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SECTION TWO
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Patients presenting as emergencies
Table 9.2 Logical thinking for patients presenting with chest pain
Potentially life- threatening
conditions—all usually causing central
chest pain Other causes of central chest pain Causes of pleuritic chest pain
Coronary artery disease (myocardial
infarction or acute coronary syndrome)
Massive pulmonary embolus (PE)
Thoracic aortic dissection: severe, tearing
in nature, radiating to interscapular area
Pneumothorax (particularly tension)
Oesophageal rupture
Pericarditis
Gastro- oesophageal reflux disease (GORD)
Muscular or skeletal
Anxiety
Pericarditis
PE (more likely to be smaller and more
peripheral)
Pneumothorax
Pneumonia (reactive pleuritis)
Empyema
Viral pleuritis
Malignant involvement of chest wall
(including mesothelioma)
Rib trauma, fracture or metastases
Inflammatory pleuritis (e.g. rheumatoid
arthritis, systemic lupus erythematosus)
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artery disease, it is this potential diagnosis that often
dominates the initial thoughts of the assessing doctor.
This is why patients presenting with chest pain who
appear unwell or in need of immediate resuscitation
should have an electrocardiogram (ECG) recorded
before the initial history and examination are complete.
The outcome from attempts to open an occluded
coronary artery depends on the speed with which
arrangements can be made for either thrombolysis or
angioplasty, so little is to be gained (and much to be
lost) from a prolonged assessment. However, in some
patients with critical coronary artery disease the initial
ECG recording may be normal, so it is essential that a
careful history and examination are performed on all
patients with chest pain not obviously in immediate
need of resuscitation or intervention. Patients with
chest pain are, understandably, often anxious about
the possibility of underlying serious heart disease and
an important part of the doctor’s role is to project
calm reassurance.
Chest pain that has a life- threatening cause
(Table 9.2) is usually central and of sudden/
rapid onset. Certain features may be diagnostically
helpful; these include radiation of the pain to the
left arm and/or jaw (myocardial ischaemia) or the
interscapular area (aortic dissection); accompanying
breathlessness (massive pulmonary embolus or
pneumothorax); or a clear temporal association
with prolonged vomiting (oesophageal rupture).
In pericarditis, the pain may be ‘classic’ (central
pain relieved by sitting forward) or pleuritic. The
features of chest infections and viral infections
should be obvious. Pneumonias not infrequently are
associated with headache. Important examination
features to note during the initial, rapid assessment
of an ill patient with chest pain include the fine
crepitations of pulmonary oedema, the hyperresonant percussion and tracheal deviation of
pneumothorax or the asymmetric blood pressure
readings consistent with thoracic aortic dissection.
Box 9.1
Risk factors for coronary heart disease
Age
Blood pressure
Smoking
Cholesterol
Diabetes
Racial grouping
Family history of coronary artery disease or stroke before
the age of 60
Girth (obesity)
If ‘ABC’ interventions are not required for
resuscitation, if the patient is stable and no other
features are requiring immediate action (e.g.
peripheral cyanosis), then a more considered
assessment is appropriate. In addition to the history,
the risk factors for coronary artery disease and
pulmonary embolism (PE) may be factored into the
diagnostic process (Box 9.1 and Table 9.3). The blood
pressure should be taken in both arms, particularly if
the arm pulses feel unequal. Unequal blood pressure
measurements in the arms raise the possibility of
aortic dissection and serious consideration should
be given to appropriate urgent imaging (usually
thoracic CT scanning). A raised jugular venous
pressure may suggest early heart failure. Precordial
auscultation may reveal a pericardial rub. There may
be classic signs of pneumonia. It can be difficult to
differentiate between pleuritic and musculoskeletal
chest pain from the history, but pain exacerbated
by palpation and posture changes more than by
inspiration is more likely to be musculoskeletal.
Signs of deep venous thrombosis automatically raise
the clinical suspicion of a PE.
The serious nature of many of the diagnoses of
patients who present with chest pain dictates that
the threshold for certain investigations is often low.
In addition to being a crucial test at the moment of
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9
Patients presenting as emergencies
Table 9.3 Modified Wells criteria for assessing the risk
of pulmonary embolism (PE) in a patient with symptoms
consistent with pulmonary embolism
Clinical parameter Score
Clinical evidence of deep vein thrombosis
(DVT)
No alternative diagnosis likely other than PE 3
Heart rate greater than 100 per minute 1.5
Surgery or immobility in preceding 4 weeks 1.5
Previous confirmed DVT or PE 1.5
Haemoptysis 1
Active malignancy 1
Total score Risk
> 6 High
2–6 Moderate
2 Low
initial assessment, the ECG has additional value when
it is repeated over a period of time, looking for any
evolution in its appearance (often called ‘dynamic
changes’). Detailed description and explanations of
the possible ECG features of myocardial infarction
and pulmonary embolism are given elsewhere. The
chest X- ray may show features of pneumothorax,
pneumomediastinum (from oesophageal rupture),
heart failure, widened mediastinum (often seen in
thoracic aortic dissection), pneumonia, rib fractures/
destruction and pleural effusions. In the emergency
unit, measurement of troponin in blood (a protein
released when cardiac myocytes undergo ischaemic
necrosis) is performed on many patients with chest
pain. It is not a diagnostic test of cardiac chest pain,
but ‘negative’ results (below a certain threshold)
indicate that the risk of a serious acute cardiac event
in the ensuing 30 days is extremely low. A negative
troponin test does not obviate the need to make a
detailed clinical assessment; a patient with a typical
history of ‘crescendo angina’ (worsening in severity
and/or frequency, occurring at rest or on minimal
exertion over days to weeks) should still be treated as
an emergency even if the troponin result is reassuring.
3
The breathless patient
When life- threatening conditions present with
breathlessness, it should be rapidly established
whether immediate and resuscitative interventions
are required whilst simultaneously making a clinical
assessment to establish the cause (Table 9.4).
The patient should be placed in a safe, monitored
(ECG and pulse oximetry) environment and
clinicians should act quickly if there is evidence of
visible distress, the usage of accessory muscles of
respiration, high respiratory rate, high pulse rate,
cyanosis or observable low oxygen saturations. The
Table 9.4 Potentially life- threatening conditions presenting
as breathlessness
Potentially life- threatening
Clinical assessment
Stridor (may be mistaken
for wheeze)
Audible wheeze (one
should listen very
carefully, as it may be very
quiet)
Diffuse features Pneumonitis
Significant asymmetry of
findings in a whole lung
on percussion and/or
auscultation
Focal features of
consolidation
No obvious abnormality Pulmonary embolism (hypoxia
immediate response should be to administer highflow oxygen to the patient with any of the above
findings, unless there is good evidence that this
has on this occasion, or previous occasions, caused
breathing difficulties (most commonly patients with
chronic obstructive pulmonary disease, COPD). In
the majority of cases, arrangements for urgent ECG
and chest X- ray (CXR) will be made immediately,
before the initial clinical assessment is complete.
There may even be certain clinical scenarios (e.g.
upper airway obstruction, tension pneumothorax) in
which immediate clinical intervention is necessary.
conditions
Partial obstruction of trachea
or major airway
Severe asthma
Anaphylaxis
Acute bronchitis
Pulmonary oedema
Widespread pneumonia
Pulmonary oedema
Pneumothorax
Massive pleural effusion
Total lung collapse
Lobar collapse from tumour,
foreign body or mucus plug
Pneumonia
often present)
Metabolic acidosis (hypoxia
often absent)
General principles
A rapid clinical assessment will establish if detailed
history taking is going to be realistic. A conscious,
alert patient who is able to speak in full sentences
is reassuring. Features suggestive of an obstructed
airway include complete absence of airway
sounds (complete obstruction) or added sounds of
laboured breathing where air entry is diminished
(partial obstruction). Tachycardia and tachypnoea
may reflect respiratory distress. Use of accessory
muscles of respiration is typical in the partially
obstructed airway, and signs include a tracheal tug
(a slight downward movement of the trachea with
each inspiratory effort), paradoxical chest and
abdominal movement (‘see- sawing’—the chest wall
moves inwards during inspiration and outwards in
expiration and there is dyssynchrony between the
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Patients presenting as emergencies
129
rib cage and the abdomen), with supraclavicular and
intercostal ‘in- drawing’. Irritability, agitation and a
reduced consciousness level may reflect hypoxaemia
and carbon dioxide retention. Do not rely on
cyanosis as a feature in identifying an obstructed
airway as this is a very late pre terminal sign. Observe
or ask about ‘best breathing position’. Be aware that
the patient may have positioned himself for optimal
airflow in the setting of airway obstruction; moving
the patient into a supine position may precipitate
loss of the airway altogether. Low pulse oximetry
readings (SpO2) reflect inadequacy of oxygenation,
which is not the same as ventilation. Arterial blood
gas sampling may be helpful but should not delay
treatment. Respiratory acidosis, with a high carbon
dioxide tension (PaCO2) and reduced pH, reflects
alveolar hypoventilation. When assessing patients,
look carefully for these signs and symptoms and
always call for help early from an anaesthetist if
airway compromise is suspected. The young can
compensate well initially, masking impending
desaturation and hypoxaemia. Be mindful of injuries
that will compromise the airway, such as facial burns,
bleeding and foreign bodies obstructing the airway.
Always provide high flow oxygen with a reservoir bag
at 15 litres/minute, and reassess frequently, looking
for signs of deterioration, which may be caused by
deterioration of the underlying condition, or excess
oxygen in a patient with chronic CO2 retention.
In the emergency situation of the acutely breathless
patient it is helpful to consider the potential
problem in one of two ‘groupings’: upper airway
obstruction and cardiopulmonary pathologies that
affect ventilation and/or gas exchange (Table 9.5).
Airway obstruction
Most commonly, airway obstruction occurs in a
patient with a decreased level of consciousness with
resultant loss of the cough reflex used to clear normal
bronchial secretions. Such patients are also at risk of
aspiration of gastric contents because of depression
of other reflexes that control the competence of the
tracheo- oesophageal junction. Pragmatically, this
can be easily inferred by the patient’s response to
insertion of an adjunct, such as an oropharyngeal
(Guedel) airway. Fully conscious patients, in whom
laryngeal reflexes are present, will not tolerate this
airway and inserting one may precipitate gagging,
vomiting and laryngospasm. In a patient with reduced
consciousness and a threatened airway, the adjunct is
tolerated, with consequent relief of backward tongue
displacement and soft palate obstruction. Insertion
of a Guedel airway usually should be combined with
manoeuvring the patient into the recovery (lateral)
position (the effect of which is to push the tongue
and jaw forward under gravity, thereby improving
the airway) (Fig. 9.1).
The second, less common scenario of airway
obstruction is the patient presenting with stridor—
the term used to describe the harsh, high- pitched
musical breathing noise caused by narrowing
of the upper airways with impending complete
obstruction. It may be inspiratory, expiratory or
biphasic, although it is most commonly heard just
during inspiration. Inspiratory stridor indicates
laryngeal obstruction, because the negative
intrathoracic pressures exacerbate extrathoracic
obstruction during inspiration. Intrathoracic
obstruction may cause expiratory stridor, as
the airways are compressed during expiration.
Common causes of stridor include tumours
(usually laryngeal/tracheal, but also mediastinal
and oesophageal), peritonsillar and retropharyngeal
abscesses, inhalation of a foreign body and
laryngotracheobronchitis (‘croup’). Children are
more susceptible to the latter two causes owing
to the narrower diameter of their airway and the
fact that normal inquisitive behaviour often leads
to objects being inserted into their mouths. In
developed countries, vaccination programmes that
include Haemophilus influenzae type B vaccine
have led to a sharp reduction in the incidence of
acute epiglottitis—an important cause of stridor
in children in which infection by this organism
of the valve at the tracheo- oesophageal junction
causes fever, dysphagia, sore throat and (classically)
drooling of saliva as the pain of swallowing dictates
that the child will try to avoid doing this. If stridor,
as opposed to wheeze, is considered, the cause may
be evident from the history (airway cancer, foreign
body exposure or anaphylaxis). The examiner’s ear
should be placed carefully close to the mouth of
the patient to try to establish the source of airflow
limitation. Stridor of any cause in any age group
is frightening to patients; the attending doctor’s
demeanor needs to be calm and gentle whilst
simultaneously arranging emergency assistance.
Acute stridor is an airway emergency, and the teams
of intensive care, anaesthesia and ear, nose and
throat specialists should be mobilized as quickly as
possible to establish a secure airway.
Specific mention should be made of burn victims
in whom inhalation of superheated gases and toxins
of combustion causes swelling of the lining of the
tracheobronchial tree with consequent obstruction.
The history will usually be obvious, but important
clinical signs that suggest airway injury include a
hoarse voice, singed hairs of the nasal passages and
soot and erythema in the upper airway. Recognizing
this promptly should initiate measures to secure the
airway early with an endotracheal tube. The stridor
associated with the severe upper airway oedema of
anaphylaxis will be dealt with later in this chapter.
The importance of recognizing airway obstruction
as the cause of acute breathlessness is self- evident;
although provision of supplemental oxygen is a
crucial therapeutic intervention, it will not resolve
the underlying problem of hypercapnia associated
with hypoventilation.
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9
Patients presenting as emergencies
Table 9.5 Logical thinking for conditions causing breathlessness, including the emergency conditions
Clinical assessment Classification Condition
Stridor Large airway disease Partial obstruction of trachea or major airway
Bilateral or diffuse wheeze Small airway disease Asthma
Acute bronchitis (including bronchitic
component to chronic obstructive pulmonary
disease)
Anaphylaxis
Pulmonary oedema (presenting as bronchial
oedema)
Obesity hypoventilation syndrome (although
often the wheeze from obesity- related airflow
limitation is not heard)
Asymmetric features in whole lung field (tracheal
deviation, hyper- resonance to percussion and
diminished breath sounds)
Asymmetric features in whole lung field (tracheal
deviation, stony dullness to percussion and
diminished breath sounds)
Asymmetric features in whole lung field (tracheal
deviation, dullness to percussion and diminished
breath sounds)
Diffuse bilateral abnormalities (crepitations) Diffuse parenchymal
Diffuse bilateral abnormalities (bronchial
breathing)
Focal abnormality (bronchial breathing) Focal parenchymal
Focal abnormality (dullness to percussion and
diminished breath sounds)
Bilateral, focal abnormalities (basal stony
dullness and diminished breath sounds)
Bilateral, focal abnormalities (bronchial breath
sounds)
Thoracic deformity Chest wall skeletal
No obvious abnormality Pulmonary vascular
This table is not intended to be an exhaustive list. It is aimed at assisting logical thought, particularly with regard to clinical features.
Pleural disease Pneumothorax
Pleural disease Massive pleural effusion
Large airway disease Total lung collapse (tumour, foreign body, mucus
plug)
Pneumonitis
disease
Diffuse parenchymal
disease
disease
Pleural disease Pleural effusion
Pleural disease Bilateral pleural effusions
Parenchymal disease Bilateral pneumonia (e.g. bibasal pneumonia)
disease
disease
Respiratory muscle
weakness
Compensatory effort Metabolic acidosis
Psychogenic Psychogenic hyperventilation
Pulmonary oedema
Pulmonary fibrosis
Multilobar or bronchopneumonia
Pneumonia
Lobar collapse
Bronchiectasis
Scoliosis
Thoracic surgery
Pulmonary embolism
Pulmonary hypertension
Diaphragm paralysis
Neuromuscular disease
Anaemia
Acute breathlessness owing to ventilatory
and/or oxygenation defects
The sensation of breathlessness is poorly understood.
In normal respiration active inspiration is followed
by passive expiration, but in breathlessness of any
cause there is active expiration and a change in
the normal inspiration:expiration time ratio. The
diaphragm works at a mechanical disadvantage
when this ratio changes and hypoxia added to this
situation may contribute further to the discomfort
of breathlessness. The usual cause is loss of lung
compliance/elastic recoil, which requires active
expiration to compensate. This is seen either with
Figure 9.1 The recovery position.
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Patients presenting as emergencies
131
chronic damage to lung parenchyma or acutely
when the alveolar spaces are filled with material
that is less compressible than aerated lung, such as
interstitial fluid, pus or blood. In some conditions
(classically acute asthma) severe overinflation of
the lungs reduces their ability to expire effectively.
Finally, the sensation of breathlessness may occur
with conditions completely unrelated to the heart
or lungs, such as diabetic ketoacidosis. Here, a
change in blood pH is sensed by chemoreceptors in
the brainstem leading to Kussmaul’s breathing (‘air
hunger’) as an attempt is made to hyperventilate
and blow off carbon dioxide, thereby improving the
acidosis.
History taking is often limited in breathless
patients. Accompanying friends, relatives or carers
may be able to provide collateral information and
it may be possible to elicit certain key features by
asking simple ‘yes/no’ questions (‘Do you have
asthma? Have you eaten something you are allergic
to?). It may be impossible to differentiate between
the wheeze of acute asthma, anaphylaxis, bronchitis
or, rarely, pulmonary oedema, but a history of
previous asthma and atopy, fever or chest pain may
help direct the clinician to a working diagnosis. If
asthma is suspected, then early administration of
a beta- 2- adrenergic agonist can be lifesaving and
will rarely cause harm. The ability to administer
this medication, either via nebulizer or metered
dose inhaler and spacer device, is a fundamental
skill that should be familiar to all clinicians. If it is
ineffective owing to severe bronchoconstriction,
then intravenous administration can be considered
by experienced clinicians.
Clinical examination of the breathless patient may
reveal significant asymmetry in chest expansion,
percussion and/or auscultation. In general, the
side that moves less has the pathology within it.
The deviated trachea will be ipsilateral to the side
of lung collapse or focal fibrosis and contralateral
to a tension pneumothorax or very large pleural
effusion. These are differentiated by the percussion
note, which will be hyper- resonant in tension
pneumothorax and dull (some say ‘stony dull’) in
the presence a massive effusion. Breath sounds may
be absent or poorly heard in the affected lung in
all of these conditions. Relief may be immediate
with minimal aspiration of either air (tension
pneumothorax) or fluid (pleural effusion) prior to
formal drainage.
Diffuse polyphonic wheeze or indistinct
widespread coarse crackles with acute on chronic
shortness of breath is typical of an exacerbation
of COPD. Widespread bilateral unchanging fine
crepitations are most often heard with acute
pulmonary oedema. Focal features, such as tactile
fremitus, dullness to percussion, increased vocal
resonance and bronchial breathing, provide evidence
of consolidation and/or collapse and can usually be
confirmed by an urgent chest X- ray.
If there are no obvious examination abnormalities
in the acutely breathless patient, then the history
will need further clarification. Chest pain and/
or breathlessness in the presence of relevant
risk factors raise the possibility of a PE (see
Table 9.3). Investigation with an arterial blood
gas is useful in determining oxygen and carbon
dioxide exchange alongside any disturbances in
pH. Most conditions causing breathlessness are
exacerbated by lying flat and relieved by sitting
up, although this ‘orthopnoea’ is most obvious
with pulmonary oedema and respiratory muscle
weakness. Breathlessness relieved by lying flat
(platypnoea) is relatively rare and is most often
associated with PE; in this case, the supine posture
improves pulmonary perfusion and provides relief.
A cough acutely productive of purulent sputum
may support a working diagnosis of pneumonia.
Longer- standing cough may be associated with
non- purulent sputum production (asthma, chronic
COPD and bronchiectasis) or non- production
(interstitial lung disease and lung cancer). An
absent or weak cough may suggest respiratory
muscle disease. Acute, frothy sputum (occasionally
tinged with blood) may be seen in pulmonary
oedema. Frank haemoptysis may occur in PE,
lung cancer, pulmonary vasculitis, pneumonia,
tuberculosis and acute bronchitis.
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9
Patients presenting as emergencies
The patient with hypotension or shock
There are numerous definitions for ‘shock’ but a
useful one may be considered to be ‘a failure of blood
flow to provide sufficient perfusion of the major
organs’. It is often associated with hypotension.
Hypotension and shock are clinical emergencies and
require appropriate and immediate intervention.
Hypotension may be defined as ‘abnormally low
blood pressure for that given patient’, which means
interpreting the documented blood pressure in
context. For one patient, a ‘normal’ recorded blood
pressure may be ‘abnormal for him’ as it is significantly
lower compared with previous readings. In another, a
‘low’ blood pressure may be entirely normal for that
specific patient. If in doubt, a low blood pressure
should always be acted upon. For the purposes of
this chapter, it will be accepted that hypotension and
shock encompass similar pathologies and belong on
the same spectrum. Severe hypotension may lead
to shock. It is essential, therefore, that, irrespective
of aetiology, this is seen as a medical emergency,
and a joint effort is made simultaneously to initiate
resuscitative treatment and make a diagnosis. This
involves administering intravenous fluids while
other clinical features and vital observations are
elicited. The fluids may be subsequently stopped
if pulmonary oedema becomes evident. The organ
that is most sensitive to under perfusion is the brain;
confusion and decreased levels of consciousness
in the context of shock indicate poor cerebral
oxygenation, so patients should usually be nursed
lying flat to promote cerebral perfusion.
Teamwork is paramount. If more than one clinician
is available, one may focus on taking a history while
another may take responsibility for examination
and institution of treatment. Examination findings,
irrespective of the cause, may include a rapid pulse
and heart rate and a third heart sound. It should be
noted that in otherwise fit individuals, in the face
of severe hypovolaemia, there may be a prolonged
period of ‘compensation’, in which the healthy
heart maintains cardiac output and a normal blood
pressure by increasing the heart rate and the force of
contraction. Therefore, the patient with unexplained
tachycardia should be examined and investigated
thoroughly, and impending shock should not be
missed.
During resuscitation, a quick starting point is
needed when assessing the causes of shock, because
a correct diagnosis will dictate the most appropriate
intervention. One way to categorize shock is to
differentiate causes into those with a wide or a narrow
pulse pressure (‘pulse pressure’ is the difference
between systolic and diastolic blood pressure)
(Table 9.6). As a general rule, patients with widened
pulse pressure will present with warmer peripheries,
and the palpable peripheral pulse may be more
‘bounding’ in nature. Patients with narrowed pulse
Table 9.6 Logical thinking in shock
Mechanism Common or important examples
Narrow pulse
pressure
Widened pulse
pressure
Box 9.2
1. Hypovolaemic
2. Cardiogenic
3. Distributive
4. Obstructive
pressure often have cooler peripheries, with weak,
‘thready’ peripheral pulses. Although ‘normal’ pulse
pressure is often quoted as 40 mmHg, it should be
noted that during hypotension this figure should
be interpreted with caution. For example, a blood
pressure of 75/40 mmHg could be interpreted as
having a widened pulse pressure of 35 mmHg, as
this is in the context of a low systolic blood pressure.
There are varying types of shock, which need
general discrimination to apply definitive treatment
(Box 9.2). One type of shock may evolve into another,
leading to a mixed clinical picture requiring more
than one treatment strategy. For example, it is not
uncommon for septic shock (ordinarily presenting
with a widened pulse pressure) to lead rapidly
to cardiogenic shock (usually characterized by a
narrow pulse pressure) in patients with coexisting
heart disease. Septic shock is also often associated
with hypovolaemic shock. It is not uncommon for
cardiogenic shock to improve with treatment, but
then be superseded by infection and septic shock. If
it is not possible to categorize a pulse pressure into
narrow or wide, other features described below may
help identify the cause of shock.
Narrow pulse pressure associated with shock
is almost always a consequence of cardiac
failure (‘cardiogenic shock’) or hypovolaemia
(‘hypovolaemic shock’). Examination findings, in
addition to specific features described below, may
include cold and pale limb peripheries. Although there
are many general causes of widened pulse pressure
(including aortic regurgitation, thyrotoxicosis, fever,
anaemia, pregnancy, patent ductus arteriosus, aortic
dissection, raised intracranial pressure, vasodilating
drugs, Beriberi heart disease and old age), wide pulse
pressure with shock is almost always a consequence
of profound vasodilatation, usually with warm limb
peripheries. The most common cause is infection
(‘septic shock’); less common causes include
Types of shock
Hypovolaemic shock (haemorrhage,
fluid losses from enteral tract, fluid
losses from renal tract, fluid losses from
skin [burns]); cardiogenic shock from
myocardial failure (coronary ischaemia,
acute myocarditis)
Septic shock; anaphylactic shock;
neurogenic shock (all can also be known
as distributive shock)
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Patients presenting as emergencies
Table 9.7 Classes of haemorrhage
Class I Class II Class III Class IV
Blood loss (ml) Up to 750 750–1500 1500–2000 >2000
Blood loss (% Blood volume) Up to 15% 15%–30% 30%–40% >40%
Pulse rate <100 >100 >120 >140
Blood pressure Normal Normal Decreased Decreased
Pulse pressure (mmHg) Normal or increased Decreased Decreased Decreased
Respiratory rate 14–20 20–30 30–40 >35
Urine output (ml/hr) >30 20–30 5–15 Negligible
CNS/mental status Slightly anxious Mildly anxious Anxious, confused Confused, lethargic
133
anaphylaxis (‘anaphylactic shock’) and loss of
neurogenic vasomotor tone (‘neurogenic shock’).
Hypovolaemic shock
Conceptually, hypovolaemic shock is the easiest to
understand as simply insufficient circulating volume
to provide for the oxygen demands of the organs.
Typically, this is caused by haemorrhage and may
be divided into four classes (Table 9.7). External
haemorrhage is usually clinically obvious, either from
the history or from visual evidence of blood loss. The
source of internal bleeding may be more difficult to
diagnose, although the prevailing clinical picture is
common to both (Table 9.8). Cool peripheries and
corresponding changes in heart rate, blood pressure
and respiratory rate are key indicators. Simple
assessment through testing the capillary refill time
and provocative testing, such as a postural blood
pressure, is useful in unmasking compensated shock.
In the initial period following a haemorrhage, it
should be remembered that the blood haemoglobin
concentration may be preserved. Once bleeding is
suspected as the cause of hypovolaemic shock, the
clinical approach is straightforward and intuitive;
replace the blood that has been lost (as it is the best
resuscitative fluid) and stop the bleeding. External
bleeding can be controlled in most situations by locally
applied pressure. Internal bleeding often necessitates
surgical or endoscopic intervention, and interventional
radiology techniques are increasingly being applied in
a number of situations and specialist institutions.
Although external and internal bleeding are
the most common causes of hypovolaemic shock,
non- haemorrhagic causes also exist. In developing
countries gastrointestinal fluid loss (e.g. caused by
cholera) is a leading cause of death, especially in
children. Other volume- losing conditions include
salt- wasting renal conditions, burns, sequestration
of fluid into the bowel and adrenal insufficiency. As
a rule, hypovolaemic shock in the context of these
conditions takes longer to develop than, for example,
acute intra- abdominal blood loss, so a carefully taken
history is likely to be diagnostically informative.
Replacement of fluid with crystalloid in the first
instance is the most important intervention.
Table 9.8 Internal bleeding sites
Pelvis Pelvic fracture
Ectopic pregnancy
Abdomen Liver
Spleen
Kidney
Thorax Massive haemothorax
Gastrointestinal Oesophageal and/or gastric
varices
Duodenal ulcer
Retroperitoneal Ruptured abdominal aortic
aneurysm
Peripheries Long bone fractures
Cardiogenic shock
Cardiogenic shock refers to a failure of the heart to
pump blood effectively to meet peripheral oxygen
demands. It is most frequently caused by a large
myocardial infarction but may also be owing to
cardiac dysrhythmias, other causes of cardiac muscle
pump failure (e.g. myocarditis, cardiomyopathy) or
acute cardiac valve problems. In this situation, as with
hypovolaemic shock, there will usually be a narrow
pulse pressure. Cardiogenic shock may be associated
with a preceding history of chest pain, palpitations
or breathlessness (in particular orthopnoea). There
are frequently auscultatory features of pulmonary
oedema. Patients with brittle cardiac function may
present with cardiogenic shock irrespective of the
initial trigger. An ECG is often informative and may
show changes of recent infarction, dysrhythmia and
non- specific changes of pericarditis, myocarditis and
cardiomyopathy. Treatment will largely depend on
the cause; inotropic support and invasive measures
are frequently required.
Distributive shock
Distributive shock is owing to inappropriate
distribution of a normal or elevated cardiac output.
Invariably there is profound vasodilatation with
associated capillary leakage. The most common cause
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Patients presenting as emergencies
is severe sepsis, in which an overwhelming cascade
of inflammatory mediators causes distribution of
blood to inappropriate areas. The clinical history
may suggest an obvious source of infection and
examination findings may include a fever, observed
rigors, auscultatory features of lung consolidation or
abdominal features of peritonitis.
Anaphylactic shock is usually clinically easily
apparent (respiratory distress, agitation, urticarial
rash, face, mouth, tongue and orbital swelling and
wheeze), but there may not be a history of allergy
or hypersensitivity. Accompanying hypotension is
frequent, owing to marked vasodilatation, pooling of
blood and a consequent reduction in venous return to
the heart. Knowing the common causes of the allergy
and the ability to recognize urticaria are important.
Once recognized, detailed clinical assessment is
inappropriate; immediate resuscitation is required
with intramuscular adrenaline (epinephrine) and
intravenous fluids.
Neurogenic shock, another form of distributive
shock, is very rare. It is caused by disruption
of the vasomotor tone of blood vessels causing
inappropriate dilatation and pooling of blood
with a marked reduction in venous return and,
consequently, cardiac output. A history of either
spinal trauma or medical intervention (e.g. epidural
anaesthesia or autonomic blocking agents) usually
prompts its consideration as a diagnosis.
Obstructive shock
Most commonly, obstructive shock occurs with
massive pulmonary embolism in which obstruction
to blood flow through the pulmonary circulation
reduces venous return to the left atrium and ventricle
so markedly that cardiac output into the systemic
circulation falls and hypotension develops. Patients
will be breathless and usually have chest pain. The
combination of clinical signs of right- side heart
strain with hypotension and hypoxia should prompt
consideration of massive pulmonary embolism.
Obstruction to the outflow of the left ventricle occurs
with severe aortic stenosis, although usually this
condition develops over a prolonged period of time.
The patient with diminished consciousness
The definition of ‘consciousness’ may be the (waking)
state of awareness of oneself and environment. The
absence of awareness, therefore, even when one is
stimulated, may implicate diffuse or multifocal
brain dysfunction and may be defined as ‘coma’ or
‘diminished consciousness’. Although the last two
terms may be seen as synonymous, the term ‘coma’
may have widespread and conflicting implications.
In these situations, ambiguity should be avoided,
and the patient should be described as having
‘diminished consciousness’.
Consciousness is controlled by the brainstem
through a system of nerve cells and fibres
known as the ‘reticular activating system’ or the
‘ascending arousal system’. The cerebrum helps
maintain consciousness and alertness and at least
one hemisphere, as well as the reticular activating
system, must be functioning normally to maintain
consciousness. The brain’s ability to adjust its activity
and consciousness levels can therefore be impaired
in several ways, particularly when both cerebral
hemispheres are suddenly and severely damaged,
when the reticular activating system malfunctions,
when blood flow or the amount of nutrients (such
as oxygen or sugar) supplying the brain decreases or
when toxic substances impair brain function.
There are several ways to describe the conscious
state objectively, although perhaps the two bestknown ‘scores’ are the Glasgow Coma Scale (GCS)
and the ‘AVPU’ (alert, verbal, pain, unresponsive)
score (Tables 9.9 and 9.10). The GCS attributes a
score, ranging from 3 to 15. It was originally devised
to assess the level of consciousness after head injury,
although now is used for almost all acutely presenting
patients. The GCS has the advantage of being easily
and reliably administered by a range of different health
professionals. When faced with a poorly conscious
patient, the usual pairing of resuscitation and
diagnostics should be followed. Severe neurological
conditions may affect upper airway tone, respiratory
drive (e.g. Cheyne–Stokes respiration), vasomotor
tone and cardiac rhythm. Also, if the cause of the
brain dysfunction is systemic (see Table 9.11),
Table 9.9 The Glasgow Coma Scale
1 2 3 4 5 6
Eyes Does not open
eyes
Verbal Makes no
sounds
Motor Makes no
movements
Opens eyes in
response to painful
stimuli
Incomprehensible
sounds
Extension to painful
stimuli (decerebrate
response)
Opens eyes in
response to voice
Inappropriate
words
Abnormal flexion
to painful stimuli
(decorticate
response)
Opens eyes
spontaneously
Confused,
disoriented
Flexion or
withdrawal to
painful stimuli
N/A N/A
Orientated,
converses
normally
Localizes
painful stimuli
N/A
Obeys
commands
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Table 9.10 The ‘AVPU’ score (a simplification of the Glasgow Coma Scale)
*
Alert Verbal Pain Unresponsive
A fully awake (although not
necessarily oriented) patient
This patient will
spontaneously open eyes, will
respond to voice (although
may be confused) and will
possess motor function
*
APVU, alert, verbal, pain, unresponsive.
this will need to be dealt with. Therefore, it is
paramount that the ‘airway, breathing, circulation’
(ABC) algorithm is given due respect. The airway
should be supported appropriately (if necessary
with endotracheal intubation), the ‘recovery’ lateral
position may be required in the unintubated patient
to prevent aspiration, hypotension may require
vigorous intravenous fluids and monitoring will be
required for hypertension and cardiac dysrhythmias.
After resuscitation, one should focus on rapidly
identifying the cause of brain dysfunction (see Table
9.11). If a systemic cause is obvious, it should already
have been dealt with. A brief history from witnesses
may reveal preceding hemiparesis, headache, trauma,
fit, recreational drug or alcohol intake, or a history of
cancer, diabetes, liver or renal disease. Examination
should include a full body inspection for features of
trauma, fundoscopy, cranial nerves and motor function
(including power, tone and reflexes). The power,
sensory, cerebellar and visual assessments may not be
possible owing to a lack of cooperation. One should
attempt to examine for meningism by assessing nuchal
rigidity (diminished neck flexion with otherwise
retained neck movements) and knee extension with
the patient supine, with the hip and knee preflexed
(pain on knee extension is Kernig’s sign).
A very brief description of common pathologies
The patient makes some kind of
response (eyes or voice or motor) when
prompted by questions, e.g. ‘Are you
ok?’
The patient’s eyes may open, or the
response may simply be a moan or
slight movement of a limb
Table 9.11 Logical thinking in the poorly conscious patient
Primary cranial diffuse or
multifocal disease, where
structural lesions will be
obvious on imaging
Vascular
Infection
Inflammation
Tumours
Trauma
Secondary cranial disease:
systemic
Hypoxia/anoxia
Hypotension
Hypothermia
The patient makes some
kind of response (eyes or
voice or motor) when pain
stimulus is used on them
No response to voice or
pain
Primary cranial diffuse
disease where no
structural lesions will be
obvious on imaging
Infection
Inflammation
Trauma (‘concussion’)
Non- convulsive status
epilepticus or postictal state
Psychiatric (conversion,
stupor)
Secondary cranial disease:
metabolic
Alcohol
Drugs
Hypoglycaemia
Endocrine disturbance
(sodium balance, thyroid
disturbance)
Liver
Renal
Non- cranial infection
leading to changes in conscious level includes the
following:
Vascular lesions include cerebral arterial
or venous thromboses leading to infarcts.
Intracranial haemorrhages may be subarachnoid
or intracerebral. Relevant cases should be referred
early to stroke units or neurosurgeons.
Primary cranial infections may manifest as
meningitis, encephalitis or meningoencephalitis.
One may also become acutely encephalopathic
from widespread non- infective inflammatory
vascular lesions. With infective and inflammatory
pathologies, changes may or may not be evident
on cranial imaging. Treatment with antibiotics
and/or antiviral agents will be empirical initially,
and should not be withheld in favour of preceding
lumbar puncture, especially if the patient is
critically unwell.
After trauma, extradural and subdural
haematomata may be suspected, as may
subarachnoid and intracerebral haemorrhages.
The condition known as ‘diffuse axonal injury’
(DAI) refers to extensive lesions in white
matter tracts and is one of the major causes of
unconsciousness after head trauma. ‘Concussion’
is the most common type of traumatic brain injury,
where there is temporary loss of brain function
with a variety of subsequent physical, cognitive
and emotional symptoms. Usually no changes are
visible on imaging, and symptoms usually resolve
spontaneously over days or weeks. Relevant cases
should be referred early to the neurosurgical unit.
Non- convulsive status epilepticus as a cause
of altered consciousness is often overlooked.
There will often be no obvious clinical clues
other than eye deviation or involuntary eye
movements. Often, the unconscious patient who
has been intensely investigated in the emergency
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Patients presenting as emergencies
Table 9.12 Relationship of pupillary changes to site of anatomical damage
Unilateral pathological constriction
Unilateral pathological dilatation (mydriasis)
Pupillary fibres close to the origin of the third
cranial nerve are especially susceptible when
uncal herniation or a posterior communicating
aneurysm compresses the nerve.
This mydriasis is usually accompanied with
sparing of oculomotor function.
When pupillary fibres more distal in the third
cranial nerve are affected, the mydriasis usually
occurs together with oculomotor dysfunction.
(miosis) Mid- point pupil
Hypothalamic damage may lead to
ipsilateral Horner’s syndrome.
Pontine damage may lead to bilateral
miosis.
Lateral medullary and ventrolateral
cervical cord lesions may lead to
ipsilateral Horner’s syndrome.
Mid- brain damage: the midpoint pupil shows no reaction
to light.
department, and who spontaneously becomes
more alert over the subsequent hours, will have
had an unwitnessed seizure.
If opioid overdose is suspected, one may consider
administering the opioid antagonist naloxone.
This may be essential if the unconscious state is
affecting the airway. If the vital observations are
stable, however, the benefit of rapid opioid reversal
should be weighed against the disadvantages (e.g.
disorientation, aggression, vomiting, removal of
analgesia).
The psychiatric patient (with or without a known
past history) may have a poor consciousness level
from conversion disorder, or stupor secondary to
depression or schizophrenia. Often, the diagnosis
will be made after preceding exhaustive negative
tests and will need an expert assessment by the
psychiatrist.
Pupillary examination deserves special mention. As
pupillary pathways are resistant to metabolic insult,
the identification of absent pupillary reflexes usually
implies structural pathology. The brainstem areas
governing conscious level are anatomically close
to the areas controlling the pupils and so pupillary
changes help to identify brainstem pathology causing
altered conscious level (Table 9.12).
Investigations, as always, should be targeted to
the index of suspicion from clinical assessment.
Those pertaining to resuscitation, including CXR,
ECG and blood sugar, should be performed on
initial encounter. Cranial imaging (usually a cranial
CT scan) will be indicated if there is a significant
possibility of structural lesions. It should be
remembered, however, that the transfer of the
patient to the radiology department may carry
major risk, particularly if the patient requires general
anaesthesia for intubation. Therefore, the advantages
of performing neuroradiology should always be
measured against risk. A lumbar puncture may be
required; contraindications according to existing
national and local guidelines should be referred to
and, if present, the procedure should be deferred.
An electroencephalogram (EEG) may reveal
abnormalities consistent with a seizure disorder.
Plasma alcohol may easily be measured and may lend
support to a clinical diagnosis of alcohol toxicity.
Some, although not all, hospitals are able to perform
urine toxicology analyses for recreational and other
drugs. Plasma levels for paracetamol, salicylates and
anticonvulsant medications are also easily available.
These may be relevant in cases of deliberate or
inadvertent self- harm. Some plasma levels for drugs
are only available in specialist ‘poisons’ units. It is
therefore often good practice to have a saved sample
of serum, which may subsequently be transported, if
required. Tests of renal function and liver function
(including blood clotting) should be included in the
context of altered conscious level.
The syncopal patient
Syncope is a frequent cause of presentation to
hospital and the emergency department. It may be
defined as temporary loss of consciousness with rapid
onset and spontaneous recovery. The implication
is that there is temporary, global hypoperfusion to
the brain. The brevity of the event is mostly limited
to a few minutes. Although the causes of syncope
are often not sinister (the most common cause is
a vasovagal episode), the consequences may be
catastrophic if, for instance, the onset occurs while
driving. The condition should therefore always be
taken seriously (Table 9.13).
When the duration of the loss of consciousness
is unknown or thought to be prolonged, the
possibility of seizures should be considered. This
impression may be reinforced by the presence of
tongue biting, urinary incontinence, preceding aura
or unusual behaviour, ongoing drowsiness, confusion
or headache or a collateral history of involuntary
movements during the episode. The approach to
patients with seizures is discussed elsewhere in this
chapter.
The history of the syncopal event will not be
complete when told by the patient, although events
preceding and following it may be recounted. It is
important, therefore, that any witnesses of the event
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