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Ovid: Oxford Handbook of Accident and Emergency Medicine

Editors: Wyatt, Jonathan P.; Illingworth, Robin N.; Clancy, Michael J.; Munro, Philip T.; Robertson, Colin E. Title: Oxford Handbook of Accident and Emergency Medicine, 2nd Edition Copyright ©2005 Oxford University Press > Table of Contents > Chapter 8 – Major trauma Chapter 8 Major trauma P.312
Major trauma—treatment principles Patients who present with serious (or apparently serious) injuries require immediate assessment and resuscitation. The finer points of history taking may have to wait until later. However, suspect major trauma in:

  • high speed road collisions, vehicle ejection, rollover, prolonged extrication
  • death of another individual in the same collision
  • pedestrians thrown up or run over
  • falls of more than 6 metres

Management of specific injuries is outlined in subsequent pages. Although treatment should be tailored to the needs of each individual patient, many therapeutic interventions are common to all patients: Airway control Use basic manoeuvres (suction, chin lift, oropharyngeal airway) to open the airway and apply O2 by face mask (p316). Avoid tilting the head or moving the neck if there is a chance of neck injury. If the airway remains obstructed despite these measures, get expert help and consider advanced manoeuvres (p317). O2 Provide high flow O2 to all. Patients who are apnoeic or hypoventilating require assistance by bag and mask ventilation prior to tracheal intubation and IPPV. Cervical spine control This is the first priority in any patient who presents with possible spine injury (eg neck pain, loss of consciousness). Provide immediate in-line manual cervical immobilization by placing one hand on each side of the patient’s head and holding it steady (without traction) and in-line with the remainder of the spine. Whilst maintaining manual immobilization, ask an assistant to apply an appropriately sized hard cervical collar. Adhesive tape and sandbags may be applied, but may cause problems in certain patients (eg patients who are vomiting or uncooperative patients who have consumed much alcohol). IV fluids Insert 2 large cannulae in the forearm or antecubital fossae veins. If initial attempts fail, consider a femoral venous line or in a child an intraosseous line. If these fail or are inappropriate, consider a central line or a cut-down onto the long saphenous vein. However, bear in mind the difficulties and potential hazards of attempting central venous access in hypovolaemic patients. Commence IV fluids for patients with hypovolaemic shock with 1L of 0.9% saline (or Hartmann’s solution) in adults (20mL/kg in children). If further IV fluid is required, alternate crystalloid with colloid and consider urgent blood transfusion once >2L (in an adult) have been given (p166). Analgesia Adequate pain relief is often forgotten or deferred. Give morphine IV (diluted in saline to 1 mg/mL) titrated in small increments according to response. Provide an antiemetic (eg cyclizine 50mg IV) at the same time. Consider other forms of analgesia (eg regional nerve blocks, immobilization and splintage of fractures). Antibiotics Give prophylactic IV antibiotics for compound fractures and penetrating wounds of the head, chest or abdomen. Antibiotic choice follows local policy—a broad spectrum antibiotic (eg cefuroxime) is useful. Tetanus Ensure tetanus prophylaxis in all patients (p396). P.313
Advanced Trauma Life Support (ATLS®) The concept of ATLS was introduced by the American College of Surgeons in an attempt to improve the immediate treatment of patients with serious injury. The ATLS approach has enabled some standardisation of trauma resuscitation. According to ATLS, treatment of all patients with major trauma pass through the same phases:

  • Primary survey
  • Resuscitation phase
  • Secondary survey
  • Definitive care phase

A key feature of ATLS is frequent re-evaluation of the patient’s problems and the response to treatment. Any deterioration necessitates a return to evaluate the ‘ABC’ (airway, breathing and circulation). Primary survey On initial reception of a seriously injured patient, life-threatening problems are identified and addressed as rapidly as possible. An ‘ABC’ approach is adopted, with each of the following aspects being quickly evaluated and treated:

  • Airway maintenance with cervical spine control
  • Breathing and ventilation
  • Circulation and haemorrhage control
  • Disability (rapid assessment of neurological status)
  • Exposure (the patient is completely undressed to allow full examination)

With optimum staffing and direction, instead of considering each of the above aspects sequentially (from ‘A’ to ‘E’), aim to address these simultaneously. Resuscitation phase During this period, treatment continues for the problems identified during the primary survey. Further practical procedures (eg insertion of NG tube, chest drain and urinary catheter) are performed. Secondary survey This involves a head to toe examination to identify other injuries. This examination is accompanied by relevant investigations (eg X-rays). The patient is monitored throughout—any deterioration necessitates a return to the assessment of ABC. Repeated clinical assessment and a high index of suspicion are essential if occult injuries are not to be missed—this applies particularly to the severely injured and to those with a reduced conscious level. Definitive care phase The early management of all injuries is addressed, including fracture stabilization and emergency operative intervention. P.314
Investigations in major trauma Identification of injuries and their sequelae is based upon information gathered from the history, examination and investigations. Select specific investigations according to the presentation of each patient, but bear in mind that all patients with major trauma require: group and save/X-match, BMG, X-rays, ABG. BMG Performing an instant ‘stix’ test to ascertain blood glucose level, confirmed by formal laboratory sample, is mandatory for all patients with major trauma and particularly important on any patient with GCS < 15/15. SaO2 Attach a pulse oximeter on arrival in A&E, then monitor continuously (p96). Blood tests Check U&E, FBC and glucose on all patients. If there is any possibility of significant haemorrhage, request group and save/X-match. Request baseline clotting screen in patients with major haemorrhage or those at special risk (eg alcoholics or those on anticoagulants). Obtain serum amylase level in abdominal trauma and cardiac specific enzymes in significant chest trauma. X-rays Multiply injured patients often require multiple X-rays. Obtain CXR and pelvic X-rays as a minimum (these provide information which guides resuscitation). Obtain a lateral cervical spine X-ray if the patient’s condition permits, but remember that a ‘normal’ X-ray does not exclude spinal injury. Don lead aprons and gloves and remain with the patient whilst X-rays are taken—in particular, ensure satisfactory immobilization of the cervical spine throughout. Accompany the patient if he needs to be taken to the radiology department for further X-rays, but remember that resuscitation in this unfamiliar environment is difficult. Urinalysis Test the urine for blood if there is suspicion of abdominal injury. ABG This provides useful information, including the degree of hypoxia, hypoventilation and acidosis. In critically ill patients (especially those requiring ventilatory support or those destined for neurosurgery/ITU) repeat as necessary and consider inserting an intra-arterial line to continuously monitor BP. ECG Monitor all patients and record an ECG if >50yrs or significant chest trauma. CT scan This is being used increasingly to aid evaluation of head, neck, chest, abdominal and pelvic injuries. Ensure that an appropriately trained doctor accompanies the patient to the CT scanning suite and that monitoring continues. Do not transfer a patient with haemodynamic instability to the CT scanner. USS and DPL Valuable in assessing abdominal trauma, the role of USS depends to a certain extent on local policy and expertise (see p336). Other investigations Angiography is indicated in certain specific circumstances (major pelvic fracture, aortic injury). Occasionally, other tests requiring specialist expertise (eg echocardiography) may prove to be useful. P.315
Trauma scoring Much of the published research concerning the epidemiology and management of trauma uses trauma scoring. A basic understanding of the accepted system of trauma scoring may be of benefit to those treating injured patients. Injury Severity Score (ISS) The ISS is widely used to retrospectively score the anatomical injuries of an individual patient. The score is obtained by first scoring each individual injury using the Abbreviated Injury Scale (‘AIS’). The AIS attributes a score between 1 and 6 to each individual injury, as follows:

  • AIS 1 = minor injury
  • AIS 2 = moderate injury
  • AIS 3 = serious injury
  • AIS 4 = severe injury
  • AIS 5 = critical injury
  • AIS 6 = inevitably fatal injury

To calculate the ISS from an array of AIS scores for a patient, the 3 highest AIS scores in different body regions are squared then added together. ISS considers the body to comprise 6 regions: head/neck; face; chest; abdomen; extremities; external (skin). Possible ISS scores range from 1-75. Any patient with an AIS = 6 is automatically given an ISS of 75. For example, consider the following patient:

Injuries AIS (body region)
Closed linear temporal skull fracture AIS = 2 (head/neck)
Major aortic arch rupture at its root AIS = 5 (chest)
Bilateral pulmonary contusions AIS = 4 (chest)
Massive splenic rupture with hilar disruption AIS = 5 (abdomen)
Multiple widespread superficial abrasions AIS = 1 (external)

ISS = (5)2 + (5)2 + (2)2 = 54 The ISS is non-linear and some scores (eg 15) are impossible. One accepted definition of ‘major trauma’ is an ISS > 15. The Revised Trauma Score (RTS) The RTS is used to assess the physiological disturbance of a trauma patient. The score is calculated from the respiratory rate, systolic BP and GCS. Each of these parameters are assigned a code (value) to which a weighting factor is applied. The 3 resultant scores are then added together to give the RTS. The RTS ranges from 0 (worst possible) to 7.84 (best). TRISS methodology Combining the ISS with the RTS and adding a weighting factor according to the age of the patient, it is possible to calculate a ‘Probability of Survival’ (Ps) for each patient, based upon the national norm. Patients who survive with Ps < 0.5 are regarded as ‘unexpected survivors’; patients who die with Ps > 0.5 as ‘unexpected deaths’. By analysing the results of treating a large number of patients, TRISS methodology may be used to compare ‘performances’ (eg of one hospital against the national norm). P.316
Airway obstruction—basic measures Severely injured patients die rapidly unless oxygenated blood reaches the brain and other vital organs. Therefore, clear and protect the airway, ensure that ventilation is adequate and give O2 in as high a concentration as possible. The most urgent priority is to clear an obstructed airway, but avoid causing or exacerbating any neck injury: instruct someone to hold the head and neck in a neutral position until the neck has been satisfactorily immobilized. When treating any seriously injured patient, always ensure that O2, suction and airway equipment are readily available. Get anaesthetic help early if a patient with a serious airway problem arrives or is expected. Causes of airway obstruction

  • coma from any cause can result in airway obstruction and loss of protective airway reflexes
  • blood or vomit may block the airway
  • the airway may be disrupted by trauma of the face/larynx, or occluded by a haematoma or by oedema following burns

Assessment of airway obstruction Talk to the patient and see if he responds. A lucid reply shows that his airway is patent, that he is breathing and that some blood is reaching his brain, at least for the moment. Ensure that his neck does not move until it has been checked and cleared of injury (p366). Look and listen to check how the patient is breathing. Complete airway obstruction in someone still trying to breathe results in paradoxical movements of the chest and abdomen, but no breath sounds. Gurgling, snoring and stridor are signs of partial obstruction. Management of airway obstruction

  • Look in the mouth and pharynx for FBs, blood and vomit. The tip of a laryngoscope may be useful as an illuminated tongue depressor.
  • Remove any FB with Magill’s forceps and suck out any liquid with a large rigid suction catheter. See if the patient responds and has a gag reflex, but beware of precipitating coughing or vomiting.
  • If vomiting occurs, tilt the trolley head down and suck out any vomit promptly.
  • Lift the chin and use the jaw thrust manoeuvre (see below) to open the airway, but do not tilt the neck.
  • After any airway intervention, look, listen and feel to reassess the airway and breathing.
  • If the gag reflex is absent or poor, insert an oropharyngeal airway (see below). This helps to hold the tongue forwards, but can cause vomiting or coughing if there is a gag reflex. If the gag reflex is present or the patient is clenching the jaw, consider a nasopharyngeal airway. Although a nasopharyngeal airway is useful in some situations, avoid its use if there is evidence of facial or head injury.
  • If the airway is now patent and the patient is breathing, give high concentration O2 (15 litres/min via a non-rebreathing reservoir mask).
  • If the airway is patent, but breathing inadequate, ventilate the patient on O2 with a bag, valve and mask and prepare for tracheal intubation. If possible, one person should hold the mask on the face with both hands to ensure a good seal, whilst a second person squeezes the ventilation bag.

Insertion of oropharyngeal airway

  • Select the appropriate size of airway.
  • Hold an airway against the patient’s face: a correctly sized airway reaches from the angle of the jaw to the centre of the mouth. A large adult usually needs a size 4 airway, most men require size 3, some women need a size 2. An incorrectly sized airway may make the obstruction worse rather than better.
  • Open the patient’s mouth and insert a laryngoscope only far enough to depress the tongue.
  • Look in the mouth and suck out any fluid.
  • Insert the airway over the tongue until the flange touches the lips.
  • Remove the laryngoscope, check the airway and breathing and give O2.
  • Ventilate the patient if breathing is inadequate.

Insertion of nasopharyngeal airway

  • Select an appropriate airway, which is usually the same diameter as the patient’s little finger. A safety pin through the flange end will prevent displacement up the nose.
  • Lubricate the airway with water or a water-soluble lubricant.
  • Insert the tip of the airway into one nostril and direct the airway posteriorly.
  • The airway should slide easily into the nose until the flange abuts the nostril and the tip is just visible in the pharynx. Never force a nasopharyngeal airway into a nostril—any bleeding produced will markedly aggravate the airway problem.
  • Check the airway and breathing and give O2.

Jaw thrust manoeuvre The aim of this is to open the upper airway with minimum movement of the cervical spine. Place the forefingers of both hands immediately behind the angles of the mandible and push the mandible anteriorly. This will bring the tongue anteriorly and thus away from the posterior pharyngeal wall. Tracheal intubation in trauma An injured patient who has no gag reflex needs tracheal intubation to maintain the airway and protect it against blood and vomit. Intubation may also be needed because of: apnoea (after initial ventilation with bag/valve/mask), respiratory inadequacy, to prevent potential obstruction from facial burns or to allow manipulation of ventilation in patients with ↑ ICP. Intubation in such circumstances necessitates emergency anaesthesia: suitable expertise with appropriate equipment and assistance are essential (p304). An assistant must hold the head to prevent movement of the neck during intubation, whilst another assistant provides cricoid pressure (p304). Confirm correct tracheal tube placement by:

  • seeing the tube pass through the cords
  • observing symmetrical chest movement
  • listening over both axillae for symmetrical breath sounds
  • confirming placement with end-tidal CO2 monitoring

If the airway is completely obstructed, the obstruction cannot be removed and the patient cannot be intubated, an urgent surgical airway is needed (p318). P.318
Airway obstruction—surgical airway Surgical cricothyroidotomy or jet insufflation of the airway via a needle cricothyroidotomy is needed if the airway is obstructed by trauma, oedema or infection and the trachea cannot be intubated. Emergency tracheostomy is not indicated in this situation because it is too time-consuming to perform and the necessary expertise may not be available. Needle cricothyroidotomy This is a rapid temporizing measure whilst preparation is made for securing a definitive airway (eg surgical cricothyroidotomy). Jet insufflation via a cannula placed through the cricothyroid membrane can provide up to 45mins of oxygenation of a patient with partial airway obstruction.

  • Use a large IV cannula-over-needle (12 or 14G in adults, 16 or 18G in children), attached to a syringe.
  • Palpate the cricothyroid membrane between the thyroid and cricoid cartilages.
  • Pass the needle and cannula at a 45° angle to the skin through the lower half of the cricothyroid membrane into the trachea.
  • Aspirate whilst advancing the needle. Aspiration of air confirms entry into the trachea. Withdraw the needle whilst advancing the cannula down into position in the trachea.
  • Connect the cannula via a Y connector or O2 tubing with a side hole in it to wall O2 at 15L/min (in the case of children the rate should be initially set (in L/min) at the child’s age in years, increasing if necessary until capable of causing chest movement). Hold the cannula firmly in position. Occlude the side hole or the end of the Y connector with your thumb for 1 sec in 5 to give intermittent insufflation of O2. Spontaneous breathing through the small airway of a cannula is very difficult, but the patient should be able to exhale partially in the 4secs between jets of O2. However, CO2 retention occurs and limits the time that jet insufflation can be tolerated. Placing a second cannula may help.

Surgical cricothyroidotomy This technique is not appropriate in children aged <12yrs.

  • Feel the thyroid and cricoid cartilages and the cricothyroid membrane between them.
  • Clean the area and use LA (if the patient is conscious and time allows).
  • Hold the thyroid cartilage with one hand and make a transverse incision through the skin and the cricothyroid membrane.
  • Use a tracheal spreader or curved artery forceps to open the hole into the trachea.
  • Insert a tracheostomy tube (5-7mm diameter) through the cricothyroid membrane into the trachea.
  • Remove the introducer from the tracheostomy tube, inflate the cuff and connect the tube to a catheter mount and ventilation bag.
  • Ventilate the patient with O2 and secure the tracheal tube.
  • Examine the chest and check for adequacy of ventilation.
    Surgical Cricothyroidotomy

Tension pneumothorax Tension pneumothorax is a life-threatening emergency and requires prompt recognition and treatment. It occurs when gas progressively enters the pleural space but is unable to leave. Increasing pressure causes complete lung collapse on the affected side and ultimately pushes the mediastinum to the other side. Movement of the mediastinum leads to kinking of the great vessels, thereby ↓ venous return and cardiac output. Additional compromise results from compression of the lung on the other side, particularly in patients undergoing IPPV. The process leading to tension pneumothorax may occur very rapidly, culminating in cardiac arrest within minutes. Causes Tension pneumothorax is seen most frequently following trauma, but it may also occur iatrogenically after attempted insertion of a central venous line (p56). A small (perhaps unsuspected) simple pneumothorax is particularly likely to become a tension pneumothorax when IPPV is commenced. Features

  • dyspnoea, tachypnoea and acute respiratory distress
  • absent breath sounds on the affected side
  • hyper-resonance over the affected lung (difficult to demonstrate in a noisy environment)
  • distended neck veins, tachycardia, hypotension and ultimately, loss of consciousness
  • tracheal deviation away from the affected side (this is rarely clinically apparent)
  • ↑ inflation pressure in a patient receiving IPPV

Diagnosis This is entirely clinical: do not waste time obtaining X-rays. Treatment

  • Apply O2 by face mask.
  • Perform immediate decompression by inserting a 16G IV cannula just over the top of the third rib (avoiding the neurovascular bundle) into the second intercostal space in the mid-clavicular line. Withdraw the needle and listen for a hiss of gas.
  • Tape the cannula to the chest wall.
  • Insert an axillary chest drain on the affected side (p327).
  • Remove the cannula.
  • Check the patient and obtain a CXR.

Note: the risk of causing a pneumothorax by needle decompression in a patient who did not have one is approximately 10%. P.321
Chest wall injury 1 Blunt chest wall trauma is extremely common—both as an isolated injury and as part of multiple injuries. Isolated rib fracture A history of trauma with subsequent musculoskeletal pain suggests rib fracture. The diagnosis is confirmed by localised chest wall tenderness—the diagnosis of a single rib fracture is a clinical one. Check for features suggestive of pneumothorax (dyspnoea, ↓air entry, see p326), secondary pneumonia or multiple rib fractures and if any are present, obtain a CXR. Treat uncomplicated isolated rib fracture with oral analgesia (eg co-dydramol ± NSAID). Warn the patient that the rib may remain painful for ≥3 weeks and to seek medical advice if additional symptoms develop. Multiple rib fractures Observe the chest wall carefully for possible flail segment and look for clinical evidence of pneumothorax or, in late presentations, secondary pneumonia. Check SaO2, ABG and obtain a CXR. Note that up to 50% of rib fractures may not be apparent on CXR. Treat Flail segment (p324) and pneumothorax (p326). Treat patients with uncomplicated multiple rib fractures according to the presence of other injuries and pre-existing medical problems as follows:

  • in patients whose other injuries require GA and IPPV, warn the anaesthetist of the potential risk of pneumothorax
  • patients with pre-existing pulmonary disease and limited respiratory reserve require admission for analgesia and physiotherapy
  • patients with chest infection often require admission for antibiotics and physiotherapy, depending upon past medical history, clinical and radiological findings

Sternal fracture Sternal fracture frequently occurs during road traffic collisions, either due to impact against the steering wheel or seat belt. The injury may be associated with myocardial contusion, great vessel injury and spinal injury (see below). Features Anterior chest pain with localised tenderness over the sternum. Investigations

  • Place on a cardiac monitor.
  • Record an ECG to exclude arrhythmias, MI (p68) or myocardial contusion (look for ST changes, particularly elevation). Consider further investigation with echocardiography.
  • Check cardiac enzymes.
  • Request CXR and lateral sternal X-ray: the latter will demonstrate the fracture (which is usually transverse), the former associated injuries.

Treatment Provide O2 and analgesia. Admit patients who have evidence of myocardial contusion or injuries elsewhere. Only consider discharging those patients who have an isolated sternal fracture, with a normal ECG, no associated injuries and normal pre-existing cardiopulmonary function. Patients who are discharged require oral analgesia (eg co-dydramol ± NSAID) and GP follow-up. Note Rarely, forced flexion of the chest causes a displaced sternal fracture with wedge fractures of upper thoracic vertebrae. Check the spine carefully: ask about pain and look for kyphosis and tenderness (the latter may not be apparent). Since lateral thoracic X-rays often fail to show the upper thoracic vertebrae, if injury is suspected, consider requesting a CT scan. P.323
Chest wall injury 2 Flail segment Fracture of ≥3 ribs in 2 places renders a portion of the chest wall capable of independent movement. This portion is termed ‘flail’. A flail segment indicates significant injury to the underlying lung (typically pulmonary contusions). Large segments are produced laterally when the majority of ribs on one side fracture anteriorly and posteriorly. Similarly, a large anterior flail segment is produced by bilateral fractures of all ribs anteriorly—in this case, the free portion comprises the sternum, costal cartilages/medial ends of the fractured ribs. Presentation The flail segment causes pain and moves paradoxically compared with the rest of the chest wall, thereby limiting the effectiveness of respiration. The diagnosis is a clinical one, but it can be quite difficult to make. Look tangentially at the chest for areas which move paradoxically (ie inwards during inspiration and outwards during expiration). There may be associated features of respiratory distress (cyanosis, tachypnoea). Check for pneumothorax or haemothorax (p326). Investigations Assessment of the extent of respiratory compromise is largely clinical, aided by a few simple investigations:

  • SaO2 on pulse oximetry.
  • ABG—the combination of hypoxia and respiratory acidosis (↑pCO2, ↑ H+) indicates severe respiratory compromise.
  • CXR will demonstrate fractures and associated injuries (eg pulmonary contusions, pneumo-/haemothorax).


  • Provide O2.
  • Treat associated life-threatening problems.
  • Contact anaesthetist and consider the need for immediate or urgent tracheal intubation with IPPV. Careful observation and monitoring in a high dependency or ITU setting is required.
Figure. Flail Segment.

Ruptured diaphragm Left-sided ruptures predominate (75%). Major rupture of the diaphragm, with associated herniation of abdominal contents into the chest, is a severe injury resulting from a significant traumatic insult (often massive abdominal crushing). Depending upon the extent of the injuries, the patient may present with evidence of hypovolaemic shock and respiratory compromise. Note that ruptured diaphragm may have some clinical features in common with a tension pneumothorax. Call a surgeon and ITU: the patient is likely to require GA, intubation and IPPV. Minor rupture, with less dramatic herniation, may present in more subtle fashion and result from penetrating injury. The diagnosis is frequently missed, but important because:

  • it is often associated with injury to both abdominal and thoracic contents
  • there are possible late complications (eg bowel herniation/obstruction)
  • it does not heal spontaneously

Suspect it from the mechanism of injury and an abnormal or high hemi-diaphragm contour on erect CXR. Look also for stomach or bowel loops in the chest (the tip of the NG tube may sometimes be seen coiled within the intrathoracic stomach). Once suspected, resuscitate and refer to a surgeon. Oesophageal rupture Traumatic (non-iatrogenic) rupture of the oesophagus is uncommon, but may follow blunt or penetrating injury. Suspect it if the patient complains of chest and back/neck pain in the presence of a normal ECG. Look for surgical emphysema in the neck. CXR may demonstrate pneumo-mediastinum (a layer of gas around the heart/mediastinum), a left sided pleural effusion or pneumothorax. Provide O2, IV analgesia and commence IV antibiotics (eg cefuroxime 1.5g), resuscitate and treat other injuries, and refer to a cardiothoracic surgeon. Boerhaave’s syndrome is ‘spontaneous rupture’ of the oesophagus associated with overindulgence and vomiting. Patients are classically middle-aged and present with severe chest pain, subcutaneous emphysema and signs of shock. If suspected, treat as outlined for traumatic rupture above. P.326
Pneumothorax and haemothorax Traumatic pneumothorax Pneumothorax frequently results from blunt injury with associated rib fractures or from penetrating injury (stabbing or gunshot). It may also be iatrogenic, secondary to attempted insertion of a central venous line. Features Patients are likely to complain of symptoms relating to the associated injury (such as rib fractures, p322). The degree of breathlessness resulting from the pneumothorax depends largely upon its size. Other features may be present, including surgical emphysema, cyanosis, ↓ air entry over the affected lung. The presence of severe dyspnoea and distended neck veins/hypotension suggest tension pneumothorax (p320). CXR demonstrates the pneumothorax. Both inspiratory and expiratory X-rays are not required. Wherever possible, obtain CXR with the patient erect. X-rays taken with the patient lying supine may not show a free lung edge, despite a considerable pneumothorax. This is because in this position, air tends to become trapped anteriorly in the pleural space. If the patient cannot have an erect X-ray, features suggestive of pneumothorax on a supine CXR are:

  • hyperinflation of the affected hemithorax with depressed hemidiaphragm
  • double contour of a hemidiaphragm
  • basal hyperlucency of the affected lung
  • visualization of apical pericardial fat tags

CT scan obtained to exclude other injuries will easily reveal pneumothorax. SaO2 and ABG may reveal hypoxia. Treatment Tension pneumothorax is an emergency requiring immediate needle decompression (p320). Provide O2 and drain all other traumatic pneumothoraces using a chest drain after CXR, as described opposite. Haemothorax Blood may collect in the pleural cavity in association with a pneumothorax (haemopneumothorax) or without (haemothorax). A large amount of bleeding into the pleural space sufficient to produce hypovolaemic shock is termed massive haemothorax. Features Clinical presentation may be similar to that seen in traumatic pneumothorax described above, except that there may be dullness to percussion over the affected lung and in the case of massive haemothorax, clinical evidence of hypovolaemia. CXR Blood from a haemothorax usually distributes patchily under the affected lung in patients lying supine, showing up as ↑ shadowing on a supine X-ray. It may be very difficult to distinguish haemothorax from pulmonary contusions on supine X-ray, but haemothorax may produce blurring of a hemidiaphragm contour or of the costophrenic angles. Treatment Provide O2 and insert 2 large venous cannulae (sending blood for X-matching). If there is evidence of hypovolaemia, commence IV fluids before inserting a large (at least 32FG) axillary chest drain (see below). Although it is standard practice to try to direct the chest drain downwards towards the diaphragm, this seldom seems to make a difference in practice—it is much more important to ensure that a tube of sufficient calibre is selected, in order to minimize the problem of blockage. Referral to a cardiothoracic surgeon If the chest drain initially yields >1000mL of blood, or the drain subsequently produces >200mL/h, refer urgently to a cardiothoracic surgeon. P.327
Chest drain insertion Use the ‘open’ technique, as described below. Explain the procedure, obtain consent and confirm that the patient has venous access, is breathing O2 and being monitored. Ensure that all equipment is ready and a good light is available. Consider giving additional IV opioid analgesia during the procedure.

  • abduct the ipsilateral arm fully
  • clean the skin with antiseptic and cover with sterile drapes
  • identify the 5th intercostal space just anterior to the mid-axillary line (count down and across from the angle of Louis at the level of the 2nd rib)
  • infiltrate LA (1% plain lidocaine) under the skin and down to the top of the 6th rib
  • prepare the chest drain; remove and discard the trocar (in adults, use a size 28-32F; in children, use the largest size that will comfortably pass between the ribs)
  • make a 2-3cm incision in the line of the ribs
  • use blunt dissection with artery forceps to spread the tissues down to the pleural space, just above the 6th rib
  • puncture the pleura with the artery forceps
  • put the tip of a gloved finger into the pleural cavity to ensure a clear passage
  • insert the chest drain ensuring that all drainage holes are inside the chest (typically ≈15-20cm in adults)
  • connect the drain to an underwater seal
  • suture the drain securely in place (eg with 0/0 silk) and cover with a dressing and adhesive tape. Whilst securing it in place, get an assistant to hold the drain so that it does not inadvertently fall out. It is useful to insert two untied sutures at the site of exit of the chest drain, so that these can be later tied to close the exit site when the time comes to remove the drain
  • check that the underwater seal is ‘swinging’ in the tube with respiration
  • listen for air entry and check the patient
  • obtain a CXR to confirm placement: if the tube has been inserted too far (eg so that it is touching the mediastinum), pull it back slightly and re-suture and secure in place
  • afterwards, keep the bottle below the level of the patient. Avoid clamping the tube.

Note: ruptured bronchus Persistent, continuing bubbling of gas through the underwater drain may reflect a major rupture of the tracheo-bronchial tree, especially if the lung fails to re-expand. Bronchial rupture may also present with haemoptysis or tension pneumothorax. Involve a cardiothoracic surgeon at an early stage. P.328
Pulmonary contusions and aspiration Pulmonary contusions High energy transfer during blunt injury (eg high falls or road traffic collisions) often results in pulmonary contusions. Suspect them in all patients with flail chest. Clinical features Pulmonary contusions produce ventilation-perfusion mismatch which may lead to hypoxia and respiratory distress, and ↑ likelihood of ARDS. Radiological appearances Pulmonary contusions may be visible on initial CXR as patchy opacification. However, initial radiological appearances are non-specific and may be confused with those seen after pulmonary aspiration or haemothorax (p326). X-ray changes resulting from pulmonary contusions tend to be progressive and become more prominent with time. Management Provide high flow O2, check ABG to help assess the need for GA, tracheal intubation and IPPV. Refer to ITU for observation and further treatment. Pulmonary aspiration—see p110 Inhalation of vomit and other foreign material may add considerably to the damage resulting from the initial injury. Common associations

  • inhalation of vomit after head injury with ↓ conscious level and impaired protective laryngeal reflexes: gastric contents are particularly irritant to the respiratory tract
  • inhalation of blood/teeth after facial trauma
  • inhalation of water/weed after near drowning (p246)

Presentation Suspect pulmonary aspiration from the history, associated respiratory signs and X-ray appearance. The CXR may show diffuse opacification affecting one or both lungs—the distribution depends upon the position at the time of aspiration. Management

  • Check SaO2, ABG and obtain a CXR.
  • Provide high flow O2.
  • Treat other injuries.
  • Consider the need for GA, tracheal intubation and IPPV. Bronchoscopy may be needed to remove large FBs within the bronchial tree.
  • Even if there is no urgent requirement for IPPV, remember that the respiratory problem is likely to worsen (with development of infection/ARDS), so involve ITU early.
  • Do not give routine antibiotics, unless there is a specific indication (eg immersion in rat-infested water, eg sewage, with the risk of subsequent development of Weil’s disease—p229).

Penetrating chest injury 1 In the UK, unlike the US, chest ‘stabbing’ is far more frequent than ‘shooting’. Both mechanisms of injury can pose a serious threat to life. Initial assessment and resuscitation Do not be misled by seemingly ‘innocuous’ wounds. The magnitude of the external wound has no correlation with the potential for internal injury. All patients need O2, venous access (send blood for X-matching or group and save) and resuscitation according to an evaluation of the airway/cervical spine, breathing and circulation. Remove all of the patient’s clothes and log roll to check for wounds to the back of the trunk and perineum. Particularly in gunshot injuries, make a quick early check for evidence of spinal cord injury. Remember also that penetrating chest injury often involves the abdomen (and vice-versa). During the initial assessment aim to exclude or identify and treat the following:

  • tension pneumothorax (p320)
  • sucking chest wound (p332)
  • cardiac tamponade (p332)
  • massive haemothorax (p326)

Further management depends partially upon haemodynamic status: The stable patient Many patients present without overt evidence of significant injury.

  • provide O2, secure venous access and send blood for group and save
  • monitor SaO2, pulse, BP and respiratory rate
  • record an ECG
  • obtain a CXR (ideally PA erect)
  • provide IV analgesia as required (see p268)
  • consider tetanus status and the need for prophylactic antibiotics (eg 1.5g IV cefuroxime)
  • cover the chest wound with a sterile dressing (for sucking chest wound—see p332)
  • drain any pneumothorax with a chest drain (having previously aspirated if tension—p320). Do not insert the drain through the wound (this ↑ the risk of infection)
  • refer all patients for admission, observation, formal wound cleaning, exploration and closure. If the patient remains stable overnight, with no clinical or radiological abnormalities (on repeat CXR), many patients may be safely discharged with a course of oral antibiotics and arrangements for review
  • carefully document the size, position and other features of the chest wound, remembering the potential medicolegal significance (p30)

The unstable patient Haemodynamic instability may be due to tension pneumothorax, massive haemothorax, sucking chest wound or cardiac tamponade. Treat each of these as outlined on pp320-333, involving a cardiothoracic surgeon at an early stage. Indications for thoracotomy Thoracotomy in theatre will be required for significant haemorrhage, which typically means:

  • >1.5 L of free blood obtained by initial chest drainage, or
  • >200mL of blood draining per hr, via the chest drain.

Penetrating chest injury 2 Open chest injury A penetrating chest wound resulting in open communication between the pleural cavity and the outside may cause respiratory insufficiency. In sucking chest wounds, as the chest wall moves during attempted respiration, air flow resistance may be less through the open chest wound than through the nasopharynx and tracheo-bronchial tree. This limits the airflow into the tracheo-bronchial tree, as air moves preferentially directly through the chest wall into the pleural space, producing a pneumothorax. Lung collapse and hypoxia result. Features Look for respiratory insufficiency (cyanosis, tachypnoea, respiratory distress). Management

  • Provide O2.
  • Cover the chest wound with a square of polythene or sterile dressing. Secure 3 sides of the dressing to the chest wall with adhesive tape, leaving one side free. This will allow air to exit through the chest wall during expiration, but prevent air entry into the chest cavity.
  • Insert a chest drain (not through the wound) to drain the pneumothorax.
  • Provide further resuscitation as necessary.
  • Call a cardiothoracic surgeon to arrange formal wound closure.

Cardiac tamponade Haemorrhage into the pericardial sac may compromise cardiac output. Continuing accumulation of blood leads to cardiac tamponade, culminating in cardiac arrest. Cardiac tamponade most frequently follows penetrating trauma. Features Clinical diagnosis requires a high index of suspicion. The oft-quoted Beck’s triad comprises: distended neck veins, hypotension and muffled heart sounds. Identifying muffled heart sounds is rarely easy in a noisy department and neck veins may not be distended in a hypovolaemic patient. Kussmaul’s sign and pulsus paradoxus are classical, but rarely helpful. Pulsus paradoxus is a drop in systolic BP by >10mmHg during inspiration and Kussmaul’s sign is a further ↑ in venous pressure during inspiration. Investigation CXR and ECG are rarely helpful, but may exclude coexistent conditions (eg pneumothorax). If time permits, echocardiography is the investigation of choice. Treatment

  • Provide O2, insert 2 IV lines, commence IV fluid infusion and monitor ECG. Meanwhile, request that the thoracotomy tray be made ready.
  • If the patient’s condition permits, contact the cardiothoracic surgeon and arrange immediate transfer for thoracotomy in theatre.
  • If the patient deteriorates to peri-arrest, attempt pericardiocentesis using an 18G needle connected to a 20mL syringe and 3 way tap. Puncture the skin 1-2cm below the xiphisternum at 45° to the skin. Carefully advance the needle cephalad and aim towards the tip of the left scapula (some advocate aiming for the right). ST and T wave changes, widened QRS or ventricular arrhythmias imply that the needle has been advanced too far. Successful aspiration of a small amount of blood (eg 20-40mL) may improve cardiac output temporarily and ‘buy time’, whilst preparing for thoracotomy and surgery.
  • Perform thoracotomy for cardiac arrest from penetrating trauma (see below).

Thoracotomy for cardiac tamponade Thoracotomy in the A&E department may be required in certain life-threatening emergencies, including cardiac arrest due to penetrating chest injury. First exclude and treat other reversible causes of cardiac arrest (upper airway obstruction, p316; tension pneumothorax, p320). Thoracotomy is not indicated for cardiac arrest following blunt injury. Procedure

  • Summon expert help, but do not wait for it to arrive. Instead, continue:
  • Whilst the thoracotomy tray is being opened, don gloves and an apron, ensure that the patient is being ventilated with O2 via a tracheal tube and commence external chest compressions (p46). Continue rapid IV infusion via multiple lines and obtain blood for transfusion.
  • Standing on the patient’s left side, abduct the left arm, stop chest compressions and open the left chest wall. Start the incision at the medial end of the 5th intercostal space and cut laterally just above the 6th rib into the axilla. Use rib retractors to enable access to the intrathoracic organs. If necessary, improve access further by continuing the incision medially using strong scissors to cut through the sternum and into the right 5th intercostal space.
  • Identify the heart: carefully incise vertically through the bulging pericardium over its anterior surface, avoiding the phrenic nerves.
  • Evacuate blood from the pericardial sac and identify the damage.
  • Manually compress the descending aorta.
  • Place a finger over the cardiac defect and perform internal cardiac massage by compressing the heart between 2 flat hands, with fingers placed over defects. Allow the surgeon to close defects in the myocardium using interrupted 4/0 proline sutures with teflon buttresses.
  • Once appropriate sutures are in place, stop internal cardiac massage and check cardiac rhythm and output. If the heart is fibrillating, defibrillate using the small internal defibrillation paddles, by placing a paddle over each side of the heart. Start with 5J energy initially, ↑ as necessary to max of 50J.
  • Once a pulse has been restored, ensure that hypovolaemia is corrected (monitor CVP using a central venous line, see p56). Give cefuroxime 1.5g IV, insert an arterial line and urinary catheter, recheck U&E, glucose FBC and clotting.
  • The cardiothoracic surgeon will direct further surgical management.

Aortic injury The vast majority of aortic injuries (≈90%) are sustained during high energy blunt trauma (eg road traffic collisions, high falls): only a small proportion of these patients reach hospital with signs of life. The usual site of rupture is just distal to the origin of the left subclavian artery, possibly caused by differential shearing forces between the mobile arch and the fixed descending thoracic aorta. An alternative proposed mechanism is that during rapid deceleration the first rib and clavicle swing down and directly ‘nip’ the aorta (‘osseous pinch’ theory). The injury is relatively unusual in children, who are perhaps protected by having more elastic tissues. Features Patients who reach hospital alive are most likely to have a partial or contained rupture, with a haematoma confined by aortic adventitia. They may complain of chest and back pain and there may be a harsh systolic murmur, absent or ↓pulses (with differential BP between arms and legs) and evidence of hypovolaemic shock: features of other significant non-aortic injuries may predominate. Diagnosis The diagnosis of aortic injury can be difficult: adopt a high index of suspicion. An erect CXR is invaluable provided that the patient’s condition permits it. CXR features suggesting aortic injury include:

  • widened mediastinum (>8cm on PA film)
  • abnormal aortic arch contour
  • deviation of the trachea to the right side
  • deviation of NG tube to the right side (eg such that it lies to the right of T4 spinous process)
  • depression of the left main bronchus >40° below the horizontal
  • left pleural cap or fractured first/second ribs are often quoted, but are of little diagnostic value
  • the CXR may be normal!

Management Resuscitate and treat other injuries. As a minimum, provide O2, insert two IV cannulae, start IV fluids, provide analgesia, monitor vital signs and SaO2. Check U&E, glucose, FBC, clotting, ABG and X-match. Insert urinary catheter and arterial line. Involve an expert early and refer urgently for further specialist investigation (CT scan and/or aortography) and ITU care to control BP prior to definitive treatment. Historically, this has comprised open surgical repair, but some specialist centres are now reporting good short-term results using transluminal endovascular stents. P.335
Blunt abdominal trauma—evaluation Blunt injury to the abdomen may be isolated or associated with injuries elsewhere. Evaluation of the abdomen may be rendered particularly difficult in the latter situation. The mechanisms of injury responsible are diverse and include road traffic collisions, crushing injuries, high falls and direct blows (eg kicks and punches). Remember that lower chest injury may be associated with splenic or liver injuries. Examination

  • Assess for hypovolaemia. Check pulse, BP and capillary refill.
  • Look for bruising (eg ‘lap belt’ imprint). (Measurements of abdominal girth are unhelpful and unreliable as a means of assessing intra-abdominal haemorrhage).
  • Feel for tenderness and evidence of peritonism. (Listening for bowel sounds is not helpful: their presence or absence is not a discriminating feature).
  • Check for femoral pulses.
  • Log roll to check for loin tenderness and back injury.
  • Examine the perineum and perform a PR examination, checking perineal sensation, anal tone, rectal integrity/blood and in the male, the position of the prostate. A high-riding, ‘boggy’ or impalpable prostate may indicate urethral injury (see p341).

Investigations The need for and choice of investigation depend upon individual circumstances, local policy, facilities and expertise. Patients who are haemodynamically unstable or who have peritonism require immediate referral for laparotomy. Perform urinalysis in all patients. Insert a urinary catheter in patients who present with haemodynamic disturbance or who are critically ill as a result of other injuries (unless there is evidence of urethral injury, see p341). Serum amylase is required on all patients with abdominal injury, but may be normal even with major pancreatic trauma. Plain abdominal X-ray is rarely useful, unless associated bony injury or bowel perforation is suspected: free intraperitoneal gas may be demonstrated on an erect CXR. USS provides a rapid, repeatable, non-invasive bedside tool. It is operator-dependent. Haemoperitoneum is identified by scanning the hepatorenal and splenorenal fossae and the pelvis. The pericardium can also be scanned to look for tamponade. CT scan is being increasingly used to evaluate abdominal injuries as well as identifying injuries in other regions (eg retroperitoneum, brain, chest). DPL is helpful in situations where clinical evidence of intra-abdominal injury is equivocal or where CT or USS is not immediately available. It may be employed in other situations (eg to search for intra-abdominal haemorrhage in shocked head-injured patients who are unconscious or in patients whose massive pelvic fracture is being externally fixed, see p444). The open technique of DPL is shown below. The role of DPL has diminished in recent years since USS and CT scan have become more readily available. Also, particularly as far as children are concerned, certain injuries (eg ‘minor’ splenic injury) are now often treated conservatively, so a +ve DPL is of less value. P.337
How to perform diagnostic peritoneal lavage

  • Explain the procedure and obtain consent if conscious.
  • Ensure that the bladder has been decompressed by a urinary catheter.
  • Ensure that an NG tube (or if head injured, orogastric tube) has been passed.
  • Enlist an assistant and bright light.
  • Clean the skin with antiseptic and drape with sterile towels.
  • Infiltrate LA (1% lidocaine with adrenaline/epinephrine) around the proposed site of incision.
  • Make a vertical midline skin incision ≈3cm long at a point one third of the distance from the umbilicus to the symphysis pubis. However, use a supraumbilical site if the patient has lower abdominal scars, is pregnant or has a pelvic fracture. Request that the assistant exerts gentle pressure on the wound edges, in order to minimize bleeding.
  • Divide the linea alba, identify the peritoneum and grasp it between 2 clips.
  • Gently bring the peritoneum into the wound and feel its edge between finger and thumb to ensure that no bowel has been caught in the clips.
  • Make a tiny peritoneal incision and insert a peritoneal dialysis catheter (without the needle).
  • Gently twist the peritoneal clip to obtain a good seal around the catheter.
  • Attempt to aspirate any free fluid. If obvious enteric contents or >5mL blood is aspirated: stop, the DPL is +ve: the patient requires a laparotomy.
  • Infuse 1 L of warmed 0.9% saline.
  • Keep the catheter and seal in place and allow 1-2mins for the fluid to mix.
  • Allow the effluent fluid to siphon out into the empty bag placed on the floor.
  • Send fluid for laboratory analysis. Since a +ve DPL commits the surgeon to a laparotomy, an objective measurement is helpful.
  • Close the abdomen in layers.

Criteria for +ve DPL

  • aspiration of >5mls free blood or obvious enteric contents
  • RBC count >100,000/mm3
  • WBC count >500/mm3
  • the presence of food debris or other enteric contents (eg vegetable fibres)

Note: air enters the peritoneal cavity during DPL and this may be visible on subsequent X-rays. P.338
Blunt abdominal trauma—management Initial stabilization (see p312)

  • provide O2
  • treat airway and breathing problems
  • insert 2 IV lines
  • send blood for U&E, amylase, glucose, FBC and X-matching
  • give IV fluids according to initial evidence of hypovolaemia and response to treatment
  • provide IV analgesia as necessary (contrary to popular opinion, this does not compromise clinical abdominal evaluation)
  • consider the need for NG tube and urinary catheter
  • involve a surgeon at an early stage
  • inform the anaesthetist and theatre staff if an urgent laparotomy is needed

Further evaluation and treatment Following initial stabilisation and resuscitation, further evaluation and treatment will depend largely upon the clinical situation: Haemodynamically unstable Refer urgently to a surgeon for laparotomy. There is no need (or time) to attempt to define the intra-abdominal injury. Clinical peritonism Resuscitate as above, provide IV antibiotics (eg cefuroxime 1.5g) and refer urgently to a surgeon for laparotomy. Haemodynamically stable, no peritonism Refer to a surgeon for further investigation and observation. It may be appropriate to investigate some of these patients with USS or CT, whilst others may be appropriately managed with regular observations and clinical re-examination. Possible abdominal injury in the multiply injured These patients often provide a diagnostic challenge: tailor investigations and management according to individual circumstances. USS and DPL are rapid, simple and useful tools to help to exclude significant intra-abdominal haemorrhage in the multiply injured patient. CT has superior diagnostic accuracy, but is time-consuming, requires transfer and oral/IV contrast. Only consider CT scanning for those patients who are haemodynamically stable. Abdominal trauma in pregnancy Involve the obstetrician/gynaecologist at an early stage. Remember to check rhesus/antibody status—see p569. P.339
Penetrating abdominal trauma The majority of penetrating abdominal injuries result from the use of knives and guns. The extent of the external wound bears no relationship to the magnitude of intra-abdominal injuries. Many of these injuries have medicolegal implications (p30). Initial approach On receiving the patient, provide O2, secure venous access and resuscitate according to an initial assessment of:

  • Airway and cervical spine
  • Breathing
  • Circulation

Obtain complete exposure at an early stage in order to check for additional wounds to the chest, back, loins, buttocks and perineum. Evaluation of abdominal injury Unless the patient presents with hypovolaemic shock, it may be difficult to decide the extent and severity of the abdominal injury on clinical grounds. In addition to standard monitoring and palpation of the abdomen, perform a digital rectal examination and (especially in gunshot injuries) check carefully for spinal cord/cauda equina injury (p366). Investigations Urinalysis Check the urine for blood. Blood Check BM, U&E, amylase, glucose, FBC, group and save/X-match. X-rays If possible, obtain an erect CXR to check for free gas under the diaphragm and a plain supine abdominal X-ray to search for FBs (bullet fragments, tips of knives etc). DPL Although this may be of assistance in evaluating abdominal injury, do not consider this until the surgeon has assessed the patient (see below). Management

  • Give O2.
  • Insert 2 IV cannulae and send blood as outlined above.
  • Provide IV analgesia (eg titrated increments of morphine) as required.
  • Give IV antibiotics (eg cefuroxime 1.5g + metronidazole 500mg).
  • Consider the need for tetanus prophylaxis (p396).
  • Cover the wound with a sterile dressing. Never probe or explore the wound in A&E in attempt to define its depth and possible peritoneal penetration. Involve the surgeon at an early stage to decide further management. Patients who are haemodynamically unstable or who have obvious bowel contents protruding through the wound require urgent resuscitation and laparotomy. Investigation and treatment of other patients varies according to local policy. Although some patients may be managed conservatively with monitoring and close observation, wound exploration in the operating theatre will be required if omentum is seen to protrude through the wound. If omentum or bowel is protruding through the wound, do not attempt to push it back into the abdomen—cover it with a sterile swab soaked in saline.

Renal trauma Most renal injuries result from direct blunt abdominal trauma, the kidney being crushed against the paravertebral muscles or between the 12th rib and the spine. Indirect trauma (eg a fall from a height) can tear the major blood vessels at the renal pedicle or rupture the ureter at the pelvi-ureteric junction. Penetrating injuries are relatively rare. Many patients with renal trauma also have other important injuries, which may obscure the diagnosis of the renal injury. Children are particularly prone to renal injuries. Trauma may uncover congenital abnormalities, hydronephrosis or occasionally incidental tumours. Clinical features Most patients give a history of a blow to the loin or flank and have loin pain followed by haematuria (which may be delayed). The loin is tender and there may be visible bruising or abrasions. Worsening renal pain may indicate progressive renal ischaemia. Perinephric bleeding can cause loin swelling and a palpable mass. Haematuria may be absent in severe injuries in which there are renal vascular tears, thrombosis or complete ureteric avulsion. Investigations Look for and record visible haematuria and test for microscopic haematuria. Get venous access, send blood for FBC, U&E, glucose, amylase, group and save. IVU is the standard investigation if a serious renal injury is suspected. It is used to elucidate the form and function of an injured kidney and confirm a functioning contra-lateral kidney. Stable patients with microscopic haematuria do not need urgent IVU, but require review and appropriate follow-up. IVU is needed if there is frank haematuria or if the patient was initially shocked and has frank or microscopic haematuria. Involve the surgical team before arranging the IVU. An unstable patient requiring immediate laparotomy may need an intra-operative IVU to diagnose a renal injury and to check that the other kidney is functioning. Contra-indications to IVU include: previous serious reaction to injected contrast media, myeloma, sickle cell disease, currently taking metformin. Technique: preliminary KUB, then IV non-ionic low osmolar contrast media (eg Omnipaque) over 30-60secs, with full length abdominal X-ray at 15mins. The plain control X-ray film may show fractures of lower ribs or lumbar transverse processes, loss of psoas shadow/renal outline or a loin mass displacing the bowel or diaphragm. The IVU may show extravasation of contrast, distortion of the calyceal pattern or non-visualization of all or part of the kidney. Non-visualization occurs with: absent kidney, renal artery avulsion/thrombosis, massive parenchymal disruption). In those patients who are haemodynamically stable, contrast-enhanced CT provides better information and eliminates the need for IVU. USS shows renal morphology, but not function. Selective angiography is occasionally helpful. Management Most blunt renal injuries settle with bed rest and analgesia. Give prophylactic antibiotics after consulting the surgical team and according to local policies. Repeat and record pulse, BP and T°. Test serial urine samples. Patients with penetrating renal injuries and severe blunt renal trauma need urgent expert assessment ± emergency surgery: the warm ischaemic time of a kidney is only ≈2hrs. Resuscitate with IV fluids, IV analgesia + IV antibiotics. P.341
Bladder, urethral and testicular trauma Bladder injury Most bladder ruptures are into the peritoneal cavity, caused by direct blows to the lower abdomen. These injuries often occur in people with distended bladders. Bone fragments from a fractured pelvis may also penetrate the bladder (p444). Clinical features Lower abdominal pain ± peritonism may be associated with haematuria or an inability to pass urine. Look for perineal bruising and blood at the external urethral meatus. Perform a PR examination to check for the position of the prostate and the integrity of the rectum. Investigations and managment X-ray the pelvis to check for fractures. If there is no sign of urethral injury, pass a catheter to check for haematuria. Refer to the urology team. A cystogram will show extravasation from a bladder injury. Intraperitoneal ruptures need laparotomy and repair. Extraperitoneal ruptures may heal with catheter drainage and antibiotics. Urethral injuries Posterior urethral tears are often associated with pelvic fractures. Urethral injury may also result from blows to the perineum (especially falling astride). Look for perineal bruising and blood at the external urethral meatus and perform a PR examination (an abnormally high-riding prostate or inability to palpate the prostate imply urethral injury). If urethral injury is suspected, do not attempt urethral catheterization, but refer urgently to the urology team. Some urologists perform a retrograde urethrogram to assess urethral injury, but many prefer suprapubic catheterization and subsequent imaging. Penile injuries —see p501 Testicular trauma Injury to the scrotum/testis may result in scrotal haematoma or testicular rupture. Both conditions require analgesia. Further treatment depends upon the exact diagnosis. USS may help to distinguish between scrotal haematoma and testicular rupture. Scrotal haematoma may respond to conservative measures. Testicular rupture requires urgent surgical exploration and repair. Scrotal injuries Wounds involving the scrotal skin may need to be sutured (preferably with absorbable sutures)—most heal rapidly. Refer for investigation if there is complete scrotal penetration with the attendant risk of damage to the testis, epididymis or vas deferens. P.342
Head injury—introduction The size of the problem Many patients with serious or fatal trauma have suffered a head injury. Additionally, minor head injuries are a very frequent reason for attendance at A&E. Blunt injury is more common than penetrating injury. Common causes of head injury

  • road traffic collisions of all types
  • falls
  • assaults
  • sporting and leisure injuries
  • workplace injuries
  • other mishaps

Pathophysiology Brain injury may be primary or secondary. Primary injury occurs at the time of the head injury. This takes the form of axonal shearing and disruption, with associated areas of haemorrhage. This primary damage may be widespread (‘diffuse axonal injury’) or localised (eg ‘contre-coup’ frontal contusions in a fall hitting the occiput). Secondary injury occurs later and takes a variety of forms which commonly coexist. Many are preventable or treatable and are thus the focus during resuscitation:

  • hypoxia
  • hypovolaemia and cerebral hypoperfusion
  • intracranial haematoma with localised pressure effects and generalized ↑ ICP
  • other causes of ↑ ICP, including cerebral oedema and hypercapnia
  • epileptic fits
  • infection

The role of intracranial pressure Once the skull sutures have fused, the cranium is a closed box. Thus, a relatively small ↑ in volume (eg from swelling or haematoma) results in a large ↑ in ICP (see below). As ICP↑, cerebral perfusion pressure↓, since: Cerebral perfusion pressure = Mean arterial pressure – ICP Once cerebral perfusion pressure falls <70mmHg, significant secondary brain injury may occur. Control of ICP and BP (including avoiding wild swings in BP) is an important treatment goal, especially as the normal cerebrovascular autoregulatory mechanisms are impaired after head injury. Cerebral arterioles remain sensitive to pCO2, however, with an ↑ CO2 resulting in marked arterial vasodilatation and unwanted ↑ICP. Controlling pCO2 to within normal levels is therefore important. ↑ICP produces a diminishing conscious level and causes herniation of the temporal lobe through the tentorial hiatus, stretching the oculomotor nerve, resulting in ipsilateral pupillary dilatation. This may progress to contralateral hemiparesis and finally, brainstem compression with cardiorespiratory arrest. ↑ICP leads to a reflex ↑ in systemic arterial BP together with bradycardia: this combination is sometimes called the Cushing P.343
Indications for referral to hospital Any one of the following criteria indicate the need for hospital assessment:

  • impaired conscious level at any time
  • amnesia for the incident or subsequent events
  • neurological symptoms (vomiting, severe and persistent headache, fits)
  • clinical evidence of a skull fracture (CSF leak, periorbital haematoma)
  • significant extracranial injuries
  • worrying mechanism (high energy, possible NAI, possible penetrating injury)
  • continuing uncertainty about the diagnosis after first assessment
  • medical co-morbidity (anticoagulant use, alcohol abuse)
  • adverse social factors (eg alone at home)

The following are highly recommended:

  • the SIGN (Scottish Intercollegiate Guidelines Network) guideline on head injury is accessible on: http://www.sign.ac.uk
  • the NICE (National Institute for Clinical Excellence) clinical guideline (on head injury) published in 2003 and accessible on: http://www.nice.org.uk
Figure. ICP according to intracranial blood volume

Head injury—triage and monitoring Triage Every A&E department requires a system for the rapid initial assessment of head-injured patients. The exact system will depend upon local policy, expertise and facilities. It will enable patients with significant injuries to receive immediate resuscitation and promote urgent treatment of those patients liable to complications. Experienced nursing staff can quickly identify those patients in need of urgent attention, based upon:

  • the mechanism of injury
  • history from the ambulance crew
  • an assessment of vital signs
  • conscious level according to the Glasgow Coma Scale (p349)
  • limb power
  • pupil responses
  • BMG

For patients who are haemodynamically stable, alert and orientated, with no neurological deficit and an apparently minor head injury, it may be appropriate to proceed to obtaining a full history, as outlined on p346. For patients with multiple injuries and/or a serious head injury, there will be no time initially to obtain a full history. Instead, proceed rapidly to initial examination and resuscitation. During initial examination it is useful to obtain an impression of the severity of the head injury. One simple method (AVPU) is to classify patients according to their response to stimulation, as follows:

  • Alert
  • responsive to Voice
  • responsive only to Pain
  • Unresponsive

If a patient is unresponsive or responds only to pain, call for senior help and an anaesthetist, since expert airway care will be needed. Monitoring Every head-injured patient requires regular neurological observations. These should include measurements of GCS, pupil response, limb power, pulse, BP and respiratory rate on a standard chart, such as the one shown below. This monitoring is critical if complications such as intracranial haematomas, fits and hypovolaemia from other injuries are to be detected and treated at an early stage. Any deterioration in GCS is an emergency: re-examine the patient and correct identifiable problems promptly whilst obtaining urgent senior help. P.345

Figure. An example of a neurological observation chart

Head injury—history It may be impossible to obtain a complete history from the patient, particularly if there was loss of consciousness and/or amnesia. Use all available sources of information, including friends and family, other witnesses and the ambulance crew. Cover the following areas: Mechanism of injury Eliciting the exact mechanism of injury will provide an impression of the nature of the forces involved and the likelihood of subsequent complications. Consider the possibility that the head injury may have been preceded and caused by another medical problem (eg arrhythmia, epileptic fit). Time of injury This information is useful, but may not be known. Loss of consciousness/amnesia A period of unconsciousness implies a head injury of at least moderate severity. It can be difficult to establish exactly how long unconsciousness lasted, particularly if there is associated amnesia. Document the length of amnesia (both before and after injury), but remember that the full extent of the amnesia may not become apparent until much later. Subsequent symptoms Some symptoms are relatively common after head injury (eg headache and vomiting)—many patients will complain of these without being directly asked. There are a number of other symptoms, however, which the patient may not mention unless specifically asked. Enquire about the following symptoms:

  • headache
  • nausea and vomiting
  • limb weakness
  • paraesthesiae
  • diplopia
  • rhinorrhoea
  • otorrhoea

Past medical history Document pre-existing illnesses and symptoms, particularly those which may have played a role in causing the head injury (eg epilepsy, diabetes, cardiac arrhythmias), or might play a role in making the consequences more severe (eg bleeding tendency). Enquire about previous head injury (an old skull fracture visible on new X-rays may otherwise be confusing). Drug history Ask particularly about recent alcohol and other drug ingestion and establish whether or not the patient is taking anticoagulant drugs (eg warfarin). This is very important, since patients with bleeding disorders and/or on anticoagulants have a significantly higher risk of intracranial problems after head injury and need to be admitted to hospital (p354). Social history Before contemplating discharge of any head-injured patient, find out if there is a responsible adult at home, or if there is someone else with whom the patient could go and stay. Tetanus status Enquire the date of the last tetanus prophylaxis if there are any wounds. P.347
Head injury—examination Resuscitation proceeds with examination, according to problems identified in the primary survey. Follow initial brief neurological examination (GCS, pupil reactions, limb weakness) by definitive complete examination: Cervical spine injury Consider this possibility in all cases (see p312). Glasgow Coma Scale Determining the conscious level is a crucial part of the neurological examination. The adult score ranges from 3-15/15 and is calculated as shown below. Repeated GCS recordings are a crucial part of monitoring the head injured patient. A fall in GCS indicates a potentially serious deterioration in the patient’s condition and mandates a search for correctable conditions. Vital signs Record pulse, BP and respiratory rate. BMG This is essential in all patients with altered conscious level. Alcohol Record if the patient smells of alcohol. Never assume ↓GCS is due to alcohol. Eye signs Document pupil size (in mm) and reaction to light. Unilateral pupillary dilatation may reflect local orbital injury or oculomotor nerve compression due to ↑ ICP (p342). Check for a full range of eye movements and the presence of diplopia or nystagmus. Look in the fundi, although papilloedema is a late sign of ↑ ICP. If there is any suspicion of eye injury, measure VA (p512). In infants, check for retinal haemorrhages (p690). Scalp, face and head Examine the cranial nerves and search for abnormal cerebellar signs (nystagmus, hypotonia, intention tremor, dysdiadochokinesia). Carefully record scalp, ear or facial injury. Examination of facial injuries is considered on p358. The limbs Check limb tone, power, sensation and reflexes. Abnormalities (eg hemiparesis) may result from the primary brain insult or be a consequence of a developing intracranial haematoma requiring urgent intervention. Other injuries The presence of a head injury can render identification of non-cranial injuries difficult. In particular, relatively minor non life-threatening orthopaedic injuries (eg finger dislocations, wrist fractures) are easily missed. Ensure full examination, including palpation of all limbs for possible injury. Signs of base of skull fracture This is often a clinical diagnosis. One or more of the following may be seen:

  • bilateral orbital bruising confined to the orbital margin (‘panda eyes’).
  • subconjunctival haemorrhage (no posterior margin of haemorrhage seen).
  • haemotympanum or bleeding from the auditory meatus.
  • otorrhoea or rhinorrhoea (± anosmia). Fluid mixtures containing relatively similar quantities of blood and CSF will separate into a ‘double ring’ when dropped onto blotting paper.
  • Battle’s sign—bruising over the mastoid process without local direct trauma follows petrous temporal bone fracture, but takes several days to appear.

Glasgow Coma Scale (adults) The GCS assesses the level of consciousness by scoring 3 aspects of the patient’s response and adding up the scores to reach a final score.

Eye response open spontaneously 4
open to verbal command 3
open to pain 2
no response 1
Verbal response talking and orientated 5
confused/disorientated 4
inappropriate words 3
incomprehensible sounds 2
no response 1
Motor response obeys commands 6
localises pain 5
flexion/withdrawal 4
abnormal flexion 3
extension 2
no response 1
Total (GCS) range 3-15


  • Record GCS in shorthand showing its component parts (for example, GCS 10/15 (E3, V2, M5) means that the patient opens eyes to verbal commands, speaks incomprehensible sounds, localises a painful stimulus). Similarly, when communicating with other health professionals describe the total score (GCS) and its component parts.
  • Unconsciousness is generally taken to mean no eye response and GCS ≤8.
  • ‘Abnormal flexion’ implies decorticate rigidity; and ‘abnormal extension’ implies decerebrate rigidity.
  • The GCS is difficult to apply to small children, but may be modified as outlined on p677.

Head injury—imaging Traditional use of X-rays is increasingly being replaced by CT scanning. Scottish Intercollegiate Guidelines Network (SIGN) guideline on the early management of patients with a head injury (http://www.sign.ac.uk) has now been followed by National Institute for Clinical Excellence (NICE) guidance. The latter was published in 2003 and is available on http://www.nice.org.uk The role of CT scanning CT scanning is used to identify and define the brain injury and more importantly, associated intracranial haematomas amenable to surgical treatment. Ensure adequate resuscitation before transferring for CT scan. In many cases, this will include GA, tracheal intubation and IPPV. Always arrange for appropriately trained staff to accompany the patient to CT scan. When clinical features point strongly to an intracranial haematoma (eg the emergence of focal signs or a deteriorating GCS), discuss promptly with a neurosurgeon the benefits of transferring the patient to a centre which has both CT scanning facilities and an emergency neurosurgical service. Indications for CT scan Request CT scan for any of the following (see http://www.nice.org.uk):

  • GCS <13/15 at any point since injury
  • GCS 13 – 14/15 at 2hrs post-injury
  • suspected open or depressed skull fracture
  • any sign of basal skull fracture
  • post-traumatic seizure
  • focal neurological deficit
  • >1 episode of vomiting (except in children <12yrs, where clinical judgement is required)
  • amnesia for >30 mins of events before impact*
  • loss of consciousness and/or amnesia combined with one of: age >65yrs, coagulopathy (including clotting disorder, anticoagulant drug treatment) or dangerous mechanism* (eg pedestrian hit by car, fall >1metre or 5 stairs)

Most requests will be urgent (scan performed and interpreted within an hour), except for the two indications marked with an asterisk*, which if isolated, may allow CT scan to be obtained less urgently (within 8 hrs), depending upon discussion with experts. Interpretation of CT scan Ensure that CT scans are assessed by someone with appropriate training and expertise.

  • Skull fractures are obvious, as is the degree of depression of fragments.
  • Intracranial haematoma may cause midline shift and take several forms: extradural haematomas (p353) appears as a high density (white) lens-shaped lesions. Subdurals conform more to the surface of the brain (p353).
  • Cerebral contusions appear as patches of low or mixed attenuation.
  • Cerebral swelling may take some time to develop, causing the ventricles to appear smaller than normal.

Skull X-rays: rationale Skull X-rays are quick, cheap and easy to obtain. Standard views are: AP, lateral and Towne’s. They are useful to detect skull vault fractures, but do not define any intracranial lesion. Identification of skull fractures has been traditionally held to be important because of the ↑ risk of intracranial haematoma, particularly if the conscious level is impaired (see the table below). It is accepted that skull X-rays in conjunction with high quality inpatient observation have a role where CT scanning resources are unavailable. Indications for skull X-rays Traditional indications for skull X-rays (if CT is not performed) include any of the following:

  • history of significant injury
  • an inadequate history
  • loss of consciousness
  • continuing symptoms (vomiting or amnesia)
  • clinical evidence of base of skull fracture
  • full thickness scalp wounds and/or haematoma
  • GCS < 15/15

Interpretation of skull X-rays It can be difficult to distinguish fractures from vascular markings and suture lines. If in doubt, examine the relevant part of the head for sign of injury and seek a senior opinion. Linear fractures appear as sharp-edged lucent lines, which have a different appearance from vascular markings. Depressed fractures take various forms, but tangential views may demonstrate the depressed bone. Base of skull fractures are often not visible, but there may be indirect evidence in the form of an intracranial aerocoele or fluid (air/blood) level in a sinus. Check each of the main sinuses (frontal, sphenoidal, maxillary) in turn, remembering that the lateral skull X-ray is usually obtained with the patient lying supine (ie occiput downwards). This will affect the orientation of the fluid level. Risks of operable intracranial haematoma after head injury The following risks are adapted from Teasdale et al. 1990.

GCS 15/15 overall 1 in 6000
GCS 15/15 with no other features 1 in 31,300
GCS 15/15 with post traumatic amnesia 1 in 6,700
GCS 15/15 with skull fracture 1 in 81
GCS 15/15 with skull fracture and amnesia 1 in 29
GCS 9-14/15 overall 1 in 51
GCS 9-14/15 with no skull fracture 1 in 180
GCS 9-14/15 with skull fracture 1 in 5
GCS 3-8/15 overall 1 in 7
GCS 3-8/15 with no skull fracture 1 in 27
GCS 3-8/15 with skull fracture 1 in 4

Management of serious head injury Tailor management according to the needs of each individual patient. Initial management

  • Provide O2 and protect the cervical spine (p312).
  • Check breathing—provide support if necessary. Examine for serious chest injury.
  • Check BMG and treat hypoglycaemia if present (p314).
  • Insert 2 IV cannulae and send blood for X-matching, FBC, U&E and glucose. If there is any suspicion of a pre-existing clotting disorder (eg alcoholics, patients on anticoagulant therapy), request a baseline coagulation screen.
  • Correct hypovolaemia, resuscitate and treat other injuries.
  • If GCS < 8/15, the patient will require urgent airway protection with GA, tracheal intubation and IPPV (see p304). Check ABG and ventilate to pCO2 of ≈4.5kPa.
  • Liaise early with anaesthetist and neurosurgeon (see indications listed below).
  • Contact a radiologist early to arrange a CT scan with minimum delay.
  • In the multiply or seriously injured patient who will require a CT scan, concerns of opioid drugs masking pupillary signs are less important than ensuring adequate analgesia. Provide titrated IV opioid analgesia (p268), having first recorded GCS, pupil reactions and basic neurological examination.
  • Give IV antibiotics for patients with compound skull fractures. Cefuroxime 1.5g IV is a suitable choice, but be guided by local policy. Regional neurosurgical centres vary as to whether or not they advise prophylactic antibiotics for clinical base of skull fracture (there is no compelling evidence that they prevent meningitis)—again, follow local policy.
  • Clean and close scalp wounds (p392), but do not allow this to delay CT scan or neurosurgical transfer, except where it is necessary to control scalp bleeding.
  • Insert a urinary catheter.
  • Consider the need for orogastric tube. Avoid using NG tubes in facial injury or any possibility of base of skull fracture.
  • Consider the need for tetanus immunization.

Indications for neurosurgical referral

  • CT shows a recent intracranial lesion
  • patient fulfils the criteria for CT scan, but this cannot be done within an appropriate period of time
  • persisting coma (GCS < 9/15) after initial resuscitation
  • confusion which persists >4hrs
  • deterioration in conscious level after admission (a sustained drop of one point on the motor or verbal subscales, or two points on the eye opening subscale of the GCS)
  • progressive focal neurological signs
  • seizure without full recovery
  • depressed skull fracture
  • definite or suspected penetrating injury
  • CSF leak or other sign of a basal fracture

See pp20-23 on patient transfer and for an example of a Neurosurgical Referral Letter. P.353
Treating complications Early recognition and treatment of complications is essential to prevent secondary brain damage. It is crucially important to prevent hypoxia and hypovolaemia adding to the primary cerebral insult. Fits Check BMG, glucose and ABG. Treat with IV diazepam 5-10mg. Repeat this if not initially effective. Commence an IV phenytoin infusion (loading dose 10-15mg/kg IV over 30mins with ECG monitoring) to prevent further fits. Fits which continue or recur despite this initial treatment require ITU involvement and IV anaesthetic drugs (eg thiopentone). Deteriorating conscious level Having corrected hypoxia, hypercapnoea and hypovolaemia, a diminishing conscious level is likely to reflect intracranial pathology, leading to ↑ ICP, requiring urgent investigation and treatment. Bradycardia, hypertension and a dilating pupil are very late signs of ↑ ICP. Speed is of the essence. Liaise with a neurosurgeon who will advise on use of agents to ↓ICP (eg a bolus of 0.5g/kg IV mannitol—typically 200mL of 20% for an adult). Mannitol is an osmotic diuretic which may temporarily ↓ICP and ‘buy time’ to get the patient to theatre for drainage of an intracranial haematoma. Other examples of deterioration requiring urgent reassessment

  • the development of agitation or abnormal behaviour
  • the development of severe or increasing headache or persistent vomiting
  • new or evolving neurological symptoms/signs (eg limb weakness)

Intracranial haematoma Causes of neurological deterioration after head injury include hypoxia, hypovolaemia, fits, cerebral swelling, intracranial haematoma. Intracranial haematomas are important, as prompt surgery may save lives. Patients with bleeding disorders or on anticoagulants have a greatly ↑ risk of developing an intracranial haematoma after head injury. Extradural haematoma Classically, extradural haematoma is due to bleeding from the anterior branch of the middle meningeal artery after temporal bone fracture. The textbook description is of head injury with initial loss of consciousness, then return to full consciousness, before neurological deterioration occurs as intracranial haemorrhage continues and ICP↑. However, many patients deviate from this classical ‘talk and die’ description: extradural haemorrhage may occur in non-temporal sites, without skull fracture and with no initial loss of consciousness. Subdural haematoma Bleeding from bridging veins between brain and dura causes subdural haematoma. Unlike extradural haematoma (which is separated from the brain surface by the dura), subdural haematoma conforms to the brain surface. This helps to distinguish extradural from subdural haematoma on CT scan. Subdural haematoma may be acute or chronic. Acute subdural haematoma is associated with a severe brain insult. Chronic subdural haematoma often occurs in the elderly and alcoholics (↑risk perhaps due to cerebral atrophy). Chronic subdural haematoma develops over several days, often presenting with fluctuating conscious level, sometimes with an obscure (or even no) history of head injury. P.354
Minor head injury Introduction Assessment and management of patients who have sustained relatively minor primary brain insults can be difficult. This is especially true when assessment is rendered awkward by virtue of age, epilepsy, drug or alcohol ingestion. In these circumstances, adopt a cautious approach and admit the patient for observation until the picture becomes clearer. Golden rules for managing head injury are:

  • Never attribute a ↓GCS to alcohol alone
  • Never discharge a head-injured patient to go home alone
  • Admit patients with head injury and coexisting bleeding tendency (including those taking anticoagulant drugs)

Differential diagnosis Consider the possibility that other conditions may be principally responsible for the patient’s symptoms. For example, small children who vomit after head injury may be suffering from otitis media or throat infection. Otitis media may be responsible for both the vomiting (with fever) and for the head injury (by causing unsteadiness of gait, resulting in a fall). Indications for admission

  • ↓GCS (ie < 15/15), neurological deficit or post-traumatic fit
  • significant neurological symptoms (severe headache, vomiting, irritability or abnormal behaviour, continuing amnesia >5mins after injury)
  • significant medical problems, particularly bleeding tendency (including inherited diseases and anticoagulant drugs)
  • inability to assess due to epilepsy, consumption of alcohol or drugs
  • clinical or radiological evidence of skull fracture
  • no one available at home or no safe home to go to (including suspected NAI and domestic violence)

Observation of those admitted All patients require regular neurological observations (as described on p344). Act promptly if conscious level↓ or neurological deficit develops—remember that one of the principal reasons for admitting patients with apparently minor head injuries is to monitor for the possible development of intracranial problems. In this case, resuscitate, liaise with a neurosurgeon and consider urgent CT scan. If after 12-24hrs of observation, the patient is symptom-free, haemodynamically stable and is GCS 15/15 with no neurological deficit, it is reasonable to consider discharge. Patients who do not fall into this category (ie symptomatic, ↓GCS or neurological deficit) require CT scan. Discharging patients Most of the patients who present with minor head injury can be safely discharged directly from A&E. Ensure that there is a responsible adult available to accompany them home and someone to stay with them once they get home for 24hrs. Warn the patient and the accompanying adult of the potential problems following a head injury—and what to do if any of these problems are experienced. Give advice regarding analgesia. Most A&E departments have standard written instructions which are given to the patient and accompanying adult. An example of some head injury warning advice is shown below. P.355
An example of head injury warning instructions


  1. Ensure a responsible person is available to keep an eye on you for the next 24 hours and show them this card
  2. Rest for the next 24 hours
  3. Do take painkillers such as paracetamol to relieve pain and headache
  4. DO NOT drink alcohol for the next 24 hours
  5. DO take your normal medication but DO NOT take sleeping tablets or tranquilizers without consulting your doctor first
  6. If any of the following symptoms occur then you should return or be brought back to the hospital or the hospital telephoned immediately. Tel (01***)****** (24 hours):
    • Headache not relieved by painkillers such as paracetamol
    • Vomiting
    • Disturbance of vision
    • Problems with balance
    • Fits
    • Patient becomes unrousable


  1. Your child has sustained a head injury and following a thorough examination we are satisfied that the injury is not serious. Your child may be more tired than normal
  2. Allow him/her to sleep if they want to
  3. Give Calpol or Disprol (paediatric paracetamol) for any pain or headache
  4. Try to keep your child resting for 24 hours
  5. If your child should develop any of the following:
    • Headache not relieved by paediatric paracetamol
    • Vomiting
    • Altered vision
    • Irritability
    • Fits

Becomes unrousable

  1. bring him/her back to the hospital or telephone for advice immediately: Tel (01***)****** (24 hours)

Alternative suggested written advice is available from the National Institute for Clinical Excellence (http://www.nice.org.uk). P.356
Post-concussion symptoms Presentation Post-concussion symptoms are common after head injury and cause much anxiety in patients and their relatives. The most frequent complaints are:

  • headache
  • dizziness
  • lethargy
  • depression
  • inability to concentrate

Headaches occur in most patients admitted to hospital after head injuries: in ≈30% the headaches persist for >2months. The headaches are usually intermittent and become worse during the day or on exertion. Some appear to be ‘tension headaches’ and are often not significantly helped by analgesics. Migraine attacks may become more frequent or severe after a head injury. Headaches which do not fit these patterns may reflect serious intracranial pathology. Non-specific dizziness is common after concussion. Detailed questioning may distinguish dizziness from vertigo due to disturbance of the vestibular mechanisms. Dizziness may be caused by postural hypotension or by drugs (eg co-proxamol and other analgesics) or alcohol (to which patients are often more sensitive after a head injury). Diagnosis Post-concussion symptoms are diagnosed by exclusion of other problems or complications following head injury. Take a careful history, including asking questions about drowsiness, intellectual function, neck pain, photophobia, vomiting and rhinorrhoea. Examine the patient for any specific cause of the symptoms and for any neurological deficit. Look particularly for evidence of meningitis or an intracranial haematoma. Check for papilloedema. Elderly, alcoholic patients, or those with a bleeding tendency, are prone to develop chronic subdural haematomas, which may cause confusion or intellectual deterioration, often without localising signs. Obtain a CT scan in such patients. Treatment After a careful history and examination, together with appropriate investigations to exclude other problems, reassure the patient and explain that the symptoms are likely to gradually resolve. Reduced short-term memory and impaired concentration may make it difficult for a patient to return to work and cause additional stress and anxiety: give suitable explanations and discuss the provision of a sick note with the GP. Follow-up Since symptoms may last for some time, arrange appropriate follow-up. This usually involves the GP, who needs to be kept fully informed of the clinical findings and diagnosis. P.357
Maxillofacial injuries—introduction These injuries often look dramatic and can be life-threatening as well as causing significant long-term morbidity. Common causes are road traffic collisions, assaults and sport. Emergency resuscitative measures

  • Perform a rapid initial assessment to look for and treat airway obstruction (p316) or major bleeding (p312). Remember the possibility of associated neck injury. Blood may rapidly accumulate in the pharynx requiring anterior ± posterior nasal packing for control (p528).
  • Management of airway obstruction is complex, intubation often difficult and occasionally a surgical airway is required: obtain experienced anaesthetic assistance early. Use jaw thrust, chin lift and suction to gain a patent airway.
  • With bilateral mandibular fractures, the tongue may be displaced backwards. Restore airway patency by pulling the fracture segment anteriorly or by inserting a large suture in the tongue and pulling anteriorly.
  • Maxillary fractures may be displaced far enough backwards to compromise the airway by contact of the soft palate against the posterior pharyngeal wall. This can be relieved by hooking two fingers behind the hard palate and pulling forwards and upwards, but this can produce considerable bleeding.

History Important clues may be obtained from knowing the causative events both in relation to the facial injury itself and also of injury to the head, spine etc. Drug history (eg anticoagulants or bleeding tendency) may be important. Examination Inspect the face from the front, side and above (by standing above and behind the patient). Look for:

  • asymmetry
  • flattening of the cheek (depressed zygomatic fracture)
  • ‘dish face’ deformity (flattened elongated face due to posterior and downward displacement of the maxilla)
  • nasal deviation or saddle deformity. Measure the intercanthal distance: if >3.5cm suspect nasoethmoidal fracture—see below.
  • uneven pupillary levels (due to orbital floor fracture)
  • CSF rhinorrhoea (causes ‘tramline’ effect with central CSF and blood either side)
  • subconjunctival haemorrhage without a posterior border (suggests an orbital wall fracture).

Palpate the facial bones systematically. Start over the superior orbital margins. Work down feeling both sides at the same time checking for pain, deformity, crepitus and movement. Feel specifically for steps in the inferior orbital margin and zygoma. Subcutaneous emphysema implies a compound fracture—often of the maxillary sinus. Check for hypo/anaesthesia of the cheek, side of the nose and upper lip (infraorbital nerve injury) and for numbness of the upper teeth (anterior superior alveolar nerve in the infraorbital canal) and lower teeth and lip (inferior dental nerve damage due to mandibular fracture). Examine inside the mouth, checking for dental malocclusion, loose or lost teeth (this may need CXR), bruising and bleeding. Examine the eyes carefully (p514): assume any laceration below the medial canthus involves the lacrimal duct until proven otherwise. P.359
Investigations In patients with multiple injuries, X-ray of cervical spine, CXR and pelvis will take precedence. Even with ‘isolated’ facial injuries, perform X-rays of cervical spine and head, where indicated, before facial X-rays. Facial X-rays are often both difficult to perform (because of poor patient co-operation) and difficult to interpret. Get specialist advice regarding the views required and their interpretation. CT scanning is often required prior to definitive maxillofacial surgery. The commonly required views include:

  • occipitomental 10°, 30* and 45*
  • lateral
  • orthopantomogram (for mandible)

Treatment Treatment of specific facial fractures is considered on pp360-5. Remember that even in the absence of a visible fracture on X-ray, patients in whom there is a clinical suspicion of facial fracture (swelling, tenderness, asymmetry, numbness etc) require expert attention and/or follow-up. P.360
Middle third facial fractures Dento-alveolar fractures These injuries involve only the teeth and their bony support. Look for deranged occlusion and stepped malalignment of teeth, bruising of gums and palpable fracture in the buccal sulcus. Le Fort facial fractures These lie between the frontal bone, the skull base and mandible. They involve the upper jaw, teeth, nose, maxillary and ethmoid air sinuses. They are classified:

  • Le Fort I involving the tooth-bearing portion of the maxilla. Look for lengthening of the face due to dropped maxillary segment. There may be movement or a split of the hard palate, a haematoma of the soft palate/buccal sulcus and malocclusion.
  • Le Fort II involving the maxilla, nasal bones and the medial aspects of the orbits. Look for a ‘dished-in’ face, a palpable step in the infraorbital margin, infraorbital nerve damage, surgical emphysema and malocclusion. The maxilla may be floating—if the upper teeth are pulled (gently!) the maxilla may move forward. Check for epistaxis, CSF rhinorrhoea, diplopia and subconjunctival haematoma. Facial swelling occurs rapidly and is often severe. Later, bilateral periorbital bruising may be evident.
  • Le Fort III involves the maxilla, zygoma, nasal bones, ethmoid and the small bones of the base of the skull. The entire midface is fractured from the base of the skull. Features include those of type II plus: flattened zygomatic bones (which may be mobile and tender), steps over the fronto-zygomatic sutures, movement and deformity of the zygomatic arch and altered pupillary levels. There is usually severe facial swelling and bruising. Pharyngeal bleeding may severely compromise the airway and cause hypovolaemic shock.

Note that Le Fort fractures may be asymmetric (eg Le Fort II on the right and III on the left). Nasoethmoidal fractures These produce flattened nasal bridge with splaying of the nasal complex, saddle shaped deformity of the nose, traumatic telecanthus, periorbital bruising, subconjunctival haematoma, epistaxis, CSF rhinorrhoea and supraorbital or supratrochlear nerve paraesthesia. Management of middle third facial fractures

  • Resuscitate and open the airway as described on p316.
  • Refer dentoalveolar fractures for repositioning and immobilization with acrylic/metal splints ± wiring.
  • Refer all patients with middle third or nasoethmoidal fractures to the maxillofacial specialists for admission. Occasionally, continuing haemorrhage requires packing—leave this to the specialist. Tell the patient not to blow the nose (↑subcutaneous emphysema and may drive bacteria into fracture sites, soft tissues and intracranially). Prophylactic antibiotics (eg benzyl penicillin) are usually advised by maxillofacial surgeons.
  • Ensure tetanus prophylaxis (p396) as most fractures are compound.
  • Discuss patients with CSF leaks with the neurosurgeons regarding their antibiotic policy.
  • Clean and dress compound facial lacerations, but do not close them (unless actively bleeding), as they may need formal debridement and they may provide access to assess fractures.


Figure. Le Fort classification of facial fractures

Zygomatic, orbital and frontal sinus fractures Zygomatic (malar) fractures These injuries are usually due to a direct blow and are frequently associated with severe eye injuries. ‘Tripod fractures’ involve fractures through the zygomatico-temporal and zygomatico-frontal sutures and the infraorbital foramen. Examination Look for flattening of the cheek (often obscured later by swelling), palpable defect in the infraorbital margin, infraorbital nerve damage, diplopia and subconjunctival haemorrhage (especially if no posterior margin is seen). Isolated fractures of the zygomatic arch may be accompanied by a palpable defect over the arch and limited or painful jaw movement resulting from interference with the normal movement of the coronoid process of the mandible. Orbital ‘blow-out’ fractures Caused by a direct blow to the globe of the eye (commonly from a squash ball or shuttlecock) resulting in a fracture of the orbital floor and prolapse of contents into the maxillary sinus. Examination Check for diplopia due to inferior rectus entrapment (the patient cannot look up and medially), enophthalmos and surgical emphysema. Carefully check the eye itself for injury (hyphaema, retinal detachment, glaucoma, blindness). Record the visual acuity. Test infraorbital nerve function. Fracture(s) of the floor of the orbit may not be easily visible on X-ray, but can often be inferred by the soft tissue mass in the roof of the maxillary sinus (‘tear drop’ SIGN), clouding of the sinus and surgical emphysema. Management of zygomatic and orbital fractures

  • Tell the patient not to blow his/her nose.
  • Refer all patients (including those in whom a fracture is clinically suspected but not evident on X-ray) to maxillofacial specialists who will advise regarding prophylactic antibiotics and will arrange further investigation (tomography or CT scanning) and treatment.
  • Involve the ophthalmologists if local eye injury coexists.

Note Patients with orbital emphysema who complain of sudden ↓ in vision may be suffering from a build-up of air under pressure which is compromising retinal blood flow. These patients need emergency decompression. Frontal sinus fractures Presenting features include supraorbital swelling, tenderness and crepitus, occasionally with supraorbital nerve anaesthesia. CT scanning will determine whether or not there are fractures of simply the anterior wall or of both anterior and posterior sinus walls (± depressed fragments). Give IV antibiotics and refer for admission and observation, which in the case of depressed fragments, should be to the neurosurgical team. P.363
Mandibular injuries Considerable force is required to fracture the mandible, so look for concurrent head or other injuries. The mandible is often fractured at a site distant from the point of impact (eg a fall on the chin may cause a condylar fracture), and commonly multiple fracture sites are present. The temporomandibular joint may be dislocated, or the condyle driven through the temporal bone causing a skull base fracture. Symptoms and signs The patient usually presents with pain (aggravated by jaw movement or biting). Check for swelling, tenderness or steps on palpation of the mandible. Look for malocclusion, loose or missing teeth and intra-oral bruising. Numbness of the lower lip indicates injury to the inferior dental nerve where it passes through the ramus of the mandible. X-rays Request an orthopantomogram (OPG). Temporomandibular joint dislocation and condylar fractures are best shown by condylar views. Management Simple undisplaced single fractures not involving the teeth can be provided with analgesia, soft diet, prophylactic antibiotics (eg penicillin or co-amoxiclav), tetanus cover and referred to the maxillofacial outpatient department. Refer displaced or multiple fractures to the on-call specialist. Condylar fractures If there is derangement of occlusion, or the jaw deviates on opening or there are bilateral condylar fractures then refer to on-call specialist. Advise patients with unilateral asymptomatic fractures to take a soft diet and arrange outpatient follow-up. Temporomandibular joint dislocation This is almost invariably anterior, but can be uni- or bilateral. It may be caused by a direct blow to the (often open) jaw, or in patients with lax joint capsule/ligaments by yawning, eating, dystonic reactions or intubation. The patient cannot close the mouth, the jaw protrudes anteriorly and difficulty in swallowing leads to drooling of saliva. The pain is often over the temporal fossa rather than the temporomandibular joint itself. Obtain X-rays only if there is a history of direct trauma. Treatment If seen shortly after dislocation, reduction can usually be achieved simply and without anaesthesia or sedation. Explain the process to the patient. Sit in front of him/her and with your thumb(s) protected by a gauze swab press down and backwards on the lower molar teeth while gently cupping and lifting the chin with the fingers. Confirm relocation by X-ray if it was a first-time dislocation. Post-reduction advise the patient to take a soft diet, and not to yawn (difficult!) or open the mouth widely for 24hrs. Delayed presentations can be associated with muscle spasm requiring anaesthesia and muscle relaxants. P.365

Figure. Common fracture sites of the mandible
Figure. Reduction of dislocated temporomandibular joint

Spine and spinal cord injury 1 Consider the possibility of spinal injury when managing every injured patient. Injudicious manipulation or movement can cause additional spinal injury. Maintain a particularly high index of suspicion and provide spinal immobilization in patients with:

  • major trauma
  • ‘minor’ trauma with spinal pain and/or neurological symptoms/signs
  • altered consciousness after injury
  • a mechanism of injury with a possibility of spinal injury (eg road traffic collision, high fall, diving and rugby injuries)
  • pre-existing spinal disease (eg rheumatoid arthritis, ankylosing spondylitis, severe osteoarthritis, osteoporosis, steroid therapy), as significant fractures or dislocations may follow apparently minor trauma

The commonest sites of spinal injury are the cervical spine and the thoracolumbar junction. Airway management and spinal immobilization These two aspects demand immediate attention in any patient with possible spinal injury—manage them together. The neck is the commonest site of cord injury. If immobilization is not achieved with unstable injuries, it is the site at which most additional cord or nerve root damage can be produced.

  • Perform manual immobilization rapidly (without traction), keeping the head and neck in the neutral position, by placing both hands around the neck and interlocking them behind, with the forearms preventing head movement (see below).
  • Apply a hard collar with continued manual stabilization or support with sand bags placed on either side of the head and tape applied to the forehead to prevent rotation. The collar should fit securely, but not occlude the airway or impair venous return from the head. Take particular care in patients with pre-existing neck deformity (eg ankylosing spondylitis—p475) not to manipulate the neck or to force the collar into place.
  • Ensure airway patency and adequate ventilation—hypoxia compromises an injured cord. Initially in an unconscious patient, jaw thrust and suction to the upper airway can be used. Remember that oropharyngeal stimulation can provoke severe bradyarrhythmias. Simple airway adjuncts such as oro- and naso-pharyngeal airways may maintain upper airway patency, but in a (small) proportion of patients, tracheal intubation is required. This must be performed by an individual experienced in advanced anaesthetic techniques with an assistant controlling the head/neck, thereby limiting cervical spine movement. Ideally, tracheal intubation is performed under fibre-optic control.
  • Ventilation can deteriorate due to cord oedema/ischaemia, so look regularly for diaphragmatic breathing (the diaphragm is supplied by C3/4/5) and the use of accessory muscles of respiration. Perform pulse oximetry and regular ABG analysis to confirm adequate oxygenation and ventilation. Tracheal intubation and controlled ventilation may be required.
  • Usually, patients will have been transported on a spinal board, which is removed soon after the primary survey is completed and resuscitation commenced.

Suspect spinal injury in patients with ↓ consciousness if there is:

  • flaccid arreflexia
  • ↓anal tone on PR examination
  • diaphragmatic breathing
  • an ability to flex (C5/6), but not to extend (C6/7) the elbow
  • response to painful stimulus above, but not below the clavicle
  • hypotension with associated bradycardia
  • priapism
Figure. Manual immobilization of the neck
Figure. Co-ordinated 4 person lift

Spine and spinal cord injury 2 Managing the circulation Monitor the ECG and BP. Interruption of the sympathetic system in the cord causes loss of vasomotor tone, with vasodilation, ↑ venous pooling and ↓BP. Flaccidity and arreflexia, together with the absence of a reflex tachycardia or an associated (and inappropriate) bradycardia are pointers to this, but before diagnosing ‘neurogenic shock’ exclude and treat other causes of hypotension (eg blood loss, tension pneumothorax). IV crystalloids/colloids (p312) will usually correct any relative hypovolaemia, but inotropic agents may occasionally be required if, following correction of bradyarrhythmias by atropine and adequate volume replacement, ↓cardiac output persists. Consider CVP monitoring of patients in neurogenic shock to prevent fluid overload. Other considerations Insert a urinary catheter to monitor urinary output and prevent bladder distension. Provided there is no craniofacial injury, a NG tube will prevent gastric distension (ileus commonly develops after cord injury) and ↓risk of aspiration and respiratory embarrassment. With blunt injury mechanisms, up to 2/3 of individuals with spinal cord injury have major injuries at other sites. Conscious patients can usually describe a sensory level and paralysis, with pain at the level of the vertebral injury. Adopt a particularly high index of suspicion for thoracic/abdominal injury—clinical features may be obscured by sensory/motor deficits from the cord injury itself. Paralytic ileus and abdominal distension may occur and there may be no signs of peritoneal irritation. DPL, USS or CT scanning may be required. Neurological examination Carefully perform and document the neurological examination, including light touch and pinprick sensation, proprioception, muscle power, tone, co-ordination and deep tendon reflexes. Evidence of distal, motor or sensory function implies an incomplete lesion and hence the possibility of recovery. The accuracy of this baseline examination is important, since cephalad progression of abnormalities is a sensitive marker of deterioration, and in the cervical region, may lead to respiratory failure. Document muscle group strength in upper and lower limbs using the 0-5 grading system (see below). It is standard practice to record the most caudal location which has intact (normal) motor and sensory function. Examine the perineal area (sacral dermatomes) and perform a PR examination, looking for voluntary contraction and anal tone. If present, the bulbocavernosus reflex (contraction of the bulbocavernosus muscle in response to squeezing the glans penis—S2,3,4) and anal cutaneous reflex (anal contraction produced by scratching the perianal skin—S4,5) imply sacral sparing. Spinal examination Log-roll the patient. The person controlling the head and neck directs movement. Carefully examine for tenderness, step-deformity, gibbus, widening of interspinous processes and prominence of spinous processes. Note that there may not be overlying tenderness with vertebral body fracture. Remove any debris from under the patient. Keep the patient covered and warm, as loss of sympathetic vasomotor tone results in ↑ risk of hypothermia. To ↓risk of pressure sores ensure the patient does not lie for a long period on a ‘spinal board’. P.369
Incomplete cord injury patterns There are several recognized patterns of incomplete spinal cord injury. Although the resultant physical signs can be predicted from a detailed knowledge of neuroanatomy, bear in mind that some patients present with an atypical injury and therefore an atypical pattern of injury. Anterior cord syndrome Loss of power and pain sensation below the injury, with preservation of touch and proprioception. Posterior cord syndrome Loss of sensation, but power preserved. Brown-Séquard syndrome Hemisection of the cord producing ipsilateral paralysis and sensory loss below the injury, with contralateral loss of pain and temperature. This syndrome occurs more frequently after penetrating injury than after closed injury. Central cervical cord syndrome Typically seen in elderly patients following extension injuries to the neck, with degenerative changes being the only X-ray abnormality. It is characterized by incomplete tetraparesis which affects the upper limbs more than the lower limbs (as nerves supplying the upper limbs lie more centrally within the cord). Sensory deficits are variable. Spinal cord injury without radiographic abnormality (SCIWORA) A significant proportion of children with spinal cord injury have no radiographic abnormality. The extent of both the neurological deficit and recovery is variable. Adults may similarly have spinal cord injury due to traumatic herniation of an intervertebral disc, epidural haematoma or ligamentous instability, yet plain radiographs appear normal.

Grading of muscle power
0 Total paralysis
1 Palpable or visible contraction
2 Movement with gravity eliminated
3 Movement against gravity
4 Weaker than usual
5 Normal strength
Muscles supplied by various nerve roots
C5 shoulder abductor (deltoid)
C6 wrist extensors (extensor carpi radialis)
C7 elbow extensor (triceps)
C8 middle finger flexor (flexor digitorum profundus)
T1 little finger abductor (abductor digiti minimi)
L2 hip flexors (iliopsoas)
L3 knee extensors (quadriceps)
L4 ankle dorsiflexors (tibialis anterior)
L5 big toe extensor (extensor hallucis longus)
S1 ankle plantar flexors (soleus, gastrocnemius)

Spine and spinal cord injury 3 Imaging (see indications under ‘whiplash’—p440) X-rays are readily available, but interpretation can be difficult. Whenever possible get senior expert help. Cord injury can occur without X-ray abnormality. This may be due to ↑ soft tissue elasticity allowing excessive movement, or cord compression caused by disc prolapse (eg younger patients and children), or vascular involvement or spondylosis in older patients. Cervical spine Request AP, lateral (must show C7/T1 junction: apply arm traction or get swimmer’s view if necessary) and open-mouth odontoid peg views. Displacements (subluxations/dislocations) and fractures of vertebral bodies, spinous processes and peg are often best seen on lateral X-ray. Unifacet dislocation causes vertebral displacement anteriorly ≤50% AP diameter of vertebral body. Greater displacement suggests bilateral facet dislocation. Look specifically at prevertebral soft tissue shadows for evidence of prevertebral haematomas. AP views show injuries to the pedicles, facets and lateral masses. Open-mouth odontoid view usually demonstrates peg fractures. Extension/flexion views to assess neck stability are questionable in the early post-injury period, as muscle spasm may inhibit movement and there is potential to aggravate cord damage. Obtain senior advice before requesting these views. Never perform them if any fracture or subluxation is seen on the standard 3 views, or if any neurological symptoms or deficit is present. A senior doctor must directly supervise, and the patient should move the neck himself. Stop if symptoms such as paraesthesiae occur. Thoraco-lumbar spine Standard views are AP and lateral. In the thoracic region overlapping structures may make interpretation difficult and necessitate other imaging. Provided X-rays are of diagnostic quality, visualization of fractures (usually compression or burst fractures) and displacements is rarely difficult, but these bear little predictive value to the degree of cord injury present. CT scan and MRI CT scanning delineates bony abnormalities and the extent of spinal canal encroachment. It is also useful if, despite swimmer’s views or tomography, the lower cervical/upper thoracic spine is poorly visualized. CT or MRI are useful for patients in whom there is clinical suspicion of injury (persistent pain, positive neurology) despite normal X-rays. Further treatment Immobilize cervical injuries using a firm, well-fitting cervical collar, pending a decision to undertake skeletal traction. Skeletal traction using Gardner-Wells calipers or skull halo devices and pulley/weight systems may be undertaken by orthopaedic/neurosurgical staff to reduce fracture-dislocations and improve alignment of the spine with the aim of decompressing the cord. Thoraco-lumbar fracture-dislocations are normally treated by bedrest with lumbar support. In specialist units, unstable injuries may be surgically fixed. For patients seen within 8hrs of non-penetrating cord injury, high dose steroid therapy (methylprednisolone 30mg/kg given over 15mins followed 45mins later by a continuous infusion of 5.4mg/kg/hr for 23hrs) may improve motor function, but consult the local neurosurgeon before starting this. With penetrating injuries to the spine, if the object is still in place, leave it undisturbed until it can be removed in theatre where the relationship and potential injury to the spinal cord/canal can be directly seen. P.371
Assessment of spinal X-rays Interpreting spinal X-rays can be difficult. If in any doubt, get senior expert help. A systematic approach helps to prevent injuries from being missed:

  • Check the alignment of the vertebrae. The spine should be straight or follow gentle curves and should not exhibit any ‘steps’. On the lateral X-ray assess the alignment by checking in turn: anterior vertebral border, posterior vertebral border, posterior facets, anterior border of spinous processes, posterior border of spinous processes. Look also at interspinal distances.
  • Check alignment on the AP film by following the spinous processes and the tips of the transverse processes. Look for rotational deformity and asymmetry.
  • Assess the integrity of each spinal vertebra, including the vertebral bodies, laminae and pedicles.
  • Be vigilant in assessing the odontoid peg view, looking for asymmetry/ displacement of the lateral masses of C1. Distinguish fractures (limited to bone area) from overlying soft tissue shadows (extend beyond area of bone). Note that the atlanto-odontoid distance should be ≤3mm in adults and ≤5mm in children.
  • Look for indirect evidence of significant spinal injury (↑prevertebral space). The normal soft tissue prevertebral thickness at the antero-inferior border of C3 (ie distance between pharynx and vertebral body) is <0.5cm.
    Figure. Lateral cervical spine
    Figure. AP cervical spine
    Figure. Odontoid peg view

Dermatomes Knowledge of dermatomes is a prerequisite for making sense of neurological signs.

Figure. Dermatomes front


Figure. Dermatomes back

Gunshot injuries An understanding of wound ballistics is helpful in the medical care of patients with gunshot injuries. Wounds produced by bullets/missiles are determined by kinetic energy (KE) transfer, missile flight characteristics and the tissue injured. Kinetic energy transfer The KE of a missile is directly proportional to its mass and to the square of its velocity (KE = 1/2mv2). Thus, tissue injury depends more upon the bullet’s velocity than its mass. At velocities > speed of sound, the rate of dissipation of KE becomes proportional to the velocity3 or even higher powers. Bullets travelling a >1,000 ft/sec (300m/sec) are considered to be ‘high velocity’. The tissue itself Tissue density affects the retardation of the passage of a missile and ↑ energy dissipation and tissue destruction. Bone involvement may cause additional retardation as well as bony fragments themselves causing secondary injury. Cavitation When high velocity bullets enter the body, energy is transmitted to the tissues, compressing and accelerating them at right angles away from the track. This leads to cavity formation around the bullet and its track. Over a few micro-seconds the cavity enlarges, then collapses. Tissue elasticity perpetuates a process of cavity reformation/collapse, with rapidly ↓amplitude oscillations until all KE is expended. This causes highly destructive stretching, tearing and shearing of tissues, which may produce injury many times the size of the bullet. Since the pressure in the cavity is sub-atmospheric, debris and organisms are sucked in. Clinical aspects The principles of resuscitation of a patient with gunshot injury are identical to those for any major trauma case. Specific aspects to consider are:

  • Consider staff safety: check the patient for weapons.
  • The magnitude of the external wounds may bear little relationship to the severity of internal injury. Remove the patient’s clothes and examine the entire body surface for entrance/exit wounds. These are commonly missed in hairy areas (eg scalp, axillae and perineum).
  • Patients are often young and fit: signs of hypovolaemia may be delayed.
  • Chest injuries are commonly associated with pneumothorax (p326). PEA cardiac arrest should prompt rapid exclusion of tension pneumothorax. If there is still no improvement, consider cardiac tamponade (p332).
  • Abdominal wounds are associated with a high incidence of internal injury and require laparotomy and antibiotic cover.
  • Gunshot wounds are prone to anaerobic infection (especially tetanus and gas gangrene): clothing/fragments spread widely through tissues distant from the wound track. Extensive surgical debridement (wide excision/fasciotomy) is often required to remove devitalized tissue and foreign material. All high velocity injuries need delayed primary closure with grafting or suture at 3-5days.
  • Ensure tetanus cover and give prophylactic antibiotics.
  • X-ray (AP + lateral) one body region above and one body region below any wound, as well as the one involved to search for metallic FBs.

Blast injuries Blast injuries may be due to explosions involving domestic gas, industrial sites (eg mines/mills) or bombs. Often several mechanisms coexist to cause injury. Blast wave This is an extremely short-lived pressure wave (lasting a few milliseconds only) which expands outwards from the explosive focus. It is produced by intense compression of air at the interface of the rapidly expanding hot gases. The effects can be dramatically aggravated and reinforced by reflection from solid surfaces, such as buildings. Blast wave injuries are caused by 3 mechanisms:

  • Disruption at air/tissue interfaces (especially lungs and ears, producing blast lung and tympanic membrane rupture respectively).
  • Shearing injuries at tissue/tissue interfaces causing subserous/submucosal haemorrhage.
  • Implosion of gas-filled organs leading to perforation of the GI tract and cerebral/coronary air embolism.

Blast winds These are fast moving columns of air which follow the initial blast wave. Their destructive force can be immense, leading to traumatic amputation or even complete dismemberment. Blast winds also carry debris (masonry, glass etc) which can act as secondary missiles causing fragmentation injuries. Fragmentation injuries Objects from a bomb (eg nails, casing, nuts and bolts) or flying debris (masonry, wood, glass) cause lacerations or penetrating injuries. Flash burns These are usually superficial, affecting exposed skin in those close to the explosion. Smoke inhalation may also be present in these patients. Crush injuries These may result from falling masonry, building collapse etc. Psychological Even in individuals with no physical injuries, the psychological effects of blast injury are often severe, comprising acute fear, anxiety and the potential for later chronic sequelae. General aspects of treatment The principles of blast injury treatment are identical to those for patients with other causes of major trauma (p312). Clinical features in blast injuries may be delayed, both in terms of onset and development of clinical signs. This particularly relates to lung and intra-abdominal complications, therefore observe all patients for at least 48hrs. Search particularly for (and treat promptly): pneumothorax (may be tension), respiratory failure/ARDS, peritonitis, abnormal neurological signs (suggesting air embolism), eardrum perforation, anosmia (direct olfactory nerve damage). Note that ventilation of patients with blast injuries is a highly specialist area, with potential risks of producing tension pneumothoraces and air embolism. Other aspects For forensic reasons, ensure that all the patient’s clothes, belongings and any missile fragments are carefully retained, bagged, labelled and kept secure until given to police officers. P.376
Burns—assessment Types of burns

  • thermal
  • chemical
  • electrical (p248)
  • radiation (p250)

History Determination of the circumstances resulting in the patient being burned is essential in order to appreciate the nature of the insult and potential associated risks. Do not, however, delay resuscitation in an attempt to obtain a full history. Consider the following questions:

  • Was there an explosion? (risk of blast injuries)
  • What was the burning material? (polyurethane burns to release hydrogen cyanide)
  • Was the fire in an enclosed space? (high risk of CO poisoning)
  • When did the fire start?
  • When was the patient removed from the fire?
  • How long was the patient exposed for?
  • Was there a history of loss of consciousness?
  • What is the patient’s past medical history and tetanus status?

Initial assessment This proceeds with resuscitation. Check: Airway, Breathing and Circulation. Particular problems associated with burns are:

  • airway burns—suggested by hoarseness, stridor, dysphagia, facial and mouth burns, singeing of nasal hair, soot in nostrils or on palate
  • spinal injury—particularly seen with blast injuries and in those who have jumped from buildings to escape fire
  • breathing problems—contracting full thickness circumferential burns (‘eschar’) of the chest wall may limit or prevent chest movement during attempted respiration
  • circulatory problems—hypovolaemic shock is a feature of severe burns and may also result from other associated injuries

Assessing extent Estimation of the percentage of body surface area burnt is difficult for non-experts. Use Lund and Browder charts appropriate for the age of the patient (see below). The palmar surface of the patient’s palm (not including the fingers) represents ≈0.75% body surface area. Assessing depth The depth of a burn depends upon the temperature of heat applied and how long it is applied for. Superficial (first and second degree) burns range from relatively minor (but painful) erythema (first degree) through painful erythema with blistering to deep partial thickness (second degree) burns, which do not blanch on pressure. Full thickness (third degree) burns may be white, brown or black in colour and have a ‘leathery’ appearance. They do not blister and have absent sensation. On the day of the injury it may be difficult to distinguish deep superficial (second degree) burns from full thickness (third degree) burns, but correctly making this distinction does not alter the initial management. P.377

Figure. Assessing extent of burns—Lund and Browder charts
Adults rule of 9’s: head = 9%
each arm = 9%
each leg = 18%
front of trunk = 18%
back of trunk = 18%
perineum = 1%
Infants rule of 5’s: head = 20%
each arm = 10%
each leg = 20%
front of trunk = 10%
back of trunk = 10%

Major burns—resuscitation Prehospital first aid measures

  • Ensure rescuer safety first—be guided by the fire crew.
  • Remove the patient from the burning environment. If clothes are still smouldering, apply copious amounts of cold water and remove them, unless adherent.
  • Provide O2. Apply clean sheets to the burns.

Airway and cervical spine protection

  • Treat airway obstruction (p316).
  • Continue O2 and apply a hard cervical collar if there is any possibility of spinal injury—in this case cervical spine X-rays will be required subsequently.
  • If there is evidence of impending airway obstruction (stridor, oropharyngeal swelling—see p316), call immediately for senior help (and/or a senior anaesthetist). Urgent tracheal intubation under GA may be life-saving.


  • Obtain IV access with two large peripheral cannulae.
  • Send blood for X-matching, FBC, COHb, U&E, glucose and coagulation.
  • Provide analgesia (eg IV morphine titrated according to response).
  • Provide an anti-emetic (eg IV cyclizine 50mg).

Fluid resuscitation

  • Give IV fluids. Start with isotonic crystalloid (eg 0.9% saline) at a rate of 2-4mL of crystalloid per kg body weight per % body surface area burned over the first 24hrs following injury. Give half of this volume in the first 8hrs.
  • Check pulse, BP and respiratory rate every 10-15mins initially.
  • Insert a urinary catheter and test the urine. Patients with myoglobinuria are at particularly high risk of acute renal failure—reduce this risk by adequate fluid resuscitation. Urine output is a guide to continuing fluid therapy.
  • Review the rate of IV volume replacement frequently over the initial resuscitation period and adjust it according to haemodynamic parameters, in order to maintain a satisfactory urine output (>50mL/hr in adults; >1mL/kg/hr in children).
  • Some burns units prefer a colloid (eg Gelofusin® or albumin) to form a component of the initial volume replacement: follow local policy.
  • Patients with full thickness burns of body surface area >10% may require red cell transfusion in addition to the above measures.


  • Check COHb and ABG.
  • Circumferential full thickness chest burns restricting chest movement require escharotomy. Cut the burnt areas (as shown below) down to viable tissue to release the constriction. Cutting diathermy may be helpful here.
  • Obtain a CXR.

The burn

  • Measure the area of the burn as a % of body surface area.
  • Irrigate chemical burns with warmed water (see p383).
  • Protect the burn by the application of cling film or dry sterile sheets. Do not apply extensive burns dressings before assessment by a burns specialist.
  • Involve a burn specialist at an early stage—in the UK, the National Burn Bed Bureau will help to locate a suitable bed (Telephone 01384 215576).
  • Ensure tetanus prophylaxis, but avoid ‘routine’ prophylactic antibiotics.

The burnt patient in cardiac arrest

  • follow standard guidelines
  • give a large bolus of IV fluid
  • if there is a strong possibility of cyanide poisoning (eg burnt plastic furniture in a house fire), give appropriate antidote (eg IV dicobalt edetate 20mL of 1.5%) as outlined on p201).

Vascular impairment to limbs and digits Consider the need for longitudinal escharotomies. These are occasionally needed if ischaemia causes severe pain: get advice from a burns specialist.

Figure. Escharotomy

Inhalation injury The commonest form of inhalation injury is smoke inhalation accompanying burns in house fires. In addition to causing death itself, inhalation injury ↑ mortality for a given body surface area of burn. Smoke is a complex and unpredictably variable mixture of solid, liquid and gas constituents. Common components of inhalation injury include:

  • direct thermal injury
  • soot particles cause local injury to the cilia of the respiratory tract and obstruct small airways
  • CO ≈85% of fire deaths are caused by CO (p202)
  • gas products of combustion—oxides of sulphur, nitrogen, ammonia, chlorine, hydrogen cyanide, phosgene, isocyanates, ketones and aldehydes are highly irritative. They cause lacrimation, blepharospasm and laryngospasm. Some react with water in the respiratory tract producing strong acids which cause bronchospasm, mucosal injury and oedema.

The nature of the inhaled insult determines the site, severity and systemic features. The upper respiratory tract can dissipate heat efficiently, so that direct thermal injury to the lower respiratory tract is rare unless steam/vapours are inhaled. In the lower airway, toxic components such as CO, oxides of sulphur, nitrogen, hydrogen cyanide, hydrogen chloride cause direct injury and may act as systemic poisons. Clinical features Suspect smoke inhalation if any of the following features are present: exposure to smoke or fire in an enclosed space, confusion or altered/loss of consciousness, oropharyngeal burns, hoarseness/loss of voice, singed nasal hairs, soot in nostrils or sputum, wheeze, dysphagia, drooling or dribbling, stridor. Investigations Peak flow rate Determine this in all patients. ABG Detection of hypoxia, hypercapnia and acidosis may be helpful, but does not correlate well with the severity of inhalation injury. Note that pulse oximetry has limited value because of the difficulty in distinguishing between oxyhaemoglobin and COHb. CXR Usually normal initially, later features of ARDS may develop. Carboxyhaemoglobin (COHb) CO poisoning cannot be detected by physical examination, SaO2 or pO2. Either arterial or venous COHB can be measured. Clinical features correlate poorly with COHb levels. Use the nomogram opposite to estimate COHb levels at the time of exposure. The management of CO poisoning is covered in detail on p202. ECG CO binds to myoglobin 3x more avidly than to Hb and by affecting the myocardium may produce arrhythmias, ischaemia or even MI. Fibreoptic bronchoscopy, xenon lung scanning, ventilation-perfusion scans or lung function testing may be subsequently required to assess lung problems due to inhalational injury. P.381
Management Signs of upper airway problems (facial burns, stridor, dysphagia, drooling, ↓consciousness) indicate the need for early tracheal intubation (usually using inhalation anaesthesia) by an experienced doctor with appropriate training. Mucosal swelling in the oropharynx and epiglottis can progress rapidly and necessitate a surgical airway (p318). Flexible bronchoscopy may help to assess thermal injury to the upper airway and help intubation. Assisted ventilation with PEEP or IPPV may be indicated. Give the highest possible concentration of humidified O2. Hyperbaric O2 may be indicated for CO poisoning, but remains controversial (p202). If bronchospasm is present, give nebulized ß2 agonist (salbutamol 5mg) via an O2 powered nebulizer. ↑ in microvascular permeability leads to pulmonary oedema 2-3days after injury and to pneumonia after 7-14days. Pulmonary fibrosis is common among survivors. Inadequate IV fluid resuscitation is associated with greater pulmonary oedema. IV fluid requirements to maintain cardiac and urine output are greater when smoke inhalation has occurred in burns patients. Inhalation of HCN from smouldering plastics (eg polyurethane) results in rapid systemic absorption. Measurement of blood CN concentration is difficult and takes several hours. Cyanide poisoning may be suggested by a severe metabolic acidosis, a high lactate and ↑ anion gap. Consider cyanide antidotes (p201), but they are potentially toxic so do not use blindly. There is no proven benefit from steroid therapy. Nomogram of decay of COHb with time This nomogram (adapted from Clark et al. 1981) allows back-calculation estimation of the likely peak COHb level. It will considerably under-read for children and patients who received high prehospital FiO2.

Figure. Nomogram of decay of COHb with time.

Management of smaller burns Assessment—as on p376 First aid measures Separate the patient and burning agent. Cool affected area with copious quantities of cold water, but beware hypothermia in infants and young children. Need for admission Admit patients with large burns or significant smoke inhalation for IV fluids, resuscitation and analgesia. In the UK, the National Burn Bed Bureau will search for an appropriate bed (Telephone 01384 215576). Also refer for admission burns of suspected NAI origin and patients who would be unable to cope at home (eg an elderly person or if living in difficult social circumstances). Referral to a burns specialist Refer patients with the following:

  • airway burns
  • significant full-thickness burns, especially over joints
  • burns >10%
  • significant burns of special areas (hands, face, perineum, feet)

The burn wound Leave full thickness burns uncovered and refer to a specialist. Do not de-roof partial thickness burns with blistering—consider simple aspiration. Most can be cleaned and covered with an appropriate dressing (see below). Hand burns Consider traditional covering with silver sulphadiazine cream inside a polythene bag or glove sealed at the wrist, changed after 24hrs. Simple paraffin/tulle dressings are an alternative—follow local policy. Elevate to minimize swelling. Facial burns Leave uncovered, or consider application of soft paraffin. Eye burns Check VA and refer to a specialist (p514), with prior irrigation if chemical burns (p516). Burns dressings The ideal burns dressing is sterile, non-adherent and encourages wound healing in a moist environment. The diversity of dressings available reflects the fact that this ideal dressing remains elusive. Allow senior nursing staff to advise on local preference and policy. Accumulation of fluid means that many dressings need to be changed at ≈48hrs—often this is appropriately done at a GP surgery. Analgesia and tetanus Unless there is a contraindication and/or if the patient is elderly, NSAID is appropriate and effective analgesia for many burns which do not require admission. Ensure prophylaxis against tetanus. Burns in children and non-accidental injury Unintentional burns are common in children—use the opportunity to offer advice regarding injury prevention. A minority of burns may result from NAI. Suspect NAI (p690) and seek senior help in the following situations:

  • when the explanation does not fit the burn
  • late presentation
  • other suspicious injuries
  • stocking and glove distribution scalds (± sparing of the buttocks)—this implies forced immersion in hot water
  • circular full thickness burns ≈ 0.75cm diameter may represent cigarette burns

Chemical burns Initial assessment is notoriously difficult. Alkalis tend to produce more severe burns and can continue to penetrate even after initial irrigation. Treat chemical burns with copious irrigation with water, continued for at least 20mins in alkali burns. Hydrofluoric acid burns Hydrofluoric acid is used industrially in a number of processes. Contact with the skin causes particularly severe burns, often with significant tissue damage and severe pain. This is because hydrofluoric acid rapidly crosses lipid membranes and penetrates the tissues deeply, where it releases the highly toxic fluoride ion. Fluoride ions may gain access to the circulation and produce a variety of systemic problems by a variety of mechanisms, including interfering with enzyme systems and producing hypocalcaemia by binding to calcium. Manage hydrofluoric acid burns as follows:

  • provide copious lavage to the affected skin then apply iced water (this provides better pain relief than calcium gluonate gel)
  • call a plastic surgeon at an early stage
  • check serum Ca2+ and Mg2+ and U&E
  • record an ECG and place on a cardiac monitor
  • treat hypocalcaemia

Cement burns Wet cement or concrete can cause chemical burns due to the alkali contact. These are usually partial thickness, but may be full thickness. Involve a specialist at an early stage. Phenol burns Phenol may be absorbed through the skin, resulting in systemic toxicity and renal failure. P.384
Crush syndrome A spectrum of conditions characterized by skeletal muscle injury (rhabdomyolysis). Common causes include the following:

  • Direct injuries and severe burns causing muscle damage.
  • Compartment syndromes: ‘true’ crush injuries produced by entrapment, or ‘self-crushing’ (eg an unconscious individual from drug overdose or alcohol excess lying on a hard surface). A vicious cycle is established where ↑ muscle compartment pressure obstructs blood flow, the muscles become ischaemic and oedematous, further ↑ compartment pressure and ↓blood flow leading to more ischaemia and muscle cell death.
  • Non-traumatic causes: metabolic disorders (diabetic states, ↓K +, ↓PO43 -), myxoedema, neuroleptic malignant syndrome, myositis due to infection or immunological disease.
  • Exertional: from undue exertion, grand mal fitting, rave dancing (particularly associated with ecstacy/cocaine use), often complicated by hyperthermia.

Clinical features Adopt a high index of suspicion. Symptoms depend on the underlying cause, but muscle pain, tenderness and swelling may not be present at the time of admission. In the lower limbs, the condition is commonly confused with DVT. The classic compartment syndrome with pain on passive muscle stretching and sensory deficits may take several days to develop and pass unnoticed. The presence of distal pulses does not rule out a compartment syndrome. Investigations ↑ CPK levels reflect muscle damage. Check U&E, PO43 -, Ca2+ and urate. 70% have myoglobinuria and pigmented granular casts (urinary stix tests do not differentiate between Hb and myoglobin). However, absence of myoglobinuria does not exclude rhabdomyolysis, as myoglobin clears rapidly from plasma and its presence in urine depends upon the release rate, the degree of protein binding, GFR and urine flow. If DIC is suspected, check a coagulation screen. Treatment Local problems Urgent orthopaedic referral is needed for compartment syndromes. If the difference between intracompartmental and diastolic pressures is <30mmHg, fasciotomy, excision of dead muscle and even distal amputation may be required. These procedures may induce life-threatening electrolyte shifts, bleeding, local infection and later generalized sepsis. Systemic complications Severe metabolic complications start after revascularization. Hyperkalaemia may be life-threatening (p158). Hypocalcaemia is common initially, but is rarely symptomatic. Acute renal failure can be produced by pre-renal, renal and obstructive elements. Following restoration of circulation or release from entrapment, fluid leaks into damaged areas ↓circulating plasma volume. Intracellular muscle contents enter the circulation and myoglobin and urate crystals can block the renal tubules. This process is aggravated by the ↓intravascular volume and associated metabolic acidosis. DIC and drugs which inhibit intra-renal homeostatic mechanisms (eg NSAIDs and ß-blockers) may also contribute. Prompt correction of fluid deficits and acidosis (often with CVP monitoring) and establishing a good urinary flow is essential. Alkalinization of the urine may be required: early use of mannitol has been advocated, but can cause pulmonary oedema if renal impairment is already present. If renal failure is established, dialysis may be needed, but prospects for full renal recovery are good.

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