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The clinical manifestations of critical illness (Box 19.1)
THE CRITICALLY ILL
19.3 Common causes of acute cardiovascular
19.5 SBAR framework for communication
• Cardiac arrest
• Acute myocardial infarction or ischaemia
• Acute valve dysfunction, e.g. endocarditis, mechanical valve
failure or obstruction
• Pericardial tamponade
• Cardiomyopathy: viral, alcohol-related, postpartum
Identify yourself, identify the patient and give the reason for
your concern – what is the problem?
Your observations and evaluation of patient’s current state.
What are the current issues?
• Dissection, or rupture, of abdominal or thoracic aortic
• Mesenteric infarction
Massive pulmonary embolus
• Upper: varices, peptic ulcer, tumour, Mallory–Weiss tear,
non-steroidal anti-inlammatory drugs (NSAIDs)
• Lower: diverticular disease, angiodysplasia, ischaemic
bowel, Meckel’s diverticulum, tumour
• Overt: wounds, especially to scalp, face; long bone or
• Concealed: chest – haemothorax; abdomen – splenic and/
or hepatic injury, retroperitoneal
• Obstetric/gynaecological: placenta praevia, miscarriage,
ectopic pregnancy, trauma, tumour
• Anticoagulant use or bleeding diathesis
What is this patient’s background? What is the recent history of
What should be done to respond to the current situation? (This
may even be a simple request for assistance)
19.6 Key preliminary data
Past medical history
Events leading up to presentation and environment
Electric shock/lightning injury
Envenomation (bites or stings from snakes, insects, jellyish)
19.4 Common causes of altered conscious state
Non-central nervous system causes
Drugs and poisons, e.g. opioids, alcohol, carbon monoxide,
benzodiazepines, tricyclic antidepressants
• Type II respiratory failure (↑PaCO2), hepatic or renal failure
• Thyrotoxicosis/myxoedema/addisonian crisis, non-ketotic
• Hypothermia or hyperthermia
Central nervous system causes
• Intracranial haemorrhage, e.g. subarachnoid haemorrhage
• Ischaemia: thrombosis, embolism
• Trauma: concussion, white-matter shearing (diffuse axonal
injury), haemorrhage (extradural, subdural and/or
• Infections: meningitis, encephalitis, cerebral malaria
• Primary or secondary tumour
• Hypertensive encephalopathy
The patient may be unable to give a history, so use
all possible sources of information (Box 19.6). Include
previous primary care or hospital records, relatives,
friends, bystanders and emergency or ambulance personnel. Look for diabetic/steroid/anticoagulant cards
and medications, and Alert bracelets/necklaces (Fig.
3.3). If possible, contact the patient’s GP, who is often a
key source of current and background information.
Managing your resources
Identify your available resources: which staff can help?
What is their level of seniority and experience and what
can they do? If you have others to help you, identify
roles and responsibilities. If you are team leader, communicate your thinking to the whole team clearly and
The primary survey, investigations and interventions
should take 5–10 minutes, unless you have to undertake
a life-saving intervention such as tracheal intubation.
The patient may be unable to sit up. If this is the case
examine him supine throughout.
The ABCD approach
Approach the patient so that he can see you if conscious.
Speak slowly and clearly and assess his response.
If the patient talks to you normally, the airway is clear and
there is perfusion of the brain; if his speech is lucid, cerebral
function is adequate.
Give a high inspired concentration of oxygen by mask, and
move on to B (breathing).
If there is no response to speech, usually because the patient
has altered consciousness, perform a more detailed
assessment of the airway. Look, listen and feel. Open his
mouth and remove secretions, blood, vomit or foreign material
by gentle suction with a Yankauer catheter (Fig. 19.1) under
direct vision. Leave well-itting dentures or dental plates in
place to maintain the normal airway anatomy. If they are loose
or poorly itting, remove them.
Listen for upper airway noises (Box 19.7). Gurgling, snoring or
stridor suggests partial airway obstruction. Grunting respiration
may be a sign of respiratory muscle fatigue, or an attempt to
slow expiration in a patient with a lail segment (see below).
Absent breath sounds indicates either complete airway
obstruction or absence of breathing.
Open the airway by tilting the patient’s head and lifting his chin
(Fig. 19.2). If you suspect neck injury, do not move the neck.
Control the head and neck by manual in-line control and open
the airway using the jaw lift technique (Fig. 19.3). Appropriately
19.7 Airway noises
No noise (the ‘silent airway’)
• Implies complete airway obstruction and/or absence of, or
minimal, respiratory effort
• Caused by partial upper airway obstruction from soft tissues
of the mouth and oropharynx
• Caused by luids (secretions, blood or vomit) in the
• A grunt during expiration is a sign of respiratory muscle
fatigue. It may be present after chest wall trauma with a lail
segment. Grunting improves gas exchange by slowing
expiration and preventing alveolar collapse by ↑ positive
• Caused by partial laryngeal obstruction associated with
• A ‘musical’ noise, best heard on auscultation
• When loudest in expiration, relates to obstruction in the small
bronchi and bronchioles, most often in asthma and COPD
• A harsh noise, usually loudest in inspiration, caused by
partial obstruction around the larynx or main bronchi
• In febrile patients, consider epiglottitis or retropharyngeal
• Other causes are foreign bodies, laryngeal trauma, burns or
Fig. 19.1 Yankauer suction catheter. This may have a small hole to
control airlow – if present, occlude this with your thumb to generate
Fig. 19.3 Manoeuvres in patients with suspected neck injury.
Fig. 19.2 Opening the airway by tilting the head and lifting the chin.
(A) Control the head and neck manually. (B) Open the airway using the
jaw thrust technique. N.B. A rigid cervical collar will normally then be
THE CRITICALLY ILL
Fig. 19.4 Airway adjuncts. Guedel airway (top); nasopharyngeal airway
(bottom). Note the ‘safety pin’ is to prevent migration of the proximal end
of the airway beyond the nasal oriice.
Fig. 19.5 Administering oxygen using a mask with reservoir bag.
19.9 Situations in which SpO2 may give
19.8 Principal indications for emergency
advanced airway and ventilation techniques
• Airway obstruction
• Inability to maintain airway with simple manoeuvres/
• Facial trauma, uncontrolled vomiting/bleeding
• Glasgow Coma Scale <9
• Potential for subsequent clinical deterioration, e.g. facial/
• Oxygenation and ventilation
• Raised intracranial pressure
• Potential environmental risk, e.g. ambulance transfer,
CT/MR imaging scan
sized airway adjuncts, such as nasopharyngeal or
oropharyngeal (Guedel) airways, can maintain the airway in
patients with altered consciousness (Fig. 19.4). Do not use a
nasopharyngeal airway if you suspect a skull base fracture, if
epistaxis, nasal trauma or deformity is present, or if the patient
is taking anticoagulants. Tracheal intubation may be needed if
the patient cannot maintain a patent airway. This should only
be performed by an experienced clinician (Box 19.8).
Hypotension/poor peripheral perfusion
Nail varnish, false ingernails
Abnormal haemoglobins, e.g. carboxyhaemoglobin,
methaemoglobin or sulphaemoglobin
• Skin pigmentation or excessively dirty ingers
Hypoxia hastens and causes death. Central cyanosis is a late,
unreliable sign of hypoxia. Even in critical hypoxia, cyanosis may
be absent because of severe anaemia or massive blood loss.
■ Attach a pulse oximeter probe to a ingertip (Fig. 7.25) or
earlobe. Pulse oximetry (SpO2) can non-invasively assess
peripheral oxygenation simply (Box 19.9). Use an oxygen mask
with reservoir bag and adjust the oxygen low rate to maintain
an SpO2 of 94–98% (Fig. 19.5). If the oxygen mask ‘mists’ on
exhalation, the patient has (some) respiratory effort. The only
exception to this initial treatment is if you know the patient has
chronic obstructive pulmonary disease with CO2 retention (type
II respiratory failure). These patients may lose the hypoxic
stimulus to breathe if given high concentrations of oxygen. In
these patients aim to maintain an SpO2 of 88-92%.
■ Look for movements of the chest, the accessory muscles and
the abdomen. Paradoxical respiration is movement of the
abdomen exactly out of phase with that of the chest and
indicates respiratory compromise. It is most often due to
fatigue of the diaphragm and/or airway obstruction. In patients
with chronic airlow obstruction a breathing pattern with
abnormal abdominal movements is associated with a much
poorer prognosis. Look for other abnormal breathing patterns
Seek signs of injury (bruising, pattern imprinting, wounds) and
of lail segment in trauma patients. In a lail segment the
affected area moves paradoxically: it moves outwards from the
chest wall during expiration and inwards during inspiration.
■ Kneel at the patient’s side and look tangentially across the
chest. A lail segment is often well localised and, if present,
implies that at least three ribs are broken in at least two
places (Fig. 19.6). Underlying lung injury is common.
Assess the position of the trachea in the suprasternal notch.
In a trauma patient, systematically and gently palpate the chest
to identify any areas of injury. Rib and sternal fractures are
associated with localised discomfort. Subcutaneous
emphysema feels like ‘crackling’ under your ingers. Examine
for consolidation, pneumothorax, pleural effusion and
haemothorax (Ch. 7).
Auscultate for breath sounds and added sounds. Critically ill
patients may not have the signs you expect. For example,
a patient with life-threatening asthma may have little or no
wheeze (a silent chest) because airlow into the lungs is poor.
Expose the chest, back, axillae and abdomen. Look for wounds
(usually gunshot or stab) producing an open defect in the chest
wall (Fig. 19.7). Recognise and treat open pneumothorax or a
pneumothorax under tension. An open chest wound equalises
The ABCD approach
19.10 Respiratory patterns: common causes
• Cardiac arrest
• Central neurological causes
(stroke, head injury)
• Left ventricular failure
• Central neurological causes
(stroke, head injury)
• Overdose (barbiturates,
• Metabolic acidosis
– diabetic ketoacidosis
• Hepatic failure
• Shock (lactic acidosis)
• Overdose (methanol,
ethylene glycol, salicylate)
• Respiratory failure
• Guillain–Barré syndrome
Fig. 19.7 Wound producing an open defect in the chest wall.
• High spinal cord lesions
ventilated). The diagnosis is clinical. The patient appears acutely
breathless and agitated, has tachycardia and may be cyanosed.
Hypotension, bradycardia and altered consciousness are
preterminal features. Quickly examine for jugular venous
distension, tachycardia and absent breath sounds on the affected
side. If the patient is in extremis, insert a large-bore intravenous
(IV) cannula through the second intercostal space in the midclavicular line on the affected side. Remove the needle from the
cannula. A hiss of air, with rapid clinical improvement, conirms
the diagnosis. Tube thoracostomy with underwater seal drainage is
Fig. 19.6 Flail chest. (A) A direct blow (arrowed) that fractures several
ribs at two points will result in a lail segment. (B) A severe blow to the
sternum (arrowed) may cause multiple bilateral costochondral fractures,
resulting in a lail chest.
pressure between the pleural space and atmosphere, and the
affected lung is unable to expand or contract normally with
respiration. During inspiration and expiration, you may hear air
movement and see a spray of blood at the wound. Cover the
wound with a sterile occlusive dressing secured on three sides.
A formal tube thoracostomy with underwater seal drainage is
Suspect tension pneumothorax in any patient who rapidly
develops severe respiratory and cardiovascular distress. It
occurs when lung injury produces a one-way valve effect
(Fig. 19.8). On inspiration air escapes from the lung and
accumulates in the pleural space. As the pleural pressure
increases, the ipsilateral lung progressively collapses and the
increased intrathoracic pressure reduces venous return to the
heart, eventually causing cardiac arrest.
It occurs most commonly in chest injury, during positivepressure ventilation or in underlying lung disease (especially when
Feel for a central (carotid or femoral) pulse for 10 seconds. If
you cannot feel a pulse and the patient is unresponsive, treat
as for cardiac arrest (for current guidelines from the
International Liaison Committee on Resuscitation on how to
manage cardiac arrest, see www.ilcor.org) (Fig. 19.9).
In responsive patients, feel for a peripheral (radial or brachial)
pulse. If you cannot palpate a peripheral pulse, this suggests
that the patient is signiicantly hypotensive.
Note the pulse rate, rhythm, volume and character.
Assess peripheral perfusion; press on the ingertip pulp for a
few seconds, remove your inger and estimate the capillary
reill time (normal <2 seconds).
Attach an ECG monitor to the patient. Note the ventricular rate
and the rhythm.
Control external blood losses from wounds or open fractures by
direct irm pressure with a sterile dressing placed over the site.
Minimise blood loss from long bone fractures (femur, tibia/
ibula, humerus and forearm) by splintage.
Insert a large-bore (16 FG, 1.7 mm internal diameter or bigger)
IV cannula and tape it securely to the skin. In trauma patients
and when you suspect hypovolaemia, insert and secure two
large-bore cannulae. Take initial blood samples (Box 19.11)
from the cannula and then attach an IV luid-giving set.
Commence volume replacement, if needed, with warmed 0.9%
saline or Ringer’s solution.
THE CRITICALLY ILL
Wound in lung
Air in pleural space
Fig. 19.8 Tension pneumothorax following penetrating injury. Air enters the pleural cavity via the punctured lung during inspiration. The chest wall
and lung defects act as one-way valves. Air cannot escape from the pleural cavity during expiration. The right intrapleural pressure increases, collapsing
the right lung, impeding venous return to the heart and occasionally shifting mediastinal structures to the contralateral side.
19.11 Initial venous blood samples
• Stix test for blood glucose
and formal blood glucose
• Blood grouping and save
• Full blood count
• Urea, creatinine and
Shout for help
• Liver function tests
• Blood cultures
• Cardiac biomarkers, e.g.
troponin, creatine kinase
NOT BREATHING NORMALLY?
Examine the jugular venous pressure (JVP) (Fig. 6.19). In a
sitting or semirecumbent patient, elevation of the JVP in the
presence of shock suggests a major problem with the heart’s
pumping ability, such as acute heart failure, cardiac
tamponade, massive pulmonary embolus, tension
pneumothorax or an acute valvular problem.
Check the blood pressure (p. 113).
Examine the precordium and heart, identifying the presence of
added heart sounds or murmurs.
Insert a urinary catheter (unless there is evidence of urethral or
prostatic injury – blood at the urethral meatus and/or a
high-riding, ‘boggy’ prostate on rectal examination) to monitor
Shock implies that the oxygen and blood supply to an organ
or tissue is inadequate for its metabolic requirements. It is
recognised clinically by a combination of features (Box 19.12). The
extent to which each feature is present depends upon the cause
(Box 19.13) and the time course. Signs of shock may be delayed
or obscured in athletes, pregnant women, those on vasoactive
drugs (beta-blockers, calcium channel blockers, angiotensinconverting enzyme inhibitors), those with pacemakers and the
very young and old.
2 rescue breaths
Fig. 19.9 Adult basic life support algorithm.
Tachycardia (heart rate >100 bpm) and hypotension (systolic
blood pressure <100 mmHg) are not required to diagnose shock:
the heart rate may be normal or low in hypoxic shocked patients
or those on drugs such as beta-blockers. Blood pressure may be
temporarily maintained by sympathetic activity and peripheral
vasoconstriction. In critically ill patients non-invasive cuff blood
pressure measurements are often inaccurate.
The ABCD approach
19.12 Clinical features of shock
19.14 Glasgow Coma Scale
Altered consciousness, confusion, irritability
Pallor, cool skin, sweating
Heart rate >100 bpm
Hypotension (systolic blood pressure <100 mmHg):
N.B. Hypotension is a late sign
• Respiratory rate >30 breaths/min
• Oliguria (urine output <0.5–1 ml/kg/h)
Confused: talks in sentences but disorientated
Verbalises: words, not sentences
Vocalises: sounds (groans or grunts), not words
19.13 Classiication of shock
• Blood loss: trauma, gastrointestinal or obstetric haemorrhage,
abdominal aortic aneurysm rupture
• Fluid loss: burns, gastrointestinal loss (diarrhoea, vomiting),
severe dehydration, diabetic ketoacidosis, ‘third space’
losses, e.g. sepsis, pancreatitis, ischaemic bowel
Localises to pain, e.g. brings hand up beyond chin to
Flexion withdrawal to pain: no localisation to supraorbital
pain but lexes elbow to nail bed pressure
Abnormal lexion to pain
Extension to pain: extends elbow to nail bed pressure
• Arrhythmia, myocardial infarction, myocarditis, acute valve
failure, overdose of negatively inotropic drugs, e.g. calcium
channel blocker or beta-blocker
Record the GCS as a total and its three separate
components: e.g. GCS 9/15: E3, V2, M4
• Major pulmonary embolism, tension pneumothorax, cardiac
tamponade, acute valve obstruction
• Major cerebral or spinal injury
• Toxic causes: carbon monoxide, cyanide, hydrogen sulphide,
poisons causing methaemoglobinaemia
Do not concentrate on absolute igures of systolic or diastolic
blood pressure. Readings of 90/50 mmHg are normal in many
healthy young women, while 120/70 mmHg indicates signiicant
hypotension in a patient whose pressures are usually
195/115 mmHg. Trends in pulse and blood pressure give far more
information than initial or isolated readings. If the patient has a
rising pulse rate, with a falling blood pressure and reduced urine
output, this strongly implies continuing volume loss and inadequate
In trauma the most likely cause of shock is blood loss. External
blood loss from wounds and compound fractures is usually
apparent, but haemorrhage into the abdomen and chest, or from
closed long bone or pelvic fractures, is often missed.
Assess the patient’s Glasgow Coma Scale (GCS). Separately
record the three components: eye opening, verbal response
and motor response (Box 19.14).
Examine the limbs for localising signs or paraplegia.
Check the pupils for size, reactivity and equal reaction to light.
In structural causes of coma (intracranial haemorrhage,
infarction) the light relex is usually absent; in metabolic causes
(poisoning, hypoglycaemia, sepsis) it is usually present. A
difference in pupil diameters >1 mm suggests a structural
cause. The GCS can be misleading in some types of nontraumatic brain injury, for example stroke.
Fig. 19.10 Monitoring blood glucose with a testing strip and meter.
Check the blood glucose using a Stix test (Fig. 19.10).
Hypoglycaemia usually causes a global neurological deicit
with reduced consciousness, but may present with irritability,
erratic or violent behaviour (sometimes mistaken for alcohol
or drug intoxication), seizures or focal neurological deicits,
■ If the stix test reading is <3 mmol/l, take a venous sample
for formal blood glucose measurement, but treat before you
get the result. Give 25–50 ml of 50% dextrose IV. If you
cannot obtain venous access rapidly, give 1 mg glucagon
by intramuscular (IM) injection. The conscious level should
start to improve in 10–20 minutes if hypoglycaemia is the
cause of the altered mental state. Repeat the stix test to
conirm correction of hypoglycaemia.
Persistent altered consciousness where hypoglycaemia has
been adequately corrected implies coexistent pathology, e.g.
THE CRITICALLY ILL
stroke, or cerebral oedema from prolonged neuroglycopenia.
In patients with hypoglycaemia where you suspect chronic
alcohol use or withdrawal, or malnutrition, give 100 mg IV
thiamine to prevent and treat Wernicke’s encephalopathy
(confusion, ataxia and eye signs – nystagmus and conjugate
If you cannot clearly identify a cause for the patient’s altered
conscious state, consider drug overdose. The most common
acutely life-threatening drugs are opioids, which cause altered
consciousness, respiratory depression (reduced respiratory rate
and volume) and small pupils.
■ Titrate 0.8–2 mg IV naloxone (a speciic opioid antagonist) as
a diagnostic aid and deinitive treatment to any patient with
no clear cause for altered consciousness. In opioid
intoxication, the patient responds within 30–60 seconds of IV
administration. If IV access is dificult, give naloxone IM. If the
patient responds, give further doses, as naloxone has a short
duration (minutes), while the half-life of most opioids and their
active metabolites is hours/days.
■ Give immediate treatment to stop active focal or generalised
seizures. First-line therapy is IV lorazepam (0.5–1 mg/min
up to 4 mg) or diazepam (1–2 mg/min up to 10–20 mg). If
seizures continue despite this, other agents may be required,
■ Manage seizures in pregnancy using the ABCDE approach but
consider the fetus as well. Seek senior obstetric and neonatal
support immediately. Place women >20 weeks’ gestation in
the left lateral position by placing one or two pillows under the
right hip. This prevents the gravid uterus from obstructing
venous return to the heart with consequent hypotension.
Eclamptic seizures in pregnant and postpartum patients are
associated with hypertension (diastolic blood pressure
>100 mmHg), oedema (usually generalised and often affecting
hands and face) and proteinuria. IV magnesium sulphate is a
E: Exposure and environment
If the patient is not already fully undressed, remove remaining
clothing. Cover the patient with a gown and warm blankets to
prevent hypothermia and maintain dignity. Critically ill patients
lose heat rapidly and cannot maintain normal body
Trauma patients may arrive on a rigid spinal board with neck
immobilisation. Remove them from the board to reduce
pressure sores and facilitate radiological examination. If the
patient is conscious, explain what you are going to do before
the patient is ‘log-rolled’ and lifted (Fig. 19.11). The process
needs ive people. One holds the head/neck and directs the
procedure; one removes the spinal board and other debris, and
examines the back and spine; the remaining three roll and hold
While the patient is rolled, perform a rectal examination,
assess anal tone and perianal sensation, and check the core
temperature (p. 189).
Examine the patient’s skin surface rapidly but comprehensively.
Look for bruises and wounds. In particular, examine the scalp,
perineum and axillae. Note open fractures and rashes, e.g. the
non-blanching purpuric rash of meningococcal septicaemia
(Fig. 17.1) and hyperpigmentation (hypoadrenalism).
Fig. 19.11 Deployment of personnel and hand positions used when
‘log-rolling’ a patient from the supine to the lateral position. The
person (A) controlling the cervical spine should direct the manoeuvre.
See Box 19.15.
19.15 The primary survey: investigations
Administer high-low oxygen
Measure respiratory rate and SpO2
Monitor the electrocardiogram (ECG) continuously and
measure blood pressure every 5 minutes
Insert and secure large-bore intravenous cannula(e) and
take blood samples
Record Glasgow Coma Scale
Record pupil size and reactivity
Stix test for blood glucose
Measure temperature (rectal or tympanic membrane)
• Arterial blood gas measurement
• 12-lead ECG
• Chest X-ray (+ pelvic and cervical spine views in multiply
• Urinary catheter* (and measure urine output hourly)
• Urinalysis (stix test) for blood, protein, glucose, ketones,
nitrite, bilirubin and urobilinogen
• Urine pregnancy test in females
• Nasogastric tube†
*Contraindicated if urethral injury is suspected.
Contraindicated if skull base fracture is suspected.
The secondary survey reassesses the patient after the
primary survey is complete. This is a systematic, detailed
top-to-toe examination that fully documents additional
signs and identiies injuries in the trauma patient. Only
start the secondary survey once you are conident that
there is no immediate need for further resuscitation and
the patient does not require immediate transfer for
deinitive care, e.g. to theatre for a patient with a
ruptured abdominal aortic aneurysm. Continually
re-evaluate to assess the response to treatment. If the
patient deteriorates or you are unsure about clinical
status, return to the primary survey.
Give adequate analgesia to all patients in pain. There
is no ‘standard’ dose. Slowly titrate an opioid drug, e.g.
morphine IV in 1–2 mg aliquots to achieve pain relief.
The amount needed varies according to the patient’s
response and adverse effects, e.g. respiratory depression, hypotension.
Examine the entire body surface. The skin appearance may
suggest an underlying diagnosis, e.g. pallor (blood loss or
anaemia), jaundice (hepatic failure), vitiligo or pigmentation in
sun-exposed areas, recent scars and skin creases (Addison’s
Look for rashes (in particular, the non-blanching purpuric rash
of meningococcal disease) (Fig. 17.1), foci of infection
(cellulitis, abscesses, erysipelas), bruising and wounds.
Perform a systematic top-to-toe examination, starting with
the head. In a trauma patient palpate the scalp for swelling,
and look for wounds which may be hidden in thick or
Look for signs of skull base fracture. These include periorbital
bruising (‘raccoon’ or ‘panda’ eyes; Fig. 19.12A),
subconjunctival haemorrhage (usually without a posterior
margin; Fig. 19.12B), otorrhoea or rhinorrhoea, and most
commonly bleeding from the ear or behind the tympanic
membrane (haemotympanum). Battle’s sign (bruising over the
mastoid process; Fig. 19.12C) may take 1–3 days to develop.
Examine the eyes for foreign bodies, including retained contact
lenses (remove them at this stage), and signs of chronic
disease, such as jaundice or anaemia. If you suspect corneal
abrasions, stain the eye with luorescein to identify them
Assess the pupils for size, shape, reactivity to light and
Examine the eye movements, visual acuity and optic fundi.
Urgently refer any patient with penetrating injury, disruption of
the globe or loss of vision to a specialist ophthalmologist.
Smell the patient’s breath. The sweet odour of ketones in
diabetic ketoacidosis is characteristic, but not everyone can
detect it. Severe uraemia causes a ‘ishy’ smell, and hepatic
failure a ‘mousy’ smell (fetor hepaticus) due to dimethyl
sulphide. Note whether a patient smells of alcohol, but
never attribute altered conscious level to alcohol alone.
Look in the mouth for injury to the palate, tongue and teeth.
Check the ears and throat for potential sources of infection.
Assume that the spine and/or spinal cord is injured in all
trauma patients, especially those with altered consciousness.
Conscious patients may complain of localised neck or back
pain, but may be distracted by pain from other injuries.
Maintain spinal immobilisation until you can exclude underlying
injury. This is rarely possible in the initial assessment period,
and many cases require imaging to exclude cord or
If there is no history of trauma, ask the patient to lex his neck
to touch his chin on his chest. If this causes discomfort, gently
Fig. 19.12 Signs of skull base fracture. (A) Periorbital bruising
(‘raccoon’ or ‘panda’ eyes). (B) Subconjunctival haemorrhage. (C) Battle’s
THE CRITICALLY ILL
lex his neck passively. Meningeal irritation causes spasm of
the paraspinal neck muscles with neck stiffness. Meningitis
and subarachnoid haemorrhage are common causes and may
be associated with photophobia and a positive Kernig’s sign
(p. 248). Neck stiffness may be absent early in these
conditions or with altered consciousness.
Re-examine the chest and precordium in detail (Chs 6 and 7).
Examine the abdomen, including the pelvis and perineum.
Perform a rectal and vaginal examination if necessary. Remove
any tampon in a menstruating female and consider toxic shock
syndrome as a cause of her symptoms. Rectal examination is
mandatory in patients presenting with signs of hypovolaemia,
to help identify gastrointestinal bleeding. In trauma patients
examine the perineum, rectum and urethral oriice before
inserting a urinary catheter.
Check perianal sensation and rectal sphincter tone to assess
potential spinal cord injury.
Clinical assessment of pelvis injury is often misleading.
Palpation may identify fractures, but do not ‘spring’ the
pelvis to assess stability, as this may precipitate further
Examine each limb in turn. Look for wounds, swelling and
bruising; palpate all bones and joints for tenderness and
crepitus, and assess passive and active joint movements.
Undisplaced long-bone fractures are easily missed in trauma
patients. Always examine the neurovascular integrity of the
limb distal to any injury.
Perform a full neurological examination. This is particularly
important in patients with altered conscious level or possible
Examine joints for swelling suggesting septic or reactive
arthritis (Box 19.16).
Speciic investigations will depend upon the presentation involved, e.g. CT for head injury. A 12-lead ECG
and chest X-ray are standard and in patients with
blunt trauma the initial X-rays should, as a minimum,
include views of the cervical spine, chest and pelvis.
19.16 Pupil changes and structural
A dilated pupil (>1 mm in size between the pupils, anisocoria)
in a patient with coma strongly suggests a structural
Touda Y, Nakazato N, Stein GH. Pupillary evaluation for differential diagnosis
of coma. Postgrad Med 2003;79:49–51.
Perform a urinary pregnancy test in all women of childbearing age.
Ensure tetanus prophylaxis for all trauma patients
who are non-immune. Give IV antibiotic therapy to
patients with presumed meningococcal disease, septic
shock and open fractures.
Document all investigations, therapy and response to
treatment. Stop the assessment process if the patient
needs immediate deinitive care or investigation. Let the
receiving team know exactly which stage of the assessment process you have reached when you hand over
care of the patient.
Once stable, the patient is moved to a critical care area,
theatre, scanning room or another hospital. This is highrisk and there must be suficiently trained staff accompanying the patient. The critically ill patient needs to be
adequately monitored and as ‘stable’ as possible. All
relevant documentation and investigation results should
accompany the patient, with clear lines of communication between clinicians.
If you discover that the patient is terminally ill and
that this crisis is not unexpected, it may not be appropriate for the patient to be given aggressive or ‘heroic’
treatment. It may be dificult to recognise and prepare
for a patient’s death but it is essential and humane. Communicate with the family, the GP and the senior clinician
previously involved in the patient’s care. Care for the
patient in a digniied manner, with the emphasis on
analgesia, relief of distressing symptoms and the highest
quality of nursing care.
SECTION 3 EXAMINATION IN SPECIFIC SITUATIONS
EXAMINATION TO CONFIRM DEATH 424
Brainstem death 425
What to do after you have conirmed
EXAMINATION TO CONFIRM DEATH
Look for respiratory effort and
listen for breath sounds for
Examine for pupillary response
to light and corneal reflexes
Feel the carotid pulse
for at least 1 minute
Listen for heart sounds
for at least 1 minute
General observation 1
• Pallor over face and lips
• Open staring eyes, cornea may be cloudy
• Lack of movement, particularly