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1

What affects the accumulation of fluid in the interstitium? How does this fluid differ from plasma? What happens to excess fluid? How does oedema develop?

The formation of fluid in the interstitium is governed primarily by Starlings Forces (not the same as Starlings Law!). These consist of forces from the within the capillary; the capillary pressure itself and the plasma colloid oncotic pressure. This is counterbalanced by forces within the interstitium which comprise the interstitial fluid pressure and the interstitial fluid osmotic pressure. There is normally a balance between these forces so that most of the fluid that passes out of the capillary is subsequently re-absorbed. It has a similar electrolyte profile to plasma. However, protein is not usually present as their high molecular weight precludes their filtration. Excess fluid is usually returned to the vascular system via the lymphatic route. Oedema is characterised by an excessive quantity of fluid in the extracellular space. Factors which favour its development include: Increased hydrostatic pressure Hypoproteinaemia (lower plasma oncotic pressure) Venous/ lymphatic obstruction Endothelial changes in the capillary bed (for example in acute inflammation) Starlings forces: About one sixth of the body consists of spaces between cells. The fluid within these spaces is termed interstitial fluid. This fluid is formed by filtration and diffusion from capillaries. It contains almost the same constituents as plasma with the exception of proteins as these are not filtered due to their high relative molecular mass. The pressure in the capillaries tends to force fluid and its dissolved substances through capillary pores and into this space. In contrast the osmotic pressure exerted by plasma proteins (colloid osmostic pressure) tends to favor movement from the interstitial spaces back into the vascular compartments (capillaries) themselves. The lymphatic system returns back to the circulation the small amounts of protein that do leak into the interstitium. There are four primary forces that determine fluid movement through a capillary membrane (Starlings forces): Capillary pressure - forces fluid out of the capillary Interstitial fluid pressure- which tends to force fluid inwards through the capillary membrane (when it is positive) Plasma colloid osmotic pressure- favors influx into the capillary Interstitial fluid osmotic pressure- favors efflux from the capillary into the interstitum

2

How is the respiratory rhythm generated? What is the Hering-Breur reflex? What is the most important factor in controlling respiration? In what situations is this altered?

There are 2 groups of medullary neurones, the dorsal and ventral respiratory groups, that discharge action potentials with an intrinsic rhythm that corresponds to the respiratory cycle. These upper motor neurones have efferents to the diaphragm by way of the contralateral phrenic nerve. 

These neurones receive inputs from higher centres in the CNS including the cerebral cortex and the pons. They also receive inputs from the aortic and carotid bodies. They also have a vagal input which is the sensory afferent from the lung itself. Inspiration is initiated from the dorsal respiratory group.

 

Hering-Breur reflex: When the lung is inflated, receptors send impulses to the dorsal respiratory neurones via the vagus. With high tidal volumes this serves to regulate inspiration. In humans, it is not generally activated until volumes exceed 800ml. It is therefore generally only active during exercise.

 

The most important factor controlling respiration is the partial pressure of carbon dioxide in the plasma. Within the CNS, carbon dioxide results in generation of hydrogen ions that stimulate central chemoreceptors. In the periphery, the receptors are located in the aortic and carotid bodies.

 

Patients with chronic lung disease may become less sensitive to changes in carbon dioxide levels and their respiratory drive is hypoxia driven. In this small group of people, administration of excessive oxygen may dampen the respiratory stimulus.

 

Control of ventilation: 

  • Coordinated by the respiratory centres, chemoreceptors, lung receptors and muscles.
  • Automatic, involuntary control of respiration occurs from the medulla. 
  • The respiratory centres control the respiratory rate and the depth of respiration. 


Respiratory centres

  • Medullary respiratory centre: Inspiratory and expiratory neurones. Has ventral group which controls forced voluntary expiration and the dorsal group controls inspiration. Depressed by opiates.
  • Apneustic centre: Lower pons. Stimulates inspiration - activates and prolongs inhalation. Overridden by pneumotaxic control to end inspiration.
  • Pneumotaxic centre: Upper pons, inhibits inspiration at a certain point. Fine tunes the respiratory rate.


Ventillatory variables

  • Levels of pCO2 most important in ventilation control
  • Levels of O2 are less important.
  • Peripheral chemoreceptors: located in the bifurcation of carotid arteries and arch of the aorta. They respond to changes in reduced pO2, increased H+ and increased pCO2 in ARTERIAL BLOOD.
  • Central chemoreceptors: located in the medulla. Respond to increased H+ in BRAIN INTERSTITIAL FLUID to increase ventilation. NB the central receptors are NOT influenced by O2 levels.


Lung receptors include:

  • Stretch receptors: respond to lung stretching causing a reduced respiratory rate
  • Irritant receptors: respond to smoke etc causing bronchospasm
  • J (juxtacapillary) receptors

3

What is meant by the term inotrope? How do they work? What is the difference between inotropes and vasoconstrictors? What haemodyanamic parameters need to be monitored to allow the use of inotropes? How are inotropes administered and why? What is the main functional difference between adrenaline and nor adrenaline when used therapeutically?

Inotropes are agents which affect the contractility of the myocardium. Both positive and negative inotropes are recognised. However, the former group are more clinically useful.

Many inotropes work by increasing intracellular calcium levels and thus contractility. Many, such as adrenaline, act via beta receptors and increase cellular cAMP levels with subsequent mobilisation of calcium. Some, such as dopexamine, act indirectly by increasing the level of endogenous noradrenaline by inhibition of its neuronal re-uptake.

Inotropes principally act centrally and predominantly on the myocardium. The commonly used catecholamine type agents achieve this through agonism of the beta 1 receptor. Vasoconstrictors such as nor adrenaline exert most of their effects peripherally via alpha receptor agonism. Intropes are predominantly used where there is depression of myocardial function, they increase cardiac output and often blood pressure and this in turn can improve myocardial perfusion. This dual action is important since chronotropic effects alone may worsen rather than improve myocardial ischaemia. Vasoconstrictors are mainly used where there is a peripheral problem such as leaky capillary beds and vasodilation such as may occur in sepsis. In clinical practice it is sometimes necessary to use a combination of drugs.

 

Generally, mean arterial pressure and the central venous pressure need to be known and monitored.

Inotropes are administered centrally this ensures that they enter a high flow system directly and allows for the most reliable dosing.

Adrenaline mainly works as a beta 1 receptor agonist and therefore most of its effects are cardiac. Noradrenaline is a predominantly an alpha receptor agonist and works peripherally.

 

Inotropes are a class of drugs which work primarily by increasing cardiac output. They should be distinguished from vasoconstrictor drugs which are used specifically when the primary problem is peripheral vasodilatation. 

Catecholamine type agents are commonly used and work by increasing cAMP levels by adenylate cyclase stimulation. This in turn intracellular calcium ion mobilisation and thus the force of contraction. Adrenaline works as a beta adrenergic receptor agonist at lower doses and an alpha receptor agonist at higher doses. Dopamine causes dopamine receptor mediated renal and mesenteric vascular dilatation and beta 1 receptor agonism at higher doses. This results in increased cardiac output. Since both heart rate and blood pressure are raised, there is less overall myocardial ischaemia. Dobutamine is a predominantly beta 1 receptor agonist with weak beta 2 and alpha receptor agonist properties. Noradrenaline is a catecholamine type agent and predominantly acts as an alpha receptor agonist and serves as a peripheral vasoconstrictor.

Phosphodiesterase inhibitors such as milrinone act specifically on the cardiac phosphodiesterase and increase cardiac output. 

  • Adrenaline: α-1, α-2, β-1, β-2
  • Noradrenaline: α-1,( α-2), (β-1), (β-2)
  • Dobutamine: β-1, (β 2)
  • Dopamine: (α-1), (α-2), (β-1), D-1,D-2

Minor receptor effects in brackets

Effects of receptor binding

α-1, α-2: vasoconstriction

β-1: increased cardiac contractility and HR

β-2: vasodilatation

D-1: renal and spleen vasodilatation

D-2: inhibits release of noradrenaline

4

What is meant by the term transplant? What type of transplant is a renal transplant from an unrelated donor? How do xenografts and autografts differ from an allograft? Can you name any examples of xenografts and autografts?

The transposition of tissue from one anatomical region to another.

It is an allograft. This refers to the transplant of an organ or tissue from one individual to another unrelated individual of the same species. If the donor was an identical twin then this would be termed an isograft. Xenografts are transplants from one species to another. Autografts are transplants from one site to another on the same individual.

A porcine heart valve is an example of a xenograft. The use of long saphenous vein as a conduit in coronary artery bypass grafting could be termed an autograft.

 

Transplantation of solid organs: A number of different organ and tissue transplants are now available. In many cases an allograft is performed, where an organ is transplanted from one individual to another. Allografts will elicit an immune response and this is one of the main reasons for organ rejection. 

Graft rejection occurs because allografts have allelic differences at genes that code immunohistocompatability complex genes. The main antigens that give rise to rejection are:

ABO blood group

Human leucocyte antigens (HLA)

Minor histocompatability antigens

ABO Matching
ABO incompatibility will result in early organ rejection (hyperacute) because of pre existing antibodies to other groups. Group O donors can give organs to any type of ABO recipient whereas group AB donor can only donate to AB recipient.

HLA System: The four most important HLA alleles are:  

HLA A

HLA B

HLA C

HLA DR

An ideal organ match would be one in which all 8 alleles are matched (remember 2 from each parent, four each = 8 alleles). Modern immunosuppressive regimes help to manage the potential rejection due to HLA mismatching. However, the greater the number of mismatches the worse the long term outcome will be. T lymphocytes will recognise antigens bound to HLA molecules and will then become activated. Clonal expansion then occurs with a response directed against that antigen.
The extent to which an organ needs to be accurately cross matched depends on the organ type. For example, the liver is less immunogenic than the kidney and thus HLA matching is not commonly undertaken.

Allograft: Transplant of tissue from genetically non identical donor from the same species - Solid organ transplant from non related donor

Isograft: Graft of tissue between two individuals who are genetically identical - Solid organ transplant in identical twins

Autograft: Transplantation of organs or tissues from one part of the body to another in the same individual - Skin graft

Xenograft: Tissue transplanted from another species - Porcine heart valve

5

What is meant by the term HLA and how is it relevant in renal transplantation?

The term HLA stands for human leucocyte antigen. It is encoded by a loci of genes the proteins of which are exposed on the cell surface and form the basis of the immune system. The proteins encoded by HLAs are those on the outer part of body cells that are (in effect) unique to that person. There are three major HLA (MHC class I) genes these are A, B and C. The three major MHC class II genes are HLA DP, DQ and DR. The immune system uses the HLAs to differentiate self cells and non-self cells. Any cell displaying that person's HLA type belongs to that person and, therefore, is not an invader. Cells displaying non self HLA antigens are identified as foreign and thus become targets for the immune system. This is of major importance in renal transplantation as the rejection of the graft is directly linked to the number of HLA mismatches between donor and recipient.

Transplantation of solid organs: A number of different organ and tissue transplants are now available. In many cases an allograft is performed, where an organ is transplanted from one individual to another. Allografts will elicit an immune response and this is one of the main reasons for organ rejection. 

Graft rejection occurs because allografts have allelic differences at genes that code immunohistocompatability complex genes. The main antigens that give rise to rejection are:

  • ABO blood group
  • Human leucocyte antigens (HLA)
  • Minor histocompatability antigens

ABO Matching
ABO incompatibility will result in early organ rejection (hyperacute) because of pre existing antibodies to other groups. Group O donors can give organs to any type of ABO recipient whereas group AB donor can only donate to AB recipient.

HLA System: The four most important HLA alleles are:  

  • HLA A
  • HLA B
  • HLA C
  • HLA DR

An ideal organ match would be one in which all 8 alleles are matched (remember 2 from each parent, four each = 8 alleles). Modern immunosuppressive regimes help to manage the potential rejection due to HLA mismatching. However, the greater the number of mismatches the worse the long term outcome will be. T lymphocytes will recognise antigens bound to HLA molecules and will then become activated. Clonal expansion then occurs with a response directed against that antigen.
The extent to which an organ needs to be accurately cross matched depends on the organ type. For example, the liver is less immunogenic than the kidney and thus HLA matching is not commonly undertaken.

  • Allograft: Transplant of tissue from genetically non identical donor from the same species - Solid organ transplant from non related donor
  • Isograft: Graft of tissue between two individuals who are genetically identical - Solid organ transplant in identical twins
  • Autograft: Transplantation of organs or tissues from one part of the body to another in the same individual - Skin graft
  • Xenograft: Tissue transplanted from another species - Porcine heart valve

6

Describe the key features demonstrated in the x-ray. Outline the processes by which a fracture usually heals. What features determine the rate of fracture union?

This image demonstrates a displaced, comminuted fracture of the humerus with callus formation.

Fracture healing typically follows four key stages. In the first stage, there is the formation of haematoma at the fracture site. Microvessels proliferate and enter the haematoma and granulation tissue forms. In the second stage, new woven bone is formed from the periosteum and forms a collar around the end of each bony fragment. Eventually, bridging callus is formed. As this processes proceeds, the fracture site becomes progressively more stable. In the third stage, the fracture site is reasonably inflexible and the cortical bone unites. In the final stage, the fracture site remodels along the lines of stress and Haversian systems are laid down.

Factors affecting Union:

  • Site of fracture, cancellous bone unites faster than cortical bone
  • The presence of contamination 
  • Degree of soft tissue loss or destruction
  • Poor blood supply
  • Loss of periosteum
  • Degree of displacement
  • Degree of comminution
  • Persistent mobility of the fracture site due to inadequate immobilisation
  • Co-morbidities, including age

The healing of uncomplicated fractures typically follows the processes outlined in the table below. The timing of these events, even in uncomplicated cases, is affected by the type of bone, degree of displacement and co-morbidities. Fractures involving cancellous bone typically unite rapidly and by six weeks, union is often sufficiently advanced to resist normal stresses. In contrast, fractures involving cortical bone, such as the tibia, are slower to unite and it is not uncommon for tibial fractures to take up to 16 weeks to unite, some femoral fractures may take up to 6 months.

  • Stage I: Formation of fracture site haematoma. Angiogenesis. Formation of granulation type tissue. Deposition of mineral salts
  • Stage II: Formation of sub periosteal bone. Bone formation in medullary cavity of the fracture. Eventual formation of bridging callus
  • Stage III: Endosteal bone formation
  • Ingrowth of callus from medually cavity into fibrous tissue at fracture site
  • Stage IV: Occurs following union of cortical bone at fracture site. Remodelling occurs. Haversian systems are laid down along lines of stress. Osteoclasts remove bridging callus


Complications:

  • Stage I: Poor blood supply or excessive mobility favors cartilage formation instead of callus
  • Stage II: Displaced fractures inhibit bridging callus formation
  • Stage III: These stages are slow even in the normal setting, if internal fixation is used, bridging callus is less likely to form and this can delay the onset of mechanical stability
  • Stage IV: Remodelling is less effective at correcting rotational deformity and the overall process is less effective in the elderly and when factors are present that inhibit healing

 

7

What is the commonest malignant bone tumour?

The commonest malignant bone tumour is metastatic cancer from another primary site.
A common pitfall is to answer this question stating that osteosarcoma is the commonest malignant bone tumour
Clearly if the question is : "What is the commonest primary malignant bone tumour?". Then the answer is osteosarcoma. Ensure you listen carefully to the examiner.

 


Giant cell tumour of bone
These lesions sit between benign and malignant. Most are benign. They are relatively rare. They consist of multinucleated giant cells (osteoclast like). Malignancy in these lesions is rare and is of the order of 2%. They account for 20% of benign bone tumours. The lesions may present as an enlarging mass, with pain or pathological fracture. On imaging, these lesions have an epiphyseal location and have a characteristic "soap bubble" appearance. They do not normally demonstrate sclerosis and have a sharply defined border. Histologically, they demonstrate multinucleated giant cells. Treatment is challenging since these lesions are locally aggressive and have a high rate of local recurrence following excision.

Malignant bone tumours
The commonest malignant bone tumour is bone metastasis from another solid organ malignancy. Metastatic lesions to bone are significantly more common than primary bone tumours which are extremely rare.

Osteosarcoma
This is the most common form of primary bone tumour. It typically affects males in their second decade. They typically present as a painful expanding mass affecting a long bone such as the femur, in close proximity to a joint. Imaging demonstrates a lesion with mixed sclerotic and lucent zones in the metaphysis bone formation within the tumour is often visible. All patients will be fully staged at presentation with CT, MRI and often PET scanning. There is a high rate of metastasis to the lungs and most patients will receive chemotherapy. Surgical excision is the main treatment.

Ewings sarcoma
Ewings sarcomas typically affect long bones and typically occurs during the first two decades of life. They are complex tumours and have overlap with primitive neuroectodermal tumours. They have a predilection for the lower extremity. They typically present as a painful swelling affecting a long bone. Inflammatory markers such as the ESR are sometimes raised and this is associated with a poorer prognosis. On plain films, the tumour shows evidence of bone destruction with a periosteal reaction (onion skin) appearance. As the condition progresses the periosteal findings can change as the tumour invades the periosteum. Treatment is with excisional surgery and chemotherapy. 

Secondary malignant tumours of bone
Metastatic bone tumours may be described as blastic, lytic or mixed. Osteoblastic metastatic disease has the lowest risk of spontaneous fracture when compared to osteolytic lesions of a similar size. 
Lesions affecting the peritrochanteric region are most prone to spontaneous fracture (because of loading forces at that site). 
The factors are incorporated into the Mirel Scoring system to stratify the risk of spontaneous fracture for bone metastasis of varying types.

8

Which tumours classically metastasise to bone?

Breast 
Lung
Thyroid
Renal 
Prostate

 


Giant cell tumour of bone
These lesions sit between benign and malignant. Most are benign. They are relatively rare. They consist of multinucleated giant cells (osteoclast like). Malignancy in these lesions is rare and is of the order of 2%. They account for 20% of benign bone tumours. The lesions may present as an enlarging mass, with pain or pathological fracture. On imaging, these lesions have an epiphyseal location and have a characteristic "soap bubble" appearance. They do not normally demonstrate sclerosis and have a sharply defined border. Histologically, they demonstrate multinucleated giant cells. Treatment is challenging since these lesions are locally aggressive and have a high rate of local recurrence following excision.

Malignant bone tumours
The commonest malignant bone tumour is bone metastasis from another solid organ malignancy. Metastatic lesions to bone are significantly more common than primary bone tumours which are extremely rare.

Osteosarcoma
This is the most common form of primary bone tumour. It typically affects males in their second decade. They typically present as a painful expanding mass affecting a long bone such as the femur, in close proximity to a joint. Imaging demonstrates a lesion with mixed sclerotic and lucent zones in the metaphysis bone formation within the tumour is often visible. All patients will be fully staged at presentation with CT, MRI and often PET scanning. There is a high rate of metastasis to the lungs and most patients will receive chemotherapy. Surgical excision is the main treatment.

Ewings sarcoma
Ewings sarcomas typically affect long bones and typically occurs during the first two decades of life. They are complex tumours and have overlap with primitive neuroectodermal tumours. They have a predilection for the lower extremity. They typically present as a painful swelling affecting a long bone. Inflammatory markers such as the ESR are sometimes raised and this is associated with a poorer prognosis. On plain films, the tumour shows evidence of bone destruction with a periosteal reaction (onion skin) appearance. As the condition progresses the periosteal findings can change as the tumour invades the periosteum. Treatment is with excisional surgery and chemotherapy. 

Secondary malignant tumours of bone
Metastatic bone tumours may be described as blastic, lytic or mixed. Osteoblastic metastatic disease has the lowest risk of spontaneous fracture when compared to osteolytic lesions of a similar size. 
Lesions affecting the peritrochanteric region are most prone to spontaneous fracture (because of loading forces at that site). 
The factors are incorporated into the Mirel Scoring system to stratify the risk of spontaneous fracture for bone metastasis of varying types.

9

Radiologically, how to the bony metastatic lesions of breast and prostate cancer differ? What is the functional relevance of this?

Most breast cancer metastasis are radiolucent, those of prostate cancer are sclerotic. Radiolucent lesions have a higher intrinsic risk of pathological fracture.


Giant cell tumour of bone
These lesions sit between benign and malignant. Most are benign. They are relatively rare. They consist of multinucleated giant cells (osteoclast like). Malignancy in these lesions is rare and is of the order of 2%. They account for 20% of benign bone tumours. The lesions may present as an enlarging mass, with pain or pathological fracture. On imaging, these lesions have an epiphyseal location and have a characteristic "soap bubble" appearance. They do not normally demonstrate sclerosis and have a sharply defined border. Histologically, they demonstrate multinucleated giant cells. Treatment is challenging since these lesions are locally aggressive and have a high rate of local recurrence following excision.

Malignant bone tumours
The commonest malignant bone tumour is bone metastasis from another solid organ malignancy. Metastatic lesions to bone are significantly more common than primary bone tumours which are extremely rare.

Osteosarcoma
This is the most common form of primary bone tumour. It typically affects males in their second decade. They typically present as a painful expanding mass affecting a long bone such as the femur, in close proximity to a joint. Imaging demonstrates a lesion with mixed sclerotic and lucent zones in the metaphysis bone formation within the tumour is often visible. All patients will be fully staged at presentation with CT, MRI and often PET scanning. There is a high rate of metastasis to the lungs and most patients will receive chemotherapy. Surgical excision is the main treatment.

Ewings sarcoma
Ewings sarcomas typically affect long bones and typically occurs during the first two decades of life. They are complex tumours and have overlap with primitive neuroectodermal tumours. They have a predilection for the lower extremity. They typically present as a painful swelling affecting a long bone. Inflammatory markers such as the ESR are sometimes raised and this is associated with a poorer prognosis. On plain films, the tumour shows evidence of bone destruction with a periosteal reaction (onion skin) appearance. As the condition progresses the periosteal findings can change as the tumour invades the periosteum. Treatment is with excisional surgery and chemotherapy. 

Secondary malignant tumours of bone
Metastatic bone tumours may be described as blastic, lytic or mixed. Osteoblastic metastatic disease has the lowest risk of spontaneous fracture when compared to osteolytic lesions of a similar size. 
Lesions affecting the peritrochanteric region are most prone to spontaneous fracture (because of loading forces at that site). 
The factors are incorporated into the Mirel Scoring system to stratify the risk of spontaneous fracture for bone metastasis of varying types.

10

What is the commonest primary malignant tumour of bone? How are they diagnosed, staged and treated? What is the commonest benign bone tumour?

Osteosarcoma - commonest malignant bone primary

Diagnosis is made by a combination of imaging and biopsy. Imaging with plain films and CT scanning will usually characterise the lesion. Biopsy is carefully planned such that the biopsy tract can be subsequently resected. Staging is performed with PET/CT scanning of the chest. The lungs are a common site of disease extension and most patients are treated with a combination of chemotherapy and resectional surgery.

 

Osteochondroma are one of the commonest benign bone tumours. Osteochonroma is a common non familial developmental aberration with the majority of cases presenting in the first two decades of life. The lesion is thought to arise as a result of herniation of cartilage through the growth plate and this followed by endochondral ossification typically results in a cartilage capped bony protuberance. They are typically located on long bones, usually the distal end of the femur.

 


Giant cell tumour of bone
These lesions sit between benign and malignant. Most are benign. They are relatively rare. They consist of multinucleated giant cells (osteoclast like). Malignancy in these lesions is rare and is of the order of 2%. They account for 20% of benign bone tumours. The lesions may present as an enlarging mass, with pain or pathological fracture. On imaging, these lesions have an epiphyseal location and have a characteristic "soap bubble" appearance. They do not normally demonstrate sclerosis and have a sharply defined border. Histologically, they demonstrate multinucleated giant cells. Treatment is challenging since these lesions are locally aggressive and have a high rate of local recurrence following excision.

Malignant bone tumours
The commonest malignant bone tumour is bone metastasis from another solid organ malignancy. Metastatic lesions to bone are significantly more common than primary bone tumours which are extremely rare.

Osteosarcoma
This is the most common form of primary bone tumour. It typically affects males in their second decade. They typically present as a painful expanding mass affecting a long bone such as the femur, in close proximity to a joint. Imaging demonstrates a lesion with mixed sclerotic and lucent zones in the metaphysis bone formation within the tumour is often visible. All patients will be fully staged at presentation with CT, MRI and often PET scanning. There is a high rate of metastasis to the lungs and most patients will receive chemotherapy. Surgical excision is the main treatment.

Ewings sarcoma
Ewings sarcomas typically affect long bones and typically occurs during the first two decades of life. They are complex tumours and have overlap with primitive neuroectodermal tumours. They have a predilection for the lower extremity. They typically present as a painful swelling affecting a long bone. Inflammatory markers such as the ESR are sometimes raised and this is associated with a poorer prognosis. On plain films, the tumour shows evidence of bone destruction with a periosteal reaction (onion skin) appearance. As the condition progresses the periosteal findings can change as the tumour invades the periosteum. Treatment is with excisional surgery and chemotherapy. 

Secondary malignant tumours of bone
Metastatic bone tumours may be described as blastic, lytic or mixed. Osteoblastic metastatic disease has the lowest risk of spontaneous fracture when compared to osteolytic lesions of a similar size. 
Lesions affecting the peritrochanteric region are most prone to spontaneous fracture (because of loading forces at that site). 
The factors are incorporated into the Mirel Scoring system to stratify the risk of spontaneous fracture for bone metastasis of varying types.

11

Is a pathological fracture purely a sign of a malignant bone tumour?

No, pathological fractures can complicate a number of bone disease including benign bone tumours and intrinsic disorders of the bone such as osteoporosis.

 


Giant cell tumour of bone
These lesions sit between benign and malignant. Most are benign. They are relatively rare. They consist of multinucleated giant cells (osteoclast like). Malignancy in these lesions is rare and is of the order of 2%. They account for 20% of benign bone tumours. The lesions may present as an enlarging mass, with pain or pathological fracture. On imaging, these lesions have an epiphyseal location and have a characteristic "soap bubble" appearance. They do not normally demonstrate sclerosis and have a sharply defined border. Histologically, they demonstrate multinucleated giant cells. Treatment is challenging since these lesions are locally aggressive and have a high rate of local recurrence following excision.

Malignant bone tumours
The commonest malignant bone tumour is bone metastasis from another solid organ malignancy. Metastatic lesions to bone are significantly more common than primary bone tumours which are extremely rare.

Osteosarcoma
This is the most common form of primary bone tumour. It typically affects males in their second decade. They typically present as a painful expanding mass affecting a long bone such as the femur, in close proximity to a joint. Imaging demonstrates a lesion with mixed sclerotic and lucent zones in the metaphysis bone formation within the tumour is often visible. All patients will be fully staged at presentation with CT, MRI and often PET scanning. There is a high rate of metastasis to the lungs and most patients will receive chemotherapy. Surgical excision is the main treatment.

Ewings sarcoma
Ewings sarcomas typically affect long bones and typically occurs during the first two decades of life. They are complex tumours and have overlap with primitive neuroectodermal tumours. They have a predilection for the lower extremity. They typically present as a painful swelling affecting a long bone. Inflammatory markers such as the ESR are sometimes raised and this is associated with a poorer prognosis. On plain films, the tumour shows evidence of bone destruction with a periosteal reaction (onion skin) appearance. As the condition progresses the periosteal findings can change as the tumour invades the periosteum. Treatment is with excisional surgery and chemotherapy. 

Secondary malignant tumours of bone
Metastatic bone tumours may be described as blastic, lytic or mixed. Osteoblastic metastatic disease has the lowest risk of spontaneous fracture when compared to osteolytic lesions of a similar size. 
Lesions affecting the peritrochanteric region are most prone to spontaneous fracture (because of loading forces at that site). 
The factors are incorporated into the Mirel Scoring system to stratify the risk of spontaneous fracture for bone metastasis of varying types.

12

What is an osteoclastoma? What is a chondroma and what features would favor a benign over a malignant lesion?

Osteoclastoma: These are multinucleated giant cell tumours affecting the bone. They are locally aggressive lesions with a low metastatic potential. They have a classical soap bubble appearance on x-ray.

 

Chondromas a benign cartilaginous lesions and are also very common. These are most typically located in the hands and upper limbs and are rarely found within the axial skeleton, a fact that helps to distinguish these from their sarcomatous counterparts. They are located either within the medulla (endochondroma) or on the periosteal surface (juxtacortical chondroma).
Central location, rapid change in size and irregular borders are all clinical features that would raise the suspicion of sarcoma.

 

Benign bone tumours
These are relatively common and typically occur in the young. Most will cease growth once skeletal maturity is attained. A key aspect to managing benign bone tumours lies in the exclusion of a malignant bone tumour. Plain films, CT, MRI and sometimes a bone biopsy may be required.

  • Osteoid osteoma: M>F
    • Commonest between 10 and 25 years
    • Severe pain that responds to NSAIDS
    • Femur and tibia usually affected
    • Lesion affects cortex and radiologically consists of a lucent centre surrounded by reactive sclerosis
    • Usually smaller than 1cm
  • Chondroma: Common benign tumour
    • Endochondroma are central lesions that may cause cortical thinning
    • Ecchondroma project beyond the cortex
    • May cause pathological fracture
    • Rarely found in large bones
  • Osteochondroma: One of the commonest benign bone tumours
    • Usually occurs on the surface of a metaphysis (usually femur, proximal humerus or tibia)
    • Pedunculated lesion arising from metaphysis
    • Long standing lesions
    • Do not grow once skeletal maturity reached
  • Bone cyst: Commonest in adolescent boys
    • Occur in proximal femur and humerus
    • May result in pathological fracture
    • Does not affect growth plate
    • On imaging appears as ovoid radiolucent area with surrounding cortical thinning


Giant cell tumour of bone
These lesions sit between benign and malignant. Most are benign. They are relatively rare. They consist of multinucleated giant cells (osteoclast like). Malignancy in these lesions is rare and is of the order of 2%. They account for 20% of benign bone tumours. The lesions may present as an enlarging mass, with pain or pathological fracture. On imaging, these lesions have an epiphyseal location and have a characteristic "soap bubble" appearance. They do not normally demonstrate sclerosis and have a sharply defined border. Histologically, they demonstrate multinucleated giant cells. Treatment is challenging since these lesions are locally aggressive and have a high rate of local recurrence following excision.

Malignant bone tumours
The commonest malignant bone tumour is bone metastasis from another solid organ malignancy. Metastatic lesions to bone are significantly more common than primary bone tumours which are extremely rare.

Osteosarcoma
This is the most common form of primary bone tumour. It typically affects males in their second decade. They typically present as a painful expanding mass affecting a long bone such as the femur, in close proximity to a joint. Imaging demonstrates a lesion with mixed sclerotic and lucent zones in the metaphysis bone formation within the tumour is often visible. All patients will be fully staged at presentation with CT, MRI and often PET scanning. There is a high rate of metastasis to the lungs and most patients will receive chemotherapy. Surgical excision is the main treatment.

Ewings sarcoma
Ewings sarcomas typically affect long bones and typically occurs during the first two decades of life. They are complex tumours and have overlap with primitive neuroectodermal tumours. They have a predilection for the lower extremity. They typically present as a painful swelling affecting a long bone. Inflammatory markers such as the ESR are sometimes raised and this is associated with a poorer prognosis. On plain films, the tumour shows evidence of bone destruction with a periosteal reaction (onion skin) appearance. As the condition progresses the periosteal findings can change as the tumour invades the periosteum. Treatment is with excisional surgery and chemotherapy. 

Secondary malignant tumours of bone
Metastatic bone tumours may be described as blastic, lytic or mixed. Osteoblastic metastatic disease has the lowest risk of spontaneous fracture when compared to osteolytic lesions of a similar size. 
Lesions affecting the peritrochanteric region are most prone to spontaneous fracture (because of loading forces at that site). 
The factors are incorporated into the Mirel Scoring system to stratify the risk of spontaneous fracture for bone metastasis of varying types.

13

What is the commonest malignant colonic lesion? What is the commonest anatomical site for colonic cancers to develop? What are the commonest presenting symptoms of colorectal cancer? What diagnostic modalities are available to investigate the colon? Once colonic cancer is diagnosed, how is the patient staged?

Adenocarcinoma. Other rare lesions include melanomas, carcinoid tumours and in the distal anal canal squamous cell cancers. Up to 70% of colonic cancers occur in the sigmoid colon and upper rectum.

The commonest symptoms include change in bowel habit and rectal bleeding. Other symptoms include abdominal pain, weight loss and those related to anaemia resulting from chronic occult blood loss.

 

Investigations: Colonoscopy, CT colonoscopy, Barium enema, CT scanning with faecal tagging
Colonoscopy is the most sensitive and specific test.

 

All colonic cancers are staged with CT scanning of the chest, abdomen and pelvis. MRI scanning of the rectum is performed if the cancer lies below the peritoneal reflection.

 

Patients diagnosed as having colorectal cancer should be completely staged using CT of the chest/ abdomen and pelvis. Their entire colon should have been evaluated with colonoscopy or CT colonography. Patients whose tumours lie below the peritoneal reflection should have their mesorectum evaluated with MRI. 

Once their staging is complete patients should be discussed within a dedicated colorectal MDT meeting and a treatment plan formulated.

Treatment of colonic cancer
Cancer of the colon is nearly always treated with surgery. Stents, surgical bypass and diversion stomas may all be used as palliative adjuncts. Resectional surgery is the only option for cure in patients with colon cancer. The procedure is tailored to the patient and the tumour location. The lymphatic drainage of the colon follows the arterial supply and therefore most resections are tailored around the resection of particular lymphatic chains (e.g. ileo-colic pedicle for right sided tumours). Some patients may have confounding factors that will govern the choice of procedure, for example a tumour in a patient from a HNPCC family may be better served with a panproctocolectomy rather than segmental resection. Following resection the decision has to be made regarding restoration of continuity. For an anastomosis to heal the key technical factors include; adequate blood supply, mucosal apposition and no tissue tension. Surrounding sepsis, unstable patients and inexperienced surgeons may compromise these key principles and in such circumstances it may be safer to construct an end stoma rather than attempting an anastomosis. 
When a colonic cancer presents with an obstructing lesion; the options are to either stent it or resect. In modern practice it is unusual to simply defunction a colonic tumour with a proximal loop stoma. This differs from the situation in the rectum (see below). 
Following resection patients with risk factors for disease recurrence are usually offered chemotherapy, a combination of 5FU and oxaliplatin is common.

Rectal cancer
The management of rectal cancer is slightly different to that of colonic cancer. This reflects the rectum's anatomical location and the challenges posed as a result. Tumours located in the rectum can be surgically resected with either an anterior resection or an abdomino - perineal resection. The technical aspects governing the choice between these two procedures can be complex to appreciate and the main point to appreciate for the MRCS is that involvement of the sphincter complex or very low tumours require APER. In the rectum a 2cm distal clearance margin is required and this may also impact on the procedure chosen. In addition to excision of the rectal tube an integral part of the procedure is a meticulous dissection of the mesorectal fat and lymph nodes (total mesorectal excision/ TME). In rectal cancer surgery invovlement of the cirumferential resection margin carries a high risk of disease recurrence. Because the rectum is an extraperitoneal structure (until you remove it that is!) it is possible to irradiate it, something which cannot be offered for colonic tumours. This has a major impact in rectal cancer treatment and many patients will be offered neoadjuvent radiotherapy (both long and short course) prior to resectional surgery. Patients with T1, 2 and 3 /N0 disease on imaging do not require irradiation and should proceed straight to surgery. Patients with T4 disease will typically have long course chemo radiotherapy. Patients presenting with large bowel obstruction from rectal cancer should not undergo resectional surgery without staging as primary treatment (very different from colonic cancer). This is because rectal surgery is more technically demanding, the anastomotic leak rate is higher and the danger of a positive resection margin in an unstaged patient is high. Therefore patients with obstructing rectal cancer should have a defunctioning loop colostomy.

In the emergency setting, where the bowel has perforated, the risk of an anastomosis is much greater, particularly when the anastomosis is colon-colon. In this situation, an end colostomy is often safer and can be reversed later. When resection of the sigmoid colon is performed and an end colostomy is fashioned the operation is referred to as a Hartmans procedure. Whilst left sided resections are more risky, ileo-colic anastomoses are relatively safe even in the emergency setting and do not need to be defunctioned.

14

What is this investigation, what does it show and what is the treatment?

This is a double contrast barium enema. It demonstrates an "apple core" lesion of the ascending colon. This is most likely to represent a right sided colonic adenocarcinoma. Ideally, it should be biopsied using a colonoscope and staged with CT scanning of the chest abdomen and pelvis. It should be treated with a right hemicolectomy.

Patients diagnosed as having colorectal cancer should be completely staged using CT of the chest/ abdomen and pelvis. Their entire colon should have been evaluated with colonoscopy or CT colonography. Patients whose tumours lie below the peritoneal reflection should have their mesorectum evaluated with MRI. 

Once their staging is complete patients should be discussed within a dedicated colorectal MDT meeting and a treatment plan formulated.

Treatment of colonic cancer
Cancer of the colon is nearly always treated with surgery. Stents, surgical bypass and diversion stomas may all be used as palliative adjuncts. Resectional surgery is the only option for cure in patients with colon cancer. The procedure is tailored to the patient and the tumour location. The lymphatic drainage of the colon follows the arterial supply and therefore most resections are tailored around the resection of particular lymphatic chains (e.g. ileo-colic pedicle for right sided tumours). Some patients may have confounding factors that will govern the choice of procedure, for example a tumour in a patient from a HNPCC family may be better served with a panproctocolectomy rather than segmental resection. Following resection the decision has to be made regarding restoration of continuity. For an anastomosis to heal the key technical factors include; adequate blood supply, mucosal apposition and no tissue tension. Surrounding sepsis, unstable patients and inexperienced surgeons may compromise these key principles and in such circumstances it may be safer to construct an end stoma rather than attempting an anastomosis. 
When a colonic cancer presents with an obstructing lesion; the options are to either stent it or resect. In modern practice it is unusual to simply defunction a colonic tumour with a proximal loop stoma. This differs from the situation in the rectum (see below). 
Following resection patients with risk factors for disease recurrence are usually offered chemotherapy, a combination of 5FU and oxaliplatin is common.

Rectal cancer
The management of rectal cancer is slightly different to that of colonic cancer. This reflects the rectum's anatomical location and the challenges posed as a result. Tumours located in the rectum can be surgically resected with either an anterior resection or an abdomino - perineal resection. The technical aspects governing the choice between these two procedures can be complex to appreciate and the main point to appreciate for the MRCS is that involvement of the sphincter complex or very low tumours require APER. In the rectum a 2cm distal clearance margin is required and this may also impact on the procedure chosen. In addition to excision of the rectal tube an integral part of the procedure is a meticulous dissection of the mesorectal fat and lymph nodes (total mesorectal excision/ TME). In rectal cancer surgery invovlement of the cirumferential resection margin carries a high risk of disease recurrence. Because the rectum is an extraperitoneal structure (until you remove it that is!) it is possible to irradiate it, something which cannot be offered for colonic tumours. This has a major impact in rectal cancer treatment and many patients will be offered neoadjuvent radiotherapy (both long and short course) prior to resectional surgery. Patients with T1, 2 and 3 /N0 disease on imaging do not require irradiation and should proceed straight to surgery. Patients with T4 disease will typically have long course chemo radiotherapy. Patients presenting with large bowel obstruction from rectal cancer should not undergo resectional surgery without staging as primary treatment (very different from colonic cancer). This is because rectal surgery is more technically demanding, the anastomotic leak rate is higher and the danger of a positive resection margin in an unstaged patient is high. Therefore patients with obstructing rectal cancer should have a defunctioning loop colostomy.

In the emergency setting, where the bowel has perforated, the risk of an anastomosis is much greater, particularly when the anastomosis is colon-colon. In this situation, an end colostomy is often safer and can be reversed later. When resection of the sigmoid colon is performed and an end colostomy is fashioned the operation is referred to as a Hartmans procedure. Whilst left sided resections are more risky, ileo-colic anastomoses are relatively safe even in the emergency setting and do not need to be defunctioned.

15

What are phaeochromocytomas? What hormones do they secrete? What symptoms do they cause? How is the diagnosis made? How would you image a suspected phaeochromocytoma? What is the operation of choice for a phaeochromocytoma?

These are hormonally active tumours of the adrenal medulla. They are derived from chromaffin cells. They secrete catecholamines. The classical symptoms include headache, palpitations and sweating. Some are discovered incidentally or during the diagnostic work up of hypertension.

A 24 hour urine collection of catecholamine hormones and their metabolites is undertaken and in patients with phaeochromocytoma the levels vastly exceed the normal range.

Investigating: I would use a combination of CT, MRI and I-MIBG scanning. The previous concerns about contrast agents precipitating crises is no longer valid, should there be concerns, blockade can be used.

Surgical Mx: Laparoscopic adrenalectomy

 

These are tumours of the adrenal medulla and are derived from chromaffin cells. They are able to secrete catecholamines. Some present with hypertension although only 0.6% of patients with hypertension will be found to have a phaeochromocytoma. Others may be found incidentally during imaging performed for another reason. Approximately 5% of incidental tumours are found to be phaeochromocytomas. Some phaeochromocytomas are linked to genetic syndromes these include; MEN II, von Hippel Lindau and neurofibromatosis type I.

The classical presenting symptoms that are associated with phaeochromocytomas include headache, palpitations and sweating. 

Diagnosis of phaeochromocytoma includes 24 hour urine collection for adrenaline, nor adrenaline, metanephrine and nor metanephrine levels. Imaging is with MRI and CT, the latter investigation was previously associated with concerns about the relationship of crises related to the use of contrast media. This risk is now acknowledged to be rare. However, where concerns are raised, adrenergic blockade may be used. Radionucleotide imaging with I-MIBH (meta iodobenzylguanidine) scanning will localise many pheochromocytomas and detected extra adrenal lesions. 

Treatment is with surgical excision, laparoscopic adrenalectomy is the favoured approach. The preoperative preparation of these patients is important. It is crucial that the patient is given alpha blockers prior to surgery (phenoxybenzamine). Some patients require additional beta blockade but these are not commenced until alpha blockade has been achieved.

16

What is the normal arterial pH? How is it maintained within such a narrow range?How is arterial pH usually measured? What is the difference between bicarbonate and standard bicarbonate? What is meant by the term anion gap and why is it used?

It is between 7.35 and 7.40

A number of physiological processes are involved in maintaining pH. Within the blood itself, bicarbonate is present and will tend to combine readily with hydrogen ions to form carbonic acid. This dissociates to form carbon dioxide and water. The lungs and the kidneys provide the main sites of acid base excretion and conservation. Via the lungs, changes in respiratory rate allow for the retention or excretion of carbon dioxide with associated implications for pH. In the kidneys, bicarbonate is retained and over the longer term, hydrogen ion excretion can be increased to address increases hydrogen ions.

Arterial pH is usually measured by a method of arterial blood gas sampling and analysis. ABG machines also directly measure oxygen, carbon dioxide, sodium, potassium and chloride - the bicarb is calculated from the other known parameters. 

The bicarbonate value is that which is actually present at the time. However, this can be affected by various respiratory processes. These can be corrected for by adjusting the carbon dioxide level to 5.3kPa. This can change the value of the bicarbonate, which is known as the standard bicarbonate.

 

Anion Gap: Within the plasma, the balance of cations and anions usually ensures electrochemical neutrality. However, only a proportion of anions are measured, these include bicarbonate and chloride. Other anions are not measured (but are present) and these account for the anion gap. In patients with metabolic acidosis, knowledge of the anion gap is helpful since it can help to distinguish between acidosis resulting from bicarbonate loss (where the anion gap is normal) or acid gain (when it increases).

The normal arterial pH is between 7.35 and 7.40, this corresponds to a hydrogen ion concentration of 40nmol/L. The pH of the body is controlled by a number of physiological mechanisms. Blood and tissue buffering is one of the most ubiquitous systems. Hydrogen ions combine with bicarbonate to form carbonic acid which dissociates under the influence of carbonic anhydrase to form carbon dioxide and water. The control of bicarbonate ion concentration is renal and that of carbon dioxide by the lungs. 

In response to acid accumulation, increases in respiratory rate facilitate the excretion of carbon dioxide. Over the longer term, the kidney is able to increase hydrogen ion excretion. 
Within the kidney, the proximal convoluted tubule re-absorbs 85% of filtered bicarbonate. In the distal nephron, hydrogen ions are secreted into the collecting duct by an H+ ATPase pump. The excreted acid is generated in the tubular cells from the formation of carbonic acid. When it dissociates, the hydrogen ion is excreted and the bicarbonate ion is retained. Urinary buffers such as ammonium ions serve to address this hydrogen ion load. However, in the normal situation, urine is slightly acidic with a pH of between 5 and 6. 

Interpretation of acid base changes
Clinically, the most useful method of assessing acid base balance is through the measurement of arterial blood gases. These are collected from a main artery (usually radial) into a syringe that contains an anticoagulant. The pO2, pH and pCO2 are directly measured and the bicarbonate is calculated using the Henderson Hasselbach equation The Henderson Hasselbach equation is pH=pK+log [HCO3]/[H2CO3]. The pK for the bicarbonate/ carbonic acid system is 6.1 and the carbonic acid is usually viewed as being synonymous with carbon dioxide. The key message about the equation is that it illustrates that the pH depends upon the ratio of bicarbonate to carbon dioxide. One value that is provided by arterial blood gas measurements is the standard bicarbonate. The standard bicarbonate is the value that is obtained when the pCO2 is corrected to 5.3kPa, it has the effect of removing any respiratory component. Usually, the standard bicarbonate is between 22 and 26 mmol/L increases are consistent with metabolic alkalosis and values below this range suggest metabolic acidosis. 

Anion gap
Other ions measured with arterial blood gas machines are sodium, potassium and chloride. Chloride and bicarbonate carry a negative charge and are thus anions. Extracellular fluid is normally electrochemically neutral. However, the cations and anions that are measured do not usually balance precisely, the difference arises because there are other anions in the plasma that are not usually measured. This difference is termed the anion gap. Metabolic acidosis can arise through two main mechanisms, bicarbonate loss or acid gain. In the former, there is an increase in plasma chloride levels so that the anion gap remains constant. However, in the latter, where there is an increased production of acid, there is an increase in the anion gap.

 

It is not uncommon for patients to have more than one disturbance of acid base metabolism. For example they may have a respiratory acidosis due to a narcotic overdose and a metabolic alkalosis due to vomiting. In these situations, the pH will represent the sum total of all processes combined. Careful interpretation of the arterial blood gases will allow the underlying causes to be elucidated.

17

What are the key macroscopic differences between ulcerative colitis and Crohn's disease? What key histological feature helps distinguish ulcerative colitis from Crohns disease?

Macroscopic: Ulcerative colitis is confined to the colon and spreads in a progressive fashion from the rectum proximally. Crohn's disease is patchy in its distribution with the terminal ileum being the commonest site of disease. Indeed, Crohn's can affect any segment of the GI tract from mouth to anus. At the disease site, ulcerative colitis is a condition that predominantly affects the mucosa, Crohn's disease is transmural.

 

Histological: Epitheliod granulomas which are more likely to be found in associated with Crohns disease.

 

Ulcerative colitis is a form of inflammatory bowel disease. Inflammation always starts at rectum, does not spread beyond ileocaecal valve (although backwash ileitis may occur) and is continuous. The peak incidence of ulcerative colitis is in people aged 15-25 years and in those aged 55-65 years. It is less common in smokers.

The initial presentation is usually following insidious and intermittent symptoms. Features include:

  • bloody diarrhoea
  • urgency
  • tenesmus
  • abdominal pain, particularly in the left lower quadrant
  • extra-intestinal features:  include sclerosing cholangitis, iritis and ankylosing spondylitis. Arthritis is the most common extra-intestinal feature in both CD and UC

Common to both Crohn's disease (CD) and Ulcerative colitis (UC):

  • Related to disease activity: Arthritis (pauciarticular, asymmetric), Erythema nodosum, Osteoporosis, Episcleritis (more common in Crohns disease)
  • Unrelated to disease activity: Arthritis (polyarticular, symmetric), Pyoderma gangrenosum, Clubbing, Primary sclerosing cholangitis (much more common in UC), Uveitis (more common in UC)


Pathology

  • Red, raw mucosa, bleeds easily
  • No inflammation beyond submucosa (unless fulminant disease)
  • Widespread superficial ulceration with preservation of adjacent mucosa which has the appearance of polyps ('pseudopolyps')
  • Inflammatory cell infiltrate in lamina propria
  • Neutrophils migrate through the walls of glands to form crypt abscesses
  • Depletion of goblet cells and mucin from gland epithelium
  • Granulomas are infrequent


Barium enema

  • Loss of haustrations
  • Superficial ulceration, 'pseudopolyps'
  • Long standing disease: colon is narrow and short -'drainpipe colon'


Endoscopy

  • Superficial inflammation of the colonic and rectal mucosa
  • Continuous disease from rectum proximally
  • Superficial ulceration, mucosal islands, loss of vascular definition and continuous ulceration pattern.


Management

  • Patients with long term disease are at increased risk of development of malignancy
  • Acute exacerbations are generally managed with steroids, in chronic patients agents such as azathioprine and infliximab may be used
  • Individuals with medically unresponsive disease usually require surgery- in the acute phase a sub total colectomy and end ileostomy. In the longer term a proctectomy will be required. An ileoanal pouch is an option for selected patients

18

What colonic complications may occur in association with ulcerative colitis? What is the treatment of choice for a patient with ulcerative colitis who is acutely unwell and whose condition has failed to respond to steroids? How and why does this surgical strategy differ from the elective treatment of choice for definitive disease management?

These include the development of colorectal cancer (six fold increased risk)
Bleeding 
Toxic megacolon
Colonic perforation
Medically resistant disease

 

Failure to respond to steroids (UC) : Acutely -  sub total colectomy and end ileostomy

The definitive surgical strategy for the management of ulcerative colitis is a pan proctocolectomy. This differs from a sub total colectomy in that the rectum is removed. Resection of the rectum is not undertaken in the emergency setting because this carries considerable increased risk that is not justified in the emergency setting. It should be noted that a sub total colectomy is not the definitive management and that even where a sub total colecotmy is performed, a resection of the rectum will be required subsequently.

 

Ulcerative colitis is a form of inflammatory bowel disease. Inflammation always starts at rectum, does not spread beyond ileocaecal valve (although backwash ileitis may occur) and is continuous. The peak incidence of ulcerative colitis is in people aged 15-25 years and in those aged 55-65 years. It is less common in smokers.

The initial presentation is usually following insidious and intermittent symptoms. Features include:

  • bloody diarrhoea
  • urgency
  • tenesmus
  • abdominal pain, particularly in the left lower quadrant
  • extra-intestinal features:  include sclerosing cholangitis, iritis and ankylosing spondylitis. Arthritis is the most common extra-intestinal feature in both CD and UC

Common to both Crohn's disease (CD) and Ulcerative colitis (UC):

  • Related to disease activity: Arthritis (pauciarticular, asymmetric), Erythema nodosum, Osteoporosis, Episcleritis (more common in Crohns disease)
  • Unrelated to disease activity: Arthritis (polyarticular, symmetric), Pyoderma gangrenosum, Clubbing, Primary sclerosing cholangitis (much more common in UC), Uveitis (more common in UC)


Pathology

  • Red, raw mucosa, bleeds easily
  • No inflammation beyond submucosa (unless fulminant disease)
  • Widespread superficial ulceration with preservation of adjacent mucosa which has the appearance of polyps ('pseudopolyps')
  • Inflammatory cell infiltrate in lamina propria
  • Neutrophils migrate through the walls of glands to form crypt abscesses
  • Depletion of goblet cells and mucin from gland epithelium
  • Granulomas are infrequent


Barium enema

  • Loss of haustrations
  • Superficial ulceration, 'pseudopolyps'
  • Long standing disease: colon is narrow and short -'drainpipe colon'


Endoscopy

  • Superficial inflammation of the colonic and rectal mucosa
  • Continuous disease from rectum proximally
  • Superficial ulceration, mucosal islands, loss of vascular definition and continuous ulceration pattern.


Management

  • Patients with long term disease are at increased risk of development of malignancy
  • Acute exacerbations are generally managed with steroids, in chronic patients agents such as azathioprine and infliximab may be used
  • Individuals with medically unresponsive disease usually require surgery- in the acute phase a sub total colectomy and end ileostomy. In the longer term a proctectomy will be required. An ileoanal pouch is an option for selected patients

19

What restorative strategies are available following a sub total colectomy for ulcerative colitis?

The only restorative option is completion proctectomy and formation of an ileoanal pouch. This is usually anastomosed to the anal verge. Very rarely, some surgeons will offer a continent Koch pouch ileostomy. Ileo-rectal anastomosis is not an accepted treatment for ulcerative colitis. Many patients choose not to undergo pouch surgery with its associated lifestyle restrictions. These will be left with a permanent end ileostomy.

 

Ulcerative colitis is a form of inflammatory bowel disease. Inflammation always starts at rectum, does not spread beyond ileocaecal valve (although backwash ileitis may occur) and is continuous. The peak incidence of ulcerative colitis is in people aged 15-25 years and in those aged 55-65 years. It is less common in smokers.

The initial presentation is usually following insidious and intermittent symptoms. Features include:

  • bloody diarrhoea
  • urgency
  • tenesmus
  • abdominal pain, particularly in the left lower quadrant
  • extra-intestinal features:  include sclerosing cholangitis, iritis and ankylosing spondylitis. Arthritis is the most common extra-intestinal feature in both CD and UC

Common to both Crohn's disease (CD) and Ulcerative colitis (UC):

Related to disease activity: Arthritis (pauciarticular, asymmetric), Erythema nodosum, Osteoporosis, Episcleritis (more common in Crohns disease)

Unrelated to disease activity: Arthritis (polyarticular, symmetric), Pyoderma gangrenosum, Clubbing, Primary sclerosing cholangitis (much more common in UC), Uveitis (more common in UC)


Pathology

  • Red, raw mucosa, bleeds easily
  • No inflammation beyond submucosa (unless fulminant disease)
  • Widespread superficial ulceration with preservation of adjacent mucosa which has the appearance of polyps ('pseudopolyps')
  • Inflammatory cell infiltrate in lamina propria
  • Neutrophils migrate through the walls of glands to form crypt abscesses
  • Depletion of goblet cells and mucin from gland epithelium
  • Granulomas are infrequent


Barium enema

  • Loss of haustrations
  • Superficial ulceration, 'pseudopolyps'
  • Long standing disease: colon is narrow and short -'drainpipe colon'


Endoscopy

  • Superficial inflammation of the colonic and rectal mucosa
  • Continuous disease from rectum proximally
  • Superficial ulceration, mucosal islands, loss of vascular definition and continuous ulceration pattern.


Management

  • Patients with long term disease are at increased risk of development of malignancy
  • Acute exacerbations are generally managed with steroids, in chronic patients agents such as azathioprine and infliximab may be used
  • Individuals with medically unresponsive disease usually require surgery- in the acute phase a sub total colectomy and end ileostomy. In the longer term a proctectomy will be required. An ileoanal pouch is an option for selected patients

20

What is a malignant melanoma? What are the risk factors for the development of melanoma? What types of melanoma are recognised? When a melanoma is resected, what single pathological variable correlates most closely with prognosis? 

It is a malignant tumour arising from the epidermal melanocyte.

Risk Factors: Both environmental and phenotypical features are recognised. The former include; Intermittent sun exposure associated with sun burn and use of sun beds at young age. The strongest phenotypical risk factor is increased numbers of melanocytic naevi and dysplastic naevus syndrome.

The commonest variant is the superficial spreading melanoma, typically the female leg or male back are usually affected, these account for 65% of lesions. About 28% of lesions are nodular melanoma This term should be strictly applied to those lesions that have no horizontal growth phase. Approximately 7% of lesions are lentigo maligna melanoma, these lesions have a long and relatively latent horizontal growth phase. Acral and subungual melanomas may be encountered. The former comprise 10% of all melanomas on white skin, but up to 50% on darker skinned persons and are thus not uncommon. In contrast, subungual melanomas are rare, they are most frequently found in the thumb or toe, they arise from the nail plate and thus produce nail discolouration.

 

The Breslow thickness, this is a pathological measurement of the vertical growth phase of a melanoma and correlates with survival. Lesions <0.78 mm have a 10 year survival of 95%. In contrast, a depth of >3.6mm has a 10 year survival rate of 30%.

 

Malignant melanoma: The main diagnostic features (major criteria):

  • Change in size
  • Change in shape
  • Change in colour

Secondary features (minor criteria)

  • Diameter >6mm
  • Inflammation
  • Oozing or bleeding
  • Altered sensation


Treatment

  • Suspicious lesions should undergo excision biopsy. The lesion should be removed in completely as incision biopsy can make subsequent histopathological assessment difficult.
  • Once the diagnosis is confirmed the pathology report should be reviewed to determine whether further re-excision of margins is required (see below):


Margins of excision-Related to Breslow thickness

  • Lesions 0-1mm thick: 1cm
  • Lesions 1-2mm thick: 1- 2cm (Depending upon site and pathological features)
  • Lesions 2-4mm thick: 2-3 cm (Depending upon site and pathological features)
  • Lesions >4 mm thick: 3cm

Further treatments such as sentinel lymph node mapping, isolated limb perfusion and block dissection of regional lymph node groups should be selectively applie

21

What staging is performed for patients with melanoma? How are patients with nodal disease in the groin typically managed? If you were clinically suspicious of a subungual melanoma, what site would you biopsy?

Rather interestingly, little or no staging is performed either before or following resection of primary melanomas. In those patients with worrisome lesions, there is a role for sentinel lymph node biopsy. Patients with nodal disease or relapse at any site, are then fully staged with CT scanning of the head, chest, abdomen and pelvis. PET scanning is also used.

 

Nodal disease groin: This depends upon the overall disease stage. However, isolated groin nodal disease is usually managed by a block dissection of the groin.

 

Subungual melanomas are rare and originate in the nail bed. Therefore, suspicious lesions are managed by removal of the nail and biopsy of the nail bed. If the diagnosis is confirmed then specialist surgical resection is required. Rarely, this may involve amputation of the affected digit.

 

Malignant melanoma: The main diagnostic features (major criteria):

  • Change in size
  • Change in shape
  • Change in colour

Secondary features (minor criteria)

  • Diameter >6mm
  • Inflammation
  • Oozing or bleeding
  • Altered sensation


Treatment

  • Suspicious lesions should undergo excision biopsy. The lesion should be removed in completely as incision biopsy can make subsequent histopathological assessment difficult.
  • Once the diagnosis is confirmed the pathology report should be reviewed to determine whether further re-excision of margins is required (see below):


Margins of excision-Related to Breslow thickness

Lesions 0-1mm thick: 1cm

Lesions 1-2mm thick: 1- 2cm (Depending upon site and pathological features)

Lesions 2-4mm thick: 2-3 cm (Depending upon site and pathological features)

Lesions >4 mm thick: 3cm

22

How are the adrenal glands organised? From which amino acid are adrenaline and nor adrenaline derived? What provides the stimulus for the release of adrenaline and nor-adrenaline?

The paired adrenal glands consist of a cortex and medulla. The former region is divided into three distinct histological zones; the glomerulosa, fasciculata and reticularis. These secrete (in order); mineralocorticoids, glucocorticoids and androgens. The medulla contains chromaffin cells and secretes adrenaline and nor adrenaline - made from tyrosine - release stimulated by the sympathetic nervous system via pre gangionic fibres from the thoracic spinal cord.

 

Adrenal medulla 
The chromaffin cells of the adrenal medulla secrete the catecholamines noradrenaline and adrenaline. The medulla is innervated by the splanchnic nerves; the preganglionic sympathetic fibres secrete acetylcholine causing the chromaffin cells to secrete their contents by exocytosis. 
Phaeochromocytomas are derived from these cells and will secrete both adrenaline and nor adrenaline. 
The glucocorticoids and aldosterone are mostly bound to plasma proteins in the circulation. Glucocorticoids are inactivated and excreted by the liver.

23

What is cryoprecipitate? What are the main constituents of cryoprecipitate? When is it typically used? Is cross matching necessary?

It is a blood product obtained by the centrifugation of plasma.

Main constituents: Fibrinogen, von Willebrand factor, factor VIII, factor XIII and fibronectin.

Used in bleeding due to haemophilia when factor concentrates are not available. Bleeding following massive transfusion.

Cross matching is not strictly necessary, though it is commonly done. For plasma products its the reverse of the blood group.

 

  • Blood product made from plasma
  • Usually transfused as 6 unit pool
  • Indications include massive haemorrhage and uncontrolled bleeding due to haemophilia


Composition:

  • Factor VIII: 100IU
  • Fibrinogen: 250mg
  • von Willebrand factor: Variable
  • Factor XIII: Variable

24

One of the complications following tonsillectomy is haemorrhage. Describe the different types of haemorrhage that may occur following tonsillectomy and explain why they occur?

Tonsillectomy is a recognised cause of both primary and secondary haemorrhage. This is a particular problem in this patient group for two reasons, firstly because the tonsillar bed is highly vascular and secondly because excessive bleeding can result in airway compromise. Both primary and secondary haemorrhage can complicate tonsillectomy. Primary haemorrhage is the result of vessel injury or dislodgement of a clot. When guillotine tonsillectomy was popular, pressure haemostasis and clot formation was the usual haemostatic method employed. In the immediate post operative period the clot would dislodge and brisk haemorrhage would then ensue. Secondary haemorrhage is usually a delayed event and typically occurs 7-14 days following surgery. In the case of tonsillectomy, the tonsillar bed becomes infected and then bleeds as a result of sloughing of vessel walls.

 

Uncontrolled haemorrhage will ultimately result in hypovolaemic shock. This can be the starting point for a complex cycle of tissue hypoperfusion, localised hypoxia and acidosis which further inhibits tissue metabolism and localised hypothermia. Since these factors inhibit the effective functioning of the coagulation cascade they can all contribute to the progression of haemorrhage. In addition, significant haemorrhage can result in the consumption of clotting products which further exacerbates the problem. It is therefore important to both identify and treat haemorrhage promptly. In surgical practice haemorrhage can be described as primary and secondary, surgical and non surgical. Primary haemorrhage is an immediate or early event and is either the result of technical failure (e.g. knot slippage) , unrecognised vessel trauma or dislodgement of clot. Secondary haemorrhage is caused by the sloughing of a vessel wall and typically occurs 7-14 days post operatively. Causes of secondary haemorrhage include infection, pressure necrosis or malignancy. Surgical haemorrhage typically occurs as a direct result of the surgical process. Non surgical haemorrhage is the generalised oozing that can be seen from all raw surfaces and is often due to coagulopathy. The practical relevance of these categories is that primary, surgical haemorrhage usually calls for an immediate surgical solution. Intra operatively, the usual method is to control the bleeding through use of ligatures, clips or stapling devices. Occasionally, the cause of bleeding is from exposed raw surface, iatrogenic splenic injury is a classic cause of this, and such events may require use of additional agents such as haemostatic therapies such as argon plasma coagulation or application of topical haemostatic agents. Primary non surgical haemorrhage should usually be avoided by anticipating and treating coagulopathy before it becomes established. The only realistic option in such circumstances is to pack the affected area and return the patient to a critical care environment to normalise their physiology for 24 hours or so prior to returning to theatre and removing the packs. Identification of haemorrhage in the post operative patient can be surprisingly difficult and in addition to standard bedside haemodynamic parameters (pulse, BP, capillary refill and urine output) it is worth checking devices such as drains and the wound itself to ensure that bleeding is not being overlooked

25

Imagine that you are called to review a 74 year old man following a revision total hip arthroplasty because the nursing staff are concerned that there may be a post operative haemorrhage. Outline how you would assess such a patient.

I would assess their airway, breathing and circulation. I would pay particular attention to their temperature, pulse , blood pressure and capillary refill. I would inspect the wound for evidence of bleeding and if a drain had been inserted I would check that it was on free drainage and that there was no blood present in it. I would check the patients FBC. However, it is not uncommon for this to be normal initially.

 

Uncontrolled haemorrhage will ultimately result in hypovolaemic shock. This can be the starting point for a complex cycle of tissue hypoperfusion, localised hypoxia and acidosis which further inhibits tissue metabolism and localised hypothermia. Since these factors inhibit the effective functioning of the coagulation cascade they can all contribute to the progression of haemorrhage. In addition, significant haemorrhage can result in the consumption of clotting products which further exacerbates the problem. It is therefore important to both identify and treat haemorrhage promptly. In surgical practice haemorrhage can be described as primary and secondary, surgical and non surgical. Primary haemorrhage is an immediate or early event and is either the result of technical failure (e.g. knot slippage) , unrecognised vessel trauma or dislodgement of clot. Secondary haemorrhage is caused by the sloughing of a vessel wall and typically occurs 7-14 days post operatively. Causes of secondary haemorrhage include infection, pressure necrosis or malignancy. Surgical haemorrhage typically occurs as a direct result of the surgical process. Non surgical haemorrhage is the generalised oozing that can be seen from all raw surfaces and is often due to coagulopathy. The practical relevance of these categories is that primary, surgical haemorrhage usually calls for an immediate surgical solution. Intra operatively, the usual method is to control the bleeding through use of ligatures, clips or stapling devices. Occasionally, the cause of bleeding is from exposed raw surface, iatrogenic splenic injury is a classic cause of this, and such events may require use of additional agents such as haemostatic therapies such as argon plasma coagulation or application of topical haemostatic agents. Primary non surgical haemorrhage should usually be avoided by anticipating and treating coagulopathy before it becomes established. The only realistic option in such circumstances is to pack the affected area and return the patient to a critical care environment to normalise their physiology for 24 hours or so prior to returning to theatre and removing the packs. Identification of haemorrhage in the post operative patient can be surprisingly difficult and in addition to standard bedside haemodynamic parameters (pulse, BP, capillary refill and urine output) it is worth checking devices such as drains and the wound itself to ensure that bleeding is not being overlooked

26

You are involved in a challenging cholecystectomy. The gallbladder is densely adherent to surrounding structures and during the course of surgery there is damage to the common hepatic artery will significant blood loss and a time consuming repair. Finally, the surgeon dissects the gallbladder off the liver and following this process there is an on-going and constant ooze from the raw liver surface. What are the principles that should govern the management this?

The patient has undergone a long and complex procedure with significant blood loss. Coagulopathy is likely. It is reasonable to apply topical haemostatic agents in an attempt to control the situation. However, if this is not rapidly achieved, then the safest option is to pack the liver and normalise the physiology before returning to theatre to remove the packs 24 hours later.

 

Uncontrolled haemorrhage will ultimately result in hypovolaemic shock. This can be the starting point for a complex cycle of tissue hypoperfusion, localised hypoxia and acidosis which further inhibits tissue metabolism and localised hypothermia. Since these factors inhibit the effective functioning of the coagulation cascade they can all contribute to the progression of haemorrhage. In addition, significant haemorrhage can result in the consumption of clotting products which further exacerbates the problem. It is therefore important to both identify and treat haemorrhage promptly. In surgical practice haemorrhage can be described as primary and secondary, surgical and non surgical. Primary haemorrhage is an immediate or early event and is either the result of technical failure (e.g. knot slippage) , unrecognised vessel trauma or dislodgement of clot. Secondary haemorrhage is caused by the sloughing of a vessel wall and typically occurs 7-14 days post operatively. Causes of secondary haemorrhage include infection, pressure necrosis or malignancy. Surgical haemorrhage typically occurs as a direct result of the surgical process. Non surgical haemorrhage is the generalised oozing that can be seen from all raw surfaces and is often due to coagulopathy. The practical relevance of these categories is that primary, surgical haemorrhage usually calls for an immediate surgical solution. Intra operatively, the usual method is to control the bleeding through use of ligatures, clips or stapling devices. Occasionally, the cause of bleeding is from exposed raw surface, iatrogenic splenic injury is a classic cause of this, and such events may require use of additional agents such as haemostatic therapies such as argon plasma coagulation or application of topical haemostatic agents. Primary non surgical haemorrhage should usually be avoided by anticipating and treating coagulopathy before it becomes established. The only realistic option in such circumstances is to pack the affected area and return the patient to a critical care environment to normalise their physiology for 24 hours or so prior to returning to theatre and removing the packs. Identification of haemorrhage in the post operative patient can be surprisingly difficult and in addition to standard bedside haemodynamic parameters (pulse, BP, capillary refill and urine output) it is worth checking devices such as drains and the wound itself to ensure that bleeding is not being overlooked

27

What is an open fracture? Do you know of any grading systems for open fractures? What is the usual immediate management of open fractures?

A fracture that occurs in communication with the breach of the surrounding skin or viscera.

The Gustilo and Anderson is a commonly used system and is relatively reproducible. The system considers three grades of injury, 1-3, depending upon the size of the wound, degree of contamination and bony disruption. The third category is subdivided to consider the effects of contamination and vascular injury.

Mx: Careful assessment and management of associated injuries. It is important to determine the nature and extent of injury with imaging and clinical examination. This should be followed by administration of antibiotics and tetanus toxoid. Early debridement of the wound and temporary fracture stabilisation should usually occur within 6 hours or on the following trauma list.

 

The term open fracture refers to a disruption of the bony cortex associated with a breach in the overlying skin. Any wound that is present in the same limb as a fracture should be suspected as being representative of an open fracture. One of the main problems with open fractures is the associated injuries to the surrounding soft tissues. Whilst the skin is usually relatively resistant to trauma, underlying muscle can be damaged or devitalised, nerves, blood vessels and periosteum may all be disrupted the degree to which this occurs correlates with the severity of the injury and the outcome. These can be graded using the Gustilo and Anderson system (see below).
 

GradeInjury

  • 1: Low energy wound <1cm
  • 2: Greater than 1cm wound with moderate soft tissue damage
  • 3: High energy wound > 1cm with extensive soft tissue damage
    • 3 A Adequate soft tissue coverage
    • 3 B Inadequate soft tissue coverage
    • 3 C Associated arterial injury


In Type IIIc injuries, the mangled extremity scoring system (MESS) can help to predict the need for primary amputation. 

Initial management should focus on careful patient examination to check for associated injuries, control of haemorrhage and the extent of injury. The area should be carefully imaged, distal neurovascular status established the wound covered with a dressing and antibiotics administered. Early debridement is the cornerstone of the management of open fractures. The aim of the debridement is to remove foreign material and devitalised tissue. In most cases the wound is left open. The wound should be irrigated, generally, 6 litres of saline is used. The fracture should be stabilised and an external fixator is often used in the first instance

28

How would you debride an open fracture? In what circumstances should the wound be closed primarily?

Under general anaesthesia I would carefully debride all non viable skin and the wound edges as a minimum. I would assess the underlying muscle for its viability and remove any non viable fat or muscle. I would remove all foreign material and bony fragments. Having completed this process I would irrigate the wound with at least 6 litres of saline and stabilise the fracture with an external fixation device.

With the exception of small uncontaminated type I wounds, they should not be primarily closed and re-look and plastic surgical reconstruction is usually needed.

The term open fracture refers to a disruption of the bony cortex associated with a breach in the overlying skin. Any wound that is present in the same limb as a fracture should be suspected as being representative of an open fracture. One of the main problems with open fractures is the associated injuries to the surrounding soft tissues. Whilst the skin is usually relatively resistant to trauma, underlying muscle can be damaged or devitalised, nerves, blood vessels and periosteum may all be disrupted the degree to which this occurs correlates with the severity of the injury and the outcome. These can be graded using the Gustilo and Anderson system (see below).
 

GradeInjury

  • 1: Low energy wound <1cm
  • 2: Greater than 1cm wound with moderate soft tissue damage
  • 3: High energy wound > 1cm with extensive soft tissue damage
    • 3 A Adequate soft tissue coverage
    • 3 B Inadequate soft tissue coverage
    • 3 C Associated arterial injury


In Type IIIc injuries, the mangled extremity scoring system (MESS) can help to predict the need for primary amputation. 

Initial management should focus on careful patient examination to check for associated injuries, control of haemorrhage and the extent of injury. The area should be carefully imaged, distal neurovascular status established the wound covered with a dressing and antibiotics administered. Early debridement is the cornerstone of the management of open fractures. The aim of the debridement is to remove foreign material and devitalised tissue. In most cases the wound is left open. The wound should be irrigated, generally, 6 litres of saline is used. The fracture should be stabilised and an external fixator is often used in the first instance

29

What is meant by the term neurogenic shock? At what level(s) would you consider spinal cord injury to be compatible with the development of neurogenic shock? In what setting would neurogenic shock be accompanied by bradycardia and why? How is neurogenic shock managed?

This is a form of distributive shock characterised by hypotension where the underlying cause is a loss of systemic vascular resistance owing to a damage to the sympathetic outflow tract following spinal cord injury.

Injury to levels T6 and above. Injuries significantly below this level seldom produce sufficient sympathetic disruption to cause significant neurogenic shock and an alternative cause for shock should be carefully considered in such circumstances.

Injuries above T1 are associated with bradycardia owing to unopposed vagal activity on the heart.

In the first instance conventional resuscitation with intravenous fluids is commenced with the intention of the expanding the circulating blood volume. Thereafter, some patients may require vasopressor infusion and those with bradycardia may benefit from administration of atropine.

 

Spinal cord injury may produce hypotension due to loss of peripheral sympathetic vasopressor tone. Because of the possibility that hypovolaemia may co-exist with neurogenic shock (since spinal transection is seldom isolated), this should be addressed initially with appropriate fluid resuscitation. Neurogenic shock may mask the normal physiological response to hypovolaemia. An associated head injury is present in up to 25% of spinal cord injury patients. 

Neurogenic shock classically occurs in spinal injuries above the level of T6 and is due to loss of sympathetic autonomic outflow below this level. The main presenting feature of all cases of distributive shock occurs secondary to loss of SVR. The CVP is usually unaffected unless there is co-existing hypovolaemia. Cardiac output remains the same or may even be elevated. Where the injury is above the level of T6 there is hypotension and when the level is above T1 there is an associated bradycardia because there is then the added component of unopposed vagal tone. 

Management is with intravenous fluid resuscitation to expand the circulating volume and administration of supplementary oxygen. The use of nor adrenaline and / or atropine may also be necessary.

30

What clinical features are suggestive of a haemothorax? How much blood needs to be present for signs to appear on an erect CXR? What is meant by the term massive haemothorax? What are massive haemothoraces usually due to ?

  • Dyspnoea 
  • Chest pain 
  • Haemodynamic compromise 
  • Decreased air entry 
  • Dull percussion note

Approximately 400ml is needed to blunten the costophrenic angle.

The term massive haemothorax refers the initial drainage of 1000-1500ml of blood or the drainage of 200-250ml of blood per hour for 3-4 hours. - usually due to major vessel injury. 

 

Haemothorax can result from blunt or penetrating chest trauma and small haemothoraces are common. The source of bleeding depends upon the mechanism of injury and ranges from damage to minor intercostal vessels through to disruption of the great vessels. One of the challenging features of significant haemothoraces is that the causative structure is seldom readily accessible for simple compression. Parenchymal lacerations are often low pressure bleeds and will often cease spontaneously. However, significant bleeding is usually suggestive of hilar disruption and the need for surgical exploration. Massive haemothorax is defined as the initial drainage of 1000-1500ml or a drainage rate of 200-250ml per hour over 3-4 hours. On clinical examination the signs of a significant haemothorax are often very obvious. Collapsed neck veins and signs of haemorrhagic shock all suggest blood loss and this coupled with decreased air entry and a dull percussion note together will a history of chest trauma should prompt consideration of the diagnosis. The only pitfall is failing to appreciate its appearances on a supine chest film as there will not be a meniscus and the hazy opacity of the affected lung may not be appreciated. On erect CXR volumes of blood >400ml will usually obscure the costophrenic angle. The widespread use of FAST scanning has led to earlier detection of haemothoraces. The treatment of a haemothorax is insertion of a widebore intercostal chest tube. Massive haemothorax is usually an indication for thoracotomy.