
ITP causes splenic sequestration of platelets. Therefore a platelet transfusion should
be carefully timed. Too soon and it will be ineffective. Too late and unnecessary
bleeding will occur. The optimal time is after the splenic artery has been ligated.
Splenectomy
Indications
Trauma: 1/4 are iatrogenic
Spontaneous rupture: EBV
Hypersplenism: hereditary spherocytosis or elliptocytosis etc
Malignancy: lymphoma or leukaemia
Splenic cysts, hydatid cysts, splenic abscesses
Post splenectomy changes
Platelets will rise first (therefore in ITP should be given after splenic artery
clamped)
Blood film will change over following weeks, Howell Jolly bodies will appear
Other blood film changes include target cells and Pappenheimer bodies
Increased risk of post splenectomy sepsis, therefore prophylactic antibiotics
and pneumococcal vaccine should be given.
Post splenectomy sepsis
Typically occurs with encapsulated organisms
Opsonisation occurs but then not recognised
A 19 year old man has a skin lesion excised from his back. He is reviewed clinically
at 4 months post procedure and the surgeon notes that the scar has begun to contract.
Which of the following facilitates this process?
, A. Myofibroblasts
B. Neutrophils
C. Granuloma formation
D. Macrophages
E. Fibroblasts
As wounds mature the fibroblast population differentiates into myofibroblasts, these
have a contractile phenotype and therefore help in contracting the wound. Immature
fibroblasts, though able to adhere to the ECM, do not have this ability.
Wound healing
Surgical wounds are either incisional or excisional and either clean, clean
contaminated or dirty. Although the stages of wound healing are broadly similar their
contributions will vary according to the wound type.
The main stages of wound healing include:
Haemostasis
Vasospasm in adjacent vessels, platelet plug formation and generation of
fibrin rich clot.
Inflammation
Neutrophils migrate into wound (function impaired in diabetes).
Growth factors released, including basic fibroblast growth factor and vascular
endothelial growth factor.
Fibroblasts replicate within the adjacent matrix and migrate into wound.
Macrophages and fibroblasts couple matrix regeneration and clot substitution.
Regeneration
Platelet derived growth factor and transformation growth factors stimulate
fibroblasts and epithelial cells.
Fibroblasts produce a collagen network.
Angiogenesis occurs and wound resembles granulation tissue.
Remodeling
Longest phase of the healing process and may last up to one year (or longer).
, During this phase fibroblasts become differentiated (myofibroblasts) and these
facilitate wound contraction.
Collagen fibres are remodeled.
Microvessels regress leaving a pale scar.
The above description represents an idealised scenario. A number of diseases may
distort this process. It is obvious that one of the key events is the establishing well
vascularised tissue. At a local level angiogenesis occurs, but if arterial inflow and
venous return are compromised then healing may be impaired, or simply nor occur at
all. The results of vascular compromise are all too evidence in those with peripheral
vascular disease or those poorly constructed bowel anastomoses.
Conditions such as jaundice will impair fibroblast synthetic function and overall
immunity with a detrimental effect in most parts of healing.
Problems with scars:
Hypertrophic scars
Excessive amounts of collagen within a scar. Nodules may be present histologically
containing randomly arranged fibrils within and parallel fibres on the surface. The
tissue itself is confined to the extent of the wound itself and is usually the result of a
full thickness dermal injury. They may go on to develop contractures.
Image of hypertrophic scarring. Note that it remains confined to the boundaries of the
original wound:
Image sourced from Wikipedia
Keloid scars
Excessive amounts of collagen within a scar. Typically a keloid scar will pass beyond
the boundaries of the original injury. They do not contain nodules and may occur
following even trivial injury. They do not regress over time and may recur following
removal.
, Image of a keloid scar. Note the extension beyond the boundaries of the original
incision:
Image sourced from Wikipedia
Drugs which impair wound healing:
Non steroidal anti inflammatory drugs
Steroids
Immunosupressive agents
Anti neoplastic drugs
Closure
Delayed primary closure is the anatomically precise closure that is delayed for a few
days but before granulation tissue becomes macroscopically evident.
Secondary closure refers to either spontaneous closure or to surgical closure after
granulation tissue has formed.
hich of the following blood products can be administered to a non ABO matched
recipient?
A. Whole blood
B. Platelets
C. Packed red cells
D. Fresh frozen plasma
E. Cryoprecipitate
