Essential Notes for MRCS - Book 2(B)

Circulation

Recognition of shock may be difficult due to the great physiological reserve of children. Often the only
signs are reduced peripheral perfusion and tachycardia. Greater degrees of shock may manifest as
decreased consciousness and reduced responses to pain.


Remember
CO = SV × HR
CO is cardiac output, SV stroke volume, HR heart rate.
In infants the SV is small and relatively fixed, so CO varies with HR. Thus the primary response to
hypovolaemia is tachycardia and the response to fluid resuscitation is blunted.
Caution: increased HR is compounded by pain and fear.
Other useful features in assessing paediatric circulation are:
Pulse volume
End-organ perfusion (skin perfusion, respiratory rate, urine output, mental status) • Temperature (toe–core
gap)


NORMAL VALUES OF BP, HEART AND RESPIRATORY RATES, AND URINE OUTPUT IN
CHILDREN


PHYSIOLOGICAL RESPONSES OF CHILDREN TO HAEMORRHAGE

Intravenous access in paediatric trauma

After two attempts at percutaneous access, consider:

In children aged <6 years: intraosseous needle (anterior surface of tibia 2 cm below tuberosity) • In
children aged >6 years: venous cut-down

Fluid resuscitation in paediatric trauma

Give initial bolus of 20 ml/kg crystalloid (warmed whenever possible). Reassess, looking continually for
a response to the bolus:
Decreased HR
Increased BP
Increased pulse pressure
Increased urine output
Warm extremities
Improved mental status

If there is no improvement with the bolus, give 20 ml/kg colloid (usually Haemaccel). Children who do
not respond to fluids may require blood (10 ml/kg).

Disability after paediatric head trauma

A child’s brain is different from that of an adult. The brain grows rapidly over the first 2 years and has an
increased water content. The subarachnoid space is relatively smaller and so the brain is surrounded by
less CSF to cushion it in the event of impact.

The outcome of head trauma is worse in children aged <3 and these children are particularly vulnerable
to secondary brain injury. Children with an open fontanelle are more tolerant to an expanding mass
because the ICP does not rise as easily (a bulging fontanelle may be palpated).

The GCS is still useful in children aged >4. In children aged <4 the verbal response score must be
modified (eg 5 = appropriate for age, 4 = crying consolably, 3 = crying inconsolably, 2 = agitated, 1 =
noiseless).

Exposure

Remember that the relatively large surface area to weight ratio of children means that they lose heat
quickly. Overhead heaters and blankets are essential.

Note: remember that all drug dosages should be worked out per kilogram of body weight. The weight
estimate in kilograms for those <10 is calculated by: (age + 4) × 2.

Thoracic trauma in children

This occurs in 10% of children (and two-thirds of these will have concurrent injury to the head or
abdomen).
The chest wall is more compliant, so children can have pulmonary contusions without rib fracture;
therefore you should actively look for injury (rib fracture requires proportionally more force in a child
than in an adult)
Mobility of the mediastinal structures makes the child more sensitive to tension pneumothorax and flail
segments • Chest drain insertion is performed in the same way as for an adult but a smaller diameter tube
is used

Abdominal trauma in children

Decompress the stomach with an NG or orogastric tube (crying causes swallowing of air) • Children are
often managed non-surgically with repeated observation and examination (unless haemodynamically
unstable)

Certain injuries are more prevalent in the child:
Duodenal and pancreatic injuries due to handlebar trauma
Mesenteric small-bowel avulsion injuries
Bladder rupture (shallower pelvis)
Fall-astride injuries to the perineum

Non-accidental injury

Always be aware of the possibility that trauma has been caused by non-accidental injury (NAI). It is
estimated that up to 2% of children may suffer NAI during childhood. A number of features should raise
your suspicion.

In the history:
Late presentation
Inconsistent story
Injury not compatible with history (eg long bone fracture in children under walking age) • Repeated
injuries

In the examination:
Abnormal interaction between child and parents
Bizarre injuries (eg bites, burns and shape of injury such as fingertip bruising) • Perioral injuries
Perianal/genital injuries
Evidence of previous injuries (old scars, healing fractures)

You must refer on to the appropriate authorities, even if in doubt (via your immediate senior and the
paediatrics service – these children should be seen by a senior paediatrician). Ensure that your notes are
clear and accurate. Describe what you see, not what you infer, eg say ‘four circular bruises approximately
1 cm in diameter around the upper arm’ rather than ‘bruising from fingertips’.

The following investigations should be performed in any case of suspected physical abuse:
Full skeletal survey – radiology of the whole skeleton to look for old or undiagnosed fractures • Tests of
clotting function, including FBC for platelets
Biochemistry, including bone biochemistry
Appropriate investigations of the head if indicated
Medical photography of any affected area

5.3 Trauma in pregnancy

In a nutshell ...

Treatment priorities are the same as for the non-pregnant patient – treat the mother first as the fetus is

reliant on her condition. Resuscitation and stabilisation need modification to account for the anatomical
and physiological changes that occur in pregnancy. The fetus may be in distress before the mother
shows outward signs of shock.

Anatomical changes in pregnancy

First trimester: uterus is relatively protected by bony pelvis and thick-walled uterus • Second trimester:
uterus becomes intra-abdominal and more vulnerable to injury; amniotic fluid cushions fetus • Third
trimester: relative decrease in amniotic fluid and thickness of uterus, so fetus is more vulnerable to blunt
and penetrative trauma

The placenta contains no elastic tissue and is vulnerable to shearing forces, resulting in incidences of
placental abruption and damage to dilated pelvic veins.

Physiological changes in pregnancy

Oestrogen and progesterone have the following effects:
smooth muscle tone: decreased gastric emptying with lower oesophageal sphincter reflux, so risk of
aspiration
PaCO2: to 4 kPa (30 mmHg). This is the ‘physiological hyperventilation of pregnancy’ secondary to the
respiratory stimulant effect of progesterone. Forced expiratory volume in 1 s/forced vital capacity
(FEV1/FVC) remains the same, but tidal volume increases by 40%
pulse rate
BP: by 10–15 mmHg in the second trimester (normalises near term)
plasma volume: by 50%
cardiac output: by 1.0–1.5 l/min (CVP is usually normal despite the increased total volume)

This means that pregnant women have to lose more of their total circulating volume before signs of
hypovolaemia develop. Blood is shunted away from the uterofetal circulation to maintain the mother’s
vital signs. Therefore the fetus may be shocked before maternal tachycardia, tachypnoea or hypotension
develop. For these reasons, vigorous fluid replacement is required.

Aortocaval compression

The enlarged uterus can compress the inferior vena cava (IVC) and impair venous return, reducing
cardiac output by up to 40%. This can cause a drop in BP unless the pressure is minimised by placing
patients in the left lateral position.

Secondary survey in pregnancy

Urgent radiographs (eg of C-spine) are still taken because the priority is to detect life-threatening injuries.
The uterus can be protected with lead for all imaging except the pelvic film.

Special considerations in pregnancy

Search for conditions unique to the pregnant patient:

Blunt/penetrating uterine trauma
Placental abruption
Amniotic fluid embolism
DIC
Eclampsia
Uterine rupture
Premature rupture of membranes in labour
Isoimmunisation: prophylactic anti-D should be given to rhesus-negative mothers within 72 hours • The
Kleihauer–Betke test (maternal blood smear looking for fetal red blood cells) is specific but not very
sensitive, and is therefore of little use

5.4 Post-traumatic stress disorder



In a nutshell ...

This occurs when a person has experienced a traumatic event involving actual or threatened death or
injury to themselves or others. The individual will have felt fear, helplessness or horror. There are
three classic symptoms that usually cluster:
Intrusions: re-experiencing the event via flashbacks or nightmares • Avoidance: the person attempts to
reduce exposure to people, places or things that exacerbate the intrusions • Hyperarousal:
physiological signs of increased arousal, including hypervigilance and increased startle response

These symptoms must persist for more than 1 month after the event to qualify as PTSD, causing significant
distress or impairment of social or occupational situations.

Other symptoms include:
Insomnia
Anorexia
Depression with low energy
Difficulty in focusing
Social withdrawal

Lifetime prevalence in the USA is 5–10% (Kessler et al, 1995). This value increases to more than 20% in
inner city populations.

Management of PTSD

If symptoms are mild and present for less than 4 weeks, then a period of watchful waiting is
recommended.

Psychological therapy: trauma-focused cognitive behavioural therapy should be offered to those with
either severe post-traumatic symptoms or severe PTSD in the first month after the traumatic event. These
treatments should be offered to everyone with PTSD over the subsequent months and should normally be
provided on an individual outpatient basis.

Drug therapy: this should be administered only by a specialist and usually involves antidepressants such
as paroxetine.

5.5 Brainstem death

The diagnosis of brainstem death

Definition of brainstem death

Irreversible cessation of brainstem function
In the UK, diagnosed by specific tests

Preconditions for diagnosis of brainstem death

Apnoeic coma requiring ventilation
Known cause of irreversible brain damage (eg head injury, cerebral haemorrhage)

Exclusions from diagnosis of brainstem death

Hypothermia (temperature <35°C)
Depressant drugs (eg sedatives, opiates, muscle relaxants)
Metabolic derangements (eg sodium, glucose, hepatic encephalopathy)

Tests of brainstem death

These look for activity in the cranial nerves (CNs).
Pupil responses: CN II. No direct or indirect reaction to light • Corneal reflex: CN V and CN VII. Direct
stimulation with cotton wool • Pain reflex: in facial distribution; motor; CN V and CN VII. Reflexes
below the neck are ignored as they may be spinal reflexes • Caloric test: instillation of cold water into
the auditory canal, looking for nystagmus towards the stimulation; CN VIII, CN III and CN VI. Check that
canal is not blocked with wax first
Gag reflex: CN IX and CN X
Apnoea test: pre-oxygenate with 100% O2 then disconnect from the ventilator. Insufflate oxygen into the
trachea via catheter at 4 litres/min. Observe for any sign of respiration for 10 minutes until PaCO2 is
>6.65 kPa. May need to stop test if sats drop or becomes bradycardic and unstable

If the patient shows no response to the above tests then brain death can be diagnosed after two sets have
been performed. Legal time of death is after the first set.

The tests are performed by two doctors, both 5 years post-registration, one of whom must be a consultant,
and neither doctor should be a member of a transplant team. There is no set time between the two sets but
at least 6 hours should have elapsed between the onset of coma and the first set.

Organ donation after brainstem death

The possibility of donation must be discussed with the relatives, usually after the first set of tests. If they
agree to donation then the local transplant coordinator is contacted, who arranges viral and
histocompatibility testing. They will come to the hospital and talk in detail with the relatives and liaise
with the transplant surgeons. See Chapter 7, Transplantation in Book 2.

5.6 Complications of intravascular drug abuse

Types of drugs which are injected for recreational drug use are: morphine, heroin, cocaine, amphetamine
and methamphetamin. Injecting preparations not intended for this purpose is particularly dangerous
because of the presence of excipients (fillers), which can cause blood clots. Injecting codeine into the
bloodstream directly is dangerous because it causes a rapid histamine release, which can lead to
potentially fatal anaphylaxis and pulmonary oedema. Dihydrocodeine, hydrocodone, nicocodeine, and
other codeine-based products carry similar risks. To minimize the amount of undissolved material in
fluids prepared for injection, a filter of cotton or synthetic fiber is typically used, such as a cotton-swab
tip or a small piece of cigarette filter.

Following prolonged drug administration peripheral venous access becomes increasingly difficult due to
phlebitis associated with repeated non-sterile injection. The addict eventually attempts to administer
drugs into a major deep vein, commonly the groin, with a substantial probability of vascular injury
occurring. Direct intra-arterial injection can lead to limb ischaemia, either primarily as a consequence of
direct local arterial injury and occlusion or as a result of distal small vessel damage. Infective vascular
complications may also result with peri-vascular abscess or formation of an arterial or venous
pseudoaneurysm.

Intra-arterial Injection

The effects of intra-arterial injection arise as a combination of particulate emboli, vasospasm in distal
vessels, and endothelial injury leading to small vessel vasculitis and venous thrombosis. These changes
produce a diffuse tissue ischaemia, which may be exacerbated if the patchy muscle necrosis that results
leads to the development of a compartment syndrome with major muscle necrosis. It is predominantly
small vessel and venous damage that gives rise to the clinical picture of limb mottling and swelling with
muscle tenderness, in the presence of a full complement of pulses.

Supportive medical therapy with systemic heparin is, the best treatment in patients with a full complenient
of limb pulses following intra-arterial injection. In the few patients who present with an absent major
limb pulse at the site of injection it is probable that thrombosis has been initiated following direct
mechanical and chemical injury of the vessel. Unless major proximal limb pulses are absent investigation
with a view to reconstructive vascular surgery are not indicated.

Infective Complications

Superficial thrombophlebitis and deep vein thrombosis are prevalent in injecting drug addicts Venous
pseudoaneurysm is usually present with groin pain, fever, leucocytosis and, sometimes, a fluctuant groin.
Preoperative investigation rarely enables the diagnosis to be made before surgery, which consists of
excision of the infected pseudoaneurysm with excision and ligation of the infected vein, in most cases this
is the common femoral vein.

Arterial infected pseudoaneurysm or ‘aneurysmal abscess’ is the commonest vascular complications
found in drug addicts. The majority of infected pseudoaneurysms develop in the femoral artery although
they have been reported to occur in brachial and radial arteries Pseudoaneurysm commonly presents as a
painful swelling, with fever and leucocytosis, it may present with intermittent bleeding and, occasionally,
massive haemorrhage. The features of an indurated, erythematous swelling may be mistaken for a simple
abscess on initial presentation the majority of pseudoaneurysms are pulsatile on examination, with an
audible bruit over the swelling. Infected pseudoaneurysms of the upper limb vessels seem to require

neither revascularization nor amputation after excision and ligation. Revascularization following ligation
and resection of an infected femoral aneurysm often requires the use of a synthetic graft because of the
lack of good quality vein in drug abusers, this has been associated with a significant incidence of graft
infection and occlusion.

Duplex ultra-sonography should be performed on any swelling in the vicinity of a major vessel to
determine whether or not the lesion contains flowing blood, confirming the diagnosis of pseudoaneurysm.

Bacterial endocarditis should always be considered when assessing intravenous drug users.

5.7 Human and animal bites

Human Bites

Any form of bite should be considered a contaminated wound and management is as for all traumatic
wounds. Thorough lavage, removal of foreign bodies and debridement should be performed.

Infection is the major complication of bite wounds and infections of poorly vascularized structures, such
as ear cartilage, may be difficult to treat. Other serious infectious complications such as osteomyelitis of
the skull vault, necrotizing fasciitis, infectious tenosynovitis, and septic arthritis have been associated
with human bites.

Bacteria that often contaminate human bites include streptococci, Staphylococcus aureus, Haemophilus
spp, Eikenella corrodens and Bacteroides spp and other anaerobes. Transmission of viruses (e.g. hepatitis
B, hepatitis C, HIV, HTLV-1) following human bites is much less common.

Animal Bites

Dog attacks kill approximately 10-20 people annually in US, most of these fatalities are young children.
Local infection and cellulitis are the leading causes of morbidity, sepsis is a potential complication of
bite wounds, particularly C canimorsus (DF-2) sepsis in immunocompromised individuals. Dog bites
typically cause a crushing-type wound because of their rounded teeth and strong jaws.

The sharp pointed teeth of cats usually cause puncture wounds and lacerations that may inoculate bacteria
into deep tissues. Infections caused by cat bites generally develop faster than those of dogs. Pasteurella
multocida infection is the most common pathogen contracted from cat bites and may be complicated by
sepsis.

Other complications include meningitis, osteomyelitis, tenosynovitis, abscesses, pneumonia, endocarditis,
and septic arthritis. When rabies occurs, it is almost uniformly fatal.

CHAPTER 6

Trauma
Part 2: Musculoskeletal

Nigel W Gummerson

Pathophysiology of fracture healing
1.1 Primary bone healing
1.2 Secondary bone healing
1.3 Delayed bone healing
1.4 Systemic effects of trauma

Classification of fractures
2.1 Describing fractures
2.2 Imaging of fractures
2.3 Describing plain trauma radiographs

Principles of management of fractures

Complications of fractures
4.1 Early general complications of fractures
4.2 Early local complications of fractures
4.3 Late local complications of fractures

Common fractures
5.1 Upper limb
5.2 Lower limb
5.3 Pelvic fractures
5.4 Thoracolumbar spinal injuries
5.5 Cervical spine trauma

Fractures and related injuries in children
6.1 Paediatric bone
6.2 Epiphyseal injuries
6.3 Forearm bone fractures
6.4 Supracondylar fractures
6.5 Condylar fractures
6.6 Femoral fractures in children

Soft-tissue injuries and disorders
7.1 Soft-tissue injuries of the knee
7.2 Soft-tissue injuries of the ankle

Compartment syndrome
8.1 Pathogenesis and physiology
8.2 Diagnosis and treatment

SECTION 1

Pathophysiology of fracture healing

Bone is unique in its ability to repair itself without scarring, using the processes that occur during normal
bone formation and bone turnover. Bone healing may be primary or secondary.

1.1 Primary bone healing Primary bone healing occurs when the fracture gap is
small and there is minimal motion between the fracture fragments. This situation is
achieved after anatomical reduction and rigid fixation with absolute stability (eg
open reduction and internal fixation [ORIF] of forearm fracture with
interfragmentary compression).

New vessels will cross the fracture gap and bone remodelling occurs across the fracture gap with little or
no callus formation. Primary bone healing requires a blood supply, and extensive soft-tissue stripping at
the time of injury or at the time of surgery will impede the process.

1.2 Secondary bone healing Secondary bone healing occurs in three phases (others
may further subdivide these phases). There is considerable overlap between these
phases:

Inflammatory phase
Reparative phase
Remodelling phase

Inflammatory phase

At the time of injury there will be bleeding from both the vessels in the medullary cavity and the vessels
in the periosteum. Blood clot will form and the bleeding will stop. Cytokines (platelet-derived growth
factor [PDGF], interleukins IL-1 and IL-6, transforming growth factor ß [TFG-ß], fibroblast growth factor
[FGF], insulin-like growth factor [IGF] and bone morphogenetic proteins [BMPs]) are released from the
clot, marrow, periosteum and bone, recruiting inflammatory cells (macrophages and neutrophils),
fibroblasts and osteoprogenitor cells. This process begins immediately and is well established by day 7,
which represents the peak of cellular proliferation at the fracture site. Cell proliferation declines to day
14.

Reparative phase

Fibroblasts, recruited to the fracture site, will lay down a disordered matrix of type II collagen.
Chondrocytes will mature and begin chondrogenesis around day 9–14. This produces callus, initially a
soft material, which bridges the fracture ends. This soft callus will become mineralised (from day 14),
increasing in stiffness and strength, to become hard callus. This process is similar to the embryonic
process of endochondral ossification. The osteoblasts, which mediate this process, are derived from
periosteum, marrow and fracture site. Ossification is enhanced by early motion and (protected) weight
bearing. During this time neovascularisation occurs, with new vessels growing into the fracture site.

As ossification continues the callus becomes woven bone. Unlike the bone before injury, the woven bone
has a random orientation of collagen and haversian systems.

Remodelling phase

Remodelling takes many (1–4) years. it is a normal physiological process for the entire skeleton, allowing
it to respond to changes in loading patterns. After injury, remodelling converts woven bone to lamellar
bone which has an internal architecture ordered in response to the loads across it. This change in bone
internal structure in response to load is Wolff’s law.

As a very general rule fractures of the upper limb (in adults) take 6–8 weeks to unite. In the lower limb it
takes 12–14 weeks.

1.3 Delayed bone healing There are many factors that can delay bone healing. After
internal fixation this may manifest as failure of the instrumentation. For
conservatively treated fractures delayed union may manifest as persisting pain and
motion or with radiological signs such as hypertrophic callus formation and a
persistent fracture gap (suggesting insufficient immobilisation of the fracture) or
atrophic/hypotrophic callus (suggesting a biological reason for delayed union).

Factors that delay bone healing

Systemic patient factors

Diabetes
Vascular insufficiency • Malnutrition
Disorders of vitamin D, calcium or phosphate metabolism • Drugs, non-steroidal anti-inflammatory drugs
(NSAIDs) and steroids

Local factors

Infection
Inadequate immobilisation • Loss of local blood supply

1.4 Systemic effects of trauma There is a well-recognised inflammatory response
after trauma or surgery. The cytokines that stimulate the inflammatory response at
the fracture site can also be measured in the circulation where it is thought that
they contribute to the systemic response to trauma (particularly IL-6 and TGF-ß).

Injured patients will have a rise in cytokine levels immediately after the incident. The cytokine levels will
rise again after any surgical procedure. The most frequently studied situation is femoral nailing for
femoral fractures. It is thought that this ‘second hit’ can precipitate acute respiratory distress syndrome
(ARDS) or multiorgan failure (MOF). Measurement of cytokines may help determine the optimal timing
of reconstructive surgery to minimise the pro-inflammatory systemic effects of the trauma and subsequent
surgery.

SETION 2

Classification of fractures

In a nutshell ...

Fracture classification
Nine things to talk about when you describe a fracture • Eleven things to say about the radiograph

Many different classification systems have been developed for use in trauma. They each try to describe
one or more of the following areas:
Mechanism of injury
Location of injury
Injury morphology
Functional or physiological consequences of injury • Damage to surrounding structures in zone of injury

Fracture classifications tend to focus on the location and morphology of injury. Some fracture
classifications attempt to provide a comprehensive framework that allows classification of any fracture in
any anatomical area (eg the AO classification of long-bone fractures); others are specific to one
anatomical location (eg the Garden classification of intracapsular proximal femoral fractures).

There are pros and cons to all these systems. In general any classification system should be reliable,
reproducible and relevant – and have some bearing on treatment and prognosis.

Remember, it is more useful for a trainee to be able to describe a fracture accurately than to learn one of
the many classification systems.

The age of the patient can help determine which injuries are more or less likely (see box overleaf).


Fracture pattern related to age
The same mechanism of injury may result in a different pattern of pathology depending on the age of the
patient. This is because different structures are vulnerable at different stages of development and the
weakest structure tends to be injured, eg:
At age 10–14 years growth plate is vulnerable • At age 16–35 years ligaments rather than bone are
vulnerable • At age 40–70 years bone is weakest

A fall on the outstretched hand therefore results in typical injuries.
Typical injury from a fall on an outstretched hand at different ages

Age (years) Typical injury

Child <10 Greenstick fracture (distal radius or radius and ulna)

10–14 Physeal injury (typically Salter–Harris II fracture)

16–35 Fractured scaphoid Scaphoid ligament injury Intra-articular radial head fracture

40–70+ Colles’ fracture of the distal radius

2.1 Describing fractures

Nine things to talk about

. General features: age of patient, mechanism of injury, general condition of patient, medical history, etc
2. Anatomical site: which bone? Which part of the bone?

. Type: traumatic, pathological or stress fracture?
Traumatic fracture identified by mechanism of injury and absence of pathological features • Stress
fractures develop slowly in bones subjected to repetitive loads (eg sports training, military marching) •
Pathological fractures are low-energy injuries (not sufficient to fracture a normal bone) resulting in
fracture of a bone altered by a disease process that can be:
• Systemic (osteoporosis, metabolic bone disease, Paget’s disease) • Localised (primary bone tumour,
haematopoietic disorder, metastatic disease) 4. Intra-articular or extra-articular
. Joints: congruent, subluxed or dislocated 6. Physeal injury (if growth plate still open) 7. Fracture
pattern:
Simple (spiral, oblique or transverse)
Wedge fracture
Multifragmentary
. Deformity and displacement:
Rotational deformity
Shortening or distraction
Translation (occurs in two planes: for a distal radius this is volar/dorsal and radial/ulnar) • Angular
deformity (occurs in two planes) • Articular steps
. Associated soft-tissue injury:
Condition of skin, muscle and tendon
Open or closed (fracture site communicates with open wound) • Neurovascular status
Ligamentous injuries

2.2 Imaging of fractures

Plain radiographs

Standard investigation to confirm/exclude fracture or dislocation • Always two views of whole bone with
its proximal and distal joints • If one bone of a pair is broken, look very carefully at the other one • If
there is no fracture look for dislocation • Look for soft-tissue injuries on radiographs

CT

Image intra-articular fractures (good resolution of articular fragments) • Useful for spinal and pelvic
injuries
Can be used to create three-dimensional reconstructions that help preoperative planning

MRI

The investigation of choice for suspected hip fracture when the plain films are equivocal (NICE guideline)
• Can be used to image articular surface
Gives information on soft tissues (eg ligamentous and meniscal injuries with tibial plateau fracture)

2.3 Describing plain trauma radiographs It is possible that you’ll be shown a
radiograph of a trauma case or complication of a fracture. There are too many
possibilities to be covered in this book, but nothing can replace experience in a busy
A&E or orthopaedics job. (To refresh your memory we recommend the book
Practical Fracture Management by Ronald McRae. This has an excellent overview of
all the common fractures and their management and includes many radiographs of
the more common injuries.) If in doubt, follow the guidelines below for looking at a
radiograph.



Looking at a radiograph
Check the label (this is the radiograph of William Rhodes who is 40, taken on 20 October 2012) • Name

the bone or joint, side and the view (eg it is an anteroposterior [AP] view of the left femur) • Describe
the obvious abnormality, if there is one
Describing a fracture on a radiograph
If shown only one film, ask if there are any other views • Site: side, bone and level (divide long bones
into proximal, middle and distal thirds) • Pattern: transverse, oblique, spiral, complex (in children,
greenstick or buckle fractures) • Comminution: simple, wedge or complex (comminuted) • Special
features: eg avulsion fracture, depressed, involving the articular surface • Displacement: estimate
percentage of fracture surface in contact and shortening • Angulation* or tilt
Axial rotation: you need to see the joint above and below the fracture • Associated features:
dislocation, soft-tissue swelling, obvious compound (not easy to determine on radiograph unless
dramatic), foreign bodies and pathological fracture
Do NOT say ‘angulation’ unless you have read up on it and fully understand it; it means the opposite to
what most people think – saying ‘fracture of the mid-shaft of the tibia with 20° of medial angulation’
means ‘the distal end of the distal fragment has swung LATERALLY’! (Use the word ‘tilt’ instead – ‘the
distal fragment is tilted laterally by about 20°’. This means what it says – much safer during exam
stress!)

SECTION 3

Principles of management of fractures

In a nutshell ...

Principles of fracture management
Resuscitation
Reduce (if necessary)
Hold
Rehabilitate the limb and the patient

When discussing any given fracture consider the following six points:

1. Initial emergency measures

2. Does the fracture require reduction?
3. If reduction of the fracture is required, how will it be achieved?
4. What support is required, and for how long?
5. Consideration of soft-tissue injury?
6. Does the patient need to be admitted?

This allows you time to organise your thoughts, gives you a framework for discussing your answer, and
allows the examiners to steer you to the points that they want you to discuss, without the feeling that you
have missed out any important principles. You can then address the fracture that you have been asked to
assess with reference to each relevant principle in greater detail.

Initial emergency measures

Resuscitation following ATLS guidelines for all major trauma • Temporary splint (eg sandbags, inflatable
splints) • Reposition deformed limbs immediately if overlying skin at risk • If open fracture take
photographs and swabs, cover with sterile dressings, give antibiotics and tetanus prophylaxis • Assess
clinically and radiologically

Does the fracture require reduction?

No it does not:
If undisplaced
If displacement likely to be corrected by remodelling (eg in children) • If risks of anaesthesia outweigh
disadvantage of deformity

Yes it does:
If slight displacement in functionally vital area (eg articular surface) • If significantly displaced, angled or
rotated (criteria vary for each fracture)

As a general principle, lower-limb injuries need anatomical reduction to maintain the normal weight-
bearing axis of the limb. The function of the upper limb is to place the hand in space; the shoulder and
elbow both have a large range of motion and small residual deformities can be accommodated.

Deformity in the same plane as the joint (eg flexion extension of a femoral fracture is in the same plane as
the knee) is better tolerated than deformities perpendicular to the joint (eg varus– valgus malalignment of
the femur changes the weight-bearing axis through the knee). Rotation is poorly tolerated in any fracture.

How will reduction be achieved?

Closed (manipulation under anaesthesia or MUA) • Open reduction:
• If MUA has failed
• If internal fixation is required (for unstable fracture configuration and to allow early mobilisation) • If
fracture is open
Continuous traction – rarely used except in cervical spine and femur

What support is required, and for how long?

Non-rigid support:
• Broad-arm slings for support of distal limb where support of the fracture is needed (eg clavicle
fractures) • Collar and cuff for support of distal limb where traction is desirable (eg shaft or neck of
humerus) • Cast immobilisation: typically plaster back-slab initially, completed or changed to
lightweight cast when the swelling subsides • Internal fixation: eg compression plates and screws or
intramedullary devices

Internal fixation

Indications for internal fixation
Fractures requiring open reduction • Unstable fractures
Intra-articular fractures
Multiply injured patients

Advantages of internal fixation
Anatomical reduction, absolute stability • Allows primary bone healing • Earlier mobilisation of joints •
Earlier discharge from hospital

Complications of internal fixation
Infection
Anaesthetic risk
Failure of fixation
Malposition of metalwork

External fixation

Advantages of external fixation
Rapid application
Useful for multiple injuries • Stabilises comminuted fractures that are unsuitable for internal fixation •
Provides fixation outside zone of injury for open fractures and allows access to the wound

Disadvantages of external fixation
Cumbersome
Pin-track infection/colonisation • May hold fracture in slight distraction resulting in non-union/delayed
union

Ilizarov circular frame

Advantages of Ilizarov circular frame
Allows fine and continuous control of position, compression and distraction • Facilitates gradual
correction of deformity

Disadvantages of Ilizarov circular frame
Requires close supervision and frequent adjustment • Wire-track infection
Requires specialist skills

Continuous traction

Skeletal or skin traction
Skeletal pins (eg Steinman or Denham pins) • Adhesive skin traction
Now used for temporary preoperative stabilisation of adult femoral fractures and as definitive treatment of
some paediatric (and a small number of adult) femoral fractures

Disadvantages of skeletal or skin traction
Requires constant monitoring and adjustment • Patient immobilised for many weeks, resulting in weakness
and stiffness • Risks of pressure sores, chest infection and thromboembolism

Cast bracing

After first few weeks of cast immobilisation (allowing formation of soft callus) conversion to hinged cast
allows mobilisation of joint • Used for fractures around the elbow and the knee

Consideration of soft-tissue injury

Consider if there are open fractures, crush injury, contusions or neurovascular injury.

Open fractures

Initial measures as above (swab, photograph, dressing, IV antibiotics, tetanus prophylaxis) • Debridement
and lavage under GA (ideally within 6 hours for heavily contaminated wounds and 24 hours for an
isolated open fracture) • Assess skin cover and plan closure (primary, split-skin graft, local flap, free
flap) • Infection risk is inversely related to time to definitive closure

Open fracture of the tibia and fibula
Classification according to the soft-tissue defect left after debridement (Gustilo and Anderson’s [1976]
classification of open fractures).

Type I
Wound <1 cm long
Little soft-tissue damage
Simple fracture pattern with little comminution

Type II
Wound >1 cm long
No extensive soft-tissue damage • Moderate contamination and fracture comminution

Type III
Extensive soft-tissue damage • Contamination and fracture comminution • Type A: soft-tissue coverage is
adequate. Comminuted and segmental high-energy fractures are included regardless of wound size • Type
B: extensive soft-tissue injuries with massive contamination; and severe fracture comminution require a
local or free flap for coverage
• Type C: arterial injury requires repair

Crush injury and severe contusion
Beware of compartment syndrome • Assess and treat neurological and vascular damage • Reconstructable
injury?


Mangled extremity severity score (MESS)

1–4 Energy of injury

1–3 Limb ischaemia (double score if time >6 hours)

0–2 Shock

0–2 Age of patient

MESS score >7 is indication for amputation.

Does the patient need to be admitted?

GA or other inpatient treatment required • Observation (eg comorbidity, multiple trauma) • Nursing care
(bed-bound, bilateral limb fractures) • Mobilisation with physiotherapy • Social factors (eg elderly
person) • Child abuse suspected

SECTION 4

Complications of fractures

Complications of fractures
Early general complications
Hypovolaemic shock
DIC
SIRS
Fat embolism syndrome
Early local complications
Arterial injury
Nerve injury
Compartment syndrome
Infection
Soft-tissue compromise
Late general complications
Deep venous thrombosis (DVT)
Pulmonary embolism (PE)
Urinary tract infection (UTI)
Respiratory tract infection
Disuse atrophy
Psychosocial/economic factors
Late local complications
Delayed union/non-union/malunion • Infection
Joint stiffness
Secondary osteoarthritis
Avascular necrosis
Myositis ossificans
Complex regional pain syndrome – aka reflex sympathetic dystrophy or Sudeck’s atrophy

4.1 Early general complications of fractures Fractures and hypovolaemic shock

For more details on shock in trauma see Chapter 6, Part 1. Approximate blood loss in closed fracture:
Pelvis 1–5 litres
Femur 1–2.5 litres
Tibia 0.5–1.5 litres
Humerus 0.5–1.5 litres

Fractures and disseminated intravascular coagulation

DIC is associated with trauma and massive transfusions. It causes consumption of clotting factors and
platelets, resulting in uncontrolled bleeding from injured sites. It is treated by replacement of platelets and
clotting factors, with surgical control of bleeding if required. Hypothermia will exacerbate any
coagulation problem. Therefore consideration of the patient’s exposure and environment in the
resuscitation room and operating theatre is of great importance.

Fractures and systemic inflammatory response syndrome This is the systemic
response to major trauma, mediated by changes in the autonomic nervous system
and the immune system. Some patients are more susceptible to it as a result of their
genetics and immune system.

Features of SIRS (must have two or more):
Pyrexia >38°C or <36°C
Tachycardia >90 beats/minute • Tachypnoea >20 beats/minute or PaCO2 <4.26 kPa (32 mmHg) • WCC
>12 000 cells/mm2 or 10% immature (bands) forms

Patients with signs of SIRS should not be subjected to major surgery until their condition improves. The
additional (surgical) trauma may exceed their physiological capacity to autoregulate the local organ and
systemic circulation. This is the ‘second-hit’ hypothesis of trauma, and applies in particular to the
intramedullary nailing of long bones, which provokes a large immunological response in patients.

Fractures and fat embolism syndrome

This complication of long-bone (especially femur) fracture presents with a petechial rash, confusion and
hypoxia. The pathophysiology is not completely understood. Fat embolism syndrome is thought to occur
as a result of:
Release of lipid globules from damaged bone marrow fat cells • Increased peripheral mobilisation of fatty
acids • Increased synthesis of triglycerides by liver
It results in embolism of the microvasculature with lipid globules. As any part of the microvasculature
can be affected, the clinical manifestations are varied:
Pulmonary: ventilation/perfusion mismatch • Cerebral: ischaemia, infarction, oedema • Cardiac:
arrhythmias and impaired mechanical performance • Renal: ischaemic glomerular/tubular dysfunction •
Skin: capillary damage, petechial haemorrhage
Diagnosis is made by detection of fat globules in body fluids in association with pulmonary and
failure/dysfunction of at least one other organ system. Treatment is to maintain adequate tissue
oxygenation. The incidence may be reduced by early stabilisation of long-bone fractures.

4.2 Early local complications of fractures Fractures and arterial/nerve injury


COMMON SITES OF NERVE AND ARTERIAL INJURY
Examples of common sites of injury Structures at risk

Proximal humeral fractures/shoulder
dislocation

Axillary nerve
Humeral shaft (middle and distal third)

Radial nerve

Radial nerve (most common), median nerve, ulnar nerve or
brachial artery

Paediatric supracondylar fracture
Median nerve (acute carpal tunnel syndrome)

Distal radial fracture
Lumbar–sacral plexus, iliac vessels or superior gluteal artery

Pelvic fracture
Acetabular fractures/hip dislocation

Sciatic nerve
Popliteal artery and common peroneal nerve

Knee dislocation

Any lower leg artery or nerve

Open tibial fracture

Priorities in management of bleeding pelvic injury

Pelvic stabilisation can be achieved with a temporary pelvic binder, or more permanently with an
external fixator. Operative surgical control of the bleeding pelvic injury has now largely been replaced by
interventional vascular radiological control of bleeding.

Priorities in management of neurovascular limb injury

Haemorrhage control
Arterial/venous shunt
Wound debridement
Skeletal stabilisation
Arterial/venous reconstruction • Soft-tissue coverage
Fasciotomy (if required after reperfusion)

Nerve injuries

Nerve repair may be deferred, but it is suggested that best results are obtained if it is undertaken within
10 days of injury.


Neuropraxia: conduction block, axon and nerve sheath intact. Usually full recovery by 6 weeks •
Axonotmesis: axon divided, nerve sheath intact. May recover (at rate of 1 mm/day), but fibrosis may
prevent full recovery (exploration and neurolysis may be indicated)
Neurotmesis: axon and nerve sheath divided. Little chance of recovery unless primary surgical repair or
nerve grafting. Unlikely to achieve full recovery, even with surgical treatment.

For further discussion of nerve repair see Trauma, Part 1.

Fractures and infection

In a nutshell ...

Fractures may be associated with:
Cellulitis
Gas gangrene
Tetanus
Necrotising fasciitis

Cellulitis

Features of cellulitis
There is infection of the dermis and subcutaneous tissues • Limbs are commonly affected (usually the
lower leg) • Erythema occurs with blurred demarcation to normal tissue

Microbiology of cellulitis
Cellulitis is commonly caused by ß-haemolytic streptococci (Streptococcus pyogenes)

Risk factors for cellulitis
Lymphoedema
Tinea fungal infections of the feet

Treatment of cellulitis
Rest and elevation
IV antibiotics

Gas gangrene

Features of gas gangrene
Shock and septicaemia, with tachycardia, fever, confusion and rigors • Limb is initially cool, becoming
discoloured • Bubbles of trapped CO2 produce crepitus and may be visible on plain radiographs • Even
with the best available treatment, mortality rates are around 25%

Microbiology of gas gangrene
Caused by Clostridium spp. (C. perfringens in 80–95% of cases): • Gram-positive, spore-forming rods •
Anaerobic but will tolerate aerobic conditions • Exotoxins produced include toxin a (responsible for
haemolysis and tissue necrosis) • Gas produced by anaerobic metabolism causes reduced tissue blood
flow and acceleration of tissue necrosis • Enzymes produced include collagenase • Can spread by 2–3
cm/hour

Risk factors for gas gangrene
After amputation of ischaemic limbs • Deep penetrating injuries with tissue necrosis (eg battlefield
injuries) • GI sepsis with tissue necrosis • Failed illegal abortion

Treatment of gas gangrene
Surgical debridement (amputation) • High-dose antibiotics (penicillin) • Hyperbaric oxygen therapy
(increasing the PO2 in tissues inhibits bacteria metabolism and reduces tissue necrosis)

Tetanus

Features of tetanus
Symptoms begin 3 days to 3 weeks from infection (typically after 7–8 days):
Headache
Muscle stiffness around the jaw • Rigid abdominal muscles
Sweating and fever

Tetanus often results from deep penetrating wounds with soil contamination. Mortality rate is
approximately 50%.