General Surgery

The Concept

A wound is any break in the normal structure and continuity of a tissue. Wound healing is the body's response to that injury — a remarkably organised, overlapping cascade of cellular and biochemical events whose goal is to restore the barrier and, as far as possible, the function of the tissue. It is important to understand that these 'phases' are not separate boxes that finish one after another; they overlap continuously, and a problem in an early phase (say, ongoing infection prolonging inflammation) holds up every later phase. Understanding the sequence explains almost everything about why wounds heal well or badly.

Phase 1 — Haemostasis (immediate)

The moment a vessel is cut, it constricts to limit blood loss, and platelets stick to the exposed collagen of the damaged wall, aggregating into a platelet plug. The coagulation cascade then lays down fibrin, converting the plug into a stable clot. This clot does two jobs at once: it stops the bleeding, and it forms a temporary scaffold along which the repair cells will later migrate. Crucially, activated platelets also release growth factors (PDGF, TGF-β) that summon inflammatory cells — so haemostasis is not merely 'stopping bleeding', it is the trigger that starts the whole healing programme.

Phase 2 — Inflammation (0–3 Days)

Neutrophils arrive first, over the first day or two, to kill bacteria and clear debris. From about day 2–3 the macrophage takes over and becomes the key orchestrating cell of healing: it phagocytoses dead tissue and bacteria, and secretes the growth factors (PDGF, TGF-β, VEGF, FGF) that call in fibroblasts and drive new blood-vessel formation. This is why inflammation is a double-edged sword — too little (as in immunosuppression or steroid use) means poor debridement and weak signalling, while too much or too prolonged (as with persistent infection or a foreign body) traps the wound in this phase and prevents it moving on.

Phase 3 — Proliferation (3–21 Days)

Now the wound is rebuilt. Fibroblasts migrate in and synthesise collagen (initially the weaker type III) and ground substance. At the same time, new capillaries sprout (angiogenesis), and together the new vessels and collagen form granulation tissue — the red, granular, slightly bleeding tissue seen in an open healing wound; its redness is simply the many capillary loops, and healthy granulation is the essential bed on which a wound epithelialises or accepts a skin graft. Epithelial cells then migrate across the surface from the wound edges and any surviving skin appendages (epithelialisation), and specialised contractile fibroblasts (myofibroblasts) draw the wound edges together (contraction), shrinking the defect.

Phase 4 — Maturation / Remodelling (3 Weeks – Up to 1 Year)

The wound is now closed but weak. Over months, the disorganised type III collagen is progressively replaced by stronger, cross-linked type I collagen, and the fibres reorganise along the lines of mechanical stress. This is why a wound keeps gaining strength long after it looks healed — yet even a fully mature scar regains only about 70–80% of the original tissue's tensile strength. The scar also becomes paler and flatter as its excess capillaries regress.

Types of Wound Healing

How a wound heals depends chiefly on how much tissue is lost and whether the edges can be brought together:

The logic is simple: apposed edges (primary) have almost no gap to bridge, so healing is quick with a neat scar; an open wound (secondary) must laboriously fill a defect with granulation and pull itself closed, which takes longer and scars more.

Factors That Impair Healing — and WHY

Local factors act right at the wound:

• infection prolongs inflammation and consumes resources
• a foreign body is both a mechanical barrier and a nidus for infection
• ischaemia/poor blood supply starves the wound of the oxygen collagen synthesis needs
• tension or movement repeatedly disrupts the fragile new tissue
• a haematoma separates the edges and is an ideal culture medium
• previous irradiation damages the local fibroblasts and blood vessels.

Systemic factors act through the whole patient:

• malnutrition deprives the wound of the protein needed for collagen and of key cofactors (vitamin C for cross-linking, zinc for enzymes)
• diabetes mellitus impairs healing on several fronts (microangiopathy, poor perfusion, neutrophil dysfunction, and high glucose feeding bacteria)
• corticosteroids and immunosuppression blunt the inflammatory phase and directly suppress collagen synthesis (an effect partly reversed by vitamin A)
• smoking, anaemia, advanced age, malignancy, jaundice and uraemia all reduce the wound's capacity to repair.

Complications of Healing

Healing can go wrong by being excessive — producing a hypertrophic scar or keloid — or deficient — producing a chronic non-healing ulcer or wound dehiscence. Secondary healing across a joint can cause a disabling contracture, and a long-standing scar or chronic ulcer can rarely undergo malignant change into a Marjolin's ulcer (a slow-growing squamous cell carcinoma).

Wound strength never exceeds about 80% of the original tissue.

• Four overlapping phases: haemostasis (clot + growth factors) → inflammation (macrophage is key) → proliferation (granulation, collagen III, epithelialisation, contraction) → remodelling (collagen III→I, strength rises to ~80% over months).
• Healing types: primary (apposed, fine scar), secondary (open, granulation + contraction, more scar), tertiary (delayed primary closure).
• Collagen synthesis needs oxygen + vitamin C — explains why ischaemia, smoking, anaemia and scurvy impair healing.
• Local factors: infection, foreign body, ischaemia, tension, haematoma; systemic: malnutrition, diabetes, steroids, smoking.
• Complications: excess (keloid/hypertrophic), deficient (ulcer/dehiscence), contracture, Marjolin's ulcer.

The Concept

A surgical site infection (SSI) is an infection that develops at or near a surgical incision within 30 days of the operation (or within 90 days if a prosthesis or implant is left in place). It is one of the commonest hospital-acquired infections, and it matters because it causes pain, prolongs hospital stay, can lead to wound breakdown or incisional hernia, and occasionally progresses to life-threatening sepsis. Almost everything about preventing SSI follows from one idea: infection occurs when the load and virulence of contaminating bacteria overwhelm the patient's local defences. Every preventive measure either reduces the bacterial load or strengthens the host — so if you understand that balance, you can reason out the whole management.

How It Develops

Every surgical wound is contaminated to some degree, but infection only follows when the bacterial inoculum is large enough (classically around 10⁵ organisms per gram of tissue) or when host resistance is lowered. A foreign body or dead tissue dramatically lowers the number of bacteria needed to establish infection, because it shelters organisms from the immune system — which is why implants, sutures and devitalised tissue are such important risk factors. The infection typically declares itself around the 5th–7th postoperative day, and the commonest organism is Staphylococcus aureus.

CDC Classification (BY Depth)

The CDC classifies SSI by the anatomical depth involved, which guides how it is managed:

Surgical Wound Classification (predicts Risk)

Wounds are graded by how contaminated they are at operation — and the expected infection rate rises accordingly, because a dirtier field means a higher bacterial load:

This classification is practically useful: it tells you which operations genuinely benefit from antibiotic prophylaxis and which patients need especially careful technique.

Risk Factors

Patient factors that lower resistance include diabetes, obesity (fat is poorly perfused and prone to infection), malnutrition, smoking, immunosuppression, and any distant untreated infection. Operative factors that raise the bacterial burden or reduce local defence include prolonged surgery, poor haemostasis or rough technique, contamination, a foreign body/implant, and intra-operative hypothermia (which impairs the neutrophils that fight infection).

Prevention — the Reasoning Behind Each Step

Because SSI is a battle between bacterial load and host defence, prevention attacks both sides:

• Optimise the patient — control blood glucose, correct malnutrition and anaemia, and stop smoking; each strengthens the host's ability to resist infection.
• Remove hair by clipping, not shaving — shaving with a razor causes microscopic cuts that quickly become colonised with bacteria, so shaved patients have higher infection rates than clipped ones; this is a classic, counter-intuitive exam point.
• Skin antisepsis — a chlorhexidine or povidone-iodine prep reduces the resident skin flora before incision.
• Antibiotic prophylaxis timed within 60 minutes before incision — the aim is a high tissue drug level at the moment of incision, when contamination occurs; given too early or after the incision it is far less effective. It is a single dose (re-dosed only for long operations or major blood loss), not a prolonged course, because the goal is to cover the operative window, not to treat an established infection.
• Maintain normothermia and good oxygenation intra-operatively — neutrophil bacterial killing is an oxygen-dependent process, so a warm, well-oxygenated patient fights contamination better.

Management of an Established Ssi

The principle mirrors that of any pus collection: open and drain the wound to release the pus and reduce the bacterial load, send a specimen for culture and sensitivity, and debride any dead tissue. The wound is then managed with regular dressings to heal by secondary intention. Antibiotics are given for spreading cellulitis or systemic sepsis, guided by culture — but, as with an abscess, they are an adjunct and cannot replace drainage of a collection.

• Prophylaxis — a single IV dose of an appropriate agent (e.g. A cephalosporin; add metronidazole for colorectal surgery) within 60 minutes before incision.
• Established infection — culture-guided antibiotics; empirical anti-staphylococcal cover pending sensitivities.

Timing of prophylactic antibiotic within 60 minutes of incision matters most.

• SSI = infection at the surgical site within 30 days (90 days with an implant); commonest organism S. Aureus, usually presents day 5–7.
• Infection = bacterial load/virulence overwhelming host defence; a foreign body/dead tissue lowers the inoculum needed.
• CDC depth: superficial incisional / deep incisional / organ-space. Wound classes clean→dirty predict rising risk.
• Prevent by attacking both sides: optimise patient (glucose, nutrition, smoking); clip don't shave; skin antisepsis; prophylactic antibiotic within 60 min; normothermia/oxygenation.
• Treat established SSI by opening/draining + culture-guided antibiotics; antibiotics can't replace drainage.

WHY These Are Feared

Both conditions are rapidly progressive, life-threatening soft-tissue infections that can kill within hours to days. The single most important lesson is that the visible skin changes badly underestimate the true extent of the disease underneath — so the surgeon who waits for obvious skin necrosis before operating is already too late. The governing principle is 'time is tissue': survival depends on recognising the infection early and taking the patient to theatre for radical surgery, because antibiotics alone cannot reach or remove dead, avascular tissue.

Necrotising Fasciitis — the Mechanism

Necrotising fasciitis is infection that spreads along the fascial planes — a relatively avascular, low-resistance layer that offers little barrier, so the infection races along it far faster than the overlying skin reveals. As it spreads, it thromboses the small perforating vessels that supply the skin from below; the skin, cut off from its blood supply, becomes dusky, then blisters (haemorrhagic bullae) and finally necroses. This also explains the hallmark early sign — pain out of all proportion to the visible findings — because the disease under the surface is far more extensive than the modest redness on top.

It is usefully divided by microbiology: Type I is polymicrobial (a synergistic mix of aerobes and anaerobes, typically in diabetics and the elderly, where the enzymes of one organism assist another), while Type II is monomicrobial, classically due to Group A Streptococcus (Streptococcus pyogenes). Fournier's gangrene is the name given to necrotising fasciitis of the perineum and scrotum.

Clinical Features

• Severe pain out of proportion to the visible signs — the earliest and most valuable clue.
• Oedema spreading beyond the margin of erythema, dusky discoloured skin, haemorrhagic bullae, and sometimes crepitus (gas in the tissues).
• Marked systemic toxicity — fever, tachycardia, hypotension and rapid clinical deterioration, out of keeping with the modest skin appearance.

Management — WHY Surgery, Not Antibiotics, Comes First

The definitive treatment is urgent, radical surgical debridement of all necrotic tissue, repeated as often as needed ('re-look' operations). The reason antibiotics cannot do this job is that the infected tissue is dead and thrombosed — it has no blood supply, so no drug can reach the bacteria within it; only the knife removes the source. Around this, the patient needs broad-spectrum IV antibiotics covering Gram-positives, Gram-negatives and anaerobes, with clindamycin added specifically to switch off bacterial toxin production, plus aggressive resuscitation and organ support in intensive care and correction of the underlying condition (e.g. Diabetes).

Gas Gangrene (clostridial Myonecrosis)

Gas gangrene is a fulminant infection of muscle caused by Clostridium perfringens, a spore-forming anaerobe that thrives in deep, contaminated, poorly-oxygenated wounds. Its alpha-toxin (a lecithinase) destroys cell membranes, killing muscle and releasing gas — felt as crepitus — while the toxins cause profound, often fatal, toxaemia. The wound is intensely painful, oedematous and produces a thin foul discharge, with a bronze discolouration of the overlying skin.

Treatment again rests on urgent debridement or amputation to remove the dead muscle, combined with high-dose penicillin plus clindamycin (clindamycin, again, suppresses toxin synthesis), full resuscitation, and — where available — hyperbaric oxygen, which works because these organisms are anaerobes for which oxygen is toxic.

Investigations — But Don't Delay Surgery

Necrotising fasciitis is fundamentally a clinical diagnosis, and the cardinal error is to wait for tests before operating. Investigations support but never replace judgement: markedly raised inflammatory markers (CRP, white cell count), deranged sodium and renal function, and imaging (X-ray or CT) that may show gas tracking along the fascial planes. The LRINEC score (using CRP, total leucocyte count, haemoglobin, sodium, creatinine and glucose) helps stratify risk, but a low score does not exclude the diagnosis. The definitive diagnosis is often made at operation, where the surgeon finds grey, oedematous, non-bleeding fascia that separates easily on a finger sweep, with thin 'dishwater' pus and a lack of the normal healthy resistance and bleeding of living tissue.

Differential & Prognosis

The main differentials are severe cellulitis and a simple abscess — but pain out of proportion, rapid spread, systemic toxicity and skin necrosis point firmly to a necrotising infection. Prognosis is directly tied to time: mortality rises sharply with every hour of delay to debridement, and is worse with delayed presentation, extensive disease, older age and comorbidity. After the sepsis is controlled by repeated debridements, the patient needs nutritional support and later reconstruction/skin grafting of the large tissue defects created.

• Gas gangrene — high-dose IV benzylpenicillin + clindamycin (clindamycin for its anti-toxin effect).
• Necrotising fasciitis — broad-spectrum (e.g. Piperacillin-tazobactam or a carbapenem) + clindamycin, then de-escalate by culture.

Pain out of proportion to appearance is the earliest warning sign.

• Both are surgical emergencies — the skin signs underestimate the deep extent; 'time is tissue'.
• Necrotising fasciitis spreads along avascular fascia and thromboses skin vessels → dusky skin, bullae; pain out of proportion is the early clue. Type I polymicrobial, Type II Group A Strep; Fournier's = perineum.
• Treat by urgent radical debridement (antibiotics can't reach dead, thrombosed tissue) + broad-spectrum antibiotics + clindamycin + resuscitation.
• Gas gangrene: Clostridium perfringens alpha-toxin → muscle necrosis + gas (crepitus) + toxaemia.
• Gas gangrene: debridement/amputation + penicillin + clindamycin ± hyperbaric oxygen (O₂ is toxic to the anaerobe).

The Concept

An ulcer is a break in the continuity of the covering epithelium — of skin or of a mucous membrane. Ulcers are extremely common in surgical practice, and the whole art of managing them lies in reading the ulcer to work out its cause, because the treatment of a venous ulcer, an arterial ulcer, a diabetic ulcer and a malignant ulcer are completely different. The clinical appearance — especially the edge — is not just description for its own sake; each feature is a direct clue to the underlying pathology.

Classification

Ulcers can be described in two complementary ways. Clinically, by their current behaviour — a spreading ulcer (actively enlarging, inflamed edge), a healing ulcer (with a sloping, bluish, epithelialising edge), or a callous/chronic ulcer (long-standing, indurated, making no attempt to heal). Aetiologically, by cause — venous, arterial (ischaemic), neuropathic (trophic/diabetic), pressure (decubitus), traumatic, infective (tuberculous, syphilitic), malignant (Marjolin's, squamous or basal cell carcinoma), and tropical.

Reading the Edge — the Key Skill

The edge tells you what the ulcer is doing, and therefore what is causing it:

So a punched-out ulcer on the tip of a toe with absent pulses is almost certainly ischaemic; the same punched-out ulcer on the sole of a diabetic foot, but painless and surrounded by callus, is neuropathic. The reasoning is the appeal, not rote memory.

Understanding the Common Ulcers

Venous ulcers arise from chronic venous hypertension (failing valves): the sustained high pressure damages the skin capillaries in the 'gaiter' area around the medial malleolus, producing the typical shallow, sloping-edged ulcer with surrounding pigmentation and lipodermatosclerosis. Arterial (ischaemic) ulcers come from an inadequate blood supply, so they occur at the most distal, pressure-exposed points (toes, heel), are painful and punched-out, with absent pulses. Neuropathic (diabetic) ulcers result from loss of protective sensation — the patient does not feel repeated minor trauma, so a painless, punched-out ulcer forms at pressure points on the sole, often with surrounding callus.

Marjolin's Ulcer — Never Forget It

Marjolin's ulcer is a squamous cell carcinoma arising in a chronic wound, scar or sinus — classically in an old burn scar or a long-standing ulcer. Because it grows in scar tissue that has no nerves and few lymphatics, it is characteristically painless and slow to metastasise, and its edge becomes everted. This is the single most important reason why the edge of any chronic, non-healing ulcer must be biopsied — to catch malignant change before it is missed.

Investigations

A wound swab identifies infecting organisms, but the crucial test in a chronic ulcer is biopsy of the edge to exclude malignancy. Vascular ulcers need assessment of the arterial supply with Doppler and the ankle-brachial pressure index (ABI) — this must be done before applying compression, since compressing an ischaemic limb is dangerous. Blood glucose is checked for diabetes, and X-ray looks for underlying osteomyelitis.

Management

The overriding principle is to treat the cause, alongside good local wound care — debridement of slough, appropriate dressings and control of infection. The cause-specific treatments follow directly from the pathology: compression therapy for venous ulcers (to reverse venous hypertension), revascularisation for arterial ulcers (to restore blood supply), and offloading plus tight glucose control and infection management for diabetic foot ulcers, with pressure relief and nursing care for decubitus ulcers. Once a clean, healthy granulating bed is achieved, a skin graft or flap may be used to close a large defect, supported by good nutrition.

How to Examine an Ulcer

A methodical examination is what generates the clues above. On inspection, note the site (e.g. Gaiter area suggests venous, toe tip suggests arterial, sole suggests neuropathic), size, shape, number, the all-important edge, the floor (its tissue — healthy pink granulation, or slough, or malignant tissue), and the discharge. On palpation, assess the base for induration (a hard base suggests malignancy or chronic fibrosis), tenderness, and fixity to deeper structures, and — crucially — examine the regional lymph nodes and the vascular and neurological status of the limb, since these determine both cause and management.

Pressure (decubitus) Ulcer

A pressure ulcer forms over a bony prominence (sacrum, heel, ischial tuberosity, greater trochanter) in an immobile, bedridden or unconscious patient. Sustained pressure exceeds the capillary filling pressure, cutting off the blood supply to the skin and causing ischaemic necrosis. The lesson is that prevention — regular repositioning, pressure-relieving mattresses, good nutrition and meticulous skin care — is far easier and more effective than treating an established ulcer.

Principles of Management (summary)

Identify and treat the underlying cause → Optimise host factors — nutrition, glucose, tissue perfusion → Local wound care — debride slough, dress, control infection → Biopsy the edge of any chronic ulcer to exclude malignancy → Definitive cover (skin graft/flap) once a healthy granulating bed is achieved

The edge of the ulcer usually reveals its underlying nature.

• Ulcer = break in covering epithelium; the skill is reading the ulcer to find the cause.
• Classify clinically (spreading/healing/callous) and by cause (venous, arterial, neuropathic, pressure, infective, malignant).
• Edge clues: sloping (healing/venous), punched-out (ischaemic/trophic/syphilitic), undermined (TB), everted (SCC), pearly (BCC).
• Marjolin's = SCC in a chronic scar/ulcer — painless, slow to spread; always biopsy the edge of a chronic ulcer.
• Assess vascular status (ABI before compression) and glucose; treat the cause — compression (venous), revascularisation (arterial), offloading (diabetic) — plus wound care.

The Concept

These three terms describe distinct pathological structures that students often confuse, yet the distinction is simple once you picture them. A cyst is a closed sac; a sinus is a blind-ending tract with one opening; and a fistula is a tract connecting two surfaces with two openings. The key to managing sinuses and fistulae is understanding why they refuse to heal — because a tract will keep discharging as long as something is driving it.

CYST

A cyst is a closed sac with a definite epithelial or endothelial lining containing fluid or semisolid material. The lining is what distinguishes a true cyst from a mere fluid collection (a pseudocyst). Cysts are either congenital — such as a dermoid (from ectoderm buried along embryonic fusion lines), a thyroglossal cyst (a midline neck swelling that classically moves with swallowing and tongue protrusion because of its attachment to the hyoid and tongue), or a branchial cyst — or acquired, such as a retention cyst (e.g. A sebaceous cyst, formed when a gland's outlet is blocked), a distension cyst, a cystic tumour, or a parasitic (hydatid) cyst.

Sinus

A sinus is a blind tract, lined by granulation tissue or epithelium, connecting a deep focus of disease to a surface — it has only one opening. The vital point is that a sinus persists because something at its deep end keeps it discharging — dead tissue, a foreign body, or chronic infection. Common examples are a pilonidal sinus (in the natal cleft, driven by ingrown hair — 'jeep-driver's disease' in hairy young men), a tuberculous sinus, chronic osteomyelitis (with a sequestrum of dead bone at the bottom), and a suture/foreign-body sinus. Treat the discharge by removing the cause at the deep end — otherwise it simply recurs.

Fistula

A fistula is an abnormal communication between two epithelial (or endothelial) surfaces — either between two hollow organs (e.g. A colovesical fistula) or between an organ and the skin (e.g. An enterocutaneous fistula, or a fistula-in-ano). It has two openings. Fistulae may be congenital (e.g. A branchial fistula) or acquired (following surgery, inflammation such as Crohn's disease, malignancy or trauma).

WHY a Sinus or Fistula Won't Heal — 'friends'

A tract heals only when the factor sustaining it is removed. The causes of persistence are captured by the mnemonic friends, and it is worth understanding each rather than merely listing them:

• F — Foreign body (including sutures, dead bone): a constant nidus for infection and discharge.
• R — Radiation: irradiated tissue has poor blood supply and cannot heal.
• I — Infection / Inflammation (e.g. Tuberculosis, Crohn's disease): ongoing inflammation keeps the tract open.
• E — Epithelialisation of the tract: once the tract lines itself with epithelium, it behaves like a permanent channel and will not close spontaneously.
• N — Neoplasm: a tumour in the tract prevents healing.
• D — Distal obstruction: if flow beyond the tract is blocked, pressure forces contents out through the fistula, keeping it patent.
• S — Steroids / immunosuppression (and high output): impair healing generally.

Investigations & Management

A sinogram or fistulogram (contrast injected into the opening), or cross-sectional imaging such as MRI for a fistula-in-ano, defines the tract and its connections before any surgery. Management then follows logically: identify and remove the perpetuating factor (foreign body, infection, distal obstruction, treat Crohn's, etc.), and excise the tract (fistulectomy or sinus excision) once the cause is controlled. A high-output fistula (> 500 mL/day, typically a proximal enterocutaneous fistula) additionally demands careful attention to fluid, electrolyte and nutritional support and protection of the surrounding skin — because losing large volumes of intestinal content is itself dangerous.

Sebaceous CYST — a Common Example

A sebaceous (epidermoid/pilar) cyst is a retention cyst that forms when the outlet of a skin gland is blocked, so keratin and sebum accumulate behind it. It presents as a smooth, spherical swelling that is tethered to the skin at a central punctum (the blocked opening) but freely mobile over the deeper tissues. It may become infected, ulcerate, or (rarely) form a fungating mass called Cock's peculiar tumour. Treatment is complete excision of the cyst wall — leaving any wall behind leads to recurrence, because the lining regenerates the cyst.

Pilonidal Sinus — a Common Example

A pilonidal sinus is a sinus in the natal cleft that contains hair, seen typically in hirsute young men ('jeep-driver's disease', because prolonged sitting and friction drive broken hairs into the skin). It presents with a discharging sinus, or with an acute pilonidal abscess. Management is to drain any abscess first, then definitively excise the sinus tract with attention to hygiene and hair removal to prevent recurrence — again illustrating the rule that the perpetuating cause (here, hair) must be dealt with.

A fistula has two openings; a sinus has only one.

• Cyst = closed sac with an epithelial/endothelial lining (congenital: dermoid, thyroglossal, branchial; acquired: sebaceous, hydatid).
• Sinus = blind tract, one opening (pilonidal, TB, osteomyelitis, foreign body) — persists because of a deep nidus.
• Fistula = abnormal communication between two surfaces, two openings (congenital or acquired).
• Persistence follows friends: Foreign body, Radiation, Infection/Inflammation (Crohn's/TB), Epithelialisation, Neoplasm, Distal obstruction, Steroids.
• Image the tract (sinogram/fistulogram/MRI); remove the perpetuating cause + excise; support fluids/nutrition in high-output fistulae.

The Concept — What Shock Actually Is

Shock is a state of acute circulatory failure in which the delivery of oxygen to the tissues is inadequate to meet their metabolic needs. The single most important idea to grasp is that shock is about tissue perfusion, not blood pressure — a patient can be in established shock with a still-normal blood pressure. When cells are starved of oxygen they switch to anaerobic metabolism, producing lactic acid; if perfusion is not restored, this progresses to cell death, organ failure and, ultimately, death. Everything else follows from thinking about what determines oxygen delivery.

Oxygen delivery depends on cardiac output (heart rate × stroke volume) and the oxygen content of the blood. Stroke volume in turn depends on preload (the volume returning to the heart), contractility (the pump), and afterload (the vascular resistance). Shock arises whenever one of these fails — and that gives us a logical classification.

Classification — BY the Mechanism That Fails

Pathophysiology & Stages — WHY Early Shock Hides

Understanding the stages explains the clinical signs. In the compensated stage, baroreceptors detect the falling pressure and trigger a sympathetic response: the heart speeds up (tachycardia) and the peripheral vessels constrict to divert blood to vital organs. This is why an early-shock patient is tachycardic with cool, clammy skin, a prolonged capillary refill and reduced urine output — yet a still-normal blood pressure. The body is holding the pressure up by squeezing. In the decompensated stage, these mechanisms are exhausted, so blood pressure finally falls, perfusion worsens and acidosis deepens. If this continues, the irreversible stage supervenes — widespread cell death and multi-organ failure that no longer respond to treatment.

Clinical Features

The typical picture is tachycardia, a weak thready pulse, cool/pale/mottled clammy skin, prolonged capillary refill (> 2 s), tachypnoea, oliguria and altered mental state (anxiety → confusion → drowsiness), with hypotension appearing late. One important exception is early distributive (septic or anaphylactic) shock, where widespread vasodilatation makes the patient warm, flushed and bounding ('warm shock') before they eventually become cold as it decompensates.

Management — Restore Perfusion, Treat the Cause

Resuscitation follows the ABC approach. Secure the airway and give high-flow oxygen; insert two large-bore IV cannulae (wide and short cannulae allow the fastest flow); and attach full monitoring. Then two things happen in parallel — restore the circulation and identify/treat the cause:

• Hypovolaemic/distributive shock — rapid fluid resuscitation with isotonic crystalloid boluses, reassessing after each; give blood for haemorrhage.
• Cardiogenic shock — fluids are given cautiously (the failing pump is easily overloaded); inotropes support contractility.
• Distributive/refractory shock — vasopressors (noradrenaline first-line) restore vascular tone once volume is replaced.
• Obstructive shock — relieve the obstruction (needle/tube decompression of a tension pneumothorax, pericardiocentesis for tamponade).
• Treat the cause definitively — stop the bleeding, give antibiotics and achieve source control for sepsis, adrenaline for anaphylaxis.

Response is judged not by blood pressure alone but by improving perfusion: a falling heart rate, warming peripheries, urine output above 0.5 mL/kg/hour, restored mental state and a clearing lactate.

Distinguishing the Types at the Bedside

• Although the initial resuscitation is similar, reading the clinical pattern points to the type and therefore the definitive treatment.
• Hypovolaemic shock gives cold peripheries with an obvious source of loss (bleeding, vomiting, burns) and a low CVP.
• Cardiogenic shock also has cold peripheries but with signs of a full circulation — a raised CVP/JVP, basal crackles, a gallop — because the problem is the pump, not the volume.
• Distributive (septic/anaphylactic) shock is classically warm and vasodilated early with a low CVP.
• Obstructive shock shows a high CVP with specific signs — tracheal deviation and absent breath sounds (tension pneumothorax), or muffled heart sounds (tamponade).

Complications of Prolonged Shock

If perfusion is not restored quickly, sustained tissue hypoxia damages every organ: the kidneys develop acute tubular necrosis (acute kidney injury), the lungs develop acute respiratory distress syndrome (ARDS), the gut mucosal barrier breaks down (allowing bacterial translocation and worsening sepsis), the clotting system may tip into DIC, and ultimately multi-organ dysfunction syndrome (MODS) supervenes. This cascade is precisely why early recognition and rapid restoration of perfusion — before the compensated stage fails — saves lives.

Shock is defined by inadequate perfusion, not by blood pressure alone.

• Shock = acute circulatory failure with inadequate tissue oxygen delivery; it is about perfusion, not blood pressure.
• Types (by mechanism): hypovolaemic (commonest), cardiogenic, distributive (septic/anaphylactic/neurogenic), obstructive.
• Compensated stage keeps BP normal by tachycardia + vasoconstriction → cool clammy skin, prolonged CRT, oliguria; hypotension is a late sign.
• ABC + high-flow O2 + two large-bore cannulae; restore volume (crystalloid/blood) + treat the cause; inotropes/vasopressors for cardiogenic/refractory.
• Judge response by perfusion — heart rate, urine output >0.5 mL/kg/h, mental state, lactate clearance.

Start with the Compartments — It Explains Everything

To prescribe fluids sensibly you must first know where water sits in the body, because this determines where any fluid you infuse will end up. Total body water is about 60% of body weight — roughly 42 litres in a 70 kg man. Of this, two-thirds is intracellular (ICF, ~28 L) and one-third is extracellular (ECF, ~14 L). The ECF is itself split, with three-quarters in the interstitium (~10.5 L) and only one-quarter in the plasma/intravascular space (~3.5 L). That last figure is the key: the intravascular compartment — the one that keeps the circulation going — is small, and different fluids reach it to very different degrees.

Types of Fluid — and Where Each One Goes

This is the heart of the topic. Fluids are either crystalloids or colloids:

• Isotonic crystalloids (0.9% saline, Ringer lactate/Hartmann's) — distribute throughout the whole ECF. Since only about a quarter of the ECF is intravascular, only ~25% of what you infuse stays in the circulation — so you need roughly 3 times the volume of blood lost to refill the intravascular space. These are the fluids for resuscitation and replacement.
• 5% dextrose — the glucose is quickly metabolised, leaving free water that distributes across total body water. Almost none stays intravascular, so it is useless for resuscitation; it is used to provide free water for maintenance.
• Colloids (albumin, gelatins, starches) — contain large molecules that exert oncotic pressure and so stay in the intravascular space longer, expanding plasma volume with a smaller infused volume — but they are costlier and carry specific risks (allergy; starches are now largely avoided).

The Three Purposes of Fluid Therapy

Every fluid prescription serves one of three distinct purposes, and muddling them causes errors:

Maintenance Requirements

A person at rest needs roughly 30–35 mL/kg/day of water, about 1–2 mmol/kg/day of sodium, and about 1 mmol/kg/day of potassium, plus some glucose to limit ketosis. In children the Holliday-Segar ('4-2-1') rule is used: 4 mL/kg/h for the first 10 kg, 2 mL/kg/h for the next 10 kg, and 1 mL/kg/h for each kg thereafter.

Assessing Fluid Status

Good prescribing depends on assessment. Look for dehydration (thirst, dry mucous membranes, reduced skin turgor, tachycardia, low JVP/CVP, oliguria, and in severe cases hypotension) or overload (raised JVP, oedema, basal crackles, gallop rhythm). Combine the history, a careful examination, the urine output, and where needed the CVP and biochemistry, then reassess frequently — fluid therapy is a continuous adjustment, not a single decision.

Composition of Common IV Fluids

Complications of Fluid Therapy

Fluids are drugs and can harm. Under-resuscitation leaves the patient in shock with organ hypoperfusion. Over-resuscitation causes pulmonary and peripheral oedema, and tissue oedema that impairs wound and gut healing; large volumes of 0.9% saline additionally cause a hyperchloraemic metabolic acidosis (which is why balanced solutions like Hartmann's are often preferred). The remedy is careful assessment and frequent reassessment rather than a fixed prescription.

'third-space' Losses

In major surgery, sepsis or bowel obstruction, fluid is sequestered into a non-functional 'third space' (the inflamed gut wall, peritoneal cavity or interstitium). This fluid is lost from the circulation even though it remains in the body, causing hypovolaemia that must be replaced — and it later mobilises back into the circulation during recovery, a shift that must be anticipated to avoid overload.

Total body water is two-thirds intracellular, one-third extracellular.

• Total body water ≈ 60% of weight; 2/3 intracellular, 1/3 extracellular; of the ECF only ~1/4 (≈3.5 L) is intravascular.
• Isotonic crystalloid distributes through the ECF (only ~25% stays intravascular → need ~3× volume lost); 5% dextrose spreads across all body water (useless for resuscitation); colloids stay intravascular longer.
• Resuscitate with isotonic crystalloid/blood, never 5% dextrose.
• Three purposes: maintenance (normal losses), resuscitation (restore volume), replacement (match abnormal losses).
• Maintenance ≈ 30–35 mL/kg/day water + Na 1–2 mmol/kg + K 1 mmol/kg (children: 4-2-1 rule); assess status clinically + urine output/CVP and reassess.

The Concept — WHY We Use Components

Modern practice almost never transfuses whole blood. Instead a single donation is separated into components, for two good reasons: one donation can then treat several different patients, and each patient receives only the part they actually need, avoiding the risks of the rest. Understanding what each component contains tells you exactly when to use it.

Blood Components & Their Uses

Indications — a Restrictive Approach

Because transfusion carries real risks, a restrictive threshold is used: red cells are generally given when haemoglobin falls below about 7 g/dL (a slightly higher trigger of ~8 g/dL in patients with cardiac disease), or in acute blood loss causing haemodynamic compromise. The decision rests on the patient's symptoms and physiology, not the number alone.

Grouping & Cross-matching — the Safety Step

Every transfusion must be ABO and Rhesus (Rh) compatible. Group O negative is the universal donor (no A, B or Rh antigens to react against) and is used in dire emergencies; AB positive is the universal recipient. Before a routine transfusion, the patient's serum is cross-matched against the donor cells to detect any incompatibility. The commonest cause of a fatal reaction is a clerical error — the wrong unit given to the wrong patient — which is why bedside identity checks are non-negotiable.

Transfusion Reactions — Classified BY Timing

It helps to think of reactions as immediate or delayed:

• Acute haemolytic reaction (the most dangerous) — usually ABO incompatibility from a clerical error. Recipient antibodies destroy the donor cells (intravascular haemolysis), causing fever, loin/back pain, hypotension, haemoglobinuria, DIC and acute renal failure. Stop the transfusion immediately.
• Febrile non-haemolytic reaction — recipient antibodies against donor white-cell antigens cause fever and chills; common and benign (reduced by leucodepletion).
• Allergic / urticarial — a reaction to donor plasma proteins; ranges from urticaria to anaphylaxis (classically in IgA-deficient recipients).
• TACO (transfusion-associated circulatory overload) — too much volume too fast → pulmonary oedema, especially in the elderly/cardiac patient.
• TRALI (transfusion-related acute lung injury) — donor antibodies trigger acute lung injury with hypoxia and pulmonary infiltrates.
• Delayed — delayed haemolytic reaction (days later), infection transmission (hepatitis B/C, HIV — now very rare with screening), and iron overload with repeated transfusion.

Managing a Suspected Reaction

The immediate steps are the same whatever the cause: stop the transfusion, keep the IV line open with saline, re-check the patient's and unit's identity, and resuscitate (oxygen, fluids, support blood pressure). Then treat specifically — for a severe acute haemolytic reaction, maintain urine output and manage DIC and renal failure — and report the reaction, returning the unit and a fresh sample to the blood bank for investigation.

Changes in Stored Blood (WHY Fresh Differs)

Understanding what happens to blood during storage explains several transfusion complications. Over its storage life, red cells progressively leak potassium (so stored blood is potassium-rich), 2,3-DPG falls (temporarily reducing oxygen offloading), platelets and clotting factors degrade (so stored blood does not correct coagulopathy), the blood becomes acidic and cold, and microaggregates form. These changes underlie the complications of massive transfusion.

Autologous Transfusion

A patient can sometimes receive their own blood — collected pre-operatively (predeposit), salvaged and returned during surgery ('cell salvage'), or by haemodilution. This eliminates the risks of incompatibility and transmitted infection, which is its main appeal, though it is not suitable in cancer or infected fields.

Principles of Safe Transfusion

Because the deadliest reactions come from giving the wrong blood to the wrong patient (a clerical error), safety rests on rigorous checks: correct sample labelling at the bedside, formal group-and-cross-match, and a final bedside identity check of patient and unit by two people before starting. The transfusion is observed closely, especially in the first 15 minutes when severe reactions declare themselves.

Most fatal reactions arise from clerical error, not immunology.

• Component therapy: one donation treats several patients, each getting only what they need.
• Packed cells (anaemia, 1 unit ≈ +1 g/dL Hb), FFP (clotting factors), platelets (thrombocytopenia + bleeding), cryoprecipitate (fibrinogen).
• Restrictive trigger ≈ Hb <7 g/dL (<8 in cardiac disease); O-negative = universal donor, AB-positive = universal recipient; always cross-match.
• Acute haemolytic reaction (ABO incompatibility, usually clerical error) is the most dangerous — fever, loin pain, haemoglobinuria, DIC, renal failure; stop the transfusion.
• Also: febrile non-haemolytic, allergic/anaphylaxis, TACO (overload), TRALI (lung injury), infection. First step for any reaction = stop transfusion, saline, recheck identity, resuscitate, report.

The Concept

Haemorrhage is the escape of blood from the circulation. It matters in surgery both as an emergency in its own right and as the commonest cause of hypovolaemic shock. Classifying a haemorrhage — by its source, its timing and the amount lost — is not academic: each classification directly guides how urgently and how you must act.

Classification BY Source

• Arterial — bright red blood spurting in pulsatile jets (high pressure).
• Venous — darker blood welling out in a steady flow.
• Capillary — a generalised ooze from raw surfaces.

Classification BY Timing — a High-yield Idea

The timing of bleeding after an injury or operation points to its cause, which is why this classification is so useful:

• Primary haemorrhage — occurs at the time of injury or surgery.
• Reactionary haemorrhage — occurs within 24 hours, typically as the blood pressure recovers after resuscitation and dislodges a clot, or a ligature slips.
• Secondary haemorrhage — occurs 7–14 days later, when infection erodes a vessel wall. Recognising this mechanism explains its delayed timing and its association with sepsis.

Classes of Haemorrhagic Shock (atls)

The ATLS system grades acute blood loss by physiology, and reading it carefully teaches an important point about compensation:

Management — 'stop the Bleeding, Restore the Volume'

The two priorities run together. Control the bleeding by direct pressure and elevation, a tourniquet for a limb, definitive surgery, or interventional radiology (embolisation). Simultaneously, restore circulating volume through two large-bore cannulae — initially with warmed isotonic crystalloid, then blood for significant loss. In major trauma, modern practice uses damage-control resuscitation: permissive hypotension (accepting a lower blood pressure until surgical control, so as not to 'pop the clot'), a massive transfusion protocol giving red cells, FFP and platelets in a balanced ~1:1:1 ratio, and tranexamic acid early. Throughout, one aims to avoid the 'lethal triad' of hypothermia, acidosis and coagulopathy, which reinforce one another and make bleeding impossible to stop.

Methods of Arresting Haemorrhage

Bleeding is stopped by natural and artificial means. The body's own response is vessel retraction and constriction, then platelet plug and clot formation. Surgically, control is achieved by direct pressure and elevation first, then definitive measures — ligation or clipping of the vessel, diathermy (electrocautery), suture, topical haemostatic agents, a tourniquet for a limb, or angiographic embolisation by interventional radiology. Choosing the method depends on the vessel and the situation.

Concealed (internal) Haemorrhage

Not all serious bleeding is visible. Concealed haemorrhage into the chest, abdomen, pelvis or around a long-bone fracture can rapidly cause shock with no external blood loss — so in a shocked trauma patient one must actively look for hidden bleeding (e.g. With fast ultrasound of the abdomen). This is why the shocked patient with no obvious wound still needs a systematic search for the source.

Assessing Blood Loss

Blood loss is estimated from the physiological response (the ATLS class — heart rate, pulse pressure, mental state and urine output), rather than from the visible blood alone, because young patients compensate so well that a large loss may be masked until sudden collapse.

Reactionary VS Secondary — the Mechanism Matters

It is worth dwelling on why the timing tells you the cause. Reactionary bleeding appears within hours because the event that caused it is mechanical — as the patient warms and the blood pressure is restored by resuscitation, a small vessel that had gone into spasm reopens, a clot is washed away, or a ligature slips. Secondary bleeding appears a week or two later because the cause is biological — infection in the wound gradually erodes the wall of a vessel until it gives way. So the same symptom (bleeding) at different times demands different thinking: re-explore and secure the vessel for reactionary bleeding; control infection and often ligate the vessel more proximally for secondary bleeding.

Blood pressure falls late — tachycardia comes first.

• Haemorrhage = escape of blood from the circulation; classify by source, timing and amount.
• By source: arterial (bright, spurting), venous (dark, steady), capillary (ooze).
• By timing: primary (at injury), reactionary (<24 h, clot dislodges/ligature slips), secondary (7–14 d, infection erodes vessel).
• ATLS classes I–IV by % loss; pulse pressure narrows in Class II before systolic falls in Class III — hypotension is late.
• Stop the bleeding (pressure/tourniquet/surgery/embolisation) + restore volume (crystalloid then blood); trauma → permissive hypotension, 1:1:1 massive transfusion, tranexamic acid, avoid the lethal triad.

The Concept — a Dysregulated Response

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. The crucial word is dysregulated: the damage in sepsis is done not only by the microbe but by the body's own overwhelming inflammatory reaction to it. Septic shock is the most severe form — sepsis with profound circulatory and metabolic derangement, defined as persistent hypotension requiring vasopressors to maintain a mean arterial pressure ≥ 65 mmHg together with a raised lactate (> 2 mmol/L) despite adequate fluid resuscitation — and it carries a high mortality.

Pathophysiology — WHY the Patient Is 'warm' Then Cold

Infection triggers a massive release of inflammatory mediators that act on the circulation in several damaging ways at once: widespread vasodilatation (which drops the blood pressure and, early on, makes the patient warm and flushed), increased capillary permeability (fluid leaks out of the vessels, worsening the effective hypovolaemia), microvascular thrombosis (which can progress to DIC), and myocardial depression. The result is tissue hypoperfusion and cellular hypoxia even though the cardiac output may initially be high — this is why septic shock is the classic 'warm' (distributive) shock early, turning cold as it decompensates.

Recognition

Sepsis should be suspected in any patient with a likely infection who develops fever or hypothermia, tachycardia, tachypnoea, altered mental state, and signs of poor perfusion (mottling, oliguria, a rising lactate). Bedside tools such as qSOFA (respiratory rate ≥ 22, altered mentation, systolic BP ≤ 100) flag patients at higher risk who need urgent assessment.

Management — the First Hour ('sepsis Six')

Sepsis is a time-critical emergency; the evidence is that acting within the first hour saves lives. A simple, memorable bundle is to take three and give three:

• Give — high-flow oxygen; IV broad-spectrum antibiotics (immediately after cultures); and IV fluid resuscitation (a crystalloid bolus, about 30 mL/kg).
• Take — blood cultures (before antibiotics if possible); serum lactate; and monitor urine output.

Ongoing Care

If hypotension persists despite adequate fluids, vasopressors (noradrenaline first-line) are started to restore vascular tone and maintain a mean arterial pressure ≥ 65 mmHg. The patient is managed in a high-dependency/intensive care setting with organ support as needed, guided by repeated assessment of perfusion and lactate clearance.

Sirs and the Spectrum

Historically, sepsis was framed around the Systemic Inflammatory Response Syndrome (SIRS) — two or more of: temperature > 38 or < 36 °C, heart rate > 90, respiratory rate > 20, and abnormal white-cell count. SIRS plus a source of infection defined sepsis. Current definitions focus instead on organ dysfunction (measured by the SOFA score) as the marker that separates dangerous sepsis from an uncomplicated infection, because it is organ dysfunction that predicts death.

Organ Dysfunction in Sepsis

The dysregulated response and hypoperfusion damage organs in a recognisable pattern — acute kidney injury (oliguria), acute lung injury/ARDS (hypoxia), altered mental state, deranged clotting/DIC, and hepatic and cardiovascular dysfunction — which together constitute multi-organ dysfunction syndrome (MODS), the common final pathway and the reason mortality is so high.

Prevention in Surgical Patients

Much surgical sepsis is preventable: asepsis, appropriate antibiotic prophylaxis, prompt treatment and drainage of infections, removal of infected devices, and early recognition of the deteriorating patient all reduce its incidence and severity.

WHY Early Antibiotics and Source Control Save Lives

The evidence in sepsis is stark: every hour of delay in effective antibiotics increases mortality, because the dysregulated response feeds on the ongoing infection. But antibiotics act on the bacteria in the blood and tissues — they cannot penetrate a walled-off collection of pus or sterilise dead tissue. This is the surgical crux: a septic patient with an abscess, an anastomotic leak, dead bowel or an infected implant will not recover on antibiotics and fluids alone, however aggressive, until the source is physically controlled — drained, resected or removed. Recognising the surgical source early, and dealing with it, is often the decisive intervention.

• Fluid resuscitation — crystalloid bolus ≈ 30 mL/kg, reassessing.
• Vasopressor — noradrenaline infusion, titrated to map ≥ 65 mmHg.
• Broad-spectrum antibiotics per local protocol, immediately after cultures.

The hour-1 bundle — cultures, antibiotics, fluids, lactate — drives survival.

• Sepsis = life-threatening organ dysfunction from a dysregulated host response to infection; septic shock = sepsis + vasopressor-requiring hypotension + lactate >2 despite fluids.
• Mediator storm → vasodilatation (warm shock), capillary leak, microthrombi (DIC), myocardial depression → tissue hypoperfusion.
• Recognise: fever/hypothermia, tachycardia, tachypnoea, altered mentation, mottling, oliguria, high lactate (qSOFA).
• First hour 'Sepsis Six': give O2, IV antibiotics, IV fluids (30 mL/kg); take cultures, lactate, urine output.
• Source control is the surgical key (drain pus/debride/remove device); noradrenaline for fluid-refractory hypotension, target map ≥65.

The Concept — Treat the Greatest Threat First

Trauma kills in a predictable order: an obstructed airway kills faster than a breathing problem, which kills faster than bleeding, which kills faster than a brain injury. The ATLS primary survey is built entirely around this fact — it looks for and treats the most rapidly lethal problems in sequence, and you do not move to the next step until the current one is controlled. The sequence is ABCDE, and the governing rule is 'treat first what kills first', reassessing constantly because a patient can deteriorate at any point.

A — Airway with Cervical-spine Control

The first question is whether the airway is patent. A patient who can talk clearly has, for that moment, a patent airway and adequate breathing. Look for obstruction — blood, vomit, a foreign body, or the tongue falling back in an unconscious patient — and listen for stridor or gurgling. Clear and open the airway with suction, a jaw thrust (not head tilt) and airway adjuncts, proceeding to a definitive airway (intubation) if needed. Throughout, the cervical spine is protected (manual in-line stabilisation, then collar and blocks), because any airway manoeuvre could move an unstable neck and cause cord injury — so airway and C-spine are managed together.

B — Breathing & Ventilation

With the airway secure, expose the chest and give high-flow oxygen, then look, feel and listen for the immediately life-threatening chest injuries that impair ventilation: a tension pneumothorax (decompress immediately — do not wait for an X-ray), an open pneumothorax (seal), a massive haemothorax, and a flail chest. Monitor oxygen saturation. The point of doing this in 'B' is that these injuries kill within minutes if missed.

C — Circulation with Haemorrhage Control

Now address bleeding — the commonest cause of preventable trauma death. Control external haemorrhage with direct pressure or a tourniquet, and assess perfusion (pulse rate and character, blood pressure, capillary refill, skin, mental state). Insert two large-bore cannulae (or intraosseous access) and give warmed fluid and, for significant loss, blood. Crucially, look for concealed haemorrhage — remembered as 'blood on the floor and four more': the chest, abdomen, pelvis and long bones — using a fast scan and a pelvic binder. In trauma, hypotension is due to haemorrhage until proven otherwise.

D — Disability (neurological Status)

A rapid neurological assessment follows: the Glasgow Coma Scale, pupil size and reaction, any lateralising signs, and a blood glucose (hypoglycaemia mimics head injury). A falling GCS or an unequal pupil signals a serious intracranial problem needing urgent CT and neurosurgical input; a GCS of 8 or less mandates a definitive airway.

E — Exposure & Environment

Finally, fully undress the patient to find every injury, while actively preventing hypothermia with warming and warmed fluids. This matters because hypothermia, together with acidosis and coagulopathy, forms the 'lethal triad' that makes bleeding impossible to stop.

Adjuncts & What Follows

Adjuncts to the primary survey include full monitoring, blood tests (including cross-match), chest and pelvis X-rays, fast, and — with appropriate caution — a urinary catheter and gastric tube. Only once the ABCDE is complete and the patient is stabilising does the secondary survey (a head-to-toe examination with an ample history) begin. Any sudden deterioration means going back to A and reassessing the whole sequence.

The Secondary Survey & Ample History

Once the primary survey is complete and the patient is responding to resuscitation, the secondary survey begins — a thorough head-to-toe examination (including the back via a log-roll, and every orifice) to identify every injury, not just the life-threatening ones. It is paired with an ample history — Allergies, Medications, Past medical history, Last meal, and Events/environment of the injury — which shapes anaesthesia, drug choices and the search for occult injuries. The golden rule is that the secondary survey never begins until the primary survey is complete and any deterioration has been re-addressed from 'A'.

Special Patient Groups

The ABCDE approach is universal but modified by physiology. The pregnant patient is nursed with a left lateral tilt (to lift the uterus off the vena cava) and remembered as 'two patients'. Children compensate extremely well and then crash suddenly, so subtle tachycardia must be taken seriously. The elderly may be on beta-blockers (masking tachycardia) or anticoagulants (worsening bleeding) and tolerate injury poorly. Recognising these differences prevents false reassurance.

Common Pitfalls

Preventable trauma deaths often follow predictable errors: missing a tension pneumothorax by waiting for an X-ray, underestimating concealed haemorrhage (a young patient maintains their blood pressure until a sudden collapse), failing to prevent hypothermia, and being distracted by a dramatic but non-lethal injury (an open fracture) while a quiet abdominal bleed goes unnoticed. Disciplined adherence to the sequence, and frequent reassessment, guards against all of these.

Treat the greatest threat to life first, in strict order.

• ATLS primary survey = ABCDE, treating the most rapidly lethal problem first, in sequence, reassessing constantly.
• A — airway patency (a talking patient is patent) with cervical-spine protection; jaw thrust, adjuncts, definitive airway; GCS ≤8 → intubate.
• B — high-flow O2 + find/treat tension pneumothorax, open pneumothorax, massive haemothorax, flail chest immediately.
• C — control external bleeding + assess perfusion + 2 large-bore cannulae + warmed fluid/blood; find concealed bleeding ('chest, abdomen, pelvis, long bones'); hypotension = haemorrhage until proven otherwise.
• D — GCS, pupils, glucose; E — expose fully but prevent hypothermia (lethal triad); then adjuncts and secondary survey.

The Concept — Prevent the Second Injury

The brain is enclosed in a rigid skull, which is the key to understanding head injury. Damage occurs in two phases. The primary injury happens at the instant of impact (contusion, laceration, diffuse axonal injury) and cannot be undone. The secondary injury develops over the following minutes to days — from hypoxia, hypotension, an expanding haematoma, raised intracranial pressure, and seizures — and, critically, much of it is preventable and treatable. The entire management of head injury is therefore aimed at preventing secondary brain injury.

WHY Pressure Is the Enemy — the Monro-kellie Doctrine

Because the skull is a fixed box containing brain, blood and CSF, any new volume — a haematoma or swelling — must be offset by squeezing out CSF and venous blood. This buys time (the patient may look deceptively well), but once this compensation is exhausted the intracranial pressure (ICP) rises steeply. Since cerebral perfusion pressure = mean arterial pressure − ICP, a rising ICP (or a falling blood pressure) chokes off the brain's blood supply, causing ischaemia; unchecked, the brain is forced through the tentorium or foramen magnum (herniation), which is fatal. This is why hypoxia and hypotension are so dangerous — they compound an already threatened blood supply.

Types of Head Injury

• Skull fractures — linear, depressed, or base-of-skull (signs: 'raccoon eyes', Battle's sign, and CSF leak from the nose or ear).
• Intracranial haematomas — extradural (arterial, lucid interval), subdural (venous), subarachnoid, and intracerebral.
• Diffuse injuries — concussion, cerebral contusion, and diffuse axonal injury (from rotational shearing).

Assessment

The core tools are the Glasgow Coma Scale (which grades severity — mild 13–15, moderate 9–12, severe ≤ 8), the pupils (a fixed, dilated pupil suggests uncal herniation compressing the third nerve), lateralising limb signs, and the mechanism of injury. Deterioration is judged by a falling GCS, which is why serial observation is essential.

Signs of Raised Icp

Warning signs include a falling conscious level, headache and vomiting, pupillary changes, and the ominous, late Cushing's response — hypertension with bradycardia and irregular breathing, a reflex attempt to maintain cerebral perfusion that signals critically high ICP and impending herniation.

Investigation & Management

A CT head is the investigation of choice, showing haematoma, fracture, midline shift and effacement of the basal cisterns. Management is directed squarely at preventing secondary injury: maintain oxygenation and blood pressure (avoid hypoxia and hypotension at all costs), nurse head-up, secure the airway (intubate if GCS ≤ 8), and treat raised ICP with mannitol or hypertonic saline, controlled ventilation, sedation and seizure control. A significant haematoma requires urgent neurosurgical evacuation, and ICP may be monitored directly in severe cases.

The Intracranial Haematomas in Detail

Understanding the haematomas by their source clarifies their behaviour. An extradural haematoma is arterial (middle meningeal artery, temporal fracture), collects fast, and gives the classic lucid interval — appearing biconvex on CT. A subdural haematoma is venous (bridging veins), commoner in the elderly and anticoagulated, may be acute or chronic, and appears crescent-shaped. A subarachnoid haemorrhage layers blood in the CSF spaces, and an intracerebral haematoma/contusion lies within the brain itself. Each raises ICP and may need evacuation.

WHO Needs a CT Scan?

Not every head injury needs imaging, and structured criteria (such as NICE or the Canadian CT Head rules) select those at risk of a significant lesion. High-risk features prompting an urgent CT head include a GCS below 13 at any point (or below 15 at 2 hours), a suspected skull fracture, any focal neurological deficit, more than one episode of vomiting, a post-traumatic seizure, and dangerous mechanisms — with a lower threshold in patients on anticoagulants.

Concussion & Complications

Concussion is a transient disturbance of brain function after injury (headache, confusion, amnesia) with a normal CT; it is managed with rest and graded return to activity, with caution about repeated injury. Longer-term complications of significant head injury include post-traumatic epilepsy, chronic subdural haematoma, CSF leak with meningitis risk, cognitive and behavioural change, and post-concussion syndrome — which is why follow-up matters even after apparent recovery.

• Mannitol 0.25–1 g/kg IV, or hypertonic saline, for acutely raised ICP.
• GCS severity: mild 13–15, moderate 9–12, severe ≤ 8 (intubate).
• Target: avoid hypoxia (SpO₂ > 94%) and hypotension (maintain cerebral perfusion).

Secondary injury is preventable — that is where treatment acts.

• Primary injury (at impact, irreversible) vs secondary injury (hypoxia, hypotension, haematoma, raised ICP — preventable); management targets the secondary injury.
• Monro-Kellie: fixed skull; a mass is compensated by displacing CSF/blood until ICP rises steeply → falling cerebral perfusion (CPP = map − ICP) → ischaemia → herniation.
• Assess with GCS (severe ≤8), pupils (fixed dilated = herniation), lateralising signs; lucid interval suggests extradural haematoma.
• Raised ICP: falling GCS, vomiting, pupillary change, Cushing's response (hypertension + bradycardia — late).
• CT head is investigation of choice; maintain O2 and BP, head-up, intubate if GCS ≤8, mannitol/hypertonic saline, evacuate significant haematoma.

The Concept

Chest injuries kill by interfering with the two vital functions the thorax performs — ventilation (getting oxygen in) and circulation (the heart and great vessels). A small number of injuries are immediately life-threatening and must be found and treated during the primary survey ('B' and 'C'), often on clinical grounds alone. Reassuringly, the great majority of chest trauma is managed not by opening the chest but by a simple chest drain and supportive care.

Immediately Life-threatening Injuries

These must be identified and treated at once:

• Tension pneumothorax — air enters the pleural space through a one-way valve and cannot escape, so it accumulates, collapses the lung and pushes the mediastinum across, kinking the great veins and obstructing venous return (obstructive shock). Signs: severe respiratory distress, absent breath sounds and hyperresonance on one side, tracheal deviation away, distended neck veins and hypotension. It is a clinical diagnosis treated by immediate needle or finger decompression, then a chest drain — never wait for an X-ray.
• Open pneumothorax ('sucking chest wound') — a chest-wall defect through which air moves preferentially, impairing ventilation; cover with a dressing sealed on three sides (a flutter valve) and insert a chest drain.
• Massive haemothorax — > 1500 mL of blood in the pleural cavity; dullness with absent breath sounds and shock; treat with a chest drain, blood transfusion, and thoracotomy if bleeding continues.
• Flail chest — two or more adjacent ribs each broken in two places create a free segment that moves paradoxically; the real danger is the underlying lung contusion causing hypoxia. Treat with oxygen, good analgesia, physiotherapy and ventilation if needed.
• Cardiac tamponade — blood in the pericardium compresses the heart and prevents filling (obstructive shock); look for Beck's triad — hypotension, muffled heart sounds and raised JVP — and treat by pericardiocentesis or thoracotomy.

Potentially Life-threatening Injuries

Detected during the secondary survey and imaging, these include pulmonary contusion, traumatic aortic rupture, tracheobronchial injury, blunt cardiac injury, diaphragmatic rupture and oesophageal injury. They are less immediately dramatic but can be lethal if missed.

Management Principles

The reassuring principle is that most chest trauma is managed with oxygen, analgesia and a chest drain, which re-expands the lung and drains blood or air; only a minority — continued massive bleeding, tamponade, major airway or vascular injury — require thoracotomy. Adequate analgesia (including regional blocks) is more important than it sounds, because pain prevents the patient breathing and coughing, leading to atelectasis and pneumonia.

Ventilation Versus Circulation — a Useful Framework

Chest injuries are easier to remember if grouped by the function they threaten. Injuries that primarily impair ventilation (tension and open pneumothorax, flail chest with contusion) present with respiratory distress and hypoxia. Injuries that primarily impair circulation (massive haemothorax, cardiac tamponade) present with shock. Tension pneumothorax straddles both — it starts as a ventilation problem and becomes an obstructive-shock circulation problem as the mediastinum shifts. This framework directs the examination.

The Intercostal Chest Drain

Because the chest drain is the workhorse of thoracic trauma, its principles are worth knowing. It is inserted in the 'safe triangle' (bordered by the lateral edge of pectoralis major, the anterior border of latissimus dorsi and a line at the nipple level), passing over the top of the rib to avoid the neurovascular bundle that runs under each rib. The drain is connected to an underwater seal, which acts as a one-way valve allowing air and blood out while preventing anything being drawn back in — re-expanding the lung. Swinging of the fluid level confirms a patent drain, and bubbling indicates an air leak.

When Thoracotomy Is Needed

A thoracotomy (surgically opening the chest) is reserved for the minority of injuries the drain cannot control: an immediate drainage of > 1500 mL of blood, or ongoing losses of > 200 mL/hour, cardiac tamponade, and major airway or great-vessel injury. A resuscitative (emergency) thoracotomy is a last-resort procedure in select patients who arrest from penetrating chest trauma.

Assessing the Chest-injured Patient

• A structured examination detects these injuries quickly.
• Inspection looks for bruising, the pattern of a seat-belt, a flail segment, an open wound and the respiratory rate
• palpation feels for tenderness, crepitus (subcutaneous emphysema, implying an air leak) and tracheal position
• percussion distinguishes the hyperresonance of a pneumothorax from the dullness of a haemothorax
• auscultation reveals reduced or absent breath sounds and the character of the heart sounds. This pattern — tracheal position, percussion note and breath sounds together — is what separates a tension pneumothorax from a massive haemothorax at the bedside, before any imaging.

Tension pneumothorax is a clinical diagnosis — do not wait for imaging.

• Chest trauma kills by impairing ventilation or circulation; the life-threatening injuries are found/treated in the primary survey, often clinically.
• Immediately life-threatening: tension pneumothorax (needle/finger decompression + drain), open pneumothorax (3-sided seal + drain), massive haemothorax (drain + blood ± thoracotomy), flail chest (O2/analgesia/physio, treat lung contusion), cardiac tamponade (Beck's triad → pericardiocentesis/thoracotomy).
• Tension pneumothorax and tamponade cause obstructive shock — diagnose clinically, do not wait for imaging.
• Potentially life-threatening (secondary survey): pulmonary contusion, aortic rupture, tracheobronchial/cardiac/diaphragmatic/oesophageal injury.
• Most chest trauma is managed with O2, analgesia and a chest drain; only a minority need thoracotomy.

The Concept — the Hidden Bleeder

The abdomen is one of the great 'hidden' sites of major haemorrhage: a trauma patient can be in profound hypovolaemic shock from bleeding into the abdomen with no external sign at all. The central clinical decision in abdominal trauma is deceptively simple to state — does this patient need a laparotomy, and how urgently? — and answering it depends chiefly on the patient's haemodynamic stability.

Mechanisms & the Organs at Risk

Blunt trauma (road-traffic accidents, falls, assault) most often injures the solid organs — the spleen and liver — which bleed. Penetrating trauma divides into stab wounds (relatively predictable tracks; liver and small bowel commonly injured) and gunshot wounds (unpredictable, more destructive, usually requiring exploration). Recognising the mechanism predicts the likely injuries.

Clinical Assessment

Abdominal signs can be subtle or masked (by head injury, intoxication or distracting injuries), so a high index of suspicion is vital. Look for abdominal pain, distension, guarding or rigidity, the imprint of a seat-belt ('seat-belt sign'), bruising, and referred pain to the shoulder tip (from diaphragmatic irritation by blood). Because signs evolve, serial examination is important.

Investigations — Matched to Stability

• Fast scan (Focused Assessment with Sonography in Trauma) — a rapid bedside ultrasound that detects free fluid (blood) around the organs and heart; ideal in the unstable patient because it is immediate and does not require moving them.
• CT of the abdomen — the investigation of choice in the stable patient; it grades solid-organ injury precisely and detects other injuries, allowing non-operative management.
• Diagnostic peritoneal lavage — now largely replaced by fast and CT.

Management — Decided BY Stability

The management flows directly from the patient's physiology:

• Haemodynamically unstable with a positive fast → immediate laparotomy; do not delay for a CT scan.
• Haemodynamically stable → CT, after which many solid-organ (spleen/liver) injuries are managed non-operatively (close observation, sometimes with angiographic embolisation), preserving the organ.
• Penetrating trauma with evisceration, peritonitis or instability → laparotomy; most gunshot wounds are explored.
• In the exsanguinating patient, damage-control surgery is used — rapidly stop the bleeding and contamination, pack the abdomen, close temporarily, resuscitate and rewarm in intensive care, and return for definitive surgery once physiology is restored.

Pelvic & Retroperitoneal Haemorrhage

Two 'hidden' sites deserve special mention because they cause exsanguination that a laparotomy does not directly control. A major pelvic fracture can bleed massively into the retroperitoneum from the rich venous plexus and cancellous bone; the first-line manoeuvre is a pelvic binder to close the pelvic ring and tamponade the bleeding, followed by angiographic embolisation or surgical packing. Retroperitoneal haematoma from renal or vascular injury behaves similarly — bleeding that is concealed from both external view and simple examination.

Patterns of Organ Injury

Knowing which organ is likely injured guides the search. The spleen is the most commonly injured organ in blunt trauma (left upper quadrant pain, referred left shoulder-tip pain — Kehr's sign) and is graded on CT. The liver is next and, like the spleen, is often managed non-operatively if stable. Hollow-viscus (bowel) injury is easily missed and presents later with peritonitis; the duodenum and pancreas are injured in handlebar/seat-belt injuries; and bladder or urethral injury is suggested by blood at the urethral meatus, a high-riding prostate or inability to pass urine — a contraindication to blind catheterisation.

Serial Assessment & the Missed Injury

Because abdominal signs evolve and imaging is imperfect, the haemodynamically stable but suspicious patient is admitted for serial examination rather than discharged. A rising pulse, developing peritonism or a falling haemoglobin over the following hours may be the first sign of a bowel injury or delayed splenic rupture — the reason a single normal examination is never taken as final.

Signs That Should Raise Alarm

Certain findings flag serious intra-abdominal injury and mandate close monitoring or surgery. Peritonism (guarding, rigidity, rebound tenderness) indicates hollow-viscus perforation or significant bleeding; abdominal distension with shock suggests major intra-abdominal haemorrhage; a seat-belt sign across the abdomen is associated with bowel and mesenteric injury; and bruising in the flanks (Grey-Turner's) or around the umbilicus (Cullen's) suggests retroperitoneal bleeding. In penetrating trauma, evisceration of bowel or omentum, or an implement in situ (which is left in place until theatre) are clear indications for exploration.

Haemodynamic stability decides between CT and immediate laparotomy.

• The abdomen is a hidden site of major haemorrhage; the key question is whether a laparotomy is needed, decided mainly by haemodynamic stability.
• Blunt trauma → solid organs (spleen, liver) bleed; penetrating → stab (liver/bowel) or gunshot (explore).
• Signs may be subtle: pain, distension, guarding, seat-belt sign, shoulder-tip pain; examine serially.
• Unstable + positive fast → immediate laparotomy (no CT); stable → CT, then often non-operative management (± embolisation).
• Exsanguinating patient → damage-control surgery (stop bleeding/contamination, pack, resuscitate, definitive surgery later).

The Concept — Two Early Killers

Burns are dangerous out of all proportion to how they look, and two threats dominate the early hours: airway compromise from inhalation injury, and the massive fluid shift that causes 'burn shock'. Everything in initial management flows from assessing the extent (percentage of body surface burnt) and the depth of the burn, and from protecting the airway before it swells shut.

Assessing the Extent (% Tbsa)

The percentage of total body surface area (TBSA) burnt is estimated with Wallace's Rule of Nines in adults — head 9%, each arm 9%, each leg 18%, the front of the trunk 18%, the back 18%, and the perineum 1%. In children the head is relatively larger and the legs smaller, so a Lund-Browder chart is used for accuracy. A quick rule for scattered burns is that the patient's palm is about 1%. (Simple erythema, as in sunburn, is not counted.)

Assessing the Depth

The Airway — Assess and Secure Early

Inhalation injury is the priority because airway swelling can close the airway within hours. Suspect it with facial or neck burns, singed nasal hairs, soot in the mouth or sputum, hoarseness, stridor, or a fire in an enclosed space. The rule is to intubate early — before oedema makes intubation impossible. Also consider carbon monoxide and cyanide poisoning in enclosed-space fires (give high-flow oxygen).

Fluid Resuscitation — and WHY

A significant burn (> 15–20% TBSA in adults, > 10% in children) causes a massive inflammatory capillary leak, so plasma pours out of the circulation into the burnt and surrounding tissues, producing hypovolaemic 'burn shock'. This is replaced using the Parkland formula: 4 mL × body weight (kg) × %TBSA of Ringer lactate over the first 24 hours, giving half in the first 8 hours (timed from the moment of the burn) and the rest over the next 16 hours — with maintenance fluid added in children. The formula is only a starting estimate; the resuscitation is titrated to urine output (0.5–1 mL/kg/h in adults, higher in children), which is the best bedside marker of adequate perfusion.

Other Management

Give generous IV opioid analgesia; clean the wounds and apply a topical antimicrobial (e.g. Silver sulfadiazine) with dressings; give tetanus prophylaxis; and start early high-calorie, high-protein nutrition because burns cause an intense hypermetabolic state. A circumferential full-thickness burn forms a rigid eschar that constricts — of a limb (compromising circulation) or the chest (restricting breathing) — and needs an urgent escharotomy (incising the eschar to release it). Deep burns require early excision and skin grafting, and major burns are transferred to a specialist burns unit.

Types of Burn & Their Special Problems

• The cause of the burn changes the management.
• Thermal (flame/scald) burns are commonest.
• Electrical burns are deceptive — small entry/exit wounds hide extensive deep tissue damage along the current's path, causing rhabdomyolysis (myoglobinuria and renal failure) and cardiac arrhythmias, so they need cardiac monitoring and generous fluids with a higher urine-output target.
• Chemical burns require prolonged irrigation with water (removing the agent), with alkalis penetrating more deeply than acids. Recognising the type prevents underestimating the injury.

The Pathophysiology of Burn Shock

It is worth understanding why burns cause such profound fluid loss. The burn triggers release of inflammatory mediators that make capillaries leaky, not just locally but systemically, so protein-rich fluid escapes into the interstitium; combined with the loss of the skin's water barrier (huge evaporative losses), the circulating volume falls dramatically over the first 24–48 hours. This is a distributive and hypovolaemic 'burn shock', and it is why fluid resuscitation is front-loaded into the first 8 hours when the leak is greatest.

Complications & Referral

Major burns carry many complications: burn shock, inhalation injury, infection and sepsis (the leading cause of later death), acute kidney injury, hypothermia, a Curling's (stress) gastric ulcer, and later contractures and hypertrophic scarring. Certain injuries warrant transfer to a specialist burns unit — large burns (> 10% in children, > 15–20% in adults), full-thickness burns, burns of the face, hands, feet, perineum or over joints, and electrical, chemical or inhalation injuries.

• Parkland formula — 4 mL/kg/%TBSA of Ringer lactate over 24 h (half in the first 8 h); add maintenance in children.
• Titrate to urine output 0.5–1 mL/kg/h (adults), 1–1.5 mL/kg/h (children).
• Topical silver sulfadiazine; IV opioid analgesia; tetanus prophylaxis.

Urine output, not the formula, is the true guide to resuscitation.

• Two early killers: inhalation airway injury and burn shock (capillary-leak hypovolaemia); assess extent + depth.
• Extent: Rule of Nines (adult), Lund-Browder (children — larger head), palm ≈ 1%. Depth: superficial → full-thickness (full-thickness is painless, leathery, needs grafting).
• Airway: suspect inhalation injury (facial burns, soot, hoarseness, enclosed fire) → intubate early before oedema; consider CO/cyanide.
• Parkland: 4 mL/kg/%TBSA Ringer lactate/24 h (half in first 8 h) + maintenance in children; titrate to urine output.
• Also: opioid analgesia, silver sulfadiazine + dressings, tetanus, high-calorie nutrition, escharotomy for constricting circumferential burns, early excision/grafting, burns-unit referral.

The Concept & Risk Factors

Breast carcinoma is the commonest cancer in women, and understanding it begins with the idea that most cancers are oestrogen-driven — anything that increases a woman's lifetime exposure to oestrogen raises her risk. This explains the classic risk factors: early menarche and late menopause (a longer reproductive span), nulliparity or a first pregnancy after 30 (pregnancy is protective), obesity (fat converts androgens to oestrogen after menopause), and prolonged hormone use. Added to these are increasing age, a family history, and the inherited BRCA1/BRCA2 gene mutations, which confer a very high lifetime risk.

Pathology

Most cancers arise from the ducts. The key distinction is between carcinoma in situ (malignant cells confined by the basement membrane — DCIS, a premalignant/non-invasive stage) and invasive carcinoma (cells breached the basement membrane and can metastasise). The commonest is invasive ductal carcinoma (no special type), followed by invasive lobular carcinoma. Every tumour is assessed for three receptors that guide treatment: oestrogen (ER) and progesterone (PR) receptors, and HER2.

Clinical Features

The commonest presentation is a painless, hard, irregular, fixed lump, usually in the upper outer quadrant. Signs of local advancement teach the anatomy of spread: skin tethering or dimpling and nipple retraction (infiltration of the ligaments of Cooper and ducts), peau d'orange (skin oedema from dermal lymphatic blockage), fixation to the chest wall, and palpable axillary nodes. Distant spread is to bone, lung, liver and brain.

Triple Assessment & Staging

Any breast lump is worked up by triple assessment — clinical examination, imaging (mammography ± ultrasound), and needle biopsy (core biopsy) — which together give a near-certain diagnosis. Staging uses the TNM system (tumour size, nodal involvement, metastasis), and the axillary nodes are the single most important prognostic factor.

Management — a Multimodal Approach

Treatment combines surgery, radiotherapy and systemic therapy, tailored to stage and receptor status:

• Surgery — either breast-conserving surgery (wide local excision) for smaller tumours (always followed by radiotherapy), or mastectomy for larger/multifocal tumours. The axilla is staged by sentinel lymph node biopsy; if involved, an axillary clearance is done.
• Radiotherapy — after conservation surgery and after mastectomy for high-risk disease, to reduce local recurrence.
• Endocrine therapy for ER-positive tumours — tamoxifen (premenopausal) or an aromatase inhibitor (postmenopausal), exploiting the oestrogen dependence.
• Chemotherapy for higher-risk/node-positive disease, and trastuzumab (Herceptin) for HER2-positive tumours.

Routes of Spread

• Understanding how breast cancer spreads explains both its staging and its clinical signs.
• Local spread invades the skin (tethering, ulceration, peau d'orange) and the pectoral muscle/chest wall.
• Lymphatic spread — the main early route — is chiefly to the axillary nodes (and less commonly the internal mammary and supraclavicular nodes), which is why axillary status is so central to prognosis.
• Blood-borne spread seeds the classic sites — bone (the commonest, causing pain and pathological fractures), lung, liver and brain. This is why staging investigations in advanced disease target these organs.

Prognostic Factors

Prognosis is estimated from several factors combined (e.g. In the Nottingham Prognostic Index): lymph node status (the most powerful), tumour size, and histological grade, together with receptor status. A small, low-grade, node-negative, ER-positive tumour carries an excellent outlook, whereas a large, high-grade, node-positive or triple-negative tumour does far worse — and it is this profile, not the diagnosis of 'cancer' alone, that guides how aggressively the patient is treated.

Screening

Because early, impalpable cancers (especially DCIS, detected as microcalcification) are far more curable, population mammographic screening is offered to women in the target age band (typically ~50–70 years, three-yearly in many programmes). High-risk women (strong family history, BRCA carriers) are screened earlier and with MRI. The principle is that detecting cancer before it is palpable improves survival.

Locally Advanced & Metastatic Disease

Not all breast cancer is operable at presentation. Locally advanced disease (large fixed tumours, skin/chest-wall involvement, matted nodes, or inflammatory cancer) is usually treated first with neoadjuvant chemotherapy to shrink the tumour and make surgery possible, followed by surgery and radiotherapy. Metastatic disease is not curable but is very treatable, and the aim shifts to controlling the disease and maintaining quality of life with endocrine therapy, chemotherapy, targeted agents (e.g. Trastuzumab), and bone-directed treatment (bisphosphonates) for skeletal metastases. This palliative-but-active philosophy means many women live for years with controlled metastatic disease.

Breast Reconstruction & the MDT

Modern breast cancer care is delivered by a multidisciplinary team (surgeon, oncologist, radiologist, pathologist, specialist nurse) that individualises treatment to the tumour biology and the patient's wishes. Reconstruction — immediate or delayed, using an implant or the patient's own tissue (latissimus dorsi or DIEP flap) — is an integral part of mastectomy care, restoring body image. Psychological support, genetic counselling for BRCA carriers, and clear discussion of the risks and benefits of each option are all part of a comprehensive, patient-centred plan rather than surgery in isolation.

• Tamoxifen 20 mg daily for ER-positive disease (usually 5–10 years).
• Sentinel node biopsy is the standard for staging a clinically negative axilla.
• Axillary nodal status = the single most important prognostic factor.

Axillary node status remains the strongest prognostic factor.

• Mostly oestrogen-driven; risk rises with lifetime oestrogen exposure (early menarche/late menopause, nulliparity), age, family history, BRCA1/2.
• Pathology: DCIS (in situ, premalignant) vs invasive (ductal commonest); always test ER, PR, HER2.
• Painless hard irregular fixed lump (upper outer quadrant); skin tethering, nipple retraction, peau d'orange, axillary nodes; spreads to bone/lung/liver/brain.
• Diagnose by triple assessment; stage by TNM; axillary nodes = most important prognostic factor.
• Multimodal: conservation+radiotherapy or mastectomy, sentinel node biopsy; tamoxifen/aromatase inhibitor (ER+), trastuzumab (HER2+), chemotherapy (high-risk/triple-negative).

The Concept — Andi

Most breast lumps and symptoms are benign, and the modern way to understand them is the concept of ANDI — Aberrations of Normal Development and Involution. The insight is that the breast is not a static organ: across a woman's life it develops, cycles monthly, and involutes, and most 'benign breast disease' is simply a minor aberration of these normal processes rather than true disease. This reframing explains why these conditions are so common, age-related, and usually need reassurance rather than aggressive treatment.

Fibroadenoma — an Aberration of Development

A fibroadenoma arises from a single lobule that overgrows, and occurs in young women (15–30). It is the classic 'breast mouse' — a smooth, firm, highly mobile, painless lump. It is benign with negligible malignant potential; after triple assessment confirms it, small ones may simply be observed, with excision for larger, growing or symptomatic ones.

Fibrocystic Change — an Aberration of Cycling

Fibrocystic change reflects an exaggerated response to the monthly hormonal cycle, and occurs in the 30–50 age group. It causes cyclical breast pain (mastalgia), lumpiness and nodularity that worsen premenstrually. It is benign; management is reassurance, a supportive bra, and simple analgesia, with cysts aspirated if symptomatic.

Breast CYSTS — an Aberration of Involution

Cysts are common in the perimenopausal years (35–50) as lobules involute and their ducts become distended with fluid. They present as a smooth, sometimes tender, discrete lump. On ultrasound they are clearly fluid-filled; a simple cyst is aspirated and, if the fluid is not bloodstained and the lump disappears completely, needs no further action. Bloodstained fluid or a residual lump requires biopsy to exclude malignancy.

Other Benign Conditions

• Duct ectasia — dilated, shortened ducts in older women, causing thick cheesy nipple discharge and nipple retraction (a benign mimic of cancer).
• Fat necrosis — a firm lump after trauma that can mimic cancer and needs triple assessment to distinguish.
• Galactocele — a milk-filled cyst during lactation.
• Duct papilloma — a benign wart-like growth in a duct, the commonest cause of blood-stained nipple discharge.

Mastalgia (breast Pain)

Breast pain is one of the commonest reasons women present, and separating it into types guides management. Cyclical mastalgia (linked to the menstrual cycle, bilateral, part of fibrocystic change) is the commonest and responds to reassurance, a supportive bra and simple analgesia. Non-cyclical mastalgia may arise from the breast (e.g. Duct ectasia) or from the chest wall (costochondritis — Tietze's syndrome). The reassuring message is that breast pain alone is rarely a symptom of cancer, so the main task is to exclude a lump and reassure.

Fat Necrosis & Galactocele

Two specific benign lumps are worth knowing. Fat necrosis follows trauma (often forgotten by the patient) and produces a firm, sometimes tethered lump that can mimic carcinoma clinically and on mammography — so it requires triple assessment to be sure. A galactocele is a milk-filled cyst occurring during or after lactation, presenting as a smooth cystic lump that resolves on aspiration.

The Principle of Safe Reassurance

Across all benign conditions the governing rule is the same: a lump or symptom is labelled benign only after triple assessment has excluded malignancy, after which the patient can be confidently reassured and spared unnecessary surgery. Over-treating benign disease and under-investigating a 'benign-feeling' cancer are the two errors this discipline prevents.

Clinical Approach to a Benign Lump

Bringing the conditions together, the practical approach to a woman with a breast lump is: take a focused history (age, duration, cyclical change, pain, discharge, risk factors), examine both breasts and the regional nodes, and arrange triple assessment matched to age (ultrasound if young, mammography added if older). The age of the patient is itself a strong clue — a mobile lump at 20 is most likely a fibroadenoma, cyclical nodularity at 40 is fibrocystic change, a smooth lump at 45 is often a cyst, and a hard fixed lump at 60 must be treated as cancer until proven otherwise.

A Practical Diagnostic Framework

In the clinic the age of the patient plus the character of the lump usually predicts the diagnosis before investigation: a highly mobile firm lump at 20 suggests a fibroadenoma; cyclical nodularity at 40 suggests fibrocystic change; a smooth discrete lump at 45 suggests a cyst; and a hard, irregular, fixed lump at 60 must be treated as cancer. This framework does not replace triple assessment — it directs it — and it embodies the safe principle that the 'benign' label is only ever confirmed after imaging and needle biopsy, never on clinical impression alone.

Most benign breast change is an aberration of normal processes.

• ANDI = Aberrations of Normal Development and Involution — most benign breast disease is a minor aberration of normal breast processes.
• Fibroadenoma (young, 15–30): smooth, firm, very mobile painless 'breast mouse'; benign.
• Fibrocystic change (30–50): cyclical mastalgia, lumpiness, nodularity; reassurance + supportive bra + analgesia.
• Cysts (perimenopausal, 35–50): fluid-filled; aspirate — biopsy if bloodstained fluid or residual lump.
• Also duct ectasia, fat necrosis, galactocele, duct papilloma (commonest cause of bloody discharge); confirm 'benign' only after triple assessment.

The Concept — WHY Three, Not One

Triple assessment is the cornerstone of breast diagnosis: every discrete breast lump or suspicious symptom is evaluated by three independent methods — clinical assessment, imaging, and pathology (needle biopsy). The logic is that no single test is perfect — each has false negatives — but when all three agree, the diagnosis is near-certain (accuracy > 99%). Combining them means a cancer is very unlikely to be missed and a benign lump can be confidently reassured, ideally in a single 'one-stop' clinic visit.

Clinical Assessment

A careful history notes the lump's duration and change, relation to the menstrual cycle, pain, nipple discharge, and risk factors. Examination inspects for asymmetry, skin changes (dimpling, peau d'orange), and nipple retraction, then palpates the lump (size, consistency, mobility, fixation) and the axillary and supraclavicular nodes. Findings are scored (e.g. P1 normal to P5 malignant). Clinical assessment alone can be misleading, which is exactly why the other two components exist.

Imaging

Imaging is chosen by age because breast density differs:

• Mammography — the imaging of choice in women over about 35, whose breasts are less dense. It detects masses and, importantly, microcalcifications — a key sign of DCIS not palpable clinically.
• Ultrasound — preferred in younger women (< 35) with dense breasts, and used in all ages to characterise a lump as solid or cystic and to guide biopsy.
• MRI — reserved for specific situations (e.g. Screening BRCA carriers, assessing lobular cancer or implants).

Imaging is also scored (M1–M5 / U1–U5).

Pathology (needle Biopsy)

Tissue diagnosis is obtained by needle:

• Core needle biopsy — the preferred method, because it takes a core of tissue that shows the histological architecture, distinguishes invasive from in-situ disease, and allows receptor (ER/PR/HER2) testing — all essential for planning treatment.
• Fine needle aspiration cytology (FNAC) — quicker but only gives cells (cytology, C1–C5), and cannot tell invasive from in-situ; now largely superseded by core biopsy.

Interpreting the Results

The three arms are considered together. Concordant results (all benign, or all malignant) give a confident diagnosis. Discordance — for example a clinically suspicious lump with a benign biopsy — is a red flag that must never be ignored; it prompts repeat biopsy or diagnostic excision, because it may reflect a sampling error missing a cancer.

The One-stop Clinic

Triple assessment is ideally delivered in a 'one-stop' breast clinic, where clinical examination, imaging and needle biopsy are all performed at a single visit, with results discussed the same day where possible. This design reflects the whole philosophy of the approach: rapid, combined assessment minimises the anxiety of waiting and the risk of losing patients to follow-up, and reaches a reliable diagnosis quickly.

Scoring Systems

Each arm is given a numerical score so the team can integrate them objectively: clinical P1–P5, imaging M1–M5 (mammography) and U1–U5 (ultrasound), and pathology B1–B5 (core biopsy) or C1–C5 (cytology) — in each case 1 being normal/benign and 5 being malignant. Concordant high scores confirm cancer and allow definitive treatment to be planned; concordant low scores allow discharge.

Limitations & the Role of Excision Biopsy

No test is infallible: mammography is less sensitive in the dense breasts of younger women, and needle biopsy can miss a small or heterogeneous lesion (sampling error). When the arms are discordant, or a lesion is scored as indeterminate/atypical (e.g. B3), a diagnostic excision biopsy (often after image-guided wire localisation for impalpable lesions) is performed to obtain the definitive answer.

Impalpable Lesions

Screening detects many impalpable abnormalities (a cluster of microcalcification, or a small mass seen only on imaging). These cannot be felt, so they are sampled under image guidance — stereotactic or ultrasound-guided core biopsy — and, if excision is needed, localised first with a guidewire or radioactive/magnetic seed placed by the radiologist so the surgeon can remove the correct area, with a specimen X-ray confirming the lesion has been excised. This is how modern practice deals with cancers found before they are ever palpable.

Special Clinical Scenarios

Triple assessment adapts to particular situations. In pregnancy and lactation, ultrasound is the first-line image (avoiding radiation) and any suspicious lump is still biopsied, because pregnancy-associated cancers are easily missed. In the screening-detected impalpable lesion, the whole process is image-led — stereotactic core biopsy, and wire or seed localisation for excision. In a young woman with a classic fibroadenoma, clinical assessment plus ultrasound and core biopsy may permit safe conservative management. The method flexes to the context while never abandoning its three-arm principle.

Discordance between the three demands further investigation.

• Triple assessment = clinical + imaging + needle biopsy for every discrete lump; combined accuracy >99%.
• Clinical: history + examination of lump and regional nodes (scored P1–P5).
• Imaging: mammography if >35 (detects microcalcification/DCIS), ultrasound if <35 or to characterise solid/cystic; MRI selectively.
• Pathology: core biopsy preferred (shows architecture, invasive vs in-situ, ER/PR/HER2) over FNAC.
• Concordant results confirm the diagnosis; discordance mandates re-biopsy/excision — never ignore it.

The Concept

A breast abscess is a localised collection of pus in the breast, almost always the end-result of mastitis (inflammation/infection of breast tissue) that has not resolved. Understanding the two settings in which it occurs — lactational and non-lactational — explains the different organisms, sites and management, and the general surgical principle that pus must be drained applies throughout.

Lactational (puerperal) Mastitis & Abscess

This is the common form, occurring in breastfeeding mothers, typically a few weeks postpartum. The mechanism is milk stasis plus a cracked nipple that lets skin bacteria — usually Staphylococcus aureus — enter and infect stagnant milk, which is an ideal culture medium. It presents with a painful, red, hot, swollen, wedge-shaped area and fever. If a fluctuant collection develops, an abscess has formed.

Non-lactational Abscess

This occurs outside lactation and is strongly associated with smoking and duct ectasia/periductal mastitis. It tends to be periareolar (around the nipple) and is more prone to recur and to form a mammary duct fistula. The organisms are often mixed, including anaerobes, so antibiotic choice differs.

Management

Management follows the stage:

• Cellulitis/mastitis (no pus yet) — antibiotics (flucloxacillin for lactational; co-amoxiclav/metronidazole cover for non-lactational anaerobes), analgesia, and — importantly in lactational mastitis — continued breastfeeding or expression to relieve the milk stasis that drives it.
• Established abscess (fluctuant/pus) — antibiotics alone will not cure a collection, so it must be drained. The modern first-line is ultrasound-guided needle aspiration (repeated as needed), reserving incision and drainage for large or multiloculated abscesses.
• A biopsy of the abscess wall is taken in non-lactational or atypical cases to exclude an underlying inflammatory carcinoma.

Pathogenesis of the Lactational Abscess

The sequence in a breastfeeding mother is worth spelling out because it guides prevention. Milk stasis (from poor latch, missed feeds or blocked ducts) provides a stagnant, nutrient-rich medium; a cracked or fissured nipple provides the portal of entry for skin Staphylococcus aureus; the organism multiplies, causing cellulitic mastitis, which — if not relieved by continued drainage of milk and antibiotics — progresses to a walled-off collection of pus, the abscess. Good latch, frequent feeding and nipple care therefore prevent the whole cascade.

WHY Continue Breastfeeding?

A point that surprises students: mothers with lactational mastitis or even an abscess are generally encouraged to continue breastfeeding or expressing from the affected side. This is because the underlying driver is milk stasis — emptying the breast removes the culture medium and helps resolution — and the milk is not harmful to the infant. Stopping abruptly causes engorgement and worsens the problem.

Complications

Untreated or recurrent disease can lead to a chronic abscess, a mammary duct fistula (especially in the non-lactational, smoking-related periductal disease), scarring and distortion of the breast, and — the diagnosis never to miss — a mistaken label of 'abscess' on what is actually an inflammatory carcinoma, which is why non-resolving lesions are always biopsied.

A Note on the Neonatal & Adolescent Breast

Breast infection is overwhelmingly a condition of the lactating adult, but abscesses occasionally occur in neonates (from maternal-hormone-stimulated breast tissue) and adolescents; these are managed conservatively where possible, with careful incision (avoiding the developing breast bud) if drainage is essential. In all age groups the principle is unchanged — antibiotics for cellulitis, drainage for an established collection, and biopsy for anything that does not behave as expected.

A Note on Recurrent & Atypical Infection

Recurrent periareolar infection in a smoker points to periductal mastitis and duct ectasia, and definitive cure often requires total duct excision plus smoking cessation rather than repeated courses of antibiotics. Any breast inflammation that fails to resolve as expected — persistent erythema, an underlying mass, or skin changes — must be imaged and biopsied to exclude inflammatory carcinoma, a cancer that characteristically mimics infection with a red, swollen, peau-d'orange breast. Vigilance for this mimic is the single most important safety point in managing 'breast infection'.

Breastfeeding is generally continued from the affected side.

• Breast abscess = collection of pus, usually following unresolved mastitis; drain the pus.
• Lactational: milk stasis + cracked nipple → Staphylococcus aureus; painful red wedge-shaped area + fever; keep breastfeeding/expressing.
• Non-lactational: smoking + duct ectasia/periductal mastitis; periareolar, mixed/anaerobic organisms, recurs, may form duct fistula.
• Mastitis (no pus) → antibiotics; established abscess → ultrasound-guided aspiration (first-line) or incision and drainage.
• Biopsy the wall / image if atypical or non-resolving — exclude inflammatory carcinoma; stop smoking in non-lactational disease.

The Concept — the Key Questions

Nipple discharge is common and usually benign, but it can occasionally signal cancer, so the assessment is a structured attempt to answer a few key questions: is it from one duct or many, one breast or both, spontaneous or only on squeezing, and what colour is it? The answers separate the reassuring physiological discharge from the discharge that needs investigation. Broadly, bilateral, multi-duct, non-spontaneous discharge is benign; unilateral, single-duct, spontaneous or blood-stained discharge is 'suspicious' and must be worked up.

Physiological & Galactorrhoea

Physiological discharge — small amounts of milky or greenish fluid from multiple ducts of both breasts, only on squeezing — is benign and needs only reassurance. Galactorrhoea is a copious milky discharge unrelated to lactation, caused by hyperprolactinaemia — from a pituitary prolactinoma, drugs (dopamine antagonists), or hypothyroidism — so it is investigated with a serum prolactin, thyroid function and, if raised, pituitary imaging.

Pathological Causes BY Colour

• Blood-stained (or serosanguinous) — the most important to investigate. The commonest cause is a benign duct papilloma, but it can also be duct ectasia or an underlying carcinoma (especially DCIS).
• Thick, cheesy, green/brown, multi-duct — typical of duct ectasia in an older woman.
• Purulent — suggests infection (abscess/periductal mastitis).
• Milky — physiological or galactorrhoea (see above).

Assessment & Management

A patient with suspicious (single-duct, spontaneous or bloody) discharge undergoes triple assessment — examination (looking for a lump and identifying the discharging duct), imaging (mammography ± ultrasound), and testing the discharge (for blood) with biopsy of any mass. Where no cause is found but the discharge is troublesome or suspicious, the discharging duct(s) are excised — microdochectomy (single duct, to preserve breastfeeding in the young) or total duct excision (Hadfield's procedure) (multiple ducts in the older woman) — which is both diagnostic and therapeutic.

The Duct Papilloma

Since it is the commonest cause of the most worrying discharge, the intraductal papilloma deserves emphasis. It is a small, benign, wart-like epithelial growth within a large subareolar duct, and as it is friable it bleeds, producing spontaneous, unilateral, single-duct, blood-stained discharge — often with no palpable lump. It is diagnosed and treated by microdochectomy (excising the affected duct), which also provides histology to confirm it is benign and exclude a papillary carcinoma.

A Structured Approach

Faced with nipple discharge, a logical scheme is: first decide if it is galactorrhoea (bilateral, milky, multi-duct → check prolactin/thyroid and drugs); if not, decide whether it is benign-type (bilateral, multi-duct, on pressure, green/brown → reassure ± treat duct ectasia) or suspicious-type (unilateral, single-duct, spontaneous, bloody → full triple assessment and duct excision). This algorithm ensures the small number of sinister discharges are always investigated while the majority are reassured.

Investigations

Useful investigations include examination to identify the discharging duct and any lump, testing the fluid for blood, mammography and ultrasound (and, for a single discharging duct, sometimes ductography or ductoscopy), and cytology of the fluid (though a negative cytology does not exclude cancer). A discrete lesion is biopsied.

A Note on Malignant Causes

Although most nipple discharge is benign, the features that raise concern for an underlying malignancy (usually DCIS, occasionally invasive or papillary carcinoma) are a bloody or serous single-duct discharge in an older woman, an associated mass, or associated microcalcification on mammography. This is why the 'suspicious' discharge is never simply reassured: even though the commonest cause (duct papilloma) is benign, only triple assessment and, where indicated, duct excision can safely exclude cancer.

A Structured Diagnostic Algorithm

Faced with nipple discharge, a stepwise scheme keeps the assessment safe: first identify galactorrhoea (bilateral, milky, multi-duct → check prolactin, thyroid function, drug history); then separate clearly benign-type discharge (bilateral, multi-duct, on expression, green/brown → reassure, treat duct ectasia) from suspicious discharge (unilateral, single-duct, spontaneous, blood-stained → full triple assessment and, where needed, duct excision). This algorithm reliably investigates the small proportion of sinister discharges while reassuring the majority, and it always ends by excluding an underlying carcinoma before a benign cause is accepted.

Blood-stained single-duct discharge requires investigation.

• Key questions: single vs multiple ducts, unilateral vs bilateral, spontaneous vs on squeezing, and colour.
• Benign/physiological: bilateral, multi-duct, on squeezing, milky/green — reassure.
• Galactorrhoea (milky, non-lactational) = hyperprolactinaemia (prolactinoma, drugs, hypothyroidism) → prolactin, TFTs, pituitary imaging.
• Suspicious: unilateral, single-duct, spontaneous, blood-stained → triple assessment; commonest cause of bloody discharge is duct papilloma (but exclude carcinoma/DCIS).
• Treat by microdochectomy (single duct) or total duct excision/Hadfield's (multiple ducts) when needed.

The Concept — the Central Question Is Cancer

A solitary thyroid nodule is a discrete swelling within one lobe of an otherwise normal-feeling thyroid. It is a common presentation, and the entire work-up is built around answering one question: is it malignant? The reassuring background fact is that only about 5–10% of clinically solitary nodules are cancerous — the great majority are benign — but because a missed thyroid cancer is very treatable when caught, every solitary nodule is assessed systematically rather than dismissed.

What a 'solitary' Nodule Actually Is

It is worth knowing that many apparently solitary nodules are not truly solitary: the commonest finding is a dominant or prominent nodule within an occult multinodular goitre, or a benign colloid nodule. Genuinely discrete lesions include a benign follicular adenoma, a thyroid cyst, an area of thyroiditis, and — the one to exclude — a thyroid carcinoma.

Clinical Red Flags for Malignancy

The history and examination look specifically for features that raise the probability of cancer:

• Age extremes (under 20 or over 60) and male sex.
• Rapid growth, or a hard, irregular, fixed nodule.
• Hoarseness (suggesting recurrent laryngeal nerve infiltration) or dysphagia/stridor.
• Cervical lymphadenopathy.
• A history of neck irradiation in childhood, or a family history of thyroid cancer or men syndrome.

Investigations

The nodule is worked up with a logical sequence of tests:

• Thyroid function tests (TSH, T3, T4) — assess function; a functioning ('toxic') nodule that suppresses the TSH is rarely malignant.
• Ultrasound of the neck — characterises the nodule (solid vs cystic) and looks for suspicious features (microcalcification, hypoechogenicity, irregular margins, increased internal vascularity, taller-than-wide shape) and abnormal nodes.
• Fine-needle aspiration cytology (FNAC) — the single most important investigation, giving a cytological category (Thy/Bethesda) that guides management.
• Radioisotope scan — reserved for a nodule with a suppressed TSH: a 'hot' (functioning) nodule is almost always benign, whereas a 'cold' (non-functioning) nodule carries a ~15–20% malignancy risk.

Management — Guided BY Cytology

Treatment follows the FNAC result. A benign (Thy2) nodule is reassured and observed, with surgery only for size, symptoms or cosmesis. A malignant or suspicious (Thy4/Thy5) nodule is treated by thyroidectomy. The crucial category is the follicular lesion (Thy3): because FNAC cannot distinguish a benign follicular adenoma from a follicular carcinoma, these patients undergo a diagnostic hemithyroidectomy (lobectomy) so the whole lesion can be examined histologically. A simple cyst is aspirated, with excision if it recurs or the fluid is bloodstained.

The Cytology Categories

FNAC results are reported in standardised categories (the Thy or Bethesda system) that directly drive management: Thy1 non-diagnostic (repeat the aspirate), Thy2 benign (reassure/observe), Thy3 follicular/indeterminate (diagnostic hemithyroidectomy), Thy4 suspicious of malignancy, and Thy5 diagnostic of malignancy (proceed to appropriate thyroidectomy). This categorisation is why cytology sits at the centre of the pathway — it converts a lump into a management plan.

The Approach in Summary

Put together, the assessment of any solitary nodule is a disciplined sequence: clinical evaluation for red flags → thyroid function tests → ultrasound → FNAC (with an isotope scan only if the TSH is suppressed). The great value of this scheme is that it confidently reassures the ~90% with benign disease while reliably selecting the ~10% who need surgery — and it never relies on clinical impression alone, because a hard fixed nodule can occasionally be benign and a deceptively soft one malignant.

Clinical Examination of the Nodule

Examination of the neck contributes real information that guides the work-up. The nodule is assessed for size, consistency (soft, firm or hard), surface, mobility, and whether it moves on swallowing (confirming a thyroid origin). The examiner palpates for cervical lymphadenopathy (raising the suspicion of malignancy, especially papillary carcinoma), checks for tracheal deviation and retrosternal extension, listens for a bruit, and assesses the patient's clinical thyroid status. A hard, fixed nodule with palpable nodes and hoarseness is clinically worrying, whereas a soft, mobile, solitary nodule that moves freely is more reassuring — though, as always, imaging and cytology, not clinical feel alone, make the diagnosis.

• Malignancy risk of a clinically solitary nodule ≈ 5–10%; of a 'cold' nodule on scan ≈ 15–20%.
• Follicular lesion on FNAC (Thy3) → diagnostic hemithyroidectomy.
• Hot/toxic nodule → almost always benign.

Most solitary nodules are dominant nodules of a multinodular gland.

• Solitary thyroid nodule: the central task is to exclude malignancy (~5–10% are malignant).
• Red flags: age <20 or >60, male, rapid growth, hard/fixed, hoarseness, nodes, neck irradiation, family history/men.
• Investigate with TFTs, ultrasound, FNAC (most important); isotope scan if TSH suppressed (hot = benign, cold = ~15–20% malignant).
• FNAC cannot distinguish follicular adenoma from carcinoma → follicular lesion needs diagnostic hemithyroidectomy.
• Benign → observe; malignant/suspicious → thyroidectomy; cyst → aspirate (excise if recurs/bloody).

The Concept — Classify BY Cell of Origin & Behaviour

Thyroid cancers are best understood by their cell of origin, because this determines their behaviour, spread, prognosis and treatment. Most arise from the hormone-producing follicular cells and are called 'differentiated' (papillary and follicular) — these behave well. A distinct group arises from the calcitonin-producing parafollicular C cells (medullary carcinoma), and a rare, lethal group is undifferentiated (anaplastic). Holding this classification in mind makes the whole topic coherent.

The Types

A rare thyroid lymphoma can also arise, characteristically in a gland affected by Hashimoto's thyroiditis.

Clinical Features

Most present as a thyroid nodule or swelling, sometimes with features of malignancy — a hard fixed lump, cervical lymphadenopathy, hoarseness (recurrent laryngeal nerve involvement), or dysphagia. Anaplastic carcinoma presents dramatically with a rapidly enlarging hard mass causing stridor, dysphagia and hoarseness from local invasion. Medullary carcinoma may additionally cause flushing and diarrhoea (from calcitonin and other secreted peptides).

Investigations

The nodule is assessed by ultrasound and FNAC with thyroid function tests. For suspected medullary carcinoma, serum calcitonin is a tumour marker, and — critically — the patient is screened for men 2 and an associated phaeochromocytoma (plasma/urinary metanephrines) must be excluded and treated before any thyroid surgery, to avoid a hypertensive crisis on the table.

Management

• Differentiated (papillary/follicular) — total thyroidectomy (hemithyroidectomy for small, low-risk papillary tumours), with neck dissection for involved nodes; radioiodine (I-131) ablation of residual/metastatic thyroid tissue; lifelong thyroxine to suppress TSH (removing the growth stimulus); and serum thyroglobulin as a follow-up marker of recurrence.
• Medullary — total thyroidectomy with central compartment node dissection; it does not take up iodine, so radioiodine is ineffective; follow up with calcitonin.
• Anaplastic — usually palliative (airway protection/tracheostomy, external radiotherapy, chemotherapy), as cure is rarely possible.

Staging & Prognostic Factors

Prognosis in differentiated cancer depends less on the tumour type than on patient and tumour factors captured in scoring systems (such as AMES/ages): Age (older patients do worse), Metastases, Extent of the primary/extrathyroidal spread, and Size. This is why a young woman with node-positive papillary cancer still has an excellent outlook, whereas the same histology in an older patient with extrathyroidal extension is treated far more aggressively.

Follow-up & Recurrence

After treatment of differentiated cancer, follow-up exploits the biology: having removed all normal thyroid tissue, any detectable serum thyroglobulin (or a rising level) signals recurrent or residual tumour, and whole-body radioiodine scans can localise it. For medullary cancer the equivalent markers are calcitonin and CEA. Lifelong follow-up is standard because differentiated cancers can recur years later, and recurrence is often still curable.

Management of Advanced & Recurrent Disease

Advanced differentiated cancer with distant metastases is still often treatable because the tissue may take up radioiodine: metastases in bone or lung can be targeted with therapeutic I-131 after total thyroidectomy, alongside TSH-suppressive thyroxine. Where tumours dedifferentiate and lose iodine avidity, or in progressive medullary and anaplastic disease, newer targeted kinase inhibitors (e.g. Against the RET or BRAF pathways) have a role. External-beam radiotherapy is used for unresectable or symptomatic local disease. The overarching principle is that differentiated thyroid cancer, even when advanced, frequently follows an indolent course and is managed with a long-term outlook.

A Note on Presentation Via Nodes

An important clinical pearl is that differentiated thyroid cancer, especially papillary, may first present as a lateral cervical lymph node rather than a thyroid lump — a firm neck node in a young adult should prompt assessment of the thyroid. Conversely, the finding of thyroid cancer mandates careful assessment of the neck nodal levels, because nodal disease guides the extent of surgery. This bidirectional relationship between the gland and the neck nodes is central to planning the correct operation.

• Differentiated cancer: total thyroidectomy + radioiodine ablation + TSH-suppressive thyroxine; thyroglobulin as marker.
• Medullary: total thyroidectomy + central node dissection; calcitonin marker; NO radioiodine.
• Exclude phaeochromocytoma before medullary/men thyroid surgery.

Papillary spreads by lymphatics; follicular by blood.

• Classify by origin: differentiated (papillary, follicular — follicular cells), medullary (C cells), anaplastic (undifferentiated), lymphoma (Hashimoto's).
• Papillary (commonest, young, lymphatic spread, excellent prognosis); follicular (blood spread to bone/lung, needs histology).
• Medullary: secretes calcitonin, sporadic or men 2 (RET) — screen for phaeochromocytoma first; anaplastic: elderly, rapidly fatal.
• Differentiated → total thyroidectomy + radioiodine + TSH suppression + thyroglobulin follow-up.
• Medullary → total thyroidectomy + central node dissection, no radioiodine; anaplastic → palliative.

The Concept & Classification

A goitre is simply an enlargement of the thyroid gland, and the many causes become manageable if classified along two axes: whether the gland is diffusely enlarged or nodular, and whether it is toxic (overactive) or non-toxic. This grid organises the whole subject.

How a Simple Goitre Becomes Multinodular

Understanding the natural history explains most nodular goitres. Iodine deficiency (or increased demand at puberty/pregnancy) lowers thyroid hormone output, so the pituitary secretes more TSH, which drives diffuse hyperplasia — a soft, smooth simple goitre. Over years of fluctuating stimulation and involution, the gland becomes nodular (multinodular goitre), with some nodules eventually becoming autonomous (toxic MNG) and others developing haemorrhage, cystic change or calcification. This is why endemic (iodine-deficient) regions have so much goitre, and why simple goitres evolve into nodular ones.

Clinical Features

A goitre is a neck swelling that characteristically moves upwards on swallowing (because the thyroid is bound to the larynx by the pretracheal fascia) — the sign that identifies it as thyroid. Examination assesses its size, surface (diffuse or nodular), consistency, lower border (whether it can be felt, or extends retrosternally), any tracheal deviation or compression, cervical nodes, a bruit, and the patient's thyroid status.

Complications

These are high-yield and follow from a mass in the neck:

• pressure effects — dysphagia (oesophagus), dyspnoea and stridor (tracheal compression), and hoarseness (recurrent laryngeal nerve)
• retrosternal extension causing thoracic-inlet obstruction
• secondary thyrotoxicosis (toxic change)
• malignant change
• haemorrhage into a nodule, causing sudden painful enlargement that may acutely compress the airway.

Investigations & Management

Investigate with thyroid function tests, ultrasound, FNAC of any dominant/suspicious nodule, and CT (without iodinated contrast if radioiodine may be needed) to assess retrosternal extension and tracheal compression. A non-toxic simple goitre is usually observed (correcting iodine deficiency). Surgery (total or subtotal thyroidectomy) is indicated for pressure symptoms, retrosternal extension, cosmetic concern, suspected malignancy, or toxic change; toxic goitres are additionally managed with antithyroid drugs or radioiodine.

The Thyroiditides

• Several forms of thyroiditis cause a diffuse goitre and are worth distinguishing.
• Hashimoto's thyroiditis is an autoimmune condition causing a firm diffuse goitre and eventual hypothyroidism (and carries a small risk of thyroid lymphoma).
• De Quervain's (subacute) thyroiditis is a painful goitre following a viral infection, with a transient thyrotoxic phase and a raised ESR, that is usually self-limiting.
• Riedel's thyroiditis is a rare, dense fibrosis producing a hard, fixed ('woody') gland that mimics cancer and can compress adjacent structures.

Retrosternal Goitre

A retrosternal (substernal) goitre is one that extends behind the sternum into the mediastinum, usually as a lower extension of a multinodular goitre. It matters because the confined thoracic inlet means it readily causes tracheal compression and venous obstruction (revealed by Pemberton's sign). It is an indication for surgery, and although it looks alarming, the great majority can be delivered through a standard neck (cervical) incision.

Assessment of Thyroid Status & Airway

Any goitre is assessed for two practical things beyond its size: the patient's thyroid status (euthyroid, hypothyroid or thyrotoxic — because a toxic goitre must be controlled before surgery) and the airway. Longstanding large goitres, especially retrosternal ones, may compress or deviate the trachea and, over time, weaken the tracheal cartilage rings (tracheomalacia), which can collapse when the supporting goitre is removed. Pre-operative assessment therefore includes flow-volume loops or CT where compression is suspected, and the anaesthetist is forewarned, because airway management is the key peri-operative risk in large goitre surgery.

Hashimoto's & the Risk of Lymphoma

Hashimoto's thyroiditis deserves a further note because, besides being the commonest cause of hypothyroidism and a firm diffuse goitre, it carries a small but definite risk of primary thyroid lymphoma. A rapidly enlarging goitre in a patient with known Hashimoto's should therefore raise this suspicion and prompt biopsy, illustrating how a benign autoimmune goitre can occasionally harbour a serious complication.

Retrosternal extension causes tracheal compression and needs assessment.

• Goitre = thyroid enlargement; classify as diffuse vs nodular and toxic vs non-toxic; moves up on swallowing.
• Iodine deficiency → ↑TSH → diffuse hyperplasia (simple goitre) → over years → multinodular goitre → can become toxic.
• Complications: pressure (dysphagia, stridor/dyspnoea, hoarseness), retrosternal extension (Pemberton's sign), toxic change, malignancy, haemorrhage into a nodule.
• Investigate: TFTs, ultrasound, FNAC of dominant nodule, CT for retrosternal/tracheal compression.
• Surgery for pressure symptoms, retrosternal extension, cosmesis, suspected malignancy or toxic change.

The Concept

Thyrotoxicosis is the clinical state produced by an excess of circulating thyroid hormone, and its features flow directly from the fact that thyroid hormone drives the body's metabolic rate and amplifies sympathetic activity. The commonest cause is Graves' disease, an autoimmune condition in which TSH-receptor stimulating antibodies continuously activate the gland — explaining both the diffuse overactivity and the unique extrathyroidal features.

Causes

The main causes are Graves' disease (diffuse, autoimmune — commonest), toxic multinodular goitre (autonomous nodules in an older patient), toxic adenoma (a single hot nodule), and thyroiditis (a transient release of stored hormone). Recognising the cause matters because it determines treatment.

Clinical Features

The hypermetabolic, sympatho-active state produces a characteristic picture: weight loss despite a good appetite, heat intolerance and sweating, palpitations with tachycardia or atrial fibrillation, a fine tremor, anxiety and irritability, diarrhoea, oligomenorrhoea, warm moist skin, and proximal muscle weakness. A goitre is usually present.

Features Specific to Graves' Disease

Because Graves' is autoimmune, it has extrathyroidal signs not seen in other causes, which are diagnostic:

• eye disease (Graves' ophthalmopathy) — exophthalmos/proptosis, lid retraction and lid lag, and, in severe cases, ophthalmoplegia and sight-threatening optic-nerve compression
• pretibial myxoedema (thickened skin over the shins)
• thyroid acropachy (clubbing-like changes)
• a diffuse goitre with an audible bruit (from its vascularity).

Investigations

Confirm with thyroid function tests — a suppressed TSH with raised free T3/T4. TSH-receptor antibodies confirm Graves'. A radioiodine uptake scan distinguishes the causes: diffusely increased uptake in Graves', patchy uptake in toxic MNG, and a single hot area in a toxic adenoma.

Management — Three Modalities

• Antithyroid drugs — carbimazole (or propylthiouracil) block hormone synthesis and render the patient euthyroid, given as a titrated dose or 'block-and-replace'; a 12–18 month course achieves lasting remission in about half of Graves' patients. A beta-blocker (propranolol) rapidly controls the sympathetic symptoms. Patients must be warned that a sore throat may signal agranulocytosis and to have a blood count checked.
• Radioiodine (I-131) — a definitive outpatient treatment that ablates thyroid tissue; it commonly results in hypothyroidism, and is avoided in pregnancy and active eye disease.
• Surgery (thyroidectomy) — for a large or compressive goitre, suspected malignancy, failed drug therapy, or patient choice. The gland must be rendered euthyroid before operation and given Lugol's iodine pre-operatively to reduce its vascularity.

Choosing Between the Three Treatments

• Each modality has trade-offs that guide the choice.
• Antithyroid drugs are non-invasive and can achieve lasting remission in Graves' but require prolonged treatment and carry a relapse rate and the risk of agranulocytosis.
• Radioiodine is simple and definitive but usually leads to lifelong hypothyroidism and is unsuitable in pregnancy or active eye disease.
• Surgery gives rapid, definitive control and is preferred for large/compressive goitres, suspected malignancy, or when the other options fail or are contraindicated, at the cost of the operative risks. The decision is individualised to the cause, goitre size, eye disease, pregnancy plans and patient preference.

Graves' Ophthalmopathy & Pregnancy

Graves' eye disease is autoimmune and runs a course partly independent of the thyroid; it is worsened by smoking and by radioiodine, and severe, sight-threatening disease needs high-dose steroids, orbital radiotherapy or surgical decompression. In pregnancy, propylthiouracil is generally preferred in the first trimester and radioiodine is contraindicated — an important safety point.

Thyrotoxicosis in Special Situations

Two situations deserve emphasis. In pregnancy, thyrotoxicosis must be controlled to protect mother and fetus, but radioiodine is absolutely contraindicated (it crosses the placenta and ablates the fetal thyroid), so antithyroid drugs are used — propylthiouracil in the first trimester — at the lowest effective dose, with surgery reserved for drug failure. In the elderly, thyrotoxicosis may present atypically as 'apathetic thyrotoxicosis' — with weight loss, atrial fibrillation and lethargy rather than the classic hyperkinetic picture — so it must be actively considered as a cause of new atrial fibrillation or unexplained weight loss in older patients.

• Carbimazole to render euthyroid; propranolol for sympathetic symptoms; warn re agranulocytosis (sore throat → FBC).
• Lugol's iodine ~10 days pre-op to reduce gland vascularity.
• Radioiodine avoided in pregnancy and active Graves' eye disease.

Ophthalmopathy occurs only in Graves disease, not other causes.

• Thyrotoxicosis = excess thyroid hormone → hypermetabolic + sympathetic features; Graves' (autoimmune, TSH-receptor antibodies) is commonest.
• Causes: Graves', toxic MNG, toxic adenoma, thyroiditis.
• Features: weight loss with good appetite, heat intolerance, palpitations/AF, tremor, anxiety, diarrhoea; Graves'-specific: eye disease, pretibial myxoedema, acropachy, diffuse goitre with bruit.
• Diagnose: low TSH + high T3/T4, TSH-receptor antibodies, radioiodine uptake scan (diffuse/patchy/single-hot).
• Treat with antithyroid drugs (carbimazole) + propranolol, radioiodine, or surgery; render euthyroid + Lugol's iodine before surgery to prevent thyroid storm.

The Concept — Anatomy & Timing

The complications of thyroidectomy are best learned through the anatomy of the structures the surgeon works around and the timing at which each appears. The thyroid is intimately related to the recurrent and external laryngeal nerves, the parathyroid glands, the trachea and major vessels, and damage to any of these produces a characteristic, often examinable, complication.

Haemorrhage & Tension Haematoma

Reactionary haemorrhage into the closed neck space is the most urgent early complication. Because the neck is a confined compartment, an expanding tension haematoma compresses the trachea and causes rapid airway obstruction — a true emergency. The life-saving action is to open the wound immediately at the bedside (removing skin and strap-muscle sutures) to release the haematoma and relieve the airway, before returning to theatre.

Nerve Injuries

• Recurrent laryngeal nerve (RLN) — runs in the tracheo-oesophageal groove near the inferior thyroid artery. Unilateral injury causes hoarseness (a paralysed vocal cord); bilateral injury is an emergency causing stridor and airway obstruction (both cords paralysed near the midline), often requiring re-intubation or tracheostomy.
• External (superior) laryngeal nerve — near the superior thyroid pedicle; injury weakens the cricothyroid muscle, causing loss of vocal pitch and voice fatigue — particularly disabling for singers.

Hypocalcaemia

The parathyroid glands may be inadvertently removed or devascularised, causing hypoparathyroidism and a fall in serum calcium, typically at 24–72 hours. This produces neuromuscular irritability — perioral tingling, paraesthesiae, carpopedal spasm, and positive Chvostek's and Trousseau's signs — and, if severe, tetany and laryngospasm. It is usually transient but can be permanent after total thyroidectomy.

Airway Problems & Thyroid Storm

Airway obstruction can result from a haematoma, bilateral RLN palsy, laryngeal oedema, or tracheomalacia (softened tracheal rings after a long-standing large goitre, collapsing when support is removed). In an inadequately prepared thyrotoxic patient, the operation can precipitate a thyroid storm.

Late Complications

Later problems include hypothyroidism (inevitable after total thyroidectomy; may also develop after subtotal resection), recurrent thyrotoxicosis or goitre after subtotal surgery, permanent hypoparathyroidism or RLN palsy, and a hypertrophic or keloid scar.

Types of Thyroidectomy

The operation performed depends on the pathology, and each carries its own risk profile. A hemithyroidectomy (lobectomy) removes one lobe (diagnostic for a follicular lesion, or treatment for benign unilateral disease). A total thyroidectomy removes the whole gland (for cancer or large bilateral goitre) but carries the highest risk of bilateral nerve injury and permanent hypoparathyroidism. A subtotal thyroidectomy (leaving a remnant) was traditionally used for Graves'/goitre to preserve function but risks recurrence. Matching the operation to the disease balances cure against the risk of these complications.

Prevention & Post-operative Monitoring

Most complications are minimised by careful technique — identifying and preserving the recurrent laryngeal nerves and parathyroid glands (with auto-transplantation of a devascularised parathyroid), meticulous haemostasis, and pre-operative preparation of thyrotoxic patients. Post-operatively the patient is watched for airway compromise and neck swelling (with clip-removers/suture-cutters kept at the bedside for a haematoma), and serum calcium is checked; vocal-cord function is assessed if the voice is abnormal.

Minimising Risk & Consent

Because these complications are well defined, safe thyroid surgery rests on prevention and informed consent. The surgeon routinely identifies and preserves the recurrent laryngeal nerves and parathyroid glands, uses meticulous haemostasis to prevent a haematoma, and prepares thyrotoxic patients to be euthyroid. Some units use intra-operative nerve monitoring to help protect the recurrent laryngeal nerve. The patient should be consented specifically for the risks of voice change (nerve injury), low calcium (hypoparathyroidism), bleeding, and lifelong thyroxine, so that these recognised outcomes are understood in advance rather than discovered afterwards.

• Airway-threatening neck haematoma → open the wound at the bedside immediately.
• Check serum calcium post-op; severe hypocalcaemia → IV calcium gluconate + oral calcium/vitamin D.
• Unilateral RLN palsy → hoarseness; bilateral → stridor/airway emergency.

Tension haematoma is the emergency — open the wound at the bedside.

• Learn complications by anatomy (nerves, parathyroids, trachea, vessels) and timing (immediate/early/late).
• Tension haematoma → rapid airway obstruction → open the wound at the bedside immediately (emergency).
• RLN injury: unilateral = hoarseness, bilateral = stridor/airway emergency; external laryngeal nerve = loss of voice pitch (singers).
• Hypocalcaemia (parathyroid injury) at 24–72 h: perioral tingling, carpopedal spasm, Chvostek's/Trousseau's → calcium ± vitamin D.
• Also airway obstruction (haematoma/bilateral RLN/tracheomalacia), thyroid storm (unprepared), and late hypothyroidism/recurrence/keloid.

The Concept & a Useful Rule

Salivary gland tumours arise mostly in the parotid gland (about 80%), less often in the submandibular gland, and least in the minor salivary glands. There is a single elegant rule that organises the topic: the smaller the gland, the more likely a tumour in it is malignant. So most parotid tumours are benign (~80%), whereas about half of minor salivary gland tumours are malignant. This inverse relationship guides how worried you are about any given salivary swelling.

Classification

Clinical Features — Benign VS Malignant

A benign tumour is typically a slow-growing, painless, smooth, mobile lump — a pleomorphic adenoma classically appears as a swelling over the angle of the jaw or in the parotid tail. The features that signal malignancy are the ones to look for actively: rapid growth, pain, a hard or fixed lump, skin or deep-structure infiltration, cervical lymphadenopathy, and — most importantly for a parotid mass — a facial nerve palsy, because the facial nerve runs through the parotid and a malignant tumour infiltrates it.

Investigation

Assessment uses FNAC (to obtain a tissue diagnosis), ultrasound, and MRI (to define the extent and whether the deep lobe or facial nerve is involved). An important principle is to avoid open incisional biopsy of a parotid mass, because it risks seeding tumour and damaging the facial nerve — the diagnosis is made by needle, and the definitive excision provides the full histology.

Management

• Benign parotid tumour (pleomorphic adenoma) — superficial parotidectomy (removing the superficial lobe containing the tumour) with careful preservation of the facial nerve. Simple enucleation is avoided because the tumour has microscopic extensions through an incomplete capsule and recurs.
• Submandibular tumour — excision of the whole gland.
• Malignant tumour — radical excision (sacrificing the facial nerve only if it is directly involved), neck dissection for nodal disease, and post-operative radiotherapy.

The Facial Nerve & Parotid Anatomy

The facial nerve is the central character in parotid surgery: it enters the gland and divides it into an artificial superficial and deep lobe, its branches fanning out over the face. This is why a superficial parotidectomy — which removes the part of the gland superficial to the nerve — can treat most benign tumours while sparing facial movement, and why identifying and preserving the nerve trunk (found at landmarks such as the tragal pointer) is the crux of the operation. Deep-lobe tumours are more challenging and may present as a parapharyngeal swelling.

Complications of Parotidectomy

The complications follow the anatomy: facial nerve injury (temporary neuropraxia or permanent palsy), Frey's syndrome (gustatory sweating from aberrant nerve regeneration), a salivary fistula or sialocele, greater auricular nerve numbness of the ear lobe, and haematoma. Knowing these allows proper consent and post-operative care.

Deep-lobe & Parotid Duct

Beyond the common superficial tumour, a deep-lobe parotid tumour may grow medially into the parapharyngeal space and present as a swelling of the soft palate or tonsil pushing it towards the midline, rather than as an obvious facial lump — a presentation worth recognising. The parotid also drains via Stensen's duct, which opens opposite the second upper molar; obstruction or a tumour here can cause recurrent parotid swelling. These anatomical facts explain the varied ways parotid pathology presents and why imaging (MRI) is used to map the deep lobe before surgery.

Staging, Grading & Prognosis

Malignant salivary tumours are staged by the TNM system (size, nodal spread, metastasis) and graded histologically, both of which drive treatment intensity and prognosis. High-grade tumours (high-grade mucoepidermoid, adenoid cystic, salivary duct carcinoma) behave aggressively with nodal and distant spread, whereas low-grade tumours may be cured by surgery alone. Facial nerve involvement, extra-glandular extension and positive nodes all worsen the outlook. This is why the pre-operative assessment (FNAC grade, MRI extent, nodal status) matters so much: it separates the patient who needs only a superficial parotidectomy from the one who needs radical surgery, neck dissection and radiotherapy.

A Clinical Summary

In summary, the assessment of a salivary swelling asks three questions: which gland, benign or malignant, and (for the parotid) is the facial nerve involved? A slow, painless, mobile parotid lump with an intact nerve is very likely a pleomorphic adenoma treated by superficial parotidectomy; pain, fixation, rapid growth, nodes or nerve palsy signal malignancy needing radical surgery and radiotherapy. This simple triad — gland, behaviour, nerve — organises the whole topic for the viva.

• Parotid ~80% of tumours and ~80% benign; the smaller the gland, the higher the malignancy risk.
• Facial nerve palsy + parotid mass = malignancy until proven otherwise.
• Pleomorphic adenoma → superficial parotidectomy (not enucleation); avoid open biopsy of the parotid.

The smaller the gland, the greater the chance of malignancy.

• Most salivary tumours are in the parotid (~80%) and benign; the smaller the gland, the higher the malignancy risk.
• Benign: pleomorphic adenoma (commonest, recurs if enucleated), Warthin's tumour (older men, bilateral, cystic). Malignant: mucoepidermoid (commonest malignant), adenoid cystic (perineural, lung mets).
• Malignant features: rapid growth, pain, hard/fixed, skin/node involvement, and facial nerve palsy (parotid).
• Investigate with FNAC, ultrasound, MRI; avoid open incisional biopsy of the parotid.
• Pleomorphic adenoma → superficial parotidectomy preserving the facial nerve; malignant → radical excision ± nerve sacrifice + neck dissection + radiotherapy.

The Concept — a System for a Common Problem

Neck swellings are common and have a wide differential, so the key skill is a systematic approach rather than memorising a long list. Three simple axes narrow the diagnosis quickly: the anatomical location of the swelling, the age of the patient, and the pathological category. Combining these, together with a focused examination, usually points to the diagnosis before any investigation.

BY Location — Midline VS Lateral

Location is the first great divider. Midline swellings are few and specific: a thyroglossal cyst, a thyroid isthmus mass, a dermoid cyst, or a submental lymph node. Lateral swellings are far more numerous and are further localised by the anterior and posterior triangles — for example, a branchial cyst lies at the anterior border of sternocleidomastoid, while a cystic hygroma classically occupies the posterior triangle.

BY Age

Age powerfully shifts the probabilities. In children and young adults, think of congenital lesions (thyroglossal cyst, branchial cyst, cystic hygroma) and reactive lymphadenopathy. In older adults, the emphasis shifts firmly towards neoplasia — a metastatic lymph node or lymphoma — which is why the same lump is approached very differently at 15 and at 65.

BY Pathology

It also helps to run through pathological categories: congenital (thyroglossal/branchial cyst, cystic hygroma), inflammatory (reactive or tuberculous lymphadenitis), neoplastic (metastatic node, lymphoma, salivary or thyroid tumour), and swellings of specific structures (thyroid, salivary glands, vascular such as a carotid body tumour).

History & Examination

The history notes duration and growth, pain, and associated symptoms (fever, weight loss, night sweats; ENT symptoms such as hoarseness, dysphagia or nasal obstruction). Examination defines the swelling's site, size, shape, consistency, mobility, fluctuation and transillumination (cystic lesions), pulsatility (vascular), and its movement on swallowing (thyroid) or tongue protrusion (thyroglossal cyst). Crucially it includes examining the likely primary sites — the scalp, oral cavity, and upper aerodigestive tract — and all other node groups.

Investigation

FNAC and ultrasound are the first-line investigations; CT/MRI defines extent, and in a suspected metastatic node an ENT panendoscopy searches for the primary. Blood tests are added as indicated.

Special Examination Techniques

Certain bedside tests clinch specific diagnoses and are worth listing: transillumination (a cystic hygroma lights up brilliantly), pulsatility and a bruit (a carotid body tumour or aneurysm), movement on swallowing (thyroid) versus movement on tongue protrusion (thyroglossal cyst), compressibility and emptying (a vascular malformation), and side-to-side but not vertical mobility (a carotid body tumour). Eliciting the right sign often makes the diagnosis clinically before any scan.

A Note on Levels

Surgeons describe cervical nodes by anatomical levels (I–VI), which matters because the level of a metastatic node predicts the likely site of the primary tumour — for example, upper (level II) nodes often relate to oropharyngeal primaries, and a left supraclavicular (Virchow's) node classically points to an abdominal (e.g. Gastric) primary. This orderly drainage is what makes the neck examination so informative.

Working Through a Differential

In practice the clinician combines the axes: a midline swelling moving on tongue protrusion in a child is a thyroglossal cyst; a brilliantly transilluminable posterior-triangle swelling in an infant is a cystic hygroma; a fluctuant swelling at the upper anterior border of sternocleidomastoid in a young adult is a branchial cyst; a pulsatile lump splaying the carotid is a carotid body tumour; and a hard fixed node in an older smoker is a metastasis. Rehearsing these pattern-recognitions turns a daunting differential into a short, targeted list once the site, age and physical signs are known.

Investigations in Sequence

A logical investigation ladder avoids both under- and over-testing. Ultrasound with FNAC is the first-line workhorse — it distinguishes solid from cystic, characterises nodes, and yields cytology at the same sitting. Cross-sectional imaging (CT/MRI) then maps the extent, deep structures and other nodes. Blood tests (full blood count, and specific serology or LDH if lymphoma or infection is suspected) are added selectively, and an ENT panendoscopy is arranged for a suspected metastatic squamous node. The guiding idea is that each test is chosen to answer a specific question raised by the clinical assessment, not ordered reflexively.

Putting It Together

The value of the systematic approach is that it converts anxiety about a long differential into a confident, targeted plan: define the swelling by location, age and physical signs; place it in a pathological category; confirm with FNAC and ultrasound; and, in any adult over 40, treat a persistent lump as a metastatic node until the upper aerodigestive tract has been cleared. Applied consistently, this scheme rarely misses a serious diagnosis.

Anatomical location narrows the differential more than any test.

• Approach a neck swelling systematically by location, age and pathology.
• Midline: thyroglossal cyst, thyroid isthmus, dermoid, submental node. Lateral: localise by anterior/posterior triangle.
• Children/young: congenital + reactive nodes; older adults: think neoplastic (metastatic node, lymphoma).
• Examine for consistency, fluctuation/transillumination, movement on swallowing/tongue protrusion, and the primary sites (scalp, oral cavity, aerodigestive tract).
• FNAC + ultrasound first; over-40 lump = metastatic node until proven otherwise (panendoscopy for the primary); avoid blind excision biopsy (except suspected lymphoma).

The Concept

Enlargement of the cervical lymph nodes is extremely common, and the whole art is separating the trivial from the sinister. The causes fall into three broad groups — reactive/inflammatory, specific infection (notably tuberculosis), and neoplastic (metastatic carcinoma or lymphoma) — and the character of the nodes plus the patient's age usually indicates which group is responsible.

Causes

• Reactive (inflammatory) — the commonest: acute tender nodes accompanying an upper respiratory, throat or dental infection, and chronic reactive nodes. These are soft, tender and mobile.
• Tuberculous lymphadenitis — a chronic, often matted group of nodes that may caseate to form a 'cold abscess', which can point through the deep fascia as a 'collar-stud' abscess and discharge as a chronic sinus. Other specific infections include HIV, toxoplasmosis and cat-scratch disease.
• Metastatic carcinoma — typically a hard, fixed node, most often squamous carcinoma from a head-and-neck primary (also thyroid and, at the left supraclavicular Virchow's node, from the abdomen).
• Lymphoma — characteristically rubbery, multiple, non-tender nodes, often with systemic 'B symptoms' (fever, night sweats, weight loss).

Assessment

The examination reads the nodes like a diagnostic text: their number and site, consistency (soft = reactive, rubbery = lymphoma, stony-hard = metastatic), mobility or fixity, tenderness, and matting (suggesting TB). One then searches for a primary in the head and neck and assesses for systemic features.

Investigations

FNAC is the first-line test and ultrasound characterises the nodes. For a suspected metastatic squamous node, an ENT panendoscopy with biopsy hunts for the primary. If lymphoma is suspected, an excision biopsy of a whole node is required — because diagnosis and subtyping depend on the architecture, which FNAC cannot show. Tuberculous nodes are confirmed by Ziehl-Neelsen staining, culture and histology (caseating granulomas).

Management

Treatment is directed at the cause: antibiotics for bacterial lymphadenitis, a full course of anti-tuberculous chemotherapy for TB, treatment of the primary plus neck dissection for metastatic carcinoma, and chemotherapy/radiotherapy for lymphoma.

Tuberculous Lymphadenitis in Detail

TB cervical nodes (scrofula) deserve emphasis in this setting. They typically present as a chronic, painless, matted mass of nodes in a young adult, which may progress through stages: firm discrete nodes → matting → caseation forming a fluctuant 'cold' abscess (cold because it lacks the heat of acute inflammation) → the pus tracking through the deep fascia to form a 'collar-stud' abscess → discharge as a chronic non-healing sinus. Diagnosis is by FNAC/biopsy (caseating granulomas, acid-fast bacilli) and treatment is a full course of anti-tuberculous chemotherapy, not primarily surgery.

Lymphoma — WHY Excision Biopsy

The reason lymphoma demands an excision (or generous core) biopsy rather than FNAC is fundamental: classifying a lymphoma — and therefore choosing treatment — depends on the nodal architecture and immunohistochemistry, which need an intact node. A cytology smear showing lymphocytes cannot distinguish reactive change from lymphoma or subtype it, so a suspicious rubbery node with systemic symptoms goes to excision biopsy.

The Metastatic Neck Node — a Structured Search

When a node is judged metastatic, the search for the primary is systematic: a thorough examination of the scalp, skin, oral cavity, oropharynx, nasopharynx, larynx and hypopharynx, followed by examination under anaesthesia with panendoscopy and biopsy of any suspicious mucosa, and cross-sectional imaging (CT/MRI) and increasingly pet-CT to find an occult primary. Only when a primary is truly not found (a genuine 'occult primary') is the neck itself treated. This disciplined hunt reflects the principle that treating a metastatic node without addressing its source is futile.

Virchow's Node & Distant Primaries

Not every metastatic cervical node comes from a head-and-neck primary. The classic exception is Virchow's node — an enlarged left supraclavicular node (Troisier's sign) — which receives thoracic-duct drainage and characteristically signals an abdominal or thoracic primary, most famously gastric carcinoma (also pancreatic, oesophageal, testicular, or lymphoma). Finding such a node therefore redirects the search to the abdomen and chest rather than the upper aerodigestive tract, a distinction that examiners like to test and that changes the entire investigative pathway.

A Summary of the Approach

The safe endpoint is a firm rule set: read the nodes by consistency and matting; investigate with FNAC and ultrasound; excision-biopsy only for suspected lymphoma; panendoscopy to find the primary of a metastatic squamous node; and never blindly excise an undiagnosed node. Treatment then follows the cause. This discipline reliably distinguishes the benign reactive node from the tuberculous mass and the sinister metastasis.

In adults, a hard fixed node is metastatic until proved otherwise.

• Three groups: reactive/inflammatory, specific infection (TB), neoplastic (metastatic carcinoma, lymphoma).
• Consistency reads the cause: soft/tender = reactive, rubbery/multiple = lymphoma, stony-hard/fixed = metastatic; matted ± cold abscess = TB.
• FNAC + ultrasound first-line; panendoscopy to find the primary of a metastatic squamous node.
• Suspected lymphoma → excision biopsy (architecture needed), not FNAC; TB → ZN stain, culture, caseating granulomas.
• Treat the cause: antibiotics / anti-TB therapy / treat primary + neck dissection / chemo-radiotherapy for lymphoma.

The Concept — WHY the Submandibular Gland?

Salivary calculi (sialolithiasis) form overwhelmingly in the submandibular gland (about 80%), and understanding why explains the whole condition. The submandibular gland produces thicker, more mucinous, more alkaline saliva rich in calcium, and its duct (Wharton's duct) is long and runs uphill against gravity to open in the floor of the mouth — a perfect recipe for stasis and stone formation. A stone then obstructs salivary flow, causing swelling and predisposing to infection.

Salivary Calculi — Clinical Features

The hallmark is painful swelling of the gland at mealtimes: eating (or even the sight of food) stimulates salivation, but the obstructing stone prevents outflow, so the gland swells and aches, then gradually settles between meals. A stone may be palpable in the floor of the mouth along the duct. Recurrent obstruction predisposes to recurrent sialadenitis.

Salivary Calculi — Diagnosis & Treatment

Diagnosis is by bimanual palpation of the floor of the mouth, a plain X-ray (most submandibular stones are radio-opaque), and ultrasound, sialography or CT. Treatment depends on the site: a stone near the duct orifice can be removed intra-orally (by incising the duct), whereas a stone within the gland or a gland damaged by recurrent infection is treated by excision of the submandibular gland. Sialendoscopy is a modern minimally-invasive option.

Sialadenitis

Sialadenitis (inflammation of a salivary gland) has several forms:

• Acute bacterial (suppurative) parotitis — classically in a dehydrated, elderly or post-operative patient with poor oral hygiene, where reduced salivary flow allows Staphylococcus aureus to ascend the duct. There is a painful, hot, swollen, tender parotid, and pus may be expressed from the duct.
• Viral — mumps, typically causing bilateral parotid swelling.
• Chronic / recurrent — from obstruction, or autoimmune disease (Sjögren's syndrome).

Acute bacterial parotitis is treated with rehydration, antibiotics, oral hygiene and salivary stimulation, with drainage if an abscess forms — and, importantly, it is largely preventable by keeping post-operative patients well hydrated with good mouth care.

Complications of Obstruction

Persistent salivary obstruction has consequences beyond the mealtime pain: recurrent acute sialadenitis, formation of an abscess, and eventually chronic sialadenitis with irreversible fibrosis and atrophy of the gland (which is then best excised). Understanding this progression explains why a symptomatic stone within the gland, or a gland damaged by repeated infection, is treated by gland excision rather than repeated conservative measures.

Submandibular Gland Excision

When excision is needed, the surgeon must be aware of three nearby nerves at risk: the marginal mandibular branch of the facial nerve (injury droops the corner of the mouth), the lingual nerve (tongue sensation and taste), and the hypoglossal nerve (tongue movement). Careful technique to preserve these is central to the operation.

Viral & Autoimmune Sialadenitis

Two non-bacterial forms round out the topic. Mumps, a paramyxovirus, causes painful bilateral parotid swelling in children, and is important for its complications (orchitis, meningitis, pancreatitis). Sjögren's syndrome is an autoimmune destruction of salivary and lacrimal glands causing dry mouth and dry eyes (sicca syndrome), often with bilateral gland enlargement and a raised risk of salivary lymphoma in the long term. Recognising these prevents mislabelling every swollen gland as a stone or bacterial infection.

The practical upshot across sialadenitis is that the history usually reveals the type — mealtime pain suggests obstruction, an acutely hot tender gland in a dehydrated patient suggests bacterial infection, bilateral childhood swelling suggests mumps, and chronic dryness suggests Sjögren's — which then directs the appropriate investigation and treatment.

Principles of Management Summarised

Pulling the salivary infections and stones together, management follows three principles. First, relieve obstruction — remove a stone or dilate a stricture so saliva can flow. Second, treat infection — antibiotics, hydration and oral hygiene for acute bacterial sialadenitis, with drainage of any abscess. Third, remove the diseased gland when it is irreversibly damaged by recurrent infection or harbours a proximal stone. Underlying all of these is the recognition that salivary stasis is the common enemy, so measures that keep saliva flowing (hydration, sialogogues, good oral care) both treat and prevent these conditions.

A Summary of Principles

Across salivary obstruction and infection the theme is that salivary stasis is the common enemy: relieve obstruction, treat infection, and excise an irreversibly damaged gland — while keeping saliva flowing (hydration, sialogogues, oral hygiene) to both treat and prevent disease. Mealtime submandibular swelling means a stone; a hot tender parotid in a dehydrated post-operative patient means bacterial parotitis.

Submandibular gland is most affected — viscous mucous saliva, uphill duct.

• Salivary stones form mostly in the submandibular gland (~80%) — thick mucinous alkaline saliva + long uphill duct (Wharton's).
• Classic feature: painful gland swelling at mealtimes, settling between meals; stone often palpable in the floor of the mouth.
• Diagnose by palpation, plain X-ray (radio-opaque), ultrasound/sialography; treat by intra-oral removal (distal stone) or gland excision (proximal/recurrent).
• Acute bacterial (Staph) parotitis: dehydrated/elderly/post-op patient, hot tender parotid, pus from duct → hydration, antibiotics, oral hygiene, drainage.
• Also viral (mumps, bilateral) and autoimmune (Sjögren's); prevent bacterial parotitis with hydration and mouth care.

The Concept — a Developmental Remnant

A branchial cyst is a developmental swelling arising from remnants of the branchial (pharyngeal) apparatus — the embryonic structures that form the head and neck. Most arise from incomplete obliteration of the second branchial cleft. Understanding this embryological origin explains its characteristic location and its occurrence in young people, and distinguishes it from acquired neck lumps.

Branchial CYST — Clinical Features

It typically presents in a young adult (20–30 years) as a smooth, soft, fluctuant swelling at the junction of the upper third and lower two-thirds of the sternocleidomastoid muscle, deep to its anterior border. It is often noticed when it enlarges or becomes infected (painful and inflamed). Aspiration classically yields fluid containing cholesterol crystals. The diagnosis is supported by ultrasound and FNAC.

Branchial Fistula & Sinus

A branchial fistula results when both ends of the branchial cleft persist, leaving a track between the skin and the pharynx; a sinus opens at one end only. The external opening is characteristically at the lower third of the neck, at the anterior border of sternocleidomastoid, and may discharge mucus or become recurrently infected. A complete fistula runs upward to open internally near the tonsillar fossa.

Management

The treatment of both cyst and fistula is complete surgical excision of the lesion and any tract; incomplete removal leads to recurrence, and excision is best done when the lesion is not acutely inflamed. Care is taken because the tract of a fistula runs close to important structures (the carotid vessels and cranial nerves).

The Important Caveat in Older Patients

A crucial teaching point: while a branchial cyst is a genuine diagnosis in the young, a cystic lateral neck swelling appearing for the first time in a patient over 40 must not be assumed to be a branchial cyst — it may be a cystic metastasis from a head-and-neck squamous carcinoma (often from an HPV-related oropharyngeal primary, e.g. The tonsil), which can present as a cystic node. Such patients need full investigation (FNAC, imaging, panendoscopy) rather than simple excision.

Other Branchial Anomalies & the Differential

The second cleft is much the commonest, but anomalies of the first, third and fourth branchial arches also occur and present at characteristic sites (a first-cleft anomaly near the ear/angle of jaw; third/fourth-arch sinuses low in the neck, sometimes causing recurrent thyroiditis). The differential for the classic branchial cyst includes a cold abscess, lymph node, or cystic metastasis, which is why FNAC and imaging are used before excision.

Principles of Excision

Complete excision requires removing the entire lining and tract; a fistula tract is best defined (sometimes with a probe or dye) and excised in continuity, occasionally needing a second, higher 'step-ladder' incision to follow it up towards the pharynx. Because the second-arch tract passes between the internal and external carotid arteries and near cranial nerves, meticulous dissection is essential.

Embryology Made Simple

A brief grasp of the embryology makes the anomalies memorable. The branchial (pharyngeal) apparatus consists of a series of arches separated externally by clefts and internally by pouches; each arch forms particular structures (muscles, cartilages, nerves) of the head and neck. Normally the clefts are obliterated; when a remnant of the second cleft persists it forms the classic branchial cyst, sinus or fistula in the upper lateral neck. This is why these lesions lie along a predictable line and in young people, before acquired pathology becomes common.

Timing & Outcome of Surgery

The timing of excision matters: an acutely infected branchial cyst is treated first with antibiotics (and drainage if it abscesses), with definitive excision deferred until the inflammation settles, because operating in an inflamed field risks incomplete removal and injury to adjacent structures. With complete excision the outcome is excellent and recurrence uncommon; incomplete removal of a tract is the usual reason for recurrence. In every case in an older patient, the histology of the excised 'cyst' is reviewed to ensure a cystic metastasis has not been missed — closing the loop on the key safety caveat.

A Summary for the Viva

The examinable essence is: a fluctuant swelling at the upper-third anterior border of sternocleidomastoid in a young adult is a branchial cyst (cholesterol crystals on aspiration), treated by complete excision; a fistula opens at the lower-third anterior border and runs up towards the tonsillar fossa; and — the safety caveat — a new cystic lateral neck swelling after 40 may be a cystic squamous metastasis, so investigate before excising.

Classically presents in the second or third decade.

• Branchial cyst = developmental remnant, usually of the 2nd branchial cleft; young adults (20–30).
• Smooth, fluctuant swelling at the junction of upper 1/3 and lower 2/3 of sternocleidomastoid, deep to its anterior border; aspirate shows cholesterol crystals; may get infected.
• Branchial fistula/sinus: external opening at the lower-third anterior border of SCM; complete fistula runs up to the tonsillar fossa.
• Treat both by complete surgical excision of the lesion/tract.
• Caveat: a new cystic lateral neck swelling in a patient >40 may be a cystic squamous metastasis — investigate (panendoscopy), don't just excise.

The Concept — Two Cancers in One Organ

Oesophageal carcinoma is really two different diseases that share an organ, and grasping this distinction organises the whole topic. The two histological types — squamous cell carcinoma and adenocarcinoma — differ in their site, their risk factors and their epidemiology. Both share a grim feature, however: because the oesophagus has no serosal covering and a rich submucosal lymphatic network, the tumour spreads early and presents late, so the prognosis is generally poor.

The Two Types

The key link to remember is that adenocarcinoma arises from Barrett's oesophagus — the metaplastic change caused by chronic acid reflux — which is why long-standing GORD is a cancer risk.

Clinical Features

The cardinal symptom is progressive dysphagia — difficulty swallowing that begins with solids and advances to liquids as the lumen narrows — accompanied by marked weight loss. Other features include odynophagia (painful swallowing), regurgitation, and anaemia from chronic bleeding. Late or advanced disease may cause hoarseness (recurrent laryngeal nerve involvement), a cough on swallowing (a tracheo-oesophageal fistula), and supraclavicular lymphadenopathy.

Spread

• The routes of spread explain the late, incurable presentation.
• Direct spread invades the mediastinum, trachea and aorta (unchecked by any serosa).
• Lymphatic spread is early and extensive through the submucosal plexus, producing 'skip lesions' away from the main tumour.
• Blood-borne spread reaches the liver and lungs, and transcoelomic spread can occur for lower tumours.

Investigation & Staging

Upper GI endoscopy with biopsy is the diagnostic test, directly visualising the tumour and providing tissue. Staging then determines whether cure is possible: CT of the chest and abdomen (distant spread), endoscopic ultrasound (EUS) (the depth of invasion, T stage, and local nodes, N stage), pet-CT (occult metastases), and staging laparoscopy for lower/junctional tumours (peritoneal disease).

Management

• Curative treatment — possible only in early, localised disease: oesophagectomy (e.g. The Ivor-Lewis or transhiatal approach), usually preceded by neoadjuvant chemotherapy or chemoradiotherapy to improve outcomes.
• Palliative treatment — for the majority who present late, the goal is to relieve dysphagia and maintain quality of life with a self-expanding metal stent, radiotherapy or chemotherapy, laser recanalisation, and nutritional and supportive care.

Nutrition & the Multidisciplinary Approach

Because dysphagia and cachexia dominate the illness, nutritional support is central — many patients need feeding via a fine-bore nasogastric tube, a feeding jejunostomy, or a stent to restore swallowing before and during treatment. Care is delivered by a multidisciplinary team (upper-GI surgeon, oncologist, radiologist, pathologist, dietitian and specialist nurse) that decides between curative and palliative pathways based on stage and fitness. Given that most patients present with incurable disease, honest discussion of prognosis and early involvement of palliative care are as important as the technical options.

Alarm Features & Early Detection

The lesson from the poor prognosis is the value of acting on 'alarm' symptoms: any patient over ~55 with new dysphagia, weight loss, persistent vomiting, gastrointestinal bleeding or iron-deficiency anaemia needs urgent endoscopy. In patients with long-standing reflux, recognising and surveilling Barrett's oesophagus offers the chance to detect adenocarcinoma at a curable, early stage — the main opportunity to improve on the generally dismal outcomes of established disease.

A Note on Palliation

Since most patients are incurable, effective palliation is a large part of oesophageal cancer care. The dominant problem is dysphagia, best relieved by a self-expanding metal stent placed endoscopically, which restores swallowing quickly; radiotherapy (external beam or brachytherapy) and chemotherapy shrink the tumour and prolong relief, and laser or argon-plasma coagulation can recanalise an obstructing tumour. Managing pain, nutrition, and a distressing tracheo-oesophageal fistula (with a covered stent) are central goals, delivered with early palliative-care involvement.

• Diagnostic test = upper GI endoscopy + biopsy; stage with CT, EUS, pet-CT ± staging laparoscopy.
• Curative option = oesophagectomy (± neoadjuvant chemo/chemoradiotherapy) in localised disease only.
• Adenocarcinoma arises from Barrett's oesophagus (chronic GORD).

Site predicts the histological type and the risk factor.

• Two types: squamous (upper/mid third; smoking, alcohol, achalasia) and adenocarcinoma (lower third/GOJ; from Barrett's/GORD, obesity).
• No serosa + rich submucosal lymphatics → early spread, late presentation, poor prognosis.
• Progressive dysphagia (solids→liquids) + weight loss ± hoarseness/cough (fistula)/anaemia.
• Diagnose by endoscopy + biopsy; stage with CT, EUS (T/N), pet-CT, staging laparoscopy.
• Curative: oesophagectomy ± neoadjuvant therapy (early disease only); most get palliation (stent, chemo/radiotherapy).

The Concept — a Failed Valve

Gastro-oesophageal reflux disease (GORD) is the reflux of acidic gastric contents into the oesophagus in sufficient amount to cause symptoms or mucosal damage. It arises when the normal anti-reflux mechanism fails. That mechanism is not a single sphincter but a combination: the tone of the lower oesophageal sphincter (LOS), the acute angle of His where the oesophagus meets the stomach (a flap valve), the pinch of the diaphragmatic crura, and a short intra-abdominal segment of oesophagus. When these are disrupted — often by a hiatus hernia — reflux occurs.

Risk Factors

Anything that lowers LOS tone or raises intra-abdominal pressure promotes reflux: obesity, hiatus hernia, pregnancy, smoking, alcohol, fatty or large meals, and drugs that relax the LOS. Understanding these explains why lifestyle change is central to treatment.

Clinical Features

The classic symptom is heartburn — a retrosternal burning that is worse on lying down, bending or after meals — with acid regurgitation and waterbrash (excess salivation). Atypical presentations are important: chronic cough, hoarseness, nocturnal asthma and dental erosion can all be due to reflux. New dysphagia suggests a complication (stricture) and warrants endoscopy.

Complications

Chronic reflux damages the oesophagus in a recognisable sequence: oesophagitis → peptic stricture (causing dysphagia) → Barrett's oesophagus (columnar metaplasia, a premalignant change carrying a risk of adenocarcinoma), and bleeding with iron-deficiency anaemia. It is the risk of Barrett's and cancer that makes persistent reflux more than a nuisance.

Hiatus Hernia — the Types

A hiatus hernia is herniation of part of the stomach through the oesophageal hiatus of the diaphragm into the chest, and its two types behave very differently:

Investigation & Management

Investigation includes upper GI endoscopy (to grade oesophagitis, detect Barrett's and exclude cancer), 24-hour pH monitoring (the gold standard for confirming reflux), oesophageal manometry, and a barium swallow for the hernia. Management is stepwise:

• Lifestyle — weight loss, elevating the head of the bed, avoiding trigger foods and late meals, stopping smoking.
• Medical — proton pump inhibitors (PPIs) are the mainstay, with antacids and H2-blockers as adjuncts.
• Surgical — for refractory symptoms, volume reflux or complications: a Nissen fundoplication (wrapping the gastric fundus around the lower oesophagus to recreate a valve), with repair of the hiatus.

WHY the Anti-reflux Mechanism Fails

It is worth expanding on the physiology, because it explains both symptoms and surgery. Normally, transient reflux is prevented by the resting tone of the LOS and reinforced by the flap-valve effect of the acute angle of His and the 'pinchcock' action of the diaphragmatic crura during rises in intra-abdominal pressure. A sliding hiatus hernia pulls the junction into the chest, flattening the angle of His and separating the sphincter from the crural support — so the several layers of protection fail together, which is why hernia and reflux so often coexist and why surgery aims to restore this anatomy.

Surgery & its Complications

Nissen fundoplication (a 360° wrap of fundus around the lower oesophagus) recreates a competent valve and is highly effective, but the patient must be counselled about its characteristic side-effects: dysphagia (if the wrap is too tight), 'gas-bloat' syndrome and inability to belch or vomit, and flatulence. Careful patient selection — ideally those with proven acid reflux on pH testing who responded to PPIs — gives the best results, and a partial (e.g. Toupet) wrap may be chosen where oesophageal motility is poor.

A Note on Atypical & Extra-oesophageal Reflux

Reflux does not always present as heartburn. 'Silent' or extra-oesophageal reflux can present to other specialties — as chronic cough, recurrent laryngitis and hoarseness, throat clearing, or worsening asthma — because refluxed acid irritates the larynx and airway. Recognising this prevents prolonged mistreatment of a 'respiratory' or 'ENT' complaint that is actually GORD, and a trial of PPI or pH testing confirms the link.

• PPIs are the mainstay of GORD; 24-hour pH monitoring is the gold-standard diagnostic test.
• Surgery = Nissen fundoplication for refractory reflux/complications.
• Rolling (para-oesophageal) hernia → surgical repair (strangulation risk).

Barrett oesophagus is the premalignant endpoint of chronic reflux.

• GORD = reflux causing symptoms/damage from failure of the anti-reflux mechanism (LOS tone, angle of His, crura, intra-abdominal oesophagus).
• Heartburn worse lying/bending/after meals + regurgitation; atypical: cough, hoarseness, asthma; new dysphagia = complication.
• Complications: oesophagitis → stricture → Barrett's (→ adenocarcinoma) → bleeding.
• Hiatus hernia: sliding (90%, reflux) vs rolling/para-oesophageal (strangulation/volvulus risk).
• Lifestyle + PPIs (mainstay); Nissen fundoplication for refractory disease; repair a rolling hernia surgically.

The Concept — a Balance Tipped

A peptic ulcer is a breach in the mucosa of the stomach or duodenum that penetrates the muscularis mucosae, occurring wherever mucosa is exposed to acid and pepsin. The unifying idea is an imbalance between aggressive and defensive factors: aggression from acid, pepsin, Helicobacter pylori and NSAIDs, versus defence from mucus, bicarbonate, mucosal blood flow and prostaglandins. Anything that increases aggression or weakens defence produces an ulcer, and this framework explains both the causes and the treatment.

Aetiology

• Helicobacter pylori — the dominant cause: a Gram-negative spiral bacterium found in the great majority of duodenal (~95%) and gastric (~70%) ulcers. It damages the mucosa directly and disturbs acid regulation.
• NSAIDs — inhibit cyclo-oxygenase and hence prostaglandins, removing a key mucosal defence.
• Others — smoking, severe physiological stress (Cushing's ulcer after head injury, Curling's ulcer after burns), steroids, and the rare gastrin-secreting tumour of Zollinger-Ellison syndrome.

Duodenal VS Gastric Ulcer

Clinical Features

The typical symptom is epigastric pain — burning or gnawing — with a characteristic relationship to food (relieved by eating in duodenal ulcers, worsened in gastric ulcers), along with nausea and dyspepsia. Sometimes a complication (bleeding or perforation) is the first presentation, which is why dyspepsia with alarm features is investigated.

Investigation

Upper GI endoscopy is the key investigation — it visualises the ulcer, and importantly every gastric ulcer is biopsied to exclude malignancy and tested for H. Pylori (rapid urease/CLO test, histology). Non-invasive H. Pylori tests include the urea breath test and stool antigen. A fasting serum gastrin is measured if Zollinger-Ellison syndrome is suspected.

Management

• Eradicate H. Pylori — triple therapy: a PPI plus two antibiotics (e.g. Amoxicillin and clarithromycin) for 1–2 weeks — which cures most ulcers and prevents recurrence.
• Acid suppression — a PPI to heal the ulcer.
• Remove precipitants — stop NSAIDs and smoking; use gastroprotection if NSAIDs are essential.
• Surgery — now rare, reserved for complications or truly refractory disease (historically vagotomy and antrectomy).