General Surgery

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.

• 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).

• 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; and 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.

• 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.

• 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.

• 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.