Surgery - Circulation: Classification of Haemorrhagic Shock

Class 1 Shock

Blood pressure: Systolic blood pressure is unchanged and diastolic blood pressure is unchanged.

Pulse: The pulse is high-normal in rate and normal in volume.

Capillary refill time: Capillary refill time is normal.

Respiratory rate: Respiratory rate is normal.

Urine output: Urine output remains greater than 30 mL/hour.

Extremities: The extremities retain a normal colour.

Complexion: The complexion remains normal.

Mental state: The patient remains alert.

Blood loss: Blood loss is less than 15%, approximately 750 mL.

A useful tennis analogy is “love-fifteen.”

Class 2 Shock

Blood pressure: Systolic blood pressure is usually normal, while diastolic blood pressure may be raised.

Pulse: The pulse rate is approximately 100–120 beats/minute, with a generally normal pulse volume.

Capillary refill time: Capillary refill is slow, usually taking more than 2 seconds.

Respiratory rate: Tachypnoea develops.

Urine output: Urine output falls to approximately 20–30 mL/hour.

Extremities: The extremities become pale.

Complexion: The patient appears pale.

Mental state: The patient may become anxious.

Blood loss: Blood loss is approximately 15–30%, corresponding to around 800–1500 mL.

A useful tennis analogy is “fifteen-thirty.”

Class 3 Shock

Blood pressure: Both systolic and diastolic blood pressure are reduced.

Pulse: The pulse is greater than 120 beats/minute and becomes thready.

Capillary refill time: Capillary refill remains slow, usually more than 2 seconds.

Respiratory rate: The respiratory rate is greater than 20 breaths/minute.

Urine output: Urine output falls to approximately 10–20 mL/hour.

Extremities: The extremities are pale.

Complexion: The patient appears pale.

Mental state: The patient may become aggressive or drowsy.

Blood loss: Blood loss is approximately 30–40%, corresponding to around 1500–2000 mL.

A useful tennis analogy is “thirty-forty.”

Class 4 Shock

Blood pressure: Systolic blood pressure is very low, while diastolic blood pressure is very low or may be unrecordable.

Pulse: The pulse is greater than 120 beats/minute and is very thready.

Capillary refill time: Capillary refill may be undetectable.

Respiratory rate: The respiratory rate is greater than 20 breaths/minute.

Urine output: Urine output falls to approximately 0–10 mL/hour.

Extremities: The extremities are pale and clammy.

Complexion: The patient may appear ashen.

Mental state: The patient becomes drowsy or confused.

Blood loss: Blood loss exceeds 40%, corresponding to more than 2000 mL.

A useful tennis analogy is “game over.”

Surgery - Circulation

Shock

Shock is a clinical state in which the circulation is inadequate to maintain sufficient tissue perfusion.

As a result, the metabolic demands of the body are not met, oxygen delivery to tissues becomes inadequate, and abnormal cellular and organ physiology develops.

Types of Shock

Hypovolaemic shock occurs when there is a reduction in intravascular volume, most commonly due to haemorrhage.

Cardiogenic shock occurs when the heart fails as an effective pumping mechanism. This may result from primary cardiac damage or secondary causes such as cardiac tamponade.

Septic shock results from infection and the release of inflammatory mediators, causing vasodilatation and abnormal distribution of intravascular volume.

Neurogenic shock results from loss of sympathetic vascular tone due to disruption of neurological pathways, such as following spinal cord injury.

Anaphylactic shock results from a severe allergic reaction with mediator release, causing vasodilatation, increased vascular permeability, and maldistribution of circulating volume.

Common Feature of Shock

All forms of shock ultimately result in inadequate effective circulation and insufficient delivery of oxygen to tissues for cellular uptake and aerobic metabolism.

Shock in Trauma

In a shocked trauma patient, hypovolaemic shock secondary to haemorrhage should be assumed until proven otherwise.

Obvious Haemorrhage

Obvious external haemorrhage may occur with open or compound fractures.

Digital or limb amputation may cause severe visible blood loss.

Arterial puncture wounds may also produce rapid and potentially life-threatening haemorrhage.

Hidden Haemorrhage

Closed long-bone fractures may conceal a considerable volume of blood within the surrounding tissues.

Thoracic trauma may result in blood accumulating within the pleural or thoracic cavity.

Abdominal trauma may produce significant intraperitoneal or retroperitoneal haemorrhage.

Closed pelvic fractures can cause massive concealed haemorrhage within the pelvis and retroperitoneum.

Penetrating Wounds

Penetrating wounds involving the neck or mediastinum should be treated with a high index of suspicion.

These injuries may damage major blood vessels or penetrate the heart, potentially producing severe haemorrhage, cardiac tamponade, or cardiogenic shock.

Clinical Assessment of Shock

Clinical assessment of shock should be systematic and include inspection, auscultation, palpation, and bedside monitoring.

Inspection

Peripheral or central cyanosis may indicate inadequate oxygenation or poor tissue perfusion.

A shocked patient may appear cold and clammy because sympathetic activation causes peripheral vasoconstriction and reduced skin perfusion.

Distended jugular veins may suggest an obstructive or cardiogenic cause of shock, such as cardiac tamponade.

Visible trauma should be assessed for evidence of active or previous haemorrhage.

Respiratory rate should be assessed. A normal adult respiratory rate is approximately 12–20 breaths per minute, and tachypnoea may be an early feature of shock.

Confusion, agitation, aggression, drowsiness, or coma may develop as a result of reduced cerebral perfusion or hypoxia.

The jugular venous pressure may provide additional information, although it may be difficult to assess reliably during the rapid evaluation of a trauma patient.

Auscultation

Muffled heart sounds may suggest cardiac tamponade in the appropriate clinical setting.

Pulse Assessment

The pulse should be assessed for rate, rhythm, and volume.

A normal resting adult pulse is approximately 60–100 beats per minute.

The pulse may be bounding, weak or thready, irregular, or absent depending on the patient’s condition.

If a radial pulse cannot be palpated, the carotid and femoral pulses should be assessed.

If no central pulse is present, cardiac arrest should be recognised and appropriate resuscitation commenced immediately.

Capillary Refill Time

Capillary refill time provides a rapid estimate of peripheral perfusion.

Pressure may be applied to the sternum or another appropriate site until the area blanches.

Normal colour should generally return within approximately 2 seconds.

A prolonged capillary refill time may suggest impaired peripheral perfusion and shock.

Bedside Investigations and Monitoring

Blood pressure should be measured and monitored.

Oxygen saturation should be assessed using pulse oximetry.

Continuous cardiac monitoring and an ECG rhythm trace should be obtained where appropriate.

Urine output should be monitored as an important marker of organ perfusion, usually after urinary catheterisation when appropriate during the subsequent trauma assessment.

Estimation of Blood Loss

The clinical findings of pulse, blood pressure, respiratory rate, mental status, and urine output can be used together to estimate the severity of haemorrhagic shock.

Traditional haemorrhagic shock classifications are based on an average 70-kg adult with an estimated circulating blood volume of approximately 5 litres.

Initial Management of Shock

In trauma, shock should initially be treated as haemorrhagic hypovolaemia until another cause has been established.

Management focuses on restoring effective circulation while identifying and controlling the source of bleeding.

Intravenous Access

Two large-bore peripheral intravenous cannulae should be inserted, preferably into the antecubital veins.

Large-bore access, such as 14–16G cannulae, allows rapid administration of fluids and blood products.

If antecubital access cannot be obtained, other accessible peripheral veins should be cannulated using the largest practical bore.

If peripheral venous access is unsuccessful, alternative access such as intraosseous access or central venous access may be required depending on the patient’s age, condition, and available expertise.

A surgical venous cut-down involves direct surgical exposure and cannulation of a vein, traditionally the great saphenous vein, although this is now much less commonly required.

Intraosseous access can provide rapid vascular access in both children and adults when conventional intravenous access cannot be established promptly.

Central venous access using a large-bore catheter or the Seldinger technique may be used by experienced clinicians when indicated.

Initial Fluid Resuscitation

Initial fluid resuscitation should use warmed fluids when appropriate, while avoiding unnecessary large-volume crystalloid administration in actively bleeding trauma patients.

Fluid or blood products may be administered rapidly using pressure-assisted systems when clinically indicated.

Balanced crystalloid solutions such as Hartmann’s solution, also known as Ringer’s lactate, may be used when crystalloid resuscitation is required.

Seldinger Technique

The Seldinger technique is used to insert a catheter into a blood vessel.

A needle is inserted into the desired vessel, and a guidewire is passed through the needle.

The needle is then removed while the guidewire remains in place.

A dilator and catheter are subsequently passed over the guidewire into the vessel, after which the wire is removed and the catheter is secured.

Blood Sampling During Cannulation

Blood should ideally be collected when intravenous access is obtained and before large-volume fluid administration.

A sample should be sent for group and save or group and cross-match, depending on the severity of bleeding and anticipated transfusion requirements.

A full blood count should be obtained to provide baseline haemoglobin, haematocrit, platelet count, and other haematological information.

Urea, electrolytes, and creatinine should be measured as baseline investigations.

Blood glucose should also be checked, either using a bedside glucose meter or laboratory testing.

Additional serum samples may be stored if further investigations are likely to be required.

Adjunctive Measures

Adequate oxygenation and ventilation must be ensured because restoring circulation alone will not correct tissue hypoxia if oxygenation remains inadequate.

Supplemental oxygen should be provided when indicated, and airway protection with intubation may be necessary in severely injured or unconscious patients.

External haemorrhage should be controlled promptly using direct pressure over the bleeding site.

Elevation of an injured limb may occasionally help reduce venous bleeding where appropriate, although direct pressure and definitive haemorrhage control remain more important.

Fluids and Blood Products

Hartmann’s solution or Ringer’s lactate is a balanced crystalloid that may be used for volume replacement.

Other crystalloids, such as normal saline, are also available, although large-volume administration may have disadvantages.

Colloid solutions have historically been used for intravascular volume expansion, but they have a limited role in modern trauma resuscitation.

Blood products provide both circulating volume and, in the case of red blood cells, oxygen-carrying capacity.

Indications for Blood Transfusion

Blood products are indicated when there is significant or ongoing haemorrhage, particularly when the patient shows evidence of severe haemorrhagic shock.

Patients with substantial blood loss may require activation of a major haemorrhage or massive transfusion protocol.

Emergency Blood

When blood is required immediately and the patient’s blood group is unknown, group O red blood cells may be used.

Group O negative red cells are traditionally regarded as universal donor red cells and are commonly prioritised for certain patients, although institutional emergency transfusion protocols may also use group O positive blood in selected circumstances.

Emergency uncross-matched blood can be given without waiting for full compatibility testing when life-threatening haemorrhage is present.

Type-Specific Blood

Type-specific blood can usually be provided once the patient’s ABO and Rh blood group has been determined.

This blood is matched to the recipient’s major blood group but may be issued before full cross-matching is complete when urgent transfusion is required.

Fully Cross-Matched Blood

Fully cross-matched blood undergoes ABO typing, antibody screening, and compatibility testing to maximise compatibility with the recipient.

A patient blood sample must be sent to the laboratory before fully cross-matched blood can be prepared.

Definitive Treatment of Shock

Once initial resuscitation has begun, management should focus on identifying and treating the specific underlying cause of shock.

In haemorrhagic shock, definitive haemorrhage control may require surgery, interventional radiology, endoscopy, fracture stabilisation, or other targeted treatment.

Cardiac Tamponade

Cardiac tamponade is a life-threatening circulatory problem that must be recognised during the primary survey.

It occurs when blood or other fluid accumulates within the pericardial sac and exerts pressure on the heart.

This pressure interferes with diastolic filling, reduces stroke volume, and may result in obstructive shock and cardiovascular collapse.

Traumatic cardiac tamponade most commonly follows penetrating or blunt cardiac injury.

Recognition of Cardiac Tamponade

Beck’s triad consists of hypotension, muffled heart sounds, and raised jugular venous pressure.

These classical findings may not all be present in a trauma patient, particularly in the presence of significant blood loss.

Bedside ultrasound, particularly the FAST or eFAST examination, can rapidly identify pericardial fluid in an unstable trauma patient.

Kussmaul’s Sign

Kussmaul’s sign refers to a paradoxical rise or failure of the jugular venous pressure to fall during inspiration.

Although it may occur in disorders that impair right ventricular filling, it is not a reliable classical sign of acute traumatic cardiac tamponade.

Management of Cardiac Tamponade

Management begins with the ABCDE approach and simultaneous resuscitation.

Definitive treatment requires urgent relief of pericardial pressure and control of the underlying cardiac injury.

Pericardiocentesis may be used as a temporary emergency measure in selected situations when definitive surgical treatment is not immediately available.

In traumatic tamponade, emergency thoracotomy or operative pericardial decompression may be required, particularly when penetrating cardiac injury is suspected.

Emergency Department Thoracotomy

Emergency department thoracotomy may be considered in selected patients with penetrating thoracic trauma who initially had signs of life and then deteriorate into profound shock or cardiac arrest.

It may also be used in exceptional circumstances to control catastrophic intrathoracic haemorrhage, relieve cardiac tamponade, perform open cardiac massage, or temporarily cross-clamp the descending thoracic aorta.

The procedure should only be undertaken in appropriately selected patients by teams with the necessary trauma and surgical expertise.

Situations Where Emergency Thoracotomy Is Unlikely to Be Beneficial

Emergency thoracotomy has a very poor outcome after prolonged cardiac arrest without signs of life.

Outcomes are particularly poor following severe blunt trauma with prolonged absence of vital signs.

The decision depends on the mechanism of injury, duration of resuscitation, presence or absence of signs of life, available expertise, and local trauma protocols.

Surgery - Disability

Immediate Neurological Assessment

Neurological status should initially be assessed rapidly using the AVPU system, followed by a more definitive assessment using the Glasgow Coma Scale (GCS).

AVPU System

A – Alert: The patient is spontaneously alert and responsive. This is approximately equivalent to a GCS of 14–15.

V – Voice: The patient responds to verbal stimuli. This is approximately equivalent to a GCS of 9–10.

P – Pain: The patient responds only to painful stimuli. This is approximately equivalent to a GCS of 7–8.

U – Unresponsive: The patient does not respond to verbal or painful stimuli. This may correspond to a GCS as low as 3.

Glasgow Coma Scale

The Glasgow Coma Scale (GCS) provides a more detailed assessment of the patient’s level of consciousness.

It consists of three components: eye response, verbal response, and motor response.

The patient’s best response in each category is recorded, giving a maximum total score of 15.

Best Eye Response

No eye opening – 1 point.

Eye opening to painful stimuli – 2 points.

Eye opening to verbal stimuli – 3 points.

Spontaneous eye opening – 4 points.

Best Verbal Response

No verbal response – 1 point.

Incomprehensible sounds or noises – 2 points.

Inappropriate words – 3 points.

Confused conversation – 4 points.

Orientated and lucid response – 5 points.

Best Motor Response

No motor response – 1 point.

Abnormal extension to pain (decerebrate response) – 2 points.

Abnormal flexion to pain (decorticate response) – 3 points.

Withdrawal from pain – 4 points.

Localising to pain – 5 points.

Following commands – 6 points.

Highest GCS Score

The highest possible GCS score is 15.

A patient with a GCS of 15 is fully alert, awake, orientated, and appropriately responsive.

Lowest GCS Score

The lowest possible GCS score is 3, not zero.

A patient with a GCS of 3 is deeply unconscious and demonstrates no eye, verbal, or motor response.

GCS and Intubation

A GCS of 8 or less indicates severe impairment of consciousness and should prompt assessment of the patient’s ability to protect their airway.

In trauma, the traditional principle is “GCS 8, intubate,” although the decision to intubate should also take into account the patient’s airway, ventilation, oxygenation, clinical trajectory, and other injuries.

Reassessment of GCS in Trauma

The GCS should be reassessed frequently in a trauma patient, traditionally every 15 minutes during the acute phase.

Every GCS assessment should be clearly documented so that any improvement or deterioration in neurological status can be identified.

Surgery - Exposure

Patient Exposure

The patient should be fully exposed from head to toe so that injuries anywhere on the body can be identified. Clothing may need to be removed using shears when necessary.

Full exposure is important because visual clues may reveal otherwise unsuspected injuries. For example, seatbelt marks may indicate significant underlying chest or abdominal trauma, including possible sternal injury.

Log-Roll

Following exposure, a log-roll should be performed when indicated. The patient is rolled onto their side while maintaining spinal alignment and immobilisation throughout the manoeuvre.

A coordinated team is required to perform the log-roll safely, traditionally involving up to five people, particularly when spinal injury is suspected.

Assessment During Log-Roll

During the log-roll, the back, buttocks, posterior thighs, posterior legs, and spine should be carefully examined.

The spine should be assessed for deformity, focal tenderness, bruising or ecchymosis, wounds, and other evidence of injury.

A digital rectal examination (DRE) may be performed when clinically indicated, particularly when pelvic, rectal, urethral, or spinal injury is suspected.

Digital Rectal Examination

Anal tone may be assessed during DRE. Reduced anal tone can occur with spinal cord or neurological injury.

The examination should assess for blood, which may indicate anorectal or pelvic trauma.

The prostate may be assessed in male patients. A high-riding or non-palpable prostate has traditionally been associated with urethral injury.

Palpable bony fragments or spicules may suggest an associated pelvic fracture.

Prevention of Hypothermia

Hypothermia must be avoided once the patient has been exposed.

Following examination and log-roll, the patient should be covered and appropriately insulated as soon as possible while still allowing access for continued assessment and treatment.

Core Body Temperature

Core body temperature should be monitored using an appropriate core-temperature measurement method. Rectal temperature is one method of assessing core temperature, although other core sites may be used depending on the clinical situation.

Raising Core Temperature in Hypothermia

In mild hypothermia, external warming can be provided using forced-air warming devices such as Bair Hugger® systems, together with blankets and appropriate covering.

Warmed intravenous fluids may be administered to prevent further heat loss and assist rewarming when fluid resuscitation is required.

In more significant hypothermia, active internal rewarming techniques may be considered depending on severity and available expertise.

These techniques can include warmed lavage or irrigation through appropriate routes, such as gastric, bladder, peritoneal, or other body cavities, although their use depends on the clinical circumstances and current trauma protocols.

Medicine – Primary Hyperlipidaemia Disorders

Primary hyperlipidaemias are inherited disorders of lipoprotein metabolism that cause abnormal elevation of LDL cholesterol, triglycerides, or both. They are important because they can lead to premature atherosclerotic cardiovascular disease, pancreatitis, or characteristic lipid deposits such as xanthomas.

The major disorders in the original notes are familial hypercholesterolaemia, familial hypertriglyceridaemia, lipoprotein lipase deficiency, and familial combined hyperlipidaemia.

1. Familial Hypercholesterolaemia

Familial hypercholesterolaemia – FH is an inherited disorder characterised by markedly elevated:

LDL cholesterol.

The classic form is usually inherited in an:

Autosomal dominant pattern.

2. Genetic Basis of Familial Hypercholesterolaemia

Most classical cases are caused by pathogenic variants affecting the:

LDL receptor – LDLR.

Other genes can also produce a similar phenotype, including:

APOB

and

PCSK9.

The underlying problem is impaired removal of LDL particles from the circulation.

3. LDL Receptor Defect

Normally LDL particles bind to:

LDL receptors on hepatocytes

and are removed from the blood.

When LDL receptor function is reduced:

LDL clearance falls.

Therefore LDL remains in the circulation for longer.

This leads to:

Markedly elevated plasma LDL cholesterol.

So the original statement that the LDL half-life is prolonged is broadly correct.

4. Heterozygous Familial Hypercholesterolaemia

A person with one affected allele typically has:

Heterozygous familial hypercholesterolaemia – HeFH.

The original prevalence of:

About 1 in 500

is an older traditional estimate.

Modern population studies suggest HeFH is more common, approximately:

Around 1 in 200–300 people, though prevalence varies between populations.

5. Cholesterol Levels in Heterozygous FH

The original notes give total cholesterol of:

9–15 mmol/L.

Patients with HeFH can indeed have very high cholesterol, but a fixed range is not required for diagnosis.

More important is:

Markedly elevated LDL cholesterol, especially from a young age, together with family history or physical signs.

6. Cardiovascular Risk in Heterozygous FH

Untreated HeFH greatly increases the risk of:

Premature atherosclerotic cardiovascular disease.

This includes:

Coronary artery disease.

Myocardial infarction.

The exact relative risk varies, so the older statement of a universal:

“six- to eightfold increase”

should be regarded as an approximate historical teaching point rather than a fixed figure.

7. Tendon Xanthomas

One of the most characteristic clinical signs of FH is:

Tendon xanthomas.

These are cholesterol deposits within tendons, especially:

Achilles tendons.

Extensor tendons of the hands.

They strongly suggest:

Familial hypercholesterolaemia.

8. Xanthelasma

Xanthelasma refers to yellow cholesterol-rich plaques around the eyelids.

It may occur in FH, but it is:

Less specific than tendon xanthomas.

Xanthelasma can also occur in people without severe inherited hypercholesterolaemia.

9. Corneal Arcus

Another possible feature is:

Corneal arcus.

In older adults this can be physiological, but in a young person it may support the presence of:

Severe hypercholesterolaemia.

10. Homozygous Familial Hypercholesterolaemia

Homozygous familial hypercholesterolaemia – HoFH is much rarer and far more severe.

Patients have profoundly impaired LDL receptor pathway function.

This results in extremely high LDL cholesterol from:

Early childhood.

11. Childhood Xanthomas

The original notes correctly describe:

Xanthomas in early childhood.

Children with HoFH can develop widespread xanthomas because cholesterol levels are extremely high from birth.

Sites may include:

Tendons.

Skin.

Pressure areas.

12. Childhood Cardiovascular Disease

Untreated HoFH can cause severe atherosclerosis very early in life.

Complications may include:

Aortic root disease.

Coronary artery disease.

Myocardial infarction during childhood or adolescence.

Therefore HoFH is a severe medical condition requiring specialist treatment.

13. Familial Hypercholesterolaemia and Atherosclerosis

The central complication of FH is accelerated:

Atherosclerosis.

Persistently high LDL penetrates the arterial wall, contributing to plaque development and progressive narrowing or plaque rupture.

This explains why reducing LDL exposure as early as possible is a major goal in FH.

14. Treatment of Familial Hypercholesterolaemia

The original notes correctly include:

Diet

and

HMG-CoA reductase inhibitors – statins.

However, modern treatment is usually more intensive than diet plus statin alone.

Lifestyle measures remain useful, but genetic FH generally cannot be adequately treated by dietary modification alone.

15. Statins

Statins inhibit:

HMG-CoA reductase

in the liver.

This reduces hepatic cholesterol synthesis and increases hepatic expression of:

LDL receptors.

Therefore:

STATIN → ↑ LDL RECEPTOR ACTIVITY → ↓ PLASMA LDL.

High-intensity statin therapy is commonly a cornerstone of treatment.

16. Additional LDL-Lowering Therapy

If LDL remains elevated despite maximally tolerated statin therapy, additional agents may include:

Ezetimibe.

PCSK9-targeted therapy.

Other LDL-lowering treatments may be used in selected severe cases.

Patients with HoFH often need specialist treatment, potentially including more intensive pharmacological strategies and occasionally:

Lipoprotein apheresis.

17. Familial Hypertriglyceridaemia

Familial hypertriglyceridaemia is an inherited tendency toward elevated:

Triglycerides, usually carried mainly in VLDL particles.

It is often described as having:

Autosomal dominant familial clustering.

However, the genetics are usually more complex than a simple single-gene dominant disorder.

18. Turbid Plasma

When triglycerides are markedly elevated, plasma may appear:

Turbid or milky.

This is caused by large numbers of triglyceride-rich lipoprotein particles.

The more severe the triglyceride elevation, the more obvious the turbidity may become.

19. Eruptive Xanthomas

Severe hypertriglyceridaemia can cause:

Eruptive xanthomas.

These are small yellow-red papules, often appearing over:

Buttocks.

Back.

Extensor surfaces.

They can appear rapidly when triglycerides are extremely elevated.

20. Hypertriglyceridaemia and Pancreatitis

A major complication of severe hypertriglyceridaemia is:

Acute pancreatitis.

Risk increases substantially when triglycerides become very high.

Therefore:

SEVERE HYPERTRIGLYCERIDAEMIA + ABDOMINAL PAIN → CONSIDER ACUTE PANCREATITIS.

21. Hepatosplenomegaly

Very severe triglyceride-rich lipoprotein accumulation can produce:

Hepatomegaly

and sometimes:

Splenomegaly.

This is especially associated with severe chylomicronaemia syndromes rather than ordinary moderate familial hypertriglyceridaemia.

22. Retinal Changes

Severe hypertriglyceridaemia may produce:

Lipemia retinalis, where retinal vessels develop a creamy appearance.

The original note lists:

Retinal vein thrombosis.

Thrombotic events can occur in various metabolic settings, but lipemia retinalis is the more classic ocular association of extreme hypertriglyceridaemia.

23. Treatment of Familial Hypertriglyceridaemia

Treatment starts with:

Dietary modification.

Weight management.

Reduction or avoidance of alcohol.

Treatment of diabetes or other secondary contributors.

For significant persistent hypertriglyceridaemia, medications such as:

Fibrates

may be used.

24. Fibrates

Fibrates activate:

PPAR-α.

This increases fatty-acid oxidation and enhances metabolism of triglyceride-rich lipoproteins.

The overall effect is:

Lower plasma triglycerides.

Therefore:

FIBRATES → PARTICULARLY USEFUL FOR HIGH TRIGLYCERIDES.

25. Lipoprotein Lipase Deficiency

Lipoprotein lipase – LPL deficiency is a rare inherited disorder causing severe impairment of triglyceride-rich lipoprotein metabolism.

It is classically inherited in an:

Autosomal recessive pattern.

26. Normal Function of Lipoprotein Lipase

LPL is located on vascular endothelial surfaces, especially in:

Adipose tissue.

Skeletal muscle.

It hydrolyses triglycerides contained in:

Chylomicrons

and

VLDL.

This releases fatty acids for uptake into tissues.

27. LPL Deficiency

When LPL activity is severely deficient:

Chylomicrons cannot be cleared normally.

Therefore chylomicrons accumulate in plasma.

The result is:

Severe hypertriglyceridaemia.

This is part of the syndrome often termed:

Familial chylomicronaemia syndrome.

28. Clinical Features of LPL Deficiency

Patients may develop symptoms from childhood, including:

Recurrent pancreatitis.

Eruptive xanthomas.

Lipemia retinalis.

Hepatosplenomegaly.

Blood or plasma may appear:

Milky or lactescent.

29. Pancreatitis in LPL Deficiency

Recurrent acute pancreatitis is one of the most important complications.

Therefore:

CHILD/YOUNG PERSON + EXTREME TRIGLYCERIDES + RECURRENT PANCREATITIS → THINK FAMILIAL CHYLOMICRONAEMIA.

30. Treatment of LPL Deficiency

Management differs from ordinary hypertriglyceridaemia.

The cornerstone is a:

Very-low-fat diet

to reduce formation of dietary chylomicrons.

Alcohol and other triglyceride-raising factors should be avoided.

Because the primary defect is severe impairment of the LPL pathway, traditional triglyceride-lowering drugs such as fibrates may have:

Limited effectiveness in true complete LPL deficiency.

This is an important distinction from ordinary familial hypertriglyceridaemia.

31. Familial Combined Hyperlipidaemia

Familial combined hyperlipidaemia – FCHL is a common inherited dyslipidaemia associated with increased production of:

ApoB-containing lipoproteins.

Affected family members may show different lipid patterns.

32. Lipid Pattern in Familial Combined Hyperlipidaemia

Patients may have:

High LDL cholesterol.

High triglycerides.

or

Both elevated cholesterol and triglycerides.

The lipid phenotype may vary over time and between relatives.

Therefore the original description of:

Elevated cholesterol and triglycerides

is broadly correct, but not every patient necessarily has both raised simultaneously.

33. ApoB in Familial Combined Hyperlipidaemia

A characteristic feature is often:

Elevated apolipoprotein B – ApoB.

This reflects an increased number of:

Atherogenic lipoprotein particles.

This contributes to the disorder’s strong association with premature cardiovascular disease.

34. Atherosclerosis in Familial Combined Hyperlipidaemia

The major clinical concern is:

Premature atherosclerosis.

Patients have increased risk of:

Coronary artery disease

and other atherosclerotic cardiovascular disease.

Unlike classic FH, tendon xanthomas are generally:

Not characteristic.

35. Familial Combined Hyperlipidaemia and Metabolic Factors

FCHL often coexists with features such as:

Obesity.

Insulin resistance.

Hypertension.

These factors may worsen the lipid phenotype and cardiovascular risk.

36. Treatment of Familial Combined Hyperlipidaemia

Treatment focuses on reducing overall cardiovascular risk.

This includes:

Diet and weight management.

Exercise.

Smoking cessation.

Management of diabetes and hypertension.

LDL-lowering therapy, often with statins.

Additional triglyceride-lowering therapy may be considered according to the lipid pattern.

37. Familial Hypercholesterolaemia – Note Form

Inheritance:

Usually autosomal dominant.

Typical defect:

LDL receptor pathway.

↓

Reduced LDL clearance.

↓

Markedly increased LDL cholesterol.

Heterozygous FH:

Commoner than old 1:500 estimate; roughly 1:200–300 in many populations.

Premature coronary disease.

Tendon xanthomas.

Xanthelasma may occur.

Premature corneal arcus may occur.

Homozygous FH:

Very rare.

Extremely high LDL from childhood.

Childhood xanthomas.

Very premature coronary and aortic atherosclerosis.

MI can occur in childhood/adolescence.

Treatment:

Lifestyle measures.

High-intensity statin.

Ezetimibe.

PCSK9-targeted therapy when needed.

Specialist therapy/apheresis in severe HoFH.

38. Familial Hypertriglyceridaemia – Note Form

Main abnormality:

Raised triglycerides, usually VLDL predominant.

Possible features when severe:

Turbid plasma.

Eruptive xanthomas.

Pancreatitis.

Lipemia retinalis.

Hepatomegaly ± splenomegaly.

Treatment:

Diet.

Weight loss where appropriate.

Avoid excess alcohol.

Control diabetes.

Fibrates for suitable patients.

39. Lipoprotein Lipase Deficiency – Note Form

Inheritance:

Autosomal recessive.

Defect:

LPL pathway failure.

↓

Failure to clear chylomicron triglyceride normally.

↓

Extreme hypertriglyceridaemia.

Clinical features:

Childhood onset.

Milky plasma.

Eruptive xanthomas.

Lipemia retinalis.

Hepatosplenomegaly.

Recurrent pancreatitis.

Treatment:

Very-low-fat diet is central.

Traditional fibrates may be relatively ineffective in complete LPL deficiency.

40. Familial Combined Hyperlipidaemia – Note Form

Lipid abnormality:

↑ LDL cholesterol.

or

↑ Triglycerides.

or

↑ Both.

Typical additional clue:

↑ ApoB.

Major complication:

Premature atherosclerotic cardiovascular disease.

Tendon xanthomas:

Generally absent, helping distinguish it from classical FH.

41. Important Corrections to the Original Notes

The traditional prevalence:

“Heterozygous FH ≈ 1 in 500”

is now considered too low.

Modern estimates are closer to:

ABOUT 1 IN 200–300, depending on the population.

The original fixed cholesterol range:

9–15 mmol/L

can occur in HeFH, but diagnosis is not based on a single universal cholesterol range. The key abnormality is:

MARKEDLY ELEVATED LDL FROM A YOUNG AGE.

The older statement of:

“six- to eightfold increased IHD risk”

captures the substantial risk but should not be treated as a fixed value for every patient.

The clinically important message is:

UNTREATED FH → MARKEDLY INCREASED PREMATURE ASCVD RISK.

For severe hypertriglyceridaemia, the classic retinal manifestation is:

LIPEMIA RETINALIS

rather than retinal vein thrombosis as the defining association.

LPL deficiency should be distinguished from ordinary familial hypertriglyceridaemia.

In true LPL deficiency:

CHYLOMICRONS ACCUMULATE MASSIVELY

and treatment is centred on:

STRICT DIETARY FAT RESTRICTION.

Familial combined hyperlipidaemia may cause raised cholesterol, triglycerides, or both—not necessarily both in every affected person.

Key Clinical Pattern

For rapid recall:

FAMILIAL HYPERCHOLESTEROLAEMIA → VERY HIGH LDL + TENDON XANTHOMAS + PREMATURE CORONARY DISEASE.

HOMOZYGOUS FH → CHILDHOOD XANTHOMAS + VERY EARLY ATHEROSCLEROSIS/MI.

FAMILIAL HYPERTRIGLYCERIDAEMIA → HIGH TG + PANCREATITIS RISK.

LPL DEFICIENCY → AR + CHYLOMICRONS + EXTREME TG + RECURRENT PANCREATITIS.

FAMILIAL COMBINED HYPERLIPIDAEMIA → ↑ LDL AND/OR ↑ TG + ↑ ApoB + PREMATURE ATHEROSCLEROSIS.

The easiest final distinction is:

TENDON XANTHOMA → THINK FAMILIAL HYPERCHOLESTEROLAEMIA.

ERUPTIVE XANTHOMA + PANCREATITIS → THINK SEVERE HYPERTRIGLYCERIDAEMIA.

Medicine – Causes of Secondary Hyperlipidaemia

Secondary hyperlipidaemia means elevated blood lipids caused by an underlying disease, medication, lifestyle factor, or physiological state rather than by a primary inherited lipid disorder.

The pattern may be predominantly:

Raised cholesterol, especially LDL cholesterol,

or

Raised triglycerides,

although mixed abnormalities are common.

⸻

1. Mainly Raised Cholesterol

Conditions that predominantly increase cholesterol include:

Hypothyroidism.

Cholestasis.

Nephrotic syndrome.

Renal transplantation.

⸻

2. Hypothyroidism

Hypothyroidism commonly causes:

Raised total cholesterol

and

Raised LDL cholesterol.

The major mechanism is reduced hepatic expression and activity of:

LDL receptors.

This decreases clearance of LDL particles from the circulation.

Therefore:

HYPOTHYROIDISM → ↓ LDL CLEARANCE → ↑ LDL CHOLESTEROL.

⸻

3. Lipid Pattern in Hypothyroidism

The typical pattern is:

↑ LDL cholesterol.

↑ Total cholesterol.

Triglycerides may also rise, especially in more severe disease, so the abnormality is not always purely hypercholesterolaemic.

⸻

4. Clinical Importance

When otherwise unexplained hypercholesterolaemia is found, particularly with symptoms such as:

Fatigue.

Weight gain.

Cold intolerance.

Constipation.

it is reasonable to consider:

Hypothyroidism.

Treating the thyroid disorder may improve the lipid profile.

⸻

5. Cholestasis

Cholestasis means impaired formation or flow of bile.

It can produce marked:

Hypercholesterolaemia.

This may occur in:

Extrahepatic biliary obstruction

or

Intrahepatic cholestatic disease.

⸻

6. Mechanism in Cholestasis

An important abnormal lipoprotein can appear in cholestasis:

Lipoprotein X – Lp-X.

This cholesterol-rich particle contributes to the marked increase in measured serum cholesterol.

Therefore:

CHOLESTASIS → Lp-X ACCUMULATION → MARKED HYPERCHOLESTEROLAEMIA.

⸻

7. Clinical Clues to Cholestasis

Associated features may include:

Jaundice.

Pruritus.

Dark urine.

Pale stools.

Raised alkaline phosphatase.

Thus a high cholesterol concentration in a jaundiced patient may reflect:

Cholestasis rather than a primary lipid disorder.

⸻

8. Nephrotic Syndrome

The original notes correctly include:

Nephrotic syndrome.

The classic nephrotic picture consists of:

Heavy proteinuria.

Hypoalbuminaemia.

Oedema.

Hyperlipidaemia.

⸻

9. Mechanism of Hyperlipidaemia in Nephrotic Syndrome

Loss of albumin in urine lowers plasma oncotic pressure and stimulates increased hepatic synthesis of proteins and lipoproteins.

At the same time, lipid clearance may also be impaired.

This produces increases in:

LDL.

VLDL.

Total cholesterol.

Triglycerides.

Therefore nephrotic syndrome may produce:

Mixed hyperlipidaemia, not only isolated hypercholesterolaemia.

⸻

10. Typical Lipid Pattern in Nephrotic Syndrome

The most striking finding is often:

Markedly raised cholesterol.

However, triglycerides can also rise.

Therefore:

NEPHROTIC SYNDROME → ↑ CHOLESTEROL ± ↑ TRIGLYCERIDES.

⸻

11. Renal Transplantation

Hyperlipidaemia is common after:

Renal transplantation.

The lipid pattern may include:

Raised total cholesterol.

Raised LDL.

Raised triglycerides.

So, again, it may be:

Mixed rather than purely cholesterol-predominant.

⸻

12. Why Renal Transplantation Causes Dyslipidaemia

Several factors contribute, including:

Immunosuppressive medications.

Persistent CKD.

Weight gain.

Diabetes.

Hypertension.

Reduced physical activity.

⸻

13. Immunosuppressive Drugs

Important transplant medications that can worsen lipid profiles include:

Corticosteroids.

Ciclosporin.

Sirolimus and related mTOR inhibitors.

Tacrolimus tends to have a less pronounced lipid effect than ciclosporin, although metabolic complications can still occur.

⸻

14. Mainly Raised Triglycerides

Conditions that predominantly increase triglycerides include:

Obesity.

Insulin resistance.

Diabetes mellitus.

Chronic alcohol excess.

Several other secondary causes can also produce hypertriglyceridaemia.

⸻

15. Obesity

Obesity, particularly:

Visceral or central obesity,

is strongly associated with:

Insulin resistance.

Insulin resistance increases release of free fatty acids from adipose tissue and promotes hepatic synthesis of:

Triglycerides and VLDL.

Therefore:

OBESITY → INSULIN RESISTANCE → ↑ VLDL → ↑ TRIGLYCERIDES.

⸻

16. Insulin Resistance

Insulin normally suppresses:

Lipolysis in adipose tissue.

With insulin resistance, this suppression becomes less effective.

More free fatty acids reach the:

Liver.

The liver uses these fatty acids to synthesise:

Triglycerides.

These are exported mainly in:

VLDL particles.

⸻

17. Metabolic Syndrome Pattern

The typical dyslipidaemia of insulin resistance includes:

Raised triglycerides.

Low HDL cholesterol.

Small dense LDL particles.

This pattern is often seen in:

Metabolic syndrome.

⸻

18. Diabetes Mellitus

Poorly controlled diabetes, especially with marked insulin deficiency or resistance, can cause:

Hypertriglyceridaemia.

The mechanism includes:

Increased lipolysis.

Increased hepatic VLDL production.

Reduced triglyceride-rich lipoprotein clearance.

⸻

19. Severe Hypertriglyceridaemia in Diabetes

Very poorly controlled diabetes can occasionally produce:

Severe hypertriglyceridaemia.

When triglycerides become extremely high, there is an increased risk of:

Acute pancreatitis.

Therefore severe triglyceride elevation should prompt assessment for:

Uncontrolled diabetes.

⸻

20. Chronic Alcohol Excess

The original notes correctly include:

Chronic alcohol excess.

Alcohol increases hepatic:

Fatty acid synthesis

and

Triglyceride production.

It can therefore increase:

VLDL secretion.

⸻

21. Alcohol and Triglycerides

The typical pattern is:

Raised triglycerides.

The rise may be particularly marked when alcohol excess occurs together with:

Obesity.

Diabetes.

High carbohydrate intake.

⸻

22. Pancreatitis Risk

Alcohol excess can therefore contribute to pancreatitis in two different ways:

Direct alcohol toxicity

and

Severe hypertriglyceridaemia.

This becomes particularly relevant when triglycerides are very high.

⸻

23. Other Important Causes of Secondary Hypertriglyceridaemia

Important additional causes include:

Pregnancy.

Chronic kidney disease.

Certain medications.

Excessive refined carbohydrate intake.

Some endocrine disorders.

⸻

24. Pregnancy

During pregnancy, especially later pregnancy, triglycerides physiologically increase because of changes in:

Oestrogen.

Insulin resistance.

Hepatic lipoprotein production.

Usually this is physiological, but in susceptible individuals triglycerides can become markedly elevated.

⸻

25. Chronic Kidney Disease

CKD commonly causes abnormalities in triglyceride-rich lipoprotein metabolism.

The typical pattern may include:

Raised triglycerides.

Reduced HDL.

LDL concentration may be normal or variably elevated.

⸻

26. Medications Causing Hypertriglyceridaemia

Drugs that may increase triglycerides include:

Corticosteroids.

Oestrogens.

Retinoids.

Some antipsychotics.

Certain HIV therapies.

Some beta-blockers.

Thiazide diuretics, particularly at higher doses.

The degree of effect varies considerably between patients and agents.

⸻

27. Mixed Secondary Hyperlipidaemia

Many secondary causes do not fit neatly into a single “cholesterol” or “triglyceride” category.

Examples include:

Nephrotic syndrome.

Renal transplantation.

Diabetes.

CKD.

These can produce:

Mixed dyslipidaemia.

Therefore the original classification is useful for memorisation but should not be considered absolute.

⸻

28. Mainly Raised Cholesterol – Note Form

Hypothyroidism:

↓ LDL receptor activity.

↓

↓ LDL clearance.

↓

↑ LDL cholesterol.

⸻

Cholestasis:

Lipoprotein X accumulation.

↓

Marked hypercholesterolaemia.

⸻

Nephrotic syndrome:

↑ Hepatic lipoprotein synthesis + impaired clearance.

↓

↑ Cholesterol ± ↑ triglycerides.

⸻

Renal transplantation:

Immunosuppressive drugs + metabolic factors.

↓

Often mixed dyslipidaemia.

⸻

29. Mainly Raised Triglycerides – Note Form

Obesity:

Insulin resistance.

↓

↑ Free fatty acids.

↓

↑ Hepatic VLDL.

↓

↑ Triglycerides.

⸻

Diabetes mellitus:

Insulin resistance or deficiency.

↓

↑ VLDL production + impaired clearance.

↓

↑ Triglycerides.

⸻

Chronic alcohol excess:

↑ Hepatic triglyceride synthesis.

↓

↑ VLDL.

↓

↑ Triglycerides.

⸻

30. Important Corrections and Clarifications

The original division into:

“mainly raised cholesterol”

and

“mainly raised triglycerides”

is useful for revision, but many secondary causes produce overlapping abnormalities.

⸻

Nephrotic syndrome often produces:

BOTH HIGH CHOLESTEROL AND HIGH TRIGLYCERIDES, although cholesterol may be especially prominent.

⸻

Renal transplantation can also produce:

MIXED DYSLIPIDAEMIA, rather than isolated hypercholesterolaemia.

⸻

Diabetes particularly raises triglycerides when metabolic control is poor, and it often produces the characteristic insulin-resistant pattern of:

↑ TG + ↓ HDL + SMALL DENSE LDL.

⸻

Key Clinical Pattern

For rapid recall:

HYPOTHYROIDISM → ↑ LDL CHOLESTEROL.

CHOLESTASIS → ↑ CHOLESTEROL, OFTEN VIA LIPOPROTEIN X.

NEPHROTIC SYNDROME → ↑ CHOLESTEROL ± ↑ TRIGLYCERIDES.

RENAL TRANSPLANT → MIXED DYSLIPIDAEMIA, OFTEN DRUG-RELATED.

OBESITY / INSULIN RESISTANCE / DIABETES → ↑ TRIGLYCERIDES.

ALCOHOL EXCESS → ↑ TRIGLYCERIDES.

A useful final distinction is:

CHOLESTEROL-PREDOMINANT → THINK HYPOTHYROIDISM, CHOLESTASIS, NEPHROTIC SYNDROME.

TRIGLYCERIDE-PREDOMINANT → THINK INSULIN RESISTANCE, DIABETES, OBESITY, ALCOHOL.

Surgery - Secondary Survey

Objectives of the Secondary Survey

The secondary survey begins after immediate life-threatening injuries have been identified and treated.

Its purpose is to obtain a definitive history, perform a thorough examination, assimilate relevant investigations, and formulate an appropriate management plan.

The patient should be examined systematically from head to toe, including both the front and back of the body.

A thorough assessment includes examination of all relevant orifices where indicated, traditionally summarized by the phrase “fingers and tubes in every orifice.”

A detailed history of the incident should be obtained, including collateral information from witnesses, paramedics, or accompanying persons when available.

A complete medical history should also be obtained.

All directed investigations should be reviewed and incorporated into the overall clinical assessment.

The secondary survey should conclude with the formulation of a definitive management plan.

Investigations

Any investigations relevant to the patient’s injuries and clinical condition should be performed.

At the very least, a trauma imaging series should be obtained or considered as appropriate, together with basic blood investigations and an electrocardiogram (ECG).

Further investigations should be directed by the mechanism of injury, examination findings, and the patient’s clinical condition.

History

A paramedic handover should be obtained to establish the mechanism of injury, events at the scene, pre-hospital findings, and any treatment already given.

A collateral history should be obtained from witnesses or accompanying persons whenever possible.

The patient’s own history should be obtained whenever their clinical condition allows.

An AMPLE medical history should also be obtained.

A – Allergies: Any known drug, food, or other relevant allergies should be identified.

M – Medications: Current medications should be documented.

P – Past Medical History: Relevant previous medical conditions, operations, and comorbidities should be established.

L – Last Meal: The timing of the patient’s last meal or oral intake should be determined.

E – Events Leading to the Situation: The events and circumstances leading to the injury or current situation should be clarified.

Deterioration During the Secondary Survey

If there is any change or deterioration in the patient’s clinical condition during the secondary survey, assessment should immediately return to the ABCDE approach.

Any newly identified life-threatening problem should be evaluated and treated as necessary.

The secondary survey should only be resumed once the patient has been sufficiently stabilized.

Surgery - Pelvis

Clinical Findings Suggesting Pelvic Injury

Obvious deformity or an open injury may indicate significant pelvic trauma.

Localised pelvic pain or limb paraesthesia may suggest associated bony or neurological injury.

Signs of retroperitoneal haemorrhage include bruising of the scrotum, buttocks, or along the line of the inguinal ligament, known as Fox’s sign.

Signs of urethral injury include blood at the urethral meatus, a high-riding prostate, and an inability to void urine.

Rectal examination may reveal blood or palpable bony fragments.

Reduced anal tone may indicate associated neurological or lumbosacral injury.

Abnormal pelvic stability on clinical assessment may also suggest disruption of the pelvic ring.

Types of Pelvic Injury

External rotation of the hemipelvis occurs with disruption of the pubic symphysis and is typically associated with anteroposterior compression.

This injury pattern may be caused by a direct anteroposterior compression force.

It may also result from a direct posterior blow to the iliac spines.

Forced external rotation of the lower limb can also produce this pattern of pelvic injury.

Internal rotation of the hemipelvis is associated with compression fractures of the pubic rami and usually results from lateral compression.

This pattern is typically caused by a lateral impact producing medial compression of the pelvis.

Vertical shear injury involves fracture-dislocation of the hemipelvis with superior and posterior displacement.

It is caused by a vertical loading force that fractures the pubic rami and disrupts the sacroiliac joint, resulting in displacement of the affected hemipelvis.

Pelvic Springing

Pelvic springing is a clinical test used to assess the stability and integrity of the pelvic ring.

It involves gentle compression of the iliac wings.

The aim is to identify pelvic instability that may suggest a fracture before imaging is obtained.

Main Concern in Pelvic Fracture

The major concern in pelvic fracture is uncontrolled haemorrhage into the pelvic cavity.

The pelvis can accommodate several litres of blood, so significant haemorrhage may occur before it becomes externally apparent.

Interim Management of Unstable Pelvic Fractures

A sheet may be placed beneath the buttocks and wrapped anteriorly around the pelvis, with the ends secured to provide a basic temporary splint.

Anterior external fixation may be used by inserting two pins into the anterior border of the ilium on each side and connecting them with a rigid external frame.

Posterior external fixation may involve pin insertion along the line between the anterior superior iliac spine and posterior superior iliac spine, with the pins connected using a reduction clamp.

External fixation should be performed by an experienced orthopaedic surgeon because of the risk of iatrogenic neurovascular injury.

Surgery - Musculoskeletal

Musculoskeletal Injuries Contributing to Shock

Several musculoskeletal injuries can result in significant blood loss and contribute to haemorrhagic shock. These include arterial bleeding, pelvic fractures, large vessel puncture, limb amputation, and long bone fractures. Long bone fractures can conceal substantial amounts of blood loss. A humeral fracture may be associated with approximately 0.5–1.5 litres of blood loss, a tibial fracture with approximately 0.5–1.5 litres, and a femoral fracture with approximately 1.0–2.5 litres.

Musculoskeletal Assessment in the Secondary Survey

The primary survey and ABCs should always be addressed first. Once the patient is stable, the musculoskeletal system can be assessed systematically during the secondary survey. This includes taking a focused history and examining the patient using the principles of look, feel, and move.

History

The history should include the position of the patient when first found or on arrival, any obvious or suspected trauma, and the mechanism of injury. In road traffic accidents, important details include seatbelt use, airbag deployment, whether the patient was able to mobilise after the accident, and the direction of impact. It is also useful to determine whether the patient was found close to or away from the accident site.

An AMPLE history should be taken, including allergies, medications, past medical history, last meal, and events surrounding the injury. Previous joint or limb pathology should also be identified. Osteoporosis and osteopenia are especially important because they increase susceptibility to fractures following relatively minor trauma.

Inspection

The patient should be appropriately exposed and both sides of the body compared. Look for open fractures, which may involve exposed bone but are not always immediately obvious. Other important features include swelling, deformity, bruising, wounds, and changes in the colour of the limb distal to the injury.

Palpation

Both sides should be compared while assessing the temperature of the distal limb, the presence of crepitus, joint effusions, haemarthroses, and capillary refill time. In a conscious patient, pain and tenderness should also be assessed. Neurological integrity should be checked by assessing fine touch sensation, motor function, and sweating of the skin, or hidrosis.

Movement

Range of active movement should be assessed in a conscious patient. Passive movement may be considered in an unconscious patient where appropriate. However, an obvious or suspected fracture should not be manipulated before X-ray imaging, as this does not add significantly to the diagnosis and may worsen the injury. Joint dislocations should generally be reduced as soon as clinically appropriate. Weight-bearing may be assessed as tolerated when relevant.

Investigations

Plain X-rays are the standard initial investigation for uncomplicated musculoskeletal trauma. Imaging should be selected according to the suspected site and type of injury.

Rule of Twos

The rule of twos is a useful principle when assessing fractures radiologically. Two joints should be considered, meaning the joint above and the joint below the injury should be assessed where appropriate. Two views, usually an anteroposterior and lateral view, should be obtained to assess displacement and angulation accurately. If doubt remains, the opposite side may occasionally be imaged for comparison, although this is rarely required.

Surgery - Glossary of Surgical Terminology

Abduct

Abduct means movement of an extremity away from the midline of the body.

Adduct

Adduct means movement of an extremity towards the midline of the body.

Adeno-

The prefix adeno- refers to glands or glandular tissue.

Afferent

Afferent means travelling or conducting towards a central structure.

Anastomosis

An anastomosis is a surgically created connection between two tubular structures, such as two segments of bowel or two blood vessels.

Angio-

The prefix angio- refers to blood vessels.

Anomalous

Anomalous means deviating from what is considered normal or expected.

Aseptic

Aseptic refers to the complete absence of disease-causing microorganisms or to measures used to prevent microbial contamination.

Atelectasis

Atelectasis refers to collapse of the alveoli, resulting in partial or complete loss of lung volume in the affected area.

Atresia

Atresia is the congenital absence or abnormal narrowing of a normal opening or lumen. The adjective is atretic.

Biopsy

A biopsy is a sample of tissue obtained from the body and sent for histopathological examination to establish a diagnosis.

Cachexia

Cachexia is generalized wasting and loss of body mass associated with chronic disease or malignancy. A patient affected by this condition may be described as cachectic.

Calculus

A calculus is a stone or solid concretion formed within the body, such as a renal or biliary calculus.

Calor

Calor is one of the classic signs of inflammation and refers to increased warmth in the affected area.

Caseation

Caseation is the breakdown of diseased tissue into a soft, cheese-like material. The adjective is caseous.

Caudal

Caudal means relating to or directed towards the lower part of the body.

Cephal-

The prefix cephal- refers to the head.

Cicatrix

A cicatrix is a scar formed after healing of damaged tissue.

Colic

Colic is pain that occurs in waves, usually due to contraction or obstruction of a hollow or tubular organ.

Curettage

Curettage is the scraping of the internal surface of an organ or body cavity using a spoon-shaped surgical instrument known as a curette.

Cyst

A cyst is an abnormal sac lined by epithelium and containing fluid or semi-solid material.

Diaphoresis

Diaphoresis refers to excessive or profuse sweating.

Diverticulum

A diverticulum is a small sac or pouch projecting from the wall of a hollow organ. A true diverticulum contains all the layers of the parent organ, as in Meckel’s diverticulum. A pseudodiverticulum contains only some of the normal wall layers, as commonly seen in diverticular disease of the colon.

Dolor

Dolor is one of the classic signs of inflammation and refers to pain.

Dysphagia

Dysphagia means difficulty swallowing. It should be distinguished from odynophagia, which means painful swallowing.

Ecchymosis

Ecchymosis refers to bruising caused by bleeding into the tissues beneath the skin.

-ectomy

The suffix -ectomy means surgical removal of an organ or structure. For example, parotidectomy is surgical removal of the parotid gland.

Epistaxis

Epistaxis means bleeding from the nose, commonly referred to as a nosebleed.

Excision Biopsy

An excision biopsy is a biopsy in which the entire lesion or tumour is removed for histopathological examination.

Fistula

A fistula is an abnormal epithelialized communication between two epithelial surfaces, organs, or body cavities.

Frequency

Urinary frequency refers to abnormally frequent urination.

Functio Laesa

Functio laesa is one of the classic signs of inflammation and refers to loss or impairment of function.

Haemangioma

A haemangioma is a benign tumour or proliferation of blood vessels.

Haematemesis

Haematemesis means vomiting of blood, usually indicating bleeding from the upper gastrointestinal tract.

Haematoma

A haematoma is a localized collection of blood within tissues that forms a swelling or mass. It may resolve spontaneously or may become secondarily infected.

Haematuria

Haematuria refers to the presence of blood in the urine.

Haemoptysis

Haemoptysis refers to coughing up blood originating from the respiratory tract.

Haemothorax

A haemothorax is the accumulation of blood within the pleural space.

Hesitancy

Urinary hesitancy refers to difficulty in initiating the flow of urine.

Icterus

Icterus is another term for jaundice, characterized by yellow discoloration of the skin, sclerae, and mucous membranes due to elevated bilirubin levels.

Incisional Biopsy

An incisional biopsy is a biopsy in which only part of a lesion or tumour is removed for histopathological examination rather than removing the entire lesion.

Induration

Induration refers to abnormal hardening of a tissue or organ, often caused by inflammation, infiltration, or fibrosis.

Intussusception

Intussusception occurs when one segment of the bowel telescopes into an adjacent segment of bowel, potentially causing intestinal obstruction and impairment of blood supply.

Laparoscopy

Laparoscopy is the visualization of the peritoneal cavity using a laparoscope inserted through small incisions. It uses optical technology to allow inspection and surgical procedures within the abdomen.

Laparotomy

A laparotomy is the surgical opening of the abdominal cavity through an incision.

Lumen

The lumen is the cavity or internal space within a tubular organ, such as the bowel or a blood vessel. The adjective is luminal.

Melaena

Melaena refers to black, tarry stools caused by digested blood, most commonly due to bleeding from the upper gastrointestinal tract.

Nocturia

Nocturia refers to abnormal urination during the night, typically requiring the patient to wake from sleep to pass urine.

Obstipation

Obstipation is the complete inability to pass either stool or flatus and may indicate severe intestinal obstruction.

Odynophagia

Odynophagia means painful swallowing.

Orchid-

The prefix orchid- refers to the testis or testicles.

-orrhaphy

The suffix -orrhaphy refers to surgical repair by suturing. For example, herniorrhaphy is the surgical repair of a hernia.

-ostomy

The suffix -ostomy refers to the surgical creation of an opening or stoma. For example, a colostomy is a surgically created opening of the colon onto the abdominal wall.

-otomy

The suffix -otomy refers to a surgical incision into an organ or structure. For example, a laparotomy involves making an incision into the abdominal cavity.

-pexy

The suffix -pexy refers to the surgical fixation of an organ or structure. For example, orchidopexy is surgical fixation of the testis.

Phlegmon

A phlegmon is a solid, swollen, inflamed mass of tissue. In pancreatitis, the term may be used to describe an inflammatory pancreatic mass.

Pneumaturia

Pneumaturia refers to the passage of gas or air in the urine. It may occur in conditions such as an enterovesical fistula.

Pneumothorax

A pneumothorax is the presence of air within the pleural space, which may cause partial or complete collapse of the affected lung.

Pus

Pus is a thick fluid produced during inflammation, particularly bacterial infection, and consists of inflammatory cells, microorganisms, and tissue debris. The correct adjective is purulent.

Rubor

Rubor is one of the classic signs of inflammation and refers to redness of the affected area.

Sinus

A sinus is an abnormal, blind-ending epithelialized tract that connects a deeper focus of disease to an epithelial surface.

Stenosis

Stenosis means abnormal narrowing of a lumen, passage, or opening.

Suppuration

Suppuration refers to the formation or discharge of pus.

Transection

Transection means transverse or complete division across a structure.

Volar

Volar refers to the surface of the palm of the hand or, in some anatomical contexts, the corresponding flexor surface.